Skip to main content

Full text of "Scientific integrity and federal policies and mandates : case study 3--EPA's dioxin reassessment : hearing before the Subcommittee on Energy and Environment of the Committee on Science, U.S. House of Representatives, One Hundred Fourth Congress, first session, December 13, 1995"

See other formats


SCIENTinC INTEGRin AND FEDERAL POUCIES 
AND MANDATES: CASE STUDY 3-EPA'S DIOXIN 
REASSESSMENT 



Y 4. SCI 2:104/39 



Scientific Integrity and Federal Po... 

HEARING 

BEFORE THE 

SUBCOMMITTEE OX ENERGY AND EN^^RONMENT 

OF THE 

COMMITTEE ON SCIENCE 
U.S. HOUSE OF REPRESENTATR^S 

ONE HUNDRED FOURTH CONGRESS 

FIRST SESSION 



DECEMBER 13, 1995 



[No. 39] 



Printed for the use of the Committee on Science 




JUL 2 6 1996 

Boston Public Library 

government Poruments Dept. 




23-557CC 



U.S. GOVERNMENT PRINTING OFFICE 
WASHINGTON : 1995 



For sale by the U.S. Government Printing Office 

Superintendent of Documents, Congressional Sales Office, Washington, DC 20402 

ISBN 0-16-052655-8 



SCIENTinC INTEGRITY AND FEDERAL POLICIES 
AND MANDATES: CASE STUDY 3-EPA'S DIOXIN 
REASSESSMENT 



Y4.SCI 2:104/39 



Scientific Integrity and Federal Po... 

HEARING 

BEFORE THE 

SUBCOMMITTEE OX ENERGY AND EXMROXMEXT 

OF THE 

COMMITTEE ON SCIENCE 
U.S. HOUSE OF REPRESENTATR^S 

ONE HUNDRED FOURTH CONGRESS 
FIRST SESSION 



DECEMBER 13, 1995 



[No. 39] 



Printed for the use of the Commitiee on Science 



Superintendent Of Documents 
DEPOSITORY 



t or Documents I 
JITORV 

6 1996 



JUL 2 6 1996 

Boston Public Library 

bovefoment Do rumftntc; Oeot. 




U.S. GOVERNMENT PRINTING OFFICE 
23-557CC WASHINGTON : 1995 

For sale by the U.S. Government Printing Otfice 

Superintendent of Documents, Congressional Sales Office, Washington, DC 20402 

ISBN 0-16-052655-8 



COMMITTEE ON SCIENCE 



ROBERT S. WALKER, 
F. JAMES SENSENBRENNER, Jr., 

Wisconsin 
SHERWOOD L. BOEHLERT, New York 
HARRIS W. FAWELL, Illinois 
CONSTANCE A. MORELLA, Maryland 
CURT WELDON, Pennsylvania 
DANA ROHRABACHER, California 
STEVEN H. SCHIFF, New Mexico 
JOE BARTON, Texas 
KEN CALVERT, California 
BILL BAKER, California 
ROSCOE G. BARTLETT, Maryland 
VERNON J. EHLERS, Michigan** 
ZACH WAMP, Tennessee 
DAVE WELDON, Florida 
LINDSEY 0. GRAHAM, South Carolina 
MATT SALMON, Arizona 
THOMAS M. DAVIS, Virginia 
STEVE STOCKMAN, Texas 
GIL GUTKNECHT, Minnesota 
ANDREA H. SEASTRAND, California 
TODD TIAHRT, Kansas 
STEVE LARGENT, Oklahoma 
VAN HILLEARY, Tennessee 
BARBARA CUBIN, Wyoming 
MARK ADAM FOLEY, Florida 
SUE MYRICK, North Carolina 

David D. Clement, Chief of Staff and Chief Counsel 

Barry Beringer, General Counsel 

TiSH Schwartz, Chief Clerk and Administrator 

Robert E. Palmer, Democratic Staff Director 



Pennsylvania, Chairman 
GEORGE E. BROWN, Jr., California RMM* 
RALPH M. HALL, Texas 
JAMES A. TRAFICANT, Jr., Ohio 
JOHN S. TANNER, Tennessee 
TIM ROEMER, Indiana 
ROBERT E. (Bud) CRAMER, Jr., Alabama 
JAMES A. BARCIA, Michigan 
PAUL McHALE, Pennsylvania 
JANE HARMAN, California 
EDDIE BERNICE JOHNSON, Texas 
DAVID MINGE, Minnesota 
JOHN W. OLVER, Massachusetts 
ALCEE L. HASTINGS, Florida 
LYNN N. RIVERS, Michigan 
KAREN McCarthy, Missouri 
MIKE WARD, Kentucky 
ZOE LOFGREN, California 
LLOYD DOGGETT, Texas 
MICHAEL F. DOYLE, Pennsylvania 
SHEILA JACKSON LEE, Texas 
WILLIAM P. LUTHER, Minnesota 



Subcommittee on Energy and Environment 

DANA ROHRABACHER, Cahfornia, Chairman 



HARRIS W. FAWELL, Illinois 
CURT WELDON, Pennsylvania 
ROSCOE G. BARTLETT, Maryland 
ZACH WAMP, Tennessee 
LINDSEY 0. GRAHAM, South Carolina 
MATT SALMON, Arizona 
THOMAS M. DAVIS, Virginia 
STEVE LARGENT, Oklahoma 
BARBARA CUBIN, Wyoming 
MARK ADAM FOLEY, Florida 
STEVEN H. SCHIFF, New Mexico 
BILL BAKER, California 
VERNON J. EHLERS, Michigan 
STEVE STOCKMAN, Texas 



DAVID MINGE, Minnesota 

JOHN W. OLVER, Massachusetts 

MIKE WARD, Kentucky 

MICHAEL F. DOYLE, Pennsylvania 

TIM ROEMER, Indiana 

ROBERT E. (Bud) CRAMER, Jr., Alabama 

JAMES A. BARCIA, Michigan 

PAUL McHALE, Pennsylvania 

EDDIE BERNICE JOHNSON, Texas 

LYNN N. RIVERS, Michigan 

KAREN McCarthy, Missouri 



*Ranking Minority Member 
**Vice Chairman 



(II) 



CONTENTS 



WITNESSES 

Page 

December 13, 1995: 

William H. Farland, Director, National Center for Environmental Assess- 
ment, Office of Research and Development, U.S. Environmental Protec- 
tion Agency 15 

Michael Gough, Former Government Expert Member of Dioxin Reassess- 
ment Review Committee, EPA Science Advisory Board 36 

George W. Lucier, Director, Environmental Toxicology Program, National 

Institute of Environmental Health Sciences 46 

Kay H. Jones, President, Zephyr Consulting, Seattle, Washington 58 

Admiral Elmo E. R. Zumwalt, Jr., United States Navy (Retired), Agent 

Orange Coalition, Arlington, Virginia 85 

Appendix I — Additional Statements and Material 

Additional comments submitted for the record by Dr. Michael Gough 181 

Additional statement for the record submitted by Mr. C.T. Howlett, Managing 

Director of the Chlorine Chemical Council 185 

Correspondence submitted for the record by Dr. Kay Jones, Captain USPHS 

(retired), and President of Zephyr Consulting, Seattle, Washington 187 

Comments submitted for the record by Dr. Genevieve Matanoski, Chair, 

Science Advisory Board, Environmental Protection Agency 207 

Documents supplied for the record by Admiral E.R. Zumwalt, Jr., at the 
request of Congressman George Brown 213 

July 19, 1995, Wall Street Journal article by Dr. Robert Huggett, Assistant 
Director for Research and Development at the Environmental Protection 
Agency, regarding EPA's review of dioxin 249 

Response by Dr. Morton Lippmann, Professor, New York University Medical 
Center, and Chair, Science Advisory Board review committee for EPA's 
Dioxin Reassessment Review to the July 19, 1995, Wall Street Journal 
article 250 

Appendix II— Correspondence 

Response by the Environmental Protection Agency regarding additional ques- 
tions submitted in a letter dated February 14, 1996 from Chairman 
Rohrabacher to Dr. William Farland, Director, National Center for Environ- 
mental Assessment, Office of Research and Development 251 

Correspondence between Congressman Doyle and Mr. Paul Sutton, Chief, 

Homeless Veterans' Housing Programs 256 

Correspondence between Congressman George Brown and Dr. Donald G. 
Barnes, Science Advisory Board, Environmental Protection Agency (with 
attachments) 265 

(III) 



SCIENTIFIC INTEGRITY AND FEDERAL POLI- 
CIES AND MANDATES: CASE STUDY 3— EPA'S 
DIOXIN REASSESSMENT 



WEDNESDAY, DECEMBER 13, 1995 

U.S. House of Representatives, 

Committee on Science, 
Subcommittee on Energy and Environment, 

Washington, DC. 

The subcommittee met at 10:15 a.m. in Room 2318 of the Ray- 
burn House Office Building, the Honorable Dana Roharabacher, 
Chairman of the Subcommittee, presiding. 

Mr. Rohrabacher. This hearing of the Energy and Environment 
Subcommittee will come to order. 

Let me begin by apologizing that we are late today. There are 
certain events in the world that sometimes take precedence over 
daily business. 

One of the things that will take precedence over daily business 
is the deplo3rment of American troops in great numbers to an area 
of conflict, and the Republican Party, which now dominates the 
House of Representatives, now the majority party, is trying to de- 
termine its policy as to what we will do in terms of the deployment 
of 20,000 American groimd troops to Bosnia. 

Obviously, this chairman and the other Republican members felt 
that letting this hearing start 45 minutes late was the thing to do 
rather than not to debate the issue of this troop deployment to the 
degree it was required. 

We finished that vote, and we had a vote in the conference to de- 
cide the Republican position, and just for those who are interested, 
it was an overwhelming vote favoring the opposition to sending 
those troops to the Balkans, an opposition which would be substan- 
tial rather than just posturing and would be opposing the spending 
of any funds. Federal funds, in order to send American troops to 
the Balkans. 

Whereas I was participating in that debate and felt strongly 
about it, that is why we are late. 

I apologize, but that was the circumstance, and I hope you will 
understand. 

This is a third in a series, and I apologize to my members as 
well, and this will not happen again and this was, I thought, a 
monumental issue that deserved my attention. 

So I apologize. I am sorry. 

(1) 



Okay. This is the third in a series of hearings on how science is 
being used in Federal agencies to formulate policies and mandates. 
Today we will look at the EPA's dioxin reassessment. 

Scientists have struggled to quantify the effects of dioxin com- 
pounds for over 20 years. It is particularly difficult because dioxin 
is a generic name given to 210 different compounds. Dioxin can 
only be produced by the high-temperature combustion of certain 
elements. 

The EPA's reassessment began in 1991, after questions were 
raised about the scientific foundation for certain regulations. 

A draft document was not produced until 1994, which was sub- 
mitted to the EPA's Science Advisory Board. As a result, the 
board's recommendations, and that is of the board's recommenda- 
tions, parts of the report will be revised, which the EPA says may 
take another year, lengthening the reassessment process to five 
years. 

There is no question good science was produced in the EPA's doc- 
ument. 

The EPA issued an open call to the best scientists in the field 
to participate, and many of them did. In many respects, the early 
stages of this process were a model of peer review and sound 
science, and the EPA is to be commended for it. 

As a matter of fact, that is what the Republicans have been call- 
ing for. And yet this happened on its own, and we do commend 
them for it. 

But when it came time to write the critical portion of the health 
effects of the document, it appears that the doors were closed and 
the EPA drew its own conclusions. 

Of course, it is the end product that gets the attention and is 
used as the foundation for future regulations. 

In a remarkable letter to Science magazine a year ago, 18 of the 
scientists who worked on the early portions of this reassessment 
said the EPA's conclusions are, and I quote, "are heavily dependent 
on many unproved assumptions and untested hypotheses." 

They went on to urge, they went on to urge, "urge EPA to clearly 
distinguish regulatory policy from matters of scientific fact." 

It is remarkable because most scientists, this is remarkable be- 
cause most scientists are loath to air their concerns in public. 

A number of the signatories, in fact, turned down an invitation 
to testify today, telling this committee they did not want to partici- 
pate in the "political process," and that it could affect their work 
with the EPA. 

It is clear these scientists feel strongly about the validity of the 
reassessment process used by the EPA. 

There are no easy answers to the health questions raised by 
dioxin, and we are not here to imply that there are easy answers. 

Instead we will take a look at how the EPA distinguishes regu- 
latory policy from scientific fact, using the reassessment as a case 
in study. 

To do that, we have a panel of scientists with differing views who 
are highly qualified on the topic. 

Again, we have, this is the way I like to do things, instead of 
having just one side present their case and then perhaps having 
somebody down, you know, as the last witness whom nobody hears 



presenting another case, we have tried to put people on both sides 
of this issue on the same panel so we can have an honest discus- 
sion. 

Dr. William Farland directs the office of health and environ- 
mental assessment at the EPA and was charged with coordinating 
the reassessment. 

Dr. Michael Gough served as a Federal expert consultant to the 
EPA's Science Advisory Board's health effects panel and has 15 
years of experience at the Office of Technology Assessment in 
dioxin research. 

Dr. George Lucier is director of the environmental toxicology pro- 
gram at the National Institute of Environmental Health Sciences 
and also contributed to the reassessment document. 

Dr. Kay Jones is president of Zephyr Consulting and has worked 
on stationary and mobile-source combustion issues at the EPA, the 
Council on Environmental Quality, the World Health Organization, 
and Drexel University. 

Later we will hear from Admiral Elmo Zumwalt, who, as chair- 
man of the Agent Orange Coordinating Council, who has very 
strong feelings about the health effects of dioxin. 

[The opening statement of Chairman Rohrabacher follows:] 



OPENING STATEMENT 

REP. DANA ROHRABACHER 

EPA'S DIOXIN REASSESSMENT 

DECEMBER 13, 1995 

This is the third in a series of hearings on how 
science is being used in Federal agencies to formulate 
policies and mandates. Today we will look at EPA's 
Dioxin Reassessment. 

Scientists have struggled to quantify the effects 
of dioxin compounds for over 20 years. It is 
particularly difficult because dioxin is a generic neime 
given to 210 different compounds. Dioxin can only be 
produced by the high temperature combustion of certain 
elements . 

The EPA's reassessment began in 1991 after 
'questions were raised about the scientific foundation 
for certain regulations. 

A draft document was not produced until 1994, 
which was submitted to EPA's Science Advisory Board. 
As a result of the Board's recommendations, parts of 
the report will be revised, which the EPA says may take 
another year, lengthening the reassessment process to 
five years . 



2. 

There is no question good science was produced in 
the EPA's document. 

The EPA issued an open call to the best scientists 
in the field to participate and many of them did. In 
many respects, the early stages of this process were a 
model of peer review and sound science and the EPA is 
to be commended for it . 

When it came time to write the critical portion of 
the Health Effects document, however, it appears the 
doors were closed and the EPA drew its own conclusions. 

Of course, it is the end product that gets the 
attention and is used as the foundation for future 
regulations. 

In a remarkable letter to Science Magazine one 
year ago, 18 of the scientists who worked on early 
portions of this reassessment said the EPA's 
conclusions "are heavily dependent on many unproved 
assumptions and untested hypotheses . " 

They went on to "urge EPA to clearly distinguish 
regulatory policy from matters of scientific fact." 



3. 

It is remarkable because most scientists are 
loathe to air their concerns in public. A nvimber of 
the signatories turned down an invitation to testify 
today, telling this committee they did not want to 
participate in the "political process" and that it 
could affect their work with EPA. 

It's clear these scientists feel strongly about 
the validity of the reassessment process used by the 
EPA. 

There are no easy answers to the health questions 
raised by dioxin, and we are not here to imply there 
are. 

Instead, we will take a look at how the EPA 
distinguishes regulatory policy from scientific fact, 
using the reassessment as a case study. 

To do that, we have a panel of scientists with 
differing views who are highly qualified on the topic. 

Dr. William Farland directs the Office of Health 
and Environmental Assessment at the EPA and was charged 
with coordinating the reassessment. 



4. 

Dr. Michael Gough served as the Federal Expert 
Consultant to the EPA's Science Advisory Board's Health 
Effects Panel and has 15 years of experience 
at the Office of Technology Assessment in dioxin 
research. 

Dr. George Lucier is Director of the Environmental 
Toxicology Program at the National Institute of 
Environmental Health Sciences and also contributed to 
the reassessment document. 

Dr. Kay Jones is the President of Zephyr (Zeh'fir) 
Consulting and has worked on stationary and mobile 
source combustion issues at EPA, the Council on 
Environmental Quality, the World Health Organization 
and Drexel University. 

Later we will hear from Admiral Elmo Zumwalt, 
Chairman of the Agent Orange Coordinating Council, who 
has strong feelings about the health effects of dioxin. 

« # # 



8 

Mr. ROHRABACHER. Before we turn to our first panel, I will ask 
our distinguished, I guess it is acting ranking minority member, 
Mr. Roemer, for an opening statement. 

Mr. Roemer. Thank you, Mr. Chairman. I appreciate being rec- 
ognized, and thank you for having this hearing this morning. 

As you know, I am a strong supporter of risk assessment as an 
important tool to help agencies craft reasonable, cost-effective regu- 
lations. 

I think it is very appropriate for the Subcommittee to review the 
risk assessment practices of the Federal agencies so that we can 
better understand the promises and limitations of risk assessment, 
the opportunities to improve it, and the potential impacts of pend- 
ing risk assessment and regulatory reform legislation. 

The dioxin risk assessment is probably the most expensive, com- 
plex, and scientifically challenging risk assessment ever under- 
taken by the EPA. 

EPA deserves being commended for undertaking this reevalua- 
tion of the science and for making such unprecedented efforts to 
open the process up for public participation and scientific peer re- 
view. 

It is, however, a very complicated model. Some modifications and 
suggested improvements for EPA are in order, and we hope to hear 
those today. Some mistakes have been made in the process. Even 
a cursory review of the testimony shows that the science underly- 
ing the assessment is very complicated and subject to dispute even 
among respected experts. 

Significant scientific uncertainties remain. 

Given the potentially enormous costs associated with further 
EPA dioxin regulations, it shouldn't be all that surprising that var- 
ious interest groups have been busy spinning the EPA risk assess- 
ment £ind the Science Advisory Board review of EPA's works. 

Faced with scientific disputes, we can't act as a science court. Ul- 
timately, we have to leave the resolution of scientific issues to the 
scientific process. 

The question is whether that process has been fair and whether 
the risk assessment fairly represents the science on which it has 
been based. 

In putting together its risk assessment chapter, EPA initially 
consulted with outside experts to identify the key risk assessment 
and risk characterization issues. 

It then worked, together with experts from other Federal regu- 
latory agencies, to draft the risk assessment chapter. 

In September 1994 EPA published a public review draft of the 
risk assessment and not only asked for public comments but also 
held five public hearings across the country to obtain those com- 
ments. 

EPA submitted the draft report and the extensive public com- 
ments it received to EPA's scientific advisory board for an inde- 
pendent scientific peer review. 

A special 39-member SAB panel, representing a variety of dis- 
ciplines and viewpoints, was appointed, met, and issued a report. 
EPA is now in the process of rewriting its assessment to meet the 
concerns expressed by the SAB. 



While EPA's process could probably be improved, I look forward 
to hearing suggestions in the testimony for such specific improve- 
ments. 

It certainly appears that the process was open for full public par- 
ticipation, debate, and scientific peer review. 

As far as I can tell, the process seems to be working. It seems 
somewhat premature to judge EPA's efforts until the final product 
is complete. 

I am also interested to know what effect the passage of a bill like 
H.R. 1022 would have on future risk assessments, taking the 
dioxin risk experience into account. 

The dioxin risk assessment has already taken over four years, in- 
volved hundreds of scientists, generated mountains of reports, and 
cost the taxpayers a lot of good money. 

I am particularly concerned that, without a provision like the 
amendment I offered on the Floor to prevent expansive, new judi- 
cial review of risk assessments, we wouldn't even be this far along. 

Instead, the environmental groups or the industry groups would 
have hauled EPA into court, where lawyers and judges instead of 
scientists would be trying to resolve some of these scientific dis- 
putes. 

Mr. Chairman, I would ask unanimous consent that a statement 
to the Committee from the EPA Science Advisory Board be made 
part of the record, and, Mr. Chairman, if there is any remaining 
time on our side, I would like to yield to the gentleman, our former 
chairman, Mr. Brown. 

Mr. ROHRABACHER. Your letter will be, without objection, will be 
made part of the record. 

[The prepared statement of Congressman Roemer follows:] 



10 



Statement of the Hon. Tim Roemer 
Hearing on EPA Dioxin Reassessment 
Energy and Environment Subcommittee 

December 13, 1995 

Thank you, Mr Chairman. As you know, I am a strong supporter of risk 
assessment as an important tool to help agencies craft reasonable and cost-effective 
regulations. I think it is very appropriate for the Subcommittee to review the risk 
assessment practices of the federal agencies so that we can gain a better understanding of 
the promises and limitations of risk assessment, the opportunities to improve it, and the 
potential impacts of pending risk assessment and regulatory reform legislation. 

The dioxin risk assessment is probably the most expensive, complex and 
scientifically-challenging risk assessment ever undertaken by the EPA. EPA deserves 
commendation for undertaking this reevaluation of the science and for making such 
unprecedented efforts to open the process up for public participation and scientific peer 
review. 

Even a cursory review of the testimony shows that the science underlying the 
assessment is very complex arid subject to dispute even among respected experts. 
Significant scientific uncertainties remain. Given the potentially enormous costs 
associated with further EPA dioxin regulations, it shouldn't be all that surprising that 
various interest groups have been busy "spinning" the EPA risk assessment and the 
Science Advisory Board review of EPA's work. 

For the most part, we are not scientists on this Subcommittee. Faced with scientific 
disputes, we can't act as a "science court." Ultimately, we have to leave the resolution of 
scientific issues to the scientific process. The question is whether that process has been 
fair and whether the risk assessment fairly represents the science on which it is based. 

In putting together its risk assessment chapter, EPA initially consulted with outside 
experts to identify the key risk assessment and risk characterization issues It then worked 
together with experts from other federal regulatory agencies to draft the risk assessment 
chapter. In September, 1994, EPA published a public review draft of the risk assessment 
and not only asked for public comments, but also held five public hearings across the 
country to obtain comments 

EPA submitted the draft report and the extensive public comments it received to 
EPA's Scientific Advisory Board for an independent scientific peer review A special 39- 
member SAB panel representing a variety of disciplines and viewpoints was appointed, 
met, and issued a report. EPA is now in the process of rewriting its assessment to meet 
the concerns expressed by the SAB. 



11 



While EPA's process could probably be improved ~ and I look forward to hearing 
suggestions in the testimony for such improvements — it certainly appears that the process 
was open for full public participation, debate, and scientific peer review. As far as I can 
tell, the process seems to be working It seems somewhat premature to judge EPA's 
efforts until the final work product is complete. 

I also am interested to know what effect the passage of a bill like H.R. 1022 would 
have on future risk assessments, taking the dioxin risk experience into account The 
dioxin risk assessment has already taken over 4 years, involved hundreds of scientists, 
generated mountains of reports, and cost the taxpayers a lot of good money I am 
particularly concerned that without a provision like the amendment I offered on the floor 
to prevent expansive new judicial review of risk assessments, we wouldn't even be this far 
along. Instead, the environmental groups or the industry groups would have hauled EPA 
into court where lawyers and judges instead of scientists would be trying to resolve some 
of these scientific disputes. 

Thank you, Mr. Chairman, and I would yield any remaining time to the ranking 
member of the full Committee, Mr Brown. 



12 

Mr. ROHRABACHER. We very happily would like to hear from 
former distinguished chairman, Mr. Brown of California. 

Mr. Brown. Mr. Chairman, I compliment you on scheduling this 
risk assessment hearing. This is an invaluable part of both main- 
taining oversight over a complex subject and providing an oppor- 
tunity for members to become familiar with a debate which I have 
been participating in for 15 years and still don't fully understand. 
And our members are going to need all the help they can get in 
mastering this. 

I want to merely raise one point, Mr. Chairman, which I hope is 
not construed as being overly critical. In the charter for this hear- 
ing it was indicated that we would have a witness from the Science 
Advisory Board. 

We have a letter from the Science Advisory Board signed by its 
executive director indicating they would like to provide a witness 
if the committee desires. 

And yet we do not have a witness from the Science Advisory 
Board on the panel. 

We have a very good substitute in the form of Dr. Gough, but I 
think he would be the first to admit he is not a member of the 
Science Advisory Board. 

Mr. ROHRABACHER. Thank you, Mr. Brown. I would just like to 
let you know Morton Lipman, Dr. Morton Lipman, the chairman of 
the health effects panel, was the first person that was invited to 
testify. 

He was unable to attend. We have done our utmost to get the 
most qualified people on both sides of the argument to be on the 
panel. 

I mean, this is something we strove to do. Strove, is that the 
right word? Strove? Strived? We strove. 

No, we didn't strove, we strived. 

Mr. Brown. Mr. Chairman, I am not criticizing the makeup of 
the panel. I think you do have a balanced panel. 

Mr. ROHRABACHER. All right. 

Mr. Brown. But I was merely pointing out that we could have 
asked for another member of the panel, and they have offered to 
provide such a member. 

But I am sure that this will not damage the value of this hearing 
substantially. 

Mr. ROHRABACHER. Thank you very much. 

Now I guess we have Mr. Doyle, who would like to have an open- 
ing statement. Certainly. 

Mr. Doyle. Thank you, Mr. Chairman. 

I want to thank you for calling today's hearing, and I don't want 
to take up a lot of the subcommittee's time, but there are a couple 
points I feel compelled to make before we begin. 

First, I want to commend those in industry who have put forth 
great effort to minimize dioxin use. 

In particular, the record of the pulp and paper industry is espe- 
cially commendable. 

I am hopeful that Congress will in some way move to address the 
regulatory issues which seem to be based on a particular outcome 
of the ongoing research on dioxin. 



13 

While I think we need to honestly examine how EPA is conduct- 
ing this research, we must also not presuppose its outcome. 

Secondly, as the only member of the Science Committee who also 
serves on the Veterans' Affairs Committee, I can tell you that there 
are very few times that an issue of interest to both committees. 

However, the subject of today's hearing is one of those occasions. 

The issue of dioxin is of special importance to our Nation's veter- 
ans, due, in large part, to the controversy surrounding the effects 
of Agent Orange exposure during the Vietnam War. 

This is widely known by all Members of Congress. So I was 
somewhat surprised that the veterans community had no voice in 
the initial list for this hearing. 

I would like to thank Chairman Rohrabacher for recognizing this 
omission and inviting Admiral Zumwalt to be with us here today. 

I have also taken the liberty of contacting Dr. Paul Sutton of the 
Vietnam Veterans of America about today's hearing, and I would 
like to ask unanimous consent to include in the record our cor- 
respondence, as well as a statement on behalf of WA. 

Thank you, Mr. Chairman, and I 3rield back my time. 

Mr. Rohrabacher. Without objection, that correspondence will 
be included in the record. 

[The prepared statement of Congressman Doyle follows:] 



14 



OPENING STATEMENT OF REP. MIKE DOYLE 

SUBCOMMITTEE ON ENERGY & ENVIRONMENT 

HEARING ON EPA'S DIOXEV REASSESSMENT 

December 13,1995 



Mr. Chairman, I want to thank you for calling today's hearing. 

I don't want to take up a lot of the Subcommittee's time, but there a couple points I feel 
compelled to make before we begin. 

Fiist, I want to commend those in industry who have put forth great effort to minimize 
dioxin use. In particular, the record of the pulp and paper industry is especially 
commendable. I am hopeful Congress will, in some way, move to address the regulatory 
issues which seem to be based on a paiticular outcome of the ongoing research on dioxin. 
While I TbiTilf we need to honestly examine how EPA is conducting this research, we must 
also not presuppose its outcome. 

Secondly, as the only member of the Science Committee who also serves on the Veterans' 
Affairs Committee, I can tell you that there are very few times that an issue that is of 
interest to both Committees. However, the subject of today's hearing is one of those 
occasions. 

The issue of dioxin is of special importance to our nation's veterans, due m large part to 
controversy surrounding the effects of Agent Orange exposure during the Vietoam War. 
This is widely known by all Members of Congress, so I was somewhat surprised that 
veterans' commimity had no voice in the initial witness list for this hearing. I would hke 
to thank Chairman Rohrbacher for recognizing this omission and inviting Admiral 
Zumwalt to be here with us today. 

I also have taken the hberty of contacting Dr. Paul Sutton of the Vietnam Veterans of 
America about today's hearing. I would like to ask unanimous consent to include in the 
record our correspondence as well as his statement on behalf of WA. 
Again, thank you Mr. Chairman, and yield back my time. 



15 

Mr. ROHRABACHER. This hearing is supposed to be focused on the 
process, the reassessment process, and that is our authority. 

That's what this committee has authority over, our subcommittee 
has committee authority over. And we do not, we are not tr5dng to 
determine the toxicity or lack of toxicity of dioxin. 

And because we felt that your request was, you know, heartfelt 
and thought out but not necessarily under the jurisdiction of the 
committee but we went ahead with your request, and that's why 
Admiral Zumwalt will be testifying today, as a courtesy to those 
who feel so strongly on this issue. 

However, let me repeat, our jurisdiction is simply over the reas- 
sessment process, and we are not here to determine dioxin itself, 
whether or not that is a toxic material or not. 

So, with that, I think we should proceed with our first witness, 
and again I will apologize to our witnesses for being late, and some 
of my other Republican colleagues, who are probably still partici- 
pating in that conference, will be joining us shortly. 

Mr. ROHRABACHER. Dr. Farland. 

STATEMENTS OF WILLIAM H. FARLAND, PH.D., DIRECTOR, NA- 
TIONAL CENTER FOR ENVIRONMENTAL ASSESSMENT, OF- 
FICE OF RESEARCH AND DEVELOPMENT, U.S. ENVIRON- 
MENTAL PROTECTION AGENCY, ACCOMPANIED BY LINDA 
BIRNBAUM, DIRECTOR, DIVISION OF EXPERIMENTAL TOXI- 
COLOGY, NATIONAL HEALTH AND ENVIRONMENTAL EF- 
FECTS LABORATORY 

Dr. Farland. Good morning. I am Dr. William Farland, the Di- 
rector of the National Center for Environmental Assessment within 
the Office of Research and Development at the U.S. EPA. 

I am accompanied here today by Dr. Linda Birnbaum, the Direc- 
tor of the Division of Experimental Toxicology at our National 
Health and Environmental Effects Laboratory and EPA's chief re- 
search scientist on dioxin and related compounds. 

Linda is also an internationally recognized expert on the topic. 

Mr. Chairman, as you mentioned, I have the agency lead on the 
current dioxin reassessment project, and I have worked on evaluat- 
ing the risks of dioxin and related compounds since the early 
1980s. 

I, along with Dr. James Witlock, the Chair of the Department of 
Molecular Pharmacology at Stanford, was responsible for the mech- 
anisms of action chapter in the health reassessment. 

In addition, I was the principal author of the risk characteriza- 
tion chapter, along with Dr. Birnbaum, my colleagues from EPA, 
from several agencies of the Department of Health and Human 
Services and from the U.S. Department of Agriculture and several 
scientists from academic institutions. 

As you no doubt know by now, scientists from the U.S. Environ- 
mental Protection Agency, other Federal agencies, and the general 
scientific community have been involved in a comprehensive sci- 
entific reassessment of dioxin-related compounds since 1991. 

Two thousand pages of external review documents, drafts, were 
made available in September 1994 by the agency for public com- 
ment and review by the EPA's Science Advisory Board. 



16 

This process has been a model for open participatory environ- 
mental health assessment. Peer review has been an integral part 
of the entire reassessment process. 

Extensive comments have been received and will be the basis for 
revisions to the draft docimients. 

These documents and subsequent comments highlight a number 
of issues which are of broad scientific interest. 

Now, in answer to the questions that were posed on page 2 of 
the hearing charter, I have discussed these in my written testi- 
mony, but, in brief, the EPA believes that the risk characterization 
was consistent with the scientific findings contained in the earlier 
chapters; secondly, that contrary to the implication of the charter, 
the question, the risk characterization was informed by input from 
a panel of external reviewers of the draft chapters, drafted by Fed- 
eral scientists, and it was peer reviewed. It, like the rest of the re- 
port, involved both EPA and non-EPA drafters and reviewers. 

EPA's risk characterization does not rely solely on high levels of 
exposure to animals, but integrates animal data with limited 
human information. 

Animal data have been obtained at levels of exposure that are 
comparable to human exposures. The human information has been 
obtained on populations exposed at background levels and above. 

Finally, while the regulatory impacts assessments are carried out 
on every regulation that might be issued, no analysis of potential 
economic impacts on regulations that may be based on this reas- 
sessment will be conducted until the reassessment is complete and 
a comprehensive agencywide strategy has been developed. 

As you mentioned, dioxin is the term used for a group of chemi- 
cal compounds with similar chemical structure, which are inadvert- 
ently created through a number of activities, including combustion, 
certain types of chemical manufacture, chlorine bleaching of pulp 
and paper, and other industrial processes. 

They are produced in very small quantities compared to other 
pollutants; we estimate less than 30 pounds of toxic equivalents an- 
nually in the U.S. 

However, because they are highly toxic, they have been treated 
as significant environmental pollutants since the early 1970s. 

In 1985 EPA published a scientific review of the health effects 
of 2,3,7,8-TCDD, the most toxic of the dioxin compounds. That as- 
sessment has served as the scientific basis for dioxin risk estimates 
for ail U.S. EPA programs. 

In 1991 the EPA announced that it would conduct a comprehen- 
sive scientific reassessment of the health risks of exposure to the 
family of compounds generally known as dioxin. 

EPA has undertaken this task in light of significant advances in 
scientific understanding of the mechanisms of dioxin toxicity, sig- 
nificant new studies of dioxin's carcinogenic potential in humans, 
and increased evidence of other adverse effects. 

The reassessment is part of the agency's goal to improve its re- 
search and science base and to incorporate this knowledge into 
EPA decisions. 

The reassessment consists of two documents, each of about a 
thousand pages long and each published in several volumes. 



17 

One of these documents addresses the human health effects of 
dioxin. The second focuses on sources and levels of exposure. 

The reassessment is a scientific document and does not address 
regulatory policy or issues. 

Volume 3 of the health effects document is the risk characteriza- 
tion chapter. This chapter integrates the findings of both the effects 
and exposure documents, outlines important inferences and science 
policy assumptions made in the absence of complete information, 
and describes potential hazards and risks posed by dioxin. 

The draft study not only updates the '85 document but also rep- 
resents an ongoing process to build a scientific consensus regarding 
the question of dioxin's potential to produce toxic effects. 

To help foster this consensus, EPA has worked to make each 
phase of the dioxin reassessment an open and participatory one. 

These efforts have included the involvement of outside scientists 
as principal authors of chapters, numerous public meetings to take 
comments on our plans and progress, publication of earlier drafts 
of our public work for public comment and review. 

The current external review draft has been made available for 
public comment and full scientific review. Results of this review, 
which took place from September 1994 to October 1995, will be 
used to revise and update the drafts over the next year. 

When this process is completed, we anticipate having an up-to- 
date and thorough scientific evaluation of dioxin that is on the cut- 
ting edge of environmental toxicology and exposure assessment. 

My written testimony has extensive details about the findings 
and issues contained in the draft Health Assessment of Dioxin and 
Related Compounds. 

Regarding health risks, the draft study affirms the association of 
dioxin and cancer. In its 1985 assessment, EPA concluded that 
dioxin is a proven animal carcinogen and a probable human car- 
cinogen under some conditions of exposure. 

The current draft reaches the same conclusions but with greater 
confidence because of additional published human data and en- 
hanced understanding of dioxin's mode of action. 

The SAB agreed with these conclusions. Based upon both animal 
and human evidence, EPA's estimate of dioxin cancer potency is es- 
sentially unchanged from that of 1985. 

The draft reassessment differs significantly from the 1985 docu- 
ment in its evaluation of dioxin's noncancer effects. 

Today we have a stronger body of evidence to suggest that, at 
some dose, dioxin exposures can result in a number of effects in hu- 
mans and some of these effects may even have an adverse impact 
on health. 

These effects may include developmental and reproductive ef- 
fects, immune suppression and disruption of regulatory hormones. 

We currently have limited direct evidence to show that any of 
these noncancer effects occur in humans at everyday levels of expo- 
sure. However, new studies are appearing which support earlier 
findings. 

We can infer from the information on levels of dioxin and related 
compounds that persist and recycle in the environment and are 
found in minute quantities in food and in people that average ev- 



18 

eryday exposure levels are close to exposures that are known to 
cause such effects in laboratory animals. 

Humans exposed to dioxin at several times average background 
levels in the general population have also shown indications of sub- 
tle effects which may or may not represent an adverse effect to 
health. 

In addition, the exposure document provides the first comprehen- 
sive survey of U.S. sources of dioxin and related compounds. 

A large variety of sources of dioxin have been identified, and oth- 
ers may exist. The available information suggests the presence of 
dioxin-like compounds in the environment has occurred primarily 
as a result of industrial practices and is likely to reflect changes 
in release over time. 

The principal identified sources of environmental release may be 
grouped into four major types, combustion and incineration 
sources; chemical manufacturing and processing sources; industrial 
and municipal processes; and reservoir sources. 

Although the current draft suggests that municipal and hospital 
waste incineration may account for the majority of the known re- 
leases, comments suggest the need to reevaluate these estimates 
based on changes in the number of active facilities and technologies 
applied to incineration in the past few years. 

Additional complex issues associated with the assessment include 
the air-to-food-to-humans pathway of exposure, the concept of tox- 
icity equivalence, background exposures, and dioxin's mode of ac- 
tion which make it similar to an environmental hormone. 

Other issues, such as the meaning of subtle and perhaps adapt- 
ive rather than adverse effects of dioxins and the calculations of 
margins of exposure, have also been discussed in my written testi- 
mony. 

The risk characterization. Chapter 9, for dioxin and related com- 
pounds was developed as an integrated analysis of information 
from the exposure document and fi-om the eight health effects 
chapters. 

Key assr.mptions were identified and discussed, and uncertain- 
ties attendant to the findings of the report were highlighted in the 
integrated analysis and the risk characterization summary. 

Issues to be discussed in the risk characterization chapter 
emerge directly fi*om the previous assessment work carried out by 
external authors as well as EPA scientists, were articulated by 
commenters on the process of the reassessment in numerous public 
meetings, and specifically came from recommendations made by 
peer panel reviewers of earlier versions of the reassessment chap- 
ters in 1992. 

This process led to the development of a draft risk characteriza- 
tion, primarily by EPA authors but with the assistance of some 
outside scientists. 

This early draft was reviewed extensively within the EPA and by 
numerous Federal agencies. The interagency review resulted in the 
formation of a drafting team from EPA, HHS, and USDA to ad- 
dress the comments of the reviewers. 

An unauthorized and unintended release of the interagency re- 
view draft also produced a round of unsolicited external comments 
in June and July of 1994. 



19 

All of this input formed the basis for the external review draft 
of the risk characterization which was released in September of '94 
for broad public comment. 

Despite the question raised in the charter of this hearing, the 
risk characterization is consistent with the findings contained in 
the earlier chapters. Any minor inconsistencies identified by peer 
review will be rectified in the revised version of the document. 

In its October 1995 report to the administrator, the SAB noted 
a number of strengths in the risk characterization. 

First, "by focusing serious attention on the various noncancer ef- 
fects, the agency has dispelled any misconception that EPA's risk 
assessment process is overly preoccupied with carcinogenic effects." 

Second, "by evaluating an entire group of compound classes with 
a common attribute rather than a single compound, the agency re- 
sponds to the generally mistaken criticism that its risk assessment 
process can only address issues on a chemical-by-chemical basis." 

Third, "in the opinion of most committee members, a useful com- 
parative perspective is provided in the draft conclusions where the 
agency highlights the fact that the margin of safety between the 
background exposures and the levels of exposure where effects 
have been seen in test animals for dioxin-like compounds is smaller 
than EPA usually sees from amy other compounds." 

On the other hand, the SAB noted three major weaknesses. First, 
the presentation, this is a quote, "The presentation portrayed in 
the draft conclusion is not balanced." This statement is footnoted 
with the following. "Several members of the committee do not agree 
with the statement and regard the EPA presentation and the infer- 
ences drawn as appropriately conservative within the context of 
public health protection." 

Second, "Important uncertainties associated with the agencj^s 
conclusions are not fully recognized and subjected to feasible analy- 
ses. 

Third, "The characterization of noncancer effects is not per- 
formed in a manner that allows meaningful analysis of the incre- 
mental benefits of risk management alternatives." This statement 
also was footnoted with the following statement. "A minority with- 
in the committee finds the noncancer risk characterization to be 
appropriate for use within a public health perspective. 

However, they agree that the reassessment's characterization is 
not performed in a manner which will be very useful in the analy- 
sis of the incremental benefits of risk management by those who 
will be concerned with microlevel incremental costs." 

These comments, with their specified examples as well as more 
specific comments on the other chapters, will be dealt with in the 
revision process. 

EPA is now in the process of addressing the comments on the ex- 
ternal review draft of the dioxin reassessment. Comments from the 
SAB will be considered along with those from the broader scientific 
community and the public. 

Details of our proposed process for dealing with the comments is 
contained in my written testimony. 

With regard to timing of these events, the revision process has 
already begun. Drafting of the chapter summaries and the revised 



20 

dose-response chapter and the risk characterization are anticipated 
to be complete by March 1996. 

Peer panel meetings are expected to be held on these documents 
early in May, particularly on chapter 8, the dose-response chapter 
and chapter 9, the characterization chapter. 

Documents will be referred to the SAB in June, with a review 
meeting to be held as soon as possible thereafter. 

Final documents are targeted for printing in August, with release 
occurring in September 1996. 

Obviously, this assumes that no major new issues arise during 
the revision process that would require extensive additional analy- 
sis or obviate the current approach for assessing dioxin risk. 

While the science of the reassessment is undergoing further peer 
review, EPA will be examining the reassessment's policy implica- 
tions to determine what changes, if any, are needed in existing pro- 
grams. 

While regulatory impact assessments are carried out on every 
regulation that might be issued, no estimates of the economic im- 
pact to the public from regulations that may be based on this reas- 
sessment have yet been carried out. Throughout the reassessment 
process, the agency has repeatedly stated that existing EPA efforts 
and programs will not be changed on the basis of this draft reas- 
sessment. 

However, they may change significantly after the completion of 
the report. 

EPA is committed to developing an agencjrwide strategy for man- 
aging dioxin risks concurrent with completion of the dioxin reas- 
sessment. 

As with the reassessment, we want to provide an opportunity for 
public input into our policy evaluations. 

I thank you for the time this morning, and I will be glad to take 
questions whenever it is appropriate. 

Mr. ROHRABACHER. Yes. 

Dr. Farland, we actually, the committee would like to have had 
a shorter presentation, but I let you go on because I think that 
what you are sajdng is basically the basis of what this discussion 
is supposed to be about. 

So I was very happy to have you have a little longer time to 
present your case. 

Dr. Farland. Thank you, Mr. Chairman. 

[The prepared statement of Dr. Farland follows:] 



21 



Testimony of 

William H. Farland, Ph.D. 

Director, 

National Center for Environmental Assessment 

Office of Research and Development 

U.S. Environmental Protection Agency 

before the 

Energy and Environment Subcommittee 

of the 

Committee on Science, 

House of Representatives 

December 13, 1995 

Introduction 

Scientists from the U.S. Environmental Protection Agency (USEPA), other 
Federal agencies and the general scientific community have been involved in a 
comprehensive scientific reassessment of dioxin and related compounds since 1991. 
External review drafts of the reassessment documents entitled "Estimating Exposure to 
Dioxin and Related Compounds" and "Health Assessment of 2, 3.7,8- 
tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds" were made available in 
September, 1994 by the Agency for public comment and review by the EPA's Science 
Advisory Board (SAB). This process has been a model for open, participatory 
environmental health assessment. Peer review has been an integral part of the entire 
reassessment process. Extensive comments have been received and will be the basis 
for revisions to the draft documents. These documents and subsequent comments 
highlight a number of issues which are of broad scientific interest. Answers to the 
questions posed on page 2 of the Hearing Charter are discussed in the text that follovi^. 
In bnef, 1) the EPA believes that the risk characterization was consistent with the 
scientific findings contained in the eariier chapters; 2) contrary to the implication of the 
question, the risk characterization was informed by input from a panel of extemal 
reviewers of the draft chapters, drafted by Federal scientists and was peer reviewed. It, 
like the rest of the report, involved both EPA and non-EPA drafters and reviewers; 3) 
EPA's risk characterization does not rely solely on high levels of exposure to animals, 
but integrates animal data with limited human infomriation. Animal data have been 
obtained at levels of exposure comparable to human exposures, and human 
information has been obtained on populations exposed at background levels and 
above; and 4) while regulatory impact assessments are carried out on every regulation 
that might be issued, no analysis of the potential economic impact on regulations that 
may be based on this reassessment will be conducted until the reassessment is 
complete and a comprehensive Agency-wide strategy has been developed. 



22 



Background 



Dioxins are a group of chemical compounds inadvertently created through a 
number of activities including: combustion, certain types of chemical manufacture, . 
chlorine bleaching of pulp and paper, and other industrial processes. Dioxin is 
produced in very small quantities compared to other pollutants (around 30 pounds 
TEQ^ annually in the U.S.); however, because it is highly toxic, it has been treated as a 
significant environmental pollutant since the early 1970's. U.S. EPA first took action 
against dioxin as a contaminant of the herbicide 2,4, 5-T in 1979. Since then, EPA has 
expanded its dioxin control efforts to each of its major programs. 

In 1985 EPA published a scientific review of the health effects of 2,3,7,8-TCDD, 
the most toxic of the dioxin compounds. That assessment has served as the scientific 
basis for dioxin risk estimates for all U.S. EPA programs. In April 1991, EPA 
announced that it would conduct a comprehensive scientific reassessment of the health 
risks of exposure to the family of compounds generally known as dioxin (2,3,7,8-TCDD 
and other dioxin-like compounds, including certain dioxin-like polychlorinated biphenyls 
(PCBs)). EPA has undertaken this task in light of significant advances in our scientific 
understanding of mechanisms of dioxin toxicity, significant new studies of dioxin's 
carcinogenic potential in humans, and increased evidence of other adverse health 
effects. The reassessment is part of the Agency's goal to improve its research and 
science base and to incorporate this knowledge into EPA decisions. In September, 
1994, EPA released a "public review draft" of its dioxin reassessment. This release 
marked a mid-point in EPA's effort to reevaluate the scientific understanding of dioxin. 
While the reassessment has been underway, EPA has continued to move forward in 
implementing its dioxin control programs, based on the 1985 assessment and, in most 
cases, applying technology-based rather than risk-based solutions. In the past fifteen 
years, EPA has taken action under every one of its major statutes to control the risks of 
dioxin. No regulatory action has been undertaken by the Agency based on the results 
of this draft reassessment. Throughout the reassessment process the Agency has 
repeatedly stated that existing EPA efforts and programs will not be changed on the 
basis of this draft reassessment, but they may change significantly after the completion 
of the report. 



1TEQ = Toxic Equivalents. TEQ is an internationally recognized convention for 
expressing the toxicity of a complex mixture of multiple dioxin-like compounds, varying 
in their toxicity, as an equivalent amount of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 
the reference compound for this class. 



23 



Science Reassessment 



In September 1994, the EPA released the public review draft of the full 
reassessment. The reassessment consists of two documents, each about a thousand 
pages long, and each published in several volumes. One of these documents 
addresses the human health effects of dioxin; the second focuses on sources and 
levels of exposure. The reassessment is a scientific document and does not address 
regulatory policy or issues. An effort to address regulatory policy issues raised by the 
reassessment will be carried out in separate, public discussions in the winter and spring 
of 1996. Volume three of the health effects document is the Risk Characterization 
chapter . This chapter integrates the findings of both the effects and exposure 
documents, outlines important inferences and science policy assumptions made in the 
absence of complete information, and describes the potential hazards and risks posed 
by dioxin. 

The draft study not only updates the 1985 document, but also represents an 
ongoing process to build a broad scientific consensus regarding the question of dioxin's 
potential to produce toxic effects . To help foster this consensus, EPA has worked to 
make each phase of the dioxin reassessment an open and participatory process. 
These efforts have included the involvement of outside scientists as principal authors of 
several chapters, numerous public meetings to take comment on our plans and 
progress, and publication of eariier drafts of our work for public comment and review. 
The current "external review" draft has been made available for public comment and full 
scientific review. Results of this review, which took place from September, 1994 to 
October, 1 995, will be used to revise and update the drafts over the next year. When 
this process is completed, we anticipate having an up-to-date and thorough scientific 
evaluation of dioxin that is at the cutting edge of environmental toxicology and exposure 
assessment. 

Regarding health risks, the draft study reaffirms the association of dioxin and 
cancer. In its 1985 assessment, EPA concluded that dioxin is a proven animal 
carcinogen and a probable human carcinogen. The cun-ent draft report reaches the 
same conclusion, but with greater confidence because of additional published human 
data and enhanced understanding of dioxin's mode of action. Based upon both animal 
and human evidence, EPA's estimate of dioxin's cancer potency is essentially 
unchanged from that of 1985. 

The draft reassessment differs significantly from the 1985 document in its 
evaluation of dioxin's non-cancer effects. Today we have a stronger body of evidence 
to suggest that at some dose, dioxin exposure can result in a number of non-cancer 
effects in humans, and that some of these effects may have an adverse impact on 
health. These effects may include developmental and reproductive effects, immune 
suppression, and disruption of regulatory homriones. We currently have very limited 



24 



direct evidence to show that any of these non-cancer effects occur in humans at 
everyday levels of exposure. However, we can infer from the infbmiation on levels of 
dioxin and related compounds in the environment, in food, and in people that average 
everyday exposures are close to exposures that are known to cause such effects in 
laboratory animals. Humans exposed to dioxins at several times average background 
levels in the general population have also shown indications of subtle effects which may 
or may not represent an adverse impact on their health. 

U.S. Exposure Survey 

The Exposure Document provides the first comprehensive survey of U.S. 
sources of dioxin and related compounds. A large variety of sources of dioxin have 
been identified and others may exist. The available information suggests that the 
presence of dioxin-like compounds in the environment has occurred primarily as a 
result of industrial practices and is likely to reflect changes in release over time. The 
principal identified sources of environmental release rhay be grouped into four major 
types: combustion and incineration sources; chemical manufacturing/processing 
sources; industrial/municipal processes; and reservoir sources. Although the current 
draft suggests that municipal and hospital waste incineration may account for the 
majority of known releases, comments suggest the need to reduce these estimates 
based on changes in numbers of active facilities and technologies applied to 
incineration in the past few years. Also, additional sources have been identified and will 
be further addressed in future versions of the document. 

Because dioxin-like chemicals are persistent and accumulate in biological 
tissues, particularly in animals, the scientific community has hypothesized since the late 
1980's that the major route of human exposure is through ingestion of foods containing 
minute quantities of dioxin-like compounds. The EPA reassessment document adopts 
this hypothesis. This pathway results in wide-spread, low-level exposure of the general 
population to dioxin-like compounds. Certain segments of the population may be 
exposed to additional increments of exposure by being in proximity to point sources or 
because of dietary practices. The actual levels of dioxin and related compounds in the 
environment and in food in the U.S. are based on relatively few samples and must be 
considered quite uncertain. However, they seem consistent with levels measured in a 
number of studies in Western Europe and Canada. The consistency of these levels 
across industrialized countries provides reassurance that the U.S. estimates are 
reasonable. Collection of additional data to reduce uncertainty in U.S. estimates of 
dioxin-like compounds in the environment and in food represents an important data 
need. Data collection is currently underway in a series of studies being carried out by 
EPA and U.S. Department of Agriculture (USDA) scientists. Recent data on levels of 
dioxin-like compounds in the fat of beef suggests similar, if not slightly lower, levels 
compared to previous information. Additional food products are being collected and 
dioxin levels are being analyzed. 



25 



Air to Food Hypothesis 



This assessment adopts the hypothesis that the primary mechanism by which 
dioxin-like compounds enter the terrestrial food chain is via atmospheric deposition. 
Dioxin and related compounds enter the atmosphere directly through air emissions or 
indirectly, for example, through volatilization from land or water or from re-suspension of 
particles. Deposition can occur directly onto soil or onto plant surfaces. At present, it is 
unclear whether atmospheric deposition represents primarily current contributions of ■ 
dioxin and related compounds from all media reaching the atmosphere, or whether it is 
past emissions of dioxin and related compounds which persist and recycle in the 
environment. Understanding the relationship between these two scenarios will be 
particulariy important in understanding the relative contributions of individual point 
sources of these compounds to the food chain and assessing the effectiveness of 
control strategies focussed on either current or past emissions of dioxins in attempting 
to reduce the levels in food. Commentors have also highlighted the importance of 
better understanding atmospheric transfomnation processes in order to adequately 
model fate and transport of these compounds from source to receptor (human or 
ecological). 

Toxicity Equivalents 

Because the assessment of dioxin and related compounds involves the 
evaluation of approximately eighteen major persistent chemicals and hundreds of 
others, often occurring as complex environmental mixtures, an approach has been 
developed to overcome the lack of information on individual members of this class. 
Throughout the reassessment, concentrations of dioxin and related compounds have 
been presented as TCDD equivalents (TEQs). TCDD is the best studied of this class of 
compounds and is the reference compound with regard to determination of toxicity 
equivalence factors (TEFs). Other dioxin-like compounds are assigned TEFs based on 
inspection of available physical, chemical and toxicologic infomnation. Other 
approaches to evaluating the toxicity of dioxin-like compounds such as assuming that 
all are as toxic as 2,3,7,8-TCDD, or assuming that they do not contribute significantly to 
the toxicity of this family of compounds given 2,3,7,8-TCDD's potency are generally 
considered to be unacceptable. Therefore, the international scientific community, as 
represented by Worid Health Organization (WHO) and NATO scientific committees, the 
EPA and several states have adopted the TEF approach as a useful, albeit uncertain, 
procedure in the face of incomplete data on this family of compounds, and with the 
prospects of ever filling all of the data gaps improbable. 

The strengths and weaknesses as well as the uncertainties associated with the 
TEF/TEQ approach have been discussed in detail in the documents but further 
attention will be needed to provide appropriate perspective on their use. In particular. 



26 



additional care will be given to delineating the contribution of TCDD, the best studied of 
these compounds, to estimated TEQ. The assessment of toxicity of dioxin and related 
compounds presents a difficult "complex mixture' problem. Use of the TEFs for dioxin- 
like PCBs in estimating total TEQ has received-extensive comment As noted, the use 
of the TEQ approach is fundamental to the evaluation of this group of compounds and 
as such represents a key assumption upon which many of the conclusions in this 
reassessment hinge. Additional data are being collected to evaluate this issue both in 
temns of the assignment of appropriate TEFs and in addressing issues such as 
additivity of the TEFs in environmental samples and food or in human blood, tissue, or 
mother's milk. 

"Background" Exposure 

The term "background" exposure has been used throughout this reassessment 
to describe exposure of the general population, who are not exposed to readily 
identifiable point sources of dioxin-like compounds. Data on human tissue levels 
suggest that body burden levels among industrialized nations are reasonably similar. 
Average background exposure leads to body burdens in the human population which 
average 40-60 pg TEQ/g lipid (40-60 ppt) when all dioxin-like dioxins, furans and PCBs 
are included. High-end estimates of body burden of individuals in the general 
population (approximately the top 10% of the general population) without additional 
identifiable exposures may be approximately 2 times higher based on available data. 
While there are some recent data to suggest that both environmental and human body 
burdens are on a downward trend, additional information will be needed to establish a 
baseline upon which to evaluate future measurements. 

In addition to general population "background" exposure, some individuals or 
groups of individuals may also be exposed to dioxin-like compounds from discrete 
sources or pathways locally within their environment. Examples of these "special" 
exposures include: occupational exposures, direct or indirect exposure to local 
populations from discrete sources, exposure to nursing infants from mother's milk, or 
exposures to subsistence or recreational fishers. Although daily exposures to these 
populations may be significantly higher than daily exposures to the general population, 
simply evaluating these exposures by averaging higher daily intakes pro-rated over a 
lifetime might obscure the potential significance of elevated exposures for these sub- 
populations, particulariy if exposures occur for a short period of time during critical times 
during development and/or growth. This has raised the issue as to the most 
appropriate "dose metric" to use for dioxin exposure. Exposure levels, intake values, 
and body burdens have all been used in the past for this purpose. While the current 
document focusses on body burden, it recognizes that other metrics of exposure may 
be more appropriate for assessing certain biological responses. In response to a 
number of comments on this issue, future versions of the report will address this issue 
more fully. 



27 



Mode of Action 



This reassessment concludes that the scientific community has identified and 
described a series of events attributable to exposure to dioxin-like compounds including 
biochemical, cellular and tissue-level changes in nomnal biological processes. Binding 
of dioxin-like compounds to a cellular protein called the "Ah receptor" represents the 
first step in a series of common biological steps and may be necessary for most if not 
all of the observed effects of dioxin and related compounds in vertebrates including 
humans. While binding to the Ah receptor appears to be necessary for all well-studied 
effects of dioxin, it is not sufficient, in and of itself, to elicit the&e responses. Many 
effects elicited by exposure to 2,3,7,8-TCDD are shared by other chemicals which have 
a similar structure and Ah receptor binding characteristics. This is the main basis for 
the assumed validity of the TEF approach. Consequently, the biological system 
appears to respond to the cumulative exposure of Ah receptor-mediated chemicals 
rather than to the exposure to any single dioxin-like compound. Based on our 
understanding of dioxin mechanism(s) to date, it is accurate to say that interaction with 
the Ah receptor is necessary, that the Ah receptor in humans is similar in stmcture and 
binding characteristics to those found in dioxin responsive animals, and that there is 
likely to be a variation between and within species and between tissues in individual 
species based on differential responses "down stream" from receptor binding. The 
potency and fundamental level at which these compounds act on biological systems is 
analogous to several well studied hormones. Dioxin and related compounds have the 
ability to alter the pattem of growth and differentiation of a number of cellular targets by 
initiating a series of biochemical and biological events resulting in the potential for a 
spectrum of responses in animals and humans. Initial simplistic attempts to describe 
dioxin's mode of action as a transcriptional regulator of gene activity fail to account for 
recent data that suggests that receptor binding may also alter levels of cellular 
phosphorylation and hormone and growth factor receptor function without impacting 
transcription. Further work will be needed to understand this complex of inter-related 
activities. Additional data available to address ther^ issues will be discussed in 
revisions to the reassessment document. 

The reassessment also finds that there is adequate evidence based on all 
available information, including studies in human populations as well as in laboratory 
animals and from ancillary experimental data, to support the inference that humans may 
have the potential to respond with a broad spectrum of effects from exposure to dioxin 
and related compounds, if exposures are high enough. These effects will likely range 
from adaptive changes at or near background levels of exposure to adverse effects with 
increasing severity as exposure increases significantly above background levels. 
Enzyme induction, changes in hormone levels and indicators of altered cellular function 
represent examples of effects of unknown clinical significance and which may or may 
not be early indicators of toxic response. Induction of activating/metabolizing enzymes 
at or near background levels, for instance, may be adaptive or may be considered 



28 



adverse since induction may lead to more rapid metabolism and elimination of 
potentially toxic compounds, or may lead to increases in reactive intermediates and 
may potentiate toxic effects. Demonstration of examples of both of these situations for 
dioxins and for other families of compounds is available in the published toxicologic 
literature. Clearly adverse effects including, perhaps, cancer may not be detectable 
until exposures exceed background by one or two orders of magnitude (10 or 100 
times) or more. The mechanistic relationships of biochemical and cellular changes seen 
at very low levels of exposure to production of adverse effects detectable at higher 
levels remains uncertain and controversial. It is this relationship in conjunction with an 
understanding of "background" exposures to dioxin-like compounds that is at the heart 
of this assessment. 

Species Sensitivity 

It is well known that individual species vary in their sensitivity to any particular 
dioxin effect. Human data provide direct or indirect support for evaluation of likely effect 
levels for several of the endpoints based primarily on animal information although the 
influence of variability among humans remains difficult to assess. Biochemical, cellular, 
and organ-level endpoints have been shown to be affected by TCDD, but specific data 
on these endpoints do not generally exist for other members of this chemical family. 
Despite this lack of specific data, there is reason to infer that these effects may occur 
for all dioxin-like compounds, based on the concept of toxicity equivalence. 

Some of the effects of dioxin and related compounds such as enzyme induction, 
changes in hormone levels and indicators of altered cellular function have been 
observed in laboratory animals and humans at or near body burden levels of people in 
the general population. Other effects are detectable only in highly exposed 
populations, and there may or may not be a likelihood of response in individuals 
experiencing lower levels of exposure. Adverse effects associated with temporary 
increases in dioxin blood levels based on short terrr^hjgh level exposures, such as 
those that might occur in animal experiments, an iouM^trial accident or in infrequent 
contact with highly contaminated environmental media, may be dependent on exposure 
coinciding with a window of sensitivity of biological processes. 

Non-Cancer Health Effects 

In tCDD-exposed men, subtle changes in biochemistry and physiology such as 
enzyme induction, altered levels of circulating reproductive honnones, or reduced 
glucose tolerance, have been detected in a limited number of the few available studies. 
These findings, coupled with knowledge derived from animal experiments, suggest the 
potential for adverse impacts on human metabolism, and developmental and/or 
reproductive biology, and, perhaps, other effects in the range of current human 
exposures. Given the assumption that TEQ intake values represent a valid comparison 

8 



29 



with TCDD exposure, some of these adverse impacts may be occurring at or within one 
order of magnitude of average background TEQ intalce or body burden levels. It seems 
reasonable to infer that, as body burdens increase within and above this range, the 
probability and severity as well as the spectrum of human non-cancer effects most lilcely 
increases. It is not currently possible to state exactly how or at what levels humans in 
the population will respond, but the margin-of-exposure (MOE) between background 
levels and levels where effects are detectable in humans in terms of TEQs is 
considerably smaller than previously estimated. These facts and assumptions lead to 
the inference that some more highly exposed members of the general population or 
more highly exposed, special populations may be at risk for a number of adverse 
effects including developmental toxicity based on the inherent sensitivity of the 
developing organism to changes in cellular biochemistry and/or physiology, reduced 
reproductive capacity in males based on change in hormone levels and, perhaps, 
decreased sperm counts, higher probability of experiencing endometriosis in women, 
reduced ability to withstand an immunological challenge and others. This inference that 
more highly exposed members of the population may be at risk for various non-cancer 
effects is supported by obsen/ations in animals, by scientific inference, and by some 
human infonnation from highly exposed cohorts. 

The deduction that humans are likely to respond with non-cancer effects from 
exposure to dioxin-like compounds is based on the fundamental level at which these 
compounds impact cellular regulation and the broad range of species which have 
proven to respond with adverse effects. Since, for example, developmental toxicity 
following exposure to TCDD-like congeners occurs in fish, birds, and mammals, it is 
likely to occur at some level in humans. It is not cun-ently possible to state exactly how 
or at what levels people will respond with adverse impacts on development or 
reproductive function. Fortunately, there have been few human cohorts identified with 
TCDD exposures in the high end of the exposure range, and when these cohorts have 
been examined, few clinically significant effects were detected. The lack of adequate 
human information and the focus of most cun-ently available epidemiologic studies on 
occupationally, TCDD-exposed adult males makes evaluation of the inference, that 
non-cancer effects associated with exposure to dioxin-like compounds may be 
occurring, difficult. It is important to note, however, that when exposures to very high 
levels of dioxin-like compounds have been studied, such as in the Yusho and Yu- 
Cheng cohorts, a spectrum of adverse effects have been detected in men, women and 
children. Some have argued that to deduce that a spectrum of non-cancer effects will 
occur in humans in the absence of better human data overstates the science; most 
scientists involved in the reassessment as authors and reviewers have indicated that 
such inference is reasonable given the weight-of-the-evidence from available data. As 
presented, this logical conclusion represents a testable hypothesis which may be 
evaluated by further data collection. 



23-557 0-96-2 



30 



Development of Margins-of-Exposure (MOE) 

The likelihood that non-cancer effects may be occuning in the human population 
at environmental exposure levels is often evaluated using a "margin-of-exposure" 
(MOE) approach. A MOE is calculated by dividing the human-equivalent animal LOAEL 
or no observed adverse effect level (NOAEL) with the human exposure level. MOEs in 
the range of 100 -1000 are generally considered adequate to mle out the likelihood of 
significant non-cancer effects occurring in humans based on sensitive animal 
responses. The average levels of intake of dioxin-like compounds in terms of TEQs in 
humans described above would result in body burdens well within a factor of 100 of 
levels representing lowest observed adverse effect levels (LOAELs) in laboratory 
animals exposed to TCDD or TCDD equivalents. Our analysis of body burdens in 
animals and humans relative to effect levels for a number of biochemical, cellular and 
clearly adverse endpoints has recently been published (DeVito, et al.,1995, 
Environmental Health Perspectives, Volume 103, Number 9) For several of the effects 
noted in animals, a MOE of less than a factor of ten, based on intake levels or body 
burdens, is likely to exist. Based on these data alone, traditional toxicologic 
approaches for deriving likely NOAELs for humans and translating them into "safe" or 
"tolerable" levels for regulatory purposes will need to be reconsidered. While it is 
unlikely that any large segment of the human population is incurring an adverse impact 
from current body burdens, MOEs are less than we once believed. This issue has been 
recognized by the WHO and an expert panel has recently (November, 1995) been 
convened to consider the need to re-evaluate the WHO statement regarding a 
"tolerable daily intake" or TDI for dioxin and related compounds. A report of this 
meeting will be available in the very near future. 

Carcinogenicity of Dioxin-Like Compounds 

With regard to carcinogenicity, EPA's weight-of-the-evidence evaluation 
suggests that dioxin and related compounds (CDDs, CDFs, and dioxin-like PCBs) are 
likely to present a cancer hazard to humans. Extension of this statement of hazard to 
this broad range of compounds based on TEFs and in the face of limited data to assess 
cancer hazard of the individual congeners is a critical issue. The epidemiological data 
alone are not yet deemed sufficient to characterize the cancer hazard of this class of 
compounds as being "known." However, combining suggestive evidence of recent 
epidemiology studies with the unequivocal evidence in animal studies and inferences 
drawn from mechanistic data supports the characterization of dioxin and related 
compounds as likely cancer hazards, that is, likely to produce cancer in some humans 
under some conditions. It is important to distinguish this statement of cancer hazard 
from the evaluation of cancer risk. The extent of cancer risk will depend on such 
parameters as route and level of exposure, overall body burden, dose to target tissues, 
individual sensitivity, and hormonal status. 



10 



31 



While major uncertainties remain, efforts of this reassessment to bring more data 
into the evaluation of cancer potency have resulted in an upper bound, risk specific 
dose estimate (1 X 10"* risk or one additional cancer in one million exposed) of 
approximately 0.01 pg TEQ/ kg body weight/ day. Estimates of exposure associated . 
vi/ith other specific risk values (10"*, 10"*,etc.) can be derived by using a low dose linear 
model. These risk specific dose estimates represent plausible upper bounds on risk 
based on the evaluation of animal and human data. These values are similar to 
previous estimates published by EPA in 1985 but which were'based on less data. 
"True" risks are not likely to exceed these values, may be less, and may even be zero 
for some members of the population. It is cun^ently not possible to estimate more 
precisely the risk to exposed individuals. The use of a linear model to provide 
probabilistic risk estimates remains controversial. Alternative approaches will need to 
be addressed in future versions of the reassessment. The SAB specifically suggested 
that the dose-response discussion in Chapter 8 should reflect consideration of 
alternative models, including those inferring a threshold for response, and their 
implications on estimates of cancer risk. 

The current evidence suggests that both receptor binding and some eariy 
biochemical events such as enzyme induction are likely to demonstrate low-dose 
linearity. The mechanistic relationship of these eariy events to the complex process of 
carcinogenesis remains to be established. If these findings imply low-dose linearity in 
biologically-based cancer models under development, then the probability of cancer risk 
will be linearly related to exposure to TCDD at low doses, and the slope of the response 
curve in the low dose region will be a critical issue for predicting risk. If they do not, 
non-linear relationships may exist between exposures and cancer risk. Until the 
mechanistic relationship between early cellular responses and the parameters in 
biologically based cancer models is better understood, the shape of the dose-response 
curve for cancer in the low-dose region can only be inferred with uncertainty. 

Associations between human exposure to dioxin and certain types of cancer 
have been noted in occupational cohorts with average body burdens of TCDD 
approximately 2 orders of magnitude (100 times) higher than average TCDD body 
burdens in the general population. The average body burden in these occupational 
cohorts level is within 1-2 orders of magnitude (10-100 times) of average background 
body burdens in the general population in terms of TEQ. Thus, there is no need for 
large scale low dose extrapolations since these body burdens are the result of 
occupational exposures added to "background" exposures experienced by the general 
population. Nonetheless, the relationship of apparent increases in cancer mortality in 
these populations to calculations of general population risk remains uncertain due to 
uncertainty in the dose-response relationship within these two orders of magnitude. 

TCDD has been clearly shown to increase malignant tumor incidence in 
laboratory animals (e.g. liver, lung, thyroid, hard palate). It also appears to decrease 

11 



32 



the incidence of sonoe honnone-sensitive cancers (uterine, mammary) in laboratory 
rodents. The reason for this decrease is unknown although some have speculated that 
it is due to dioxin's anti-estrogenic activity, while others have suggested that it is an 
indirect consequence of change in animal body weights. In addition, a number of 
studies analyzed in this reassessment demonstrate other biological effects of dioxin 
related to the process of carcinogenesis. A number of reviewers including some 
scientists on the SAB suggest that the complex impacts of dioxin on the carcinogenic 
process, causing the potential for both increases and decreases in cancer risk in 
exposed humans, need to be addressed if we are to truly appreciate the impact of 
dioxin exposures. Initial attempts to construct a biologically-based model for certain 
dioxin effects as a part of this reassessment will need to be continued and expanded to 
accommodate more of the available biology relating to potential cancer risk. In 
addition, biologically-based models to apply to a broader range of potential health 
effects associated with exposure to dioxin-like compounds will be needed in the future. 

Risk Characterization 

According to the National Research Council, who articulated the widely used risk 
assessment paradigm in their seminal, 1983 treatise on risk assessment in the Federal 
Govemment, risk characterization is the final step in the risk assessment process in 
which the first three steps (hazard identification, dose-response assessment and 
exposure assessment) are summarized and the information integrated to develop a 
qualitative or quantitative estimate of the likelihood that any of the hazards associated 
with the agent of concern will be realized in exposed people. In this step, strengths and 
weaknesses of the available data are discussed, and assumptions and uncertainties 
which are embodied in the risk assessment are articulated. This guidance has been re- 
iterated by the EPA in its own risk characterization policy on a number of occasions. 

The risk characterization (Chapter 9) for dioxin and related compounds was 
developed as an integrated analysis of information from the exposure document and 
from the eight health effects chapters. Key assumptions were identified and discussed. 
Uncertainties attendant to the findings of the report were highlighted in the integrated 
analysis and in the risk characterization summary. Issues to be discussed in the risk 
characterization chapter emerged directly from the previous assessment woric carried 
out by external authors as well as EPA scientists, were articulated by commentors on 
the process of reassessment in numerous public meetings, and specifically came from 
recommendations made by peer reviewers of the eariier versions of the reassessment 
chapters in 1992. This process led to the development of a draft risk characterization, 
primarily by EPA authors but with the assistance of some outside scientists. This eariy 
draft was reviewed extensively within the EPA and by numerous Federal agencies. 
The inter-agency review resulted in the fonnation of a drafting team from EPA, HHS, 
and USDA to address the comments of the reviewers. An unauthorized and 
unintended release of the inter-agency review draft also produced a round of 

12 



33 



unsolicited external comments in June and July, 1994. All of this input fbnned the basis 
for the external review draft of the risk characterization which was released in 
September, 1994 for broad public comment and peer review by the Agency's SAB. 
Despite the question raised in the charter for this hearing, the risk characterization is 
consistent with the findings contained in the eariier chapters. Any minor inconsistencies 
identified by peer review wilt be rectified in the revised version of the document. 

In its October, 1995 report to the Administrator, the SAB noted a number of 
strengths in the risk characterization. First, *by focusing serious attention on various 
non-cancer effects, the Agency has dispelled any mis-impression that EPA's risk 
assessment process is overly preoccupied with carcinogenic effects". Second, "by 
evaluating an entire group of compound classes (with a common attribute), rather than 
a single compound, the Agency responds to the generally mistaken criticism that its risk 
assessment process can only address issues on a chemical-by-chemical basis." Third, 
"in the opinion of most Committee Members, a useful comparative perspective is 
provided in the draft conclusions where the Agency highlights the margin of safety 
(between background exposures and levels of exposure where effects have been seen 
in test animals) for dioxin-like compounds is smaller than EPA usually sees for many 
other compounds." 

On the other hand, the SAB noted three "major weaknesses." First, "the 
presentation portrayed in the draft conclusions is not balanced." This statement was 
footnoted with the following: "Several members of the Committee do not agree with this 
statement and regard the EPA presentation and the inferences drawn as appropriately 
conservative within the context of public health protection." Second, "important 
uncertainties associated with the Agency's conclusions are not fully recognized and 
subjected to feasible analyses." Third, "the characterization of non-cancer effects is not 
perfomried in a manner that allows meaningful analysis of the incremental benefits of 
risk management altematives." This statement was footnoted with the following 
statement: "A minority within the Committee finds the non-cancer risk characterization 
to be appropriate for use within a public health perspective. However, they agree that 
the reassessment document's characterization is not perfomied in a manner which will 
be very useful in the analysis of the incremental benefits of risk management 
alternatives by those who will also be concerned with the micro-level incremental 
costs." These comments with their specified examples as well as more specific 
comments on the other chapters will be dealt with in the revision process. 

Next Steps 

The EPA is now in the process of addressing comments on the external review 
draft of the dioxin reassessment. Comments from the SAB will be considered along 
with those from the broader scientific community and the public who reviewed the report 
during the public comment period which extended from September, 1994 to January, 

13 



34 



1995. The exposure documents and the first seven chapters of the health assessment 
document will be revised an updated by EPA Chapter Managers. As suggested by the 
SAB, summaries are being prepared for each of the health assessment chapters and 
the contribution of 2,3,7,8-TCDD or other dioxin-like compounds are being delineated 
so that a greater appreciation of the uncertainty in applying TEQ to complex mixtures 
can be gained. These revised portions of the document will be subjected to additional 
internal and limited external peer review prior to being finalized. A disposition of 
comments will be prepared as the documents are completed. Chapter 8 (Dose- 
Response Chapter) is being subjected to a major re-write as suggested by the SAB. 
This re-write will be drafted by an expanded dose-response modeling team, which will 
include additional statistical expertise and the assistance of a phannacologist familiar 
with modeling receptor-mediated responses. The revised Chapter 8 will be subjected to 
a public peer panel review, containing 8-10 extemal scientific experts, prior to being 
finalized, and will be referred back to the SAB for review as suggested. The Risk 
Characterization will also be extensively revised to address public and SAB comments. 
As suggested by the SAB, public input on the revision process has been sought, 
additional experts from outside the Federal government will be enlisted to contribute to 
the revision, and a public peer review of the revised risk characterization by 
approximately 10 external scientific experts will be conducted prior to its finalization. 
The risk characterization will also be referred back to the SAB as suggested. The SAB 
can then evaluate response to their suggestions and the adequacy of the additional 
peer review conducted on the draft report. 

With regard to the timing of these events, the revision process has already 
begun. Drafting of chapter summaries and the revised dose response chapter and the 
risk characterization are anticipated to be complete by March, 1996. Peer panel 
meetings are expected to be held in eariy May. Documents will be referred to the SAB 
in June with a review meeting to be held as soon as possible thereafter. Final 
documents are targeted for printing in August with release occurring in September, 

1996. Obviously, this assumes that no major new issues arise during the revision 
process that would require extensive additional analysis or obviate the current 
approach to assessing dioxin risk. 

Summary 

Based on all of the data reviewed in this reassessment and scientific inference, a 
picture emerges of TCDD and related compounds as potent toxicants in animals with 
the potential to produce a spectrum of effects in animals and, perhaps, in humans. 
Some of these effects may be occuning in humans at very low levels, and some may 
be resulting in adverse impacts on human health. The potency and fundamental level 
at which these compounds act on biological systems is analogous to several well- 
studied hormones. Dioxin and related compounds have the ability to alter the pattern of 
growth and differentiation of a number of cellular targets by initiating a series of 

14 



35 



biochemical and biological events resulting in the potential for a spectaim of responses 
in animals and humans. Despite this potential, there is currently no clear indication of 
increased disease in the general population attributable to dioxin-like compounds. The 
lack of a clear indication of disease in the general population should not be considered 
strong evidence for no effect of exposure to dioxin-like compounds. Rather, lack of a 
clear indication of disease may be a result of the inability of our current data and 
scientific tools to directly detect effects at these levels of human exposure. Several 
factors suggest a need to further evaluate the impact of these chemicals on humans at 
or near current background levels. These are: the weight of the evidence on exposure 
and effects; an apparently low/ margin-of-exposure for non-cancer effects; and potential 
for additivity to background processes related to carcinogenicity. Critical issues relating 
to dioxin exposure and toxicity, and requiring additional attention in the reassessment 
include; sparse data to derive national means for sources/pathways; state of validation 
of exposure models; trends in environmental/body burden levels; TEFs/TEQs; impact of 
human data on hazard and risk characterization; significance of enzyme induction and 
other biochemical effects; and the relative roles of data, scientific inference, and 
science policy in informing regulatory decisions. The Agency plans to address 
comments provided by the general scientific community, the public, and the Agency's 
SAB. The current schedule, including revision and additional peer review, should allow 
completion of the dioxin reassessment by September, 1996. 

While the science of the reassessment is undergoing further peer review, EPA 
will be examining the reassessment's policy implications to detennine what changes, if 
any, are needed in existing programs. While regulatory impact assessments are 
carried out on every regulation that might be issued, no estimates of the economic 
impact to the public from regulations that may be based on this reassessment have yet 
been estimated. Throughout the reassessment process EPA has repeatedly stated that 
existing Agency efforts and programs will not be changed on the basis of this draft 
reassessment, but they may change significantly after the completion of the report. 
EPA is committed to developing an Agency-wide strategy for managing dioxin risks, 
concurrent with completion of the dioxin reassessment. As with the reassessment, we 
want to provide an opportunity for public input into our policy evaluations. This winter 
and spring, EPA will hold dioxin policy wori<shops to explore the policy implications of 
the reassessment. 



15 



36 

Mr. ROHRABACHER. Dr. Gough? 

STATEMENT OF MICHAEL GOUGH, PH.D., FORMER GOVERN- 
MENT EXPERT MEMBER OF DIOXIN REASSESSMENT REVIEW 
COMMITTEE, EPA SCIENCE ADVISORY BOARD 

Dr. GouGH. My light didn't come on. Can you hear me? Okay. 

Good morning, Mr. Chairman and committee members. I am Mi- 
chael Gough, and earlier this year, when I was employed at the Of- 
fice of Technology Assessment, I was a government expert member 
of EPA's Science Advisory Board's dioxin reassessment review com- 
mittee. 

I have been involved in analysis and writing about dioxin since 
1980, when I was put in charge of OTA's congressionally mandated 
oversight of executive branch research into possible health effects 
of exposures to dioxin-contaminated Agent Orange during the Viet- 
nam War. 

My book, "Dioxin, Agent Orange," was published in 1986 while 
I was in the private sector, and I now have a contract to write a 
second book about dioxin. 

I have written a number of papers on this subject, and I chaired 
a Department of Veterans' Affairs advisory committee about the 
care of Vietnam veterans, as well as the Department of Health and 
Human Services committee to review the United States Air Force's 
ongoing 20-year-long study of the health of the men who sprayed 
90 percent of the Agent Orange used in Vietnam. 

Mr. ROHRABACHER. What we should do is, that will be a 15- 
minute bell, if you could proceed with your testimony, as soon as 
you are done, we will then break to vote and come back and hear 
the other witnesses. 

Dr. GouGH. Okay. 

Mr. ROHRABACHER. Proceed. 

Dr. GouGH. So I should hurry. Okay. 

Since OTA closed on September 30, I have accepted a position 
with the Cato Institute that will begin at the first of the year. 

My oral testimony is abstracted from my written text. 

The letter of invitation for this hearing mentions four specific is- 
sues. I have little to say about two. I do not know why EPA wrote 
chapter 9, the risk characterization chapter, as well as part of 
chapter 8 about risk models inhouse, and I do not know why chap- 
ter 9 was less extensively peer reviewed than the other chapters 
before the committee review. 

The second issue I will not address is the economic impacts of 
dioxin regulation. 

The first issue that I will discuss is the question about inconsist- 
ency between the scientific findings in the earlier chapters and the 
analyses and conclusions in chapters 8 and 9. 

The review committee made numerous comments about such in- 
consistencies. 

To illuminate that point, I will mention some recurring themes 
in the review committee's report to the SAB. 

One, EPA adds together its estimates of the toxicity of all dioxin- 
like molecules without consideration of antagonistic interactions 
between and among them. 



37 

Moreover, the majority of the committee concluded that PCBs, 
which account for up to 50 percent of the risk EPA associates with 
dioxin-Hke molecules, are sufficiently different from dioxin "that 
they should not be part of this document." 

I must apologize. My references to page numbers are to draft 
4(A) of the committee report, which is not the final draft. So you 
just have to paw through it to find it. 

Two, almost all the toxicity data were derived at high dose levels, 
and EPA inadequately describes its methods for extrapolations to 
risks at lower doses and provides insufficient justification for its 
choice of methods. 

Three, a molecule present in every cell, the Ah receptor, is con- 
sidered important to dioxin's mechanism of action but it is not 
factored into EPA's risk assessment, nor is any other receptor mol- 
ecule. 

Four, had EPA considered a model that includes a receptor mol- 
ecule, the model would predict a nonlinear and/or a threshold con- 
taining dose-response curve. Either of those characteristics would 
have produced risk estimates lower than those produced by EPA. 

Five, EPA classifies dioxin as a complete carcinogen, a molecule 
capable of causing all the steps that led to cancer. 

The committee concludes that dioxin "is not a complete carcino- 
gen and thus to avoid confusion should not be designated as such." 

The second issue I will comment about is whether EPA's risk es- 
timates are based on results from exposing animals to high doses 
of dioxin and extrapolating fi-om those results to estimates of 
human risk at much lower exposure levels. 

In general, that is the case. To a major extent, it is inevitable. 
If toxic effects are noted in animals, concerns understandably are 
raised about possible human risk. 

The crux of the EPA reassessment is that animal studies indicate 
that toxic effects can occur at exposures 10 to 100 times above 
those experienced by humans in the general population. 

EPA goes on to say that some segments of the population may 
be exposed to such levels. 

In contrast to EPA's conclusion, the review committee concluded 
that the only human effect that is "clearly established as being re- 
lated to TCDD," that is dioxin, "exposure" is chloracne. 

That skin disease has been seen only in humans exposed to very 
high levels of dioxin. It does not result from environmental expo- 
sures. 

The committee urged EPA to consider carefully the soon to be 
published results of the Air Force study of the men who sprayed 
Agent Orange. 

As discussed at public meeting in February 1995, only a handful 
of diseases and possibly clinically significant conditions is elevated 
in the dioxin-exposed men, and any connection between dioxin and 
those end points is more of a puzzle than an explanation. 

EPA uses two methods to compare animal doses that cause toxic 
effects to human exposure levels. As can be seen by inspecting 
EPA's tables in chapter 9, conventional dose-rate comparisons as 
used by every other agency in government, so far as I know, show 
that most toxic effects in animals occur at doses 1,000 to 100,000 



38 

times higher than human exposure rates, indicating an ample mar- 
gin of safety for humans. 

On the other hand, standing apart from all other agencies in 
methods of risk estimation, EPA interprets some body burden com- 
parisons that suggest human exposures are much closer to those 
associated with toxic effects in animals. 

The committee asked that EPA review that line of reasoning and 
justify its decisions. 

EPA's summarizing statements are very dramatic. For instance, 
"It is not currently possible to state exactly how or at what levels 
humans in the population will respond. But the margin of exposure 
between background levels and levels where effects are detectable 
in humans in terms of TEQs," which is a total risk from all dioxin- 
like molecules, "is considerably smaller than previously estimated." 

This statement provides no direction for research or conclusions 
because of its vagueness. As the committee commented, "The last 
sentence of the above conclusion, re MOE, is, in the opinion of 
most, but not all, of the committee, thought to be highly specula- 
tive and needs to be reexamined. 

In effect, it states that we don't know what will occur or at what 
level this unknown response will occur, but we know that it will 
occur in terms of total dioxin exposure closer to background levels 
than previously estimated." 

Another EPA summary statement also drew a specific comment. 
This is a quote from EPA. "Based on all of the data reviewed in 
this reassessment and scientific inference, a picture emerges of 
TCDD," that is, dioxin, "and related compounds as potent toxicants 
in animals with the potential to produce a spectrum of effects. 

Some of these effects may be occurring in humans at very low 
levels, and some may be resulting in adverse impact on human 
health." 

As the committee reports states, "It is difficult to determine what 
EPA is inferring in the last sentence of the above-cited conclusion. 

If it is intended to state that adverse effects in humans may be 
occurring at near current exposure levels, it is the committee's 
judgement that EPA has not submitted findings that support ade- 
quately this conclusion." 

I want to thank you for this opportunity to testify, and I will be 
happy to answer any questions. 

[The prepared statement of Dr. Gough follows:] 



39 

Testimony of Michael Gough, PhD* 

before the 

Committee on Science 

U.S. House of Representatives 

December 13, 199 5 



* Government expert member of Dioxin Reassessii.t=n Review Committee 
of the EPA Science Advisory Board. 



40 



2 

Good morning, Mr. Chairman and Committee members. I am 
Michael Gough, and earlier this year, when I was employed at the 
Office of Technology Assessment, I was a government expert member 
of EPA's Science Advisory Board's Dioxin Reassessment Review 
Committee. I have been involved in analysis and writing about 
dioxin since 1980 when I was put in charge of OTA's congressionally 
mandated oversight of Executive Branch research into the possible 
health effects of exposures to dioxin-contaminated Agent Orange 
during the Vietnam war. My book Dioxin. Agent Orange was published 
in 1986, while I was in the private sector, and I now have a 
contract to write a second book about dioxin. I have written a 
number of papers about dioxin, and I chaired a Department of 
Veterans Affairs Advisory Committee about the care of Vietnam 
veterans and the Department of Health and Human Services Committee 
to review the United States Air Force's on-going 2 0-year-long study 
of the health of the men who sprayed 90 percent of the Agent Orange 
used in Vietnam. Since OTA closed on September 30, I have accepted 
a position at the Cato Institute that will begin at the first of 
the year. 

The letter of invitation for this hearing mentions four 
specific issues to be considered. I have little to say about two 
of those: I do not know why EPA wrote chapter 9, the Risk 
Characterization Chapter (and part of chapter 8 about risk models) 
in-house, and I do not know why chapter 9 was less extensively peer 
reviewed than the other chapters before the committee review. 
Nevertheless, the statement in the invitation letter that the 



41 



3 
chapter was not peer reviewed appears too absolute. I have seen 
comments on an earlier draft of chapter 9 that were written at the 
U.S. Department of Agriculture and at the Food and Drug 
Administration. The second issue that I will not address is the 
economic impacts of dioxin regulation. 

The first issue that I will discuss is the question about 
inconsistency between the scientific findings in the earlier 
chapters and the analyses and conclusions in chapters 8 and 9. The 
review committee made numerous comments about such inconsistencies. 
To illuminate that point, I will mention some recurring themes in 
the review committee's report to the SAB: 

1. EPA adds together its estimates of the toxicity of all 
dioxin-like molecules, without consideration of antagonistic 
interactions between and among them. The compounds other than the 
one commonly called "dioxin" account for 90 percent of EPA's risk 
estimate, and hardly anything is known about any of them. 
Moreover, a majority of the committee concluded that PCBs, which 
account for up to 50 percent of the risk EPA associates with 
dioxin-like molecules are "sufficiently different from . . . [dioxin] 
... that polyhalogenated biphenyls [PCBs and related molecules] not 
be a part of this document" (p. 59) . 

2. Almost all the toxicity data were derived at high dose 
levels, and EPA inadequately describes its methods for 
extrapolation to risks at lower doses and provides insufficient 
justifications for its choice of methods. 

3. A molecule present in every cell — the Ah receptor — is 



42 



4 
considered important to dioxin's mechanism of action, but it is not 
factored into EPA's risk assessment (nor is any other receptor 
molecule) . On the other hand, the committee also criticized EPA 
for invoking the initial binding of dioxin to the Ah receptor as a 
harbinger of many toxic effects with no evidence for any connection 
and no knowledge of any kinetics between the binding and the 
effect. 

4. Had EPA considered a model that includes a receptor 
molecule, the model would predict a non-linear and/or a threshold 
containing dose response curve. [Either of those characteristics 
would have produced risk estimates lower than those produced by 
EPA.] 

5. EPA classifies dioxin as a complete carcinogen — a 
molecule capable of causing all the steps that lead to cancer. The 
committee concludes that dioxin "is not a complete carcinogen and 
thus to avoid confusion should not be designated as such" (p. 65) . 
[This is an important distinction because low level exposures to 
incomplete carcinogens, in most people's minds, is much less risky 
than exposure to complete carcinogens.] 

The committee report is full of criticisms, but it also 
praises EPA in some places. In general, however, the praise was 
given to summaries and reviews of data, and the criticisms were 
addressed at the risk characterization. 

The second issue that I will comment about is whether EPA's 
risk estimates are based on results from exposing animals to high 
doses of dioxin and extrapolating from those results to estimates 



43 



5 

of human risk at much lower exposure levels. In general, that is 
the case. To a major extent, it is inevitable. When toxic effects 
are noted in animals, concerns, understandably, are raised about 
possible human risks. 

EPA used human data to discount possible associations between 
dioxin and many human cancers. Both EPA and the committee fix on 
soft tissue sarcomas as the only human tumor that can reasonably be 
associated with dioxin. [I disagree with that association, and I 
fully expect that it will weaken with the passage of time and 
careful consideration of available data and new data that will 
become available. ] 

The crux of the EPA reassessment is that animal studies 
indicate that toxic effects can occur at exposures 10- to 100-times 
above those experienced by humans in the general population. EPA 
goes on to say that some segments of the population may be exposed 
to such levels. 

In contrast to EPA's conclusion that segments of the 
population might be suffering multiple adverse effects from dioxin 
exposures, the review committee concluded that the only human 
effect that is "clearly established as being related to TCDD 
[dioxin] exposure" is chloracne [p. 55]. That disease has been 
seen only in humans exposed to very high levels of dioxin; it does 
not result from environmental exposures. 

The committee urged EPA to consider carefully the soon-to-be 
published results of the Air Force study of the men who sprayed 
Agent Orange. The current concentrations of dioxin in the bodies 



44 



6 
of those thousand men are known, and the data provide a rich source 
of information. As discussed at a public meeting in February 1995, 
only a handful of diseases and possibly clinically significant 
conditions is elevated in the dioxin-exposed men, and the 
connection between dioxin and those endpoints is more of a puzzle 
than an explanation. EPA's examination of the Air Force data and 
data from other studies of dioxin-exposed humans should enable the 
agency to compare its estimates from animal studies to measurements 
in humans. 

EPA uses two methods to compare animal doses that cause toxic 
effects to human exposure levels. The first is the conventional 
method, used by all other agencies and governments, that compares 
the amount of dioxin inhaled or ingested per unit of body weight 
per day. The other is a comparison of the average concentration of 
dioxin in an adult human after a life-time of low-level exposure to 
the (usually estimated) concentration in animals following a single 
exposure or exposure of a few weeks to much-higher-than-human 
exposures. 

As can be seen by inspecting EPA's tables in chapter 9, 
conventional dose rate comparisons show that most toxic effects in 
animals occur at doses 1000 to 100, 000-times higher than human 
exposure rates, indicating that there is an ample margin of safety 
for humans. On the other hand, EPA interprets some body burden 
comparisons to suggest human exposures are much closer to those 
associated with toxic effects in animals. The committee asked that 
EPA review that line of reasoning and justify its decisions. 



45 



EPA's summarizing statements are very dramatic: For instance, 

It is not currently possible to state exactly how or at 
what levels humans in the population will respond, but 
the margin of exposure (MOE) between background levels 
and levels where effects are detectable in humans in 
terms of TEQs [total risk from all dioxin-like molecules] 
is considerably smaller than previously estimated. 
(Chapter 9, p. 81) 

This statement provides no direction for research or conclusions 

because of its vagueness. As the committee commented: 

The last sentence of the above quoted conclusion (re MOE) 
is (in the opinion of most, but [not] all of the 
Committee) thought to be highly speculative and needs to 
be reexamined. In effect, it states that we don't know 
what will occur or at what level this unknown [response] 
will occur, but we know that it will occur (in terms of 
TEQs) closer to background levels than previously 
estimated (p. 92) . 

Another EPA summary statement also drew a specific comment: 

Based on all of the data reviewed in this [dioxin] 
reassessment and scientific inference, a picture emerges 
of TCDD [dioxin] and related compounds as potent 
toxicants in animals with the potential to produce a 
spectrum of effects. Some of these effects may be 
occurring in humans at very low levels, and some may be 
resulting in adverse impacts on human health (Chapter 9, 
p. 87) . 

As the committee report states. 

It is difficult to determine what EPA is inferring in the 
last sentence in the above cited conclusion. If it is 
intended to state that adverse effects in humans may be 
occurring near current exposure levels, it is the 
Committee's judgement that EPA has not presented findings 
that support adequately this conclusion (p. 94). 

I want to thank you for this opportunity to testify, and I 

will be happy to answer any questions. 



46 

Mr. ROHRABACHER. Dr. Gough, thank you very much. 
And we will recess now until after this first vote. Thank you very 
much. 

[Brief recess.] 

Mr. RoHRABACHER. This hearing is called to order. 

Dr. Lucier, would you like to proceed? 

STATEMENT OF GEORGE W. LUCIER, PH.D., DIRECTOR, ENVI- 
RONMENTAL TOXICOLOGY PROGRAM, NATIONAL INSTITUTE 
OF ENVIRONMENTAL HEALTH SCIENCES 

Dr. Lucier. Thank you. Good morning. I am George Lucier, di- 
rector of the environmental toxicology program at the National In- 
stitute of Environmental Health Sciences, one of the 17 institutes 
of the National Institutes of Health. 

My research on dioxin is attempting to identify and fill knowl- 
edge gaps which create uncertainty in risk assessment. 

These findings are published frequently in the peer reviewed sci- 
entific literature. Of my roughly 200 publications, scientific publica- 
tions, about one third of them deal wholly or in part with dioxin. 

My involvement with EPA's reevaluation of dioxin's risks has 
spanned nearly four years and contributed to the preparation of 
two of the nine chapters constituting the health effects document. 

The reevaluation of dioxin's risks by EPA represents the most 
visible effort by a U.S. regulatory agency to move away from de- 
fault methodologies and to incorporate all relevant information in 
the decision process. 

The use of information on mechanism is an important step in re- 
ducing uncertainty. 

I would now like to comment on specific scientific issues within 
the framework of risk assessment for dioxin and related chemicals. 

Regarding hazard identification, dioxin causes a number of ad- 
verse effects in experimental animals, and some of these effects 
have been associated with high dioxin exposure in humans. 

In regard to cancer, 17 studies have been conducted in rodents 
and all are positive 

Mr. ROHRABACHER. Excuse me. Could you please repeat what you 
just said a few moments just before that? 

Dr. Lucier. In regard to cancer? 

Mr. ROHRABACHER. In animals and in humans. Because that is 
something that has been disputed, I think. 

Dr. Lucier. It says dioxin causes a number of adverse effects in 
experimental animals, and some of those effects have been associ- 
ated with high dioxin exposure in humans. 

Mr. ROHRABACHER. Okay. Could you tell me what that means? 
And then you could go on. 

Dr. Lucier. That means that when you look at dioxin body bur- 
den, say, from an environmental or occupational exposure and look 
at cancer incidence in the population that has those burdens, there 
is an association between the two; dioxin concentrations, which, in 
this case, as I had said, were high, and that adverse outcome, such 
as cancer. 

Mr. ROHRABACHER. In terms of the relationship between how it 
affects animals and humans. 



47 

Dr. LuciER. My statement merely was that dioxin causes cancer 
in experimental animals. 

Mr. ROHRABACHER. Right. 

Dr. LuciER. And there is an association with high dioxin expo- 
sures in humans either from environmental or occupational set- 
tings and cancer in humans. This doesn't prove that dioxin is caus- 
ing that cancer, it merely says that there is an association. 

Mr. ROHRABACHER. Right. 

Dr. LuciER. Which means that the 

Mr. ROHRABACHER. In other words, the same dioxin that caused 
the cancer in the animals causes the health impact on humans in 
a high dose. 

Is that what you're saying? 

Dr. LuciER. Yes. 

Mr. ROHRABACHER. Okay. Go right ahead. Sorry. 

I just wanted to make sure I understood that exact point. 

Dr. LuciER. Okay. 

And I will say my next sentence even though it reiterates what 
I just said. Epidemiology studies on humans exposed to dioxin at 
high doses provide evidence that dioxin is a human carcinogen, al- 
though the influence of confounding factors cannot be entirely ruled 
out. 

Dioxin also produces a number of noncancer effects in experi- 
mental animals, such as birth defects, reproductive problems, 
neurologic disorders, and hormonal alterations. 

Recent studies in humans suggest that some noncancer effects 
may also occur in humans exposed to high doses. 

Dioxin also causes a vast array of hormonal, molecular, and bio- 
chemical effects, some of which are likely involved in the adverse 
health effects. 

It has been called, with good reason, an environmental hormone 
or endocrine disrupter. 

My bottom line on hazard identification are that dioxin should be 
considered a probable human carcinogen and that noncancer effects 
of dioxin and related compounds are a public health concern. 

Current estimates are that adults in the U.S. are exposed to ap- 
proximately 10 picograms of the prototypical dioxin TCDD every 
day. 

For reference, this amount is equivalent to about one-trillionth of 
an ounce. Dioxin exposure in the general population comes pri- 
marily from consuming contaminated foodstuffs. 

The current average exposure levels of American adults is 10 to 
20 times higher than the exposure level that EPA estimates could 
cause up to one cancer in a million people exposed over their life- 
times. 

EPA and other risk assessors acknowledge that the actual risk 
could very well be lower. 

Human risk estimates should include an evaluation of numerous 
other environmental chemicals that act through the same mecha- 
nism as TCDD. For example, there are 75 different dioxins and 
over 100 different chlorinated dibenzofurans and some dioxin-like 
PCBs. 



48 

Dioxin is a persistent chemical in the human body and in the en- 
vironment. For example, a biological half-life of dioxin in humans 
is 7 to 109 years. 

Dioxin is found preferentially in fat, which means that fatty tis- 
sues and human milk contain significant amounts of dioxin. 

Based on human milk concentration data, newborns who 
breastfeed for 6 to 12 months receive a dose of dioxin while nursing 
approximately 15 times higher than the average adult in the Unit- 
ed States. Although this exposure level is of concern, the benefits 
of breastfeeding certainly outweigh the risk. 

The summary of my comments on human exposure is that every- 
one has some dioxin in their bodies and, because of its biological 
persistence, everyone alive today will retain dioxin in their bodies 
through their lifetimes even if their exposures cease now. 

The component of risk assessment that generally creates the 
most uncertainty is dose-response evaluation, and dioxin is no ex- 
ception. 

While there is considerable data to support the claim that dioxin 
produces adverse health effects in humans, at least at high doses, 
there is legitimate scientific debate regarding health effects at 
lower doses. 

What is needed is the development of credible biologically based 
models for estimating human risk from exposure levels encoun- 
tered from day-to-day living. 

There has been debate regarding the relevance of rodent data in 
estimating human risk. I believe that there is considerable evi- 
dence to support the use of rodent data. 

First, rat or mouse cells, like human cells, contain the Ah recep- 
tor, which is necessary for most, if not all, of dioxin's effects. 

Second, the amount of dioxin-like, chemicals required to elicit 
changes in gene expression, is approximately the same in both rats 
and humans. 

Third, the spectrum of toxic effects is somewhat similar in rats 
and humans. However, the half-life of dioxin in rats is 25 days 
compared to 7 to 10 years in people. 

This means that if rats and humans each had equivalent doses 
of dioxin for 2 years, daily doses, humans would have 100 times 
more dioxin in their bodies than would rats. This needs to be 
factored in when using rodent data to estimate human risk. 

In summary, EPA has asked for and received considerable input 
from the scientific community in their reevaluation of dioxin's 
risks. 

This information raises concerns about current levels of human 
exposure to dioxin and dioxin-like chemicals. EPA's risk character- 
ization, I believe, is correct in expressing that concern. 

This conclusion is based on information present in the back- 
ground chapters which were peer reviewed in 1992 and '93. 

However, this statement does not mean that adverse health ef- 
fects have been shown to occur as a consequence of current expo- 
sures of the general population of the U.S. 

The risk characterization does suffer from the need to condense 
2,000 pages of background into a 50-page characterization. 

The selection of supporting information may have caused some of 
the concerns expressed by the Science Advisory Board. 



49 



This ongoing review, as documented by Dr. Farland, when com- 
pleted should improve the risk characterization chapter 

Fmally, EPA's reevaluation of dioxin's risk has been and remains 
a dauntmg task I believe that EPA has conducted an extraor- 
dmanly open and scientifically based assessment 

Thank you. 

[The prepared statement of Dr. Lucier follows:] 



50 



Testimony of George W. Lucier, Ph.D. 

Director 

Environmental Toxicology Program 

National Institute of Environmental Health Sciences 

Before the House Committee on Science 

Subcommittee on Energy and Environment 

December 13, 1995 

Good morning, I am Dr. George Lucier, Director of the Environmental Toxicology 
Program at the National Institute of Environmental Health Sciences (NIEHS), one of 17 
institutes at the National Institutes of Health (NIH). I have conducted research at NIEHS 
for 25 years and have published nearly 200 papers in the peer-reviewed scientific literature. 
Roughly 1/3 of them address wholly, or in part, health effects of dioxin. My current research 
on dioxin and related chemicals is attempting to identify and fill knowledge gaps which 
create uncertainty in risk assessment. These studies are multidisciplinary and attempt to 
integrate data from experimental systems, human samples and molecular mechanisms of 
action. 

My involvement with EPA's reevaluation of dioxin's risks has speinned nearly four years 
and has contributed to the preparation of two of the nine chapters constituting the health 
effects documents. I was the lead author of the "Carcinogenicity" chapter, and I co-chaired 
the committee with Dr. Mike Gallo (Environmental and Occupational Health Sciences 
Institute of New Jersey) that prepared Chapter 8 on "Dose Response Evaluations." I also 
served on a Department of Health and Human Services (DHHS) committee which reviewed 
a preliminary draft of Chapter 9, the "Risk Characterization" chapter. The Public Health 
Service has played a key role in evaluating human health consequences from dioxin and in 
the risk communications part of the reassessment and has worked with EPA on this issue. 



51 



General Issues 

The purpose of the reevaluation was to use new information on dioxin's mechanism of 
action to improve estimates of risks at various exposure levels. The centerpiece of the 
reevaluation reflects the general scientific consensus that most, if not all, of dioxin's effects 
are mediated by a cellular receptor, which functions in a manner analogous to receptors for 
steroid hormones. I will come back to this receptor system later in my testimony. I believe 
that EPA has been extraordinarily thorough in involving the best scientific minds in the 
reevaluation process as chapter authors, members of peer-review panels for individual 
chapters, or as ad hoc members of the Science Advisory Board's review of the reevaluation 
document. It is safe to say that most of the top scientists in the dioxin arena have been 
involved in one way or another. 

The reevaluation of dioxin's risks by EPA represents the most visible effort by a U.S. 
regulatory agency to move away from default methodologies for estimating human risks and 
to incorporate all relevant scientific information in the decision process. Clearly, we don't 
know all that we would like to know about dioxin, and clearly uncertainty will remain in 
human risk estimates. The use of information on mechanism is a very important step in 
reducing uncertainty. Efforts such as this one will help restore public confidence in 
regulatory actions. 

I would now like to comment on specific scientific issues within the framework of risk 
assessment that impact on human health effects of dioxin and related chemicals. 



52 



Hazard Identification 

Dioxin causes a number of adverse effects in experimental animals and some of those 
effects have been associated with high dioxin exposures in humans. In regard to cancer, 17 
studies have been conducted in rodents and all are positive. Epidemiology studies on 
humans exposed occupationally or accidentally to dioxin at high doses provide evidence that 
dioxin is a human carcinogen although the influence of confounding factors cannot be 
entirely ruled out. Dioxin also produces a number of non-cancer effects in experimental 
animals such as birth defects, reproductive problems, neurologic disorders, and hormonal 
alterations, some of which occur at low doses. Recent studies in humans suggest that some 
non-cancer effects may also occur in humans exposed to high doses. In addition to adverse 
health effects, numerous studies in the scientific literature demonstrate that dioxin causes a 
vast array of hormonal, molecular, and biochemical effects some of which are likely involved 
in the adverse health effects described above. It has been called, with good reason, an 
environmental hormone or endocrine disrupter. I will come back to dioxin's effects later in 
my comments on dose-response relationships. 

As 1 mentioned earlier, it is generally accepted by the scientific community that most, if 
not all, of dioxin's effects require an initial interaction with a cellular protein called the Ah 
receptor. The Ah receptor, when bound to dioxin, can trigger changes in the function of 
genes, and it is those changes that most scientists think are an early and necessary event in 
the ability of dioxin to cause cancer and non-cancer effects. However, our knowledge of the 
precise way that changes in gene expression lead to toxicity is far from complete. It is this 
knowledge gap that creates much of the uncertainty in risk estimation at low exposure 



53 

levels. 

My bottom lines on hazard identification are that dioxin should be considered a 
probable human cju-cinogen and that non-cancer effects of dioxin and related compounds 
are of public health concern. 
Exposure Assessment 

Dioxins are produced in a number of ways. The key point is that the opportunity for 
dioxin production and contamination is present whenever heat, chlorine, and organic 
materials are together. The most notable historical sources of dioxin have been 
contamination of herbicides (e.g. agent orange), emissions from incinerators, and bleaching 
of paper although it should be noted that American paper industries have developed and 
applied new technology to dramatically decrease dioxin emissions during the paper-bleaching 
process. 

Current estimates are that adults in the U.S. are exposed to approximately 10 
picograms of the prototypical dioxin, 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) every day. 
For reference, this amount is equivalent to about 1 trilUonth of an ounce. Although this 
number is very small, dioxin is an extraordinarily toxic chemical. Dioxin exposure comes 
primarily from consuming contaminated foodstuffs. Current average exposure levels of 
American adults is 10-20 times higher than the exposure level that EPA estimates could 
cause up to one cancer in a million people exposed over their lifetimes. EPA and other 
risk assessors acknowledge that this cancer risk estimate is clearly conservative, and that the 
actual risk could very well be lower. 

It is important to recognize that human risks from dioxin must include an evaluation of 



54 



numerous other environmental chemicals that act through the same mechanism as TCDD. 
For example, there are 75 different dioxins, over 100 different structurally related 
chlorinated dibenzofurans and some dioxin like polychlorinated biphenyls (PCBS). In 
addition, brominated analogs of dioxins and furans are environmental contaminants. 
Toxicity of these chemicals appears to be proportional to the strength of their binding to the 
Ah receptor and the length of time that the chemical remains in the body. Thus, when 
appropriate scientific information is available, it is possible to calculate the total exposure to 
dioxin-like compounds and estimate risks of that exposure. Using this approach, it appears 
that only 5-10% of our exposure to dioxin-like chemicals is from the prototypical dioxin, 
TCDD. In other words, the average person is exposed to the equivalence of 100-200pg 
dioxin per day. 

Dioxins are persistent chemicals in the human body and in the environment. For 
example, the biological half life of dioxin in humans is 7-10 years. This means that if two 
molecules of dioxin enter your body today, one will be left 7-10 years from now. Dioxin is 
found preferentially in fat which means that fatty tissues and human milk contain significant 
amounts of dioxin. Based on human milk concentration data, newborns who breast feed for 
6-12 months, receive a dose of dioxin, while nursing, approximately 15 times higher than the 
average adult in the United States. Although, this exposure level is of concern, the benefits 
of breast feeding certainly outweigh the risks. 

The summary of my comments on human exposure is that human exposure to dioxins is 
broad-based (everyone has some dioxin in their bodies), and because of its biological 
persistence, everyone alive today will retain dioxin in their bodies for their lifetimes, even if 



55 



their exposure ceased now. 
Dose-Response Evaluation 

The component of risk assessment that generally creates the most imcertainty is dose- 
response evaluation, and dioxin is no exception. While there is considerable data to support 
the cl£iim that dioxin produces adverse health effects in humans, at least at high doses, I 
believe that there is legitimate scientific debate regarding health effects at lower doses. 
Data from experimental systems provide evidence that dose-response relationships for 
dioxin's effects on gene expression are likely linear; that is a proportional relationship 
appears to exist between exposure level and effect over a wide dose range. Therefore, it is 
fairly straightforward to estimate the magnitude of these kinds of responses outside the 
range of observable data. If we were confident that health effects caused by dioxin exhibited 
the same dose-response relationships as changes in gene expression, then risk assessment 
would be easy. A linear model would estimate risk with reasonable certainty. However, this 
is not the case. Our laboratory and others have shown that dose-response relationships for 
complex responses such as disease are different than those for changes in gene expression. 
We are conducting research to better understand the molecular and biological determinants 
of dose response, but we do not yet have the answer. Neither linear models nor threshold 
models (assume that there is an exposure level below which no effect occurs) are based on 
a solid scientific base. What is needed is the development of credible biologically-based 
models for estimating health risks from exposure levels encountered from day-to-day living. 
This effort should work towards such models for both cancer and non-cancer effects since it 
could be that adverse outcomes such as reproductive toxicity occur at lower exposure levels 



56 

than cancer. 

Relevance of Animal Models for Estimating Human Risks 

There has been considerable debate regarding the relevance of rodent data in 
estimating human risks. I believe that there is convincing evidence to support the use of 
rodent data. First, rat or mouse cells, like human cells, contain the Ah receptor which, as 
discussed earlier, appears essential for dioxin responses. Second, the amount of dioxin-like 
chemicals required to elicit changes in gene expression is approximately the same in both 
rats and humans. The human data has been obtained from people who were occupationally 
or accidentally exposed to dioxin. Third, the spectrum of toxic responses caused by dioxin 
in rats is similar to the spectrum of toxic effects associated with dioxin exposure in humans 
including cancer and reproductive p£u-ameters. The problem is that we don't have adequate 
data to determine low-dose adverse effects in rats although good data on molecular effects is 
available. I am reasonably confident, however, that the rat is an appropriate model for 
estimating human risks with one exception; that is, rodents clear dioxin from their bodies 
much more rapidly than observed in people. The half-life of dioxin in rats is 25 days 
compared to 7-10 years in people. This means that the chronic exposure level which 
produces a given body burden of dioxin in humans is approximately 100 times lower than 
that needed to produce the same tissue burden in rats. Conversely, if rats and humans each 
had the same daily intake of dioxin for two years, humans would have 100 times more dioxin 
in their bodies than would rats. This needs to be factored in when using rodent data to 
estimate human risks. 



57 

Summary 

EPA has asked for and received considerable input from the scientific community in 
their reevaluation of dioxin's risk. Taken together, information on human exposures and 
heahh effects, experimental studies and levels of environmental contamination provide 
evidence that we should be concerned about current levels of human exposure to dioxin and 
dioxin-like chemicals. EPA's risk characterization, I believe, is correct in expressing that 
concern. This conclusion is supported by information present in the background chapters 
which were peer-reviewed in 1992 and 1993. However, this statement does not mezm that 
adverse health effects have been shown to occur as a consequence of current exposures of 
the general population in the United States. The risk characterization does suffer from the 
need to condense 2000 pages of background into a 50 page characterization. The selection 
of supporting information may have caused some of the concerns expressed by the Science 
Advisory Board. This ongoing review when completed should improve the risk 
characterization chapter. Finally, EPA's reevaluation of dioxin's risks has been and remains 
a daunting task. EPA should be commended for conducting an extraordinary open and 
scientifically-based assessment. 



58 

Mr. ROHRABACHER. Thank you very much. 
Dr. Jones? 

STATEMENT OF KAY JONES, PH.D., PRESIDENT, ZEPHYR 
CONSULTING, SEATTLE, WASHINGTON 

Dr. Jones. Mr. Chairman, members of the committee, thank you 
for the opportunity to testify regarding EPA's dioxin reassessment. 

My comments are in response to the hearing charter. 

I have been involved in the risk assessment of dioxin impacts for 
some 15 years, have been closely involved in the whole reassess- 
ment process as a peer reviewer. 

Although I am in almost complete agreement with the EPA 
Science Advisory Board's review findings, I would like to discuss 
some other fundamental problems with the EPA's reassessment 
documentation and its premature use in setting emissions control 
policy and the agency^s issuance of regulatory orders. 

Some specific examples which illustrate my concerns are as fol- 
lows: 

EPA claimed at their regional office public announcements in 
September 1994 that it was seeking public input and peer review 
of the reassessment documents. 

If this were the case, why were EPA spokespersons clearly stat- 
ing that hospital and municipal waste incinerators were major con- 
tributors to current human dioxin exposure? Why did the same 
spokesperson suggest that a low beef consumption diet was an ap- 
propriate health protection measure? 

This preemption of the peer review process would be unaccept- 
able outside of government. 

EPA's reassessment stated that dioxin-like PCBs are a major 
contributor to our current body burden of dioxin-like compounds. 

Despite the significance of this contribution, the reassessment 
failed to address PCB exposure in a balanced fashion relative to 
dioxins. 

EPA's ORD staff conducted a screening risk assessment of an ex- 
isting waste energy facility in Columbus, Ohio, based on a meth- 
odology which was still under peer review. EPA Region 6 issued a 
regulatory order stating that the risk assessment results dem- 
onstrated a probable imminent health endangerment to the com- 
munity in Columbus, Ohio, creating hysteria among some citizens. 

Not only was the risk assessment result grossly exaggerated, the 
use of such RAs for imminent health endangerment declarations is 
totally inappropriate. 

Despite numerous appeals by the Solid Waste Authority of 
Central Ohio, EPA has refused to withdraw that risk assessment. 

EPA was engaging in the setting of overly strict standards on the 
dioxin emissions fi-om hospital incinerators during the reassess- 
ment review process, touting such emissions as being the biggest 
single identified source in the United States. 

Although the SAB pointed out that this estimate was probably 
high, based on new information, this was not the fact of the matter. 

It should have been impossible to make a 10- to 50-fold overesti- 
mate, given the availability of the requisite data prior to Septem- 
ber 1994. 



59 

This example underscores a lack of internal checks on the tech- 
nical validity of EPA staff work. 

EPA did not carry out a good-faith effort to inventory known 
sources of dioxin emissions as the SAB politely suggested. 

The European inventories contain many more sources which are 
also common to the U.S. but were ignored by EPA. It appeared to 
me that EPA has a pre-set agenda to emphasize the contribution 
of waste incineration while downplaying or ignoring other obvious 
or potential sources. 

EPA fully recognized the sensitivity of risk assessment results to 
its new proposed model relating dioxins in air to dioxins in grass 
and beef in 1992. 

It caused previous site-specific risk assessment cancer estimates 
to increase 100- to 10,000-fold. This conceptual model result was 
used by plaintiffs in the infamous East Liverpool, Ohio, hazardous 
waste incinerator test bum hearing that EPA has not conducted 
any field measurements since 1992 to verify this model which links 
unknown rural air levels of dioxins to our beef supply. 

More recent data from European research strongly suggests that 
EPA's new air-to-beef pathway model is no more significant than 
what was modeled prior to the issuance of the reassessment. 

I think the major misconception that the authors of chapter 9 
have is that they believe that they have applied the best science 
at hand in developing policy and taken regulatory actions prior to 
the orderly completion of the risk assessment process. 

They should understand that the technical hjrpotheses produced 
by EPA, or by any researcher, for that matter, are not a contribu- 
tion to science until they have been thoroughly peer reviewed. 

Good policy can only be based on good science. It cannot be based 
on anecdotal information or personal biases. 

I firmly believe that EPA should be a risk-based agency. 

In fact, most of EPA's past regulatory decisions took risk into ac- 
count in some fashion. The dilemma is how good are EPA risk as- 
sessment procedures? This is doubly important when EPA staff at- 
tempt to misapply existing scientific work. 

Poor policies will always emerge from poor risk assessments, as 
clearly demonstrated so far in the dioxin case. 

The major issue is how can we ensure that the agency conducts 
scientifically valid and balanced risk analyses in the future? 

Some form of a strict peer review procedure must be required if 
the risk assessment and regulatory functions are to remain in the 
same agency. 

Thank you. 

[The prepared statement of Dr. Jones follows:] 



60 



Testimony of 

Kay H. Jones Ph.D. 

before the 

Subcommittee on Energy and Environment 

of the 

Committee on Science 

U.S. House of Representatives 

December 13, 1995 



Thank you for the opportunity to testify regarding EPA's dioxin reassessment. 
My comments are in response to the four issues set forth in the Hearing Charter. I 
have been involved in the risk assessment (R/A) of dioxin impacts for some fifteen 
years and have been closely involved in the whole reassessment process as a peer 
reviewer. Although I am in almost complete agreement with the EPA Science 
Advisory Board's review findings, I would like to discuss other fundamental problems 
with EPA's reassessment documentation and its premature use in setting emissions 
control policy and the Agency's issuance of regulatory orders. Some specific 
examples which illustrate my concerns are as follows: 

• EPA claimed at their 1 regional office public announcements in September 1 994 
that it was seeking public input and peer review of the reassessment documents. If 
this were the case why were the EPA spokespersons clearly stating that hospital and 
municipal waste incineration were major contributors to current human dioxin 
exposure? Why did these same spokespersons suggest that a low beef 
consumption diet was an appropriate health protection measure? This grandiose 
preemption of the peer review process would be unacceptable outside of 
government. 

• EPA's reassessment stated that dioxin like PCBs are a major contributor to our 
current body burden of dioxins. (They in fact misused the research paper in making 
its estimate of the PCS contribution. Actually more than a 50% contribution as 
opposed to the 30% contribution reported by EPA.) Despite the significance of this 
contribution, the reassessment failed to address the PCBs in a balanced fashion 
relative to dioxins. 



61 



• EPA's validation of the air to beef model was addressed by the SAB, suggesting 
that the air-plant-animal pathway... "is a worthwhile hypothesis and may well be 
true. ..it can not be proved at this time." This statement clearly questions the claim that 
they have a valid model. In fact, the papers they have published which attempt to 
show model agreement with observed data do not employ statistical methods 
required by EPA superfund regulations. Despite these issues, EPA still used the 
model for regulatory purposes. 

• EPA ORD staff conducted a screening risk assessment of an existing waste to 
energy facility in Columbus Ohio based on the unvalidated air to beef model which 
was still under peer review. EPA Region V issued a regulatory order stating that the 
R/A results demonstrated imminent health endangerment to the community in 
Columbus, creating hysteria among some citizens. Not only was the R/A result 
grossly exaggerated, the use of such R/As for an imminent health endangerment 
declaration is totally inappropriate. Despite numerous appeals by the Solid Waste 
Authority of Central Ohio, EPA has refused to withdraw the R/A. 

• EPA was engaging in the setting of overly strict standards on the dioxin emissions 
from hospital waste incinerators during the reassessment review process, touting 
such emissions as the biggest single source in the U.S., i.e., 5100 out of 9300 gms 
toxic equivalence (TEQ). Although the Science Advisory Board (SAB) pointed out 
that this estimate was probably hiah based on new information this was not the fact of 
the matter. EPA had every opportunity during the development of its inventory to 
conduct an unbiased emission inventory of this class of waste incinerators, but failed 
to do so. It should have been impossible to make a 1 to 50 fold error given the 
availability of the requisite data prior to Sept. 1 994. This example underscores the 
lack of internal checks on the technical validity of staff work. This is only one among 
many that I documented during my peer review of the exposure chapters. 

• EPA did not carry out a good faith effort to inventory known sources of dioxin 
emissions as the SAB had politely suggested. European inventories contained 
many more sources which are also common to the U.S. but were ignored by EPA. It 
appeared to me that EPA had a preset agenda to emphasize the contribution of 
waste incineration while down playing or ignoring other obvious sources, e.g., iron 
sintering plants, secondary aluminum smelting, etc.. Although they appeared to 
weigh the possible uncertainty of estimates for different sources they failed to apply 
tneir criteria in an even handed manner to all potential sources. The potential 



23-557 0-96-3 



62 



contribution of diesel fueled mobile sources is a prime example. They also did not 
discuss the potential exposure differences among the sources they did inventory. For 
example, 24 municipal waste incinerators were responsible for more than 90% of this 
source categories total inventory. It is difficult to logically relate such a few isolated 
sources to impacts on our U.S. beef industry. 

• EPA fully recognized the sensitivity of R/A results to its new proposed model 
relating dioxins in air to dioxins in grass and beef in 1992. It caused previous site 
specific R/A cancer risk estimates results, to increase 100 to 10,000 fold. This 
conceptual model result was used by plaintiffs in the infamous East Liverpool 
hazardous waste incinerator test burn hearing. EPA has modified this model protocol 
on at least three occasions prior to the issuance of the reassessment and once this 
past summer. All of these changes reflected progressively lower risks associated 
with the air to beef transfer of dioxins. Yet EPA has not conducted any field 
measurements since 1 992 to verify this model which links unknown rural air levels of 
dioxins to our beef supply. More recent data from European research strongly 
suggests that EPAs "new air to leaf to beef pathway" is no more significant than what 
was modeled prior to the issuance of the reassessment. 

I think the major misconception that the authors of Chapter 9 have is that they 
believe they have applied the best science at hand in developing policy and taking 
regulatory actions prior to the orderly completion of the reassessment process. They 
should understand that technical hypotheses produced by EPA or by any researcher 
for that matter are not a contribution to science until they have been thoroughly peer 
reviewed. Good policy can only be based on good science. It cannot be based on 
anecdotal information or personal biases. 

I firmly believe that EPA should be a risk based agency. In fact, most of EPA's 
past regulatory decisions took risk into account in some fashion. The dilemma is how 
good are EPA risk assessment procedures. This is doubly important when EPA staff 
attempt to misapply existing scientific work. Poor policies will always emerge from 
poor risk assessments as clearly demonstrated so far in the dioxin case. The major 
issue is how can we insure that the agency conducts scientifically valid and balanced 
risk analyses in the future. Some form of a strict peer review procedure must be 
required if the risk assessment and regulatory functions are to remain in the same 
agency. 



63 

Mr. ROHRABACHER. Thank you very much, Dr. Jones. 

And I am going to ask one question myself. You know, we are 
looking at this assessment and its reassessment. 

And that is, and I hate to put Dr. Farland on the spot because 
you are the one who is actually in charge of what everybody is talk- 
ing about here. So you are going to get most of the heat in this 
hearing, although that is not the purpose to put you on the hot 
spot, but to discuss how you do your job. 

And let me ask you. Why was there a different peer review proc- 
ess for the final chapter, I guess, or chapters than for the rest of 
that reassessment? 

Dr. Farland. Mr. Chairman, we laid out the process that we 
were going to use to for the reassessment back in 1991 and '92 and 
detailed that quite extensively with the public. 

The approach that we decided to use was 

Mr. ROHRABACHER. During that time, was it right off the bat 
when you set down what we're going to do, you said the final chap- 
ters were going to different in terms of their peer review? 

Dr. Farland. We said that the risk characterization chapter 
would be developed and then it would be subjected to a public com- 
ment and a peer review by the SAB. 

And our intent was to have the SAB be the peer review of that 
risk characterization chapter. 

Frankly, one has to make a cut as to when you turn something 
loose to the public, and the decision that we made was to develop 
the document internally with the help of some outside scientists to 
use the extensive scientific expertise of Federal scientists and do a 
broad inside-the-govemment review of that document and then to 
send it to the SAB, giving the SAB the benefit of all of the public 
comment that we had received over 120 days of public comment pe- 
riod. 

And the SAB would be the peer reviewer. 

Why didn't we have another peer panel convened in between the 
development of our report, the Federal review and the SAB? In 
hindsight, the SAB tells us perhaps it would have been better if we 
had done that. 

But that isn't the way that we approached it. 

The question as to whether or not we would have been given 
some 

Mr. ROHRABACHER. So it would have been better, you are conced- 
ing it would have been better to actually follow that process and 
have his outside peer review? 

Dr. Farland. Personally, Mr. Chairman, I am not positively con- 
vinced of that. The SAB suggests that, and I will take their word 
for it. 

My sense is that we might very well have gotten 

Mr. ROHRABACHER. A moment ago I thought you were conceding 
that point. Excuse me. 

Dr. Farland. I was only qualifying that to say that I do agree 
that it may have been better. 

Mr. ROHRABACHER. Okay. 

Dr. Farland. In hindsight. 

The problem I 



64 

Mr. ROHRABACHER. What about in the future when you're doing 
other type reassessments then? Will you be, you won't have to work 
in hindsight then, you have got your understanding that you have 
achieved from hindsight now. 

Dr. Farland. Right. 

Mr. RoHRABACHER. Will you be doing that when you reach, the 
conclusions that you will be including outside peer reviewers in 
your conclusion as well as the accumulation of the facts? 

Dr. Farland. I think that, given the controversial nature of this 
particular topic and given the way that this has played out, I prob- 
ably would recommend having that type of a peer review. 

We certainly are going to have that tj^je of a peer review before 
we go back to the SAB with our characterization. 

So, the answer to that is "yes." 

Mr. ROHRABACHER. All right. And the — but your contention is 
that this is your strategy all along to have an outside — not to have 
the outside peer review for the final conclusions? 

Dr. Farland. The outside peer review was the SAB review. 

Mr. ROHRABACHER. Okay. 

Dr. Farland. In other words, they — one of the issues I think that 
is important here, Mr. Chairman, is that when we do these peer 
panels, we actually decide who the peer reviewers are going to be, 
and the SAB process is an independent process. 

And we felt that it was important that the last part of the proc- 
ess have a large group of independent scientists involved in the re- 
view. 

There were a lot of debates through the course of the develop- 
ment of this process as to when and how peer reviews would be 
done. 

We made the decision to rely heavily on the SAB as an independ- 
ent peer reviewer of our final document. 

Mr. ROHRABACHER. Dr. Gough, do you have a question for Dr. 
Farland? 

Dr. GouGH. Well, yeah, I have a couple of questions. 

I was surprised when you said that — I am not surprised that you 
say you can accommodate the reviewers' comments. 

I am surprised when you said they were minor, they were sort 
of minor, because one of the criticisms of chapter 9 is its reliance 
on the default assumption of a linearized no-threshold model for 
carcinogenicity, whereas chapters 1 through 7 develop a great deal 
of information about receptors. 

And at least a majority of the people on the committee would 
think that the linearized multistage dose-response model is not ap- 
propriate for a receptor-mediated toxic event. 

And it seems to me that since this is a deviation from longstand- 
ing policy within the agency, this is not a minor change. 

Mr. ROHRABACHER. Now, the reason why that I had Dr Gough 
ask that question is because I am sure there are people in the sci- 
entific community that understand that question. 

[Laughter.] 

I don't know how many people on this panel understand it or this 
committee understand it, but I am sure it's an important question, 
and we need to make sure that people are on the record on even 
issues that the committee doesn't understand. 



65 



So, Dr. Farland, would you like to- 



Dr. GOUGH. I can make an effort to explain it, if I may. 

Mr. ROHRABACHER. All right. 

Dr. GouGH. Okay. 

Mr. ROHRABACHER. But let's not make it too long because I would 
like to ask the other panelists. 

Dr. GouGH. Well, I am also hampered. I can only gesture with 
one arm. 

[Laughter.] 

Mr. ROHRABACHER. But has someone been twisting your arm? 

[Laughter.] 

t)r. GouGH. But for most toxic events, most toxic effects, we 
think there is a threshold that you — that the human body or an 
animal can tolerate a certain number of insults without being 
pushed over into any toxic consequence. 

According to the default assumption that EPA uses for carcino- 
gens, there is no threshold, that at high doses there is a high prob- 
ability of cancer, at lower doses there is a lower probability of can- 
cer, but the probability of cancer does not reach zero until the dose 
is zero. 

And what the people on the committee for the SAB said was that 
if you consider the biology that is involved in dioxin, it seems inap- 
propriate now to use this model which associates risk, a direct rela- 
tionship between exposure and risk. 

Mr. ROHRABACHER. All right. 

Dr. Farland? 

Dr. Farland. Mr. Chairman, just a couple of comments in re- 
sponse to Dr. Gough. 

First of all, my statement was that these were perhaps minor in- 
consistencies. I said that I didn't think that there were inconsist- 
encies. 

I didn't say they were minor comments. And so, in fact, I think 
some of the comments are significant that we have, and I don't con- 
sider them to be minor. So that is just a point of clarification. 

The second point. The SAB report suggests that we used a de- 
fault approach for reaching the decision to use a linear model. 

As Dr. Gough said, the EPA's cancer guidelines suggest that in 
the absence of available information to inform you in terms of how 
to do that type of modeling, you use a linear model, which is likely 
not to underestimate the risk, probably does overestimate the risk, 
but in each case recognizing that the true risk might even be zero. 

It's an area of large uncertainty when you apply that type of a 
default, and that is recognized by the risk assessment community 
and the toxicology community. 

In the case of dioxin, in chapter 8 we developed a whole line of 
reasoning around why a linear model, not the default model, but 
a linear model was appropriate for dioxin. 

It had to do with the fact that just because it's a receptor-medi- 
ated response, there is no reason to believe that the early events 
will not be linear. 

This gets into some heavy chemistry about receptor and ligand 
interactions, but generally they follow the law of mass action, and 
that means that that event early in the process will be linear. 



66 

What we don't know is what happens after that, before you fi- 
nally get a cancer. And those may be nonlinear. But until we know 
how to draw that curve, our assumption is that because of the biol- 
ogy that is available on dioxin and because we are adding to a 
background of dioxin that we all carry around, and some effects 
that may very well be under way, an incremental exposure to 
dioxin should be modeled in a linear way, not using a default, but 
model it in a linear way. 

Mr. ROHRABACHER. Are you analyzing the cost that that t3rpe of 
approach will place on the society? 

Dr. Farland. Mr. Chairman, that comes into play when we do 
the regulatory economic analysis for these sorts of things, because 
one always wants to know how much uncertainty there is around 
these estimates and whether or not an upper-bound estimate on 
risk, like a linear model would produce, is the appropriate ap- 
proach to use, depending on the decision that will be evaluated. 

So, again, my concern right now is that we clarify in our report 
the use of whatever model that we agree with. The SAB 

Mr. ROHRABACHER. Which fits into what Dr. Lucier was saying 
about breastfeeding, I guess, that the cost, there is a risk, and even 
though it might be overestimated in analyzing, the benefits for 
your breastfeeding outweigh those. 

Dr. Farland. Absolutely. And, in fact, when we released the doc- 
ument, we also remarked that we thought that the report should 
not be the cause of people changing their diet, even though we did 
talk about dioxins in food, because the benefits of a healthy diet 
seem to us at this point to outweigh risks that may be associated 
with some small amount of dioxin in the diet for the general popu- 
lation. 

Mr. ROHRABACHER. But you are admitting that the approach that 
you are taking could well magnify the risk that is actually — the 
public is experiencing. 

Dr. Farland. There is no doubt that that is going to give an 
upper-bound estimate on risk. 

It's not likely the risk is going to be higher. It probably will be 
lower. 

Mr. ROHRABACHER. All right. 

Now, Dr. Lucier, you were complimentary of the EPA's reassess- 
ment. But yet the other scientists, you heard in my opening state- 
ment the quotes fi-om the other scientists who were not. 

Are you basically saying that you were in disagreement with 
those scientists that expressed their concerns? 

Dr. Lucier. There is clearly debate over, as you articulated in 
your opening comments, Mr. Chairman, about the dioxin issue, and 
as I stated in my testimony, that regarding dose-response relation- 
ships, there is a legitimate debate over the shape of the dose-re- 
sponse curve in the low-dose region now. 

We just had a discussion about the significance of that in rela- 
tion to receptor binding, and I have a few things to add to it. But 
I won't right at this time. 

I may come back later, if I have a chance. 

But most of the scientists who comprise the Science Advisory 
Board, it is my understanding fi*om reading it, were very com- 
plimentary about the reevaluation process. 



67 

They were especially complimentary about the background chap- 
ters which went into it and stating that they were comprehensive, 
well- written reviews. 

The main criticisms came into the risks, and those have already 
been talked about, the risk characterization chapter. 

Now, I think as I said in my testimony, I think the risk charac- 
terization did suffer from its need to condense those 2,000 pages of 
background into a much shorter document, and I think the ongoing 
review by the Science Advisory Board will help improve the risk 
characterization chapter. 

So, I don't see where my position and that of most scientists are 
in disagreement. 

Mr. ROHRABACHER. But in terms of those who did complain and 
the complaints that I acknowledged in my opening statement, you, 
I take it you disagree with those complaints? 

Dr. LuciER. Which complaint in particular, Mr. Chairman? 

Mr. ROHRABACHER. Well, let me get my opening statement. We 
will read to you the — if I can get it back, I will read you the exact 
quote that they were — while my staff is looking for that, do you 
have a question for any of the witnesses on the panel? 

Dr. LuciER. Yes. I wanted to make — it's part question and part 
comment regarding the receptor mechanisms. I will simply add to 
what Dr. Farland and Dr. Gough have already said, that if the 
changes in gene expression that are triggered by the Ah-receptor 
were clearly linked to toxic responses and we could show how they 
were linked, then the risk assessment would be easy. 

A linear model would be fairly accm-ate. 

However, we don't really understand what that link is between 
receptor binding, changes in gene expression and more complex bio- 
logical responses. 

In fact, my own laboratory has shown that the dose-response re- 
lationships for different kinds of responses to dioxin are much dif- 
ferent. 

And that has been articulated in some of the background chap- 
ters and maybe not articulated well enough in the risk character- 
ization chapter. 

Mr. ROHRABACHER. Do you have a question about that? 

Dr. LuciER. Yes. I would simply say that receptor modeling 
doesn't necessarily imply any particular shape to the dose-response 
curve. 

No dose response can be ruled in or out based solely on the 
knowledge that a response is receptor-mediated. 

Mr. ROHRABACHER. Okay. By the way, what I was asking you to 
comment on in terms of — was the letter to Science magazine a year 
ago, of the 18 scientists who worked on an early portion of the re- 
assessment which said, and I quote, that the EPA's conclusions 
"are heavily dependent on many unproved assumptions and 
untested hypotheses," and also "urge EPA to clearly distinguish 
regulatory policy from matters of scientific fact." 

I take it that you disagree with those 18 scientists? 

Dr. LuciER. Well, the 18 scientists weren't all part of the original 
process. 



68 

Some of them were involved later on. Some of them were, I 
mean, and a lot of the people who were involved did not sign that 
letter. 

I think it is consistent with the statement that there is legiti- 
mate debate in this arena. 

Mr. ROHRABACHER. So, if I can push a little bit, you think there 
is legitimate debate but you agree or disagree with what they stat- 
ed? 

Dr. LuciER. I agree with the risk characterization that current 
exposure levels of dioxin are a public health concern. 

I would be hard pressed to put a quantity to that level of con- 
cern. 

I think, as Dr. Farland and others have pointed out that and as 
I indicated in my testimony, the actual risk that is estimated may 
be much lower. 

This is clearly a conservative estimate. I would be hard pressed 
to quantitate that level of concern and wouldn't want to do that. 

Mr. ROHRABACHER. Okay. 

Dr. Jones 

Dr. Farland. Mr. Chairman? 

Mr. ROHRABACHER. Oh. Sure. Dr. Farland? 

Dr. Farland. Could I just weigh in on the issue of the science 
letter? Mr. Roemer introduced the issue of a spin to some of the 
documents that surround this reassessment, and this was one, I 
think, that has gotten a fair amount of spin, if you will allow me 
that. 

The letter basically says that these individuals were involved in 
the information collection process. Many of them were reviewers of 
drafts of the documents on panels that had been hired by various 
groups to review drafts that came out. 

Several of them were involved in our process. 

And the point, the point here that I want to make is that I agree 
that all risk assessments have these characteristics that they have 
said, and I agree with their suggestion to the scientific community 
that the broader scientific community needs to weigh in on these 
issues. 

Many of the people signed that letter because of those two 
things. 

They didn't sign it because it was critical of EPA's report. They 
signed it because we needed to involve the broader scientific com- 
munity in these issues. 

So, as much as I hate to endorse something that, because of spin 
has been suggested to be very critical of the report that I worked 
on, I do think there is some real legitimacy in the points that were 
made. 

Mr. ROHRABACHER. I think that is very well said. 

And Dr. Jones, and then I am going to turn to the rest of our 
committee here, but, Dr. Jones, would you have a question for any- 
one on the panel or a statement at this point? 

Dr. Jones. One of the things that has always been a question in 
my mind is that in the U.S. we have taken almost a totally inde- 
pendent approach to dealing with dioxin risks. 

In every other country that I am aware of, they have adopted a 
daily intake threshold of 1 to 10 picograms per kilogram per day 



69 

and have proceeded in orderly fashion to go out and find those 
sources of emissions, and usually they are specific sources, which 
may be contaminating milk or beef or something adjacent to those 
facilities, inventory those facilities, and gone about the business of 
reducing emissions from specific sources. 

I am really curious as to why we are off on that track and trying 
to treat dioxins as a zero-threshold pollutant. As you know, in 
chapter 9, it is heavily implied that we ought to make this a mini- 
mization approach and go out and control every conceivable source 
of dioxins we can find, which is obviously going to be extremely 
costly and probably misdirected. 

Mr. ROHRABACHER. Do you want to address that to Dr. Farland? 
I guess you do. 

Dr. Farland, would you like to answer that? 

Dr. Farlantd. Certainly. Just to address the last point that Dr. 
Jones made, there is nothing in chapter 9 that suggests that we 
are talking about trying to get rid of every last molecule of dioxin 
or any of the regulatory issues that are associated with dioxin. 

There are no regulatory directions given at all in this document. 

The second thing is that the World Health Organization, which 
actually determined a tolerable daily intake level for many coun- 
tries who use a World Health Organization recommendation, didn't 
rely on individual sources, didn't rely on the question of being close 
to an incinerator or something like that. 

They talked about a background level and how close that back- 
ground level was to where they saw effects in animals. 

They said that, given the fact that, in 1988, their assessment was 
that animal effects occurred at around 1 nanogram per kilogram 
per day and daily intakes were at about 10 picograms per kilogram 
per day, there was a 100-fold difference there, that was probably 
okay. About a factor of 100. 

They recognized that infants that were breastfeeding got more, 
but as Dr. Lucier said, they agreed that there were benefits to 
breastfeeding. At this time they didn't think that that exceedance 
of a tolerable daily intake should be problematic, but they would 
review it if new data came to light. 

In fact, what has happened is that new animal data suggest that 
effects are occurring at lower levels. We know more about different 
levels of dioxin and exposures in the general population and people 
on the tail of the distribution of the population, the ones that are 
more highly exposed. 

And so that margin of safety that the WHO talked about has 
shrunk. It is less than it was in 1988 when they made their state- 
ment. 

So the WHO is going back and is reevaluating whether or not 
that level, which is a management level, not a science level, it's a 
msmagement level, a tolerable daily intake, should be rethought. 

Mr. ROHRABACHER. I am going to make sure other members of 
the committee have a chance to ask. We will come back to that. 

I am very interested in this. For example, on the issue about 
whether the WHO is talking about animal effects and I know some 
people suggest that animal effects are not necessarily the human 
effects of dioxin, and when you are basing it on something like that 



70 

that those animal effects, how should we then put that into our 
own decision making process here? 

But I know that Ms. McCarthy has something to do, and if 
Chairman Brown will yield, we would be very happy to proceed. 

Ms. McCarthy? 

Ms. McCarthy. Thank you, Mr. Chairman. 

Thank you, Mr. Brown. 

Dr. Farland, I wanted to visit with you a little bit about the 
forthcoming Air Force study on Vietnam vets and their exposure to 
the spra5dng of Agent Orange during their service in the war. 

Mr. Gough raised this in his testimony, that EPA should exam- 
ine the findings of this study and therefore compare those studies 
on humans to your measurements on animals. 

I want to ask you about this forthcoming study and any limita- 
tions in it that might preclude you from actually making any un- 
ambiguous statements with regard to the effects of dioxin on 
human health. 

I am concerned that this study is a sample of men, that it does 
not deal with any of the intergenerational issues that we have been 
discussing here this morning, such as breastfeeding, and also that 
it really not take into consideration, in addition to gender dif- 
ferences, the health effects that might be different from acute expo- 
sure to high levels of dioxin versus chronic exposure to low levels 
of dioxin. 

How valuable will this forthcoming Air Force study be to you, 
and what might be any shortcomings in it that would preclude us 
finally bringing some resolution to this important issue for our vet- 
erans? 

Dr. GouGH. Ms. McCarthy, I think that you have raised a num- 
ber of the shortcomings that I would have suggested, in your com- 
ment. Again, this is adult males, and so we need to deal with the 
questions of the gender difference and certainly the age difference 
in response for dioxin. 

That is something that needs to be dealt with, and we will have 
to look for another study to deal with those. 

But that having been said, this is a very important study for us. 
The reason it's important is that these individuals have been fol- 
lowed for a number of years. 

Those individuals have given blood for dioxin analysis as well as 
being subjected to extensive clinical studies to look very carefully 
for disease, and the Air Force has done a good job in looking for 
associations between dioxin levels and various end points that they 
can measure in this particular population. 

Granted, they can't measure all of the ones we would like to look 
for in different ages and in women. 

We are working with the Air Force to look at the latest of their 
clinical evaluations. That has not yet been published. 

The evaluation took place in 1992, and it will be available soon 
in published form, and in fact we'll have some of the manuscripts 
shortly. I spoke with one of the principal investigators just within 
this past week about that. 

Secondly, I think that it is quite likely that continuing to follow 
this group will allow to look at the issue of long latency types of 
effects. 



71 

The problem that we will have is over time the dioxin levels drop 
and we don't know what happens if you have a situation like 
Saveso, Italy, where you get a very large amount of dioxin at one 
time and it drops over time, or in the case of some of our veterans 
there was an exposure over a few-year period. 

The levels are not extremely high; levels in these individuals are 
not hundreds of times higher than you and I have. 

They are higher, but they are not that much higher. 

So that those kinds of problems will make it difficult. It won't 
give us all the answers, but it will continue to be a very good study 
for us to evaluate, and we will work closely with the Air Force on 
that. 

Ms. McCarthy. So, the study itself will not resolve many of the 
uncertainties that exist but will indeed address some of them to 
your satisfaction, or it will take another ongoing study to finally re- 
solve these uncertainties? Could I have a bottom line here? 

Dr. Farland. I am not sure that we will ever be able to resolve 
all of the uncertainties with our Vietnam veterans, unfortunately. 

The situation is such that it becomes more and more difficult 
over time because the dioxins are going away as part of the natural 
process of clearing, even though that is a short time. 

But these studies will be useful to us in our understanding of the 
impact on biology. There are some effects that we can look at. 

Whether those effects are significant is something that will have 
to be very carefully analyzed in the sense that some of these may 
be adaptive responses to exposure to dioxin as opposed to some- 
thing that we would classify specifically as a health effect or an ad- 
verse impact or disease. 

So we have to sort those sorts of things out. Unfortunately, we 
will never have a definitive answer on those exposures, I am afraid. 

Ms. McCarthy. Well, the definitive answer is death, and it oc- 
curs every day to the veterans in my district. Some of them suffer- 
ing from peripheral neuropathy and other herbicide-related dis- 
eases, and our government, while we study and study and study, 
doesn't seem to share those findings in a positive way with the De- 
partment of Veterans' Affairs and others that c£in actually do some- 
thing to help these veterans. That is my overarching concern in all 
of this. 

I think the studies are necessary, but I really want to see them 
come to some sort of conclusion where we can actually then proceed 
to help the veterans who have been exposed and who have these 
diseases and are suffering. 

Dr. Farland. Yes. I would agree with you. 

Ms. McCarthy. Thank you. 

Thank you, Mr. Chairman, very much. 

Mr. ROHRABACHER. And now former Chairman Brown? 

Mr. Brown. Thank you, Mr. Chairman. 

I appreciate the testimony we have heard this morning. It is 
helped to bring me a little bit more back up to speed on a subject 
that I haven't dealt with very much in recent years. 

Let me ask you one broad question. Looking at the process as a 
whole for the review of this study and of chapter 9, would it be — 
or how would you evaluate overall the system? Is it working in a 
way reasonably close to what the Congress intended? Do we have 



72 

a process which has produced a reasonably objective and broad- 
ranging analysis of the risk involved here? Are there flaws in it? 
Is there conflicts of interest or other defects that have biased the 
study? Is there a better way we could go about it? In other words, 
are we on the right track or the wrong track with the existing risk 
assessment processes that we are using? 

And I would like each of you to comment briefly on it, not too 
long. Why don't you start out, Dr. Farland, since you've got the 
most at stake. 

[Laughter.] 

Dr. Farland. Mr. Brown, I think that we are evolving in our 
ability to do risk assessment and to involve the scientific commu- 
nity more broadly through both peer involvement and peer review. 

And so in that sense, I would say that the risk assessment proc- 
ess in bringing the best science to bear on science decisions and 
then that science into regulatory decisions is working. 

We still have some way to go. 

The biggest issue, I guess, is that we have to be sure that we 
don't find ourselves saying that one size process fits all. 

The decisions that are made daily at the EPA constitute risk as- 
sessments. Some of them turn into these multiyear efforts, like the 
dioxin assessment. 

I won't comment any further on the process that we have used 
with dioxin other than to say that I hope there won't be too many 
that will have to go through as many levels of review and working 
through consensus in the scientific community as we have done 
with dioxin. 

But clearly this is a process that is evolving. It's working, and 
it's bringing the best science to bear on these decisions. 

Mr. Brown. Working, but not perfect, then? 

Mr. Farland. I would say that is a good bottom line, sir. 

Mr. Brown. Dr. Gough? 

Mr. GoUGH. Well, the system is working, but it's not working — 
I don't think it's working so well as Dr. Farland indicates. 

In particular, as you have heard from this discussion, receptors 
are at the crux of understanding how dioxin works, and except for 
Dr. Lucier on one of the earlier chapters and not on the risk char- 
acterization chapter, I think somebody pointed out that nobody who 
wrote the risk characterization chapter was an expert in receptor 
biology. 

Moreover, no one, or very few people, on the Science Advisory 
Board's review committee was an expert on receptor biology. 

So the people who write the studies and the people who review 
the studies need to be selected with an understanding of where the 
important issues are going to be. 

The second thing that I think that I would like to comment on 
chapter 9 is that one thing that I would hope EPA walks away 
with fi-om this is that it has to exercise more discipline in its selec- 
tion of data. 

There are reports in the literature that exist, that exist as ab- 
stracts or very short papers with very little documentation and in 
some cases EPA treated those with the same seriousness as it did 
published papers that have been well replicated and with a lot 
more — with a lot more believability to them. 



73 

The last thing, and this just goes back to the chairman's com- 
ment to me about making ourselves understandable, one of the 
criticisms from the review committee was that EPA did not do a 
good job of presenting its explanations and its decision making 
process. And that, I am sure that will certainly be improved in this 
second go-round. 

Mr. Brown. Dr. Lucier? 

Dr. Lucier. Yes. Some general comments. 

Some related to the dioxin reassessment and some general issues 
regarding how we go about using more and the best science avail- 
able in the risk assessment process. 

EPA, in their reevaluation, really has, and as I said in my testi- 
mony, done an outstanding job in trying to bring all the science 
they can into the process to deal with all the areas that create un- 
certainty in risk assessment. 

I mean, one of those areas is dose response, how do we go about 
estimating low-dose human effects from higher dose animal data. 

We can only do this by bringing in the best science that is avail- 
able, not simply selecting a default approach, a linear model or 
threshold-based model which may not be necessarily based on good 
science. 

It also helps us select the most appropriate experimental system 
on which to base our human risk. Clearly, we don't want to wait 
to see adverse findings in humans before do something. 

So, if we have an experimental model because of knowledge of 
mechanism that would be predictive of what would happen in hu- 
mans, that would help us a lot in terms of improving the risk as- 
sessment process. 

The other point is sensitive subpopulations. If we know, as Dr. 
Gough said, that it's a receptor-mediated process, this does tell us 
something about whether there might be populations that might be 
unusually sensitive to dioxin's effects or whatever the chemical of 
interest is. 

Because of their genetic predisposition, they may contain a vari- 
ant of the receptor that may make them more responsive. 

They may be especially young and develop in differentiating sys- 
tems that would be more sensitive. Or there might be gender dif- 
ferences. 

Obviously, if something is acting like an environmental hormone, 
gender differences might be expected. 

It would also help us in exposure assessment in terms of picking 
up early lesions that might be predictive of response. 

What I would like to see is, after having said all that, a review 
of the process that EPA has undertook by all the interested parties 
and say we all want to use the best science possible in risk assess- 
ment, how can we streamline the process so it doesn't take quite 
so long the next time around? 

Mr. Brown. Dr. Farland, you are going to look at that question, 
aren't you, after you get all through with this? 

Dr. Farland. We are going to. 

Mr. Brown. Because it is a very important question. 

Dr. Farland. We think that is going to be very instructive for 
us in terms of future assessments. 

Mr. Brown. Dr. Jones? 



74 

Dr. Jones. I just have three comments, and I mentioned those 
in my earher testimony. 

But number one is I think that in the process the peer review 
process should go along without so much fanfare as it did during 
this risk assessment where there was a perceived policy being 
enunciated at the same time that the peer review was going on. 

I was more involved with the background and the exposure sec- 
tions of the report and not the toxicology side. And one of the prob- 
lems I had is that those particular chapters were not handled in 
the same manner as the toxicology chapters, they were all done by 
internal staff with not a lot of outside inputs. 

And I think that had that taken place, I think that a lot of the 
problems with those chapters would have not been discovered by 
the SAB. 

And I think that those are my two main comments. 

Mr. Brown. Yes. 

Let me just, would the Chair indulge me to follow up briefly 
here? 

Let me ask. Dr. Farland, how does this assessment or reassess- 
ment compare on a scale of 1 to 10 with others that EPA has to 
do? Is this a major 10 or is it a 5 or is it a 1? Where does it rank? 

Dr. Farland. Mr. Brown, this is clearly an outlier on the curve. 

Mr. Brown. It's a 15? 

[Laughter.] 

Dr. Farland. Could be. 

We have — we have kidded, and I have made the joke in a lot of 
talks that I have given, that dioxin is not a chemical, it's a career. 

Literally, the EPA has been involved since 1980 in ongoing as- 
sessment. 

Mr. Brown. Yes. 

Dr. Farland. The documents that have been produced are all 
major works for the agency. The science that goes into them rep- 
resent thousands and thousands of publications out of the scientific 
literature. 

So, there is a tremendous amount of work that is going on on 
this class of compounds. One, because it is a very exquisite molecu- 
lar tool. 

It produces responses at very, very low levels. And so you can do 
intricate molecular biology, you can do all sorts of interesting 
science with it. All of those need to be factored in. 

So this is clearly an outlier in terms of our assessment activities. 

Mr. Brown. But by the same token, isn't what you're learning 
here vital to your ability to assess other kinds of toxicological in- 
sults to humans or other organisms? 

Dr. Farland. Absolutely. And as has been discussed here, this 
whole issue of trying to do risk assessment on receptor-mediated 
types of responses, chemicals that are hormone-like or hormone- 
memtic-t)^e compounds are out there in the environment; they are 
found in a number of commercial products and so on. 

We need to understand how to do risk assessment on receptor- 
mediated types of responses and what t3rpe of biology they invoke. 
This is a very good example of trying to do just that. 

Mr. Brown. Well, I am hoping, and I am sure the chairman 
would share this hope, that you are learning a great deal of the 



75 

science that is necessary to produce better risk assessments more 
effectively and cheaper than you have in the past. And you would 
concur with that, I presume? 

Dr. Farland. Mr. Brown, one of the things that is a hallmark 
of this particular assessment that we haven't discussed is the fact 
that the agency made a concerted effort to develop some of the crit- 
ical research data that might be needed as we started out on this 
risk assessment. 

Dr. Bimbaum and her colleagues have developed some very im- 
portant data in their laboratories over the past couple of years for 
this reassessment. 

Dr. Lucier and his colleagues at NIEHS have done a similar type 
of thing. And this is science being developed, peer reviewed, pub- 
lished, and brought directly into the risk assessment. 

And that's the way things ought to happen. 

Mr. Brown. I recall, you will forgive me for mentioning it, 25 
years go I used to interrogate EPA witnesses who would say, "We 
don't know the answer to this question and we need more re- 
search," by saying, "Fine, I think you ought to have the more re- 
search, but in another 10 years when I ask you the same question, 
I would think you would have the answer." 

Now I think I was naive and I should say, "Another 50 years I 
think you should have the answers," because these are questions 
that we were asking 25 years ago and we still don't have the an- 
swers to. 

Let me ask this one further question, Mr. Chairman. 

We, of course, have suffered from not having adequate sample of 
humans that we could expose and measure the results of exposure 
to dioxin here, and even the Air Force study, as has been men- 
tioned, is likely to be inadequate from that standpoint. 

"Would it be useful, or would you comment on whether it would 
be useful, to have a very large human population that has been ex- 
tensively exposed and includes both sexes to do this study on, and, 
if such a population is available, shouldn't we be making an effort 
to do that study, if there is such a population, of course? 

Dr. Farland. Mr. Brown, the most highly exposed population 
that is really diverse in terms of age and sex and so on was the 
Seveso population. 

Mr. Brown. The which? 

Dr. Farland. Seveso, Italy, population that was exposed be- 
cause 

Mr. Brown. What about the Vietnamese population that was 
subjected to the Agent Orange spraying over a period of years and 
included all of the same population? 

Dr. Farland. Again, those individuals would not have been what 
we would call very highly exposed. Most of the individuals that 
have been sampled are shown to be exposed and are higher than 
average, and they show the profile for an Agent Orange exposure. 

But they are not extremely highly exposed individuals, relatively 
speaking. 

Mr. Brown. Are you making that statement based upon an in- 
vestigation of the level of exposure of large populations in Viet- 
nam? Or are you hypothecating that? 



76 

Dr. Farland. I am making the statement based on what I know 
from the Hmited number of samples that are available from the Vi- 
etnamese population. 

Again, I can only go by that, not by a very broad-based discus- 
sion. 

We have talked about trying to expand the number of individuals 
that we have sampled in Vietnam, and I think the opportunity may 
very well be open to us now that was not open to us years ago. 

Mr. Brown. Yes. I am going to ask further, but if you have any 
information on it, would you describe any efforts being made to es- 
tablish an agreement with the Vietnamese for a joint study of the 
population that might have been exposed on this subject? 

Dr. Farland. I think it's probably worth mentioning here that 
there was a trip to Vietnam just within the last six months. 

Dr. Lucier might describe the work that he and some of the col- 
leagues did there. 

Dr. Lucier. We were asked, the NIEHS, where I work, was 
asked, to make a determination of what types of studies would be 
valuable to conduct in Vietnam to help shed some light about what 
effects, what the human effects are of dioxin because of the situa- 
tion that you describe. 

We went there about six months ago with a multidisciplinary 
team comprised of physicians, researchers, and are in the process 
of generating a report which will identify what those opportunities 
are. Of course, as you might expect, there are a lot of difficulties 
in doing studies in Vietnam. 

We are also in the process of developing an exchange agreement 
whereby we can train Vietnamese scientists in our laboratories to 
go back and do some of that work themselves. But a report is now 
being generated regarding the existence of opportunities, what dif- 
ficulties would have to be overcome to achieve those, and once we 
identify something that is an appropriate study, we will try and 
fund that through our granting mechanism, providing funding is 
available. 

Mr. Brown. Thank you. 

I won't take more time to explore these questions at this point, 
Mr. Chairman. 

Mr. ROHRABACHER. Thank you very much, Mr. Brown. 

Mr. Brown. Would the Chair indicate whether the record might 
remain open for some written questions? 

Mr. RoHRABACHER. The record will remain open for any written 
questions. 

If the panel will please, we will pass them on to the panel, and 
we would appreciate your answers. Both the answers and the ques- 
tions will be submitted for the record. 

Just as the former chairman brought up this, and Dr. Farland 
has mentioned the town in Italy, now I understand that that town 
in Italy that there was a major, some sort of a major explosion and 
the people were exposed to very high level of dioxins. 

Is this part of your reassessment? Do they mention that? And 
was there — has there been major health repercussions to this? 

Dr. Farland. Mr. Chairman, the accident took place in 1976. 
The first studies of cancer 10 years after the accident have been 
published now. 



77 

There may be some indication of cancer there, although it's very 
uncertain at this time. 

Ten years is not a long latency period for cancer. So perhaps the 
next set of 

Mr. ROHRABACHER. It's coming close to 20 years now. 

Dr. Farland. Right. But the study that has been done that has 
actually looked at the population is only for 10 years. The next up- 
date will be coming along, and, hopefully, we will get more infor- 
mation. 

Mr. ROHRABACHER. Well, at least for the first 10 years, there 
wasn't any major health repercussions from that inundation with 
dioxin? 

Dr. Farland. If there were, it was very uncertain. The clinical 
studies don't seem to show very much in those first 10 years. 

There are a number of reports in the literature that don't show 
a lot of effects. 

Mr. ROHRABACHER. Now, is this part of your reassessment? 

Dr. Farland. It is. 

Mr. ROHRABACHER. Okay. And I am also told that the French 
Academy of Sciences has issued a report which finds that there 
have been no fatalities recorded due to dioxin exposure, and the 
only documented health effects have been some sort of a skin dis- 
order that they've gotten, chloracne or something. 

Is this the case? 

Dr. Farland. I am familiar with the French Academy report. 
They did refer to chloracne. As Dr. Gough said, that is the one dis- 
ease that we know of that is related to high doses and that is 
known to occur in human populations. All of the others have lim- 
ited information and so, therefore, are uncertain as to whether they 
occur in human populations. 

Mr. ROHRABACHER. All right. So, what we're talking about here 
is a problem that is being studied. 

That's what your reassessment is all about. And it seems to me 
that we're talking about — and the reassessment is also very aware 
of the major costs that are involved in this society if indeed we run 
off with regulatory proposals that could have an impact on our 
competitiveness and also on the funds that are available in our so- 
ciety to do other things rather than worry about this particular 
area. 

Dr. Farland. Our intent would be to give the best science that 
we can to the decision makers that have to make those difficult de- 
cisions. 

Mr. ROHRABACHER. Okay. 

Mr. Brown. Mr. Chairman? 

Mr. ROHRABACHER. I would yield. 

Mr. Brown. Would you allow me to raise one question, perhaps? 
And you might like to answer it. 

It seems to me that the conclusion that has been expressed by 
some of the witnesses that better information about the dose-re- 
sponse curve and the degree to which it is receptor-mediated would 
result in lower risk assessments; that is, it would give us a lower 
boundary of what the risk was. 

And yet that is a profoundly important scientific question that 
requires a considerable amount of research. 



78 

It would seem that we should all agree that the funds expended 
on that kind of research, which would have the inevitable effect of 
lowering risk assessments and mediating the economic cost of ex- 
cessive regulation ought to be thoroughly supported. 

Mr. ROHRABACHER. I would be — I am in total agreement with the 
distinguished former chairman on that point. I think where my 
stress is is that when you're dealing with funding research, that is 
a worthy goal, especially in areas like this where there may, espe- 
cially when you're talking about Vietnam, where people were ex- 
posed, where there may be some risk to the population, and the re- 
search is absolutely justified in that expenditure of money.. 

But before there is something is proven to be a health risk, pass- 
ing regulations that will cost billions of dollars to the American 
people, is not justified. 

And what we are looking for is to make sure, and in this process 
of determining risk and what health risks are to the American peo- 
ple, that the regulations do not precede the determination of what 
that risk is and precede the science. 

If the science proves that there is a problem, yes, we will spend 
those billions of dollars that the regulations will cost, and it will 
cost — it will cost billions, if not hundreds of billions, of dollars to 
try to regulate dioxin out of our system. 

And that may be what we're going to do, but let's make sure that 
the science indicates that that expenditure is necessary, because 
those hundreds of billions of dollars are coming right out of other — 
of education, of other kinds of health care and of other things that 
are important to our society. 

So, I agree witii you that the expenditure on that research is — 
and your idea about Vietnam, I think, is very well taken. 

Mr. Brown. May I respond briefly, Mr. Chairman? 

Mr. ROHRABACHER. Yes, sir. 

Mr. Brown. I happen to agree with you that we do need, of 
course, to make sure that our regulations are based upon reason- 
able science. 

I don't think there is any disagreement with that. 

I would point out, however, that some of the cases in which the 
greatest hardship has occurred on industry and on the public has 
been from failure to regulate, at least in the eyes of some, and I 
cite the example of the chemical Alar, which was criticized for not 
being regulated, falsely, in my opinion, but the problem there was 
both lack of regulation and lack of science which would have al- 
lowed us to adequately respond to that situation. 

Mr. ROHRABACHER. I think the former chairman makes a good 
point, in the sense that if the government isn't doing its job, panic 
in the public can actually be a cost as well. 

And, Mr. Gough, do you have a comment on that? 

Dr. GoUGH. Yes. 

Well, I have — you said you would get back to us, and I am going 
to take advantage to just make a couple of statements. 

Mr. ROHRABACHER. All right. 

Dr. GouGH. One is, the Ranch Hands, the Air Force study of the 
men who were exposed in Vietnam, those men were exposed to 10 
to 100, depending on how you calculate it, were exposed to 10 to 
100 times the amount of dioxin that most of us are exposed to. 



79 

That is exactly the range of exposure that EPA says may cause 
adverse human health effects. 

It's a terribly important study. It does not involve women, it does 
not involve very young people, and it doesn't involve very old peo- 
ple. 

But it is a terribly important study, and I am glad that Dr. 
Farland acknowledged that, because in the draft that we saw in 
May, there was no mention of the Ranch Hand study as saying this 
did not occur, this did not occur, this did not occur. 

The EPA simply went through and picked out the three things 
that were elevated and said this shows that dioxin causes these 
things. 

The second thing I wanted to comment on 

Mr. ROHRABACHER. Excuse me. Could you repeat that? 

Dr. GOUGH. Yes. There was an earlier report from the Ranch 
Hand study. 

Mr. ROHRABACHER. Right. The whole point. The last point that 
you made. 

Dr. GouGH. That instead of EPA presenting a very balanced re- 
view of the Ranch Hand study, they had gone through and picked 
out the three — three end points which might have been elevated as 
a response to exposure dioxin and had not said a word about all 
of the other end points which were completely normal. 

Mr. ROHRABACHER. Let's have Dr. Farland answer that. 

Dr. Farland. In chapter 7, which is the human noncancer epide- 
miology chapter, there is an extensive discussion and review of the 
Ranch Hand data, and discussion of the range of clinical evaluation 
that was done and the fact that a number of those are showing 
nonpositive response, no response that seems to be associated with 
it. 

Mr. ROHRABACHER. Dr. Gough is suggesting that you have under- 
scored those few areas in which there was a negative response or 
a certain type of response but ignoring the other areas that would 
say that the people did not have some sort of problem caused by 
their exposure. 

Dr. Farland. Well, the issue that we're trjdng to address here 
is whether or not there are some effects being seen in human popu- 
lations within a factor of 10 to 100. 

We are quite convinced that there are lots of things that are not 
occurring because of dioxin. 

But there are a few things that appear to be occurring, and those 
are the ones that are highlighted in the characterization chapter. 

The fact that there are changes in testosterone levels in some of 
these men, the fact that there is a change in glucose tolerance and 
diabetes incidence in some of those men, and some other clinical 
manifestations needs to be very carefully looked at because this is 
a low-level exposure. 

Mr. ROHRABACHER. Dr. Gough, is it your point that the report 
did not go state what isn't happening? 

Dr. Gough. Yes, because 

Mr. ROHRABACHER. Is that what you're saying? 

Dr. Gough. If EPA makes a prediction, as it did, that adverse 
effects to the immune system and several other systems are occur- 
ring in exposures 10 to 100 times above background and there is 



80 

a population of human beings who have been exposed to that level 
and those end points are not elevated, it needs to be mentioned. 
And it was not mentioned in the risk characterization chapter, in 
chapter 9. 

The second thing is I am glad that Dr. Farland clarified the fact 
that they are not using the default assumption to derive the linear 
risk model. 

On the other hand, I think this exhibits an incredible bias. This 
is me talking now, this is not the committee. As Dr. Lucier said, 
we — and as Dr. Farland said — we don't know what happens after 
the initial binding of dioxin to the receptor. 

Most people regard the idea that it's a linear response to be very, 
very improbable; not impossible, we don't know yet. But it's very, 
very improbable. 

Yet, EPA is using a linear model which it says exaggerates and 
overestimates the cancer risk. I think that at the very least, and 
the Science Advisory Board review committee said too, that they 
should consider other models. And granted, it's hard. 

It's difficult. But it's not fair just to take just one and say this 
is the best we can do. 

Mr. ROHRABACHER. Well, we should let Dr. Farland answer that. 

Dr. Farland. Just briefly, and then Dr. Lucier may also have 
a 

Mr. RoHRABACHER, You both have about 2 minutes, and then I've 
got to run. 

Dr. Farland. Okay. I do think that it is important that we deal 
with this issue of the dose-response curve and the early events and 
their connection to frank disease. 

I mean, that is really the issue that we are dealing with here. 

We looked at the early events and asked whether or not they 
were linear, and they appear to be. We don't know about some of 
the other events, but the slope of the curve is about the same as 
the curves that we get out of the animal studies where we actually 
measure cancer. 

Again, there is uncertainty. 

We will use additional models. We will look at the alternatives 
and write that into the characterization. 

The suggestion of the SAB will be — will be taken. 

Mr. RoHRABACHER. Dr. Lucier? 

Dr. Lucier. Yes. If I could just say something quickly about that. 

Those early events that everyone are talking about really have 
to be added onto what our current background level is. 

We are all exposed to a certain level of dioxin and will have it 
for our lifetimes. And it looks like those early events are, in fact, 
linear down to the level that people are exposed to from day-to-day 
living, and that includes data from experimental systems and also 
data from human samples from people who have been exposed to 
dioxin. 

So that there is a good body of evidence to support that. 

The difficulty, again, and I will reiterate it, is to make that link 
between those changes in gene expression and what might be 
termed an adverse health effect. 



81 

But it's very, very likely that some responses at the biochemical 
or molecular level are occurring at exposure levels that are encoun- 
tered from day-to-day living. 

Mr. ROHRABACHER. Are you gentlemen available to come back in 
one-half hour? Are you all available as a panel? It would be at 1:00. 

If you are available, what I would like to do, because I have to 
go for a vote, and I would like to reconvene this committee hearing 
at 1:00 and give you all a couple of minutes to just state your sum- 
mary of what you think you have heard today. 

And if you could, for the record. 

Now, if you could come back, we will do that at 1:00, and you 
can maybe grab a sandwich in the meantime, and then we will 
hear Admiral Zumwalt. 

So, with that, the committee is in recess till 1:00. 

[Brief recess.] 

Mr. ROHRABACHER. The subcommittee will come to order. 

I am going to suggest that our panelists each give a 2-minute, 
if you can keep it to 2 minutes, summary of some of the things that 
you think came out in today's hearing and just comments that you 
would like to make in general, summarizing what your particular 
point that you think is the most important one to come out of the 
hearing. 

I would like to — I don't believe that anyone here will really an- 
swer the question that the chairman first posed, the first question 
that I posed to the hearing today, which was. Did I strive or did 
I strove? 

[Laughter.] 

You know, I actually asked several people whether or not I 
strove to do this or I strived to do this, and I have been getting 
different answers all the way through the Congress today as to 
what is the proper English. 

Maybe I should ask a member of the press as to whether it is 
I strived? Is it "I strived" or "I strove" to do that? What is it? Okay. 

[Laughter.] 

Well, we will have to depend on the judgment of the distin- 
guished former chairman. 

Mr. Chairman, do you have an opinion on whether "I strove to 
do this" or "I strived to do this"? 

Mr. Brown. It's a matter of choice. 

Mr. ROHRABACHER. It's a matter of choice. 

[Laughter.] 

Mr. Brown. It's what we call a Solomon-like choice. 

[Laughter.] 

Mr. ROHRABACHER. Thank you. 

With that, Dr. Farland, would you like to proceed? 

Dr. Farland. Mr. Chairman, I think that the discussion this 
morning has been very useful in trying to bring out some of the is- 
sues associated with the difficulty of analyzing the very broad base 
of information, some of which is newly emerging and that uses new 
types of techniques, and all of us need to continue to look at how 
we bring these data to bear and allow the risk assessment process 
to evolve to the point where it can actually make use of this infor- 
mation. That is one of the critical points here. 



82 

We have got to keep the risk assessment process evolving so it 
can use the new science as it emerges. 

That having been said, I guess 

Mr. ROHRABACHER. Excuse me, Dr. Farland. What we will do is 
we will let you say that, and then we will give you the very last 
word as well, because you are on the hot seat today and that's the 
only fair thing to do. Thank you 

Dr. Farland. Okay. 

Mr. ROHRABACHER. Dr. Gough? 

Dr. Gough. I am going to reiterate two things I said just before 
we broke. 

One is, I think the Ranch Hand study is going to provide a great 
deal of information about men exposed to the levels that EPA is 
concerned about. 

I am delighted to hear that they are going to consider it seri- 
ously. 

I was also very happy to hear that they are going to consider al- 
ternatives to the linearized model that they used in the last draft 
of the risk assessment report. 

And then — the two things I would like to — the last comment I 
have is that science is characterized, good science, is characterized 
by very sharp h5rpotheses, very sharp statements of what we think 
is true, and then the designing of studies to find out if the reality 
agrees with what we think is true. 

The looseness, I mean risk assessment in science, you can't hold 
it to the same criteria, but I think the looseness of the conclusions 
that I read from the EPA document where we don't know — we don't 
know what's going to happen, we don't know at what level it's 
going to happen, but we're sure that it's happening at a lower level 
than we used to think. 

That sort of looseness and vagueness doesn't help anybody, it 
doesn't provide direction for research, and it certainly won't provide 
direction for decision makers. 

Mr. ROHRABACHER. Dr. Lucier? 

Dr. Lucier. Yes. Just a few comments. 

One, I think that we need to, whenever we have activities such 
as this, is to use all the information that's available, and I think 
EPA has tried to do this, information on mechanism of action, what 
happens in experimental models, what happens in humans when 
they have been exposed accidentally or occupationally to these 
chemicals such as dioxin, and to put it together in a reasonable bal- 
ance. 

Clearly, we are going to have, in most cases, more information 
at the animal level rather than the human level. I think fortu- 
nately in this case the animal models are going to be very useful 
coupled with information on human responses to help determine 
the risk of dioxin. 

I would like to see in the risk characterization chapter a sharper 
definition of what we know and what we don't know. We know a 
lot of things, there are a lot of things we don't know, and I think 
that that needs to be articulated, and I think the document is 
evolving in that way as it goes through the Science Advisory Board 
process. 



83 

Finally, I think EPA has brought the best science possible into 
the process, and is continuing to do so as it is evolving now. 

Mr. ROHRABACHER. Thank you very much, Doctor. 

Dr. Jones? 

Dr. Jones. I had a third point that I wanted to make in response 
to Congressman Brown's question earlier, and it went over my own 
head. That was the issue of promoting regulations to control 
dioxins from emissions sources before the reassessment process 
was completed. 

And a very, very good example that I raised was the fact that 
they had overestimated the emissions of dioxins from hospital in- 
cinerators by a factor of 10 to 50 to 10-50. And as a result of that, 
EPA was proceeding to establish emission limitations which essen- 
tially would cost the medical service industry somewhere between 
$2 billion and $4 billion to retrofit incinerators when, in fact, these 
incinerators probably have very little exposure capacity. 

The other point I just wanted to close with is that we have 
talked about the methodology that EPA should be using with re- 
spect to dioxins and how it will apply to other pollutants. 

And I am afraid there is another example that will come before 
you before not too long involving mercury exposure, where EPA has 
preempted the available science to suggest that mercury is a major 
problem in our society when, in fact, there is a human study done 
at human exposure levels which probably will show just the oppo- 
site. 

So I am not so sure maybe Dr. Farland can respond to that. But 
it's my understanding that EPA disinvited any comments on their 
report to Congress, on the peer review on the report to Congress 
on mercury. Thank you. 

Mr. ROHRABACHER. Dr. Farland, please feel free to have 2 min- 
utes' worth of comment and whatever you would to say. 

Dr. Farland. Well, I guess I can't let the last comment go 
unaddressed. We do have a report coming up to Congress on mer- 
cury. It was extensively peer reviewed. The peer reviews were held 
in open meetings last winter, and I think you'll find that that rep- 
resents a very good state-of-the-art assessment of the hazards of 
mercury. They are based on human studies, and so I will just stop 
with that. 

As far as this particular hearing goes, my sense here is that 
there is still some confusion about what the Science Advisory 
Board has said to EPA about their report, and I commend the re- 
port that you've received from the Science Advisory Board to your 
reading. I think it does show a good balance between some very 
significant recommendations that have been made to improve on 
the science in the report and some complementary language that 
does show that more than 80 percent of the report they have no 
need to see again. 

So, that is certainly worthwhile. 

The last point that I will make is that there have been a number 
of studies which have emerged since we finished this report and 
since the Science Advisory Board met that seemed to be continuing 
to show effects in human populations at relatively low levels of ex- 
posure. 



84 

Those will be extremely important for the revision to our report. 
These include effects in neonates, effects on the nervous system 
and the immune system. 

They are some follow-ups to cancer studies that show additional 
cancer incidence in human populations exposed to higher levels of 
exposure. This is in occupational settings. 

These will be extremely important to us so that we'll try and 
bring in the latest information in the next drafts. 

Mr. ROHRABACHER. Okay. Thank you very much, Dr. Farland. 

Finally, let me say that I made it clear earlier on that we have 
jurisdiction basically on the issue of how the research is being con- 
ducted and not the final issue as to whether or not dioxin poses a 
major threat and what price do we want to counter that threat. 

I would say this, that we have seen in the past where people 
have done reassessments and people have done studies. For exam- 
ple, I remember there was a major study that cost millions and 
millions of dollars and maybe even a hundred million dollars, about 
acid rain, and it was conducted by some of the most prestigious sci- 
entists in the United States, and it came out and then it was ig- 
nored. 

It was laid on the table, it basically — but it basically played down 
the threat of acid rain and suggested that it had been overblown 
and that it was not — that acid rain was not the problem that 
trendy scientists and trendy commentators and trendy politicians 
portrayed it as. 

I would hope that any time that the government does a study 
and any time that we look into these matters, especially things 
dealing with health, that we come up with something that is clear, 
something that is not nebulous, where you make clear statements 
that will then give us, the policymakers, something on which to 
make our judgments and that also that we that were making policy 
judgments do not ignore the science that has been brought forth in 
these reports. 

So, Dr. Farland, I especially want to thank you because I know 
that you were the one on the hot seat, and I appreciate the fact 
of your openness today and the way you have conducted yourself 

I want to thank the other panelists as well. We appreciate your 
opinions, and we appreciate you being here, and I think you have 
given us a lot of food for thought. So, thank you very much. 

Mr. ROHRABACHER. The next panel will be composed of Admiral 
Zumwalt. 

I know you have some very strong feelings on the issue of dioxin. 
We are very happy to make this forum available to you, and if you 
would like to proceed and we will just certainly whatever time you 
need and then we will and then we will follow up with some ques- 
tions after that. 

Thank you very much. Admiral. 

If I could ask our friends and staff members and others, Admiral 
Zumwalt is here, and I think that he deserves the courtesy of being 
listened to. 

Thank you. 



85 

STATEMENT OF ADMIRAL ELMO E.R. ZUMWALT, JR., UNITED 
STATES NAVY [RETIRED], AGENT ORANGE COALITION, AR- 
LINGTON, VA 

Admiral ZuMWALT. Thank you, Mr. Chairman and Members of 
the Committee. 

Mr. ROHRABACHER. Admiral, could you turn on your mike and 
pull your mike a little closer, please? 

Admiral ZuMWALT. Can you hear me now? 

Mr. ROHRABACHER. Yes, sir. 

Admiral ZuMWALT. My statement will deal primarily with EPA's 
risk assessment process. 

In 1989 Secretary of Veterans' Affairs Edward Derwinski asked 
me to do an analysis for him of the Agent Orange issue. In 1990 
I submitted a report listing numerous health effects which, in the 
judgment of my scientific advisors, were as likely as not to result 
from exposure of Vietnam veterans to Agent Orange and its dioxin 
contaminant. 

This report commented, first, on the flawed nature of the sci- 
entific analyses done by the statutory committee advising the Sec- 
retary of Veterans' Affairs, whose deliberations had been heavily 
weighted by those of its members who had associations with cor- 
porations whose production generated dioxin. 

Second, that it had been the policy of the U.S. Government in the 
early '80s to instruct government agencies that it would be most 
unfortunate if a correlation between Agent Orange and health ef- 
fects were to be found. 

Soon thereafter, the House Committee on Government Oper- 
ations, on August 9 of 1990, submitted its 12th report, entitled 
"The Agent Orange Coverup. A Case of Flawed Science and Politi- 
cal Manipulation," which constituted the devastating indictment of 
the U.S. Government's interference with science. 

I quote two of the findings from that report: 

"The White House compromised the independence of the CDC 
and undermined the study by controlling crucial decisions in guid- 
ing the course of research at the time it had secretly taken a legal 
position to resist demands to compensate victims of Agent Orange 
exposure and industrial accidents." 

"The Federal Government has suppressed or minimized findings 
of ill-health effects among veterans that could be linked to Agent 
Orange exposure." 

My report stated that respected nonindustry scientists concluded 
there were 28 diseases which met the statutory test that exposure 
to Agent Orange caused them. 

President Bush overruled the Bureau of the Budget, as a result 
of which the first three diseases were approved as diseases for 
which the Vietnam veterans or their families should receive com- 
pensation, finally, after 15 years of industry manipulation. 

Congress reassigned the responsibility for Agent Orange studies 
to the National Academy of Sciences, which contracted with the In- 
stitute of Medicine, lOM, to produce such studies. 

Dr. Kenneth Shine, lOM president, established the policy that no 
scientists would be on the panel who had taken a position pro or 
con on the correlation between exposure to Agent Orange and 
health effects. 



86 

In July of 1993 the lOM panel issued its first report, as a result 
of which seven more diseases have been authorized for compensa- 
tion. 

Thus, in the case of the study of dioxin done by lOM to get objec- 
tive conclusions, the elimination of scientists who had corporate 
conflicts has led to a total of 10 diseases being found associated 
with exposure to dioxin. 

It is a source of deep concern that the Science Advisory Board 
reviewing EPA's draft reassessment of dioxin has not been selected 
on the same basis as the lOM panel but rather contains members 
and consultants, scientists who have accepted in one form or an- 
other financial support from corporations who have a strong inter- 
est in finding negative correlation between dioxin and health ef- 
fects. 

The Science Advisory Board review of EPA dioxin reassessment 
has thus been tilted in some respects away from proper scientific 
conclusions for the purpose of making the findings of EPA less than 
objective in places for the benefit of interested corporations. 

In summary, regarding the reassessment process, the EPA, with- 
out the manipulation of company docs, came up with scientifically 
objective results. The SAB, with company doc members, denigrated 
and manipulated EPA's outcome. 

Notwithstanding that, objective scientists have peer reviewed the 
significant portion of EPA's work in the study by Drs. DeVito, 
Bimbaum, Farland, and Gastowitz in the publication "Environ- 
mental Health Perspective." 

The process that lOM has used, using only scientists who have 
no conflicts, has resulted in a situation where one Cabinet depart- 
ment, VA, recognizes the harmful effects of exposure to dioxin in 
the case of 10 diseases. 

I strongly urge Congress enact a requirement that future mem- 
bership of the Science Advisory Board contain no scientists whose 
research or livelihood in main or in part is dependent upon finan- 
cial support from corporations. 

Vietnam veterans have been denied for over 20 years the benefits 
which the law would have provided had scientific truth prevailed 
over pseudo-scientific manipulation. 

Surely it is not too much to ask that the financial conflicts of in- 
terest of the members and consultants of the Science Advisory 
Board and of today's industry witnesses be published within the 
final record of the hearing. 

Thank you, Mr. Chairman. 

[The prepared statement and attachments of Admiral Zumalt fol- 
low:] 



87 



V 



E. R. ZUMWALT, JR. 

ADMIRAL. V S. NAVY (RET.) 



8TATEMEMT BY 

Admiral E. R. 2UBwalt, Jr., USM (Rat.) 

Chairman, Agant Oranga Coordinating Council 

bafora tha 

Houaa subooBBittaa on Bnargy and Bnvironaant 

Dacaabar 13, 1995 

I am here in my capacity as Chairman of the Agent Orange 
Coordinating Council whose membership consists of most of the 
veterans and veteran-related organizations. I became involved in 
great detail in the Agent Orange issue in the following manner. 

I commanded U.S. Naval Forces, Vietnam, from 1968 until 1970 
and had further responsibilities for forces fighting in Vietneun 
while I served a member of the Joint Chiefs of Staff from 1970 to 
1974. 

In 1989 the Secretary of Veterans Affairs, The Honorable 
Edward Derwinski, asked me to serve as an unpaid special assistant 
to do an analysis for him of the Agent Orange issue. I spent seven 
months, in conjunction with respected scientists, reviewing the 
studies on dioxin. In May 1990, I submitted a report which listed 
numerous health effects which, in my judgement and that of my 
scientific advisors, were as likely as not to result from exposure 
of Vietnam veterans to Agent Orange and its dioxin contaminant. 

This report, among other things, commented on the flawed 
nature of the scientific analyses done by the statutory committee 
advising the Secretary of Veterans Affairs, the Committee on 
Environmental Health Hazards, whose deliberations had, in my 
opinion, been heavily weighted by those of its members who had 
associations with corporations whose products generated dioxin. 

In addition, I was able to establish that it had been the 
policy of the U.S. Government in the early '80s to instruct 
government agencies involved in Agent Orange studies that it would 
be most unfortunate if a correlation between Agent Orange and 
health effects were to be found. 

A copy of my report to Secretary Derwinski is attached. 

Soon thereafter, the House Committee on Government Operations 

■ 1 



on August 9, 1990, submitted its 12th report entitled The Agent 
Orange Coverup: A Case of Flawed Science and Political 

Manipulation, copy attached, which, in my judgement, constituted a 
devastating indictment of the U.S. Government's interference with 
science. 

I quote two of the findings of that report: 

"The White House compromised the independence of the CDC 
and undermined the study by controlling crucial decisions 
and guiding the course of research at the same time it 
had secretly tedcen a legal position to resist demands to 
compensate victims of Agent Orange exposure and 
industrial accidents." 

"The Federal Government has suppressed or minimized 
findings of ill health effects among Vietnam veterans 
that could be linked to Agent Orange exposure." 

I should note that industry weighed in by insuring that a 
minority of the committee took issue with the findings concerning 
the interference of the government with science. 

My report stated that based on my review with respected 
scientists of all available studies, there were 28 diseases which 
met the statutory test that it was "as likely as not" that exposure 
to Agent Orange caused them. At about the same time, the Agent 
Orange Scientific Task Force, commissioned by veterans 
organizations to study the issue, found that a large number of 
diseases were as likely as not a result of exposure to Agent 
Orange. 

To his credit, President Bush on being apprised of the 
foregoing overruled the Bureau of the Budget and accepted Secretary 
Derwinski's recommendations, as a result of which three diseases: 
chloracne, soft tissue sarcoma, and non-Hodgkin lymphoma were 
approved as diseases for which Vietnam veterans or their families 
should receive compensation. 

Soon after the foregoing events. Congress disestablished the 
Committee on Environmental Health Hazards and assigned the 
responsibility for Agent Orange studies to the National Academy of 
Sciences which contracted with the Institute of Medicine (lOM) to 
produce such studies. 

Dr. Kenneth Shine, President of the Institute of Medicine, 
agreed to establish the policy that no scientists would be on the 
panel who had taken a position pro or con on the correlation 
between exposure to Agent Orange and health effects. Highly 
credible scientists who had not previously taken such positions 
were named to a panel which reviewed all the literature. In July 



89 



of 1993, the lOM panel issued its first report as a result of which 
seven more diseases have been authorized for compensation. 

Thus in the case of the study of dioxin done by lOH to get to 
objective conclusions for veterans exposed to Agent Orange, the 
elimination of scientists who had corporate conflicts has led to a 
total of ten diseases being found, as likely as not, associated 
with such exposure. 

It is a source of deep concern that the Science Advisory Boeurd 
reviewing EPA's draft reassessment of dioxin has not been selected 
on the seune basis as the lOM panel, but rather contains as members 
and consultants scientists who have accepted in one form or another 
financial support from corporations who have a strong interest in 
finding negative correlation between dioxin and health effects. 

In my judgement, based on consultation with scientists for 
whom I have great respect, the Science Advisory Board review of EPA 
dioxin reassessment, is, like the work of the flawed Committee on 
Environmental Health Hazards, tilted in some respects away from 
proper scientific conclusions, for the purpose of making the 
findings of EPA less than objective in places, for the benefit of 
interested corporations. 

I regret that the practice of inviting scientists with obvious 
conflicts of interest to testify is being continued by this 
committee. 

I strongly urge that your committee cause Congress to enact by 
statute a requirement that future membership of the Science 
Advisory Board contain no scientists whose research or livelihood, 
in main or in part, is dependent upon financial support from 
corporations. We have learned that such scientists can be less 
than objective. The result is that Vietnam veterans have been 
denied for over 20 years the benefits which the law would have 
provided had scientific truth prevailed over pseudo-scientific 
manipulation. 

With regard to the present hearing, surely it is not too much 
to ask that the financial conflicts of interest of the members and 
consultants of the Scientific Advisory Board be published within 
the final record of the hearing. 

With regard to the substantive outcome of these hearings, I am 
aware of the great pressures brought to bear by lobbyists for the 
corporations who produce dioxin as a by-product of the operations. 
As a representative of the major veterans groups by virtue of my 
chairmanship of their Agent Orange Coordinating Council, I am also 
aware that thousands of Vietnam veterans and their families are 
equally convinced that corporate and government manipulation of 
science has delayed for years their obtaining appropriate 
compensation for tfhe diseases resulting from exposure to Agent 



90 



Oremge. By and large such veterems have supported the efforts that 
I have Bade to initiate joint research of Agent Orange using the 
heavily exposed Vietnamese people to obtain further evidence of 
health effects. The veterans, by and large, have recognized that 
the tine has come to put the war behind us with the restoration of 
diplomatic relations with the former enemy regime. They clamor for 
the final step in such closure to teOce place. That final step is 
to establish the scientific truth with regard to their exposure to 
Agent Orange. 

This hearing, if it does not interfere with the objective 
scientific analysis carried out by EPA in its draft dioxin risk 
reassessment, will have contributed to the achievement of that 
final step. 

Sincerely, 



fhu 



E. R./)Zumwalty Jr. 

Admiif^l, USN (Ret.) 

Chairman, Agent Orange Coordinating Council 

1000 Wilson Boulevard, Suite 3105 
Arlington, VA 22209-3901 

Tel: (703) 527-5380 
Fax: (703) 528-5795 

Enclosures 



91 



REPORT TO THE SECRETARY OF THE DEPARTMENT OF VETERANS AFFAIRS 

ON THE ASSOCIATION BETWEEN ADVERSE HEALTH EFFECTS 

AND EXPOSURE TO AGENT ORANGE 



As Reported by Special Assistant 

Admiral E.R. Zunwalt, Jr. 

May 5, 1990 



92 



I. INTRODUCTION 

On October 6, 1989 I was appointed as special assistant to 
Secretary Derwinski of the Department of Veterans Affairs to 
assist the Secretary in determining whether it is at least as 
likely as not that there is a statistical association between 
exposure to Agent Orange and a specific adverse health effect. 

As special assistant, I was entrusted with evaluating the 
numerous data relevant to the statistical association between 
exposure to Agent Orange and the specific adverse health effects 
manifested by veterans who saw active duty in Vietnam. Such 
evaluations were made in accordance with the standards set forth 
in Public Law 98-542, the Veterans' Dioxin and Radiation Exposure 
Compensation Standards Act and 38 C.F.R. § 1.17, regulations of 
the Department of Veterans Affairs concerning the evaluation of 
studies relating to health effects of dioxin and radiation 
exposure . 

Consistent with my responsibilities as special assistant, I 
reviewed and evaluated the work of the Scientific Council of the 
Veterans' Advisory Committee on Environmental Hazards and 
commissioned independent scientific experts to assist me in 
evaluating the validity of numerous human and animal studies on 
the effects of exposure to Agent Orange and/or exposure to 
herbicides containing 2,3,7,8 tetrachlorodibenzo-para-dioxin 
(TCDD or dioxin) . In addition, I reviewed and evaluated the 
protocol and standards employed by government sponsored studies 



93 



to assess such studies' credibility, fairness and consistency 
with generally accepted scientific practices. 

After reviewing the scientific literature related to the 
health effects of Vietnam Veterans exposed to Agent Orange as 
well as other studies concerning the health hazards of civilian 
exposure to dioxin contaminants, I conclude that there is 
adequate evidence for the Secretary to reasonably conclude that 
it is at least as likely as not that there is a relationship 
between exposure to Agent Orange and the following health 
problems: non-Hodgkin ' s lymphoma, chloracne and other skin 
disorders, lip cancer, bone cancer, soft tissue sarcoma, birth 
defects, skin cancer, porphyria cutanea tarda and other liver 
disorders, Hodgkin's disease, hematopoietic diseases, multiple 
myeloma, neurological defects, auto-immune diseases and 
disorders, leukemia, lung cancer, kidney cancer, malignant 
melanoma, pancreatic cancer, stomach cancer, colon cancer, 
nasal/pharyngeal/esophageal cancers, prostate cancer, testicular 
cancer, liver cancer, brain cancer, psychosocial effects and 
gastrointestinal diseases. 

I further conclude that the Veterans' Advisory Committee on 
Environmental Hazards has not acted with impartiality in its 
review and assessment of the scientific evidence related to the 
association of adverse health effects and exposure to Agent 
Orange. 

In addition to providing evidence in support of the 
conclusions stated above, this report provides the Secretary with 



23-557 0-96-4 



94 



a review of the scientific, political and legal efforts that have 
occurred over the last decade to establish that Vietnam Veterans 
who have been exposed to Agent Orange are in fact entitled to 
compensation for various illnesses as service-related injuries. 

II. AGENT ORANGE USAGE IN VIETNAM 

Agent Orange was a 50:50 mixture of 2,4-D and 2,4,5-T. The 
latter component, 2,4,5-T, was found to contain the contaminant 
TCDD or 2,3,7,8-tetrachlorodiben2o-para-dioxin (i.e. dioxin) , 
which is regarded as one of the most toxic chemicals known to 
man.^ 

From 1962 to 1971 the United States military sprayed the 
herbicide Agent Orange to accomplish the following objectives: 1) 



' See CDC Protocol for Epidemiologic Studies on the Health 
of Vietnam Veterans (November, 1983), p. 4 ( The CDC Protocol also 
contains a literature review as of 1983 of the health effects on 
animals and humans exposed to herbicides and dioxin, pp. 63-78. The 
literature review documents health problems such as chloracne, 
immunological suppression, neurological and psychological effects, 
reproductive problems such as birth defects, carcinogenic effects 
such as soft tissue sarcomas, lymphomas and thyroid tumors, and 
various gastrointestinal disorders) ; See also General Accounting 
Office, "Report by the Comptroller General: Health Effects of 
Exposure to Herbicide Orange in South Vietnam Should Be Resolved," 
GAO-CED-79-22 at 2 (April 6, 1979) [hereinafter GAO Report, 1979]. 

Dioxin is a family of chemicals (75 in all) that does not 
occur naturally, nor is it intentionally manufactured by any 
industry. The most toxic dioxin is called 2,3,7,8 - TCDD. Dioxins 
are produced as byproducts of the manufacture of some herbicides 
(for example, 2,4,5-T), wood preservatives made from 
trichlorophenals, and some germicides. Dioxins are also produced 
by the manufacture of pulp and paper, by the combustion of wood in 
the presence of chlorine, by fires involving chlorinated benzenes 
and biphenyls (e.g. PCBs) , by the exhaust of automobiles burning 
leaded fuel, and by municipal solid waste incinerators. 



95 



defoliate jungle terrain to inprove observation and prevent enemy 
anbush; 2) destroy food crops; and 3) clear vegetation around 
military installations, landing zones, fire base camps, and 
trails.^ 

Unlike civilian applications of the components contained in 
Agent orange which are diluted in oil and water, Agent Orange was 
sprayed undiluted in Vietnam. Military applications were sprayed 
at the rate of approximately 3 gallons per acre and contained 
approximately 12 pounds of 2,4-D and 13.8 pounds of 2,4,5-T.^ 

Although the military dispensed Agent Orange in 
concentrations 6 to 25 times the manufacturer's suggested rate, 
"at that time the Department of Defense (DOD) did not consider 
herbicide orange toxic or dangerous to humans and took few 
precautions to prevent exposure to it."* Yet, evidence readily 
suggests that at the time of its use experts knew that Agent 
Orange was harmful to military personnel.* 



See Bruce Myers, "Soldier of Orange: The Administrative, 
Diplomatic, Legislative and Litigatory Impact of Herbicide Agent 
Orange in South Vietnam," 8 B. C. Env't. Aff. L. Rev. 159, 162 
(1979) . 

' See GAO Report, 1979 at 2, 3 n.l; See also Myers, 8 B.C. 
Env't Aff. L. Rev, at 162. In contrast, civilian applications of 
2,4,5-T varied from 1 to 4 pounds per acre. 

* General Accounting Office, "Ground Troops in South Vietnam 
Were in Areas Sprayed with Herbicide Orange," FPCD 80-23, p.l 
(November 16, 1979) . 

* Letter from Dr. James R. Clary to Senator Tom Daschle 
(September 9, 1988). Dr. Clary is a former government scientist 
with the Chemical Weapons Branch, BW/CW Division, Air Force 
Armament Development Laboratory, Eglin AFB, Florida. Dr. Clary was 
instrumental in designing the specifications for the A/A 45y-l 
spray tank (ADO 42) and was also the scientist who prepared the 



96 



Th« bulk of Ag«nt Orang* harblcldas used in Vlatnan war* 
raportadly aprayad from "Oparatlon Ranch Hand" flxad wing 
aircraft. Smaller quantitlaa vara appliad from hallcoptara, 
trucks, rivarboata, and by hand. Although voluminoua racorda of 
Ranch Hand nlaaiona ara contained In computer records, otherwlac 
known aa the HERBS and Service HERBa tapes, a algnlf leant. If 
not major aource of expoaura for ground forcea was from non- 
racordad, non Ranch Hand operations.' 

Widespread use of Agent Orange coincided with the massive 
buildup of U.S. military personnel In Vietnam, reaching a peak in 



final report on Ranch Hand: Herbicide Operations In SEA, July 1979. 
According to Dr. Clary: 

When we (military acientiata) Initiated the herbicide program 
in the 1960 'a, we were aware of the potential for damage due 
to dioxin contamination in the herbicide. We were even aware 
that the 'military' formulation had a higher dioxin 
concentration than the 'civilian' version due to the lower 
cost and speed of manufacture. However, because the material 
waa to be used on the 'enemy', none of us were overly 
concerned. We never conBidorad a scenario in which our own 
paraonnel would become contaminated with the herbicide. And, 
If we had, we would have expected our own government to give 
aaslstance to vaterana so contaminated. 

Sec also notes 13, 73-75 and accompanying text Infra for 
additional information of the manufacturer's awareness of the 
toxicity of Agent Orange. 

* Combat units, such as the "Brown Water Navy," frequently 
conducted "unofficial" sprayings of Agent Orange obtained from out 
of channel, and thus unrecorded sources. Additionally, as 
Commander, U.S. Naval Forces, Vietnam, 1 was aware that Agent 
Orange Issued to Allied forces was frequently used on unrecorded 
missions. 



97 



1969 and •ventually stopping in 1971 / Thus, according to an 
official of the then Veterans Administration, it was 
"theoretically possible that about 4.2 million American soldiers 
could have made transient or significant contact with the 
herbicides because of [the Ranch Hand Operation]." ' 

A. REASONS FOR PHASE OUT 

Beginning as early as 1968, scientists, health officials, 
politicians and the military itself began to express concerns 
about the potential toxicity of Agent Orange and its contaminant 
dioxin to humans. For instance, in February 1969 The Bionetics 
Research Council Committee ("BRC") in a report commissioned by 
the United States Department of Agriculture found that 2,4,5-T 
showed a "significant potential to increase birth defects." 
Within four months after the BRC report, Vietnamese newspapers 
began reporting significant increases in human birth defects 
ostensibly due to exposure to Agent Orange. 



^ GAO Report 1979, supra note 1, at 29. pee also note 82 and 
accompanying text infra for a discussion of the correlation between 
the spraying of Agent Orange and the hospitalization of Vietnam 
soldiers for disease and non-battle related injuries. 

* House Comm. on Veteran's Affairs, 95th Cong., 2d Sess., 
Herbicide "Aoent Orange". Hearings before the Subcommittee on 
Medical Facilities and Benefits . (Oct. 11, 1978) (Statement of Ma j . 
Gen. Garth Dettinger USAF, Deputy Surgeon General USAF at 12). 

' Myers at 166. 

" Id- While birth defects did significantly increase in 
Saigon, critics contend that Saigon was not an area where the 
preponderance of defoliation missions were flown and argue that 
such increases were due primarily to the influx of U.S. medical 
personnel who kept better records of birth defects. Subsequent 



98 



By- October, 1969, the National Institute of Health confirmed 
that 2,4,5-T could cause nalfomations and stillbirths in mice, 
thereby prompting the Department of Defense to announce a partial 
curtailment of its Agent Orange spraying." 

By April 15, 1970, the public outcry and mounting scientific 
evidence caused the Surgeon General of the United States to issue 
a warning that the use of 2,4,5-T might be hazardous to "our 
health"." 

On the same day, the Secretaries of Agriculture, Health 
Education and Welfare, and the Interior, stirred by the 
publication of studies that indicated 2,4,5-T was a teratogen 
(i.e. caused birth defects), jointly announced the suspension of 
its use around lakes, ponds, ditch banks, recreation areas and 



studies in Vietnam confirm the incidence of increased birth defects 
among civilian populations exposed to Agent Orange. See e.g. 
Phuong, et. al. "An Estimate of Reproductive Abnormalities in Women 
Inhabiting Herbicide Sprayed and Non-herbicide Sprayed Areas in the 
South of Vietnam, 152-1981 18 Chemosphere 843-846 (1989) 
(significant statistical difference between hydatidiform mole and 
congenital malformations between populations potentially exposed 
and not exposed to TCDD) ; Phuong, et. al., "An Estimate of 
Differences Among Women Giving Birth to Deformed Babies and Among 
Those with Hydatidiform Mole Seen at the OB-GYN Hospital of Ho Chi 
Minh City in the South of Vietnam," 18 Chemosphere 801-803 (1989) 
(statistically significant connection between frequency of the 
occurrence of congenital abnormalities and of hydatidiform moles 
and a history of phenoxyherbicide exposure) ; Huong, et. al., "An 
Estimate of the Incidence of birth Defects, Hydatidiform Mole and 
Fetal Death in Utero Between 1952 and 1985 at the OB-GYN Hospital 
of Ho Chi Minh City, Repxiblic of Vietnam," 18 Chemosphere 805-810 
(1989) (sharp increase in the rate of fetal death in utero, 
hydatidiform mole (with or without choriocarcinoma) and congenital 
malformations from the pre 1965-1975 period, suggesting possible 
association to phenoxyherbicide exposure) . 

" Myers at 167 

'' Id. 



99 



hones and crops intended for human consumption.^^ The DepartBttnt 
of Defense simultaneously announced its suspension of all uses of 
Agent Orange.'* 

B. HEALTH STUDIES 

As Agent Orange concerns grew, numerous independent studies 
were conducted between 1974 and 1983 to determine if a link 
exists between certain cancerous diseases, such as non-Hodgkin ' s 
lymphoma and soft-tissue sarcomas, and exposure to the chemical 
components found in Agent Orange. These studies suggested just 
such a link. 

In 1974, for example. Dr. Lennart Hardell began a study 
which eventually demonstrated a statistically significant 
correlation between exposure to pesticides containing dioxin and 
the development of soft tissue sarcomas.'* 



" Id. Although Dow Chemical Company, the primary manufacturer 
of 2,4,5-T and 2,4-D, denied this teratogenicity, Dow's own tests 
confirmed that when dioxin was present in quantities exceeding 
production specifications, birth defects did occur. See J. 
McCullough, Herbicides; Environmental Health Effects; Vietnam and 
the Geneva Protocol; Developments Purina 1979 . 13 (1970) 
(Congressional Research Report No. UG 447, 70-303SP) . Pressure from 
industry subsequently led to some relaxation of the limits placed 
on the 2,4,5-T and 2,4-D. The only current uses for these chemicals 
in the United States are on rice, pastures, rangelands and rights 
of way. 

'* Id. at 167. See also Dow Chemi cal v. Ruckelshaus. 477 F. 
2d 1317, 1319 (8th Cir. 1973) (secretaries announcement quoted in 
the opinion) . 

" Hardell, L. and Sandstrom, A. "Case-control Study: Soft 
Tissue Sarcomas and Exposure to Phenoxyacetic Acids or 
Chlorophenols," 39 Brit. J. Cancer . 711-717 (1979). See also note 
89 infra for the confirming results of follow-up studies by Hardell 
and others . 



100 



In 1974 , Axelson and Sundell reported a two-fold increase of 
cancer in a cohort study of Swedish railway workers exposed to a 
variety of herbicides containing dioxin contaminants.'* 

By 1976, the Occupational Safety and Health Administration, 
established rigorous exposure criteria for workers working with 
2,4,5-T." 

In 1977 the International Agency for Research on Cancer 
(lARC) , while cautioning that the overall data was inconclusive, 
reported numerous anomalies and increased mortality rates in 
animals and humans exposed to 2,4-D or 2,4,5-T.'* 



Axelson and Sundell, "Herbicide Exposure, Mortality and 
Tumor Incidence: An Epidemiological Investigation on Swedish 
Railroad Workers," 11 Work Env't. Health 21-28 (1974). 

'^ U.S. Occupational Safety and Health Administration (1976), 
Air Contaminants; U.S. Code, Federal Register 29, Part 1910.93 at 
p. 27. 

'* With regard to 2,4-D, the lARC found the following 
anomalies: elevated levels of cancer in rats; acute and short-term 
oral toxicity in mice, rabbits, guinea pigs and rats--death, 
stiffness in the extremities, incoordination, stupor, myotonia, and 
other physical abnormalities; in monkeys, injections caused nausea, 
vomiting, lethargy, muscular incoordination and head droop, fatty 
degeneration of the liver, spleen, kidneys and heart; foetal 
anomaly increases in some species; post-birth death rates increased 
in some species; higher mortality rates and morphological 
alterations in pheasant embryos and their chicks when spraying took 
place under simulated field conditions; higher mortality rates in 
rat pups in a 3 generation exposure; gene mutation after exposure 
to high concentrations; chromosomal aberrations when cultured human 
lymphocytes were exposed; increased frequency of aberrant 
metaphases (2 to 4 times) in mice exposed to toxic concentrations. 

In humans the lARC found that: a 23 year old farming student, 
a suicide, had 6 grams of 2,4-D in his body, acute congestion of 
all organs, severe degeneration of ganglion cells in the central 
nervous system; 3 cases of peripheral neuropathy in humans sprayed 
with 2,4-D with initial symptoms of nausea, vomiting, diarrhea, 
swelling and aching of feet and legs with latency, in individual 
cases, paresthesia in the extremities, pain in the legs, numbness 
and aching of fingers and toes, swelling in hand joints, flaccid 

10 



101 



In 1978, the Environmental Protection Agency issued an 
emergency suspension of the spraying of 2,4,5-T in national 
forests after finding "a statistically significant increase in 
the frequency of miscarriages" among women living near forests 
sprayed with 2,4,5-T." 

In 1980, another provocative mortality study of workers 



parapheresis; similar case reports in agriculture workers sprayed 
by 2,4-D; workers associated with 2,4-D developed symptoms of 
somnolence, anorexia, gastralgia, increased salivation, a sweet 
taste in the mouth, a sensation of drunkenness, heaviness of the 
legs and hyperacusea, rapid fatigue, headache, loss of appetite, 
pains in the region of liver and stomach, weakness, vertigo, 
hypotension, • bradycardia, dyspeptic symptoms, gastritis, liver 
disfunction, changes in metabolic processes. 

With regard to 2,4,5-T's effect on animals the lARC found: it 
can increase the frequency of cleft palates in some strains of 
mice; fetal growth retardation may also be observed; cystic 
kidneys were observed in two strains of mice; in purest available 
form, it induced some fetal effects and skeletal anomalies in rats 
as well as behavioral abnormalities, changes in thyroid activity 
and brain serotonin levels in the progeny; increases in 
intrauterine deaths and in malformations in rats; fetal death and 
teratogenic effects in Syrian golden hamsters; chromosomal 
abnormalities . 

The lARC reported in 1977 with respect to 2,4,5-T's effects 
on humans that: workers exposed at a factory in the USSR had skin 
lesions, acne, liver impairment, and neurasthenic syndrome; similar 
findings were reported by Jerasneh, et al (1973, 1974) in a factory 
in Czechoslovakia which in 1965-68 produced 76 cases of chloracne, 
2 deaths from bronchogenic cancers. Some workers had porphyria 
cutanea tarda, urophryimuria, abnormal liver tests, severe 
neurasthenia, depression syndrome, peripheral neuropathy; in a 197 5 
accident in West Virginia, 228 people were affected. Symptoms 
included chloracne, melanosis, muscular aches and pains, fatigue, 
nervousness, intolerance to cold; 4 workers of 50 affected in a 
similar accident in the Netherlands in 1963 died within 2 years 
and at least 10 still had skin complaints 13 years later. 

" June 1979 Congressional Hearings before House Commerce 
Committee. Subcommittee on Oversight and Investigations , quoted in 
"Human Disease Linked to Dioxin: Congress Calls for 2,4,5-T Ban 
After Dramatic Herbicide Hearings", 28 Bioscience 4 54 (August 
1979) . This study, otherwise known as the Alsea Study, has been 
cited as showing the first correlation between 2,4,5-T (and 
presumably its TCDD contaminant) and teratogenic effects in humans. 

11 



102 



involved in an accident at an industrial plant which manufactured 
dioxin compounds suggested that exposure to these compounds 
resulted in excessive deaths from neoplasms of the lymphatic and 
hematopoietic tissues.^" 

On September 22, 1980, the U.S. Interagency Work Group to 
Study the Long-term Health Effects of Phenoxy Herbicides and 
Contaminants concluded "that despite the studies' limitations, 
they do show a correlation between exposure to phenoxy acid 
herbicides and an increased risk of developing soft-tissue tumors 
or malignant lymphomas. "^^ 

To be sure, there remain skeptics who insist that the 
studies failed in one respect or another to establish a 
scientifically acceptable correlation.^^ Vet, it can fairly be 
said that the general attitude both within and outside the 
scientific community was, and continues to be increasing concern 
over the mounting evidence of a connection between certain cancer 



Zack and Suskind, "The Mortality Experience of Workers 
Exposed to TCDD in a Trichlorophenol Process Accident," 22 Journal 
of Medicine . 11-14 (1980) . 

^^ See U.S. Interagency Workgroup to Study the Long-Term 
Health Effects of Phenoxy Herbicides and Contaminants (September 
22, 1980) (executive summary). 

^^ See e.g. . "The Weight of the Evidence on the Human 
Carcinogenicity of 2,4-D" (January 1990) (This report, sponsored 
by the National Association of Wheat Growers Foundation and a grant 
from the Industry Task Force II on 2,4-D Research Data, an 
association of manufacturers and commercial formulators of 2,4-D, 
concluded that the toxicological data on 2,4-D does not provide a 
strong basis for predicting that 2,4-D is carcinogenic to humans. 
Nevertheless, the panel reviewing the evidence did conclude that 
"evidence indicates that it is possible that exposure to 2,4-D can 
cause cancer in humans."). 

12 



103 



illnesstts and exposure to dioxins. 

III. VETERANS' DIOXIN AND RADIATION EXPOSURE COMPENSATION 
STANDARDS ACT OF 1984 

With the increasing volume of scientific literature giving 
credence to the belief of many Vietnam Veterans that exposure to 
Agent Orange during their military service was related to their 
contraction of several debilitating diseases — particularly non- 
Hodgkin's lymphoma, soft tissue sarcoma ("STS") (malignant tumors 
that form in muscle fat, or fibrous connective tissue) and 
porphyria cutanea tarda ("PCT") (deficiencies in liver enzymes) — 
Vietnam Veterans rightfully sought disability compensation from 
the Veterans Administration ("VA") . 

The VA determined, however, that the vast majority of 
claimants were not entitled to compensation since they did not 
have service connected illnesses.^ As a consequence. Congress 
attempted to alter dramatically the process governing Agent 
Orange disability claims through passage of the Veterans' Dioxin 
and Radiation Exposure Compensation Standards Act of 1984 



By October 1, 1983, 9170 veterans filed claims for 
disabilities that they alleged were caused by exposure to Agent 
Orange. The VA denied compensation to 7709 claimants on the grounds 
that the claimed diseases were not service connected. Only one 
disease was deemed associated with service related exposure to 
Agent Orange, a skin condition known as chloracne. See House 
Report No. 98-592, reprinted in U.S. Code Cong. & Adm. News, 98th 
Cong. 2d Sess.,1984, at 4452. See also Nehmer v. U.S. Veterans 
Administration. 712 F.Supp. 1404, 1407 (1989). 

13 



104 



(hereinafter the "Dioxin Standards Act") .** To ensure that the 
VA provided disability compensation to veterans exposed to 
herbicides containing dioxin while serving in Vietnam,^ Congress 
authorized the VA to conduct rulemaking to determine those 
diseases that were entitled to compensation as a result of a 
service-related exposure to Agent Orange.^ 

In promulgating such rules, the Dioxin Standards Act 
required the VA to appoint a Veterans' Advisory Committee on 
Environmental Hazards (the "Advisory Committee") — composed of 
experts in dioxin, experts in epidemiology, and interested 
members of the public — to review the scientific literature on 
dioxin and submit periodic recommendations and evaluations to the 
Administrator of the VA.^^ Such experts were directed to 
evaluate the scientific evidence pursuant to regulations 
promulgated by the VA, and thereafter to submit recommendations 



^^ Veterans' Dioxin and Radiation Exposure Compensation 
Standards Act, P;ib, L. 98-542, Oct. 24, 1984, 98 Stat. 2727 
(hereinafter the Dioxin Standards Act) . In passing the Act Congress 
found that Vietnam Veterans were "deeply concerned about possible 
long term health effects of exposure to herbicides containing 
dioxin, " (Section 2 (1)), particularly since "[t]here is scientific 
and medical uncertainty regarding such long-term adverse health 
effects." (Section 2 (2)). In responding to this uncertainty, 
Congress mandated that "thorough epidemiological studies of the 
health effects experienced by veterans in connection with exposure 
... to herbicides containing dioxin" be conducted, (Section 2(4)), 
especially in light of the fact that "[t]here is some evidence that 
chloracne, porphyria cutanea tarda, and soft tissue sarcoma are 
associated with exposure to certain levels of dioxin as found in 
some herbicides." (Section 2 (5)). 

^ Id. at Section 3 . 

" 1^. at Section 5. 

^' Id. at Section 6. 

14 



105 



and evaluations to the Administrator of the VA on whether "sound 

scientific or medical evidence" indicated a connection to 

exposure to Agent Orange and the manifestation of various 

diseases." 

In recognition of the uncertain state of scientific evidence 

and the inability to make an absolute causal connection between 

exposure to herbicides containing dioxin and affliction with 

various rare cancer diseases,^ Congress mandated that the VA 

Administrator resolve any doubt in favor of the veteran seeking 

compensation. As stated in the Dioxin Standards Act: 

It has always been the policy of the Veterans Administration 
and is the policy of the United States, with respect to 
individual claims for service connection of diseases and 
disabilities, that when, after consideration of all the 
evidence and material of record, there is an approximate 
balance of positive and negative evidence regarding the 
merits of an issue material to the determination of a claim, 
the benefit of the doubt in resolving each such issue shall 
be given to the claimant. 

A. NEHMER V. U.S. VETERAKS ADMINISTRATION 

Despite Congressional intent to give the veteran the benefit 
of the doubt, and in direct opposition to the stated purpose of 



" I^. at Section 5. 

" £££ Nehmer v. U.S. Ve terans Admin.. 712 F. Supp. 1404, 
1418 (N.D. Cal. (1989) wherein the court found after reviewing the 
legislative history of the Act "that Congress intended service 
connection to be granted on the basis of ' increased risk of 
incidence', or a 'significant correlation' between dioxin and 
various diseases," rather, than on the basis of a causal 
relationship. 



30 



See Dioxin Standards Act at Section 2 (13] 

15 



106 



the Dioxin Stand&rds Act to provide disability coapansation to 
Vietnam Veterans suffering with cancer who were exposed to Agent 
Orange, the VA continued to deny compensation improperly to over 
31,000 veterans with just such claims. In fact, in promulgating 
the rules specified by Dioxin Standards Act, the VA not only 
confounded the intent of the Congress, but directly contradicted 
its own established practice of granting compensable service- 
connection status for diseases on the lesser showing of a 
statistical association, promulgating instead the more stringent 
requirement that compensation depends on establishing a cause and 
effect relationship.'^ 

Mounting a challenge to the regulations. Veterans groups 
prosecuted a successful legal action which found that the VA had 
"both imposed an impermissibly demanding test for granting 
service connection for various diseases and refused to give the 



See e.g. 38 C.F.R. § 3.310(b) (compensation granted for 
cardiovascular diseases incurred by veterans who suffered 
amputations of legs or feet); Nehmer at 1418. 

The significance of the distinction between a statistical 
association and a cause and effect relationship is in the burden 
of proof that the veteran must satisfy in order to be granted 
benefits. A statistical association "means that the observed 
coincidence in variations between exposure to the toxic substance 
and the adverse health effects is unlikely to be a chance 
occurrence or happenstance," whereas the cause and effect 
relationship "describes a much stronger relationship between 
exposure to a particular toxic substance and the development of a 
particular disease than 'statistically significant association' 
does." Nehmer . 712 F.Supp. at 1416. 

Thus, the regulation promulgated by the VA established an 
overly burdensome standard by incorporating the causal relationship 
test within the text of the regulation itself. 38 C.F.R. § 3.311(d) 
("[s]ound scientific and medical evidence does not establish a 
cause and effect relationship between dioxin exposure" and any 
diseases except some cases of chloracne) (emphasis added) . 

16 



107 



veterans the benefit of the doubt in meeting the demanding 
standard." Nehmer v. U.S. Veterans Administration . 712 F. Supp. 
1404, 1423 (1989) (emphasis in original). As a result, the court 
invalidated the VA's Dioxin regulation which denied service 
connection for all diseases other than chloracne; ordered the VA 
to amend its rules; and further ordered that the Advisory 
Committee reassess its recommendations in light of the court's 
order. '^ 

Thus, on October 2, 1989, the VA amended 38 C.F.R. Part 1, 
which among other things set forth various factors for the 
Secretary and the Advisory Committee to consider in determining 
whether it is "at l6ast as likely as not" that a scientific study 
shows a "significant statistical association" between a 
particular exposure to herbicides containing dioxin and a 
specific adverse health effect." Equally important, the 



" Nehmer . 712 F. Supp at 1423. 

" 38 C.F.R. § 1.17 (b) & (d) . 38 C.F.R. § 1.17 states: 

(a) From time to time, the Secretary shall publish evaluations 
of scientific or medical studies relating to the adverse health 
effects of exposure to a herbicide containing 2,3,7,8 
tetrachlorodibenzo-p-dioxin (dioxin) and/or exposure to ionizing 
radiation in the "Notices" section of the Federal Register . 

(b) Factors to be considered in evaluating scientific studies 
include: 

(1) Whether the study's findings are statistically significant 
and replicable. 

(2) Whether the study and its findings have withstood peer 
review. 

(3) Whether the study methodology has been sufficiently 
described to permit replication of the study. 

(4) Whether the study's findings are applicable to the veteran 
population of interest. 

(5) The views of the appropriate panel of the Scientific Council 
of the Veteran' Advisory Committee on Environmental Hazards. 

(c) When the Secretary determines, based on the evaluation of 

17 



108 



regulation permits the Secretary to disregard the findings' of the 
Advisory Comnittee, as well as the standards set forth at 38 



scientific or medical studies and after receiving the advice of the 
Veteran's Advisory Committee on Environmental Hazards and applying 
the reasonable doubt doctrine as set forth in paragraph (d) (1) of 
this section, that a significant statistical association exists 
between any disease and exposure to a herbicide containing dioxin 
or exposure to ionizing radiation, SS 3.311a or 3.311b of this 
title, as appropriate, shall be amended to provide guidelines for 
the establishment of service connection. 

(d) (1) For purposes of paragraph (c) of this section a 
"significant statistical association" shall be deemed to exist when 
the relative weights of valid positive and negative studies permit 
the conclusion that it is at least as likely as not that the 
purported relationship between a particular type of exposure and 
a specific adverse health effect exists. 

(2) For purposes of this paragraph a valid study is one which: 
(i) Had adequately described the study design and methods of 

data collection, verification and analysis; 

(ii) Is reasonably free of biases, such as selection, 
observation and participation biases; however, if biases exist, the 
investigator has acknowledged them and so stated the study's 
conclusions that the biases do not intrude upon those conclusions; 
and 

(iii) Has satisfactorily accounted for known confounding 
factors. 

(3) For purposes of this paragraph a valid positive study is one 
which satisfies the criteria in paragraph (d) (2) of this section 
and whose findings are statistically significant at a probability 
level of .05 or less with proper accounting for multiple 
comparisons and subgroups analyses. 

(4) For purposes of this paragraph a valid negative study is one 
which satisfies the criteria in paragraph (d) (2) of this section 
and has sufficient statistical power to detect an association 
between a particular type of exposure and a specific adverse health 
effect if such an association were to exist. 

(e) For purposes of assessing the relative weights of valid 
positive and negative studies, other studies affecting 
epidemiological assessments including case series, correlational 
studies and studies with insufficient statistical power as well as 
key mechanistic and animal studies which are found to have 
particular relevance to an effect on human organ systems may also 
be considered. 

(f) Notwithstanding the provisions of paragraph (d) of this 
section, a "significant statistical association" may be deemed to 
exist between a particular exposure and a specific disease if, in 
the Secretary's judgment, scientific and medical evidence on the 
whole supports such a decision. 

18 



109 



C.F.R. S 1.17 (d) and determine in his ovm judgment that the 
scientific and medical evidence supports the existence of a 
"significant statistical association" between a particular 
exposure and a specific disease. 38 C.F.R. § 1.17 (f ) . 

The Secretary recently exercised his discretionary authority 
under this rule when he found a significant statistical 
association between exposure to Agent Orange and non-Hodgkin ' s 
lymphoma, notwithstanding the failure of his own Advisory 
Committee to recommend such action in the face of overwhelming 
scientific data.'* 



B. THE WORK OF THE VETERANS' ADVISORY COMMITTEE ON 
ENVIRONMENTAL HAZARDS 



To assess the validity and competency of the work of the 
Advisory Committee, I asked several impartial scientists to 



After reviewing numerous scientific studies, at least four 
of which were deemed to be valid positive in demonstrating the link 
between exposure to herbicides containing dioxin and non-Hodgkin ' s 
lymphoma, the Advisory Committee still concluded that: 

The Committee does not find the evidence sufficient at the 
present time to conclude that there is a significant 
statistical association between exposure to phenoxy acid 
herbicides and non-Hodgkin 's lymphoma. However, the Committee 
cannot rule out such an association. 

The Secretary should be interested to note that a new 
mortality study positively confirms that farmers exposed to 
herbicides containing 2,4-D have an increased risk of developing 
non-Hodgkin 's lymphoma. See Blair, "Herbicides and Non-Hodgkin ' s 
Lymphoma: New Evidence From a Study of Saskatchewan Farmers," 82 
Journal of the National Cancer Institute 575-582 (1990) . 



19 



no 



review the Advisory Connitt** transcripts. Without exception, 
the experts who reviewed the work of the Advisory Committee 
disagreed with its findings and further questioned the validity 
of the Advisory Committee's review of studies on non-Hodgkin ' s 
lymphomas. 

For instance, a distinguished group at the Fred Hutchinson 
Cancer Research Institute in Seattle, Washington, upon reviewing 
the Advisory Committee transcripts, concluded "that it is at 
least as likely as not that there is a significant association 
(as defined by the Secretary of Veterans Affairs) between 
[exposure to phenoxy acid herbicides and non-Hodgkin ' s 
lymphoma.]" '* This same group further asserts that the 
Committee's work was "not sensible" and "rather unsatisfactory" 
in its review and classification of the various studies it 
reviewed. Additionally, these scientists regarded Dr. Lathrop's 
views as "less than objective" and felt that the possibility 
exists that "his extreme views (e.g., in respect to the role of 
dose-response testing) may have unduly affected the Committee's 
work." Finally, the Hutchinson scientists argue that the issue 
of chemical-specific effects, in which animal studies have been 
sufficient to demonstrate the carcinogenicity of dioxin, is an 
important factor "not well considered by the Committee." 
(emphasis in original) 

A second reviewer of the Committee's work. Dr. Robert 



Letter to Admiral Zumwalt from Dr. Robert W. Day, Director 
of the Fred Hutchinson Cancer Research Center of Seattle, 
Washington (Feb. 20, 1990). 

20 



Ill 



Hartzaan (considered one of the U.S. Navy's top aedical 

rssearchers) , effectively confiras the views of the Hutchinson 

group. Dr. Hartzaan states that "the preponderance of evidence 

from the papers reviewed [by the Advisory Connittee] weighs 

heavily in favor of an effect of Agent Orange on increased risk 

for non-Hodgkin ' s lymphoma. "^ Dr. Hartznan also attests that: 

an inadequate process is being used to evaluate scientific 
publications for use in public policy. The process uses 
scientific words like 'significant at the 5% level' and a 
committee of scientists to produce a decision about a series 
of publications. But in reality, the Committee was so tied 
by the process, that a decision which should have been based 
on scientific data was reduced to vague impressions... 
Actually, if the reading of the rules of valid negative 
found in the transcript is correct ('a valid negative must 
be significant at the p>.05 level' that is statistically 
significant on the negative side) none of the papers 
reviewed are valid negatives. 

A third reviewing team. Dr. Jeanne Mager Stellman, PhD 

(Physical Chemistry) and Steven D. Stellman, PhD (Physical 

Chemistry) , also echo the sentiments expressed by the Hutchinson 

Group and Dr. Hartzman on the validity of the Committee's 

proceedings and conclusions. In fact, the Stellmans' detailed 

annotated bibliography and assessment of niimerous cancer studies 

relevant to herbicide exposure presents a stunning indictment of 

the Advisory Committee's scientific interpretation and policy 

judgments regarding the link between Agent Orange and Vietnam 



Letter to Admiral Zumwalt from Dr. R.J. Hartzman Capt. MC 
USN (March 7, 1990) . 



37 



I^. at p. 3. 

21 



112 



Veterans. 

A fourth reviewer, a distinguished scientist intimately 

associated with government sponsored studies on the effects of 

exposure to Agent Orange, states the same conclusions reached by 

the other reviewers: 

The work of the Veterans' Advisory Committee on 
Environmental Hazards, as documented in their November 2, 
1989 transcript, has little or no scientific merit, and 
should not serve as a basis for compensation or regulatory 
decisions of any sort... 

My analysis of the NHL articles reviewed by the committee 
reveals striking patterns which indicate to me that it is 
much more likely than not that a statistical association 
exists between NHL and herbicide exposure." 

As these various reviewers suggest, the Advisory Committee's 
conclusions on the relationship between exposure to Agent Orange 
and non-Hodgkin's lymphoma were woefully understated in light of 
the clear evidence demonstrating a significant statistical 
association between NHL and exposure to phenoxy acid herbicides 
such as Agent Orange. 

Perhaps more significant than the Committee's failure to 
make such obvious findings is the distressing conclusion of the 
independent reviewers that the Committee's process is so flawed 



See Stellman & Stellman, "A Selection of Papers with 
Commentaries Relevant to the Science Interpretation and Policy: 
Agent Orange and Vietnam Veterans," (March 1, 1990). See also note 
51 and accompanying text infra for additional discussion of the 
Stellmans' work. 

" A copy of the anonymous reviewer's analysis can be made 
available for the Secretary's personal inspection and review. In 
another paper, this same source stated: "I estimate that the 
[Vietnam] Veterans are experiencing a 40% to 50% increase in 
sarcomas and non-Hodgkin's lymphoma rates." 

22 



113 



as to be useless to the Secretary in naking any determination on 
the effects of Agent Orange. From a nere reading of Committee 
transcripts, these reviewers detected overt bias in the 
Committee's evaluation of certain studies. In fact, some members 
of the Advisory Committee and other VA officials have, even 
before reviewing the evidence, publicly denied the existence of a 
correlation between exposure to dioxins and adverse health 
effects.^" This blatant lack of impartiality lends credence to 
the suspicion that certain individuals may have been unduly 
influenced in their evaluation of various studies. Furthermore, 
such bias among Advisory Committee members suggests that the 
Secretary should, in accordance with the Dioxin Standards Act, 
appoint new personnel to the Advisory Committee. 

III. THE CDC STUDIES 

Were the faulty conclusions, flawed methodology and 
noticeable bias of the Advisory Committee an isolated problem, 
correcting the misdirection would be more manageable. But, 
experience with other governmental agencies responsible for 
specifically analyzing and studying the effects of exposure to 



For instance. Dr. Lawrence B. Hobson (Director, Office of 
Environmental Medicine, Veterans Health Services and Research 
Administration) , claims that TCDD "presents no threat from the 
exposures experienced by the veterans and the public at large," and 
virtually accuses scientists who find that such health effects do 
exist to be nothing more than witch doctors. See Hobson, "Dioxin 
and witchcraft" presented at the 5th International Symposium on 
Chlorinated Dioxins and Related Compounds (September 1985) . 

23 



114 



Agent Orange strongly hints at a discernible pattern, if not 
outright governmental collaboration, to deny conpensation to 
Vietnam veterans for disabilities associated with exposure to 
dioxin. 

A case in point is the Centers for Disease Control ("CDC"). 
As concerns grew following the first studies of h\unan exposure to 
Agent Orange, Congress commissioned a large scale epidemiological 
study to determine the potential health effects for Vietnam 
Veterans exposed to Agent Orange. Initially, this study was to 
be conducted by the VA itself. When evidence surfaced, however, 
of the VA's footdragging in commencing the study (and initial 
disavowal of any potential harm from exposure to Agent Orange) , 
Congress transferred the responsibility for the study to the CDC 
in 1983.*^ 

Unfortunately, as hearings before the Human Resources and 
Intergovernmental Relations Subcommittee or July 11, 1989 
revealed, the design, implementation and conclusions of the CDC 
study were so ill conceived as to suggest that political 
pressures once again interfered with the kind of professional, 
unbiased review Congress had sought to obtain." 

The Agent Orange validation study, for example, a study of 



See 135 Congressional Record . Statement of Senator Tom 
Daschle (November 21, 1989); See also Agent Orange Hearings at p. 
37. 

*^ Oversight Review of CDC's Agent Orange Studv: Hearing 
Before the Human Resources and Intergovernmental Relations 
Subcommittee of the Committee on Government Operations House of 
Representatives . 101st Cong., 1st Sess. at p. 71 and 330 
(1989) [hereinafter cited as Agent Orange Hearing]. 

24 



115 



the long-tenn health effects of exposures to herbicides in 
Vietnam, was supposedly conducted to determine if exposure could, 
in fact, be estimated.*' After four years and approximately $63 
million in federal funds, the CDC concluded that an Agent Orange 
exposure study could not be done based on military records.^ 
This conclusion was based on the results of blood tests of 64 6 
Vietnam Veterans which ostensibly demonstrated that no 
association existed between serum dioxin levels and military- 
based estimates of the likelihood of exposure to Agent Orange." 
Inexplicably, the CDC then used these "negative" findings to 
conclude that not only could an exposure study not even be done, 
but that the "study" which was never even conducted proves that 
Vietnam Veterans were never exposed to harmful doses of Agent 
Orange. 

Even more disturbing, when the protocol for this "study" and 
the blood test procedures were examined further, there appeared 
to be a purposeful effort to sabotage any chance of a meaningful 
Agent Orange exposure analysis. For instance, the original 
protocol for the Agent Orange exposure study understandably 
called for subject veterans to be tracked by company level 



Id . at 37; see also . Protocol for Epidemiologic Studies 
of the Health of Vietnam Veterans, Centers for Disease Control, 
Public Health Service, U.S. Department of Health and Human Services 
(November, 1983) . 

** Agent Orange Hearings at 13 (Statement of Dr. Vernon Houk) . 

" Id. at 12-13. 

25 



116 



location.^ By tracking company level units of 200 nen, rather 
than battalions of 1,000 men, the location of men in relation to 
herbicide applications would be known with greater precision, 
thereby decreasing the probeibility that study-subjects would be 
misclassified as having been or not been exposed to Agent Orange. 

However, in 1985 the CDC abruptly changed the protocol to 
have battalions, rather than companies, serve as the basis for 
cohort selection and unit location." By the CDC's own 
admission, changing the protocol to track veterans on the broader 
battalion basis effectively diluted the study for the simple 
reason that many of the 1,000 men in a battalion were probably 
not exposed to Agent Orange. Why then did the CDC change the 
protocol in 1985? 

According to Dr. Vernon Houk, Director of the Center for 
Environmental Health and Injury Control, the department within 
the CDC responsible for conducting the Agent Orange study, the 
protocol was changed because the CDC concluded that company- 
specific records were unreliable and contained too many gaps of 
information. As a result, military records could simply not be 
used to assess exposure.** 



" Id. at 41. 
" Id. at 38. 

48 



Agent Orange Hearing: Testimony of Dr. Vernon Houk at 38- 
4 and 69. Dr. Houk sports an unbounded skepticism for the health 
hazards of dioxin. He recently endorsed the lessening of the dioxin 
dumping standard in the State of Georgia at a rate 500 times more 
lenient than EPA recommended guidelines. See Letter from Dr. 
Vernon N. Houk to Leonard Ledbetter, Commissioner Georgia 
Department of Natural Resources (November 27, 1989). 

26 



117 



Richard Christian, the former director of the Environnehtal 
Study Group of the Department of Defense ("ESG") testified that 
not only was this conclusion false, but that he had personally 
informed the CDC that adequate military records existed to 
identify company-specific movements as well as spray locations.*' 
Furthermore, in a February 1985 report to the Congressional 
office of Technology Assessment, the CDC reported that in 
analyzing 21 of 50 detailed computer HERBs tapes developed by the 
ESG on company movements that it was possible to correlate the 
exposure data to areas sprayed with Agent Orange with consistent 
results.'" Indeed, a peer reviewed study sponsored by the 
American Legion conclusively demonstrated that such computerized 
data could be used to establish a reliable exposure 
classification system essential to any valid epidemiologic study 
of Vietnam Veterans.'^ 

In addition to altering the protocol from company units to 
battalions, the CDC further diluted the study by changing the 
protocol on the length of time study subjects were to have served 
in Vietnam. Whereas the original protocol required subjects to 
have served a minimum of 9 months in combat companies, the CDC 
reduced the minimum to 6 months. Furthermore, the CDC eliminated 



Agent Orange Hearing, Testimony of Richard Christian at 41. 

" Interim Report, Agent Orange Study: Exposure Assessment: 
Procedures and Statistical Issues. See also American Legion 
Magazine Special Issue, "Agent Orange" (1990) at p. 12. 

'' Agent Orange Hearing 155-220 (Testimony of Steven and 
Jeanne Stellman) ; American Legion and Columbia University Vietnam 
Experience Study, Environmental Research (December, 1988) . 

27 



118 



from consideration all veterans who served more than one tour in 
Vietnam. Finally, while the original protocol called only for 
subjects who served in Vietnam from 1967 to 1968, the years that 
Agent Orange spraying was at its height, the CDC added an 
additional 6 months to this tine period. The net effect of these 
various changes was seriously to dilute the possibility that 
study subjects would have been exposed to Agent Orange, which in 
turn would impair any epidemiological study's ability to detect 
increases in disease rate.^^ 

Although the above referenced problems cast serious 
suspicion on the work of the CDC, perhaps its most controversial 



Agent Orange Hearing at 46-49. This "dilution effect" 
is considered the classic flaw in epidemiological study design. 
Most epidemiologists would try to optimize the chances of observing 
an effect by including, rather than excluding, the subjects who are 
most likely to have been exposed to the suspected disease causing 
agent. This statistical ability to observe an effect if one is 
present is generally referred to as the "statistical power" of a 
given study. 

When the CDC chose to generalize exposure to Agent Orange to 
groups of veterans who were less likely, rather than more likely, 
to be exposed, the power of the study was diluted. For example, 
if we assume that 1 out of every 5 men who served in Vietnam was 
exposed to Agent Orange, any possible effects of the exposure will 
be diluted when the 4 non-exposed men are averaged in. If we assume 
further that exposure to Agent Orange caused a doubling of the 
incidence of cancers among the 20% of men exposed, the effect would 
largely be obscured since 80% of the group being studied would not 
have been sprayed with Agent Orange and would thus have a normal 
background rate of cancer. Consequently, only exceptionally large 
increases in the cancer rate would be discovered and or reach 
statistical significance in a study group so diluted from the 
outset. See Agent Orange Hearing at 149 (Testimony of John F. 
Sommer, Jr. , Director National Veterans Affairs and Rehabilitation 
Commission the American Legion) . 

See also Agent Orange Legislation and Oversight: Hearing 
Before the Committee on Veterans' Affairs, United States Senate, 
100th Cong. , (May 12, 1988) (Testimony of Dr. Joel Michalek) at pp. 
65, 66 and 668. 

28 



119 



action was to dataraina unilatarally that blood tasts taken aore 
than 20 yaars aftar a vataran's aarvica in Viatnan vera the only 
valid aaans of deteraining a veteran's exposure to Agent Orange. 
In addition, Dr. Houk further "assuaed" that the half-life for 
dioxin in the blood was seven years. '^ When the underlying data 
for Houk's assuaptions were recently reviewed, however, 11 
percent of the blood tests were invalid (i.e. study subjects had 
higher values of dioxin in their blood in 1987 than in 1982 even 
though the subjects had no known subsequent exposure to dioxin) 
and the half lives of dioxin in the reaaining study subjects 
ranged from a low of 2 to a high of 740 years !^ Yet despite 
this tremendous variance in the data and the high incidence of 
false results, Houk and the CDC concluded, rather remarkably, 
that a large scale exposure study was simply not possible since 
"negative" blood tests appeared to "confirm" that study subjects 
were not even exposed to Agent Orange. 

Such conclusions are especially suspect given the fact that 
scientists have consistently cautioned against the use of blood 
tests as the sole basis for exposure classification. Although 
blood and adipose tissue tests can be used to confirm that 



" Agent Orange Hearing at 59. Dr. Houk's assumption was based 
on a study of only 36 former Ranch Handers (members of "Operation 
Ranch Hand," the Air Force herbicide defoliation program) who had 
volunteered blood samples in 1982 and 1987. 

^ American Legion Magazine Reprint "Agent Orange" at 12 See 
also . Agent orange Hearing at p. 67 (testimony of Dr. Houk revealed 
that the senior statistician on the Agent Orange project believed 
that the dioxin blood analysis was so flawed there is a substantial 
likelihood that there is no correlation between the exposure scores 
and the blood levels) . 

29 



120 



Vietnam Veterans were heavily exposed to Agent Orange and the 
contaminant dioxin", even the CDC's own researchers have 
unequivocally stated that "much more has to be learned about the 
kinetics of dioxin metabolism and half-life before current levels 
can be used to fully explain historic levels of exposure."*' 

While the CDC's changes in protocol have been "justified", 
however unreasonably, on the basis of "scientific" 
explanations'^, what cannot be justified is the evidence of 
political interference in the design, implementation and drafting 
of results of the CDC study by Administration officials rather 
than CDC scientists. As early as 1986, the Subcommittee on 
Oversight and Investigations of the Committee on Energy and 
Commerce documented how untutored officials of the Office of 
Management and Budget (0MB) interfered with and second-guessed 
the professional judgments of agency scientists and 
multidisciplinary panels of outside peer review experts 



See Kahn, "Dioxins and Dibenzofurans in Blood and Adipose 
Tissue of Agent Orange Exposed Vietnam Veterans and Matched 
Controls," 259 Journal of the American Medical Association 1661 
(1988) . This report found that "Vietnam veterans who were heavily 
exposed to Agent Orange exceeded matched control subjects in both 
blood and adipose tissue levels of 2, 3,7,8-tetrachlorodiben2o-p- 
dioxin (TCDD) but not in the levels of the 12 other 2,3,7,8- 
substituted dioxins and dibenzofurans that were detected. Since 
only TCDD among these compounds was present in Agent Orange but all 
are present in the population of the industrialized world, it is 
likely that the elevated TCDD levels arose from wartime exposure." 

** Patterson, "Levels of Polychlorinated Dibenzo-p-dioxins 
and Dibenzofurans in Workers Exposed to 2,3,7,8 
tetrachlorodibenzo-p-dioxin, 16 American Journal of Industrial 
Medicine 135, 144 (1989). 



57 



See generally . Agent Orange Hearing (Testimony of Dr. 



Vernon Houk) at 44-50. 

30 



121 



effectively to alter or forestall CDC research on the effects of 
Agent Orange, primarily on the grounds that "enough" dioxin 
research had already been done.'' These Agent Orange Hearings 
revealed additional examples of political interference in the 
CDC's Agent Orange projects by members of the White House Agent 
Orange Working Group." 

Dr. Philip J. Landrigan, the former Director of the 
Environmental Hazards branch at the CDC, upon discovering the 
various irregularities in CDC procedures concluded that the 
errors were so egregious as to warrant an independent 
investigation not only of the methodology employed by the CDC in 
its validation study, but also a specific inquiry into what 
actually transpired at the Center for Environmental Health of the 
CDC.*" 

With these suspicions in mind, it should come as no surprise 
that those familiar with the CDC's work found little credence in 
the conclusions reached by the CDC in its recently released 
Selected Cancers Study. Even though the CDC has previously stated 
that it believes exposure to Agent Orange is impossible to 
assess, it found no difficultly in reporting to the press upon 
the release of the Selected Cancers Study that exposure to Agent 



0MB Review of CDC Research: Impact of the Paperwork 
Reduction Act; A Report Prepared for the Subcommittee on Oversight 
and Investigations of the Committee on Energy and Commerce, 99th 
Cong. 2nd Sess. (October 1986) . 



Houk) . 

60 



" See Agent Orange Hearing at 49-54 (Testimony of Dr. Vernon 



Agent Orange Hearing at 229 and 330. 

31 



122 



Orange do«s not cause cancer. This conclusion was reached 'despite 
the fact that the CDC nade no effort to determine, through 
military records or blood/adipose tissue tests, if study subjects 
were, indeed, exposed to dioxins; nor did the CDC attempt to 
verify exposure to Agent Orange of those study subjects who 
actually contracted cancerous diseases. In fact, according to 
scientists who have made preliminary reviews of the CDC's 
findings, the statistical power of any one cancer grouping, with 
the exception of non-Hodgkin ' s lymphoma, was so low as to make 
any conclusion virtually impossible. 

IV. RANCH HAND STUDY 

Unfortunately, political interference in government 
sponsored studies associated with Agent Orange has been the norm, 
not the exception. In fact, there appears to have been a 
systematic effort to Suppress critical data or alter results to 
meet preconceived notions of what alleged scientific studies were 
meant to find.^^ As recently as March 9, 1990 Senator Daschle 
disclosed compelling evidence of additional political 
interference in the Air Force Ranch Hand study, a separate 
government sponsored study meant to examine the correlation 
between exposure to Agent Orange and harmful health effects zunong 
Air Force veterans who participated in Agent Orange spraying 



*' See generally Agent Orange Hearing; Congressional Record . 
S 2550 (March 9, 1990); Congressional Record . (November 21, 1989) 
(Statements of Senator Thomas Daschle) . 

32 



123 



missions under Operation Ranch Hand. As Senator Daschle 

explained: 

In January 1984, the scientists in charge of the Ranch Hand 
Study issued a draft baseline morbidity report that 
described some very serious health problems in the Ranch 
Hand veterans and stated that the Ranch Handers, by a ratio 
of five to one, were generally less well than the veterans 
in the control group. The opening sentence of the draft 
report's conclusion was clearly stated: "It is incorrect to 
interpret this baseline study as 'negative.' " 

After the Ranch Hand Advisory Committee, which operates 
under the White House Agent Orange Working Group of the 
Domestic Policy Council, got its hands on the document, the 
final report was changed in some very important ways. Most 
notably, the table and exposition explaining that the Ranch 
Handers were generally less well than the controls was 
omitted, and the final conclusion was altered substantially. 
The statement that the baseline study was not negative was 
completely omitted and the study was described as 
"reassuring." " 

By altering the study's conclusion, opponents of Agent 
Orange compensation were able to point to "irrefutable proof" 
that Agent Orange is not a health problem: if those veterans most 
heavily exposed to Agent Orange did not manifest any serious 
health problems, they argued, then it could safely be deduced 
that no veteran allegedly exposed to Agent Orange in smaller 
doses could have health problems. Yet, when Senator Daschle 
questioned Air Force scientists on why discrepancies existed 
between an Air Force draft of the Ranch Hand Study and the final 
report actually released to the press, the answers suggested not 
merely disagreements in data evaluation, but the perpetration of 
fraudulent conclusions. In a word, the major premise was badly 



" See Congressional Record S 2550 (March 9, 1990) 

33 



124 



flawed. 

For example, in 1987 Ranch Hand scientists confirmed to 
Senator Daschle that an unpiiblished birth defects report shows 
that birth defects among Ranch Hand children are double those of 
children in the control group and not "minor" as originally 
reported in 1984.*' 

This increase in birth defects takes on added significance 
when one considers that the original CDC birth defects study, 
which found no increase in birth defects, merely examined birth 
defects as reported on birth certificates, rather than as 
reported by the child's parent or physician. The CDC never 
recorded hidden birth defects, such as internal organ 
malformations and other disabilities that only became apparent as 
the child developed. Consequently, it is very likely that the 
CDC's negative findings on birth defects were also vastly 
understated.*^ 

In addition to elevated birth defects. Ranch Handers also 
showed a significant increase in skin cancers unrelated to 
overexposure to the sun as originally suggested in the 1984 
report. Air Force scientists also admitted that Air Force and 
White House Management representatives were involved in 



Congressional Record . (November 21, 1989) (Statement of 
Senator Thomas Daschle) . 

*^ The CDC birth defects study was confined to Vietnam 
Veterans located in the Atlanta, Georgia region. The study was not 
an Agent Orange birth defects study since no effort was made to 
determine whether the veterans had even been exposed to Agent 
Orange. See notes 10 and 18 suora for additional information on 
birth defects. 

34 



125 



scientific decisions in spite of the study's protocol which 
prohibited such involvement." 

On February 23, 1990, the Air Force released a follow-up 
morbidity report on the Ranch Handers. That report, "1987 
Followup Examination Results," described statistically 
significant increases in health problems among Ranch Handers 
including: all cancers — skin and systemic combined, both 
verified and suspected; skin cancers alone; hereditary and 
degenerative neurological diseases and other problems. The Air 
Force concluded, however, that these and other problems cannot 
necessarily be related to Agent Orange/dioxin exposure, as they 
do not always show a "dose-response" relationship - particularly 
since the exposure index used in the data analysis "is not a good 
measure of actual dioxin exposure." " 

With this conclusion, the Air Force for the first time 
officially acknowledged that the conclusions reached in its 
original 1984 Ranch Hand study are not simply moot, but that the 
Ranch Hand study is not, at this date, an Agent Orange study at 
all since dioxin exposure could not be determined reliably in the 
first place. In other words, the Air Force could just as easily 
have concluded that the health problems associated with the Ranch 
Handers were not necessarily related to eating bear nuts. 



Congressional Record . S 2551 (March 9, 1990) (Statement 
of Senator Daschle) . 

^ Wolfe, et. al., Air Force Health Study and Epidemiologic 
Investigation of Health Effects in Air Force Personnel Following 
Exposure to Herbicides (Feb. 1990) at p. vi. 

35 



23-557 0-96-5 



126 



For the Air Force to have made the statement in 1990 of no 
evidence of a link between exposure to Agent Orange and the 
cancer problems experienced by Ranch Handers is, as Senator 
Daschle notes, "patently false. '''^. Although not yet conclusive, 
what the Ranch Hand and CDC studies demonstrate is that there is 
evidence of a link between health problems and dioxin exposures 
which may become definitive when a new and reliable exposure 
index is used to evaluate the data. 

As stated by Dr. James Clary, one of the scientists who 

prepared the final Ranch Hand report: 

The current literature on dioxin and non-Hodgkin ' s lymphoma 
and soft tissue sarcoma can be characterized by the 
following: 

1. It underestimates (reduced risk estimates) the 
effect of dioxins on human tissue systems. As 
additional studies are completed we can expect to see 
even stronger correlations of dioxin exposure and 
NHL/STS . 

2 . Previous studies were not sensitive enough to detect 
small, but statistically significant increases in 
NHL/STS. As time progresses, and additional evidence is 
forthcoming, it will be increasingly difficult for 
anyone to deny the relationship between dioxin exposure 
and NHL/STS.*^ 

V. INDEPENDENT STUDIES 

Shamefully, the deception, fraud and political interference 
that has characterized government sponsored studies on the health 



Congressional Record S. 2551 (March 9, 1990). See also 
Letter from Ma j . Gen James G. Sanders, U.S.A.F. Deputy Surgeon 
General to Senator Thomas Daschle (February 23, 1990). 

" Letter from Dr. James Clary to Senator Tom Daschle 
(September 9, 1988) . 

36 



127 



effects of sxposure to Agent Orange and/or dioxln has not escaped 

studies ostensibly conducted by independent reviewers, a factor 

that has only further compounded the erroneous conclusions 

reached by the government. 

For instance, recent litigation against the Monsanto 

corporation revealed conclusive evidence that studies conducted 

by Monsanto employees to examine the health effects of exposure 

to dioxin were fraudulent. These same fraudulent studies have 

been repeatedly cited by government officials to deny the 

existence of a relationship between health problems and exposure 

to Agent Orange. According to court papers: 

Zack and Gaffey, two Monsanto employees, published a 
mortality study purporting to compare the cancer death rate 
amongst the Nitro workers who were exposed to Dioxin in the 
1949 explosion with the cancer death rate of unexposed 
workers. The published study concluded that the death rate 
of the exposed worker was exactly the same as the death rate 
as the unexposed worker. However, Zack and Gaffey 
deliberately and knowingly omitted 5 deaths from the exposed 
group and took 4 workers who had been exposed and put these 
workers in the unexposed group, serving, of course, to 
decrease the death rate in the exposed group and increase 
the death rate in the unexposed group. The exposed group, in 
fact, had 18 cancer deaths instead of the reported 9 deaths 
(PI. Ex. 1464), with the result that the death rate in the 
exposed group was 65% higher than expected (emphasis in 
original) ." 



" Brief of Plaintiffs-appellees in Kemner. et. al . v. 
Monsanto Company . No. 5-88-0420 (5th Dist. , Illinois Appellate 
Court) (Oct. 3, 1989) (as the facts were proven at trial, the 
appeal only considered appealable matters of law). Plaintiff's 
brief refers to Zack and Gaffey, "A Mortality Study of Workers 
Employed at the Monsanto Company Plant in Nitro, WV," Human and 
Environme ntal Risks of Chlorinated Dioxins and Related Compounds 
(1983) pp. 575-591. It should be noted that the Advisory Committee 
classified this report as "negative" in evaluating compensation for 
NHL. 

The brief also states that another study of the workers 
exposed in the 1949 accident was also fraudulent (e.g. R.R. Suskind 

37 



128 



similarly, recent evidence also suggests that another .study 
heavily relied upon by those opposed to Agent Orange compensation 
to deny the existence of a link between dioxin and health effects 
was falsified. Three epidemiologic studies and several case 
report studies about an 1953 industrial accident in which workers 
at a BASF plant were exposed to dioxins concluded that exposure 
to TCDD did not cause human malignancies.^ A reanalysis of the 
data that comprised the studies, all of which was supplied by the 
BASF company itself, revealed that some workers suffering from 
chloracne (an acknowledged evidence of exposure to dioxin) had 
actually been placed in the low-exposed or non-exposed cohort 
groups. Additionally, 20 plant supervisory personnel, not 
believed to have been exposed, were placed in the exposed group. 

When the 20 supervisory personnel were removed from the 
exposed group, thereby negating any dilution effect, the 
reanalysis revealed statistically significant increases in 
cancers of the respiratory organs (lungs, trachea, etc.) and 



and V.S. Hertzberg, "Hiiman Health Effects of 2,4,5-T and Its Toxic 
Contaminants," Journal of the American Medical Association. Vol. 
251, No. 18 (1984) pgs. 2372-2380.) The study reported only 14 
cancers in the exposed group and 6 cancers in the unexposed group. 
Trial records conclusively demonstrated, however, that there were 
28 cancers in the group that had been exposed to dioxins, as 
opposed to only 2 cancers in the unexposed group. 

^ See, e.g. Thiess, Frentzel-Beyme, Link, "Mortality Study 
of Persons Exposed to Dioxin in a Trichlorophenol Process Accident 
that Occurred in the BASF AG on November 17 , 1953", 3 American 
Journal of Industrial Medicine 179-189 (1982) 

38 



129 



cancers of the digestive tract. ^^ According to the scientist who 
conducted this study, "[t]his analysis adds further evidence to 
an association between dioxin exposure and human malignancy."^ 

Recent evidence also reveals that Dow Chemical, a 
manufacturer of Agent Orange was aware as early as 1964 that TCDD 
was a byproduct of the manufacturing process. According to Dow's 
then medical director, Dr. Benjamin Holder, extreme exposure to 
dioxins could result in "general organ toxicity" as well as 
"psychopathological" and "other systemic" problems." In fact, a 



'^ Friedemann Rohleder, "Dioxins and Cancer Mortality 
Reanalysis of the BASF Cohort," presented at the 9th International 
Symposium on Chlorinated Dioxins and Related Compounds, Toronto, 
Ontario (Sept. 17-22, 1989). BASF recently published a study in 
an attempt to refute the allegations that the original studies 
related to the accident were fraudulent. See Zobier, Messerer & 
Huber, "Thirty Four Year Mortality Follow Up of BASF Employees, 62 
Occupational Environmental Health 139-157, (Oct. 19, 1989). While 
the company states that "there was no significant increase in 
deaths from malignant neoplasms," the study does conclude that: 

There was, however, a significant excess for all cancers 
combined among the chloracne victims 20 or more years after 
initial exposure when an excess would be most likely to occur. 
In addition, there is the notable finding on one case of liver 
cancer without cirrhosis in a worker with an exceptionally 
high level of TCDD in the blood. 

Id. at 155. See also id. at 139 ("In general, our results do not 
appear to support a strong association between cancer mortality and 

TCDD, but thev do suggest th at some hazard may havg been 

produced. ") (emphasis added) and 149 ("Although TCDD blood levels 
were available for only 5 of the 10 subjects, the three highest 
levels were found in subjects with liver cancer, leucosis and 
Merkell-cell carcinoma of the skin."). 

^ Wanchinski, "New Analysis Links Dioxin to Cancer," New 
Scientist . (Oct. 28, 1989) p. 24. 

" ££e L. Casten, Patterns of Secrecy; Dioxin and Agent 
Orange (1990) (unpublished manuscript detailing the efforts of 
government and industry to obscure the serious health consequences 
of exposure to dioxin) . 

39 



130 



recent expert witness who reviewed Dow Chemical corporate 
documents on behalf of a plaintiff injured by exposure to dioxin 
who successfully sued Dow'* states unequivocally that "the 
manufacturers of the chlorphenoxy herbicides have known for many 
years about the adverse effects of these materials on humans who 
were exposed to them."" 

VI. CURRENT SCIENCE ON HEALTH EFFECTS OF HERBICIDES AND DIOXIN 

Despite its poor record in carrying out its responsibility to 
ascertain the health effects of exposure to Agent Orange, the CDC 
has been candid in some of its findings. As early as 1983, for 
instance, the CDC stated in the protocol of its proposed Agent 
Orange Studies "[t]hat the herbicide contaminant TCDD is 
considered to be one of the most toxic components known. Thus 
any interpretation of abnormal findings related to 2,4,5-T must 
take into consideration the presence of varying or undetermined 



Peteet v. Dow Chemical Co. . 868 F.2d 1428 (5th Cir. 1989) 
cert denied 110 S.Ct. 328 (1989). 

" Letter from Daniel Teitelbaum, M.D., P.C. to Admiral E.R. 
Zumwalt, Jr. (April 18, 1990). Dr Teitelbaum additionally states: 

What I do think. . .may bear on the Agent Orange issue, is the 
fact that in review of Dow's 2,4-D documentation I found that 
there are significant concentrations of potentially 
carcinogenic materials present in 2,4-D which have never been 
made known to the EPA, FDA, or to any other agency. Thus, in 
addition to the problem of the TCDD which, more likely than 
not, was present in the 2,4,5-T component of Agent Orange, the 
finding of other dioxins and closely related furans and 
xanthones in the 2,4-D formulation was of compelling interest 
to me. 

40 



131 



amounts of TCDD." '* 

In 1987, after first being leaked by the New York Times , a VA 
mortality study was released indicating a 110 percent higher rate 
of non-Hodgkin ' s lymphoma in Marines who served in heavily 
sprayed areas as compared with those who served in areas that 
were not sprayed.^ The study also found a 58 percent higher 
rate of lung cancer among the same comparative groups.™ 

Also in 1987, a second VA study found a suggestive eight-fold 
increase in soft tissue sarcoma among veterans most likely to 



CDC Protocol, see note 1 supra . The CDC went on to state 
that a wide variety of health effects have been observed following 
the administration of TCDD to experimental animals including soft 
tissue sarcomas and lymphoma, nasal and nasopharyngeal cancers, 
birth defects, changes in thymus and lymphoid tissues, and other 
numerous cancers. Additionally, the CDC acknowledged the toxic 
effects of occupational exposure to dioxin, including evidence that 
exposure "may be associated with an increased risk of soft tissue 
sarcoma and lymphoma" and perhaps nasal and nasopharyngeal cancers. 

^ Breslin, et. al. "Proportionate Mortality Study of U.S. 
Army and U.S. Marine Corps Veterans of the Vietnam War," Veterans 
Administration (1987) . 

™ Id. Some scientists, including the Advisory Committee have 
attempted to denigrate these significant findings on the basis that 
Army personnel did not show similar results. The explanation for 
this lack of comparative Army findings is directly attributable to 
the dilution effect caused by including logistics personnel as part 
of the Army study. Marines were studied as a separate group. The 
Marine's logistical support personnel (i.e. the Navy), were not 
included. Thus, the increased cancers among Marines were clearly 
associated with field exposure to Agent Orange. 

The Army study, on the other hand, combined field personnel 
with personnel on logistics assignments who were unlikely to have 
been exposed to Agent Orange. As a result, the Army findings were 
drastically diluted. Additionally, Army personnel generally 
engaged the enemy and returned to base, whereas Marines 
consistently remained in areas presumably sprayed by Agent Orange 
to provide medical, health and engineering assistance to "the local 
population. Such "pacification" efforts gave Marines additional 
opportunities to be exposed to dioxins. 

41 



132 



have been exposed to Agent Orange. 

A proportionate mortality study of deaths in pulp and paper 
mill workers in New Hampshire from 1975 to 1985 showed that one 
or more of the exposures experienced by such workers (dioxin is a 
byproduct of pulp and paper production) posed a "significant 
risk" for cancers of the digestive tract and lymphopoietic 
tissues.*" 

Another case control study of fanners in Hancock County, 
Ohio, showed a "statistically significant" rise in Hodgkin's 
disease and non-Hodgkin ' s lymphoma. Although the study 
speculates that exposure to phenoxy herbicides may be the cause 
of such elevated cancers, the study recognizes that, given the 
size of its cohort, the only credible conclusion that can be 
drawn is that it "adds to the growing body of reports linking 
farming and malignant lymphoma, particularly NHL." '^ 

A study of disease and non-battle injuries among U.S. 
Marines in Vietnam from 1965 to 1972 showed a significantly 
higher rate of first hospitalizations for Marines stationed in 
Vietnam as opposed to Marines stationed elsewhere, particularly 



Kang, et. al., "Soft-Tissue Sarcoma and Military Service 
in Vietnam: A Case Control Study," 79 Journal of the National 
Cancer Institute 693 (October, 1987) . The increases were not 
statistically significant as reported. Nonetheless, the results 
are remarkable. 

*° E. Schwartz, "A Proportional Mortality Ratio of Pulp and 
Paper Mill Workers in New Hampshire," 45 British Journal of 
Industrial Medicine . 234-238 (1988). 

'^ Dubrow, Paulson & Indian, "Farming and Malignant Lymphoma 
in Hancock County, Ohio," 45 British Journal of Industrial 
Medicine . 25-28 (1988). 

42 



133 



for neoplasms, diseases of the blood and blood forming organs and 
diseases of the circulatory and respiratory systems.*^ Of 
particular significance is the fact that the rate of first 
hospitalization for disease and non-battle injuries among Vietnam 
personnel rose steadily, reaching a peak in 1969, while the rate 
of non-Vietnam personnel remained relatively constant.*^ This 
rise in hospitalization for non-combat injuries coincides exactly 
with the increased use of Agent Orange, reaching a peak in 1969, 
and declining thereafter until its elimination in 1971. 

In a recently published article entitled "2,4-D, 2,4,5 -T, 
and 2,3,7,8 -TCDD: An Overview", the authors acknowledge that at 
least three weaknesses in research related to dioxins are 
sufficient to cast doubt on the validity of any study. ** The 



Palinkas & Coben, "Disease and Non-Battle Injuries Among 
U.S. Marines in Vietnam, 153 Military Medicine 150 (March, 1988). 

^^ Id. at 151. It should be noted that the year of greatest 
combat activity, as measured by the number of personnel wounded in 
action, 1968, had the smallest disease and non-battle injury vs. 
wounded in action ratio, id. at 152. 

^ Lilienfeld and Gallo "2,4-D, 2,4,5-T and 2 , 3 , 7 , 8-TCDD: 

An Overview," Epidemiologic Review . Vol. II (1989). Three major 
criteria must be considered in evaluating the numerous 
epidemiologic studies of phenoxy herbicides and 2 , 3 , 7 , 8-TCDD: 1) 
the accuracy of exposure assessment; 2) the studies' statistical 
power; and 3) the adequacy of follow-up. Problems in any one of the 
three areas leaves the study open to criticism and subject to 
manipulation. 

For instance, in retrospective studies, various proxies of 
exposure to herbicides and 2 , 3 , 7 , 8 , -TCDD have been used such as 
military service in Vietnam or residence in an area in which the 
herbicides were sprayed. The weakness in such an approach is that 
unless the proxy corresponds to exposure, the "exposed group" is 
diluted with the individuals who have NOT been exposed, thereby 
reducing the magnitude of the strength of the association. In fact, 
such reduction may be of such a degree as to preclude detection of 
any effect. The authors note, however, that the recent development 

43 



134 



authors report that while the data on soft tissue sarcoma and 
phenoxy acids are too inconsistent to allow for any comment at 
this time, there is evidence of a strong association between STS 
and the suspect chemicals in 2 of the 8 studies analyzed in their 
article. Furthermore, the birth defect studies analyzed "suggest 
that adverse reproductive effects can be caused by [dioxin]."'^ 

Recent studies in Vietnam continue to show statistically 
significant reproductive anomalies and birth defects among women, 
and children of women presumably exposed to Agent Orange 
spraying.*^ 



of a serum marker for 2,3,7,8-TCDD by Kahn may provide the means 
of identifying persons who have been exposed. 

Furthermore, studies concerning Agent Orange have nearly all 
been conducted in the past decade. This 10 year latency period is 
generally thought to be insufficient for many cancers to be 
clinically detected. 

«^ Id. 

^ See note 10 supra . It should be noted that as early as 
1977 information about Agent Orange's potential for genetic damage 
was known to the VA. For example, a "NOT FOR RELEASE" VA document 
expressly noted Agent Orange's "high toxicity" and "its effect on 
newborn, deformed children — similar to the thalidomide 
situation." See L. Casten, Patterns of Secrecy note 73 supra at 
Department of Veteran Affairs p. 4. Similarly, in March of 1980, 
Senator Tom Daschle and Rep. David Bonior received an anonymous 
memorandum written on VA stationery which stated: 

chemical agents 2,4,5-T and 2,4-D commonly known as Agent 
Orange and Agent Blue, are mutagenic and teratogenic. This 
means they intercept the genetic DNA message processed to an 
unborn fetus, thereby resulting in deformed children being 
born. Therefore, the veteran would appear to have no ill 
effects from the exposure but he would produce deformed 
children due to this breakage in his genetic chain. . . .Agent 
Orange is 150,000 times more toxic than organic arsenic. 

Id . See also Wolfe & Lathrop, "A Medical Surveillance Program for 
Scientists Exposed to Dioxins and Furans," Human and Environmental 
Risks of Chlorinated Dioxins and Related Compounds . 707-716 (1983) 

44 



135 



In the December 1, 1989, issue of Cancer ■ a study of the 
cancer risks among Missouri farmers found elevated levels of lip 
and bone cancer as well as nasal cavity and sinuses, prostrate, 
non-Hodgkin • s lymphoma and multiple myeloma. Smaller elevations, 
but elevations nonetheless, were found for cancers of the rectum, 
liver, malignant melanoma, kidney and leukemia. According to the 
authors, evidence of the cause for the elevated risks for these 
illnesses "may be strongest for a role of agricultural chemicals, 
including herbicides, insecticides and fertilizers." ' 

Both the U.S. Environmental Protection Agency (EPA) and the 
International Agency for Research on Cancer (lARC) have concluded 
that dioxin is a "probable human carcinogen." 

In a work entitled "Carcinogenic Effects of Pesticides" to 
be issued by the National Cancer Institute Division of Cancer 
Etiology, researchers conclude that while confirmatory data is 
lacking there is ample evidence to suggest that NHL, STS, colon, 
nasal and nasopharyngeal cancer can result from exposure to 
phenoxy herbicides. 

A just released case control study of the health risks of 
exposure to dioxins confirmed previous findings that exposure to 



(Proceedings of International Symposium on Chlorinated Dioxins and 
Related Compounds, Arlington, VA, October 25-29, (1981)). The 
article explains the possible mechanism for paternally transmitted 
birth defects. 

'^ Brownson, et. al . "Cancer Risks Among Missouri Farmers," 
64 Cancer 2381, 2383 (December 1, 1989). 

" Agency for Toxic Substances and Disease Registry, pp. 7,, 
61-68, 94 reprinted in Rachel's Hazardous Waste News # 173 (March 
21, 1990) 

45 



136 

phenoxyacetic acids or chlorophenols entails a statistically 
significant increased risk (i.e. 1.80} for soft tissue sarcoma.*' 

As recently as February 28, 1990 an additional study found 
that farmers exposed to various herbicides containing 2,4-D may 
experience elevated risks for certain cancers, particularly 
cancers of the stomach, connective tissue, skin, brain, prostate, 
and lymphatic and hematopoietic systems. "'° 

This week a scientific task force, after reviewing the 
scientific literature related to the potential human health 
effects associated with exposure to phenoxyacetic acid herbicides 
and/or their associated contaminants (chlorinated dioxins) 
concluded that it is at least as likely as not that exposure to 
Agent Orange is linked to the following diseases: non-Hodgkin's 
lymphoma, soft tissue sarcoma, skin disorders/ chloracne, 
subclinical hepatotoxic effects (including secondary 
coproporphyrinuria and chronic hepatic porphyria) , porphyria 
cutanea tarda, reproductive and developmental effects, neurologic 



Eriksson, Hardell & Adami, "Exposure to Dioxins as a Risk 
Factor for Soft Tissue Sarcoma: A Population-Based Case-Control 
Study," 82 Journal of the National Cancer Institute 486-490 (March 
21, 1990) . It should be noted that in this study the median latency 
for phenoxyacetic acid and chlorophenols exposure was 29 and 31 
years respectively, thereby suggesting that many of the veterans 
who are at risk have not yet manifested symptoms of STS. 

^ Blair, "Herbicides and Non-Hodgkin's Lymphoma: New Evidence 
From a Study of Saskatchewan Farmers," 82 Journal of the National 
Cancer Institute 575-582 (1990). 

46 



137 



•f facts and Hodgkin's disease.*^ 

On the sane day that this scientific task force reported a 
statistically significant linkage between exposure to the dioxins 
in Agent orange and various cancers and other illnesses, the 
Environmental Protection Agency reported that the cancer risk 
posed by the release of such a "potent carcinogen" as dioxin in 
the production of white paper products is "high enough to require 
tighter controls on paper mills."'* 

CONCLUSIONS 

As many of the studies associated with Agent Orange and 
dioxins attest, science is only at the threshold of understanding 
the full dimension of harmful toxic effects from environmental 

93 

agents on various components of the human immune system. In 



'^ Report of the Agent Orange Scientific Task Force of the 
American Legion, Vietnam Veterans of America, and the National 
Veterans Legal Services Project, reported by McAllister, "Viet 
Defoliant Linked to More Diseases, Washington Post . May 1, 1990 at 
AS, col. 4. The report also found that there are other disorders 
for which there is evidence suggesting an association with exposure 
to Agent Orange, but for which statistically significant evidence 
is not currently available. Those diseases include: leukemias, 
cancers of the kidney, testis, pancreas, stomach, prostate, colon 
hepatobiliary tract, and brain, psychosocial effects, immunological 
abnormalities, and gastrointestinal disorders. 

'* Weisskopf, "EPA Seeking to Reduce Dioxin in White Paper: 
Cancer Risk Said to Justify Mill Restrictions," Washington Post. 
May 1, 1990 at A8, col. 1. 

'' A recent report in the Washington Post suggests that there 
is an inherent uncertainty in trying to measure the dangers posed 
by the chemicals humans eat, drink and breathe. Since human 
experimentation is impossible to assess the effect of varied doses 
of a chemical on human health, scientists are ultimately required 

47 



138 



fact, a whole new discipline - ianiinotoxicology - has developed 
to explore further the effects of environaental chemicals on 
human health and to relate animal test results to humans.^ 

Immunotoxi oology has estzdalished, however, at a minimim that 
at least three classes of undesirable effects are likely occur 
when the immune system is disturbed by environmental exposure to 
chemicals such as dioxin, including: 1} immunodeficiency or 
suppression; 2) alteration of the host defense mechanism against 
mutagens and carcinogens (one theory is that the immune system 
detects cells altered by mutagens or other carcinogenic trigger 
and destroys these cells. Thus, an impaired immune system may not 
detect and destroy a newly forming cancer) ; and 3) 
hypersensitivity or allergy to the chemical antagonist. Because 
of dioxin 's ability to be both an immunosuppressant and a 
carcinogen, as early as 1978 immunologists were suggesting that 
"[a] gents such as TCDD. . .may be far more dangerous than those 
possessing only one of these properties."*^ 

While scientists are not in agreement, some 
immunotoxicologists argue that one molecule of a carcinogenic 
agent, like dioxin in the right place and at the right time can 



to speculate or guess as to the health effects of a given chemical 
to the human body. See Measuring Chemicals' Dangers: Too Much 
Guesswork?" Washington Post . March 23, 1990. 

^ Silbergeld & Gaisewicz, "Dioxins and the Ah Receptor," 

16 American Journal of Industrial Medicine 455, 468-69 (1989). 

^ Inadvertent Modification of the Immune Response - The 

Effect of Foods, Drugs, and Environmental Contaminants; Proceedings 
at the Fourth FDA Symposixim; U.S. Naval Academy (August 28-30, 
1978) , p. 78. 

48 



139 



cause the human ininune system to turn on itself, manifestihg such 
breakdowns in the form of cancer. Indeed, even some courts have 
accepted this theory of causation in matters specifically related 
to exposure to dioxin." 

With additional evidence from Vietnam suggesting that Agent 
Orange contaminants have the ability to migrate away from actual 
spray locations via river channels and the food chain, the 
opportunity for a Vietnam Veteran to have been exposed to dioxin 
contaminant molecules increases significantly.'^ 

It cannot be seriously disputed that any large population 
exposed to chemical agents, such as Vietnam Veterans exposed to 
Agent Orange, is likely to find among its members a number who 
will develop malignancies and other mutagenic effects as a result 
of being exposed to harmful agents. 

To be sure, decisions today with regard to the seriousness 
of Agent Orange health effects must be made while the science of 



" See Peteet v. Dow Chemical Co. , 868 F.2d 1428, 1433 (5th 
Cir. 1989) cert denied 110 S.Ct. 328 (1989). 

'^ See e.g. Schecter, et. al., "Levels of 2,3,7,8-TCDD in 
Silt Samples Collected Between 1985-86 From Rivers in the North and 
South of Vietnam," 19 Chemosphere . 547-550 (1989) (suggestive 
findings that the predominant dioxin isomer in Agent Orange has 
moved into downstream rivers in the South of Vietnam) ; 01 ie, et. 
al., "Chlorinated Dioxin and Dibenzofuran Levels in Food and 
Wildlife Samples in the North and South of Vietnam," 19 Chemosphere 
493-496 (1989) (food and wildlife specimens in South Vietnam had 
a higher relative abundance of 2,3,7,8-TCDD suggesting 
contamination from Agent Orange); Schecter, et. al. "Chlorinated 
Dioxin and Dibenzofuran Levels in Food Samples Collected Between 
1985-87 in the North and South of Vietnam," 18 Chemosphere 627-634 
(1989) (Agent Orange contaminants, specifically 2,3,7,8-TCDD found 
at relatively elevated levels in food and wildlife samples 15-25 
years after environmental contamination with compound in South of 
Vietnam) . 

49 



140 



isuDunotoxicology is in its infancy. After having evaluated and 
considered all of the }cno%im evidence on Agent Orange and dioxin 
contaminants, it is evident to me that enough is knovm about the 
current trends in the study of dioxins, and their linkage with 

certain cancers upon exposure, to give the exposed Vietnam 

I 

Veteran the benefit of the doubt. 

This benefit of the doubt takes on added credence given two 
separate means for determining exposure to Agent Orange - 1) 
HERBS and Service HERBs tapes establishing troop location for 
comparison with recorded Ranch Hand spraying missions; and 2) 
blood testing from living veterans to ascertain elevated dioxin 
levels. The inexplicable unwillingness of the CDC to utilize 
this data has had the effect of masking the real increase in the 
rate of cancers among the truly exposed. There is, in my 
opinion, no doubt that had either of these methods been used, 
statistically significant increased rates of cancer would have 
been detected among the Veterans for whom exposure can still be 
verified. 

Since science is now able to conclude with as great a 
likelihood as not that dioxins are carcinogenic directly and 
indirectly through immunosuppression, and since a large 
proportion of those exposed to dioxin can be so ascertained, I am 
of the view that the compensation issue for service-related 
illnesses associated with exposure to Agent Orange should be 
resolved in favor of Vietnam Veterans in one of the two following 
ways: 

50 



141 

COMPENSATION FOR SERVICE REIATED ILLNESSES 
Alternative 1: 

Any Vietnam Veteran, or Vietnam Veteran's child who has a 
birth defect, should be presumed to have a service-connected 
health effect if that person suffers from the type of health 
effects consistent with dioxin exposure and the veteran's health 
or service record establishes 1) abnormally high TCDD in blood 
tests; or 2) the veteran's presence within 20 kilometers and 30 
days of a known sprayed area (as shown by HERBs tapes and 
corresponding company records); or 3) the veteran's presence at 
fire base perimeters or brown water operations where there is 
reason to believe Agent Orange have occurred. 

Under this alternative compensation would not be provided 
for those veterans whose exposure came from TCDD by way of the 
food chain; silt runoff from sprayed areas into unsprayed 
waterways; some unrecorded U.S. or allied Agent Orange sprayings; 
inaccurately recorded sprayings; or sprayings whose wind drift 
was greater than 2 kilometers. Predictably, problems generated 
by the foregoing oversights, the mass of data to be analyzed as 
claims were filed, and the known loss of many service records 
would invalidate many veterans' legitimate claims. 
Alternative 2; 

Any Vietnam Veteran or child of a Vietnam Veteran who 
experiences a TCDD-like health effect shall be presumed to have a 
service-connected disability. This alternative is admittedly 

51 



142 



broader than the first, and would provide benefits for some 
veterans who were not exposed to Agent Orange and whose 
disabilities are not presumably truly service-connected. 
Nevertheless, it is the only alternative that will not unfairly 
preclude receipt of benefits by a TCDD exposed Vietnam Veteran. 

Furthermore, this alternative is consistent with the 
Secretary's decision regarding the service-connection of non- 
Hodgkin's lymphoma, as well as legal precedent with respect to 
other diseases presumed by the Department of Veterans Affairs to 
be connected to one or more factors related to military service 
(i.e. veterans exposed to atomic radiation and POW's with spastic 
colon) . 
PRESUMPTIONS OF AGENT ORANGE RELATED HEALTH EFFECTS 

I have also given considerable thought to which health 
effects are to be presumed likelier than not to be related to 
TCDD exposure and therefore service-connected. Any such 
determination must be made in light of: 1) the review of the 
scientific literature, including animal studies where human data 
does not exist or has been manipulated; 2) the inappropriate 
processes of the Veterans Advisory Committee on Environmental 
Hazards; 3) the past political manipulations of Ranch Hand and 
CDC studies; and 4) the recent discoveries of manipulation by 
scientists hired by chemical manufacturers of dioxin contaminants 
to evaluate the potentially best epidemiological data concerning 
TCDD's effects on humans. 

My evaluation of the evidence has been made with just such 

52 



143 



considerations in mind. Additionally, I have conferred with 
several experts in the field. After evaluating all the evidence 
and material of record . I eun convinced that there is better than 
"an approximate balance of positive and negative evidence" on a 
series of Agent Orange related health effects. 

It can, in my judgment, be concluded, with a very high degree 
of confidence, that it is at least as likely as not that the 
following are caused in humans by exposure to TCDD: non-Hodgkin ' s 
lymphoma, chloracne and other skin disorders, lip cancer, bone 
cancer, soft tissue sarcoma, birth defects, skin cancer, lung 
cancer, porphyria cutanea tarda and other liver disorders, 
Hodgkin's disease, hematopoietic diseases, multiple myeloma, 
neurological defects and auto- immune diseases and disorders. 

In addition, I an most comfortable in concluding that it is 
at least as likely as not that liver cancer, 
nasal/pharyngeal/esophageal cancers, leukemia, malignant 
melanoma, kidney cancer, testicular cancer, pancreatic cancer, 
stomach cancer, prostate cancer, colon cancer, brain cancer, 
psychosocial effects, and gastrointestinal disease are service- 
connected. 

I have separated the two foregoing subsets subjectively 
only because there is somewhat more data to support the former 
than the latter. Nonetheless, immunological and toxicological 
theory supports both subsets and fully justifies, in my view, the 
inclusion of both subsets of the foregoing health effects in 
determining a service-connected injury. 

53 



144 



Such a resolution of the embarrassingly prolonged Agent 
Orange controversy would be on the order of decisions to 
compensate U.S. soldiers who contracted cancer after exposure to 
radiation from atomic tests and U.S. soldiers involved, without 
their knowledge, in LSD experiments. With the scientific basis 
now available for it to be stated with confidence that it is at 
least as likely as not that various health effects are related to 
wartime exposure to Agent Orange, there is the opportunity 
finally to right a significant national wrong committed against 
our Vietnam Veterans. 

RECOMMENDATIONS 

1. That the Secretary undertake a prompt reevaluation of the 
compensation decision impacting on Vietnam Veterans exposed to 
Agent Orange in light of accumulating scientific evidence that 
discredits earlier "findings" of an insufficient linkage between 
dioxin contaminants in Agent Orange and rare disease, such as 
cancer illnesses. 

2 . To the extent that the Secretary deems it necessary to 
use the Veterans' Advisory Committee on Environmental Hazards to 
assist in his reevaluation, the current members should be 
dismissed — having demonstrated a disturbing bias in their 
review to date of the scientific literature related to Agent 
Orange and dioxin — and new members should be appointed in 
accordance with Section G of the Veterans' Dioxin and Radiation 
Exposure Compensation Standards Act, including persons with 
recognized scientific and medical expertise in fields pertinent 

54 



145 



to understanding the health effects of exposure to dioxln. The 
Committee meeting currently scheduled for May 16th and May 17th 
should be cancelled. 

3. That the Secretary in making his decision regarding Agent 
Orange compensation for Vietnam Veterans do so on the basis of 
his independent evaluation of the existing scientific and medical 
evidence on the health effects of exposure to dioxins, as 
cataloged and discussed in this Report, and in full recognition 
that the standard to be applied — as mandated by both Congress 
and the courts — requires the resolution of doubts as to a 
number of cancers linked to dioxins in favor of the Vietnam 
Veteran. 



146 



Union Calendar No. 415 



lOlst Conf^resfl, 2d Session 



Houso Report 10l-fi72 



THE AGENT ORANGE COVERUP: A CASE OF FLAWED 
SCrENCE AND POLITICAL MANIPULATION 



TWELFTH REPORT 



COMMITTEE ON GOVERNMENT 
OPERATIONS 

together with 
DISSENTING VIEWS 



Av>;t'ST •.!. IV.M -CninniilU-d to tlu- Committiv of the Wholi' Mouse on llio 
Slalf ol Itu- Union and ordi'ri-d lo bf printed 



I'.S, r,l>VKHNMENT riilNTING OKKICE 
WASHINGTON : Ift'.lO 



147 



i^ 



£2 » = 
^1 = 1 

2 g 4> S 
" 0) in C 

c j: a c 

?J £ i ?i 



«'ee-^ 



£i 


< 


- 


M 


e 




«i*^ 


S 


c 


C 


3 
X 




^ ^Q 


02 




O 


3j 


2~ c 


o: 


a 


- 


2 




It! 

■«-5 


s 


1. 


o 


>> S 


a: 


O 


"^ 


j= 


1 


< 




j: 


oj 





Xco* £ 2 Sot 












a z >■ 5 " 



^^tii ^ , 



2_S 



e ° -J S : 



148 



Ifl 






c c 

ii 




ai 


« Sin ** 


O J 


"li< 






was used aa 
>uld not be cc 
Ared analysis.. 

the indepem 
oiling crucial 
ne time it ha( 
smpensate vi( 



:a-^Z£ 



E"ii.si|l|i 



|||||ll?|l3|^S^ §5 is|l5 |J5| I 



5*' 

a, Sa- S3 

l-f|f| 

1 c • • 2 I 

■sis:"! I 



•-|i|; 






I i = 



149 






s 

C8 > 

C S 

.2 g 



Cd 



5l 



HZ 

o< 

<&: 

S 



> H 

ga 
$z 

o w 
cdS 



S"! 



> c 

° ■» 



•5 = 



2 3 



.2 >H- 
go: ."o 
a « 4 <- 

0.61)0 0) 

O c^-'* 

(3 C3 CO 

col ^ 

0,'-' Q<0 

Ec c a, 

,'2 4'^*' 



< 2 

S 2 
= 3 



Ss 



||g| 

£*> « c 
o t; ^ P 

2 2)5 Q 



3-Pr^C 



3c3§ 

S 3 






c StJl-o^"^^ I ¥ o 
•Bf^t--S = EE£-s": 

I?-"- o.i "'^o-s c^ 
?. o5c^^'=•a.5«'5.T^S- 
I o- 2-g-- ?t^r2-o - 

u SIS " o— > ^c "- 

I I ^§£^ = "1-3 S- 

iii§l|illll^ 

5 o -g o s E g__^ S; » ^ : 
3 c.. o.tio5i>-" 



O o 03 <l)-o2— §.= ".T," 

S^ " g c = ^ 5 is ' 



EOO M 5 S.S 



-c 3 ■ 



150 



;*= H S)^ > :S "" S 

£ m-O C*** 3 3^ 

3^ cB o en <ac:.5 
m'" o o ♦i w 0* 

5.0-0 Sx-Ou. § 

■^S"*- -•o°'ic 



co3o'^-S_, an 

|:|sl!llHa|.c 



■" ,„ T3 i M^ m ^ 1 O I" « 



£asE"SSE.H 

* S g aO-o g 
•2 o-S g-S 4) ""-S 2 




1:saf i-S:l^-Bl-Ei 

c ££ > „ S I. H |-B " § 



C Ji c c « i 

5 CT3.2 a)S 
— cxix c 

<w oj o !rt •«-' o 

■*-* *^ Q-^ a CD 
4) -M ^ «-c__ 
ax -"*S n 2 

MC S^ £x 

-, S -, -S .ti .£ 
og «* a oo ? V 

= as a 15 

a> C S c e 
CO S° « s 

6 3 go " m 

u2"::-siss^ 

^^«1-§.2li 

i 'o3.s>x: 



E^«S2ic 

2 a-r";! a-- 



' ^ E > « o a 










"22-Sg,gQ E S2x:2 ^ S; 



:'=g§5j.|,o>.i^ 



S£E£|ts5-|3^ 




>-^T5 0-g-X 

c ag o Q o t_ 
t^-S«^|lE 

be >^ **•> 3-3 







151 






^2 ^li Jill-; mi 

£| cE£-fo.S = p°^i 
go- g *S a-S o g.S2 S^ 






E£ 



> " c = a c- o = 2 

Cd "" ■M ^ = E -' "^5 Sj ^ 

5°-S-S._°-5pSc.£o'0 

Sy£c£>.o"c_Sa).2 

3 §>g.g-l-isl2ii 



■= tj: s = a s £ * 



3:32 



ta J. 






■S.2 

i'pli 

' ■ =.5 p 

^ c 
c oi O.T: c a * - 
•S-S o "_2 Mg _ „ 

go "2.^.0— o-g 

■glo-o a'ffl'S S-c"© 
„ c .--S CO c 
4; ao^-.o .2 I 

c a t. § a>_c7>j:j: 











•o S|.S &-2-S ^■g'" £=t§| = :- = ° i^-S >>.£■§£ 3.S 
|t3|,S="" ° g ° °J i 2 i gsr g S S|| o g o^l 3 

J; a« j: S Jco c 5 c £ooS.a si u o a uSaa 




152 




o.^ g e S ^- 
"ra S o g c 

5^ 2-° EC 




153 



1 sil'i r4i:t^ i-"|i ^l-i°|! Ills- ii-^=i=" siH5 

s a":£ -2.1^1^ ^1 :^|=2 i:--si-s£o llji :=lii-2l -'Bit, 



a.2 Ji 



•j= j: 



l-gcao-oajo ■5-Sc"-' SS^.a^ = c .5 ^ 7,-5 js 









^^-="'-^1-: 1.11=1 %^m^:Uz\i nui^^^Qim- 



o a 3 



, .^ J3 •; O C 60 3 



lliPlilil:^l^i;^^?i::iiliiP^fl|.!li:il|ilOhi 



CQ 0) 



III 

n £5 

il S-o a. Q. 



c n £ o S a 



iai^ 3i-^ -: >>•? 



-s§ ji uiiiii III ii>^i?i|^t 

-■MQ ^Q. f-^J5t:_ o o-S!*^ 0.2— ^c^^JJ,, 

TB= c? Esa „„•£ u i Zi X •- S?£OMj,eo,21^^? 

•=5ouiSc3 o " SP.2 S "-^oo JacSjjCog* 




= I--- ^^ t S*""^ ■"■a S 

° tfo-o S-i £ c"" E 2C^ „-3£ 

u. o E 3 " o §TJ 8° ° -^^.r, 

M £,« c -5!*^ g^-ti-a c-2 2 S o 

„S„i coo " I'V S £ i< " ■§ S §> :i^ "^ a ? '- a S S! ?? 5; *■'-' ° (u-o h « a 5 c"S 3:2=5 •^ s 5 

|°ic '=.^gls-^^iSioS !:§ =?c>>li|««i2ll-|«i-o2£sa.^|s! ^^sl 5 I 

|„|« 2^^ -o „c p-gS g2^ rO«|>,3r at E.S-a,S^?|.£P5|°2-t \--_.i^ Zsi 






! E| S § 0, S g.S.-o = 






154 



PS 

bo;:: 
a a 



^1 



1 = 
S5 



£"0 

4) .2 

.s-s" 

as 






O-g £ "^ Q.-I 

S ^ o „ 5 ffl a; 
I aS g ^ c . " 

ill pill 

(5 3 O 4) C ., O 

«> a.^ a> a 5 c 
^ 0) n 41 ^ ^x o 
;= ffl=o Mg--^ 

^^■^'ll «^ ° 
S o si *.£"(= 

■SE-SSf.So 




a2 c ^ ^ " S" 
-irSc. -2?-" 



,r -S i; =-.2 u Sx^ 




■S i g-a c opIs„ 
xS£|.2§|-s^ 

■go' °> Ml'" 9» 

.^.S!.£-S^.S-S£ 

Oa'- 2-- i = « "= 







> S S'-'S 70 c<-S o >.-S~ ^ <u 4> 
S <u «>£•§ 2 Mii g'5 2>3 "= 2 a cu 2-i 






oiS:'- s c = «• 

:h.S2 g-gE 






155 



12 <1«^2% 



Si 

2| 

Hi 

u S 
S'5 



.2 a; a 6 5 .^ „ 

30 °! S" -Si 
a> CO . - o Q. « 






.-x .5 ?- : 



■£■503 
^ So c 



=; S: c c S £- 
o ^ M-S 3 I 8 



Sx E£w£^ 



■g 4*3 m M am 
"pS" «! !; a 



o aJ £ '- *- 



5-2 -2 ^ o 



9 about t 
d use the 
n he disc 
thought 


ase Conti 
he study, 
journals. 
e Centers 
m the Vi 
ted in the 
location9 




1 £ 

ip 
ill 


y raised question 
ly comprehend an 
ng astounded whe 
locations when it 


e Centers for Disc 
ork of ESQ from t 
th copies of daily 
personnel in tht 
he grid points fro 
; were not interes 
king for the U.S. 




imon 
cient 
I beii 
lemy 


int, th 
the VI' 
DC wi 
e, the 
irded t 
nly w< 
ire loo 




a. tc-S 


■siir: 3 ^ 






n's tes 
to suf 
■d abo 
fying ( 


t one po 
ike over 
d the C 
exercis 
trol reco 
3. Certai 
9; we we 


3 

c 




stia 
taff 
itifie 
enti 

te9. 


0. 


C ""(^ 


<*^-ria = ^ ^"^ 


c'S ? 




slsd-Si' 


& 


33 s 

^ S c 

u 


ox SD 






Cw 



E£ £ °29 0-3 Si- £ 
£ S-aa §.'• . " o ° s 

■> S,3 £ £« . 2ijt:=f 

= C03 .5.1io*OB< 

Ji-'Ss^aO .cc'-3o 
:S2^^iEofe^aox 

bfl C g J- C 3 
■- S ° 

SIS " = S '" "3 ° '•" c sr, 

°i!-S-S-=Oj: 



gS.8|- 



X a; 01 > 



■5 x.2i£ >. 
= E tmo c 



o J o. 



o =■■ 
£ -.S E 

f 2£XD. 

* ■-'-•" a 
= S >.3 ,u 

I ti<§ 

* X cyj . — 

0) — < «; 3 . 

c . MX -a 

o -ra <u c , a» 

>> ax o ^ — 

II ill! 



X oO a 



-e^q 



'* C 3 ai 

gx-°.; 

"^ a c* 3 

^Ie"? 



it^'.SPa-SS^jg. 
2 ay «.- g"-a^ 

:^iH-«>.°£xd 

s; 



Sxti^^ pxS >. 

l-sx-S S ^ 3 o It> 



3 u = », 
.Si, » 1, p 

£i>-2- 

^ cx E 
c a 3 — 



i!! -Ts a '^ 3 ■" S 

°|o-3|Eg-S'2!s 
«.|=2o--|i'3Sg 

-. cyS I S a" «J-^ 
ax:Qo«i2".c*' 
„30"5=xc-g§-- 

.S-2 ¥ ., a.2 i _: a .g. 



ao><S,=?o2a 
_c c " c^ " ax 

Sot u ¥2 So 

2Wa5&.23 3 
c ^ o ao c h,'-' 

mtUp 

3X . " -Sg C 
C CO wT3 5 Si--- 

•2gg|„s:~J 

""cS S S £ "-C 

- a «.2 c o£ " 



n O (U c 

:^£ wS 

•3>, 



: 3 a" 



S-Se| 

*J.|E 

Sill 



E is " " 



-*-r;.E iXC £ al £ 
l8oE-=ai-°.Smi.S 



;5xati. 



;86E-=ai-°.Sm|.s 



Q.C_S _'2 

o 



-o = =■;? £y r<^ 

£w i -s a S Eo oO 



"2 *' 

"x Es 



2 4 a» * 
= 6 

>S|S 

a a 2 
c I E a 

j.a'H ao 
•'S§"£ 
£==•:; -5.2 



0. 


5 <u 


- 




aO. 




4> 


aE 


c: 


S 


£ 2 





■3 


•0 u 


3 


E 


c 


L. 


3 


OCi. 


a 


■0 






c 


1-3 


£ 




> L. 






•0 


c 


E 


= ^ 


c 



lo 3 a So-g E-5 Jw2 >, ., 

£- uS g at 

.£ E ax 



„5 CIS E o- 

g 3 =!= £ E « 

.2 a S °"2 ^ 

^11^ is.! 

■£"Be"I12-§ 

°tvi * I Ic 
c ajb« „.2.2 

1 1 -=3 lie 

.'> £ E c 2.S 



HI 
O a = 

■?? x§£ 

.eII 



1= £-o 



»7 m 



^11 jJ 

>.S| 1^ 

ill --° 

Si J II 



'Ee 



III ^ 



eE 






!5-- 2 



si5 



■S'i 



ic2 ;:?>)! 



^y 






156 



■0^3821° 

1. £ Q. = c 2 .3 
o S.S *■- S = 

o 2 S 0-2 1- " 

g 2 o-^l 8 n 
o - £j:-= S g 
•o 2 ° o «'.^-° 

t:ili 1 

0, ° g MT3-- -g 

§ c lac's ^« 

^■1^.2 da-. 






'i o>-s j: 

■5 CO— g3 
>,-o5'a:= 
•o 4! = 01 









i 01 1. 3 

' *J O OJ M 



.2 S be 

"a T " 
" MX 

SfflS " 



£„£„, oiiijjp, 
■ := a; 






§^■5,0.8 : 

^1 «o « £ 2 ^-'ll g 
-oil cD S&^ " ^ B 

ii 3 no I £ S -a -^ ^ 
"« £ c ni " mS 3-c-r 
"5»'£2_<'B'oS.- 

_-^sS.2Sto23-e 

o^.i ° o^-o2 =-= 
g 8 g Si_ c = Ti ^ I 2 
a£ o.^ 2 '''^ Oi":; boa> 



■" "~ -'S°3-9'!"'"E3ig" 



•> .= 



0) « 4) " 

o m C _- 



s-^ 



S E 

°'-C eg" ^-j c 41 

SS£>>o .= .= £ 



i a— -o ^"5 I. 
*^ a a a^ 4, o-r — t3 

^|I|15s"l:e^ 



.2 J'' 
ri '■ >> 

3^ O m 



Sttg 
c g>^ 

OJ 



•Ms 

2£S 



^35 

£.2 a 

ti c 

„ a; ^^ 
M '^ c c ■ 
:.-0.2-- 

StSE 



>,3 Q." 2 

m •= e 3 
.2 I. o o > 

E «-^i:H 

S c2£*' 

Q.^ O O C3 



E^ c 

- O^ T 



w ■ 4* 2 i: 
- 2 i> a^ 



J 2 <" a_ 
a; o m.i 

o 3.2^ a 

^ ox s, 



0-0 — — " c 
V. ^ a a J u 

giM>,£:H 

— '".S'c = o 

- 3 8 c-o-a 
T} a— oS ^ 

■o S;2'S " ' 
I a g^ 



0, . II 2 i; £ 



2 -'^ 






E 

" 0) o — ^^ 
£ S a, = 2;^ 

o S o «-s 
c£ S S-o 



.5 cx^.. 

8:5-1^ >>2 

*jrs,x c 3 o 
j:: > o *J " 05 

ig<§s>. 

o ID Si t! ^ a 

■Ox 3 " ■-■- 

— *^ a -- o ~ 
S-sSo-SE 

O ° ^ 4) 03 

_f-'£-o3 a J 
g o^ S'oo 

=i " = £ "- 3 



MX 



a'So-ao S^ 

i2-^S.3 

o .^ O I. Sf'g 

_g'l.||o| 

•* V ox c « 
c aS "<2-3 

* o " -j is „ 
■^ a'H.a) 3» a 

» S XXT3X S 



X * «> «3 

£ « 5*— S i)'^ 

SO) c y-gO S 

?, C £ S 2 M .. 



E a) ots - a-s 

o£ £- o i c 
"_ SiS " I 8 

« a, < — . J, >> 

£-• c 4) S o 3~ 
"■^H a 5 



bo.L 

- <» * 
>va m 
!s c 

IP 

2 I 3 

2'^'S 

0.*' o 
E." £ 

2^3 

a.2P 

o-o 
c C J 
_ a S 
2iJ*^ 
•n c 

Ho I 



c-"8 = 

i a; ^ ,, 
2~ a§ 

a > M 

S"o.S 
c a'S 
o 3 o 

l&l 

E-o ■ 

•sas 

3 SPS 



■2|c3 



'X o 

■o a 

S.'H^ 
ai 5^ 



i- y -t ** "a a 
"-.atS c > m >• 

" c a S, c o S 
M.E a; c 5 9 
.S25a-3$o 

(u 4J jd e^ *■ 4» 
r =5 ^J bfi^ 2 ^ "■ 
a ^ M's'-'jO-^ 

3 -J O bO - 



.xC».x g 
' cOtj E 
ixO a) E 



<•= s s 2*0 

><.2 < -^ > -S 

tS-ol5P2 

<• aj a> a .S •- 

■^^ ™ S e 

l^iii-! 

8-§§E„S 
£x-s ji£ g- 
Oa|£a," 
a, ■" E_-g^ 
-Cf- a) °— 2 

E°°£ £ c £ 



01 aJi-^^2''*' "• 
S£-n MO o-o 

"> £"5-= S £- 

•s-;«-a-=ia2 
laS-|i.-st 

£K^|a|-^3 
X jj c d a 3|S 



S I ° a ° 

•sj S- 5 e V 

_«x a > 2^ 
"a" 3 "■§ 



> 
a 2 



O E- 



- flj" flj H O O 



E I g;g-o£ 

Or t- aj S 

Ec.S^2^£ 

H2.2 S 2 2 
.= EO^ a 



§.J2| 

X c.ti 



J3 



x2^ 



>^cSJa i 
3-Ha>Q§ .5! 

;o£^i3 2 
'i!, °M S 
5^g^-S -oc-S^ 
■ g " E^-S-S2"§ o£ 
-X 5 a.^ 8 8 SW?? 

J--g^"^ S"_g o g 4, -3 

S c E w d, S a)^ aj c 



S ES.S 



O Z B 

§?2 



£'5 o-o 



o-o-t: ^ 

JE Sx2 af 
O.C c 5.2 
*i o Eito-o 
2 P OJ-S a,, 
-£ Sx$^ 

3X.S2 " . c 

1 S tf f 



„S,-=2 



2|gog5^o2S,££ 



a t'i 
a) 4 c 
2 0.2 

lis 

^a-~ 



-• f" 5 

5 H O 



D O^*^ CD 0) L. O 



¥ >- "J c S 
a "-S " 
-^■5 2£° 

S o c.-s a 



2£o 
*j M 

'Kl 

o ** 

III 

^E^ 
2< 



157 










a,> ^ s £5 ? i " 



El. g-i; 



So olj 6 S 



ti :i « a Q.S ■" 

ai-o 
11 



O^ 



! 0.2 » 



:g3* 






i «j » 3 

oj3 E 3 

-•^£-° 
- S; 3 « 

*j > 0-- 



< „ « ajoS 0,35 c c ai 

2- 0^.2 c v^-o i g- «!> 



S_*''»'!ll ° = V. — T3 " 

gs-:|gi§| 

0^3^ i-S c-° «-" 



!i^ 



>f 2 ® 

a}<2 a 



Ji S~ * 3 a 3 

E g k- 2 .-o_ 
J, a ex 0X.2 

S J; Sojt; g. 

g|t|t.£2 
xl ° |5 s S 

■"=; c S o c S 



dS. " i 



~ 01 2 p= o 

Sox'^'S X 

O c «> ^ c 

■i Ct 3 C m 

^^S-OE I, 



25!SgS 

"O 3" t — 

= « S 2 2 

.- »^ J Si 
gx a '-■J 

o-^i E ° 

ill 



E-°"oi2'S. 

S 5 c " »- 
^x ° ai'S"" 
"- "^ -5 X u- — 
e u 3 2 o » 
■2-2 o 5 „ 

a'»1i a 5 3 
o c 2 ? o 

J «■£ u" J 

■o 3 X a 
^£.2S-c 
«3-S o- « 



'S 35 



O 01 4 m^" 0* 

■ a c-g 3 > c J 



60^ 

I^olgl 



u O 
3 " 



■P 3; iz 

x-s 6 » 

^ S S~ 



-■ E • 
•£ g " . S 2 ° 
•il-g^lS 

Eoiiss 

■ZSSc '" 

S >.£ =|.£ 

i|£l2| 
3aE£g^ 

5 22 E ax 
* 2.S - *■" 

•* X S?.£-2 
o*«^~j2 c y 

X '2 . 4) Of 

" g tie£ E a 

■"20 5 c — 
*^*^ . .9 o _ 



3 &■: 



,.2.2 >^ c-o 



S'>>T3 3 C 



"■5 



1^ 



i3 c 



23-557 0-96-6 



158 




alli- 
ed in 
tions 
over) 
ough 

con- 


d on 
thing 
time 
1 con- 
nt to 


stem, 
evaili 
condi 
ive c 
as r 
1, the 


S — 'o c- 


S" " c "- £ 


>> i: -^"a^ 


"O CO 3 S 3 


B o-v. c5 a) c 


O o m » 


>.xsi;§s 


3n £ 2.S 


as the spra 
those whic 
lissions, otl 
d and veg 
n only be 
In a cross 


dose wou 
sorption r 
9 such as a 
loit, and gri 

Data are 


o E S flJ ^ 


,_J3 U •" C 


.c -i- 2 y c 


Q ea o - a 


CJ _, 3 o 


TJ 


3 Sl-S 2 
§1 = 11 1 


S >.£ 1 s 






gl 2 gj"? 


^ E c ffl 0) 


■ - (0 o aJ' CO 
i^ S "S .^ <ii 


il<S"^^l-S 


ny ( 

raft 

:he 

ber 

, so 

erbi 




SsIicr^S 


5"o— 2~ 



2 £ 



ar to 
ikeli- 
with 
here- 
ween 


4) . - "W 


strictions 
scope o( 
:ta for in- 
; criteria 


^ZKl. 




^IP 



.S 3 >< § xH -2 g a. 

S.X " £ = a- ^ i 
§ff S-§.s|-s.§ 

§'i.2„-E£g_i.Sp. 



p 3 ca 

~4i 



Z Q. ai-Si'Si K P 

3'''£-ap'a.P> j; 

■^ -t;.^-- 0) c * " ^ 

« o ^ Tt. -T! ^ «, .. -r 



T3 4) - ■ P 

) m'— -P I' o.^ 



Q.<: So 






'5 t -° ' 



C 3 



:«> -S, 



.^ 



u 



S o 2 £ a,.p 0) 

J |.2iQ v" et v'' 
, =2p^.p<^.£,-§.2B 

isp'^lllfl- 






?£ u- I 

o 01— £ I- £ 

£g§§|J 



! >>•" p 



: P 3 



5, : 
is £ cu5 
: p ,o j:- 



- = ti 

; eg S 



-i.s|::°iii». 

- m2-C V^ S.S.T3 

P P .2-2 >> ., ., T) ? t.' 

II 11 illll^l 



,= 01 J) IB 

? > go 

II |e 



1^3 u c £ •^•E 



3 fci) ^"S C w 

" ^ u = a 3 3 : 
u^i-^ C ^ L , 

S 3'eqSqSi: 
i 3 



SE-K 



"ill* 
SIS',? 



•^J3 £ 

|5|| 
5.111 

o ^ P" 

.£o.c £ 

o-O'S iiS; 

|„-p.s2 
S "S .2 ^-p 

o t"-^ 



III 



ilnlfl 



159 



" D < 

>■ 9 z 



2 « 2 

<2< 



Si: 
<si 

* = ir 

3= o: ^ 

- O m 
2 J D 



O z 
! H ° 
I Z Q 



X feXx c3 o S fe S-S b^ S-c S M §-c 9 

_-4(U m C 01 ii O Xa, ^, r' Oi •-<£t«o 

cS -^ «i = ?! ,„&:. i:-2 S ,„ S S-2 -S'Si; 



3-^ C c 
-^ C = o-o 









e s - • a S ! 

"I'S'S " = Sa;~-£xo»^s 

-3 '•£>»cJ=5P3c >3C 

3., -° .2c2o2S:^3a*-^ 
^^£.ti«i.ca— o!:i-2t*'a) - 

■£Sc°-o«55"fc-2x„-3a'a 
, sf tioT: " " ■§ '5 ° 5 

.'J.- - JS aJ J= ° ^ > C ^- c — .- ■" 

.a- = ^ =-£ci 2 3-i-^ e 

2Slo-l|.s2|gS^^g-o£ 



- ^^SJs'S 



■l^li 



-° 0-? ' 



c-o O ._ C 
;— »? o ts -- 



• (0 CO ; 

il2_ 



o 3 s,^ g^ 
£S.g^|S 



'eI.s 



S 3; "1 * * M-^ 
E i S c I 2 



ti>-£-2 

ig-s» 

.§-5e° 

c o S">-2 



5 S £ So 

S Q.O 



o "^ £ 
g'oj: g 

«••= „- g 
.S g — "i 

c-a a 0) 
'5i^ to * 

^M 

Veil 

> x-o 2 



aj c o "S 

" 3 aj- 
^ £2 

£°"i 












ijjjji 



riiii? 

02s 8 



■5._ 3 01 



&3 4, 

£ „2>S"x_ 
a 2 3^ "o -S — 

.2 -r. .5 >. r*' 3 _^ o 

P* -^olc^^ 
ui? 300_o3a,3m 



C3i "^ui* 9JT3-0.i 



:5i:s..«g 



3 ^^2 



3 J a.2-o a J 



»S 



£,^E 
g c -^ 8 



»■-£.£ §S So a > 

.3 X 4 S -.. P 

^ " 8 Ji, £ ■" 

... - ^ w.-: S S-^ o = ix S ~ S 3 

3 a so 6 „•= E » £s .,■£ "-gj! g-H 



?1o 



sd 6 ?■•=££ Est;-- 



s-2ii:r >--s'?^*-^-2gfeSo 

'-•Si3-s|-S3E-_2£S^i=^o 
:=8S3m:i; it. ai -o 3 E 



V * i M 

2 cK-s 

£|.2e 

»«xx a 

H £ '=■3 
n.a c 



9-S a-3 
£ =-=.§ £ 

» S I » s 

$ i. o c ■ - 

3g.-SS§ 

cO»Ot 

a a.;^ S * 
X "-D o 3 I 

OX'S n "'O 

" S g S."o ? 
E-^ c 2 I c 

■ ll.^lag 

• = - C 3 ., S 

t g 3t. 



8 c c 



•3 aj"^? 



■a 3 p a 

i S'i g^ 



x'S E c 



o — •^•o 

•:;:^ >> a 



.5t) ax c 
c c c .11 
03 = Wo 
c o £ c a 



' w3 



55.3 



-o 5.2 

60— 



coO (0 CQ 



CT3 j:»r 
o c *-• ►^ 

"8.82 

|.£|| 
xiS£ 



c J. c S' S' 

££-°x>> 

£ 3 3" c 

*j * X TJO 

■£'e ilni 
ii 8 c a S 
:s ° c S 3.'° 

*■£ 3 = 8° 
1 sl»3 

= 8-S>a|^ 

g02 >-3° 
■z >>"■" "I 

£■3 J= _ 



■;2.22^-p 

£a^2--o 

L. «CIx-° 3 

.^la"!? 
£ ^5 



"S « i. J S s S 
o^3"l:sg| 

3 a* o aXW 



I 

2-0 

5? 



a" a|-; 



160 



8-S] 









a-& 



5PL 



P 2. _- 



^-S-S" 



it^i: 



= S « oT P 



uCauoa ion 



^ c li I- S^ 
3 >>ctj S"" 



^ "i.i: o = = 
o'_^'u m 2: y 




j3 0^ a; J - 
■5 ? fy D-o 

o « — ^ ot; 

c c c n a.> 
3 fci fci c h 

fflT3 O ^ 5X 

£2-0^ «j t c 

g g C E m 

i a||.2 So 

— "o «'•- j;-^ 

O— 01**- 



= i^ £ti sic £ 



c cii_2 = 3 S^ 

Sic "2 c m'3 3 
c S fc,S c o 



c B 
j Mg 

18 5^ §--1185 

■-o„-o£S<_o 
ire oj: S 5, ^ „ o S 
«£-" of -gg V.-0 
■-- ^c*^oi2o5 



3 J3 ^ 

3 Cj C . 

id M 

-C<-. 



loo 
Sj3 g , 



a 



- a, o-°3 



c ^'1 o fc I m^ t 

.■a >,'5 01 01 3 M 2i « 



■S-2 °3 c S-^ ^ 

llaljlsl-sl 



.2 X 



^ >>iS-"- i--c: 

iEl-li = i'^- 

u-s a X a ^ "' 
.01 o-"T) a, J- _ 

o-§l£isi||.y 






!■£ -oT — Q. 



r 01 >>r; 
,•2 g'Ouj 



o-5-Si 



c-*J 



c a* *; rt c 
E-=3gc 



3 O c 4.2 



1.2 



= |E3 






° S3 ' 

3§>;S 

c 5 .2 cm" 



S cO 

3 0) 
— .M 

o< _ 



i| Ija-J- g I c o 
: X ** .c ^-3 <u "^ o t 
'■■c 2".°'° ^'"'~ ° 



a 



'05- iS J 5-1 o^ 
r'-'^ — c — - 



c-3 — j:?' 



>T3 J, 



>,So 



:>_ ^o S.2 '"x 

I ^^-S-^u-^ oi 
ix S P c t t- 

: o ys 2033 
!5-2Hl:^lli3| 

1 3 vb. oiM*cS'-ao 



S.£E 



^>'s ap> 






":- ¥ * S 



01 I MJ= „ 3 

g „ £■- 3 S 

imh 

0) c o > 
-a tx i: as 
= 4) g 2 .2 a 

2 2c -o >, 

01 g a-o ana 
.2 a. J, -S 8 2 

■" 3 - 0.5 1: 

•3C0 £ £ c o 
01 g3i= §•§ 

bo e 4) o 
C £^ 01-0 o 



c -" Ji S 3 o 

30- ji " £ 
_ oiSx E 3 

.5 MQ 3 B 

lisp's 

g S5 "'§-.2 _. 
:5 S 4*"" "^-^ ^ 



3xx 5 Ox S; 

^.Sn a c 2 = 
2 X D. £ °--S 



J a^ o ■£ *j cx 



•^ qi _ 5 5 



o o.tix f;x o 

(J. tfl o o aj tn 2 

i: a> o a^ c-- 

J.asi-^i'o 

j,-O.2-0 3y 



ag.S|| 



frt*i c 

-2 0-- 

a o s 

X c £ 



,^i 



ia-s 



^ Sac" ° ai 



£ "-Sx =£■£ ci 
oE-o.= S— uiic 

^S.^^g:.c3 

c S >,-- 

■^ £ 3X^ O 
c~-r 41 2 <T. 



ill 

3 ax 

2 3 g 

11? 



O c ! 

T3 41 i 



I O 3 



r= "r^-?X. 






xH3_>> -S^aix 



2:2a 



o 



IS 






Z2^ 

tn V) u > 
^S ■o'l 



161 






2o^^S>5 -o "ffl 2oo^^-^ io^^o-sg =-.•>,»- „ „_ , ^ "^ " " 



t^'So" 






0:= £.2 







tii< o .Q^O=§^-.S°^ Zens'" c^=-e=5-S <i.S! ^ 5,-5 -g 5 i '^i :~ 

- = t!= ^-S-. o-a a 3^:2^.2 5-^.2 3; S E.ST.ir &.2-^fi-2 5 S S 2 ' g,^ I 



SSiS i§|S5^.2o'g = g -SSJs-l S3!i|fr-2c°l.2-£ ,I-23q|o^-^ s|J 

J- S .«) t Tst^-c o o'^O- c " >, ^2 3 J g I 4- ^I ^ OS a|-2 4.5 p «5.2^pg-;^-o .2 s^ 



162 





S=S^o-„- «-o g.SPl MO--S S'C-S >>o 

nhhiJ 1r|:|li|l.5. 11 






.ai-bo 






£|: 5 
«J!S-£-" -.2. 

-•■■--. o S °) a 



.jiS.s.£»l-S^-§!"|^.i 
l|i.s3s|£?:2Sgg 




2 >,c 

l^io a- ^ * S 

•3!,2 „ S ■= J= - „ 

_g.£<'^-2 Tj 8 >. 
cl^5| III 
c^ a, « - u c c 



•-•S I S 



$ 9 c ° 

sill 



Ili^Ssl'i 



3 t-".>-o 01 



'-■s 1^ l"- 1 E i.2=-5"g^ t K^S o £ 

SaS: S^cOG.2>ti3:5CM2°£3S!r 



!s|i 




*t §S»'2c'Sg^ 



S-S7 
CSS 



o2 o § « 

.a EffS. 



= i"i<>^T3 o "-a" S'3^ 
»«*' ,u- — S==-^ 

2g°5 = i2£^-i^ 
8 1" "I e "33^.2 

r ocS-S*-o-g| 
o., ai2SS2S»j3C 

0) 0} 01 Is u- ^ MS; 03 — •— ' 
o.> c " ° o-^ «■=.'- 

£.2! 5t) a- «)C 



5l> S" 

B £ 3 



:5g' 



«- 011= c 3-C:£7'2 
£ g "1 1 1 2 m|_ I g 

sll^llfifal 



i ^s 



163 



'■as -Sic Je3S«.i= o-S 1^ 







'•s 3 S 3 s 

t«.£Sg< g 

.£ EP s a 



= = s = :;8-s'§s"-gE 

sa»E-i|S'^|«gs 

01 ffl-a^-Ti a-a o Sii' 



c a 
£t3 S'.S 



" ^■S^-.u c*- ?■= g-^ 2 a ..*' 0. --9 ■■ 



5^ £-^ 

>g" 
E- 



fill 
§■' si 

M II 



sa^^l 







-> a, C >"■ O p " „ 

- -S X ■" 2 ■'^ — 2f S,x 
= 1^-5 ^SS|=^ 

u m ■ •- O 2 «^ 2 ^ 

"S ia ;5 - 3 3 S "a S £ 



3 



> c£aji 3 



S* aji'o^*'*^; 

III ^|!il|li 

> r^ c 3S— i: 3 e I 
^ S"-2 ct; a S w g : 
>, 5 >,-S o t c -= ^ -2 ^ 

f-s E-s " as>= >.S^ 

J a.S c 3 o>_'^ 2.,' 



- ^ « C i '2 

= Og.2S-.y 
: cO-g o " =" 



£"81 



I 3X 

Sri 



S3Sa,3S vi»^ 

ll»l!iiiir' 

8 -o §3 5- s 3 c i 



S a «! - 2 ■3 

= 3gO>^8 
' g " a o "S ■". 






a c ^H •! — 
— £ c c »; gC 



a. c 3 
__^ ID g 

'I * a^:5 ?Pc 
5 S 01 "a. <»'>■= 9 

jgX jS ,^5 

1-3 S «■ ■« "g 'x 

:a_Sgi!SS2 
>E- E >£ ao 



■g c g i«3 3 So i .£- E 
SS.i^xg^g'-i -5, eg 

Q." = 2-£'S'°x-2 2 n^g 
tj2 ° g ax S," a J, '.£.2 > 
•S ~ a - ? " = S",= S .i'o; Sf u 
g-i^S.SSS^I-SI-oJiQ. 
.|a;^-o>0-Es;|£Jo 

lIsE^Sgl'-ilsri- 

^ °-o-«= 1^ = 1"-^ Sxg 
'C 2 5 3~« i-2.2Pe,2ii *x 

•-.£ 2 S a 3 9— 1; 2 u " ' 

■«'''Oio£D.-£o— ot! 

!l|i>:Hl||l:^| 

£ a2 $43— _ " o E °J> £--'S 



a S u,"^ 9.5; 
S l<-= 3 g =" 

-° „ c ~ s a, 

fillllii 

3 M & a £ -S ?v 



«; I §x 






a 



30g5^a-2| 



c s «) c ; c~ 3 

S S o Z S?-2 -3 o 
a .s b .2_2 ■= s S 
ES, 



« '- s s"^- 

8|i°iii|:|i||i' 

so. 2 »•= a «) g-; = 9 '■ c_- 

>ta^-!r^^~Cu>^ a 

'^ = ac— Q.000— ao. 



'^ * m P £ 

=: '^ S a 
' 'J S.C "^ =■■- o 

* p « o o ^- P 
: - i|.2 a g Q.= 



L c "r -2 



5 E 



c - c S^ g-S. 



II 



J i3i 
i III 
12^1 i 



1.^ 



9 Pr-- 






164 



CO 



11.1 = 









g|-:S.£SS2^e|S2S 

£53' 



£ ■ 5 O u g 



-S"? ^ 



oc i 






. £-ni<utj»o p t- £ S ^■^ "--n = xS S°x' 



Hi! 






sS- 



i-fs.. 




5-20 

.>|x 






E" °-£^S> c $Z E-S< g| S"! o.So 5 
^r: r-^ "u. ii-T, ^ SI •" :> ^— " a 14^ i 

S i^;! E c^2 i = g I > E-^ °-^l 1^ i 



si ga.S.S 
gSS.-SJi 



a o g 

S.O.C 

o 



a-S^ E 
a-a^: 



Qx -S^-S E c 



i'' 5.o52 

ii.2 Q. 
"tj l^x 



oo"-r a, 2 ^ c boE Sixxm^x «,.5'S's o =•- 

i-'-re >;-§-5-n gs s j-3 £.E l^l six 

i^illKlilliillll#ii 



■S-B-iia 



-oS>.£g - 



'Z o 



-^. ^- >•? 



-■20 s 



a S o^tS 2-' aoT3 
X 01 5.3 ■=; ~,2 a 

"O-S'SES; aSSS 

-? 23e.5?, 2S 

I" : 51 |li!il 
fliiiiii^i^ 

ma ;i3.'2 4)a.'-2 

.^-SEii-a-°£2"J 
x-p o oj c c ^"PJ:^ 
SsE"*°"aE§«' 

i p2-p Sii.E " 
f |p.2|V£gg| 

ai£"S.~|S-^=^. 
>2< o mEc 3 ■- a g °" 

c22ag::ri£B=3 8| 

3 a»A o ■=> c ^H*— t « 



iJ! 




o S c c -o S 



165 



z ^ 



I 

3 



"eotJ- SS^SJ .?E-5« 
o:^ >.a «^ c „ 2 >,! ^- §S 

±»aj «^ = CO y «5 ™ cJ^c'oj-i; ;:. 



p S.I ^e-S-SSiSgi-a 



5315-0 



I ill I 



■0.2 c 



o E *!= £ ^.^ "I 
„S = =-3 v-° S* 
c»>,_2 c £^ S E 
■= 5-r£-5.-o£ X I 



i=.> 



S-s p-=1 



:^ 0) O.S £1-. 



2 " 

§2s 



S33 
ESS 



cp2X2£'5:S-,'S§i,S^3*'c 
g2£«§2|.i2|£8.Sg-xo 

©■ss^s .^i|s Ibis's ■^^ 

C -^ *. ^ 3 " =" ^ w __ rt. - ^ 



c £-2 

o « Jr> 






:|^ 



m "S; a ^ I 



c g.:^ g 1 



o |.S g,3 5I^_2 : 



J'E 



Jll^l 



= 31 



|E< 



at- Su^X 20 aqj E ^— - 



||i 



iS.'E 



: .§■ S-^ I 
E 3-S 



<u = S 5 i 

ES||a| 

•o > « ftj 



•3 JH- "':S 
o— .^ V a 
.- _ e o > 1) 
Tj c c 0) oj: 

Ellltl 

3-0 J CO 

t; j-g-o —i 



, J- op' 

i -■^"|2i'S.-.2 

: 5 > 2^_2 2 2! 5 s 
; 5_a £3 ■ifex-l' 

; £ >,— a c _ J c 

s 3-g.'- e!= e >.«■ 
8|||>i^|.-sj 

c-OTJ o EWi£> a 



<2s 



IcS 



TJ 2j 

Bel. 
«<Sxc 

■sjj 



C «T3 



rr X ^ *J 



sap 

c 3 o 

V 3 
•O O 



c a o 

1=1 



O.X2 



.0 

<t;o 
— 0! «> 

p "-rr 
= S p 



, § oi'3_, a 

= !=§§& 



t £|5£(£ "^ 



>.iir= oPS M* 

let -^-i 'il 

■r2o cV-. -"S 

§■£= -£2= 1,2: 

■|.2i(£jTjO^ -g- 
o- .^5 o E «> 

<i)£Ej>o-Sg?o — 
"Si,2>.8^i3<u §-0 

. S. p - ° O i § a, ^ 

3 O I ° 2 I §"° 
" - P 3 y ■ SpQ SP 



^'E^S'-E 

-3— c 3 p c p 

zi a a c > — i± „ 



"^2 -r 2 

g«-SE 
ES wli 



a ii It ^< S ^ £ 



g2> 

ill 

ana's 

^ a 1 



e'p a-S'-S 

s a,x 3 a 

Si! " f-a 
III §3 
£„-50i 



> :>.2 P 
3 e a! '^ " 

o 5 > 
p S'P^ 



2xx. -sS-ti-a 



Ess ■ "" P-o a'S S-OrS «** P Ji-2 

§aa-.|^i-xg$|i-52s^l 



E2 

> p"" 2 

!-^aS 

alii 



g^gg-Q 



"o2:|f||£| 
i-§3gPu-^i--S§ 



2?a,oO^-gg' 
x-5 ^P ..S^S- 
fe ". a -2 .i- 2 -r 5 
3:/l;aacS;<- 



^ Eo 
5 E-. 
E 8x 



--— c 
!i2 P 



= ■52 



>^.sS 



S3 3 ^^ 
|jl5 ■ 



2-o.|c-"x 






-POO, 






£§£ M° 



I. < " O 3 » 

«JxQ o^rc y a 
" E e P != £ 

X 0.-5 2-o-P.H_3 



£= i-fs" 

" " «2 p 



^■§.2 
S So J 



!J11 



:-l<?=^ 






^1 -sa 

1=5 Iq 



mil 



ii ^-. 



•i IS i-SS 






166 






:= « =■; 



, ^ a c oj, -i 
f S 6-. ^ o o 



•^S S 



■a 2 — 



3 g 



"o o 

"u 'C -' " ^^ c "a .2 

S u 2 2 M° 3i; 



So 



COM 



I il Is! 

CO .-5 - S "5 o '3 
So."? -.2 a 
a I . M E "^ — 

xcTJ-i-2 E 
' E 



cb aa'o ■^■= o" S 6 A 



= 3 
a CO 
2.E 






- 8 -^ S-j ". y 
" ""t; S 41.5" 3 * 







|'|;3-° § S « ? S bl£5 2 " cl*l ! £ " 




I g-^-G<'^ E » o g 
gas's ,„-^<S £2^ 

«? ^ go li^'S-o !! 

•5 3i2<>.S2'^fflaj 
o. .- Q**^ c oJ i 

-c ' ' 3 - . 4, a* 

Of- Q.S 5-3 % SO 









EVSS 



..UCL. « 






o c 

i> 

£ c 

c c 



53 S S i E c 

St3 g MB t O 

E C.5 a J g-^_ 

l*'"a = £c 
_o£ - »< - 



«S. 



£ = 

a a 

s5 



o c °5 

„, 2 " 'S E 

^- £ s..^ « 5 

' a i: «j S i: ■si 

= E « := ff> 

, S>.iE"5. 
E S « fe . o £? 
c'5i> * c^ — 

JJ-f C S C M^ 

, >-g.c £ S.i! c, 
= '^ a r- S*- 

C O c S"" Sir* 2 

^•S"^ES.E.|5 
E.2 g.2 £ 5 E 
OT o S §^ ^. = .5; 

o. mi a £ o > 



- 8 
> >. 

a.- 
c 3 



|£ 



22-: 

•O 3.S 

w 



■^ 2 E 5 
g« S S p 

p > '"- V 

2 E o a •; 

gSi^.2 

e:c- P o 
■3> as is 

2||l§. 

2 r oj 3 >. 

I*' »- a 
S-p o p S 

JJipS?' 



su 



't:-;^>^o<u4jpc 
£ g^p*' i;-^ ° £ 
S«2 ^ £ S^lS. 

SoP-ISOX: «j5 
-I2: 



be o ii> 
0-0 ** 



>>.a .P i; J 

■p p "^,2 

2 o-r 3X 
■0 °-^ g S 
'o aX Six 



2ol* 

O S-P « 



: x" Z^a 5 §."! s i i o 

: 5 p = 2*^ p x-g Mg o 

J a,-2' a> a.2 "^ <x £2 

j*2iii.p|x ^||« 
ji — o-o o gi 

JT, P^ g SlO-o 






S X 2 



£S:5 2 



:g^s=-g|2 

£^ 3.£ g a..^ c 
<2"S:S S 2 P " 

2 S ^ ■" 2 o £ 5 „ u. -. - 

" -^ a ■= £'o^S"p P'S'o 
i|£|g.|^25o8p| 
S.Ss!^-|^i-S§?2i-SE 



J o !^p2o g ^*-= SS 

^o-£ r p . s goP's -■' 
8-3oi8giE-^g°e>. 

^ -o-a u 3 a.B^ o 3t: 
>" gf=.io S aP a o" 

» >, = xi-E g*!2 ".§ 
V «|E-g2- 2»-5 2 

-Dc'^_ S— 0.-2 2:;; o °- 

2.ip'S|a,-3gS!l^&t; 

"gS-^fSSeSpS 

^Ms^^igi^-s; 

^S;S2il|||2j| 
3"-Sl»<»>.£>*p-| 

-J>— >OPS.S-tlO»1.2 3 

i^i§lri2g 



^oj 



a p 



2£ 



•5 p a^- 
p±> 



SOE- £^ 1 



>.-o 
xSj<""'oSb»i„J. 

|h ^ g I Mg-g'" S g:3 „- 
!-5 QEi!.£o.c.aEg5-S 



Il II 



167 



see 
*££ 

. ^ o i^i 

'g Ex 



s e; 



E-S 






icE^^j 

, « m C 



.£ S . 

■£ ^ ",2,3 ■ 
MX > c t. E 

>■§ E °-o J 

■s|8 = il 

E^H c >.S 

l.BjiB E * 
p q y a (S"0 



ix.S Ss'x 

!^-„ .is*s- 

*■ u » o o 



■o E a, 
>,E3 






"aJ 03 2 *J g « 
*^ 4) 0) ■" 

S Ex£ £- 

; o<_ s-- s5 
a 0*5*73 ♦^ 0) 

S ? *-s „-£ 

ii o E * M 
I « I c = S 



X «,:£ 
X S i- 



^'1 oW £<-2 
■5 o-"- „ c >< 



x.!i 

T3 « 



J'l|i.?l 



■=£=■*£ 









E " 3 2" 
box o' 

EC . - •: 



SS-s 






^1 
J!2 






.111 

yi 

t-X"" 

-0-3 

*|l 

3 2 

"oXX 

1 SI 

O H Q. 

1° 
III 



. J. 4) bo ft> 
£«■£■£ 

^■a 3 " 

S c-S o 

c£ 



s »: 



I -OS'S 

.oil'" 



X.£X| 

-a ^j_C)-- 



^ SiBt; Ox 



--6 £•= 



Q.O i 



« = S e 



2o2S|-= 

i SoiJ E-2 
« < •; i 5 o 
= = -9 S-* 



■^£c2cc2S 00— 



^Ifl 



5 ° 









.Six 



E-S| 
S c E 



e =-9 

< ° D. 



«4j 

* O 

o *^ 



as 
S3 



V o 



■Sit^xgigc^it j 

S 5 E "^t- t. »; o S 1- S " 
>>.£ uS 5=1 SiSc 2; 2x 



2^-2r 



o XX ■ 



,-0 q ! 



X g >.' 






= S = " * 3~ li-^ "= ^ 
Xq «— c " q.j*'j:2 ^ 

S.g>-.::*'-a*'..£„»lc 
^^^■o^Eg-^ 






=£*>^ 



tsEtJ-^sg-s^a^lEo* 

S'=£sifc,£^'Sa l^'S!^"* 
5!-S3!SS^:SJe||3>^^ 

££ = 35-5-0 = 010, . 2 a-gs-i 

J-S-o^J Sio.OX- gjjO^. -o ' 

.„ S^x g '- S « S m'SS c »i t 1 
2Ext-igisi;?,'§Sg3.Si.S.2i 



w. c aX o 

Sii £ Sx 
c 5, o = o. 
^*£1o 
.£ a.S a ., 

-o c SP« 



I ;| ss^:.i||ili| 

>* X-nOlS^JOX w^ C 

r-ti'n -— c£S"75q2ac^.5i 

■- a £ S o S E Jq => 3> 

S-So- •■ScxgScg.2 £■.!•£ 

O.bpo .2 S.|< a c g..£03 »j 



SS*E 

"I il 

■Sa o a 

^»>2.£ 



^2 



o a c m S 



>^-3iSlS 



c oiS 



:a> SiSfS E 



t-- " 



SSSS-g J- 



■2 St, a g a oJs.a fx 
ai£5as>i»2£^ 

a s * ° . = r- S>- 
E:2j=;££agg-<-s 

i-Si'^lSEE'S 






-l-lg» 

MX «"*•«£ i Ex QO 
■S 2 3.2 01 c " o gx S c 

g £■> oa-o-f £ "S ."S 

ziscsislscne 

S.2 2xS.-S-g*S.HS 







168 



"3,0 -<-' ' 






S " " « fflt'-S ^-S «== ai I- mS S-50 S x-m- S-o S o So o §-.2 J 










' ^x — 


















•S-SsS-gsi SSoSS -^^o 






i aii.S 



169 



iiilf- ^iillii-^ li 






^■^ - 5f 5 'H •- ■= t; -S Q. g- ocj:S£",= £J=t:xx 3.5 g-«,^ ¥." S ogo 

jH ""oil? s= ^:;=5?s|g |i5is£§§-SE-s3s:| ,^|.s=-=i^ s lei 
liisii mu^jiu: iliilii 1111.^^^1 !ri!lii ili!i 



i2 2>,iS--=-SS.2'; ^^Sis'SJS.S;.i:-S'S|i| >2u|<jig.§- f^ES'^ 

12|S^°=|I-SI i^-S spills S-ge^=. |£|o^lx 11 ^1^ 

2 -S o >'^-- o g 4, = c -o ^ 

■=»^«!nT'5m.. So.'-' *!:• 




u« Q.OS«.tioc3t: ai^ioOoS-2 52SS-OC. 2>0<toaa 










170 



i 2 S H < 



=g" I'll «2i"2S <3--§ it^gliss'^y ig.s 



IP ^^«ll«ll! 4|| «l«! 111! !!!i1ii?|1l IIL 



c"" c a e S' ^ -. ^ 



■% S| c^'= °|= .all %^d = ; £ « = S^ S'S^-E^ § g; 



<>s ==s 



^ P .5 3 




171 

Mr. ROHRABACHER. Thank you very much. Admiral. 

I would ask — I will reserve my time until after the other Mem- 
bers of the Committee. 

Former Chairman Brown, do you have some questions? 

Mr. Brown. Admiral Zumwalt, I think we all are aware of the 
fact that Agent Orange was not used as a means of creating dis- 
ease or illness but was intended to be used as a defoliant and that 
it was the contaminant of dioxin that caused the problems that we 
have had. 

At least we think it was that contaminant. 

There may have been other contaminants, too, I suppose, that we 
don't know about. 

But in your concern over Agent Orange, have you also reviewed 
the broader problem and its contemporary state that we are facing 
here with the ongoing concern about dioxin and its multitude of 
sources within the environment? 

Admiral Zumwalt. Yes, sir, I have. 

And you are correct that we didn't know at the time that dioxin 
was a contaminant in the Agent Orange mix. 

We know that the chemical corporations producing it knew at the 
time that it was carcinogenic. 

It is also accurate, Mr. Chairman, that I have followed very 
closely the work of the EPA and have reviewed all the studies as 
they have come out. 

And in my judgment, the EPA risk assessment was sound and 
scientific and objective, and the comments of the Science Advisory 
Board were the result of the presence on that group of representa- 
tives of industry. 

Mr. Brown. Well, I am sure the committee will want to review 
that, but this is an ongoing, this is a problem that extends far be- 
yond dioxin. 

We used to have a joke out in California that when we had a big 
oil spill that you couldn't find a petroleum geologist that didn't 
have a conflict of interest because they were all hired by the oil 
companies. 

You have similar problems with asbestos, with breast implants, 
silicone, and other things of that sort. 

I am not sure what the solution to that is, because frequently the 
most knowledgeable people are people who are hired by private in- 
dustry and sometimes they can overlook these connections and con- 
tribute to a balanced judgment about it. 

But this is going to be a problem in many areas for some time 
to come, as I am sure you realize yourself. 

Admiral Zumwalt. Yes, sir. I certainly agree with that. 

One way, for example, in which a greater degree of objectivity 
might have been achieved today is if, in counterposition to the two 
doctors who have been subsidized by industry to a certain extent, 
you had in the hearing two scientists who had not. 

Mr. Brown. Admiral Zumwalt, I wanted to particularly get your 
views on the subject of a cooperative agreement with the Vietnam- 
ese Government to do a binational study in which each country will 
participate on the effects of Agent Orange and the dioxin compo- 
nent of it. And you have far more experience on that than most 
people have. 



172 

Do you think the time might be ripe not only to cooperate in re- 
solving this or bringing more light to bear on this problem as well 
as in a more general sense establishing a research, cooperative re- 
search relationship with the Vietnamese as we do with many other 
countries, both European, Asian, and other parts of the world? Are 
we ready to go that far with the Vietnamese? And this is a subjec- 
tive judgment, but I can't think of anybody whose judgment I 
would respect more on this than you. 

Admiral Zumwalt. Yes, sir. 

In my judgment, we are. 

I might report that with the assistance of Vietnam veteran Sen- 
ator Harkin, we were able to get language in the appropriation bill 
a year ago that instructed NIEHS to do a joint research with the 
Vietnamese and the group that Dr. Lucier spoke about was the 
fruit of that language. 

Following that, I went to Vietnam for my first visit since the 
war, in September of 1994. 

I met with the former enemy general who is now president of the 
country, Le due Ann, with General Giap, with General Tran Van 
Tra, who commanded the Viet Cong forces. 

When I met him in Saigon, as an aside, I said, "General, I am 
surprised how easy it was to find you today. Twenty years ago I 
spent 2 years looking for you and never could find you." 

He laughed and said he was in Tayninh province the whole time, 
that it's just as well we didn't meet, he said, or one of us wouldn't 
be here today. 

[Laughter.] 

All of those generals plus the minister of health and the doctors 
assigned to Agent Orange issues in Vietnam have pledged total in- 
terest in and cooperation for joint research on Agent Orange. 

The Vietnam veterans strongly welcome that as a means for get- 
ting answers to the questions still unresolved about the 18 addi- 
tional diseases that the VA has not yet authorized compensation 
for. 

Mr. Brown. It's conceivable that a broad study of the Vietnam- 
ese population who not only may have been exposed 20 or 30 years 
ago but whose children or maybe even grandchildren now might 
give us some information about mutagenic or teratogenic or other 
effects that would be extremely useful if we were to undertake that 
now. 

Admiral ZuMWALT. Yes, sir. Absolutely. And in my judgment, Dr. 
Farland was in error in stating that we don't have highly exposed 
Vietnamese populations. 

We do have villagers who were very heavily exposed. 

The data that Dr. Farland has seen was compiled by Dr. Arnold 
Schechter, who was so limited in research funds that he had to 
take blood samples from a large group of people and then pool the 
blood and measure the dioxin in it, which made it impossible to 
know the individual high levels but just one average level. 

Mr. Brown. Well, I am very disturbed by — disturbed by our fail- 
ure to move aggressively on an opportunity like this, and I am also 
convinced that successful arrangements for such a joint program 
would have immeasurable benefits in terms of our own understand- 
ing as far as our veterans are concerned and be very helpful to the 



173 

Vietnamese people, who probably also have suffered a great deal of 
disease from this. 

I hope we can follow up on that aggressively in the future. 

Admiral ZUMWALT. Thank you, sir. 

Mr. ROHRABACHER. Thank you very much, former Chairman 
Brown. 

Congressman Olver? 

Mr. Olver. Thank you, Mr. Chairman. 

Admiral Zumwalt, you made a couple comments here, and I 
would like to clarify a little bit what you said toward the end of 
the testimony, and I was checking to see if it was written in exactly 
this form in your written form because I can sometimes, if I read 
things three times, understand them a little bit better. 

But you said that the companies who produced Agent Orange 
knew that it was carcinogenic. Now, I don't know whether — or close 
to that, in any case. 

Did you mean that they knew that it contained dioxin, which 
they knew was carcinogenic, or that even the broader Agent Or- 
ange is? 

Admiral Zumwalt. I have seen documents which show that there 
was knowledge within the chemical corporations that the processes 
they were using produced dioxin and that it was known that it had 
carcinogenic effects. 

Mr. Olver. I see. So you're sajdng that they knew that it con- 
tained, that it produced in the process of producing Agent Orange, 
that they knew that dioxin was in it and they also knew that was 
carcinogenic? 

Admiral Zumwalt. Yes, sir. 

Mr. Olver. All right. That clarifies that little point, in any case. 

You made several comments about the Science Advisory Board, 
and your main recommendation here, I guess, is that the Science 
Advisory Board contain no scientists that have a financial interest 
in corporations. 

The way your testimony speaks, you speak at one point of the 
Science Advisory Board reviewing EPA's draft assessment and then 
the Science Advisory Board review of EPA dioxin reassessment, 
there must be — I don't know, is that two different Science Advisory 
Boards? Did the — was there one? No, I guess that one would be the 
same one. 

Admiral Zumwalt. Yes, sir. 

Mr. Olver. But when you speak of— is this a Science Advisory 
Board created only for this particular draft assessment, reassess- 
ment of the dioxin effects? Or is it the EPA's broad Science Advi- 
sory Board? 

Admiral Zumwalt. I don't know the answer to that. I know that 
they were the board that did review this risk assessment. 

Mr. Olver. I think it would be very difficult to create a set of 
panels here that did not have some scientists who had some in- 
volvement, though I completely agree with you that if one has a 
panel set up to look at an assessment of dioxin's effect, that you 
should have nobody on it that is — that has a financial interest in 
the production of dioxin or in the production of the material, what- 
ever its major purpose is, that contains within it the dioxin. 



174 

So, it maybe that this is a very subtle difference. But we have 
a longstanding history, at least in the judicial process, of judges 
and so forth recusing themselves from involvement in decision 
making where they have some interest. 

From apparently what you say, you don't think that kind of an 
approach would apply? 

Admiral ZUMWALT. It would be better than the current approach. 
During the writing of the Science Advisory report, observers close 
to the review process have identified Drs. Greenley and Graham as 
the two members of the Science Advisory Board health panel who 
most actively and consistently challenged the validity of the dioxin 
health risk assessments contained in the EPA report. 

They were the panel members who pressed most vigorously and 
effectively for an outright rejection of the risk characterization sec- 
tion of the report, and yet they were the ones who have been sub- 
sidized by industry. 

Mr. Brown. Would the gentleman yield briefly on that? 

Mr. Olver. Sure. 

Mr. Brown. Admiral, you obviously have some documentation on 
this. 

I am not familiar with it. But could you supply that for the 
record also? 

Admiral ZuMWALT. Yes, sir, I would be glad to. 

Mr. Brown. And, of course, I would like to make the comment 
that all scientists, including my good friend Mr. Olver, are known 
to be totally objective about every subject and they don't have to 
recuse themselves from anything. 

[Laughter.] 

Mr. Olver. Okay. Just trendy, however. 

Staff has informed me in the midst of this that, in fact, it was 
a special subpanel and, of course, when put in the terms of a 
subpanel, then my mind says, well, is this a group of the overall 
panel? But I am now told that there is a science advisory panel of 
39 members that sits there. 

Now, in that science advisory panel, one I think ought to be able 
to expect scientists to recuse themselves from involvements in deci- 
sions where there is any kind of special interest. 

I am not sure that you could find a scientific panel of 39 really 
top-notch scientists who haven't at one time or another or now 
have some interest in — in a particular scientific area that had some 
financial interest of a sort. Even the academic scientists, through 
their research contracts and so forth, may well have had that. 

But when you create a subpanel for a particular reassessment, 
it seems to me that you are entirely appropriate by expecting that 
in that subpanel, which has one purpose, that there should be no 
scientists who have a financial interest in the outcome of the re- 
sult. 

They can take testimony from people on both sides. That's why 
we have panels here. You could have the two doctors in question 
on a panel to put their point of view forward and then there is a 
full — then you have a full opportunity to examine what the/re say- 
ing and from that kind of conflicts of interest they might be coming 
in that process. 



175 

But at least they aren't there voting on and persuading others 
to the particular point of view, which I think really, really causes 
serious questions in what we're doing in our — in our reviews and 
in an objective way of developing scientific panel information. 

Admiral ZUMWALT. Sir, I have two comments. 

First, not only did Drs. Greenley and Graham not recuse them- 
selves, they campaigned vigorously for and wrote the language that 
tended most to denigrate the EPA's panel risk assessment. 

Second, in the case of the lOM study panel. Dr. Kenneth Shine 
was able to identify highly respected scientists who had not been 
infected by industry subsidies and when that was done, the science 
led to the objective conclusions that there were now 10 diseases 
that, likely as not, result fi'om exposure to Agent Orange. 

The difference between a panel which has industry representa- 
tives posing as objective and a panel which has none is like night 
and day when one compares those two results. 

Mr. Olver. Can you find, Admiral, can you find testimony or 
records that shows that, in fact, it was known by that panel at the 
time that the two that were making these — taking these positions 
were — did, in fact, have a relationship to the companies that were 
producing the Agent Orange contaminated with dioxin? 

Admiral Zumwalt. Well, yes. For example, in the transcript of 
May, Dr. Greenley has said and is quoted as saying, "Those of us 
for whom dioxin supports our family, sometimes we keep looking 
for problems that aren't necessarily there because it puts food on 
the table." 

Mr. Olver. Thank you, Mr. Chairman. 

Mr. ROHRABACHER. Thank you, Mr. Olver. 

Admiral, have you heard much about this ranch hands study? 

Admiral Zumwalt. Yes, sir. And I have examined it in fairly ex- 
tensive detail. 

Mr. ROHRABACHER. Maybe you could give us your opinion of 
that? 

Admiral Zumwalt. To go back, Mr. Chairman, the — at the time 
when, as the Government Operations Committee report shows it 
was government policy to instruct agencies not to find a correla- 
tion, there was a great deal of difficulty with the early Ranch Hand 
studies. And, for example. Senator Tom Daschle had to work ardu- 
ously over a number of years to get released a study by Ranch 
Hand which was withheld because it showed that there were birth 
defects in statistically significant increased numbers. 

When one compared the veterans before they went to Ranch 
Hand who had children with the equivalent control group, they had 
a normal rate of birth defects. When one compared their children 
that they had after they returned from Vietnam with a control 
group, they had elevated numbers of birth defects. 

It took a long time to get that out, because it was being withheld. 

The second point I would make is that not very much credence 
can be put in Ranch Hand, for two reasons, with regard to carcino- 
genic effects. The number of Ranch Hand personnel involved are 
too small to produce significant numbers. It's less than 1,200. 

Second, one of the great fictions, in my judgment, about Vietnam 
is that the Ranch Hand group was the most heavily exposed. The 
Ranch Handers wore protective clothing. When they got back from 



176 

their spraying missions, they took the clothing off and took show- 
ers. The poor guys on the ground who were using Agent Orange 
themselves, my boat crews in their perimeters in the exposed 
areas, equivalent numbers in the Army and so forth, were much 
more heavily exposed. And therefore, one cannot put credence on 
Ranch Hand as being kind of the most exposed population. 

Mr. ROHRABACHER. But you do concede that they are a heavily 
exposed population? 

Admiral ZUMWALT. They are more heavily exposed than Vietnam 
veterans who did not go into combat. They are less heavily exposed 
than most who were actually in forward combat. 

Mr. ROHRABACHER. All right. 

I am in certainly no position to say one way or the other on that. 

I will do some more reading on this issue. 

However, today we were actually looking into process of evaluat- 
ing 

Admiral ZuMWALT. Yes, sir. 

Mr. ROHRABACHER. [continuing] rather than the actual outcome 
itself. 

And your point which goes into your point about company docs, 
as you call them, in my — to my way of thinking. Admiral, and with 
all due respect, what you are doing is attacking the credibility of 
someone who opposes your view rather than attacking the validity 
of their arguments. 

And quite frankly, you know, it is easier to attack the credibility 
of someone and attack someone rather than an argument, quite 
often in politics, and people move in that direction. 

And I will say that there are, quite often, people who have — I 
don't — let's say they are a Catholic, well, they may be a Catholic 
and they may be absolutely committed to the Catholic religion, but 
that doesn't make their arguments wrong or that doesn't make 
their arguments irrelevant when it comes to, for example, abortion. 
And if it's wrong to say, well, you're a Catholic, that's why you're 
against abortion, rather than talk to someone and say, well, you're 
sa5ring that life begins at conception and that's how we have to 
make our judgment, let's look at that argument. 

It seems to me that that's not the proper way to try to determine 
the truth, and the idea is to determine the truth, attacking the ar- 
guments rather than attacking the people. 

Go right ahead and respond to that, sir. 

Admiral ZuMWALT. You know, it's distasteful for me to have to 
make those points. The veterans have for 15 years seen the manip- 
ulation of studies. It has been documented that the studies were 
manipulated. We know that it was done by industry interest 
groups. And the veterans — 

Mr. ROHRABACHER. I am not suggesting that's not true. It's very 
possible that you're accurate on that. 

Admiral ZuMWALT. All right. 

Mr. ROHRABACHER. But when you're talking about government 
panels like this, for example, where you said we had two witnesses 
who had received certain support for their research in the past or 
even in the present from business, that they should be excluded. 

Admiral ZuMWALT. Yes, sir. And I am sure that my years in the 
military have made me more — less diplomatic and more accurate. 



177 

Mr. ROHRABACHER. No, no, that's fine. 

[Laughter.] 

Admiral Zumwalt. The — no mention was made of the tremen- 
dous conflicts that these two gentlemen have. Surely, at some point 
in the hearing it's appropriate. 

Mr. ROHRABACHER. Well, Dr. Farland, for example, is the head 
of the EPA, and he certainly has every reason to try to present the 
best arguments for his — for the EPA, for the bureaucracy that he 
oversees. 

Admiral ZuMWALT. I think Dr. Farland's mission in life is to 
come up with scientifically objective data, whereas the mission in 
life of the industry representatives is to reduce the exposure of 
those industries. 

Mr. ROHRABACHER. Now, are you presupposing that people who 
have worked for industry then cannot be honest people? 

Admiral Zumwalt. There are some who are honest. 

Mr. ROHRABACHER. Well, let me put this more in your own — in 
your own back yard. 

By the way, I would never say that of anybody else, some are 
honest. I would never presuppose that people are not being honest 
in their disagreement with me, even on really gut issues. 

Let me put it to you this way. You are £in admiral in the Navy. 
We have other committees that meet in determining major expend- 
itures for the United States Government. 

Now, who do we call as witnesses when we are trying to make 
those determinations? 

Well, I bet you probably testified. But you're an admiral. 

Admiral ZuMWALT. Yes, sir. 

Mr. ROHRABACHER. And your whole life came from money coming 
from — to the Navy. Now, does that mean that we shouldn't have 
military people here to advise us because they have — and we all 
know about the conflict between the Navy and the Army and the 
Air Force over where the funds should go. 

Shouldn't we have people from the military here who have the 
expertise to give us that testimony? 

Admiral ZuMWALT. Oh, absolutely they should be there. 

When I came in and testified, I identified myself as chief of naval 
operations and, therefore, responsible for and obviously in favor of 
the budgets that I submitted. 

Dr. Jones did not come in and identify himself as someone who 
has lobbied for and represented the Incinerator Association. 

I think those — that is the difference that I am referring to. 

Mr. ROHRABACHER. Okay. I think that that's fair to say that peo- 
ple who testify, that their backgrounds should be available to the 
public. 

I think that's fair. But I don't think it's fair to say that because 
someone has worked for industry, whether it's the incinerator 
burners or someone else, that they shouldn't be able to testify and 
their arguments shouldn't be considered. 

Mr. Olver. Would the chairman jdeld for a moment? 

Mr. ROHRABACHER. Well, first let the admiral answer that, and 
then I will be very happy to yield to my colleague from Massachu- 
setts. 



178 

Admiral ZUMWALT. Yes, sir. I would assert, in that regard, that 
there is widespread recognition among those scientists who do not 
take subsidies from industry that there are a subset of scientists 
who do and, therefore, come up with unobjective conclusions. 

Mr. ROHRABACHER. Well, Admiral, I am not certain that this is 
an area of your expertise, and I will say that there are people who 
are hired as consultants in any number of areas and it does not 
mean that they cannot get the honest individuals and give honest 
testimony, and if someone, for example, does some scientific re- 
search and finds something that backs up the arguments of a par- 
ticular industry, quite often the industry moves forward to try to 
help supplement that research. 

That is in — that is something that is very natural. That doesn't 
mean people are lying along the way. That just means that that's 
the natural outcome. 

For example, if the Navy was going to get cut ofi" from a certain 
amount of funding, the Navy might subsidize someone, a Ph.D. 
who was doing a study that the Navy knew would show that naval 
power was important, but that doesn't mean that researcher is 
Ijdng about the importance of naval power. 

Admiral ZuMWALT. I certainly understand that point you're mak- 
ing. 

On the other hand, I would point out that I think it is generally 
recognized now that the tobacco industry has been deceiving the 
public for years and that their scientists have been cooperating 
with them in doing so. 

Mr. ROHRABACHER. All right. Well, you see, I disagree with that 
point. 

I think that anybody, anybody in their right mind has always 
known that tobacco is Jbad for you. And from the time I was a little 
kid, common sense and everybody fi-om my church to school, every- 
body else was sajdng cigarettes, they used to call them coffin nails, 
and the tobacco industry, for them to be suggesting that, "Oh, we 
didn't, you know," to say that they in some way were tr5dng to 
cover up the fact that it was bad, they were selling a product just 
like alcohol and a lot of other things that have — that are bad for 
your health but people have the right to make the choice. 

Admiral ZuMWALT. Yes, sir, but there are scientists who practice 
voodoo science in asserting that the tobacco companies were right. 

Mr. ROHRABACHER. I think that those — I think anyone who is 
hired by a private company or has an interest, whether a financial 
interest that makes them less than honest about the conclusions, 
about conclusions of their studies or less than honest in their deci- 
sion making, those people are doing something that's wrong. 

But that doesn't mean that all people who are engaged in re- 
search and are hired by private industry all of a sudden cannot be 
honest about things that they have determined. 

Admiral Zumwalt. I agree one cannot write out a whole group. 

Mr. ROHRABACHER. But I will say also, anybody who testifies 
here and if there is a conflict or if they are, for example, if they 
have an association, their background should certainly be know. 

We certainly didn't try to cover anybody s background up. And if 
my staff didn't put that on a resume and there were groups' re- 
sumes or something that went out, I would apologize for that, but 



179 

certainly we didn't try to make someone appear to be what they 
weren't. 

But I find that the people who testified, just because they have 
had some sort of contract, research contract or whatever, with oth- 
ers in the past, I have to look at the vsdidity of their arguments. 

I can't just attack their credibility and try to attack them as a 
person. 

Mr. Olver, would you like to jump in? You had something to say? 

Mr. Olver. Yeah. I almost feel completely obfusticated from the 
previous 

Mr. RoHRABACHER. Well, that's a tough one. 

Mr. Olver. [continuing] set of comments. 

But in any case, I think the analogy isn't exactly as you have 
given it, Mr. Chairman. What we had here was not people asked 
to come in and testify where you could — where you could explore 
what their interests were and knew it when they came in. 

But you had people who were actually in the panel that was sup- 
posed to be making a quasi-judicial decision to try to come up with 
the best scientific decision that would be possible, given the best 
that you know at that time and be as objective as possible. 

It seems to me that 

Mr. ROHRABACHER. Well, I was just referring to the panelists 
today, Mr. Olver. 

Mr. Olver. Well, but your comments were related to who is 
there versus who is here. 

We serve in a quasi — we are trying to look for the best cir- 
cumstance, presuming that none of us are exactly experts in these 
areas, and all of us may have our own particular interests in it. 

But in this case, where the integrity of the process, it seems to 
me, is enormously important, it should be cleaner than a hound's 
tooth, in essence, in order to be able to — for the people, for our con- 
stituents to believe that in fact it has been as objective as the 
science can allow it to be. 

Mr. ROHRABACHER. If cleaner than a hound's tooth means that 
you don't permit people and certain arguments to be presented by 
the most 

Mr. Olver. That's not what we're saying at all. 

Mr. ROHRABACHER. But if that is 

Mr. Olver. You're taking testimony from there. What I am sug- 
gesting 

Mr. ROHRABACHER. But if that is the result, Mr. Olver. 

Mr. Olver. I am not suggesting that that's the result at all. 

We take the testimony from there and everybody on all sides gets 
heard. 

But the panel who is supposed to make an objective decision on 
it should start out at least without clear conflicts of interest within 
it. 

Mr. ROHRABACHER. Okay. 

Mr. Olver, thank you for that point. 

Admiral, we have about six minutes to go and vote. I want to 
thank you very much. 

As you can tell, it was very provocative testimony because you 
have ignited a debate even here on our committee. And I want to 
thank you very much for your testimony today. I want to thank you 



180 

very much for the service that you have rendered our country, and 
your men, we all deeply respect. Thank you, Admiral. 

Admiral ZUMWALT. Thank you, Mr. Chairman. 

Mr. ROHRABACHER. This hearing is adjourned. 

[Whereupon, at 2:00 p.m., Wednesday, December 13, 1995, the 
Subcommittee was adjourned.] 

[The following information was received for the record: 



181 



Appendix I — Additional Statements and Material 

6404 E. Halbert Rd. 
Bethesda, MD 20817 
December 29, 1995 



Mr. Larry Hart 

Subcommittee on Energy and Environment 

B-374 Raybum HOB 

U.S. House of Representatives 

Washington, DC 20515 

Dear Mr. Hart: 

Thank you again for your interest and advice during the preparation of my material 
for the hearing on the "dioxin reassessment." I have edited the transcript of my remaiks 
and returned them to Ms Disharoon. Mr. Rohrabacher stated that the hearing record 
would remain open, and I am using this letter to provide you with some additional 
comments. 

1 . As 1 remarked at the hearing. I believe the Air Force study of the Ranch Hands provides 
an enormous amount of information about men who were exposed to 10 to 100-times as 
much dioxin as the average person, the exposures at which EPA predicts an array of 
adverse effects. Moreover, 1 think that there is an etfort to discount the results of that 
study because they do not support the claims made by mam people about dioxin and 
Agent Orange. 

a. The .\ir Force study finds no clinically significant ditierences between 
the Ranch Hands and the Comparisons, and no dioxin-related increase in 
death or disease in the Ranch Hands (Public meeting of the Ranch Hand 
Advisory Committee, Philadelphia, February 14, 1995, and the complete 
report is under review for public release). The Air Force study provides no 
support for the many claims of health impacts from moderate exposures to 
dioxin and none for the EPA's projections that more highly exposed people 
in the general population are suflering disease because of dioxin. 

b. Tlie .Mr Force has published the results of investigating ever\' pregnnnc>' 
of wives and lovers and every miscarriage and live birth of children bom to 
the Ranch Hands and the Comparison group The publication also reports 
the results of investigation of every birth defect and de\'elopmental defect in 
the children of the Ranch Hands and Comparisons through the age of 1 8 or 
so. No increase in any reproductive health event can be associated with 
dioxin (Wolfe et al 1995. Epidemiolog}- 6:17-23). The study, as an 
earlier stud> of the children of veterans of the ground war in Vietnam 
(Erickson ef a/. 1984. Journal of the American Mpri'^^' Association 



182 



252:903-912), provides no support for the oft-repeated claim of elevated 
birth defects in the children of Vietnam veterans. They also offer no 
support for the reports of increased birth defects among children bom to 
members of the North Vietnamese Army who served in South Vietnam 
during the war. 

2. There was some disciission of the possibility of studying possible health effects of 
dioxin in Vietnamese populations. I regard this as unlikely to be worthwhile for three 



a. The studies of Vietnam veterans in the United States have taken years to 
do and have cost hundreds of millions of dollars in the country with the best 
medical care system in the world. How much more difQcuh and more 
expensive will such a study be in a country with much poorer medical 
services and few records from the war period? I think that those difficulties 
will cause great reliance on recall about exposures, causes of death, past 
illnesses, and impossible problems in making accurate counts of live births, 
stiU births, and miscarriages. 

b. There is no reason to believe that many Vietnamese were exposed to 
high levels of Agent Orange and dioxin except for the men who worked 
around the Ranch Hand bases or with U.S. .Army Chemical Corps xmits, 
and those men would have exposures no greater than those of the Ranch 
Hands. The published measurements of dioxin levels in Viemamese 
civilians are far lower than those in Ranch Hands and male worker 
populations and in the population of Seveso. Italy, where men, women, and 
children were exposed as a result of a chemical plant accident in 1 976. 
[There is no indication of adverse effects in the Seveso population except 
cases of chloracne and two reports of increases in certain cancers that are 
based on very small numbers, that must be regarded as tentative, that make 
no sense from dose-response considerations, and that don't fit into the 
picture of cancers that might be associated with exposures to dio.xin in the 
exposed workers.] Since elevations in disease rates are not apparent in the 
higher exposed populations, Iheie is no reason to expect any in the 
Vietnamese. 

c. Admiral Zumwah stated that some new samples of blood from Vietnam 
contained much higher levels of dioxin. So far as I know, there is no 
published report of that. I also understand that the blood samples were held 
at an airport in Vietnam by Vietnamese officials for several days after they 
were collected. lt~ the concentrations are indeed high in those samples, I 
would entertain the idea that they had been "spiked" during the time they 
were not in custody of U.S. officials. This could be checked by obtaining 
new samples and maintaining custody during the transport back to the 
United States. Such guarantees of non-tampering are standard forcnMo and 
scientific practice. 



183 



3. Admiral Zumwalt made many statements about what is known about dioxin that 
warrant comment, but I will mention only two. 

a. He said that he had seen chemical company documents that indicated the 
companies knew that dioxin was carcinogenic when the companies were 
selling Agent Orange to the government. As I understand it, the use of 
Agent Orange was discontinued in 1970 following a 1969 report that dio.xin 
caused birth defects in laboratory animals and a number of congressional 
hearings (Gough 1986. Dioxin, Agent Orange. Plenum Press, ch. 3). 
The definitive study that showed dioxin causes cancer in animals was not 
published until years later (Kociba tiZ a/. 1978. Toxicology and Applied 
Pharmacology P7: 133-140). 

The admiral may be mistaking the fact that the companies knew that 
high exposures to dioxin caused chloracne (Gough 1968. ch 13) with his 
contention that they knew dioxin was carcinogenic. If not, he has important 
information that should be made public. 

b. Admiral Zumwalt said that "combat veterans" of Vietnam were more 
highl}' exposed than Ranch Hands. There is not a shred of evidence to 
support that assertion, and everything that is known refutes it (Centers for 
Disease Control Veterans Health Study. 1988. Journal of the American 
Medical Association TdO.- 1249-1254; Kahn et al. 1988. Journal of the 
American Medical Association 1*59:1 161-1667; see Gough. 1991. 
American Journal of Public Health 57. -289-290). 



4. 1 disagree completely, as everyone would expect, with the value that Admiral Zumwalt 
places on the Institute of Medicine "study" that associated exposures to Agent Orange with 
several cancers. The lOM study was hardly menrioned during the EPA's May meeting 
about the dio.xin reassessment, and the EP.\ does not rely upon it in any way in the 
reassessment. Indeed, the lOM conclusions differ so much Irom almost everyother set of 
conclusions about Agent Orange and dioxin that they must be regarded as significant 
outliers. [I will address the lOM report in the book that I am currenUy writing.] 

5. Finally, I have some comments about Admiral Zumwalt's praise for the lOM panel that 
contained onl^' people who professed ignorance of dioxin research at the time they were 
chosen and that excluded experts from chemical companies. 

a. Advisor> committees are made up of bus) people with (typically) 
demanding jobs and professions, and serving on a committee or panel is a 
part-time affair, worked into r. crowded schedule. Committees and panels 
generally are composed of experts to reduce the time and effort necessary 
to bring everyone up to speed. As a practical matter, non-e.\perts depend 
on the staff of the committee or panel for much of their information, and I 
think that staff have too much opportunity to influence panels and 



184 



committees without experts in the area of study. Certainly, in all my years 
at OTA, I never heard ot a panel of non-experts, and I don't know what it 
would be like to staff one, but I think it would offer a lot of temptation. 

b. Admiral Zumwalt said that company experts should be allowed to testify" 
belbre committees or panels but that they shouldn't serve on ihcm. I think 
that to follow his suggestion would be to deprive certain people, because of 
their associations, with what I regard as their constitutional right to advise 
their government. If the sad history of the 20th Century teaches us 
anything, it is that accepting or rejecting individuals as "worthy" oi "fit" 
based on their associations is a doorway to abuse. 

Admiral Zumwalt appears to regard panels and committees as 
decision-making bodies; they are not. They don't make policy decisions; 
they advise elected or appointed officials who do. If they are making 
decisons, then, indeed, we need to look closely at the system, but the 
necessarj' repair is not to be found in dcnAing membership on the basis of 
associations. 

["Conflict of interest" can be seen and balanced. If conflict of 
interest is suificienl reason lo deny membersliip to a company expert, it 
should also be sufficient reason to deny membership to representatives of 
environmental organizations. The frequent lawsuits brought by such 
agencies against the Federal government represent a clear conflict of 
interest.] 

I hope that ) ou had the happiest of holidays and that the new year is very good for 
you. Please call if you have any questions or comments: my home phone is 301/229-3532, 
and my work phone is 202/789-5427. 



Sincerely, 



7^1 






Michael Gough 



185 



Chlorine Chemistkv Council 



Council 
of the 



Manufacti 



December 18, 1995 



The Honorable Dana Rohrabacher 

Chairman, Subcommittee on Energy and Environment 

House Science Committee 

2320 Raybum House Office Building 

Washington, DC 20515 

Dear Chairman Rohrabacher: 

On behalf of the Chlorine Chemistry Council, 1 appreciate the opportimity 
to submit these comments to the record for the dioxin reassessment hearing held 
on December 13, 1995. Please do not hesitate to contact me if you have any 
questions. 



Sincerely, 




C. T. "PSp" Howlett 
Managing Director 
Chlorine Chemistry Council 



Chlorine Chemistry Council • 2501 M Street, NW Washington. DC, USA 20037 • Tel. 202-887-1 100 



186 



Chlorine Chemistrv Council 



CHLORINE CHEMISTRY COUNCIL 
^ STATEMENT TO THE HOUSE SCIENCE COMMITTEE 

Council SUBCOMMITTEE ON THE ENERGY AND ENVIRONMENT 

of the 

Chemical 

Manufacturers 



SCIENTIFIC INTEGRITY AND THE PUBLIC TRUST 



Associauon THE DIOXIN REASSESSMENT 



The Chlorine Chemistry Council (CCC), a business council of the Chemical 
Manufacturers Association, supports the Environmental Protection Agency's 
efforts to reassess the sources of dioxin exposure and the effects of dioxin on 
human health. CCC has submitted extensive comments to EPA and its Science 
Advisory Board (SAB) on the draft Reassessment. In those comments, CCC 
highlighted other scientific studies and different interpretations of the critical 
literature cited by EPA. 

CCC mainly agrees with the conclusions of the SAB regarding the draft Dioxin 
Reassessment's Dose-Response and Risk Characterization chapters, and believe 
the Agency should take the substance of the SAB's comments into careful 
consideration. We endorse the SAB recommendation that Chapters 8 and 9 be 
redrafted in a reasonable and timely manner. The rewrite process begun by the 
Agency, as evidenced by its December 8, 1995, stakeholders meeting, is a good 
start. 

We support the open process in which the draft Reassessment is being reworked 
and look forward to meaningful participation by scientific experts from a 
number of disciplines and from across government, industry, environmental 
organizations and others. A scientific peer review is critical to the credibility of 
the reassessment. We will continue to work with EPA in finalizing the 
document. 



Chlorine Chemistry Council • 2501 M Street, NW Washington, DC, USA 20037 • Tel. 202-887-1100 ® 



187 



Zephyr Consulting 



January 17, 1996 



Honorable Dana Rohrabacher 

Chairman 

Energy and Environment Subcommittee 

U.S. House of Representatives 

Suite 2320, Rayburn House Office Building 

Washington D.C. 20515- 6301 



Dear Congressman Rohrabacher, 

It was indeed my pleasure to have the opportunity to testify before your 
committee on December 13, 1995 regarding the scientific integrity of EPA's dioxin 
reassessment. I hope that my comments were insightful. 

When I reviewed the testimony record I noted that Admiral Zumwalt, who 
doesn't know me, went out of his way to impugn my testimony and my professional 
integrity. I have written a letter to the Admiral challenging the statements he made in 
this regard. This self explanatory letter along with appropriate attachments are 
appended to this transmittal letter. I would greatly appreciate having this 
correspondence made a part of the hearing record. Hopefully, it will remove the 
tarnish that Admiral Zumwalt so blatantly cast upon my professional reputation. 



Respectfull 




es, PhD 
HS (retired) 



cc. Admiral Zumwalt (retired) 



(206) 328-1615 • 2600 Fairview Ave. E., Suite 18, Seattle, WA 98102 



18S 



Zephyr Consulting 






Januaiy 3. 1996 



— ..-•-,- t. 



Ajnci 



Dear Sir 

I ant deeply ofetixbed by your derogatory remarks impugning my (ttaracter 
and honesty which you made before the House Subcommittee on En^gy and 
Bivironment. Dec. 13. 1995. As a retired senior officer retiree with 20 years of 
serwica in the USAF and USPHS I have always upheld the mftary code of ethics of 
being an officef a-c a ge-t e - ?.- ?.: 32 times. I am committed to the same code of 
conduct wNch '-. ca_c~:r ; f ; :: as a recent graduate of the U.S. Air Force 
Academy (dass :- rr5 

VHtnUi a :r s: .= : fioe of my badtground arxl dstinguished 
government S6". :; sff r~_^ ; .-."aj-f; .:_ ~ace t~e '': ;.% "c -ert a~w "C'rCt 
personal attacks - - ^ j . : _ ■ e ; : ~' ; ■ . 

1. * a greater degree of obiectiv^ "-c": -a.e ree- ar- e^ec today is if in 
ooKttrposition to the two doctors who htaw :rf' f_:s::r: :> moustry to a certain 
extent..' (ines 2573. 2574) 

2. *Yes ST. And I am SLve that my years in the mitary have made me nrxxe- 
^53 *rr-=t: a-z -re arc-ate.' (ines 2876-2878.) 



0* the tremendous conflicts tr;ai tnese two 
; : -^ in the hearings it's appropriate* Qines 2881 - 



weeas "5 ~sson in ifeof r-e -o-^r. eces^-^talives is to reduce 
? : -;;e -:-stnes.* (ines 2889-2891 ) ' 



5 'T-«;'6 a;e scc^c at a-e "c-est.* (Ine 2894) 

6. '[>. Jones dkJ re: ::-e - a": dentify himself as someone who has 
lobbied for arxj represeme: -e : -ea-.y Association' (ines 2921-2923) 

7. "r-a: ree ae a i.^::f: :• s: ;-: 5:5 •. -: ;: a-; -e 5-ore come up with 



^206; J28-I615 • 2600 Fairvkw Aar. E.. Suite i« Seattk. MM 98102 



1^9 



Admiral Zunmak. you have made istse. drect and indrect accusations as to 

my professional integrity without foundation. For the record: 

1. I have -■%.%' '-ce-: '-,' '"ec'%',^'-=;-: •'% -"-r;"- '5-.-=: '.'=:' sce^ea 
Association (IWSA ,' ;- . . '^' .=:;-.- h ^h: >:.:. ^ .■ 

2. I recerve^ ^ ■■■.■.--.:■ ■.■.'■■^::-- -■■--. :-\'- ■: ■■-■■-.■■■ :■-.-■'■ -.~ .■ . :■ ■- 

sources anc ■ y ^\\h\-- h- h - ■.:: :-.. ~' --.■ , ^ v .:-■■..:- ■■■■:■ 
submitledtc "^ E=^^ :=:=: -^ =: ^^^^^ ; '.''..-. ' - ^ /- \ .■-.- \ - : ^^^ .= 
furxJing fror -^ .'.I- - : .■.^■. - h ■^' -.'■' ^■: \'.h:-.' .: -- \' '.■.:.-■■-.■ 
Rappe. Dc ,■-' '^'■'- ''-'^-' '-' ' - '■--'-:'■' - h^:^ - -.h ■ ^ ■■.-.■ \. ^-.\ .- h 
decrease ir •=; -=: . -'.-..- . ■ - -. ,■■--.■■■■ :-..■.-.. v : ;' - ; :. , : : 5tJ= 
more emph,a; i -' .--.'■.■ .., v^: - -, , :^ .e-,i 



3. My professjc' e i e; . e .^rtise with respect to c -'. i. .. -Vi: ,' 
rsk assessment of al '- - i : ^ : nation erressKins ~'e , : . - . .' 
consulling work comes ;. V ^ ^ ocal govemme^: . : -i . . - -^ 
authorities, [n the case. -^^ , .; e '--^ avendo' :e ^ 
permitting costs were a : i ' . ^ . ^ i ^ . . authority z 

cases my firm's (or my : e ., . -. - ^ :.- .'■-.-^ -.- -- . .-'. 

peer reviewed t>y State '. .'i e.^i. . c.- ^ - .. %t 

complance with Federa iui-.c i':; :>^a. :^ - -.'-i io :. -- i^:.^^:'-c-. 
guidance. 

4. In my opinKxi. the greatest test of soertrfic ce : : 
ana n a court of taw wtien appearing as an expert wtrei ^ 

^any occasons. I fuly expected to have taken the oar :. . . r -. : .- 1^: '3 
//nk*i has been customary in otfier svnilar hearings. I a~ ^ -^ ;.-.■..-=. ^ 
tempered your accusations/ remarks had you been undei oaan. 

5. I was not sponsored by the ncnerator ndustry to testify on Dec. 1 3. nor da 
the industry have any poor krxMvledge of the content of my t esf nony. 

Ihavea--.. -. . -e's of experience n the feld of protecting human heaih 
and the err/':'-c- r .; ; ess of my tenure in the government, academa or 
Dfrvate sectc- ;- e e- :r: ::ated to seerig that good soence leads to sound 
envronmer-i -::■:- = ~3i a retired Navaf 0">zs' rf ' - r ?--'» *raJ0 

attackafetc .-- . = i i i • arxJ dfehonest fas'c 




HoTKirable Dana Rotvatiactier 
Chairman of the SubcomfTWttee 



23-557 O - 9€ - 7 



190 

Zephyr Consulting 

KAY H. JONES, Ph.D. 



EDUCATION 

Ph.D. in Sanitary Engineering, (with minors in Chemical Engineering and 
Environmental Toxicology,) University of California at Berkeley, 1968 

MS, Sanitary Engineering, University of California at Berkeley, 1961 

BS, Civil Engineering, University of Washington, 1956 

EMPLOYMENT HISTORY 

1 990 - present President 

Zephyr Consulting 
Seattle, Washington 

1981 - 1990 Vice President and Practice Leader for Air Quality Management 

Roy F. Weston Inc., West Chester, PA and Seattle, WA 

1 979 - 1 981 Professor of Environmental Engineering and Deputy Director of 

The Environmental Studies Institute 
Drexel University, Philadelphia, PA 

1 975 - 1 979 Senior Advisor for Air Quality 

Council on Environmental Quality 
Executive Office of the President 
Washington D.C. 

1974 - 1975 World Health Organization (WHO) Consultant 

Ministry of Environment, State of Israel 

1967 - 1974 Senior Technical Advisor and Research Manager 

Office of Air Programs, National Air Pollution Control 
Administration (DHEW) and U.S. Environmental Protection 
Agency (EPA), Washington D.C. 

1959-1966 Bioenvironmental Engineer 

Biomedical Science Corp, U.S. Air Force 

1956 - 1959 Civil Engineer, U.S. Air Force 

1 956 Civil Engineer, Standard Oil Company of California 



\ 
(206) 328-1615 • 2600 Fairview Ave. E., Suite 18, Seattle, WA 98102 



191 



KAY H. JONES, PhD 

Page 2 

FIELDS OF COMPETENCE 

Air quality management, air pollution control engineering, risk assessment, 
government affairs and policy analysis, litigation and expert witness support, public 
participation, international program development, research management, industrial 
hygiene, radiological health, teaching. 



EXAMPLES OF PROFESSIONAL ACCOMPLISHMENTS 

• Project director on many major industrial permitting projects, including one of 
the world's largest complexes. General Motor's SATURN plant in Tennessee. 

• Directed several major projects involving the assessment of air toxics impacts 
of Superfund sites and hazardous waste disposal sites. Such assessments 
involved ambient monitohng, modeling, and risk assessment. Retained as 
expert witness for some 200 industrial defendants in major tort case involving 
a controversial Superfund site in Southern California. 

• Recognized national authority on health risks associated with combustion of 
municipal and hazardous wastes. Directed risk assessment studies on 33 
proposed projects and was technical advisor and or expert witness on 20 
additional projects. Responsible for developing and maintaining a one-of-a- 
kind worldwide data bank on emissions data for municipal incinerators. 
Authored numerous national and international papers on this subject. 
Developed innovative approach to involving the public in the risk assessment 
process. 

• Developed and maintained the only national air quality data bank outside of 
the U.S. EPA for the Motor Vehicle Manufacturer's Association (MVMA). 
Prepared three annual air quality status and trends chapters for the President's 
Council on Environmental Quality (CEQ) annual report as a consultant to CEQ. 
Prepared and presented definitive studies on ozone nonattainment issues on 
behalf of the Clean Air Working Group (CAWG), a lobbying group, 
representing some 200 U.S. industries. Co-authored several technical papers 
on this work. 

• Directed the conduct of several air quality studies that questioned the need for 
excessive air pollution control measures, in particular VOC controls, on behalf 
of local governments and industrial groups. Authored several papers 
challenging the need for auto l/M programs. Provided testimony on behalf of 
city governments to EPA and state legislative bodies. 



192 



KAY H. JONES, PhD 

Page 3 



Directed two innovative projects involving potential adverse air pollution impacts 
of alternatives to conventional home heating. Canied out an in-depth study of 
indoor air pollution at an active home using kerosene heaters. Provided definitive 
testimony before the Consumer Products Safety Commission in defense of their 
safe use. Conducted a comprehensive policy analysis of the required and local 
air quality impacts of wood stove use for the Coalition of Northeast Governors. 

At CEQ authored the Presidential Initiative on Acid Rain contained in the 
president's 1979 environmental message. This initiative was the foundation of the 
Congressionally mandated National Acid Precipitation Assessment Program 
(NAPAP). Developed an independent data system and method for assessing the 
status and trends chapters of five CEO annual reports to Congress. Developed 
computerized air pollution population exposure and risk models. Prepared and 
critiqued legislation and proposed EPA regulations. 

As a WHO consultant to Israel, established that nation's comprehensive air quality 
management program within the Environmental Protection Service. Conducted 
policy analyses on auto emission standards, ambient air quality criteria and 
standards, and stationary source air pollution control practices. Designed ambient 
monitoring programs for all major cities and assisted in the development of local 
air quality management agencies at the city government level. 

Managed research in the areas of stationary and mobile source emissions control, 
meteorology, chemistry, and physics at EPA and NAPCA. Coordinated 
intergovernmental and government/industry programs on common areas of 
research. Was agency focal point for coordinating all meteorological research 
activities and the establishment of specialized air-pollution-related meteorological 
observation programs throughout the U.S. Was vice chairman and chairman 
designee of the research programs sponsored by EPA/API/MVMA under the 
auspices of the Coordinated Research Council's (CRC's) Air Pollution Research 
Advisory Committee (APRAC). Established the first comprehensive long-range 
research needs regarding all forms of stationary and mobile-source combustion. 

Coordinated international programs on air pollution matters at EPA and NAPCA. 
Directed a major program as part of President Nixon's initiative in setting up the 
NATO Committee on the Challenges to Modern Society. This initiative led to the 
establishment of a common air quality management policy throughout NATO 
similar to the concepts and goals in the U.S. This project was the most resource- 
intensive international program ever undertaken by the EPA ($1 .7 million). Was 
also director of the U.S./Soviet bilateral program on research on control of mobile 
source emissions. 



193 



KAY H. JONES PhD 

Page 4 



Directed all environmental protection programs at the U.S. Air Force missile launch 
complex at Vandenburg AFB, California. Responsible for protection of Air Force 
personnel and the public during launches of space vehicles involving highly toxic 
propellents and nuclear materials. Designed an innovative toxic waste disposal 
system. 

In addition to the two years as a full professor at Drexel, taught for three additional 
years as an adjunct professor. Also taught environmental engineering courses 
related to air quality management at George Washington and Howard Universities 
during the period 1 970 to 1 979 (adjunct associate professor). 



PROFESSIONAL AFFILIATIONS 

American Society of Civil Engineers 

Past chairman of the Environmental Engineering Division 
Past chairman of the Air Pollution Research Committee 
Past member of the Environmental Systems Policy Committee 
Member of the Air, Noise, and Radiation Committee 
President of Student Chapter, University of Washington 

Air and Waste Management Association 

Past member and past board member of the Federal Conference of Environmental 
Engineers 

Tau Beta Pi Engineering Society 

Chi Epsilon Civil Engineering Society 



AWARDS 

Outstanding ASCE Student Member, 1956 
USAF Commendation Medal, 1966 
USPHS Commendation Medal, 1974 
USPHS Commendation Medal, 1976 



194 



IWSA's Comments on EPA's Dioxin Exposure Assessment Document 
(Estimating Exposure to Dioxin-Like Compounds 
Review Draft EPA/600/6-88/005/Ca - June 1994) 

I. EXECUTIVE SUMMARY 

The Integrated Waste Service Association has spent considerable effort researching 
worldwide data on dioxin and related compounds, including travel to Europe where Association 
members met with leading experts in the field of dioxin research. IWSA's submission to EPA 
contains 19 separate reports on dioxin fixjm the U.S., the U.K., The Netherlands, Germany, Sweden, 
and France. In addition, IWSA funded research by the leading international experts in this field to 
review and comment on the agency's findings. 

The results of IWSA's work reveal a troubling fact: that the EPA ignored existing research 
and reports when formulating the agency's conclusions about dioxin. The information contained in 
the following submittal reflects exhaustive research by hundreds of scientists. In particular, the 
Netherlands, Germany, Sweden and France approached the issue of dioxin sources in a 
comprehensive manner, unlike the EPA. For example, these European countries identified and 
measured in the field the sources of dioxin in their countries. Whereas the EPA admits it cannot 
account for between 54% and 81% of the dioxin found in the environment, Europeans have balanced 
their dioxin budget 

Unlike the U.S. EPA, European environmental policymakers look to the future. Every 
country, except the U.S., that has tackled the dioxin problem focuses its efforts on identifying efforts 
taken now that will bring down dioxin emissions in th^ future; and efforts that need to be taken in the 
future that will further decrease emissions. Whereas the EPA highlights in its report and media 
releases that municipal waste combustors (MWC) represent 3,000 g TEQ/yr, the agency gives little 
thought to explaining that a small minority of older MWCs with less efficient pollution control 
equipment emit the majority of dioxin emissions. EPA buries in its Reassessment the fact that such 
older facilities will be closed or fitted with modem pollution control equipment In fact modem 
fadUdes are more than 100 times cleaner than these older units. In the near future, MWC emissions 
will be less than SO g TEQ/yr nationwide. This is not speculation, but the cold fact of necessary 
compliance with the Clean Air Act 

Yet EPA issued a misleading statement to die media claiming 95% of all known dioxin 
emissions come from combustion without explaining the agency's clear lack of knowledge of dioxin 
sources. The simple statement left the public with the mistaken impression that municipal waste 
combustors are the only source of dioxin. Nothing coukl be further from the truth. European nations 
provide their citizens with a comprehensive inventory of dioxin sources and their individual 
contributions to the dioxin budget rather than lumping sources and issuing general statements. 



195 



Genmny has identified more than 100 sources of dioxin. Professor Rappe cautions that the 
U.S. budget misses major sources of dioxin. The production of iron, wood burning, and the earlier 
use of pentachlorophenol all may be greater dioxin sources than older, less efficient MWCs. Dr. 
Stellan Marklund of the Institute of Environmental Chemistry at the University of Umea, Sweden, 
points out the glaring onoission by EPA to test mobile sources under field conditions versus the 
testing to date done only in a lab. If Marklund is correct in his hypothesis that dioxin tailpipe 
emissions are much greater when cars using unleaded gasoline are driven in the winter when streets 
are covered with road-salt or in coastal communities, then EPA has greatiy underestimated the dioxin 
contribution of mobile sources. 

Eh-. Kay Jones takes issue with EPA's statement that tong-range transpon accounts for dioxin 
deposition in remote areas of the U.S. He suggests an alternative, reasoned hypothesis that EPA 
chose to ignore: that dioxin concentrations in agricultural crops noay be the result of local dioxin 
sources such as farm machinery, trucks, trains, and highway traffic. 

Professor R^)pe points to another fundamental problem in EPA's dioxin budget In order to 
reconcile emissions and deposition, the congener patterns in emissions should be similar to the 
congener patterns in deposition. The dioxin measured at the stack has a distinct congener pattern. 
The dk>xin measured in the soil has a distinct congener pattern. If we are to believe that what comes 
out of the stack is what we find in the soil, the two pauems should match. They do not. Professor 
Rappe points out that ambient air, soil, and sediment have a higher ratio of dioxin to furans, but 
municipal waste combustion emissions have a higher ratio of furans to dioxin. This finding clearly 
iniplies that the higher concentration of dioxin to furans in the environment cannot be explained by 
emissions from municipal waste combustors. 

EPA's rigid nMdel which predicts how emissions from a source travel, deposit and then 
become part of animals, plants, and humans is technically flawed and unacceptable in its present form. 
There is no discussion in the Reassessment that EPA has approved four different risk assessment 
models for use in predicting dioxin fate and transport. The model used in this report contains 
dramatic changes in a variety of factors without explanation. EPA has ignored its own guidance of 
focusing by focusing on the 99.9th percentile of risk. The result is that policy decisions stemming 
from application of this risk model are based on the potential harm to a fictitious person who eats, 
breaths and touches an unrealistic amount of dioxin. 

In all, IWSA and the experts who reviewed the EPA Reassessment on behalf of the 
Association have provided the agency with more than 30 specific areas of concern with the risk 
model Isjr example, EPA chose an air model, COMPDEP, as the air dispersion model despite the 
fact that COMPDEP has never been peer reviewed by the modeling community nor withstood the 
test of time similar to other air models such as ISCLT or COMPLEX 1 . The agency has not provided 
information on how COMPDEP behaves in complex terrain nor taken into account that the wet 
deposition algorithm in COMPDEP is out of date. The shortcomings of the model must be corrected 
before embracing it 



196 



Another comment concerns a set of approved chemical constants provided in the EPA 
Reassessment that ignores the range of acceptable values contained in peer review literature. EPA 
should explain how it chose the values cited in its document and how the uncertainty implicit in this 
range of values is to be incorporated into indiiea risk methodology. 

The effects of photodegradation are likely to be extremely significant when estimating dioxin 
exposure. The agency chooses to ignore photodegradation despite the strong suggestion by experts 
that photodegradation, as well as other degradation processes not discussed by EPA, are the major 
forces in determining long range transport and our background body burden matrix. 

IWSA has spent considerable time and effort to provide EPA with meaningful, accurate, and 
carefully prepared comments to assist the agency. We hope that our work will be helpful, and that 
this submission is only the beginning of a cooperative effort to understand dioxin in a comprehensive 
manner. 



197 



Zephyr Consulting 



DRAFT 



INTRODUCTION 



EPA has iised estimated annual deposition i^ates to calculate the annual TEQ dioxin 
emissions for the continental U.S. and Alaska. The range of their estimate is 20,000 - 50,000 
gm TEQ/yr. Of this amount EPA has only accounted for 9300 gm TEQ/yr. (central 
estimate). EPA believes that the difference is due to uninventoried sources or recirculation 
of historical deposition. A critical review has been made of EPA's documentation regarding 
their findings. Three questions were set forth to focus this review, these being: 

1. Are EPA's deposition estimates accurate based on the scientific evidence at hand? 

2. Are the deposition rates in the U.S. on the average higher or lower than in European 
countries? 

3. Does recirculation play a probable role in the fate and effects of current dioxin 
emissions? 

The ensuing discussion is directed at answering these three questions within the framework 
of our current state of scientific knowledge and judgment. 

R EVIEW RE SULTS 

EPA has used a nationwide deposition flux rate of 2 to 6 ng/TEQ/m^/yr to estimate the 
aggregate annual emissions from known and unknown sources. These endpoint estimates 
were synthesized from their review of the available literature (10 citations). Only 2 of the 
citations pertained to U.S. measurements or research. Only one of these 2 studies related 
to direct deposition measurements in the U.S. The other one relates to sedimentation rate 
estimates from a lake core sample. In addition to assigning the 2-6 ng/TEQ/m^/yr range 
of deposition flux rates to the lower 48 states, they assumed a 1 ng TEQ/m^/yr for Alaska 
based on a single measurement in Northern Sweden. Table 1 is a summary of EPA's 
interpretation of the data they cite. 

It is important to see if EPA properly interpreted the literature they cited in Table 1 in 
arriving at their continental deposition flux range of 2 - 6 ng TEQ/m2/yr and remote flux 
rate of 1 ng TEQ/mVyr. 

It is not clear why EPA would state that the low continental value "could be as low as 2 ng 
TEQ/mVyr (based on limited U.S. data)." They calculated the low value of 1 ng 
TEQ/mVyr from Koester & Kites and the TEQ equivalent of the 375 PCDD/PCDF 



(206) 328-1615 • 2600 Fairview Ave. E., Suite 18. Seattle. WA 98102 



198 



ng/mVyr from Smith et al.'s work is 1.75 ng/mVyr (Smith 1994). EPA provides no 
rationale as to why either of these observations would represent a continental average. 
There is also no explanation as to how they arrived at 6 ng TEQ/mVyr as an upper limit 
"(based on European data)." 

EPA did not properly report the results of the long range transport modeling results of Van 
Jaarsveld and Schutter. The lower limit of deposition at the boundary of their 1,000 by 
1,000 km grid was less than 0.5 ng TEQ/m*/yr. These low flux areas were both predicted 
for land masses and open ocean to the north of the European sources. The real important 
data contained in this paper was apparently overlooked by EPA. First, the deposition 
gradients between the urban/industrial areas and rural/remote areas should have been 
applied qualitatively to the continental U.S. Most of the U.S. does not look like Northern 
Europ>e. Most of the U.S. continental land mass does not have upwind industrial regions, 
e.g., the plains states, the Southwest, the Rockies and most of the western states. EPA could 
have applied the acid rain model for the Northeast (which they developed) in the same 
manner that was the analog for the European analysis. Secondly, this paper presented 
compatible modeled deposition and air concentrations which would allow for predictions of 
deposition flux in absence of actual deposition measurements. The range of these ratios was 
024 - 0.39 ng TEQ/mVyr per fg/TEQ/m' (mean = 029). Thirdly, but very importantly, 
the paper presented data on how localized total wet and dry deposition is relative to point 
sources, i.e., a greater than 10 fold deposition flux deCTease in 10+ km from the source. 
Had EPA applied this relationship to their low end flux estimate of 2 ng TEQ/mVyr the 
implied ambient air concentration would be 62 fg TEQ/m'. This value is only 36% of the 
level asstmied by Lorber et al. in their most recent Dioxin 94 paper on backgroimd rural air 
to beef model validation (Lorber 1994). 

Liebl et al.'s paper also contained more useful data than that reported in Table 1 by EPA. 
The same deposition flux to ambient ratio (similar to that determined from the Van 
Jaarsveld and Schutter modeling exercise) can be estimated. The average value for the 
three years of measured flux and ambient data in their rural area case is 0.056 ng 
TEQ/mVyr per fg TEQ/m'. The rural with some industry included case ratio was 0.050 ng 
TEQ/mVyr per fg TEQ/m^ The ratio for the 1992 industrial/suburban site case was 0.12 
ng TEQ/m^/yr per fg TEQ/m3 which again suggests that most deposition occurs close to 
the source of emissions. 

There are other literature citations that EPA did not include in their review. Some 
examples follow. Kfihn and Steeg (1993) reported agricultural area deposition fluxes versus 
distance from Hamburg. The fluxes were 4.5 ng TEQ/m^/yr at 2 km and 0.9 ng TEQ/mVyr 
at 9 • 18 km from Hamburg. EPA did not discuss Czuczwa and Hites (1986) Lake Siskiwit 
sediment data in this section of the report relative to atmospheric deposition rates in 
supposedly remote areas. Had EPA done so and assuming the total PCDD/PCDF to TEQ 
ratio was similar to that observed by Smith et al., they would have reported a deposition flux 
estimate of 1.09 ng TEQ/m^/yr. Several soil deposition studies were overlooked by EPA 
which reflect both the gradients in atmospheric concentrations and deposition flux. Boos 
et al. (1992) measured soil PCDD/PCDF data at 24 diverse sites in Austria, Samples were 
analyzed for a variety of settings. The remote rural background level was about l/30th of 



199 



the soil PCDD/PCDF concentration near uiban areas. Measured levels near specific industries known 
to be dioxin emitters did not show levels above those associated with the urban emissions in general. 
These data again appear to conflict with EPA's assumptions that rural ambient concentrations are 
l/5th of urban levels even assuming equatable deposition velocities. 

Based on these previous discussion jwints a more detailed subregional approach can be taken to 
iirprovc upon EPA's macro scale ^jproach although an alternative scenario is proposed later. Table 
2 shows alternative deposition flux rates for 4 categories of land use for which data is available in the 
literature. These data can then be applied to the 6 standard land use categories far the continental 
U.S. See Table 3. 

The range of the stratified estimates which have some semblance of logic relative to sources and 
receptors across the U.S. is much more in alignment with EPA's current emissions inventory of 
known sources, i.e., 9,100 gm TEQ/yr. Although this number may be at the approximate level, the 
individual sources are given incorrect contributions by EPA. There are also several other well 
recognized sources which EPA did not inventory, e.g., sintering plants, secondary aluminum smelting, 
non-highway mobile sources, etc. 

The zero deposition flux rate assigned as the lower limit for the Federal, and Rural range land use 
categories is because most of these areas are free of any significant upwind human activity as 
previously discussed. Obviously some very tow andnent levels probably exist and low end deposition 
cannot be estimated. This may also be true of some portion of the Rural Forest category because 
there are private timberlands in the more remote areas in the western half of the continent. This 
excludes the potential intermittent and localized contribution from forest fires. 

The available deposition data strongly suggests that long range transpon may not be a significant 
mechanism of widespread agricultural crop contamination as EPA suggests. The Hites ( 1 99 1 ) report 
to EPA is their only citation of evidence that long range transport of combustion related emissions 
is taking place. It should be noted there that there is an inconsistency between what Czuczwa and 
Hites (1986) and what Hites (1991) reponcd as the fate and transport mechanism. In the eariier 
citation the authors claim a high correlation between the congener profiles of the ambient data they 
used, le., Washington, D.C. and St. Louis and the Siskiwit Lake sediments. They further state that 
finding dioxins in the Siskiwit sediments "has made PCDD and PCDF ubiquitous in the environment" 
In the 1991 report a different set of ambient data were presented including that measured by the 
author et al. These data however did not show the good air and sediment congener profile 
correlations previously reported. The possible role of photodcgradation was introduced to explain 
the shift in the congener distributions between sources and sinks. Most ambient data except those 
data from the vicinity of known point sources does not exhibit the congener profiles presented in the 
latter Hites report. In fact, most U.S. urban profiles look like the Washington, D.C. and St Louis 
data. 

We believe that there is a more togk:al and compelling explanation for the levels and congener profiles 
found in Siskiwit Lake. It is not a remote lake by any stretch of the imagination when potential 
nearby sources are considered, i.e.', the Thunder Bay industry mix and commercial shipping. The 
commercial shipping in and out of Thunder Bay in 1983 involved some 1350 ships carrying 23.5 



200 



million metric tons of cargo from Thunder Bay most of which passed within 1-5 miles of the Isle 
Royale coastline. Although there have been no direct measurements of dioxins/furans from 
commercial vessel stacks there is no reason to believe that they would not be similar to those 
associated with diesel truck engines both in emission rates (ng/gal) and congener profiles. See Jones 
(1993) for a detailed discussion. 

A major shift in ship and power technology took place after 1970 when steam turbine engines were 
replaced with diesel powerplants and Great Lakes ships became bigger and more fuel efficient A 
historical fuel consunption profile in gal/mi. for the shipping past Isle Royale versus Hites' sediment 
data was estimated and is shown in Figure 1 . The annual number of ships is also shown. This latter 
indicator does not reflect the change in ton mil6 fuel economy over the transition period just 
discussed There has not been any other explanation which fits the sediment pattern as well as the 
proximate shqj fuel consunptk)n pattern. The change over to unleaded gasoline in 1975 and beyond 
has been suggested. However, the relative contribution of either leaded or unleaded gasoline 
powered vehicle dioxin emissions is insignificant in comparison to diesel powered vehicles and hence 
would not have caused such a major downward shift The advent of air pollution control on 
incinerator sources is not consistent with the sediment pattern with respect to time. Further, it is 
unlikely that municipal incinerators, being relatively few in number, could influence Siskiwit Lake's 
sedimentation. 

Smith et aL observed the same peaking and decline in sediment dioxin levels in Green Lake which is 
some 15 km east of Syracuse, New York. This lake is in a rural setting. However, it turns out that 
there are three major mobile sources which could influence the dioxin deposition in the lake as well 
as possibly explain the trend. Two of the three line sources are within 7 km and one of 16 km of 
Green Lake. They are: 

The Erie Canal through Oneida Lake, the New York Throughway and the Conrail tracks (ex Penn 
Central). Although much of the historical multi-mode traffic data was not readily available, the diend 
in transport tonnage on the Erie Canal from 1950 onward and the train fuel use from 1973 on were 
available. Throughway trafiBc data for 1988 and 1993 were used to extrapolate back to 1960. These 
data plus a composite emissions factor trend are overlaid on the sediment D^nd data in Figure 2. 
There is an apparent correlation between the decrease in the emissions and sediment dioxin levels. 

CONCI^IISIONS 

The direct answers to the three premise questions are as follows based on our critical review of 
EPA's documentation and other information we have gathered and synthesized. 

Question 1 : Are EPA's deposition estimates accurate based on the scientific evidence at hand? 

Answer No. EPA has grossly overestimated the total deposition in the U.S. Because they (a) 

did not interpret the available literature properly, (b) did not extrapolate European 
dau to the U.S. case with necessary adjustments, and (c) did not double check their 
results by ecnploying sinple mass balance analyses. If a macro scale deposition model 
approach was an acceptable approach in the U.S. case and the best estimate 



201 



subregional deposition factors were used, the annual emissions would probably fall 
in the range of 4,700 - 12,400 gm TEQ/yr. These estimates more than likely will 
encompass the inventory of known sources once EPA corrects the errors in their 
existing inventory and adds additional sources which have been well documented in 
Europe. For exanpk, EPA's inventory of hospital waste incinerator emissions is high 
by a fector of 35 while their mobile source inventory is low by a factor of at least 20. 



Question 2: 



Are the deposition rates in the U.S. on the average higher or lower than in European 
countries? 



Answer Much lower. The spacial compression between industrial, suburban and rural areas 

in Europe is a greater than most of the continental U.S. There are many subregions 
of the U.S. which have no associated upwind center of human activity which is 
primarily responsible for dioxin emissions and their subsequent transpon into rural or 
remote areas. Most of European countries experience 1 - 10 ng TEQ/m^ /yr. of 
average deposition while in the continental U.S. the range is calculated to be between 
0.6 and 1.6 ngA^Q/m?/yr. It is quite likely that remote background areas experience 
practically zero deposition flux. The EPA citation of Hites' conclusion that Siskiwit 
Lake represents a remote area is flawed because of obvious more local emissions 
sources, i.e., industry and shipping. An alternative deposition hypothesis is offered 
which does not incorporate long range transport as the principal mechanism of 
agricultural crop exposure in the U.S. Highly localized impacts due to line sources 
of mobile dioxin emissions in the form of farm machinery, transport trucks, trains, and 
highway traffic all represent equally plausible sources of crop exposure. The ambient 
air quality gradients do not exist across the major agricultural regions of the U.S. to 
support EPA's hypothesis. 



Question 3: 



Does recirculation play a probable role in the fate and effects of current dioxin 
emissions? 



Answer Probabfy not. The closure between the anticipated inventory of known dioxin 

emission sources and the best estimate range of total emissions based on deposition 
flux analyses is the most compelling counter argument 



202 

TABLE 1 
DEPOSITION RATES CITED BY EPA 



CITATION 


DEPOSITION RATES 
(ng/mVyr) 


EPA 
COMMENT/ASSUMPTIONS 


1. Koester & Hites (1992) 


370 - 540 Total PCDD/PCDF 
1-2TEQ 


Perfect isomeric distribution 


2. Smith ct aL (1993) 


375 Total FCDD/PCDF 


Dep. rate for 86 - 90 


3. Anderson ct aL (1992) 


ITEQ 


Snow in N. Sweden 


4. Fernandez et aL (1992) 


13 TEQ (nd - 0) 
17TEQ(nd- 1/2 dl) 


1 mo. urban/sub. setting 


5. Van Jaarsveld and Schutter 
(1992) 


1 - 10 TEQ 


Long range modeling of N. 
Europe 


6. Hiester et aL (1993) 


Urban 






246 - 1687 Total PCDD/PCDF 


92 measurements 




3.6 - 303 TEQ 


nd's - 




Rural 






420 Total PCDD/PCDF 






4.4 TEQ 




7. Uebl et aL (1993) 


7.6 TEQ (ind/suburb) 

IS TEQ (niral/ind) 

1.1 TEQ (rural background) 


11 mos. in 1992 


8. Fiedler (1993) 


1.8 - 73 TEQ (4.4 ave.) 


Rural areas 




73 - 36 TEQ 


Ind. areas 




1.000 TEQ 


Few areas 


9. Bowman et al. (1991) 


38 Total PCDD/PCDF 


Remote coastaL Sweden 


10. Naf et aL (1992) 


240-1,700 PCDD/PCDF 
3 - 14 TEQ 


Bothnian and Baltic Sea 
sediments 



203 

TABLE 2 
BEST ESTIMATE DEPOSITION FLUX RATES 



LAND USE 


AUTHORS 


TEQFLUX 
(ng/mVyr) 


COMMENTS/ASSUMPTION 


Remote/Rural 


Van Jaarsveld & 
Schuner 


0.25 


1/2 of modeled < 3 value 




Uebl/Boos 


0.27 


1/30 of Frankfurt 1992 dep. 
rate 

1/30 is urban/remote ratio 
from Boos^^ 


Rural 


KQhn & Steeg 


0.9 


9 - 18 km from Hamburg 




Liebl 


Z45 






Smith 


1.09 


Sediment data 


Urban/Suburban 


Uebl 


7.7 


1992 Frankfurt 




Kfihn & Steeg 


4.45 


- 2 km from Hamburg 


General 


Van Jaarsveld & 
Schuner 


11 (Belgium) 

1.1 (Denmark) 

3.8 (FRO) 

8.2 (Netherlands) 

2.4 (UJC) 


Average fluxes by country 
across Europe 


1 




53 Average 





(') Remote n.d. correction = average of all other data corrections. 



204 



TABLE 3 



ESTIMATED DIOXIN T.E. DEPOSITION RATES BY LAND USE 
AND REGIONAL CHARACTERIZATION 



REGIONAL LAND USE 
CHARACTERIZATION 


AREA 
(10* AC) 


DEPOSITION 
(no/mVyr) 


RATES 
(Om/«c/yr) 


TOTAL 
DEPOSITION 
(om/yr) | 


Developed 


773 


4.4 - 77 


17.8 - 312 X 10^ 


1376 - 2412 1 


Federal 


404.1 


0-.25 


- 1.0 X Iff* 


0-404 


Rural Crop 


422.4 


0.9 - 2.45 


3.6 - 9.9 X Iff* 


1521 - 4182 


Rural Pasture 


129.0 


0.9 - 2.45 


3.6 - 9.9 X 10* 


464- 1277 1 


Rural Range 


401.7 


0-.25 


- 1.0 X 10* 


0-402 1 


Rural Forest 


373.9 


0.9 - 2.45 


3.6 - 9.9 X 10* 


1346-3702 1 


Totals 


1,933 






4707 - 12379 1 


U.S. EPA Total 


1,933 


2-6 


8.1 - 24J X Iff* 


15,658 - 46,972 



205 



Zephyr Consulting 



S^.^.5igji 



4o 



ao 



i 




^ f 3060 












fsao 



t=y&o 






206 



Zephyr Consulting 



It.O 



I 

t 

If 



S.O 




V 



Aa> 



300 



200 



»0o 



t.'i 



\'Wo 



«T0 









i 



T5 



•50 



2.^ 



1 1^ 



^ 
1 









207 



UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 



December 12, 1995 



OFFICE OF THE ADMINISTRATOR 
SCIENCE ADVISORY BOARD 



Honorable Dana Rohrabacher 
House of Representatives 
Washington, D.C. 20515 

Dear Congressman Rohrabacher: 

I am professor of epidemiology at the School of Public 
Health at the John Hopkins University in Baltimore, MD. I also 
serve as Chair of the Executive Committee of the Science Advisory 
Board (SAB) at the Environmental Protection Agency (EPA) . The 
SAB was established by Congress nearly two decades ago to provide 
independent, objective scientific evaluation of the technical 
foundations of the EPA's positions on issues. I have been a 
member of the Board for 6 years and Chair of its Executive 
Committee for over two years. 

In that capacity I am submitting the following comments 
(which are adapted from the Executive Committee's letter 
transmitting the Board's report on dioxin) for your consideration 
and request their inclusion in the record of your hearing on the 
EPA's scientific reassessment of the rislcs associated with 
exposure to dioxin. 

In 1988, EPA released two documents addressing ris)cs from 
dioxins {A Cancer Risk-specific Dose Estimate for 2 ,3 ,7 ,8-TCDD, 
and Estimating Exposure to 2,3,7 ,8-TCDD) and requested that the 
SAB review them. The SAB report (SAB, 1989), released in 
November 1989, although not agreeing with several of the 
conclusions in the two documents, concluded that "both documents 
were carefully constructed and well written." The SAB report 
concluded with a recommendation to "...follow up on this 
excellent start..." by developing and validating new models for 
human exposure and for cancer and non-cancer risJc endpoints, and 
to pursue active research programs, resolve questions and 
incorporate new data. The Agency initiated a significant effort 
addressing dioxin exposure and risJc, and on September 13, 1994, 
released for public review and comment (59 FR 46980) a 2,400 page 
draft reassessment of the toxicity of, and human exposure to 
dioxin. 



208 



In December, 1994, the EPA Office of Research and 
Development (ORD) requested that the SAB review the reassessment 
document, and submitted a draft Charge addressing some 40 issues. 
The SAB Executive Committee approved the creation of an ad hoc 
Dioxin Reassessment Review Committee (DRRC) and appointed Drs. 
Morton Lippmann and Joan Daisey as Co-Chairs. The DRRC was 
developed by building on the SAB's Environmental Health and 
Indoor Air Quality/Total Human Exposure Committees, and adding 
{following an extensive review and recruitment process) 
additional Consultants to fill gaps in needed expertise and to 
add depth in key scientific areas. In addition to the Co-Chairs, 
37 scientists were appointed to the Dioxin Reassessment Review 
Committee, including Dr. Michael Gough (as a Federal Expert), who 
is scheduled to testify before your Committee. 

A final Charge for the review, encompassing 43 specific 
questions was adopted after discussions involving ORD and SAB 
staff, and the Co-Chairs (the detailed Charge is provided in 
section 2.2 of the enclosed report) . The DRRC subsequently met 
on May 15-16, 1995, in Herndon, Virginia to hear briefings by EPA 
staff, to receive comments by members of the public, and to 
discuss the relevant issues of the Charge. Following the public 
meeting, the Committee's report was developed through a series of 
mail reviews of successive drafts. The final report was approved 
by the SAB Executive Committee at its public meeting on September 
21, 1995. The only Members of the Dioxin Panel who participated 
in this meeting of the SAB Executive Committee were the 
Co-Chairs, Dr. Lippmann and Dr. Daisey. Admiral Elmo Zmtiwalt, 
who is scheduled to testify at your hearing, provided public 
comments at the Executive Committee meeting. 

The enclosed report provides a detailed discussion of each 
of the specific issues raised by the Charge, and addresses some 
additional related questions which arose during the course of the 
review. The following comments provide a synthesis and overall 
perspective on the Committee's findings. 

First, vis-a-vis the Exposure Assessment draft document, the 
Committee wishes to commend those responsible for doing a very 
credible and thorough job of assembling, integrating, and 
analyzing a very large body of data on dioxin source emissions, 
environmental levels, exposures, and human body burdens, all 
within the framework of human exposure assessment. The detailed 
recommendations of the DRRC largely address refinements, 
corrections and clarifications to the draft Exposure Assessment 
document, not substantive revisions. 



209 



The exposure reassessment identifies the major knovm sources 
of dioxins and provides a reasonable estimate of total emissions. 
The Committee recommends that new information on emissions from 
the incineration of medical waste (and other sources) be 
incorporated if appropriate, and that the estimates of 
uncertainties in the emissions inventory be improved for several 
emissions categories. The Committee also recommends adding an 
explicit statement to the final document noting that the 
fractional contributions of various types of emissions sources to 
total emissions cannot be assumed to be identical to the 
fractional contributions of those sources to human exposures. 
The Committee agrees with the EPA position that current levels of 
dioxin-like compounds in the environment derive primarily from 
anthropogenic sources and, based on available data, that the 
air-to-plant-to-animal pathway is most probably the primary way 
in which the food chain is impacted and humans are exposed. EPA 
should, however, take note of other potentially important 
exposure pathways, e.g., point source-to-water/sediments-to-fish 
and cigarette smoking. There is also a very large gap in our 
understanding of the potential atmospheric transformation of 
vapor-phase dioxin-like compounds and of the air-to-plant 
transfer coefficients of these compounds. 

The document's estimate of average dioxin exposure is 
reasonable, but has substantial uncertainties because of limited 
data; it thus cannot provide an estimate of the complete 
distribution of exposures for the U.S. population. The Committee 
recommends that these points be noted clearly and explicitly in 
the Summary volume for the benefit of policy makers and the 
public. The Committee commends and fully supports EPA's on-going 
efforts to develop better data on concentrations of dioxins in 
food and in human tissue and regards these as very high priority 
research needs. 

The Committee supports EPA's use of Toxic Equivalencies 
(TEQ) for exposure analysis, but also recommends that EPA 
carefully review the draft Exposure Assessment document and 
ensure that the congener-specific data are used in all instances 
(such as transport, transformation, and deposition processes) in 
which differences in the physical and chemical properties of the 
congeners are likely to be important. 

The Health Assessment draft document, in its first seven (of 
nine) chapters, provides a comprehensive review of the scientific 
literature on the biological mechanisms involved in the uptake of 
dioxin and related compounds, the binding of these agents to 
receptor sites, their metabolism and retention in tissues, and 
the biological response at the cellular, organ, organ system, and 



210 



4 

whole body levels. The Committee commends the EPA staff for this 
considerable accomplishment, and has made a number of comments 
and suggestions for relatively minor changes that should sharpen 
and clarify the content of the initial seven chapters. The 
Committee's most significant recommendations concerning these 
seven chapters center on the Agency's use of Toxic Equivalency 
Factors (TEF) to address the a broad range of dioxin-like 
compounds having the common property of binding to the Ah 
receptor, and producing related responses in cells and whole 
animals. The use of the TEFs as a basis for developing an 
overall index of public health risk is clearly justifiable, but 
its practical application depends on the reliability of the TEFs 
and the availability of representative and reliable exposure 
data. The Committee calls for clarifications in the 
specifications for TEFs of the various dioxin-like compounds for 
various health outcomes of concern, including the development of 
separate TEFs for the major compound classes, i.e., 2, 3, 7, 8-TCDD, 
other dibenzodioxins and furans, and coplanar PCBs. The 
Committee is confident that final versions of Chapters One 
through Seven will not need further review by the SAB. 

Chapter Eight, on modeling, must integrate both human and 
laboratory animal data, and is critical to the reassessment's 
overall success. The human data typically derives from accidents 
and industrial exposures, and are subject to many confounding 
factors. Animal studies often involve high-to low-dose 
extrapolations as well as cross-species extrapolation. Both 
types of such data are inadequate, by themselves, for estimating 
the human health risks of chronic, low-dose environmental 
exposures to dioxin and related compounds. Although this chapter 
reflects a great deal of effort, several Members of the Committee 
found the exposition of important points to be unclear. Chapter 
Eight is also weakened by its reliance on the standard EPA 
default assumption of a linear non-threshold model for 
carcinogenic risk. The Committee suggests that EPA consider, in 
future revisions, alternative models, allowing for minimal 
response at low environmental levels of exposure, which would be 
consistent with the body of available physiological, 
epidemiological, and bioassay data, as well as the recent 
information from pharmacokinetic modeling. 

Almost all the Members of the Committee concur with EPA' s 
judgment that dioxin, under some conditions of exposure, is 
likely to increase human cancer incidence. The conclusion with 
respect to dioxin-like compounds is less firm. In the case of 
dioxin, virtually all of the Committee believes that the animal 
studies would be categorized as "sufficient" and the studies of 
humans as "limited," providing for an overall categorization of 



211 



Bj, which would be expressed verbally as "Probably Carcinogenic 
to hiomans with limited supporting information from human 
studies." The Committee (on the basis of similar effects) would 
support the same designation for dioxin-like materials. PBBs and 
PCBs would receive ratings of Bj and Bj, respectively. 

Chapter Nine, on risk assessment, was not as thoroughly 
peer-reviewed before submission to the SAB as were the earlier 
chapters, and needs to be revised considerably to reflect the 
changes being made in Chapters 1-8 and to deal with the areas of 
weakness discussed below. The revised chapter would greatly 
benefit from an external peer review by an appropriate group. 
More specifically, the Committee identified, and wishes to 
emphasize to the Agency, particular areas of both strength and 
weakness in Chapter 9. 

Three major strengths are apparent. First, by focusing 
serious attention on various non-cancer effects (both human 
health and ecological effects), the Agency has dispelled any mis- 
impression that EPA' s risk assessment process is overly 
preoccupied with carcinogenic effects. Second, by evaluating an 
entire class of compounds, rather than a single compound, the 
Agency has responded to criticism that its risk assessment 
process can only address issues on a chemical-by-chemical basis. 
Third, a useful comparative perspective is provided in the draft 
conclusions where the Agency highlights the fact that the margin 
of safety (between background exposures and levels of exposure 
where effects have been observed in test animals) for dioxin-like 
compounds is smaller than the EPA usually sees for many other 
compounds . 

Three major weaknesses were also noted. First, the 
presentation of scientific findings portrayed in the draft 
document's conclusions is not balanced vis-a-vis the possible 
risks posed by exposure to dioxin, with a tendency to overstate 
the possibility for danger. Second, important uncertainties 
associated with the Agency's conclusions are not fully identified 
and subjected to feasible analyses. Finally, the 
characterization of non-cancer risk is not performed in a manner 
which can facilitate meaningful analysis of the incremental 
benefits of risk management alternatives. 

This letter can only highlight the major points of a 
detailed and extensive review by 39 SAB Members and Consultants 
of a 2000+ page document. Perforce, the letter cannot convey the 
many lesser, but important, findings and suggestions in the 
Committee's report. Also, it is important to note that although 
there is a broad consensus on most issues, not every 



212 



Member/consultant on the Committee agreed fully with every 
finding, which is not surprisingly given the multiplicity and 
complexity of the issues and the balanced range of views 
incorporated in the Panel. Specific instances are noted m the 
report itself. 

I hope that the information provided above will be of value 
to your Subcommittee in its deliberations. 

Sincerely, 



Dr. Genevieve Matanoski, Chair 
Science Advisory Board 



Enclosure 



213 



V 



E. R. ZUMWALT, JR. 

ADMIRAL. U S NAVY (RET ) 



December 29, 1995 



The Honorable Dana Rohrabacher 

Chairman, Subcommittee on Energy and Environment 

U.S. House of Representatives Committee on Science 

2320 Rayburn House Office Building 

Washington, DC 20515-6301 

Dear Mr. Chairman: 

Attached are the documents from which I was reading during the 
committee hearings on Scientific Integrity and Federal Policies and 
Mandates : Case Study 3--EPA's Dioxin Reassessment held on 

Wednesday, December 13, 1995, which Congressman George Brown 
requested that I provide for printing in the record. 

Thank you for your gracious comments to me. 

Sincerely, 

E. R\) Zumwalt, Jr. 

Admlr'al, USN (Ret.) 

Chairman, Agent Orange Coordinating Council 

1000 Wilson Boulevard, Suite 3105 
Arlington, VA 22209-3901 

Tel: (703) 527-5380 
Fax: (703) 528-5795 

Enclosure 

cc w/enc: The Honorable George E. Brown, Jr. 




214 



^R^eN7!Sv4C£> 



12/12/95 

TO: Admiral Elmo Zumwalt 

FROM: Rick Hind 

RE: Dioxin Hearing at Science subcommittee 

The following information may be of use to you when you testify 
tomorrow before Representative Rhohrabacher ' s subcommittee 
hearing on EPA's dioxin reassessment. 

As you know, although we nominated 7 expert witnesses to testify, 
Mr. Rhohrabacher 's hearing witness list you are the only one of 
these witnesses that will be allowed to testify. As a result, 
you are the only hearing witness representing non-governmental, 
non-industry interests. The other two non-governmental witnesses 
have consistently testified in favor of the regulated industry. 
They are Dr. Michael Gough and Dr. Kay Jones (some examples of 
their activities are described below.) 

In addition, I have attached two recently peer reviewed articles. 
The first is an article published in the September, 1995 issue of 
Environmental Health Perspectives by Michael J. Devito, Linda S. 
Birnbaum, William H. Farland and Thomas A Gasiewicz. In sum, 
this article is a peer reviewed version of Chapter 9 of EPA's 
dioxin reassessment. It's bottom line conclusion is: "Available 
human data suggest that some individuals may respond to dioxin 
exposures with cancer and noncancer effects at body burdens 
within one to two orders of magnitude of those in the general 
population . " 

The second article was a study of 1,189 chemical v/orkers in 
Hamburg, Germany published December 1, 1995 in the Johns Hopkins 
American Journal of Epidemiology by Dieter Flesch-Janys, Jurgen 
Berger, Petra Bum, Alfred Manz, Sibylle Nagel, Hiltraud Waltsgott 
and James H. Dwyer . Again, the bottom line conclusion is: 
"These findings indicate a strong dose-dependent relation between 
mortality due to cancer or ischemic heart diseases and exposure 
to polychlorinated dioxins and furans." 

Dr. Michael Gough is a consultant, formerly with the Office of 
Technology Assessment (OTA) . Earlier this year while at OTA 
Gough told the Los Angeles Times, "EPA played very fast and loose 
with it own rules in order to come to the conclusion that 
(secondhand) smoke is a carcinogen." 

In 1990 while working for the Industry Task Force II on 2,2-D (an 
herbicide) Gough disputed National Cancer Institute studies that 
showed an 8-fold increasod risk of cancer to farmers using 2,4-D. 



In 1988 Gough while working for Resources for the Future (which 
is f.unded in part by Dow Chemical, Dupont, Monsanto and the 
1436 U Street, NW • WashinQton, OC ;^0009 ' Tel (202) 402-1177 • Fax (202) 462-4507 • Tlx 89-2359 



Aic;.-i!!ii\-i ' Acilialki • Aiisl:!.i • llfliiiuiii • Bra/il • ("cin.icj • Ov.,^ • O.wh tiopulilic • Difiiiii.ii^ ■ KinUnii • ( Vtwv • Gi'riii.iny • Grc'jce • Gi.'atemala • IreUru • ii 
J.il.::ii ■ Lijx:!nboiiii| • M',;>:ilo -Th.' Mi>|i;eiliin(!s • Mo.v /le.i'.i'u' • N'.iv.ay • l-iiroi^' • S(mici • Swoutii - '-^wiI/iTla:!!.) ' Tunisia • Uiiraine • United Kingclon; • i ;- 



215 



Chemical Manufacturers Association) disputed the way in which EPA 
made its estimate of cancer risk for dioxin. 

In 1987, Gough also authored a report for the paper industry's 
research arm, the National Council on Air and Stream Improvement 
(NCASI) entitled "Executive Summary — Dioxin: A Critical Review 
of its Distribution, Mechanism of Action, Impact on Human Health, 
and Setting of Acceptable Limits." 

Also in the mid 1980s Gough worked with the consulting firm 
ENVIRON which was doing risk assessments in support of garbage 
incinerators proposals. ENVIRON is now the lead consultant for 
the American Forest & Paper Association efforts to challenge the 
EPA's reassessment of dioxin. 

Dr. Kay Jones is a frequent critic of EPA's air pollution 
program. He currently works for the Seattle based Zephyr 
Consulting firm on behalf of the incinerator industry. 

In 1989 while working for R.F. Weston, Jones urged the City of 
Detroit, Michigan to begin operating the world's largest trash 
incinerator WITHOUT adequate air pollution control systems. In 
1990, stack tests proved the need for such a system to reduce 
mercury emissions. The error cost Detroit millions in tax 
do." .^rs. 

Jones also has insisted that dioxin emissions from diesel powered 
trucks and buses is greater than dioxin emissions from 
incinerators, contrary- to the largest identified source of dioxin 
according to the EPA. 

In addition to the information on these industry witnesses, I 
have attached a segment of a recent report we did on Dow chemical 
regarding Dow's efforts to influence science and policy on 
dioxin. In particular, this report documents the chemical and 
paper industry support of work -by Dr. Greenlee and Dr. Graham. 
Greenlee and Graham were also on the recent EPA Science Advisory 
Board panel that review the dioxin reassessment and were given 
lead responsibility for writing the critiaicof Chapter 9 of the 
reassessment. As a result, their criticisms did NOT reflect the 
consensus of the SAB panel as noted by dissenting members. 



216 



Comparisons of Estimated Human Body Burdens of Dioxinlike Chemicals 
and TCDD Body Burdens in Experimentally Exposed Animals 

Michael J. DeVito,^ Linda S. Birnhaum,^ WiUiam H. Farlandr and Thomas A. Gasiewicz^ 

'Health Effects Research Labor. ..ry. U S. Eiv/iionmuntol ProtecCion Agency, Research Tnangle Park, NC 27711 USA; ^Office of Health 
and Environmental Assessment, U S- Environmental Protection Agency, Washington, DC 20460 USA; ^Department of Environmental 
(Vledicine, University Rochester School of Medicine, Rochester, NY 14642 USA 



Humans arc exposed to mixtures of polyhaJogenated iromatic hydrocarbons, and tlic potential 
health effects of these exposures are uncertain. A subset of this class of compounds produce simi- 
lar spcc:ra of loxiclcy in experimental animals as does 2.3.7.8-ietrachlorodibcnzo-;)-dioxin 
(TCDD), and these chemicals have been classified as "dioxlns." In this study, we compared the 
body burdens of dioxins that produce effects in expcrimentai animals to body burdens associated 
wiih these effects in humans. Human body burdens were estimated from Upid-adjusted serum 
concentrations of dioxins, assuming dioxins are equally distributed in body fat and an adult has 
22% body fat, The toxic equivalency factor (TEF) method was used to calculate body burdens of 
dioxins in humans. These calculations included dibenzo-/)-dioxins. dibeniofurans. and polychlo- 
rinaied biphenyls. In the general population, average background concentrations were estimated 
at 58 ng TCDD equivalents (TEQ)/kg serum lipid, corresponding to a body burden of 13 ng 
TEQ/kg body weight. Populations with known exposure to dioxins have body burdens of 
96-7.000 ng TEQ/kg body weiglit. For effects that have been clearly associated with dioxins, 
such as chJoracnc and induction of CYPIAI. humans and animals respond at similar body bur- 
dens. Induction of cancer in animals occurs at body burdens of 944-137,000 ng TCDD/kg body 
weight, wliilc noncancer effects in animals occur at body burdens of 10-12,500 ng/kg. Available 
liuman data suggest tliat some individuals may respond to dloxin exposures with cancer and 
noncancer effects at body burdens within one to zwo orders of magnitude of those in the general 
population. AVy u/ordr. dioxins, polychlorinatcd biphcnyls, risk assessment, toxic equivalency fac- 
tors. Environ He.iUh Pcrsp^ct 103:820-331 (1995) 



OvLT the last 30 years, an abundance of 
studies have clearly demonstrated chat 
2.3.7.8-tetrachlorodiben7.o-/>-dioxln 
(TCDD) is extremely toxic to experimental 
animals {l~3). Pish and wildlife arc also 
sensitive to (he toxic effects of this chemical 
(-/). TCDD is carcinogenic in male and 
female rats :ii\\\i mice, male hamsters, and 
male and female fish [5.6). Reproductive 
.ind developmental toxicity has been 
observ.'d in all experimental animals tested. 
Inimunotu.xic elfects occur in mice, rats, 
.nut nonhiiin.m primates exposed to low 
doses of TCDD {/"}. Evidence to date indi- 
cates that the actions of TCDD are mediat- 
ed by the .\\\ receptor {S.9) which functions 
as a signal transducer and transcription fac- 
tor. In many ways the actions ol the Ah 
receptor are similar to those of the steroid 
hormone receptors {10,11), although the 
.\h receptor is not a member of this super- 
family of proteins {I2JJ). Other halo- 
tjcnated dibenzo-^p-dioxins and dibenzutu- 
uiis substituted in all four lateral positions 
also have high binding afHnity to the Ah 
receptor and induce the same spectrum oi 
toxicity as TCDD (/^. In addition, certain 
polyiialogenated hiphenyls, naphthalenes, 
and diphenv! ethers are All recej)tor ago- 
nist:,. I- liif!;.uu are exposed to cuinplex mix- 



exposure to TCDD or "dioxinlike" (all 
2,3.7.8-halogenated dibenzo-/>-dioxins and 
dibenzofurans as well as the dioxinlike 
polychlorinatcd biphcnyls) chemicals is 
3-6 pg TCDD cquiv;ilcnts/kg/day in the 
United States {15.1^. The subclass of the 
polyhalogenated aromatic hydrocarbons 
with dioxinlike activity are referred to as 
dioxins in this article. 

Although the toxic effects of dioxins in 
experimental animals are unequivocal, 
their toxic effects in humans are less cer- 
tain. Cihloracne is the only toxic effect 
induced by dioxins for which there is 
unequivocal evidence linlving cx; o^lil to 
effect in humans {17). The uncertainty of 
other toxic effects of dioxins in humans is 
due to the scarcity of human populations 
with high dose exposures, limited data on 
the body burdens of dioxins present in 
these populations, the difficulty in assess- 
ing sensitive toxic endpoints in humans, 
and the lack of knowledge about likely, but 
unknown, genetic factors that may influ- 
ence the relative susceptibility of individu- 
als. Dioxins produce some of the same bio- 
chemical alterations in humans and experi- 
mental animals {IS). Several recent epi- 
demiological studies suggest an association 
between dioxin expo.sure and nuTeascil 
inckleii.e of cancer t/^'Of) and increased 



incidence of altered glucose tolerance in 
exposed populations (24,25). One way to 
determine the strength of an association 
between dioxin exposure and a toxic effect 
in humans would be to compare the dose of 
dioxin that is required to produce an effect 
in animals to the dose of dioxin in humans 
that is associated with a similar toxic effect. 
While it is clear that for some toxic effects, 
such as lethality and body weight loss, there 
are marked species differences in suscepti- 
Ldiry to dioxins. many recent studies have 
also noted that for other endpoints, such as 
reproductive and developmental effects, 
most animal species respond at similar 
doses {9.26). Thus, the dose of dioxin that 
produces a particular effect in experimental 
animals might be expected to be similar to 
the dose of dioxin associated with that same 
effect in humans. 

Although the hypothesis that toxic doses 
of dioxins in animals and humans are simi- 
lar for most responses is theoretically 
testable using data from accidentallv 
exposed human populations, there are some 
difTiculties. In particular, it is otren diffkulc 
to determine the human dosage at the time 
of exposure. In experimental studies, ani- 
mlls arc administered a known amount of 
dioxin and evaluated at a specific time ihcr 
the treatment. In humans the actual expo- 
sure is unknown and often difficult to esti- 
mate. Several epidemiological studies deter- 
mined serum concentration of dioxins in 
exposed and control populations {}9~2Sl 
Although the dose to the individuals in 
tluse studies is uncertain, the body burdens 
of dioxins in these populations can be esti- 
mated at a specific point in time. In addi- 
tion, serum and tissue dioxin concentrations 
from populations in the United States with- 

Address correspondence to M.J, DcVuo, Health 
Effects Rcscirch Laboratory, U.S. Er.viroiimcntul 
Ptotcccioii Agency. Research Triangle Park. NC 
27711 USA. 

We thank Mel Andersen. Bob Lcublce. and Ralph 
Smialowicz for critically reviewing the mjnuscript. 
This study Wis suppottcd in part bv -.he Naiionjj 
Institute of Health through a Natiot:jl Research 
Service Award (1F32 ESO5600-01i to .M D.V 
This document has been reviewed m accotdantc 
wKh U.S. Environmental Protection .\%cncf policy 
and approved for publication. Mention of trade 
names or commeccul produai does not consiitute 
endorsement or leco.nnw.njjt.on lor u^c 
Received 13 ,VljrJi rJ95; -Ktcpied J* ^!n■ 1*^^ 



217 



Reviews ' Body burdens of dioxJns in humans and animals 



out any unii5ually high exposures have been 
reported from several difterent laboratories 
(27-30). All humans in industrialized 
coiincric; are presumca to carry a body bur- 
den of dioxins based primarily on con- 
sumption of minute quantities of dioxin in 
the food supply. Here wc compare the body 
burdens of dioxins that produce efTccts in 
experimental animils to the body b- rdens 
associated with cITccrs in humans, based on 
[he clinical findings observed di ing epi- 
demiological studies. A comparison of the 
in vitro c^f^ccis of dioxins on human and 
animal tissues and cell cultures i. also pre- 
sented. This analysis suggests that some of 
the effects observed in experimental animals 
also occur in humans and that the body 
burdens of dioxins associated with these 
cf^cc:^ (adaptive and/or toxic) arc similar 
bct\veen animals and humans. 

Methods 

Comparisons of animal and human tissues 
or cell lines studied under in vitro condi- 
tions are shown in Table 1. This list is not 
meant to be exhaustive. The data presented 
are from peer-reviewed literature and 
include only those papers that compared 
animal and human tissues in the same 
study or laboratory. 

We estimated human body burdens 
based on analyses of dioxm in serum or tis- 
sue in the cited literature. Several assump- 
tions were used to derive body burdens 
from these values. Dioxins arc nssumcJ lo 
be equally distributed in the body lipid with 
all tissues having the same concentration ot 
TCDD when expressed on a lipid-adjustcd 
basis [31-33). Thu:. serum levels prescnrai 
as lipid-adjustcd arc assumed to be equiva- 
lent to adipose tissue levels expressed as 
lipid-adinstcd values. In addition, we 
assumed that for the averap.c person, 22% 
of the body weight is lipid or fat {3-f). To 
estimate body burdens in humans, lipid- 
adjusted serum or adipo.sc tissue concentra- 
tions (expressed as nt^ TCDD/kg or 
TEQ/kg) were multlplicd^iv 0.22 {3'li the 
fraction of body weight that is f.it. 

Some of the body burden estimates in 
humans presented here arc based on tissue 
concentrations of 2,3,7,8-tctrachlorodiben- 
7o-y>-dioxin alone. In all cases, humans were 
likely to have been exposed to many dioxin- 
like chemicals that bind to thf Ah receptor 
and produce the same spectrum of toxic 
effects in experimental animals as TCDD 
[2,14.26). To account for exposure to addi- 
tional dioxins. the toxic equivalency factor 
method (THD w.is used {i^i.35-38). This 
arc rel.itive potency factors used to convert 
the amount of dioxins in a sample to 
rCDD equivalents or TKQs {H,3y-38). 
ri-Ts were as.s,i;nai nnlv in .'.3.''.8-ch'orin-' 



substituted dibenzo-/>-dioxins and dibenzo- 
furans. the coplanar polychlorinated 
biphcnyl(s) (PCBs) (lUi'AC nos. 77. 81. 
126, and 169) and the mono-tJrfy;(>-substi- 
luted PCBs {lUPAC nos. 105. 114. 118. 
1S6. 157. 167. and 189). The TEF values 
used tor the dibcnzo-/>-dioxins and diben/-0- 
hirans were the U.S. EPA interim TEP val- 
ues, which represent ar. internationally 
accepted cc iventior. for ass-'vsmcnt of diox- 
ins (37.38). The TEF values used for the 
dioxinlike PCBs were the World Health 
Organization values, which resulted from a 
recent internauonal meeting of dioxin anJ 
PCD experts (38). Hence, body burdens for 
tl'.rs complex mixture of related chemicals 
are expressed in terms of TEQs. 

Body burden estimates in populations 
exposed to background levels of dioxins 
were based on published studies that mea- 
sured serum concentrations of 2,3,7,8- 
chlorine substituted dibenzo-/»-dioxins 
(CDDs) and dibenzofurans (CDPs) and 
dioxinlike PCBs In populations with no 
unusually high exposure to dioxins 
[27-30.39). Serum concentrations of 
CDDs and CDFs have been measured in a 
number of different populations from sev- 
eral studies. Schecter (27) presented data 
indicating chat the average whole-blood 
CDD/CDF concentration in U.S. {n = 
100) and German (n = 85) populations 
were similar when presented on a TEQ 
basis (41 and 42 ng TEQ/kg whole blood, 
lipid adjusted). More extensive studies of 
U.S. populations indicate that the national 
•iveragc for scrum CDD/CDF concentra- 
tions is 28 ng TEQ/kg scrum lipid (JV). 
Much smaller studies of congener-specific 
PCB seru.n or adipose tissue concentra- 
tions have been publi'^tied that indicate 



that average dioxinlike PCB concentrations 
range from 8 to 17 ng TEQ/kg tissue lipid 
in V.S. populations (28,30). The range of 
average tissue TEQ concentrations for 
CDDs/CDFs is 28-41 ng TEQ/kg lipid 
and for the PCBs the range is 8-17 ng 
TEQ/kg lipid. Based on these studies, aver- 
age background dioxin tissue concentra- 
tions range from 36-58 .-.g TEQ/kg lipid. 
In th-^e nonulatior , TC DO contribute 
apptoxirnatety !:>% of the touilTEQ. 

Body burden estimates in exposed pop- 
ulations were based on the published litera- 
IlI.c. The-t pt^rjia-; ),.s were assumed to 
h.ivc background exposures, in addition to 
the specific cxposi-res determined in the 
study. The level of dioxins in exposed pop- 
ulations were often determined years after 
the initial exposure. Body burdens were 
estimated at the time of maximal exposure 
assuming the rate of total body elimination 
of dioxins is linear with respect to time and 
dose and a assuming 7. 1 -year half-life (40). 

Determination of maximum body bur- 
dens in experimental animals was based on 
the administered dose and the rate of elimi- 
nation of dioxin from the animal. Total 
body half-life of TCDD in experimental 
animals was assumed to be first order with 
respect to time and dose. In several coses. 
body burdens in animals were based on tis- 
sue levels determined in the study. 

Eftects seen in epidemiologici! studies 
have been divided into two categories. The 
first category (Table 2) is for effects that 
have been causally associated with exposure 
to dioxins. These are effects for which there 
i\ strong evidence that the responses 
observed are due to exposure to dioxins 
and/or related compounds. Typically. 
adverse effects with demonstrated caus.ilir.' 



Tablo 1. Comparison of the eMccis of TCOD exposure on humon and ammal lissue m vitro 



Species/tissue Conceniraiion (nM) Reference Appendix note' 



TCDD binJin(][oAnreceplor(>r^l 
Induction olCYPlAl (EC^l 

Cytoloxiciry(LOEL) 

Inhibitron of proliferation (LOEL) 



Inhibition cl IqM sccreiion (LOFLI 



Mouse (C57BI/6I 

Human 

Lymphocvtes 

Mouse 

Hitman 
Embryonic palate 

f^ousc 

Rat 

Humon 
Thvmocvtes 

Mouse 

Human 
Lymphocytui 

Mouse 

Human 
Lymphocytes 

Mouse 

Human 



i47) 

(J.I 



(47) 
{47) 



LOEL, lowest observeil effect level 

''hu data and mr'tnurioluijy usi!u la do'-^fmtr 

■I'.l'cated. 



/Muc are (i.';:,on:'?d m fhi, ippc'idix 



Reviews • DeVito at al. 



218 



Tabl« 2. Responses in human 


s causally associated 1 


with 


exposure to di 


oxins and comparable 


effects in 


experimental ani 


imals 
















FjtpcrimentTl 


Body burden 




Appendix 


Elfect 


Species 


dose 




(ng/kg) 


Reference 


note' 


Chloracne 


Human 






s:>3,ooo 


(5i,5i) 


f 




Monkey 


I.IXttngftg 




1,000 


(S3) 


9 




Rabbrt 


4na/r3bbit. 
SdaysA'/eeWwe 


eks 


23 


(54) 


h 




Mouse 


4,000 ngAg, 
addys/.veeWwe 


eks 


13,900 


(55) 


' 


Downregulaaon 


Human (placenta) 




2,130 


(f«56) 


i 


of EGFR 


Rat (liver) 


125n9/l(g/d3y, 




2,582 


(57) 


k 


(maximal effect) 




30 weeks 












Mouse (live 


rl 10,000 ng/kg 




10,000 


(5S) 


1 


Induction of 


Human (placental 




2.130' 


08.56) 


i 


CYP1A1 


Rat (liver) 


125ngAg/day. 




2,582 


I5S) 


k 


(maximal effect) 




30 weeks 










Induction of liver 


Rat 


1 ng/kg 




1 


(60) 


m 


CYP1A1 (LOEL) 


Mouse 


I.SngAg/day, 




23 


(61) 


n 






5days/v«8ek/13weeks 








Hepatic 


Human 






3C0 


(63 





sequestrabon 


Rat 






100 


(63 





Background 


Human 

Rat 

Mouse 


TCDD 

PCDO/PCDF 

PCDD/PCDf/PCB 




1.1 

6-S 

8-13 

1 

4 


(67) 
(6/) 


P 
P 
P 



Abbreviations: EGFR, epidermal growth factor receptor; LOEL, lowest observed effect level; TCDD, 2,3,7.6- 

tetrachlorodibenzo-p-dioxin; PCOD, polychlorinaled dibenzodioxin; PCDF, polychlorinated dibenzofuran; 

PCB, polychlorinated biphenyl. 

The data and methodolooy used to determine each value are presented in the appendix under the letter 

indicated. 



arc aisociaccd wich high-level exposure and 
arc severe enough to clearly indicate a rela- 
tionship with such exposure. Chloracne is 
an example of such an adverse effect. In 
addition, biochemical changes such as 
induction of CYPlAl and decreases in 
EGF receptor auiophosphorylation are 
included m tins category because there is 
significant experimental evidence that these 
clTects occur through activation of the Ah 
receptor and arc therefore causally related 
to exposure to dioxinlikc chemicals. 

A second category (Table 3) was 
assigned for effects associated with dioxin 
exposure for which a causal link has not 
been definitively proven. Effects included 
in this category are decreased birth weight, 
decreased growih. delayed developmental 
niilcsioncs, cancer, decreased testosterone 
levels, and increased risk of diabetes. In 
both Tables 2 and 3, body burdens in 
experimental animals are presented for 
comparable toxic effects to those seen in 
the cpidcmiologiciJ studies. 

Table 4 presents body burdens in 
experimental animals that produce an 
effect for which no comparable human epi- 
demiological data arc yet available. The 
current epidemiological database consists 
primarily of studies on adult male popula- 
tions; few studios of women ur children arc 



available. Only effects seen at low doses or 
body burdens in experimental animals were 
chosen for this table to estimate the low 
end of the animal effect range; effects such 
as thymic atrophy, the wasting syndrome, 
or death are not included. The specific 
assumptions and data used to derive each 
value presented in Tables 1^ are presented 
in the appendbc. 

Results 

Comparisons of the in vitro effects of 
TCDD on animal and human tissues or 
cell lines arc shown in Table I. A number 
0^ investigations have found the Mi tccep- 
tor present in humans to have a similar but 
slightly lower binding affinity for TCDD 
thaii tJie A}, cf many other species {42-45). 
The concentration of TCDD required to 
produce equivalent effects in animal and 
human tissues is not significantly different 
for responses as varied as induction of 
CYPlAl in lymphocytes and thymocyte 
proliferation (Table I). For several 
responses, the effective concentration of 
TCDD differs in animal and human tissue 
by an order of magnitude or greater. 
Cytotoxic effects induced by TCDD in 
organ cultures of developing palate occur at 
concentrations 1000 times lower in mouie 
tissue than in cither human or rat tiisue 



{48\. Cultures of embryonic human and rac 
palatal shelves respond at the same concen- 
trations {43). Inhibition of lymphocyte 
proliferation and secretion of IgM in 
mouse splenic lymphocytes requires 10 
times the concentration of TCDD com- 
pared to human lonsilar lymphocyics (50). 

Cnmpiri'^ons of body burdens associat- 
ed with in vivo effects demonstrate similar 
cortclaiions between animals and humans. 
Body burden estimates in individuals with 
chloracne vary by almost two orders of 
magnitude (Tabic 2). In subjects with 
chloracne, exposures resulted from either 
industrial or accidental poisonings. In 
experimental animals, species differences 
in body burdens of TCDD that induce 
chloracne vary by almost three orders of 
magnitude, with the rabbit the most sensi- 
tive and the hairless mouse the least sensi- 
tive. The range of body burdens thac result 
in chloracne in humans (96-3.000 ng 
TEQ/kg body weight) and animals 
(23-13,900 ng TCDD/kg body wcightj 
arc similar. It should be noted that the first 
of these ranges represents interindividuai 
variation while the second includes inter- 
species variation. 

Body burdens in the general population 
were determined based on TCDD alone, 
total PCDDs/PCDFs. and total 
PCDDs/PCDFs/PCBs (Table 2). The 
average body burden of TCDD in the gen- 
eral population is approximatelv I.l ng 
TCDD/kg body weight. The average body 
burden in the general population :or total 
PCDDs/PCDFs is 9 nti TEQ/kg bodv 
weight an^ fur total PCDDs/PCDrs/PCBs 
is 13 ng TEQ/kg body weighc. 

Rice oil contaminated wiih PCDFs and 
PCBs. among other contaminants, was 
ingested by men and women from Tai\>.-a.n 
(Yu-Cheng incident); these individuals have 
been carefully studied since the poisoning 
incident {18,56.63-65). Biochemical 
changes in placentas from the "Aomcn 
exposed during the Yu-Chcng incident are 
similar to the biochemical changes in rodent 
liver from animals exposed to TCDD, Near 
mxximal down regulation of human placen- 
tal epidermal growth factor receptor 
autophosphorylation occurs at similar body 
burdens, as do comparable decreases in 
hepatic epidernul growth factor receptor in 
rats and mice (Table 2). Maximal induction 
of hepatic cytochrome P-450 lAl 
(CYPlAl) in rats and mice by TCDD 
occurs at body burdens similax co diose that 
elicit maximal increases of CYPlAl in 
human placenta from the Individuals 
(•xposed during rhc Yu-Clveng incident. The 
lowest observable effect level (LOEL) for 
en'jvn;;: induction in animals is 1 and 23 ng 
TCDn;kg body weighc in rati i6'J) and 



Volvn)o 103 Numiw 9. St'pteiT.'.rr !]-vr • ■in'tifcnn^eXJi HedU'r. 



219 



Reviews • Body burdens of dioxins in humans and animals 



Table 3. Responses in humans associated wilh dioxin exposure and comparable effects in experimental 



Body burden 
(ngAgJ 



Appendix 
Reference note* 



Cancer 


Human 
Hamster 

Rat 
Mouse 


lOOp^'kg/month/ 
6 months 

lOOnrj/Vg/day, 2years 
71 ng/Vg/day, 2years 


103-7,000 
137.000 

2.976 
94; 


1/9,23) 
(SSI 

{7a 


TtJiorpro.iiDli'.n 


natliiw) 
Mouse (skin) 


12!lngAci'day,30'/(c;ks 
7.5 ng/weck, 20 weeks 


2,5«2 
830 


{71) 
(73 


Decreased birth weight 


Human 

Rat 

Hamster 


Maternal body burden 
400 ng/kg, maternal dose 
2,0(XJngAg, 
maternal dose 


2.130 

400 

2.000 


|/S,56) 
173 

IS) 


Dectcased growth 


Human 
Rat 


Maternal body burden 
1,000 ng/kg, 
maternal dose 


1130 
1.000 


163) 
{7 SI 


Delayed developmental 
milestones 


Human 


Maternal body burden 


2.130 


IW.65) 


Object learning 


Monkey 


0.151 ng/kg/dav, 
Maternal body burden 


42 ngAg 


166) 


Decreased testosterone 


Human 
Rat 


12.500 ngAg 


44-122 
12.500 


141) 
176) 


Alteretj glucose 
homeostasis 


Human 
Guinea pig 
Rat 


30ngAg 
100ng/kg/day.30days 


99-140 

30 

2,000 


124.25) 

176) 

173) 



The data and methodology i 
indicated 


jsed to determine each valu 


e are presented in the 


appendix under the letter 


Tablo4. Lowdoseellectsin . 


animals exposed to dioxins 






Edect 


Experir 
Species do: 


nental Body burden 
;e (ng/kg) 


Appendix 
Reference note' 



Decreased oHspnng viability 


Rhesus monkey 

Rat 
Hamster 


0.76 ng/kg/day, 
4 years 
1.000 ng/kg 
18,000 ng/kg 


345 

1,000 
18,000 


ISO) 

1741 
{81) 


X 


Altered lymphocyte subsets 


Marmoset 


3ng/kg/week. 
24 weeks and 

1 5 ng/kg/week, 
12 weeks 

10 ng/kg 


10 

10 


{821 
(S3) 


cc 
cc 


Enhanced viral susceptibility 


Mouse 


10 ng/kg 


10 


(94) 


dd 


Endometriosis 


Monkey 


151 ng/kg/ 
day/4 years 


69 


IS5) 


* 


Docr';jst;d sperm count 


Rat 


6'1 ng/kg. 
maternal dose 


"■■ 


(.'51 


w 


Testis abnormalities 


Rat 
Mouse 


12,500 ng/kg 
lOOpgAg 


12,500 
100,000 


176) 
177) 


eo 



The data and methodology used to determine each value are presented in the appendix under the lener 
indicated. 



mice {61). respectively, wliich is within the 
range of background human body burdens 
of 1 3 ng TEQ/kg body weight. 

Disposition of dioxins is dose depen- 
dent in animals and humans (62). The 
body burden necessar)' for hepatic seques- 
tration is similar for rats and humans (62). 
In animals, the body burden of TCDD 
that produces a carcinogenic elTect ranges 
from 944 ng TCDD/kg body weight in 
mice (70) to I3".00n n>; TCDD/kg in 



hamsters (6S) (Table 3). Body burdens in 
animaJs exposed to carcinogenic doses of 
TCDD are 73- to 10,500-fold greater than 
background human TEQbody burdens. In 
epidemiological studies that indicate an 
association between TCDD exposure and 
increased incidence of cancer, body bur- 
dens were estimated between 109 and 
7,000 ng TCDD/kg at die time of highest 
human exposure. Background human 
ri-.Q body burdens are approximatclv 



8-540 times less than human TEQ body 
burdens estimated from the studies that 
associated dioxin exposure with increased 
cancer incidence. 

Dccicased birxh weights were rcponcd 
in children born to women exposed during 
the Yu-Cheng incident (18.56). These 
women were highly exposed and had an 
average body bt'rden of approximately' 
2.130 ng TEQ/kg body weight. Body bur- 
dens of dioxins in experimental animals 
that decrease birth weight range from 400 
to 2,000 ng TCDD/kg body weight in rati 
and hamsters (73.7'f) (Table 3). 

Children of the Yu-Cheng mothers are 
not only smaller at birth but remain smaller 
throughout childhood compared to chil- 
dren of unexposed women (6Si. In rats, 
pups of dams exposed to 1,000 ng 
TCDD/kg body weight not only have 
decreased birth weights but consistently 
weigh less than controls up to 63 days of 
age. though they do recover upon reaching 
sexual maruriry (7S). 

The Yu-Cheng children also exhibit 
delayed dcvclopmentaJ milestones (64.6Si. 
Behavioral effects after perinatal TCDD 
exposure have been observed in rhesus mon- 
keys born to mothers exposed to approxi- 
mately 5 ppt TCDD in the diet (66). Body 
' irHcns in the rhesus mothers were 42 ng 
'ICDD/kg body weight, which is approxi- 
mately 51 times less than the TEQ body 
burden in the Yu-Cheng women, but only 
3.2 times higher than average TEQ body 
burden in the general population. 

Although some of the responses seen in 
experimental animals appear to occur in 
humans at similar body burdens, there are 
significant differences in the body burden 
estimates for decreased testosterone lc\'cls 
(■//) and between human and animals. 
Based on these limited data, if decreased 
testosterone in humans is due to dioxin 
toxicity, then some humans may be 
approximately 280 times more sensitive 
than are rats for dioxin-induced decreases 
in testosterone. 

Increased incidence of diabetes in popu- 
lations exposed to dioxins has been reported 
in two studies with body burdens ranging 
from 99 to 140 ng TEQ/kg. While TCDD- 
induced diabetes has not been studied in 
expetimcntal animals, there are reports of 
altered glucose homeostasis. Alterations in 
glucose uptake in adipocytes isolated from 
guinea pigs treated with TCDD occurs at 
body burdens 3-4 times lower than human 
populations with increased incidence of dia- 
betes and altered glucose tolerance (24^5)- 
Decreased serum glucose in rats occurs at 
body burdens 14-20 times higher than the 
increased incidence of diabetes and altered 
glucose tolerance in humans. 



Envi:onn'enal r^eiWi PeitiKC'.ivef • Volume 103. Njrrber .9. September 1995 



823 



Reviews • DeVito el al. 



220 



Tabic 4 presents cscimatcJ body bur- 
dens of TCDD in experimental animals 
from studies that report low-dosc effects 
for which no comparable human studies 
are available. l,OELs for decreased off- 
spring viability/fetal viability vary from 345 
ng/kg m monkeys lo iS.OOO ng/kg m iiam- 
sters. Alterations in lymphocyn; subsets in 
juvenile inarmoscti h iO ng TCDD/kg 
body weight {82.83). Enhanced viral sus- 
ceptibility, as measured by incre.iscvi mor- 
ta,liry. occurs in mice at body burdens of 
approximately 10 ng TCDD/kg {84), 
which is cquiv.njen: to th.^ body b 'rdcn 
seen in unexposed humans and approxi- 
mately twice the level in untreated mice. 
Effects such as increased incidence of 
endometriosis in rhesus monkeys {85) and 
decreased sperm count in offspring of rats 
treated with TCDD (7^,56) occur at body 
burdens approximately five times that of 
unexposed human populations. 

Discussion 

A number of investigators have found the 
Ah receptor present in human tissues to 
have a similar, but slightly lower, affmiry 
for TCDD than those receptors present in 
many other species ('/2~*/5). For example, 
a recent study determined that the appar- 
ent binding affinity of TCDD to the AJi 
receptor ranged from 0.4 to 15 nM in 1 15 
huin.in placentas and from 1 nM in the 
TCDD responsive C57BI/6J mouse to 16 
nM in the TCDD nonrcsponsivc DBAJ2 
mouse. The binding affinity of TCDD en 
the Ah receptor is similar in mice, rats, 
hamsters, guinea pigs, and monkeys {87). 
and there is no obvious correl.uion between 
TCDD binding aff'imty to the Ah receptor 
and species sensitivity to the lethal or toxic 
effects of TCDD (57). Thus, our knowl- 
edge of the quantitative relationship 
between binding atfmity and interspecies 
responsiveness docs not provide adequate 
information to determine whether hum.uis 
are more or less responsive than other 
species based solelv on the binding affinity 
ofTCDDtothcAh receptor, 

Comparisons of human tissues or cell 
lines with similar animal tissues or cell lines 
demonstrate that from relatively simple 
responses, such as enzyme induction to 
more complex phenomena, such as cyto- 
toxicity and proliferation, human tissue 
responds in the same manner as animal tis- 
sue and at sinnlar concentrations (Table I). 
These in vitro studies suggest that humans 
will respond to dioxin and that some of 
these respon.ies may be adverse. 

The doses of dioxins that pioducc 
l'.iliality in experimcnt.1l anim.ds can vary 
by more than threi* orders of ma^nituue; 
I'l'ir.ea lu^ifi Mr the most sen.iiive and ham- 



sters arc the least sensitive [1-3). Because of 
this large variability in lethal effects, there 
has been an expectation that large species 
differences exist for all other effects. The 
diia presented in the tables indicate that for 
a particular effect, some species may be 
extremely sensitive and some rnay be resis- 
tant, but many species respond at similar 
doses (i.e., within an order of magnitude). 
All experimental mammalian species exam- 
ined respond to most of the adverse effects 
of dioxins at some dose. It i.s possible th.it 
humans may be resistant to some of the 
toxic effects of dioxins, but it seems highly 
unlikely, given the data currently available, 
that humans arc refractory to all of the toxic 
effects of these chemicals. 

Dioxins arc unequivocally potent toxi- 
cants in experimental animals, yet the 
human health effects of exposure to these 
chemicals remain controversial. Compari- 
sons of human and animal body burdens 
alone cannot prove a cause-and-effcct rela- 
tionship between toxicity and exposure in 
humans obsfrrved in an epidemiological 
study. Mowever, this intormation can be 
used to increase or decrease our confidence 
that a particular adverse health effect 
observed in an epidemiological study was 
associated with the exposure to dioxins. 

\n addition, the present analysis 
required several assumptions in estimating 
both animal and human body burdeiu. 
These assumptions were required due to 
the lack of complete d.\\x on pharmacoki- 
netics, toxic equivalency factors, species 
extrapolation, and, for humans, lack of 
information on daily dose or exposures. 
Hence, the information presented here can 
be used to direct research efforts to provide 
more accurate information on these topics. 

1 here arc some unceitainties associated 
with the assumptions used to estimate 
body burdens of dioxins in animals and 
humans. Unlike the experimental animal 
toxicology studies exaniined. humans arc 
exposed to multiple chemicals. However, 
in the epidemiological studies, many ol 
these chemicals interact with the All recep- 
tor as either agonists, partial agonists, or 
possibly antagonists. Assumptions ol the 
relative potency of the chemicals and their 
distribution in the humans will result in 
uncertainties that are difficult to quantify 
given the present database. However, these 
uncertainties are likely well within aii order 
of mat^nltudc because body burdens of 
TCDD alone rcprescnr 10% of the total 
1 FQ bodv burden due to all the PCDDs. 
PCDhs, andPCBsa"able2j. 

Human body burdens are estimated 
uiing the TEE mcthodoloi^. The TEF val- 
ues d.Tived bv the U..S. EPA and the 
•;w)ri... Ileahh Oi.'ani/.ition u.-re b.iscd un 



scientific judgment as well as experimental 
data {37M. In setting a TEF value, more 
weight was given to long-term, in vivo 
studies than to in vitro or acute in vivo 
studies {MJ6-38). In fact, although wide 
ranges of TEF values have been reported 
for specific congeners, the variabilitv is 
within a factor of 10 when the in vno data 
arc used to set the TEF value (/■/.J'j^). 

The TEF methodology assumes addi- 
tivity of toxic potential The use of the 
TEF methodology has been validated for 
complex mixtures of chlorinated dibenzo- 
/>-dioxins for effects such as enzyme induc- 
tion and tumor promotion [88). The inter- 
action of mixtures containing both dioxin- 
likc and non-dioxinlike chemicals has not 
been studied as thoroughly. There arc 
reports of antagonistic {89-91) and syner- 
gistic {92,93) interactions of dioxins and 
non-dioxinlikt PCBs. The demonstration 
of nonadditive interactions increases the 
uncertainty of these values. Finallv, the 
TEF scheme includes only full agonists or" 
the Ah receptor. The use ot TEFs and the 
assumption of additlvity have beer. 
approved by both the World Health 
Organization and the U.S. EPA as a 
default, bi't interim, approach given the 
enormity of the task to test for all possible 
interactions ot complex mixtures and in the 
relative absence of consistent data to the 
contrary {9'f}. Clearly, the TEF values and 
assumptions regarding additivity need to be 
updated as more data become available. 

Estimates of body burdens in animals 
and humans assume that the half-life o: 
elimination ot dioxins is a Hrst-orde: 
process which is independent of the body ^ 
burden or dose. There is signillcan: evi- I 
dcnce that disposition of TCDD :s io^e I 
dependent {95-97). Induction of a b:r.dii:c 
protein m the liver has been proposed b-. 
Andersen ct al. {98) to explain the dosc- 
dependent disposition of TCDD seen in 
c.>. peri mental animals. Similar dosc-deper.- 
dent hep.itic sequestration has been pro- 
posed in humans {62). These data sur^gcs: 
that elimination of these chemicals ma-, 
not be a first-order process and the uic of a 
single one-component half-life to estimate 
body burdens may not adequately predict 
these values. 

Two different methods were used to 
estimate body burdens in experimental ani- 
mals. One method involved classical phar- 
macokinetic calculations, and the second 
method used tissue concentration data pre- 
sented ill the papers. These methods result- 
ed in similar body burden estimates for 
some cases where the appropriate data we:.* 
available. For example, in mice rctcivm ■ 
1,5 ng TCDD/kg/day. estimated hudv 
burden; u.ini; cUss-cal pharm.icokincu- 



rixK'J, bcp'.jtr.iy;,' ', 



221 



Reviews ' Body burdens of dioxins in humans and animals 



calculations were 14 ng TCDD/kg body 
weight and 23 ng TCDD/kg body weight 
using TCDD tissue concentrations. Body 
burden estimates from a tumor promotion 
study with rats receiving 125 ng TCDD/ 
kg/day produces estimates of 3615 ng 
TCDD/kg body weight using pharmacoki- 
netic cdculafions and 2582 ng TCDD/kg 
body weight using TCDD tissue concen- 
trations. These results sug^.T't th.-^t the vsc 
of cither method to derive body burdens 
will result in reasonably accurate estimates. 

In estimating human body burdens, we 
assumed that dioxins distribute solely to the 
lipid portion of the body and that the con- 
centration of dioxins in serum lipid is direct- 
ly correlated to the concentration of dioxins 
in total body lipid. Several studies have 
demonstrated direct correlation between 
lipid-adjusted serum and adipose tissue con- 
centrations of dioxins from human biopsy 
samples fot die lower chlorinated d\hcnzo-p- 
dioxins and dibenzofurans (30-33)- This 
relationship is not as certain for the higher 
(six or more chlorine substitutions) chlori- 
nated analogs. Furthermore, in humans 
exposed to background levels of dioxins, the 
absolute or lipid-adjustcd concentrations of 
CDDs and CDFs in adipose tissue and liver 
arc not directly related and liver/fat ratios 
vary between 1.22 and 15. 42 depending on 
the congener and possibly on dose i99i. The 
highly chlorinated dibenzo-/)-dioxins and 
dibenzofurans are found in greater concen- 
tration in the liver compared to the fat 
(liver/fat ratio 7.4-15.42). In the same sam- 
ples. TCDD had a liver/fn ratio of approxi- 
mately 2 (9^. The human liver appears to 
accumulate these chemicals in great r pro- 
portion than adipose tissue, similar to \vha[ 
has been observed in experimental animals. 
In experimental animals, liver/fat concentra- 
tion ratios are not only different for different 
compounds, but they are dose dependent. 
As the dose of dioxins arc increased, so is the 
livcr/f.u ratio (95-P.'?). 

Usmg the assumption that dioxins are 
equally distributed in the body lipid may 
underestimate the body burden of these 
chemicals due to chemical and dose-depen- 
dent sequestration in the liver. The magni- 
tude of underestimation can be determined 
if several assumptions arc used: that the 
liver/fat ratio fot all dioxins is 15 and that 
liver is 10% of the body weight and is 10% 
lipid by weight. A liver/fat ratio of 15. as 
determined for the hcxachlorodibenzofu- 
rans in humans, is used as a worst-case sce- 
nario for hepatic sequestration. Using these 
assumptions, the present estimate of dioxin 
TEQ body burdens in background popula- 
tions wiil change from 13 to 21 ng 
TUQ/kg bodv weight. Hence, the assump- 
tion that diuiins arc equ.illv distrilmicd .n 



body lipid may slightly underestimate the 
body burdens of these chemicals, but the 
magnitude of error will be less than a factor 
of two. A better undersranding of the phar- 
macokinetic properties for this class of 
compounds in human:, is clearly indicated. 

Chloracne has been described as the halU 
mark of dioxin toxicity ir humans (17). 
Dioxin exposure in several animal species 
resultji in a chloracncgenic response and the 
body burdens which produce this response 
in animals are similar to the body burdens of 
dioxins in humans with chloracne. The 
chloracncgenic response has been thought to 
be a relatively high-dose phenomenon; how- 
ever, the variation in human sensitivity to the 
chloracncgenic effects of TCDD is almost 
two orden of magnitude. For example, there 
are individuals who developed chloracne at 
body burdens approximately three times 
background (5/)- In contrast, there are sub- 
jects widi body burdens of 1450 ngTEQ/kg 
body weight who have not developed chlo- 
racne (5/). These data suggest that humans 
differ widely in sensitivity to the chloracnc- 
genic actions of dioxins. 

There are rvvo points of caution wlien 
interpreting the chloracne data. First, 
human body burdens m.iy not be an accu- 
rate measure of chloracncgenic potential if 
point-of-contact concentrations arc impor- 
tant. For example, if dermal exposure results 
in a localized chloracncgenic response, body 
burdens estimated from scrum or adipose 
tissue levels may not accurately reflect the 
concentration of dinxins at the site of effect. 
Also, the lack of chloracne in highly exposed 
patients does not necessarily indicate that 
these individuals are resistant to all the 
effects of dioxins. In mice, gene products, in 
addition to the Ah receptor, regulate the 
chloracncgenic response (lOOi. It seems like- 
ly that multiple genetic factors may influ- 
ence the relative susceptibility of individuals 
in a response-specific fashion. 

Human respofiscs to dioxi-; . o'her than 
chloracne are not as obvious. In the Yu- 
Chcng poisoning mcident. increased rates 
of toxic effects such as miscarriages, still- 
births, low birrh weight infants, and devel- 
opmental delays have been observed in off- 
spring of women exposed to high levels of 
PCDFs and PCBs. However, it has been 
difficult to determine if the effects arc due 
to the dioxins in the mixture, the non- 
dioxinlikc PCBs, or to the combination of 
these chemicals. Researchers have tried to 
correlate effects with serum concentrations 
of either the PCDFs or PCBs (56). Birth 
weights were negatively correlated with 
PCDF levels in these individuals {56). 
Other effects such as induction of arylhy- 
drocaibon hydroxylase activity, a marker 
for CVIMAI, u^re not correlated with 



either the polychlorinated dibenzofurans or 
the PCB concentrations, but decreased pla- 
cental EGF receptor autophosphorylation 
was correlated with total PCB concentra- 
tions (56). However, due to the nature of 
the exposure, patients with high levels of 
dibenzofurans will likely have high levels of 
PCBs. making such correlations difficult to 
interpret. Also, the presence of dioxinlike 
and non-dioxinlike PCBs adds to the com- 
plexity of these correlations. 

We compared the body burdens of 
dioxins in the Yu-Cheng population to 
body burdens in experimental animals to 
determii.r the role of dioxins in the toxic 
erfects seen in these individuals. Women 
who were pregnant at the time of exposure 
or became pregnant thereafter had children 
with lower birth weights compared to unex- 
posed women, and the decrease in size per- 
sisted years after birth (63). Body burdens 
in the Yu-Cheng mothers were estimated at 
2130 ng TEQ/kg. In experimental ammals 
the body burdens that result in decreased 
birth weights range from 400 to 2000 ng 
TCDD/kg. while decreased growth occurs 
in rats at 1 .000 ng TCDD/kg. The similari- 
ties between the body burdens in animals 
and humans suggests that dioxins may plav 
a role in the dccrc;iscd birth weights. 

The behavioral effects of dioxins have 
not been thoroughly studied in experimen- 
tal animals. One study reported deficien- 
cies in object learning m rhesus monkeys 
prenatally exposed to TCDD. Delayed 
di'velopmental milestones were seen :n 
children born to Yu-Cheng mothers, bjr 
the body burdens are approximately 5! 
times higher in humans than in the mo.n- 
keys. There is recent evidence that some of 
the non-dioxinlikc PCBs m.iy h.ivc neuro- 
toxic actions (/(?/). The absence of studies 
in experimental animals examining the 
developmental behavioral toxicity of diox- 
ins makes it difficult to assess the role of 
either th;* u:^.'.ini or the non-dioxinlike 
PCBs in the developmental effects of the 
children of the Yu-Cheng patients. 

In experimental animals, some bio- 
chemical changes produced by dioxins 
occur at lower body burdens than do the 
toxic effects (57-61,71)- Induction of 
CYPlAl and decreased hepatic EGF recep- 
tor are t^vo well-characterized biochemical 
responses to TCDD. Earlier studies com- 
paring the induction of CYPlAl and 
decreaicd EGF receptor in human placcnra 
and rat liver suggested that humans may be 
more sensitive when compared on a tissue- 
dose basis (IS). However, it is possible that 
the difference in sensitivity is not entirely 
due to species differences but due to altered 
tissue sensitiviEV. For example, induction Of 
CYIMAI 1. similar in hmi-.. hvcr. .j.-.d ski:: 



v.eout ^i-i.-ilin P^isp-KU\es • Volun:e \C3. N-jocorO. Seotcmbjr W9'j 



23-557 O - 96 - 



Reviews • DeVito et al. 



222 



of mice biscd on administered dose {102). 
In contrast, when the sensitivity of these 
tissues is compared on a tissue-dose basis, 
the lung is much more sensitive than the 
liver or skin {102). The present study indi- 
cates that humans and rats arc equally sen- 
sitive to TCDD-induced biochemical 
changes when compared on a total body 
burden. Thus, when comparing the relative 
scnsiriviry of human or animal tissues to 
TCDD-induccd biochemical changes, ic 
may be more appropriate to compare body 
burdens than tissue concentrations. In 
addition, these data provide support for 
our approach. 

TCDD is clearly carcinogenic in exper- 
imental animals. All species and both sexes 
of experimental animals that have been 
chronically exposed to TCDD exhibit a 
dose-dependent increased incidence of 
tumors {S). SevctaJ tecent epidemiological 
studies have indicated an association 
between TCDD scrum concentrations and 
increased incidence of tumors {19-23). 
Body burdens in rats and mice with 
increased tumors are comparable to the 
body burdens in the human cohorts that 
have increased incidence of tumors thought 
to be associated with dioxin exposure. 
Although these data arc not conclusive, 
they arc consistent with the hypothesis that 
exposure to TCDD was an important fac- 
tor in the increased incidence of tumors in 
these cohorts. It is interesting to note th.u 
based on body burdens, mice are more sen- 
sitive to the carcinogenic effects o\ TCDD 
than arc rats. 

Carcinogenic responses are seen in 
hamsters, but the carcinogenic doses pro- 
duce body burdens 46-1300 times that 
seen either in humans, rats, or mice. 
Hamsters arc insensitive to the lethal elTccts 
of dioxins. and they may also be less sensi- 
tive to the carcinogenic response. However, 
responses such as cancer are dose depen- 
dent as well as time dependent. Thus, the 
apparent differential sensitivity ot the ham- 
ster may be due to differences in the 
dose-time regimens used in the hamster 
compared to the rat and mouse studies. It 
would be useful to compare these species 
under similar exposure protocols. 

Decreases m scrum testosterone have 
been reported in a National Institute of 
Occupational Saiety and Health (NIOSH) 
cohort {-//). There was a decrease in testos- 
terone concentrations in mdividuals with 
serum concentrations ol TCDD as low as 
20 ppt at the time of tissue sampling, which 
is 3-4 times background TCDD levels and 
only a 33% increase over total average body 
burdens. Although the decrease in testos- 
terone concentrations was statistically signif- 
icant, the decrease \v±s minor, and averji-e 



levels were still within the norm.il range. In 
addition, a clear association between serum 
TCDD concentrations and effect was not 
readily apparent in the data {41). If difFcr- 
ences in exposure patterns in the individuals 
are taken into account by b.ick-calculating 
serum 1 CDD concentrations to the time of 
exposure, there is a clearer association 
Jbetv-ecn scrum TCDD concentrations and 
lower testosterone concentrations. Here the 
lowest serum TCDD concentration associ- 
ated with decreased testosterone concentra- 
tion is 140 ppt (200 ppt TEQ). In experi- 
mental animals, high doses of TCDD 
decrease testosterone concentrations in rats 
at a body burden of 12,500 ng TCDD/kg 
body weight {75). These data suggest that 
some humans may be approximately 280 
times mote sensitive to the testosterone- 
decreasing effects of dioxins compared to 
rats. Alternatively, the decreased testosterone 
levels in die NIOSH cohort could be related 
to the concomitant exposure to other chem- 
ir.ils Involved in the m-inu fact u ring process. 
Future studies examining the sensitivity of 
other species to the testosterone-decreasing 
effects of dioxins and epidemiological stud- 
ies of other populations may provide addi- 
tional information to adequately assess the 
association between dioxin exposure and 
decreased testosterone concentrations in 
some human populations. 

Many of the effects of TCDD have 
been studied following an acute exposure 
in experimental animals. In contrast, 
humans receive low daily doses of these 
chemicals. One ol the assumptions in 
extrapolating these cltects to humans is 
that the effects arc solely related to body 
burdens. For some of these endpoints. such 
as decreased testosterone, this assumption 
has not been adequately tested. Effects such 
as cancer are clearly related to both dose 
and time. It is possible that, in addition to 
dose and body burden, length of exposure 
may also have a significant effect on toxici- 
ty. Analysis of the area under the total body 
concentration-lime curve may be a more 
appropriate marker for dose, and analysis 
of these data sets is ongoing. 

The clinical significance of some of the 
endpoints studied is uncertain. Induction 
of CYPlAl and CYP1A2 by TCDD ate 
some of the most sensitive markers of diox- 
in exposure, yet their relevance to toxicity 
is unclear. Recent studies have suggested an 
association between PAH exposure and 
CYP1A1/IA2 induction for lung and col- 
orectal cancer and athclerosclerosis 
{105-lOS)- However, these associations are 
speculative and not proven. At present, one 
could conclude that low doses of dioxins 
produce effects such as enzyme induction 
in experimental animals and that humans 



are exposed to levels of dioxins that induce 
CYPIAI/1A2 in experimental animals, but 
the relationship berween these effects and 
disease arc unceitain. 

One of the most sensitive targets for 
TCDD toxicity in experimental animals is 
the immune system. Immune alterations, 
including increased viral sensitivity in mice 
and altered lymphocyte subsets in rr.ar- 
mosets, have been reported at body bur- 
dens equivalent to human background 
exposures. However, the evidence for 
immunotoxicity of dioxins in humans is 
inconclusive. There arc reports of subtle 
immune alterations in populations heavily 
exposed to dioxins. The incidence of 
intestinal and upper respiratory tract iiuec- 
tions correlated with chloracne state and 
increased with increasing serum TCDD 
concentrations {lOG). One year after the 
Yu-Cheng poisoning episode, patients 
exhibited decreases in percentage of total 
T-cells, active T-cclls, and T-hcIpcr cells, 
which recovered by the 3-ycar follow up 
study {107). Recent studio of occupation- 
ally exposed individuals with slightly ele- 
vated body burdens of approximately 72 ng 
TEQ/kg showed no alterations In lympho- 
cyte subsets {108). However, in mice, a 
dose of TCDD that suppresses the anti- 
body response to sheep red blood cells is 
not associated with alterations in lympho- 
cyte subsets {109). Thus, immune fijncrion 
may be altered without altering K-mphoc/te 
subsets. Although some of these data iL:g- 
gest that the human immune system .-nay 
be sensitive to the effects ot d;oxins, our 
present understanding ot immunology ccts 
not support a conclusion that ihc^c a::er- 
ations are or arc not clinically significar.:. 

The present study indicates tha: :u 
vitro similar responses are seen in hu.T.an 
and animal tissues atter similar dioxin 
exposure. Human populations exposed to 
high concentrations of dioxins exhibit 
symptoms that are similar to the signs ot 
toxicir,' seen in sonvj experimental anirr..ils 
exposed to dioxins. These effects are seen at 
equivalent body burdens, strongly indicat- 
ing that dioxins are responsible ror sorr.c of 
these toxic effects in humans. For most of 
the toxic effects of dioxins, backgro-nd 
exposure is well below those associated 
with overt toxicities. However, the back- 
ground level tised in this evaluation (13 ng 
TEQ/kg body weight) is an average back- 
ground. Body burdens of dioxins appear to 
be log-normally distributed in humans 
{J 10), thus it would not be unusual to see 
populations with body burdens threr to 
four standard deviations beyond the rr.ean 
body burden. Recent studies in the 
Netherlands indicate that plasma TEQ 
concentrations in the V^th percentile ot the 



Tfe W3. NumbefS. ScpteinCur 199? • cnvifonm-3ntiji heaiin Pirspec -^s 



223 



Reviews * Body burdens of dioxjns in humans and animals 



population arc twice that of the mean 
{113), suggesting that at least 5% of the 
population has two times the mean body 
bufdcn. In addition, there are subpopula- 
tions sue!. a.s subsistence fishermen who a/e 
Wkciy to have much greater body burJcns. 
There are also some toxic effects, such as 
endometriosis and increased viraJ scnsitivi- 
'rv, whicfi occur in experimental animals at 
body hurdcns less than 10 times the aver- 
age background exposures to humans. 
Finally, human exposures that result in 
adverse health effects, such as chloracnc, 
decreased birth weights, developmental 
delays, and cancer are 3-540 times the pre- 
sent average background exposure to tliese 
chemicals. Nevertheless, the available data 
indicate that high-level human exposure to 
dioxins produce adverse health eiTccts and 
that humans are a sensitive species to the 
toxic effects of dioxins. Whether these low- 
dose effects are occurring in the general 
population or the more highly exposed 
subpopulations remains lo be determined. 

Appendix. Table Notes 

(Some notes appear in more than one 
table.) 

Table 1 

a) Apparent equilibrium binding dissocia- 
tion constants are presented (42). Under 
conditions of infinite dilution, an appar- 
ent A'^of 9 pM has been determined for 
the A^ allele in the C57BI/6 mice; this 
value is close to the estimated true Kj 

b} Splenic lymphocytes from C57B1/6 
mice and peripheral blood lymphocytes 
were isolated, cultured, and exposed to 
TCDD. Ethoxyrcsorufin-O-dcethylasc 
(RROD) .Ktivity. a marker for CYPIAI. 
w.is determined following TCDD expo- 
sure [4S). 

c) The authors [47) compared the cytotox- 
ic effects of TCOO on organ cultur* '■ 
liiim.in. mouse and rat embryonic 
palatal shelves. Embryonic palates from 
hu.-. :ii\ mouse and rat were grown in 
the same otgan culture system and 
exposed to TCDD. Cytotoxicity was 
detected using transmission electron 
microscopy. 

d) Thymocytes were isolated from either 
murine or human sources and cocul- 
turcd with either murine {48) or human 
[49) thymic epithelium culture. The 
incorporation of tritiated thymidine into 
DNA was determined in cells treated 
with TCDD following antigen stimula- 
tion. 

c) Human tonsilar lymphocytes and 
murine splenic Ivmphocytcs were used 
as J source of H-cclls. Human .md 



murine B-cells were grown under identi- 
cal conditions and exposed to TCDD. 
Proliferation and IgM secretion were 
determined in re.*:nonsc to difT-i^nt con- 
centrations of TCDD ranging from 0.3 
to30nM(5ai- 

Table 2 

The lower value, 96 ng TEQ/kg body 
weight, is the body burden c::imatc cf a 
patient with the lowest rcponed adipose 
dioxin concentration for any patient 
With chloracnc {5t). This individual was 
exposed to a mixture of CDDs and 
CDFs in 1969 and developed chloracnc. 
At the time of exposure this individual 
had adipose tissue CDD/CDF concen- 
trations of 419 ng TEQ/kg adipose tis- 
sue (5/) An additional 17 ngTEQwas 
added to this value to include the PCBs. 
The values of dioxins at the time of 
exposure were estimated by the authots 
{51). The higher of the two values repre- 
sents the average body burden of dioxins 
(TEQs) in individuals from Yusho with 
chloracnc {52). Estimates of body bur- 
dens from these individuals were deter- 
mined by Ryan ct al. (52). 

g) Rhesus monkeys were administered I 
pg/kg TCDD, and it is assumed that 
essentially no TCDD was eliminated 
when the animal developed a chloracne- 
genir response. This is a LOEL dose; no 
lower doses were tested {5S). 

h) Assumes the rabbit and the rat have the 
same rate of elimination, a half-life of 
23.7 days {8S) and that the rabbits 
weighed 2,5 kg tliroughout the experi- 
ment. This is a LOEL dose; no lower 
doses were tested {52). 

i) Assumes the h.ilf-lfr of TCDD in mice 
is I 1 d.iys and th.it the mice weigh 25 g. 
This is a LOEL dose; no lower doses 
were administered (5). 

j) In highly exposed patients from the Yu- 
Cheng incident, there is a decrcar ■ i ■; 
birch weights of children born from 
these patients compared to unexpo?;cd 
control populations {IS. 5^. In addi- 
tion, the Vu-Cheng mothers have altered 
levels of placental epidermal growth fac- 
tor receptor (EGFR) and CYPIAI. The 
data indicate that the changes in placen- 
tal EGFR and C\T1A1 in these patients 
were maximal. Body burdens deter- 
mined based on levels of 2.3.4,7,8-pen- 
tachloro-dibcnzofuran (TEF = 0.5) and 
1 .2,3.4,7,8-hexachlorodibenzofuran 
(TEF = 0.1) in placenta tissue. Lipid 
concent of the placenta is estimated at 
1% {112) and the average percent body 
fat ol a women is assumed lo be 22°/b. 
These body burden estimates were also 
uied as hodv- burdens of Yu-ChcnL-. 



mothers whose children demonstrate 
decreased growth {63) and delayed 
developmental milestones {64,65). 

k) In a rat liver tumor promotion study, 
rats initiated with diethylnitrosamine 
were exposed to doses of TCDD from 
35 to 125 ng/kg/day. Statistically signif- 
icant increases in numbers of altered 
iiepatic foci were observed in rais treated 
with 125 ngTCDD/kg/day {67). At the 
end of the study, liver concentratioru of 
TCDD were approximately 20 ppb 
{60): assumes 20% body weight is adi- 
pose tissue and that at this dose, the liver 
has three times the concentration of 
TCDD than adipose tissue. Body and 
livet weights were reported [67) for 
these animals. The body burden calcula- 
tion assumes that liver and fat account 
for 85% of the body burden in these 
animals. For tumor promotion, 125 ng 
TCDD/kg/day is the LOEL and 35 ng 
TCDD/kg/day is the NOEL for tumor 
promotion (67). For induction of 
CYPIAI {60) and downregulation of 
EGFR {59). 125 ng TCDD/kg/day was 
assumed to produce a mxximal response. 

I) Mice were administered 10 ug TCDD/ 
kg and sacrificed 7 days after trcacmcnt. 
EGFR binding was determined in 
hepatic plasma membrane {5«S). 

m) Animals received a single dose and were 
sacrificed 24 hr later. Assumes no 
TCDD eliminated at this time. 
CYPIAI induction determined by RT- 
polvmcrase chain reaction {60). The 
LOEL for CYPIAI induction was I 
ng/kg, a no observed efTect level from 
this study is 0.1 ng/kg. 

n) Animals received 1.5 ng/kg/day 5 
d.iy/week for 13 weeks (6/). Mice were 
sacrificed 3 days after l.ut dose. Hepatic, 
dermal, and pulmonary EROD activity 
were significantly induced at this dose. 
Tissue concentrations of TCDD were 
mea-^ured in liver, skin, and fat. Body 
burden estimates assumes 95% ot the 
body burden is in liver, skin, and fat. 
This is the LOEL from this study, no 
lower doses v.ere tested. 

o) Body burdens arc estimated by authors 
{62) for the increased accumulation of 
PCDD/PCDF in liver compared to adi- 
pose tissue using a pharmacokinetic 
model. 

p) Assumes average level of dioxins and 
dibenzofurans in human serum ranges 
from 28 to 4l TEQ ppt and from 8 to 
17 TEQ ppc for the PCBs. Thus, the 
average TEQ r.uiges from 36 to 58 TEQ 
ppt. Using 58 ppt as the average concen- 
tration of PCDDs, PCDFs, and PCBs 
in serum, a bodv burden of 12.76 ng 
rEQ/kj; body weight w..'; calcubtrd'. 



rit? W3. Narrccf 3. s-eote^'ib-jr i005 



Reviews • DeVito et al. 



224 



For PCDD jnd PCDF concentrations, a 
body burden of 9 ng TEQ was deter- 
mined. Average concentrations of 
TCDD in adipose tissue ire 5 ppt (lipid 
adjusted) (27). resulting in a body bur- 
den of 1.1 ngTCDD/l:£;. 

q) In control rats, PCDDs and PCDFs 
were determined at dilTcrent ages: 200- 
day-old rats had approximately 78 ppt 
TEQs in liver (tf;). This is an equivalent 
liver concentration in 60-day-old rats 24 
hr after administration of 1 ng 
TCDD/kg. 

r) Liver, fat, blood, and skin concentra- 
tio.ns of TCDD, 1,2,3,7,8-PCDD, 
2,3,7,8-TCDF, 1 ,2,3,7. 8-PCDF, 
2,3,4,7,8-PCDF, and OCDF were 
determined in 150-day-old female 
B6C3F| mice. The TEF methodology 
wa5 lised to estimate TEQ levels in these 
animals; assumes that 93% of the body 
burden is in liver, fat, and skin. 

Table 3 

s) Estimated highest body burden at time 
of last exposure. Calculations based on 
measured TCDD levels in serum (lipid 
adjusted) and assuming a first-order 
elimination kinetics and a halt-life for 
chmination of 7. 1 years. Also assumes a 
body weight of 70 kg and 22% body fat. 
Calculations for estimated serum con- 
centrations at last time of exposure per- 
formed by authors (18,2Sl. 

t) Animals administered 100 pg 
TCDD/kg 6 times every 4 weeks over a 
24-wcek period; assumes a half-life of 
14.9 days (///). Body burdens are esti- 
mated immediately after the l.isc treat- 
ment with TCDD. The administration 
of 50 pg TCDD/kg 6 times every 4 
\vceks over a 24-week period did not 
increase the incidence of any types of 
tumors in 10 hamsters {68} . 

u) Assumes a single first-order elimination 
r:.-- .---.•.Tr and a half-life for the 
whole body elimination of 23.'/ days 
(55) and a gaitrointcstinal tract absorp- 
tion of 86% (aS). Increased incidence of 
hepatocellular carcinom.is were observed 
at 100 ng/kg/day and 10 ng/kg/day is 
the NOEL {69)~ Decreased testis weiglit 
and testosterone concentrations were 
observed alter 12.5 ng TCDD/kg 7 days 
latet {76). Decreased serum glucose lev- 
els were observed in rats treated with 
100 ng/kg/day for 30 days (79). 

v) Assumes an apparent half-life of 1 1 days 
and a bt)dy weight of 20 g. Mice receiv- 
ing 71.4 ng/kg/day for 2 years had a sta- 
tistically significant increase in hepato- 
cellular carcinomas {70). 

w) ,\ssunics neonatal rats and hamsters are 
ex|)0»cd to .in equal dose of TCDD as 



are the dams on a weight basis and 
assumes all alterations arc due to the 
neonatal exposure. For decreased body 
weight in pups 400 ng/kg is the LOEL; 
a dose of 64 ng/kg to the dam was the 
NOEL for this response {73). For 
decreased sperm count the LOEL is 64 
ng/kg and no lower doses were tested 
{86). In hamsters only one dose was tcc- 
ed (2000 ng/kg) for decreased sperm 
counts {74). Decreased growth in rats is 
indicated by decreased body weights up 
to postnatal day 63 {7S). The incidence 
of fetal mortality was increased in ham- 
sters at a dose of 18 pg/kg but not at a 
dose of 6 pg/kg {81). 

x) Assumes a single first-order elimination 
rate constant and a half-life for the 
whole-body elimination of 400 days 
{SI) and a gastrointestinal absorption of 
86% {88). This is the LOEL from this 
study; no lower doses tested. Monkeys 
exposed to a diet of approximately 5 ppt 
had a daily intake of 0.151 ng/kg/day. 
Monkeys exposed to approximately 25 
ppt in the diet had a daily intake of 
approximately 0.76 ng/kg/day. For ani- 
mals with decreased object learning, the 
TCDD-exposed offspring were born 
after 16,2 months of maternal TCDD 
exposure of a diet of 0. 1 5 1 ng TCDD/ 
kg/day. Animals with increased inci- 
dence and severity of endometriosis had 
a daily intake of 0.151 ng/kg/day for 4 
years, and body burdens were deter- 
mined at the end of the exposure period. 
Monkeys exposed to 0.76 ng TCDD/ 
kg/day for 16,2 months had significant 
decreases in offspring viability. 

)■) 1 he authors extrapolated serum concen- 
trations of TCDD at the time of sam- 
[iling to initial exposures {41). Workers 
with setun\ TCDD concentrations of 
140-496 ng/kg (lipid adjusted) have a 
greater incidence of low testosterone 
concentrations ('//). Extrapolation 
assumed a lialf-Jile for TCUD of 7.1 
yeats. To estimate body burdens in these 
workers, it was assumed that the back- 
ground TEQ was 60 ng/kg, thus the 
total serum TEQ wai 1 40 ng TCDD/kg 
* 60 ng TEQ/kg = 200 ng TEQ/kg 
(lipid adjusted). 

z) Assumes that high-exposed group (>33 
ng/kg) had a background of 60 TEQ 
ng/kg. This group had at least 93 TEQ 
ng/kg. Assumes average subject was 
male, weighing 70 kg with 22% body 
fat. 

aajWorkers with increased glucose toler- 
ance and diabetes have serum levels of 
640 ppt TEQ (.?■/). 

bb) Guinea pigs itceived 30 ng TCDD/kg 
iiHrJi).nioi,-.MlK' and s.icrificed 24 hr 



after dose. Assumes that no TCDD 
was eliminated at this time. This is a 
LOEL. no other doses tested {78). 

Table A 

cc) Assu.Tiing a single first-order elimina- 
tion rate constant and a half-life of 6-8 
weeks. Bodv burdens calculated by 
authors (82). Animals treated with a 
single dose of TCDD were tested 2 
weeks after treatment (5i). 

dd) Mice were treated with TCDD and 
challenged with influenza virus 7 days 
later {84). 

ee) Mice were administered 100 pg/kg and 
examined 30 days after receiving the 
: {77). 



References 

1. Pobnd .\. JC Knutson 2.3,7,8.iciri- 
elilorodibcnio-p-dioxin action. Annu Rev 
Phiimico! Toxjcol 30;25 1-277 (1970). 

2. DcVito .M, Bitnbium LS. Toxicology of the 
dioxins ind related chemicals. In; Dioxins and 
Health (Schectcr A, cd). New York:Elsevlrr 
1994.139-162. 

3. Safe S. Compiraiivc toxicology and mecha- 
nism ot accioa of polychlofinatcd dibcnzo-p- 
dioxins and dibenzofurjns Annu Rev 
Pharmacol Toxicol 26:371-389 (19"6). 

4. U S. EPA. In.ciim report on data and nic-JloJs 
for [he lise^imeni of 2,3,7.8-telnichloiociben- 
zo-p-dioxin (TCDD) risks to aquatic otsan- 
isms and associated wildlife. EPA 60b/r- 
93/055. Washington, DC:Environm:ntal 
Ptoicction Agency, 1993. 

5. HufTJ. 2,3,7.8-TCDD: a potent and complete 

Chi-niosphere 25 173-176(1992) 

6. Johnson R. Duluth MN. Tie.ge J. Boi:s S 
Carcinogenicity of 2.3.7.8-TCDD lo medalu. 
ToMCologisi 12 476(1992). 

7. HoUapple .MP. Snyder NK. Wood SC. .Morns 
DL 2.3.7,3-Tetrachlotodiben:o-p-dioxin- 
induced changes in immutiocompetcnce; possi- 
ble mechanisms. Annu Rev Pharmacol Toxicol 
31 73-95(1991). 

8 Schuepiein RJ, Callo MA. Van dcr Hei|den 
KA. Biological basis for risk assessment of diOx 
ins and •c\-.. impounds Banbury- report 
no 35 Plainvie.v, NYCold SpnngHarbor 
LiboraioivPrcss.489-490.1991 

9, Birnbaum LS Evidence for ihe role of tl-.e .Kn 
receptor in response to dioxin. In: Reccptor- 
mediaied biological processes: implications for 
evaluating carcinogens. Progress in clinical and 
biological research, vol 387 (Spicrer HL. Slaga 
TL. Greenlee WF, McClain .M, eJs). New 
YotkWilevLiss, 1994;1.'9-154: 

10 Evans R, The steroid and thyroid hormone 
superfamily. Science 240:889-895 (1078), 

I 1 Wuiloclc JP Jr. Ccnciic and molecular aspects 
of 2.3.:',8-Icirachlorodibcnio-p-dioxin action 
Annu Rev Pharmacol Toxicol 30:251-2~- 
(1990). 

12. Burbach K.M, Poland A. Bradlleld CA. 
Cloning of the Ah-receptor cDNA reveals a 
distinctive ligand-jctivated transcription factor. 
Proc N'jrl AcjJ Sci USA 89:5185-8190 

irw2i 



iCX Number $, SeQtemcf: 



."If.?/ riciilth \'i3"cr,- 



225 



Reviews • Body burdens of dioxins in humans and animals 



Ema M. Sogjwa K, Waunibc N. Chii|nh Y. 
Matsushiia N. Goioh O. Funic Y. Fu|ii- 
Kuriyjma Y. cDNA cloning and jtrviciucc of 
mouse puiativc AS receptor Biothem Bioph/3 
ReiCommun lS-1:2'(6-253 (1992). 
Safe S Polychlotmaled biphenyls (PCBs), 
d,ben!0-p.dlo,ins (PCDDi). dibeniofurans 
(PCDFs) and related compounds: environmen- 
tai and mechanistic considerations which sup- 
p ■: ':e devclopir.ent of toxic equivalency fac- 
tors HEFs). CRC Cm Rev Toxicol 21:51-89 
(1990; 

Birnbaum IS. The mechanism of dioxin toxic- 
ity: relationship to risk assessment. Environ 
Health Perspect 102:157-167 (1994). 
Schecter A. Startin J. Wright C. Kelly M, 
Papke O. Lis A. Ball M. Olson JR. Congener- 
specific levels of dioxins and dibenzofiinans in 
U.S. food and estimated daily dioxin toxic 
equivalent intake. Environ Health Perspect 
102:962-971 (1994). 

Suskind RJL Chloracne, the hallmark of dioxin 
intoxication. Scand J Work Environ Health 
11:165-171 (1975). 

Lucier GW. Humans are a sensitive species to 
some of the biochemical effects of structural 
analogs of dioxin. Environ Toxicol Chem 
10:727-735(1991). 

Fingerhut MA. Halpern QE, Narlow BS. 
Piacetelli LA. Honchat PA. Sweeney MH. 
Cteife AL, Dill PA. Steenland K. Suruda AJ. 
Cancer mortality in workers exposed to 
2.3.7.8-tetrachlorodibenM-p-dioxin. N Engl J 
.Med 342;212-218 (1991). 
Manz A. Rarger J. Dwyer JH. Cancer monility 
among workers in chemical plant contaminat- 
:,: with dioxin. Lincet 338:959-965 (1991). 
Zobet A. Messeret P. Huber P. Thirty-four 
year mortality follow up of BA.'sF employ-ei 
exposed to 2,3.7.8-TCDD after the l'/53 acci- 
dent. )nt Arch Occup Environ Health 
62:139-157(1990). 

K\ig;viii-. M. Sanrci ^ . Winklem.n. R. 
Cancer incidence and mortality in wome.. 
occupationally exposed to chlotophenoxy her- 
bicides, chlorophenols and dioxins. Cancer 
Causes Ointrol 4:457-162 (1993). 
Bettaaii PA. Pesatori AC. Consonni D, Titoni 
A, UnJi MT. Zocchetti C. Cancer incidence 
in a population accidentally exposed to 
2.3.7.S-tetrachlorodibenio-p-dioxin, 
Epidemiology 4:397^05 ( 1993). 
Sweeney MH. Hornung RW. ^X'all DK, 
ringetli::- >"■ Hilncrin Vi'L. Prcvalencr of 
diabetes and elevated serum glucose levels in 
workers exposed to 2.3,7.3-tcttachlotodibenro- 
p-dioxin rrCDD). Presented at the 12ih intet- 
national symposium on dioxins and related 
compound*. Tampere, Finland. 24-28 August 
1992. 

Wolfe W. Michalek J. Miner ]. Needham, L 
Patterson D Jr. Diabetes versus dioxin body 
burden in veterans of operation ranch hand. 
Presented at the 12th international symposium 
on dioxins and related compounds, Tampete. 
Finland. 24-28 August. 1992, 
DeVito M, Dirnbaum IS. Dioxins: a model for 
receptor mediated toxicity. Toxicology fin 
press). 

Schecter A. Dioxins and related chemicals in 
humans and in the environment. In; Biological 
basis for risk assessment of dioxins and telated 
coinuo.iiids (Gallo iVW. Schueplien R. Vin der 
Heiidan KA. ed.). Banhurv report no 35 



Plain.iew, NY.ColdSpring Harbor Laboratory 
Press, 1991; 169-212 

Schecter A, Stanley J, Boggess K, Masuda Y, 
Mes J, Wolfr M, Furst P. Furst C, Wilson- 
Yang K, Chisholm B Polychlorinated biphenyl 
IcviU in the tissues of exposed and nonerpo^cd 



hun 



Env 



Health 



102:149-158(1994), 

Schecter A. Furst P, Furst C. Papke O. Ball .M. 
Ryan JJ, Cau HD, Dai LC, CJuynh HT, 
Cuong HQ, Pho.ing N'FN, Phiet PH, Beim 
A, Constable F, Startin J. Samedy M, Seng YK. 
Chlorinated dioxins and dibenzofurans in 
human rissue from general populations: a selec- 
tive review. Environ Health Perspect 102(suppl 
1):I59-171 (1994). 

Pittetson DG Jr. Todd GO, Turner WE, 
Maggio W, Alexander LR, Needham LL, 
Levels of non-orr*o-substituted (coplanar), 
mono- and di-orrAo -substituted polychlorinat- 
ed biphenyls, dibenzo-^dioxins, and dibenzo- 
furans in human serum and adipose tissue. 
Environ Healrh Perspecr I02(suppl 
l);195-204(1994). 

l\jhn PC. Gochfeld M, Nygren M, Hansson 
.M, Rappe C, Velez H, Ghent-Guenthet T, 
Wilson WP. Dioxins and dibenzofurans in 
blood and adipose tissue of Agent Orange- 
exposed Vietnam veterans and matched con- 
ttols. J Am Med Assoc 259:1661-1667 (1978). 
Gochfeld M. Hygren .M, Hansson .M, Rjppe 
C, Velei H, Ghent-Guenthet P. Wilson WP, 
Kjhn P Correlation of adipose and blood lev- 
els of several dioxin and dlbenzofuran con- 
geners in Agent Orange-exposed Vietnam vet- 
erans, Chemosphere 18:517-524 (1979). 
Patterson DG. Needham LL, Pirkle JL, 
Robens DW, Bagby J, Garrett WQ, Andrews 
JS Jr, Falk H, Bcrnert JT. Sampson EJ, Houk 
VN Cotrcliiion benveen setum and adipose 
tissue levels of 2.3.7.8-tctrachlorodibenio-p- 
dioxin in 50 persons from .Missouri. Arch 
Environ Contam Toxicol 1 7: 1 39-1 43 ( 1 978), 
Wnlfe Wli. .Vlicbaiek JE. .Miner JC, Pirkle JL, 
Caudill SP. Patteison DG. Jr. Needham LL. 
Determinants of TCDD half-life in veterans of 
Opetatinn Ranch Hand. J Toxicol Environ 
Health 41 431-483(1994). 
EjcIoii G. Kaminisky L. Silkwonh J, /Mdoiis K, 
Hilker D, O'Keefe P, Smith R. Cierthy J, 
Hawley J, Kim N, Decaprio A. Calculation of 
2.3.7.8-TCDD equivalent concentrations of 
complex envitonment.-d contaminant mixtuies. 
Linirr.ii Hcaltl, Perspect 70:221-22, (1976), 
Barnes D, Alford-Stevens A, Birnbaum 1. Kurr 
FK. \X'ood W, Pattoii D, Toxicity equivalency 
factors for PCBs? Quality assurance: good 
piactice, regulation and law 1:70-81 (1991), 
US, Environmental Protection Agency, 
Interim procedures for estimating risks asstxi- 
ated with exposures to mixtutes of chlorinated 
dibenzo-p-dioxins and dibenzoftirans (CDDs 
and CDFi) and 1989 update, EPA/625/3- 
89/016, NTIS PB90-I45756/XAB. 
Spiingfield. VA:National Technical 
Information Seivice. 1989. 
Ahlhourg UG. Becking GC, Birnbaum LS. 
Brnuwer A, Derb HJCM, Peeley M, Color G, 
Hannberg A, Ursen JC, Liem AKD, Safe SH, 
Schlattet C, Wacin F, Youiies M, Yrjanheikki 
E, loxic equivalency factors for dioxin-like 
PCBs. Chemosphere 28:1049-1067 (1994), 
U ,■; EPA, Chlorinated diuxins and ftirans .n 
the j-.ener,ll 1,' S popul.tio.i NH.VFS l'VS7 



tesults- EPA-560/5-9U003. Washington, 
DC;Environmental Protection Agency, 1991 
Pirkle JL, Wolfe WH, Patterson DG, 
Njeedham LL, .Michalek JE, Miner JC, 
Petersen .MR, Philips DL, Estimates of the 
half-life of 2,3.7.8-tetrachlorodibenzo-p-dioxm 
in Vietnam veterans of Operarion Ranch 
Hand, J Toxicol Environ Health 27:165-171 
(1979). 

EgelanJ GM, Sweeney MH. Fingerhut .\U, 
Halperin VXT, Willc KK. Schnoor T,M. TouJ 
serum rcstosteronc and gonadotropins in work- ' 
ers exposed to dioxin. Am J Epidemiol 
139:272-281 (1994). 

Ema M. Che N, Suzuki M, Mimura J, Sognwa 
K, Ikawa S, Fujii-Kuriyama Y Dioxin binding 
activities of polymorphic forms of mouse and 
human arylhydrocarbon receptors, J Biol 
Chem 269 27337-27343 (1994) 
Okey AB, Riddick DS, Harper PA, The Ah 
receptor: mediator of loxiciry 2,3,7,8-tetra- 
chlorodibenzo-p-dloxin (TCDD) and related 
compounds, Toxicol Lett 70:1-22 (1994). 
Wong J, Okey, AB, ,^h (dioxin) receptor in 
human populations. In: Proceedings of the 
Grear Lakes health effects program science 
workshop (Hussain ,M, ed), 1-3 March 
l994;92-95. 

Poland A, Pilen D, Glover E. Anilvsis of the 
four alleles of the murine aryl hydrocarbon 
receptoi, .Mol Pharmacol 46:9 15-92 1 (1994), 
Clark G. Tritscher A. Bell D. Lucier, GW. 
Integrated approach for evaluating species and 
inierindividual dilTerences in rcsponsiveneis to 
dioxins and struautj analogs. Environ Health 
Perspect 98:125-132 (1992). 
Abbott BD. Birnbaum LS. TCDD ctposure of 
human embryonic palatal shelves in organ cul- 
ture alters the differentiation of medial epithe- 
lial cells. Teratology 43,1 19-132 (1991), 
Gieenlee ^XT. Dold K,M. Itons RD, Osborne 
R Evidence for direct action of 2.3.".8-tetia- 
chlotodihenio-p-dioxin ITCDDl on ih.tnic 
epithelium Toxicol AppI Pharmacol 
'" 1 12-120(1975). 

Cook JC. Dold KM. Greenlee WF. .\n in vitro 
model for studying the toxicity of 2,3,7.8-te:n- 
chlorodibenzo-p-dioxin to human thvmus. 
1 oxi.ol .^ppl Pharmacol 59:256-268 (19n. 
Wood SC, Jeong HG, .Vlorns DL Holsapple 
•VIP. Direcr efTecu of 2.3.7.8-teirachlotodiben- 
zop-dioxm (TCDD) on huinin toiuillar '.ym- 
phocMes. Toxicologva: i,-!-143(l99?'.. 
lle^k H. Eckart K. .Mathar W. Levels of 
PC;DDs and PCDFs in adipose tissue of occu- 
pationally exposed workers. Chemosphere 
18:507-516(1979). 

Ryan JJ. Gisiewicz TA, Brown JR Jr. Human 
body burden of polychlorinated dibenzoftitans 
associated with toxicity based on the Yusho 
and Yucheng incidents. Fundam Appl Toxicol 
15:722(1990). 

.McNultv WP. Toxicity and fetotoxicitv of 
TCDD. TCDF, and PCB isomers in rhesus 
macj.lues (,V/.icjf.r muiirra). Environ Health 
Perspect 60:77-88 (19^5), 
Schwetz BA. Norris J.Vt. Sparschu GL. Rowe 
UK. Cehring PJ. Emerson JL. Gerbig CG 
Toxicoloi;v of chlorinated dibenzo-^dioxins. 
Environ Health Perspect 5:87-99 (19~3). 
Puvel SM. Sakamoto M. Effect of 2.3.7.8- 
tetiachl,)rodibenzo-p.dioxin on .niuiine skin ) 
Invest Oeriiiaiol 90-35-I-353 (lirS). 
S.inahaia Gl. Nels..n KG. W.inr. IK, Lucier 



••erwl ■!'Mi:lt !'ors^-oai\ei • V'jlvnit id. Wn 



Reviews • DeVito et al. 



226 



CW. Dccrcucd humin biiih weights ikct in 
utero exposure to PCBs and PCDFs ire issoci- 
jted with decreased placental EGF-slimiJated 
receptor autophospKorylation capacity. N^ol 
Pharmacol 32:572-573 (1987), 

57. Sewall CH. Lucier CW. Tritscher AM. Clark 
CC TCDD-mediated changes in hepitic epi- 
dermal gtuwtii factor receptor may be a critical 
event in the hepatocarcinogenic action of 
TCDD Carcinogenesis 14:1885-1893(1993). 

58. L,n FH. Clark C. B.rnbaum LS. Lucier GW. 
Goldstein ]A. Influence of the Ab locus on the 
effects of 2.3,7.8-tetrachlorodibcnio-p-dioxin 
on the hepatic epidermal gtowth factor recep- 
tor. Mol Pharmacol 39:307-313 (1991). 

59. Tritscher AM, Goldstein JA. Portier CJ. 
McCoy Z. Clark GC. Lucier GW. Dose- 
response relationships for chronic exposure to 
2.3.7.8-tetrachlorodibenzo-p-dioxin in a rat 
tumor promotion modcLquantification and 
immunolocaliiation of CYPlAl and CYP1A2 
in the liver. Cancer Res 52:3436-3442 (1992). 

60. Van den Heuvel JP, Clark GC. Kohn MC. 
Tritscher A,M. Greenlee WF. Lucier GW. Bell 
DA. Dioxin-rcsponsive genes: examination of 
dose-response relationships using quantitative 
reverse transcript-asc-pol/mcrase chain reaction. 
Cancer Res 54.62-68 (1994). 

61 DeVito MJ. Ma X. Bab.sb JG. Menache M. 
B.rnbaum LS. Dose-response relationships in 
mice following subchton.c exposure to 2.3,7,8- 
tetrachlorodibenio-p-dioxin: CYPIAI. 
CyPlA2. estrogen receptor and protein tyro- 
sine phosphorylation. Toxicol Appl Pharmacol 
124:82-90(1994). 



62. Ca 



Bri 



R. Erode 



Physiologically-based modeling of dse toxicoki- 
netics of polychlorinated dibcnio-p-dioxins 
and dibenzofurans in mammalians, including 
humans. I. Nonlinear disttibution of 
PCDD/PCDF body burden between liver and 
adipose tissue. Toxicol Appl Pharmacol 
131:253-266(1995). 

63 Guo YL. Lin CJ. Yao W], Ryan JJ. Hsu CC 
.Musculoskeletal changes in children prenatajly 
exposed to polychlotinated biphenyls and relat- 
ed compounds (Yu-Cheng children). J Toxicol 
Environ Health 41:83-93 (1994). 

64. Rogan W]. Gladcn BC. Hung K-l.. Koong S- 
L. Shih L-V. Taylor JS. Wu Y-C. Yang D. 
Ragan NB. Hsu C-C. Congenital poisoning by 
pdlychlofinated biphenyls and thcit contami- 
nants in Taiwan, Science 24 1 :334-336 (1978). 

r,5 Chen Y-CJ, Cou Y-L, Hsii CC, Rogan WJ. 
Cognitive development of Yu-Cheng (oil dis- 
ease) children prenatally exposed to heat- 
d^sr.ded PCBs. J Amer Med Assoc 
268:3213-3218(1992). 

66. Sch.uirz SL, Bowman RE. Learning in monkeys 
exposed perinatally to 2.3.7.8-tetrachlotodibcn- 
!0-p-dioxin (TCDD) Neutotoxicol Teratol 
11:13-19(1979). 

67. Vanden Heuvel J P. Clark GC. Tritscher AM. 
Lucier GW. Accumulation of poly<:hlorinated 
dibenzo-p-dioxins and dibcn2of\irans in livet of 
control laboratory tats. Fundam Appl Toxicol 
23 465^69(1994), 

63 Rao MS. Subbato V, Prasad JD. Scarpelli DC, 
Carcinogenicity of 2.3,7.8-tetrachlorodibenzo- 
p-dioxin in the Sytian hanistet. Carcinogenesis 
9(91:1677-1679(1978). 

69. Kociba RJ. Keyes DC. Beyer JE. Carreon R.M. 
Wade CE. Dittenbet DA. Kalnins RP. Frauson 
LE, Park CN. Barnard SD. Hummel RA. 
llumiston CG Resiihi of a iwo-ycar chioiiic 



toxicity and oncogenicity study of 2.3.7.8- 
tcttachlorodibenzo-p-dioxin in rats. Toxicol 
Appl Pharmacol 46:279-289 (1973). 
70 NTP. Bioissay of 2.3.7.8-tetiachlorodibenzo- 
/►-dioxin for possible carcinogenicity (gavage 
study). Technical report series no. 102. 
Research Triangle Park. NC:National 
Toxicology Program. 1972. 

71. Mironpot RR. Foley JF. Takahashi K. 
Goldsworlhy T. Clark G, Tiiisclier A, Portiet 
C, Lucier G. Dose response for TCDD pro- 
motion of hepatocarinogencsis in rats initiated 
with DEN: histologic, biochemical and cell 
proliferation endpoints. Environ Health 
Petspect 101:634-642(1993). 

72. Poland A, Palen D, Glover E. Tumor promo- 
tion by TCDD in skin of HRS/J hairless mice. 
Nature 300:271-275 (1972). 

73. Mably TA, Moore RW, Peterson RE. In uteio 
and lactational exposute of male rats to 
2,3,7.8-tetrachlorodibenzo-p-dioxin. 1. EflTects 
on androgenic status. Toxicol Appl Phatniacol 
114:97-107(1992). 

74. Cray LE. Jr Kelce. WR Monosson E. Ostby JS. 
Birnbaum LS, Exposure to TCDD during 
develop. .lent permanently altcts reproductive 
function in male LE rats and himstets: reduced 
ejaculated and epididyniai sperm numbers and 
sex accessory gland weights in offspting with 
normal androgenic status. Toxicol Appl 
Pharmacol 131:108-118(1995). 

75. Bjerke DL. Peteison. RE. Repioductive tn<ici- 
ty of 2.3,7,a-telrachlorodibenzo-p-dioxin in 
nule tats: different eflTccts of in utero versus 
lactational exposure. Toxicol Appl Pharmacol 
127:241-249(1994). 

76. Moore RW. Potter CL. Theobald HM. 
Robinson JA. Peteison RE. Androgenic defi- 
ciency in male tats treated with 2.3.7.8-tetta- 
chlofodibenzo-p-dioxin. Toxicol Appl 
Pharmacol 79:99-1 11 (1975). 

77. McConnell EE. Moore JA. Haseman JK, 
Hams MW. Ihe compatative toxicity of chlo- 
rinated dibeiuo-p-dioxins in mice and guinea 
pigs. Toxicol Appl Pharmacol 44:335-356 
(1978) 

78. Enan E, Liu PC, Matsumura F. 2.3,7.8- 
Tetrachlorodibenzo-p-dioxin (TCDD) causes 



:plasn 



ispofting 1 



of adipo 
pancteas ftom the guinea pig. J Biol Chcm 
267:19785-19791 (1992). 
ZinkI JG. Vos JG. Mooie JA. Gupta DN. 
Hcm.iiologic and clinical chemistry effects of 
2.3,7,3-tctiachloiodibcnro-p-dioxin in labora- 



als. En» 



Health Pe 



5:111-118(1973). 
SO. Bowman RE, Schaniz SL.. Weer.-.singhe ML. 
Baisotti DL.Chionic dietary intake of 2.3.7,8 
tetrachlorodibenio-p-dioxin (TCDD) at 5 ot 
25 patts per ttillion in the monkey: TCDD 



nddo 



cfTec 



reprt 



tive toxicity. Chemosphere 18:243-252 
(1979). 

Olson JR, McGarrigle BP, Tonucci DA. 
Schectet A. Eichelberger H. Developmental 
toxicity of 2.3.7.8-TCDD in the rat and ham- 
ster. Chemosphere 20:1 1 17-1 123 ( 1990). 
Neubett R. Golot G. Stahlmann R. Hclge H. 
Ncubert D Polyhalogenated dibenio-p-diox- 
ins and dibenzofurans and die immune system 
4. Effects of multiple dose treatment with 
2,3,7,a-letij..lilotodihcnzo-p-dioxin fPCDD) 
(Ml peripheral lyiiiphoryte subpopulatioiis of j 
non-human ptiinjie {Cjli'itljrix j.icchuj). Arch 



Toxicol 66:25(^-259 (1992). 
Neubett R, Jicob-Muller U, Stahlmann R, 
Helge H, Neuben D. Polyhalogenated djben- 
zo-p-dioxlns and dibenzofutans and th- 
immune system. 4 Effects on peripheral lym- 
phocyrc subpopulations of a non-human pri- 
mate {Cjllitiinx jatchuj) aftet tteatment with 
2,3,7, 8-tetrachlorodibcnzo.p-dioxin fTCDD). 
Arch Toxicol 64:354-359 (1990). 
Burelson CX Lebrec H, Yang Y. Ibanes JD. 
Pennington KN. Birnbaum LS Effects of 
2.3,7,8-tcttachlotodibenzo-p-dioiin (TCDD) 
on influenza host ri^istance in mice. Fundam 
Appl Toxicol (in press). 

Reier SE, Martin DC. Bowman RE. Draowski 
WP. Becker J L. Endometriosis in Rhesus mon- 
keys [Macacj mulaita) following chronic expo- 
sure to- 2.3.7.8-retrachlorodibenzo-p-dioxin. 
Fundam Appl Toxicol 21:433-441 (1993). 
Mably TA. Bjerke DL. Moore RW. Gendron- 
Fmpatrick A. Peterson R£. In uteto and lacta- 
tional exposure of male rats to 2.3.7,8-tetra- 
chloiodibenzo-p-dioxin. Ml. Effects on sper- 



and I 



abilli 



Toxicol Appl Pharmacol 1 14:108-1 16 (1992). 
Gasiewici TA. Rucci G. Cvtosolic receptor for 
2.3.7.8-retrachlorodibcnzo'-p-dioxin: evidence 

mahan specfes. Mol Pharmacol 26:90-97 
(1974). 

Schienk D. Buchmann A. Dieti K. Upp H-P. 
Brummer H. Sirma H. .Vlunzel P. Hagenmajer 
H. Gebhardt R. Bock tCW. Promotion of pre- 
neoplastic foci in tat livet with 2.3.7.8-te;ia- 
chlorodibenzo-p-dioxin. 1 ,2,3,4,6,7,8-hepat- 
achlofodibenzo-p-dioxin and a detmed mixture 
of 49 polychlorinated dibenzo-p-dioxins. 
Carcinogenesis 5:509-515 (1994). 
Davis D, Safe S. Dose-response immunotoxici- 
ties c^commetcial polychlotinated biphenvis 
(PCBs) and their intetaction with 2,3,".'s- 
tetrachlorodibenzo-p-dioxin. Toxicol Lett 
4835-42(1979) 

Bcgel L, Hatris M, Davis D, Rosengren R. 
Safe L, Safe S. 2.2'.4.4.5.5'-hexachloro- 
biphenyl as a 2.3.7.8-tetiichlofodiben20-p- 
dioxin antagonist in C57BL'6J mice. Tox:col 
Appl Pharmacol 97:561-572 (1979). 
Mortissey RE,. Harris MW, Diliberto JJ. 
Bitnbaum LS. Limited PCB antagonism of 
TCDD-induced malformations in mice. 
Toxicol Lett 60.19-26 (1990). 
van Biigelen APJM. Toxic and biochemical 
.■ ■. ■, .'v-hlorinncJ I :?;... 1.1, (PCBs) r! 
ative to and in combination »idi :.3,7,3-tetra- 
chlorodibenzo-p-dioxin in the rat: possible 
implications oi the risk asscisment (PhD Uie- 



s) Ut 



the Netherla 



,:Utl 



University, 1994. 

Bannistci R, Safe S. Synergistic interactionj of 
2,3,7,8-TCDD and 2,2',4,4',5,5'-hcxachloro- 
biphenyl in C57BL/6J and DBA/2J: role of the 
Ah receptor Toxicology 44: 159-165 (1977). 
U.S. Environmental Protection Agency- 
Guidelines on chemical mixtures. Fed Reg 
51:34014-34029(1976). 
Rose JQ. Ramsey JC. Wentzlcr TH. Hummel 
RA. Gehring PJ. The fate of 2.3.7,8-tetra- 
chlorodibenio-p-dioxin following single and 
repeated oral doses to the rat. Toxicol Appl 
Pharmacol 36:209-216(1976). 
Abraham K. Krowke R. Neubert D 
Pharmacokinetics and biologic.il activity ol 
:.3.",8tetrj.hlorodibeiiz.)-p-dioxin: 1 dose- 



: distribu 



mdu 



'/u/u(!ie /OJ. Nuinbei'X Stftembnr :f,9b • tnviioninenml Hs- : 



227 



Reviews • Body burdens of dioxins in humans and animals 



ch Tox 



hepatic cihoxyrtsorunn 0-d«thyla: 
following 1 jinglc injo 
62:348-359(1978). 

97. Van den Berg W. Dcjongh J. Olson JR. The 
loxicoliinttics and metabolism of polychlon- 
nated dibcnio p-dioxins (PCDDs) and diben- 
loRirans (PCDFs) and their relevance for toxic- 
ity. CRC Cnt Rev Toxicol 24:l-7-t (1994). 

98 Andersen. ME. Mills ]J. Garps ML Kedderis 
L. B.rnbaum LS. Neubert D. Greenlee WT. 
Modeling receptor-mediated processes with 
dioxin: implications for pharmacokinerics and 
risk assessment. Risk Anal 13:25-36 (1993). 

99. Thoma H. Mucke W. Kjuert G. Comparison 
of the polychlormatcd diben!o-p-dioxin and 
dibeniofutan in human tissue and human 
liver Chcmosphere 20:433-442 (1990). 
IQO.Knutson JC. Poland A. Response of murine 
epidermis to 2,3.7.8-tetrichlorodibenzo-p- 
dioxin: interaction of the Ah and hr loci. Cell 
30:234-348(1972). 

101. Sham W. Bush B. Seegil R. Neurotoxicity of 
polychlorinated biphcnyls: structu 
relationships of individual congenci 
AppI Pharmacol Ul:33--(2 (1991). 

102. Diliberro JJ, Akube PI. Luebke RW. Birnbau 
LS. Dose-response relationships of tissue dist 
bution and induction of CYPlAl at 
CYP1A2 eniymaiic activities following aci 
exposure to 2.3.7.8-teirachlorodibenio-p-dic 



. Toxic 



in (TCDD) in mice. Toxicol AppI Pharmacol 
130:197-208(1995). 

103. Kawajiri K. Nakachi K. Imai K. Yoshii A. 
Shinoda N. Watanabe J. Identification of 
genetically high nsk individuals to lung cancer 
by DNA polymorphisms of the cytochrome 
P450lal gene. FEBS Lett 263:131-133 (1990). 

104.Sivaraman L Lealhman MP. Yee J. Wilkens 
LR. Lau Af . Le Mirchand L CYPlAl genetic 

Cancer Res 54:3692-3695 (1994). 

105.Thirman MJ. Albrecht JH. Kcueger MA. 
Erickson RR. Cherwna DL Park SS. Gelboin 
HV. Holztman )L Induction of CYPIal and 
formation of toxic metabolites of 
benzolalpyrene by rat aorta: a possible role in 
atherogenesis. Proc Nail Acad Sci USA 
91:5397-5401(1994). 

106.Zober A. Ott MG. Mcsserer P. Morbidiry fol- 
low up study of BASF employees exposed to 
2.3.7,8-teirachlotodiben20-p-dioxin fTCDD) 
after a 1953 chemical reactor incident. Occup 
Environ Med 51:479^86 (1994). 

107. Lu Y-C. Wu Y-C. Clinical findings and 
immunological abnormalities in Yu-Cheng 
patients. Environ Health Perspect 59:17-29 
(1975). 

lOe.Zober MA, Ott MG. Papkc O. Senft K. 
Germann C. Morbidity study of ottrader per- 
sonnel with potential exposure to brominated 



dioxins and furani 1. Results of blood moni- 
toring and immunological sianu. Br] Ind Med 
49 532-544(1992). 

109 Kerkvliet NI. Brauner JA. Flow cytometric 
analysis of lymphocyte subpoplations in the 
spleen and thymus of mice exposed to an acute 
immunosuppressive dose of 2.3.7.8-tetra- 
chlorodibenio-p-dioxin. Environ Res 
52:146-164 (1990). 

llO.S.elken RL Jr. Statistical evaluations reflecting 
the skcwness in the distribudon of TCDD lev- 
els in human adipose tissue. Chemosphere 
16:2135-2140(1977). 

111. Olson JR. Gisiewia TA. Neal RA Tissue dis- 



and 1 



aboli 



of 



2.3.7.8-tetrachlorodibenlo-p-dioxin (TCDD) 

in the golden Syrian hamster. Toxicol AppI 

Pharmacol 56:78-86 (1970). 
112. Beck H. Dross A. Mathar W. PCDD and 

PCDF exposure and levels in humans in 

Germany. Environ Health Petrpect 102(supp! 

1):173-185(1994). 
1 13. Huisman M. Koopman-Esseboom C Fidler V. 

Hadders-Algra M. van der Paauw CG. 

Tuinstra LGMTh. Weisglas-Kuperus N. Saucr 



PJJ. To 
exposur 



developrr 
(1995). 



ER. Pel 



en BCL. Bi 
polychlorinated biphenyls and 
its efTeci on neonatal neurological 
It. Early Hum Dev 41:111-12? 



Society of Toxicology 

Reproductive and Developmental Toxicology Subsection 

Graduate/Postdoctoral Student Award 

We announce our intention to make awards of recognition for the best platform and/or poster preser- 
tation by graduate students or postdoctoral fellows in the areas of reproductive and developmental toxi- 
cology at the 1996 Annual Meeting of the Society of Toxicology, which will be held in Anaheim, California c^ 
March 10-14. General areas of research can include female or male reproductive toxicology, reproductive 
endocrine toxicology, teratology/developmental toxicology, and/or postnatal functional assessment. 
Candidates for these av/ards should send to the address listed below, by November 1, 1995, a copy of the 
abstract that is being submitted to the Society for this meeting. An outline of the talk or a copy of the 
poster material should also be included if possible, to assist the judges. 

The abstracts and posters should describe original research which may include applied studies, inves- 
tigations of mechanisms of toxic response, or studies of basic biochemical, physiologic, or genetic mecha- 
nisms of action. Interested individuals may request Society information and abstract forms from the 
address below. All submitted material will be treated as confidential. The winning presentations will be 
amounced at the Annual Meeting of the Specialty Subsection in Anaheim. For further information, please 
contact: 

Robert J. S.avlocl:. Ph.D. 

U.S. Environmental Protection Agency 

Health Effects Research Laboratory 

Developmental Toxicology Division (MD-71) 

Research Triangle Park. NC 2/711 .^___ 



Enwonrrerlol Heal'.h Perspxwes • VolurrK W3. NurrterS. Septerroe' :°95 



831 



228 



11^29/95 14-41 "3607 779 8623 



Amerlcsn Journal of EpitKjnjiology 

CopyWght Q 1995 by The JoJln* Hopfcm* Univer^.ty Sc\ 

All nghin feo<KV©d 



Schecter SUNY 



^ Hygten* and Public H<»aHh 



_Pe£e_i4£r-4J5lL 



3002 



Vd. 112, No. U 



Exposure to Polychlorlnated Dioxins and Furans (PCDD/F) and Mortality in a 
Cohort of Workers from a Herbicide-producing Plant in Hamburg, Federal 
Republic of Germany 



Dieter Flesch-Janys, ' Jurgen Berger." Petra Gum,' Allred Manz,' Sibylle Nagel,' Hiltraud Waltsgctt,' and 
James H. Dwyer^ 



The relation beiween mortality (all cause; cancer; cardiovascular diseases {International Classification of 
Diseases, Ninth Revision (ICD-9), codes 390-459); ischemic heart diseases (ICD-9 codes 410-414)) and 
exposure to polychiorinated dlb-^nzo-p-dioxins and -furans (PCDD/F) was investigated in a retrospective 
cohort study. The cohort consisted of 1,189 male wor)<ers in a chemical plant in Hamburg, Federal Republic 
of Germany, who had produced phenoxy herbicides, chlorophenols, and other he/bicides and insecticides 
known to be contaminaU^d with 2,3,7,8-tetrachlorcdibenzo-p-dioxi.. and uther, higher chlorinated dioxins and 
furans. TTie authors lepurled previously on cancer mortality in this cohort (or the follow-up period 1952-1989. 
The current study coveis Iha years 1952-1992 and investigates the relation of PCDD/F exposure to mortality 
using a quantitative estimate of PCDD/F exposure for the whole cohort derived from blood and adipose tissue 
levels measured in z subgroup (ri - 190), Quintlles and deciles of these estimates served as dose parameters 
in the estimation of relative nsks (RHs), using year-of-birth stratified Cox regression. An unexposed cohort of 
gas workers served as an external reference group. The total mortality was elevated in all dose groups. The 
highest relative risk was observed for the highest 2,3,7,8-tetrachlorodiben2o-p-dioiin (TCOD) decile (RR = 
2.4 J, 95% confidence internal (CI) 1 .80 to 3,29). Cancer mortality and mortality due to Ischemic heart diseases 
showed a dose-dependent relation with TCOD and all PCDD/F combined. The highest u-iative risks for cancer 
(RR = 3,30. 95% CI 2, 05 to 5. 31) and Ischemic heart diseases (RR = 2,43.95% CI 1.32 to 4.66) were observed 
in the highest PCDD/F exposure group. The pattern of effects and tests for trend were sJ.i-^ilar when the lowest 
exposure group Within the chemical worker cohort served as the reference, but the relative risks were smaller 
and the confidence intervals were larger. Potential confci inding exposures complicate the interpretation of the 
internal comparison. These findings indicate a strong dose-dependent relation between mortality due to 
cancer or ischemic heart diseases and exposure to polychlorinated dioxins and furans. Am J Epidemiol 1995. 
142:1165-75. 

dioxins; monallry: myocardial ischemia; neoplasms; occupational exposure 



7 .l,7,u-l elrachiorodiocriiX'-p-aioxin (fCDD) is ,t 
wide.<;pread environmental cont.iiuinant in food, soil, 
and water. It produce.s a vanely of toxic effects in 
experimental animals at very low doses, including 
caiciiiugenicity, immunotoxicity, teratogenicity, dis- 



Ri?celved for publication Jung 24, 1994, and in finfil form S<5p- 
tembei- 15, 199S. 

AbtwGviaiions: CI. confidence intorval. ICO-9. Intemstional Clas- 
stficsticn of Diseases, Ninth Revir.lon; PCOD/T, polychlonruted 
d)henzo-p-dioxins and -furans: RR, rekiliva risk; TCOD, 2,3,7,0- 
tetrachloradlb©nzo-p-dioAln, 

' Center for Cl-iernical Workon;' Health. Dt'partrnent of Health. 
Free and Hanseatic City ot Hamburg, Germany 

' Institute for Mathematics and Compuief Science in Modicino, 
I Iniversity Hospital Eppendort, Horrbi.i]n. Gonniioy, 

' Oepaninen- ol Prevuriti'o MedlcVie (I'iSilutfl for FrHvontior' 
He:...vrch), Un'vc;rsit-/ rf Southcn-i Cjli!om,ii, s;.t^ol ot Mo<Ji.;iM.,i. 
Lot, A/Kjuies, CA 

F'ap»int re^Ut^cis to fVoi llr i\ Mdn.'...OntfV for Cheiri'-Jil V.' jr-;- 
■y/ t- ■;i;;i,. PulilstjCr.;.-, :;ir 401. D :«-.t'.)S |i.!ilil.nir.;. (;..r,,nK- 



lurbtmces of lipid metabolism, and biochemical i-ffe£ts 
involviag drug-mcLaboUzing enzymes (1). 

However, there is an ongoing debate concerning the 
susceptibility of humans to toxic effects of this sub- 
stance. It IS Widely agreed that TCDD causes chlor- 
acnc in dose ranges comparable to those observed in 
experimental animals. The first reports on this issue 
were published in 1957 (2) and 1964 (3). With respect 
to carcinogenicity in humans, three epidemiologic 
studies witfi an exposure assessment partly based on 
dioxin levels in blood (from a subgroup) have found 
similar associations, A [ny.c US study (4) and a 
sniallrr German study (5) reported elevated risks of 
tot:il cancer mortality in group.s of workers witfi sub 
sijuii.tl cxpo.surc to TCDD (verified by measuremenrs 
of blooi* concentrations) and a latency tiirie ot aboiii 
2(J yf;y;. 0"r group rcporti'd r;.-i clevalion of ioli! 
c:mic-;i tiiort i^iw f<v > i ■^' <y" ^' . . .-'-.-r.- i" •• " • '-•■••• 



229 



11/29/95 14-42 S507 770 8623 

1166 riesch-Janyi fc!l al 



Schecter SUNY 



3003 



ical plant in Hamburg (^ = 1,184 men; ihut produced 
herbicides cutuamiiiated with TCDD and other poly- 
c.hlorinatcd dio.^ir.s and furans (6j. Thi; folTow-up pc- 
liod was iyi'i-iysy. The relative nski varied with the 
polyclilnnnated dibcnTrv/xiioxin and -furaji (PCTJD/1-") 
exposure surrogate (duration of cniploymeni, lime of 
entry into (he plant, qualitative exposure groups). In a 
subsequent analysis ( /), il was shown (hat the duration 
of employment in dillercni production departments 
with diffcreiu levels ul exposure was quamiia(ively 
related to cancer iiior(alily Significantly elevated rel- 
ative nsks for cancer mortality were observed for the 
depatlineiKS wiUi tde highest TCDD exposure. How- 
ever, no dose-response rclalions- m terms of quantita- 
tive PCDD/l exposure levels could be estimated. 

'Vht experimental and epidemiologic evidence for a 
potential relation of cardiovascular diseases, espe- 
cially ischemic heart disea.ses, to PCDD/F exposure is 
less compelling than that for cancer. There are, how- 
ever, a number of repons suggesting that TCDD may 
influence a number of risk factors for ischemic heart 
disea.ses- This possible link wis addressed in .several 
epidemiologic studies investigating outcomes related 
to ischemic heart diseases prevalence of ischemic 
heart diseases (8-11), hypertension (9, 10, 12), blood 
lipid disturbances (9. 10, 12-16), and diabetes (17, 
18). r /.vevcr, no definite conclusion can be drawn 
from iJiese studies because ol' inconsistencies m find- 
ings, uncertainties about exposure, and possible selec- 
tion bias. Several animal studies also invcsligated the 
effects of TCDD exptisurc on cardiovascular out- 
comes The reported effects include morphological 
changes in pcnpheral vessels (19, 20), funcQonal dis- 
lurbances (21-23), and dis[urbanccs in lipometabolism 
(24-27). 

Since our first report on the cohort of chemical 
workers fiorn H.imburg, new data have been collcc(ed. 
Tliese new data include an increase in (he number of 
cohort mciuberN w iih detenminalions of PCDD/F in the 
blood, data on tfie elimination velocily of PCDD/T, 
:ind extension of mortality follow-up from 19S9 to 
1992. These nev/ data allow the construction of quan- 
titative PCDD/F exposure indicators. This paper re- 
ports the findings on the quantitative relations between 
total mortality and mortality due to cancer, ischemic 
heart diseases, cardiovascular diseases, and all other 
causes and these new PCDD/1- exposure indicalofs. 

MATERIALS AND METHODS 

The cohort consisted of all regular employees of a 
rliemical ])laiu i;i Hamburg, fiorinany, employed for at 
Uast ^ months between 19.V7 and 1 984 when ih-.- plant 
v,as closed. Workers were identified by company per- 
.iunn'.-l acl union ele.;ii>in leoords and by inl'onnation 



obtained from employees. The mortality follow-t 
reported here covered the years I9.S2-1992. 

E;-posure assessment 

bxposurc (0 FCDD/1 in the plani had occurred i 
Ihe production of diffcicm herbicides and insecticide 
(2.4,5-tncliloiaptienoxyacctic acid, trichloropheno 
Dromophos, lindane; lur details see reference 6). 

For the analysis ol (he relation between PCDD/'. 
exposure and diffcieiit mortality ouicomes. a quann 
lalive expoiure variable, describing the chronic occu 
patioiial exposure to HCDD/i-' in terms of the esLiniale-. 
PCDD/F blood levels at the end of exposure abov 
Gciiiian background levels, was constructed as fol 
lows. First, definitions of 14 production department: 
of the plant were developed from an analysis of iht 
production processes by an industrial hygicnist. These 
definitions included measurements of PCDD/p level- 
in Ihe vaiious producis of the plant, in waste products 
and in different buildings within the plant. Second 
each worker \va.s assigned the time fin years' he hac 
worked in each of the 14 production depan.f.ents o; 
aicas (eg, inchlorophenoxyacetic acid production) 
These duration estimates were derived from personnel 
records supplied by the company and additional infor- 
mation elicited from workers in personal interviews 
(fur details see reference 28). Third, conccntnLions of 
PCDD/F in adipose tissue (n = 48 (29)) c- v.hol^ 
bloud (n - 142) were (jctcnnined for 190 maie work- 
ers Some ol these data (^ = 121) have been described 
previously (30). Pourth. adopting the standard assump- 
tions of a one-compartment fu^st-order kinetic model, 
we estimated PCDD/F levels at the end of exposure 
(PCDD/F'"''^') for the 190 workers with available 
determinations ot PCDD/F at various time points. This 
estimation used the halt-lives calculated from m elim- 
ination study in 48 workers from this cohort '31) and 
background levels for the German population (32). 
The contnbution ot the working tinie in each produc- 
tion department on PCDD/P wa.s then estimated 
using ordinary least-squares regression through the 
origin according to the equation 



PCDD/F,"' 



J= 1 



(1) 



where i,^ denotes the working time (iii years) for the 
/th worker in the y'th production department. Finally, 
using the values of x,^ available for all workers in ihc 
cohort and the values of /3^ obtained from tiie subgroup 
with blood/ti.ssue PCDD/F levels, wc calculated the 
i-siimated PCDD.''F levels foi all members of the co- 
hort for eacll ^oni^ener ,-\ totil tox'- eiiiiiv-'lrt.n'--. v"-- 



230 



11/29/95 15:33 C607 770 8623 



Schecter SUNY 



ud bi.lic""<. H-art Disease 



51 
11(57 



able wxs also coiiipuied lur nil illoxim dud turans 
combined I'his variable was takulaicd a', the 
wcigtited .')Um of all congeners, whcic ihe wcjgliis 
■vtie loxic equivalency factors expicbsmg tht' loxiciiy 
of eacli cor.ge:icr relalivc lo thai ol TCDD (13). 

t.xp<^5iire to ottijr carcinogctis or -usiKxled circiiv 
ogcns had occurred jr. soire production deparln'enu; of 
the piani. Of special iniportaiicc was exposure; lo tl'c 
tdcv.n carcinogen dimeiliv! sulfate in (lie opiate de- 
pa'-iraent where morphines h.id been produced. Addi- 
tionally, exposure to different liomers of hexachloio- 
cyclohexane, some suspected to be caicinogemc, h;id 
occurred in the departments Involved in tlie production 
and fi-mulation of lindane. Finally, there had liccn 
exposure U) benzene, especially in tJie syn'Jicsis of 
hexachlorocyc!ohexai;c. However, all these exposijrt;s 
occurred m production dcpartmcnls wiih low- to mid- 
range exposure to TCDD and other PCDD/F. 



Assessment of causes of death 

Vital status was .ibses.sed hy direct contact o' 
thiough comiliuniiy legislries. Causes of death wei.- 
derived from records obtained from a hospital or f,in-- 
ilv doctor by n palholo;^ist Causes nf dc.iih we;- 
coili'.,' according to the ImeniaHi'^nal Cia.^^ii'icciKan c 
Discius, Ninth RcuMon ([CD-V), by an eeperienrec 
nosologist. If no rrco:ds were available, deaih ceHif 
icates or other infonnation (life ioiurance records 
next of kin) was U'ir.J The qu.ility of ihe deterrnin:i 
iiuns of underlying cause of death wa-; a.sscssed for 
ICU-'J codes 390-'i7O .^villlable nied:c,il records o, 
deaih ceniricatcs were reviewed for 138 of 162 men- 
bers of the chemical workei cohon and a rancon' 
sample (;i = 32) of the conL'cl cohort The review w;j: 
conducted by an independent p.ilholoaist who ■a.i.- 
bliudeJ to cohort membership, llie validity ot cancer 
death dcicrminations was reported earlier (6) 



Reference group 

An exicmal control cohort served a.s an unexposed 
reference group. Tlic importance cf includirg a ccm- 
parisod group stems from several coivslderaiiciis. First, 
while cheiiucal wor.kers wiih lengthy work durations 
in heavily conlamin.itcd production depanmenu arc 
probably classifijd coiTCctly with respect to PCDD/F 
exposure, workei^ with shorter durations or work in 
"low exposure" departments coiild be subject to a 
higher probability of nusclissificaiion. Second, there 
is a potential fni negative confounding within the 
cohort This is especially problematic wiio respect to 
cancer mortality, since exposure to other carcinogens 
had occurred in die low PCDD/F exposure groups 
Finally, ihe iiiclujion of unex[.)osed controls increases 
L'le power of the study. 

The reference group consisted of a cohort of work- 
ers from a gas supply company from the same region 
of Gerrr.any as die chemical worker cohort The con- 
;rol cohoit was formerly investigated by some of us 
toUcwing the same methods in assessing vital statu'-, 
and causes of death. This gioup had served as an 
inicmal rcfereiicr i;roup of "blue-collar w-irl^ers" in a 
cancer mortality study of coke oven workers (.W). The 
socicecononiK status of the gas worker and chemical 
worker cohorts is comparable. Tiie follow-up period 
for the reference group was set from 1952 to 19H9 A 
detailed description of Uiis referent cohort w,is re- 
ported elsewhere (34). No special exposure to 
PCDD/F IS kjiown to have cccurred. so each worker of 
Ih.e referent cohort wus assigned a PCDD/F leicl of 
^e.^o above Gennan backgiouiid levels 



Rif k estimation 

Reln;ivc nsks weic estimated witii yea.'-of-b:rth 
iiratified (5-year iniervuls) Cox regression, usiiv^ 
Seven exposure levels Ithe referent cohort, the rl^^! 
four quiniiles. and the ninth and lOih deciles ^r' the 
estimated TCDD levels and total toxic equivalencies' 
for the cherrucal worker cohort. Persons with unk'nown 
vital status were excluded from the a.'talyses Tests for 
trend were performed as suggested by Rothman (35' 
Tlic calculations were perfo-Tiied with the Statistical 
Analysis System (SAS) procedure PHREG 'lb). Be- 
cause of differences between the cohorts in the distri- 
bution of total duration of employment, age. and yesr 
a! wnich einploymeiil began. liie relative nsks we.c 
adjusicd for liiese covariates In addition, an internal 
companson within the chen'.ical worker cohort wa^' 
■perfoiinsd using Lhe two lowest quintiles with respect 
10 r(?DD and total mxic equivalencies as reference 
c.itegoiy. To assess tjie potentially confo-indtng effect 
of exposure to other carcinogens, a subanalysi? with 
regard to cancer monaliiy was conducted by excluding 
workers potentially exposed to dimetiiyl sulfate 

RESUlVS 
Exposure 

Results of regressions of PCDD/F levels on duration 
of work in each production department are given in 
tabic 1 for 190 chem'cal workers with blood/lissue 
determinations The Pearson correlation coefficient 
between model-predicted and measured TCDD levels 
was r -= 0.46 (p < 0,01) The duration of employment 
in the tnctiloiophenoxyacetic acid and tlic 2,4.5-tri- 
chlorophenol (before 1957) departments showed trie 



231 



11/29/95 14:45 ©eo? 770 8623 

1168 Flesch-Janys el al 



Schecter SUNY 



Qees 



TA8L£ 1. E«dmaled ywtly incfeaM (nfl/Vg of Wood tal) InTCOD* •ndTEQ- (wiihoulTCOD) levd» due 
to working tJm« In dl(t«ont production daparl/nenU: Hamtiurg, Cormany. 1952-1992 



PrnducUon liafaAtTmfi 



TCOO 



2.4.5-Trii:ilIoroph«noxyac€lJc add 

Tridilorophanol afler or during 19S7 

Tndiloroph«noI tMtefo 19S7 

AJpha docompositjon 

Trlchtofoboftians 

6rt)nr>oph06 

HaxacWorocydohexar^ synlhesii 

Undajv 

Formulation 

Manual workara 

Unskillod wortom 

Slam and trBntport 

Administralion and others 

OpialA (mcrphlno producbon) 



75.6 (56 0lo9S2)f 
39,1 (14.9 10 63.3) 

292.1 (139.3 lo 444.9) 
0.3 (-29.7 to 30.4) 

37.7 (-67.4 lo 142.8) 
9.9 (-19.0 10 38.8) 

Ib.3 (-13.4 to 46.1) 
S.8(-19.6l0Z7.2) 

13.8 (-25.1 to 62.7) 
12.3 (-2.9 lo 27.4) 
14.8 (-61.7 10 91.2) 
-4.2 (-30.8 to 22.3) 

2.7 (-16.2 to 21.7) 
-0.1 (-S7.0to 5«.8) 



8 5 (-1.9 to 18.9) 
14.5(1.4 10 27.5) 
34.0 (-48.8 to 116 8) 
57.4 (41,7 lo 73 2) 
39.4 (-16.9 lo 95.7) 

6.1 (-7 4 to 23.6) 
32(-IZ3lo 18.7) 

7.2 (-5 3 to 19.7) 
10.4 (-12.5 to 33.3) 
12.4 (4.4 lo 20.4) 
18.8 (-21.2 10 58.8) 

5 7 (-8.4 lo 19 8) 
1 3 (-9 3 lo 12.4) 
5 4 (-26.5 10 37.5) 



• TCOO. tetrachlorodibenzo-p-diaiin; T£Q. loric equivalerxaes ol polychlorir^ated dbenzo-p-dioxins and 
lurBTS. 

t Numbers In pa/enlhesaa. 95V. conrdence interval. 



strongest a.ssociatioiis with TCDD levels (75.6 and 
292.1 ng/kg/ycar. respectively). Work durations in the 
'/,4,5-trichlorophenol department in 1957 (when the 
production procedure was modified to reduce TCDD 
contamination) or later had a smaller effect (39 1 ns>J 
kg/year). The relation for manual work (12.3 ng/kg/ 
year) was of borderline sigruficancc. The estimates for 
other departments ranged up to 37.7 ng/kg/year (tri- 
chlorobeiizene), but the standard errors were large. 
This suggests that an intake of TCDD had occurred in 
the course of work in these departments, too, but tlie 
working times alone provide only imprecise estiniatcs. 
The negative coefficients for the store and transpon 
department and opiatf department cannot be inter- 
preted as the absence of exposure. 

For the higher chlorinated dioxins, a significant 
model fit was obtained with the exception nf the hepla 
congener. The significant correlations between the ac- 
tual and the estimated PCDD/F levels ranged between 
r = 0.17 for 1,2,3,7,8,9-hcxadioxin and r = 0.79 for 
1.2,3,4,7.8-hcxadloxin. A significani model fit for the 
furans was obtained for 2,3.4,7,8-pentafuran and all 
hexa congeners except 2,3,4,6,7,8-hexafuran. The cor- 
relation coefficients were in the same range as for the 
dioxins. Expressed as toxic equivalencies, the highest 
estimated yearly increase in toxic equivalencies (with- 
out TCDD) was observed in the thermic decomposi- 
tion department (57.4 ng/kg/year of toxic equivalen- 
cies) and the irichlorobenzenc department (39.9 ng/kg/ 
year). A yearly increa.se of 12.4 ng/kg/ycar of toxic 
equivalencies for manual workers was obser/ed. For 
the trichlorophenol dt-partmeni, since 1957 liic csti 
male was 14.5 ng/kg/year. The confidence mterval.-. 
for the other dcpaiunencs included zero 



These estimates were then applied to calculate tlie 
expected PCDD/F levels for each cohort member al 
tlie end of employment m tJie plant. Tlic duration of 
employment in each department was multiplied by the 
effect estimates for the respective departmenLs. This 
yielded a mean estimated TCDD level of 141.4 ng/kg 
(median, 38.2 ng/kg) for the cohort. The mean of toxic 
equivalencies (without TCDD) was 155 ng/kg (medi- 
an, 59.2 ng/kg), and the mean of toxic equivalencies 
including TCDD (total toxic equivalencies) wa.s 296.5 
ng/kg (median, 118.3 nj/kg). 

Mortality 

Table 2 summari7>es ilic mortality of die cohorts. 
Vital status was ascertained for 1,177 of 1,189 (99.0 
percent) male chemical workers and for 2.518 of 2.528 
(99 6 percent) gas workers. A total of 414 deaths were 
observed among the chemical workers. No intorma- 
tion on tlie causes of death was irvailable for five 
decea.sed workers. Thirty percent of the deatlis were 
attributed to cancer, and 18 4 percent were attributed 
lo ischemic heart diseases. Corresponding percentages 
in the reference group were 30 percent and 21.7 per- 
cent. The .sources for diagnoses in the chemical worker 
cohort were as follows: 34 7 percent from autopsy. 
33.7 percent from hospital reports, 25 percent from 
otiicr medical sources including death certificates, and 
6.7 percent from other nonmedical sources, including 
insurance records and infonnauon from family mem- 
bers. The corresponding percentages for the referent 
group were 29.6 percent fiom autopsy, 37 percent 
irom hospital records. 2(? 5 percent from other medical 
sources, and 15 1 peiccnl from othi-r tiopniedicjl 
sources. 



232 



11/29/95 14:46 0607 770 8623 



Schecter SUNY 2)006 

Uio«in. Cancer, and Ischeriiiu Heart Disftase 116' 



TABLE 2. Numbef of workeft, vital »Ulu«, and couset o( 
death: Hamburg. Germany, 1 952-1 9M 







Chemloj/ 


Cat 






war 


«jj 




\tiij 




No. 


T. 


No 


% 


Cohort aza 




1.189 




2,52B 




Vital status 












Known 




1.177 


99,0 


2.518 


99.0 


Unk/>own 




12 


1,0 


10 


04 


Vi';»l status 












Known 




1,177 


100 


2.518 


100 


AiiM 




763 


64 -• 


1.575 


62 5 


Oscsasod 




41<1 


35,? 


0J3 


37,5 


Cancar (ICO-9' 


codas 










140-208) 




124 


30.0 


283 


30,0 


All CVD- (ICO-9 codas 










390-459) 




157 


38,0 


459 


48.6 


IHD- (ICD-9 codoj 










41CV-I14) 




76 


18,4 


205 


21,7 


Other CVD 




ei 


19,6 


254 


269 


Other causes 




133 


32.1 


201 


21,3 



• ICO-9. InlamaioraJ ClassJIicalion otDiseasas, Ninlh Revision; 
CVD. cartiovascutar diaeaso; IHO. isohemic heart disease. 



The reliability of the study detcnninatioiis of (he 
cause of death was assessed by a second pad;.:' 'jr.i. 
The confirinalion rate for cancer deaths among chem- 
ical workers wa.'; 96,5 percent as reported earlier (6). 
comparable to thai for tlie referent group (99 percent). 
The ischemic heart diseases and cardiovascular dis- 
eases diagnoses among the chemical workers were 
confirmed in 77.8 percent and S5,l percent of the 
cases, respectively. Fn the referent group of ga,<; work- 
ers, the corresponding confirmation rates were 92.9 
percent and 94.1 pcrccrr;. 

Tables 3 and 4, as well as figure 1. summ.inie the 
estimated relative risks for the mortaluy outcomes 
under consideration. These Cox regression estimates 



used data from both the chemical worker and conini 
cohorts, Ttie loial mortality was elevated in all TCDL 
and idiiil toxic equivalencies calegoiies. re;4chin" 
relative risk (RR) of 2 43 (95 pciceni confidence °jn 
terval (CI) 1.80 to .V20) in the highest TCDD exposure 
group. 

In ihc ca.sc of cancer mortality, llie monntonic in 
crease in relation to TCDD is disr\jpled m the firs 
quiniile. While for the lowest TCfJU category a rcla 
live risk of 1,59 (9,=i peiccnt C! 1.01 to 2.51) was 
observed, the cstimaie for the second quintile wa5 1.29 
(95 pctccnl CI i' '5 to 2,22), increasing to 1 70 (95 
percent Ci 0-99 to 2,9.3) in the ninth decile and 3. 30 
(95 percent CI 2.05 to .5.31) in the tenth decile. The 
test for trend is highly significant. For total toxic 
equivalencies, the deviation from a m.onotonic trend 
was observed in ihe second category, but the panem 
and the magnitude of estimates are similar to those for 

Tcnn 

While Ihe associdlion is not a.s strong as that seen 
with cancer mortality, a cle.ir pattern of increasing risk 
of cardiovasculai diseases and ischemic hcan diseases 
moilalily across exposure categories emerges fhere is 
no evidence of increased risk in the two lowest TCDD 
qutntiles. The test for trend is significant for both 
mortality outcomes. The relative risk of ischemic heart 
diseases monality increases from the ninth decile 
(RR =- 1.61. 95 percent CI 0,S5 to 3.04) to the 10th 
decile (RR = 2.48, 95 percent CI 1,32 to 4.66). For 
tot: ' toxic c;;'iiv?;?nc!es. Lfie dosc-resp<.inse pattern 
with reg.ud to cardiovascular diseases and ischemic 
heart disea.ses mortality is more pronounced ti-.an that 
observed for TCDD alone 

Other cardiovascular diseases tnorlalily (nonisch- 
emic heart diseases) showed an increase in risk with 
TCDD up to the fourth quiniile, but the risk decrea.scs 
in the ninth and 10th deciles. The same holds for total 
toxic equivalencies. The risk of death (cn\i, causes 
other th.in cancer and cirdiovasculaE diseases -..howcd 
no dose-relalcd ir^r ' 



TABLE 3. HoIiUv* rl»k ol lolal, eaneef, CVD.- IHD.' other CVD, and oihor-cou.o m< 
divided Into decilos) of estimated TCDD- kjvols (ng/Vg ol blood lul) at tho end ol ojt( 
Icvetx ucing the ctihorl of gas worketi a< rcfafcnce: Hamburg, Germany, 1952-1992 



auon to quintilom (upp«r qulntll? 
a German median background 



0-2,8 

2,81-W 4 

U,5-<9.2 

48>-156.7 

1MiAO*«,(i 

3J4y-T.aS0;' 



1,0 

1.55(1.21 lo 1,90|t 

1 30 (CMIo 1 71) 
1.47 (1 Ulo 1.90) 
1.43 (1.15 to 1.91) 
I.-'.' (I'.OTIo l.eo) 

2 4'J (I 6'Jln TK) 



1 

159(' 01 loJSI) 
1.2n (0.7S1-J 222) 
1 60(1.03 1-. 2 60) 
1.60(1.02 10 2 5?) 
I./O (0 08 10 2.90) 
:. J4T.'<1S1.--^3I) 



1 .-itO.St I 
58 (l> 54 i 
1,35 to 91 I 



J3 (0 03 lo 2-1 

ril (0 4 1 lo 1 C 
Ill'OfSlori 
*•! (0 47 10 I ? 
» ' (0 U'j lo 3 c 



1 02 (0,S4 to 1 92) 
Ole (0,4UIO 1,0?) 

1 54 (0,90 lo 2 M) 

2 •-2 (1 5;io4,c.) 



1 U 

l,79(l,lo:oi7f) 
1 70(107 1=2.70) 
1 .T8 (O ee » 2.23) 
1 Oi 10 6-.' ^.' 1 <a) 
,.71 (0 31 Ic 1.63) 



O.iil 



' Nuinl-Mirs in pur-iii!i, ■<!■., 9b% con|l.*-^fH— "M.»rvy: 



o; rcDi;, (ctfpchli: 



11/29/95 14:47 ©697 770 8623 
1 1 70 Fleacli-Janys et al 



233 



Schecter SUNY 



deev 



TABLE 4. ReUUvethkotlol»l,cinc«r, CVD,- IHD," othef CVD, irxl o*«r.cauc» mort*lliy In relation to qulntJIa* (upp« cjulnS. 
divided Into <tf>cHm%) o( ••UmaladTOTTCQ* levol. (ng/kg ol Wood f«) at iha end of •xpo»ur8 abov* Gafman m^fian backgrour 
l^oia uaing tha cohort ol gat workera aa raferenca: Hamburg, Garmary, 1952-<S92 



axvneHrtiihn 


ToJi! miv1*l»y 


Ca.v*r 




(r;D 




IHO 




C4hm CVO 


CineicMtur 




1.0 


l.u 




1 




10 




1 




t.a 


I.O-t2J 


1«.(1 11 10 1 OJ)T 


1 3U (U lAI lO 


ifJI 


u j(Oi;io 


1 SO) 


1.(72(0.54(0 


1M) 


a< (0 40 1 


a 1.74) 


2i>«(li8 1o3. 


12 3-09 5 


I 39 (1 07 lo 1 81) 


1.71(107 10 


2/«) 


92 (059 10 


l.4«) 


086(0.51 k> 


1 as) 


91 (0.« 1 


al./5) 


1.70(lx»loi; 


SB 0-98.9 


li^ (1.20 10 1.97) 


1.50 (0^ lo 


2.42) 


1.43(1.01 10 2.1T) 


0S7 (0 52 10 1 81) 


2uS (1^ li 


= 3.36) 


1 a (0.99 lo Z.< 


CS 0-278.3 


1J*(1.W lo 1.74) 


1 M (I 00 lu 2 <3) 


lis (107 10 


2.24) 


1 13(0b4 10 


;iou) 


ao/ (I.-2' 10 J JOl 


ur2(ojsu>i- 


Z7BO-!iiCa 


105(IJ!Olo2 25) 


1.71 (OMlu 


2 94) 


1-U(1.0l 10 


2.64) 


1 73 (0 82 lo 


■JM) 


iia(o,/ji 


3.20) 


1-52 (u*l 10 2.: 


MO.i-<jai 9 


2^8(1 87 10 3 12) 


a.27 a.at 10 


5.2«) 


2 06(1^10 3.45) 


2 /2 (V4'J 10 4 9«) 


1.10(0.44 1 


3J6) 


i>4«(or2io3i: 


plor troTK] 


0.01 


<0.01 




<:,01 




<.3r ! 




0.iD 




02} 



* CVO, cardio\'<,v.ij!3r dui^awi; IHD, Isctiamic haart disaaaa; TOi ii^u, toxic equivatancias of poh/chlonnatsd cib0n2o-p<^3xjis t 
hjmn3. 

-f Numbars in pa/antheua, 95% conlidanaa Iniarval. 




1,000 



ill loi ,Lu Coneantrallon (ng/l^g) 



FIGURE 1 . Tolal. cjrcer, ischemic heart disease (IHD). and other causa mortality in relation lo quintiles (upper quintila divided into isc 
u( KjUinalad tolal lomc equivalence (TOTTEQ) levels abovo median German iMcliground levels using the c^rfiort of gas workers as referer 
Hamburg, Geiinany. 195^-19^2. 



Tables 5 and 6 s'low (he relative risks from calcu- 
lations using only the daU from the l'CUL)/F-exposcd 
cohort alone. In general, the esliiiiale.s were lower 
compared with the analysis including the referent co- 
hort, and the confidence intervals were larger, lotal 
mortality aiid cancer mortality are elevated in ihc 
highc-st TCDD category. For ischemic heart di.sease.s 
morLtlity, the highest nsk was also observed in the 
highest ICUU and loial toxic enuivjlencits exposure 
groups. The test ot ircnd is significant for ischctru': 
liean diseusr-s and tolal toxic equivalencies, indicjliii;; 



a dose-dependent relation. OtJicr cardiovascular d 
eases and other causes showed no dose-related paat 
in this analysis. 

The results of a second.'xy analysis of cancer mt 
talily addressing tlie question of potential confound' 
by exposure to dimethyl sulfate in the opiate dq^a 
ment arc preseuurd in table 7. Tne 149 workers w 
non/rtio employment durations in tliis departmc 
were exclude*! from tlie anslysis. Note thai ii mc 
pronounced dose-response pattern for TCDD and to 
to.^ic equivalencies is cbciincd. The r'ffc- c" catu- 



234 



U/29/95 14:47 ©607 770 8623 



Schecter SUNY @008 

Dioxin Cancer, and Ischemic Heart Disease 117 



TAaL£ S. Relaliv* risk of total, cancer, CVD,* IHO,' olhor CVD, and oth«-cau«o mortality In relation to quintilaa (upper quinfiu 
dlviiiwl Into dsciles) of acUmaied TCDO* lovclt (ng/Vg of blood tat) at ih« end of expoturo abova Girman madian background 
level* (chemical iworkare only, two lowott calcgorlei combined ac reference); Hamburg, Germany, 1952-1992 



14 S-40J 

4S3-IS0.7 
130 0-3*4 
DM.7-0.0»0^ 



I.Ub (U.UUID 1.3«)t 
0.94 (O.COlo 1.J«1 
0.83 (0.C7 to 1.19) 
1.4T (0 97 to 2.03) 



1^4 (0.73 Id 2 C8) 
1.02(0J9to 177) 
95(0 50 10 1 81) 
2.03(1.10 10 3.75) 



1.34 (0.05 lo 2.10) 
125(0 78 10 1.S9) 
1 10(0 S3 10 1.S2) 
1.28(0.87 10 2.48) 



1 r,;(0.5»to2.16) 
Oi«(OJl 10 1.41) 
1 18(0.50 10 2 41/) 
1.59(0 71 10 3.58) 



l.ba (0.B5IO2.B9) 
2 01 (1 0710 3.77) 
1 02 (D.4S lo 2.31) 
78 (024 lo 2. AS) 



78 (0^9 lo 1 J<) 
0.6S(0J<UH.1S) 
0/4/(02010 1.11) 
1J1 (0 6410 2^7) 



• CVO. cartiiovasojiar disease; IHD, Ischemic heart dioeas^; TCOD. lelrochlo-odibenjo-p-dioxin. 
t Numbers in pareniheiea. 95% conddonca inisrval 



TAOLE 6. Relalivs risk of total, cancer, CVD,' IHO,* other CVD, and ofhar-cauea morlaliry in relation to quintila* (upper qubtta* 
divided Into deciles) of eaUmalod TOTTEQ* leve4< (n^g of blood fat) at the end of exposure above German median back^ound 
levelt (chemical worker* only, two loweet categorlee combined as reference): Hamburg, Germany, 1952-1902 



TOTTKQ 
osncentralbn 


Taal monaiBy 


Career 


CVO 


IHU 


OfarCVD 


Other cauus 


1.19-39.5 
39 6-90.9 
99.0-278,5 
Z7oe-5452 
S4S3-4.361.9 

p lot trend 


1.0 

97 (0.74 10 1.29)1 
0.74 (0 &4 lo 1 08) 

92(0 6210 1.35) 

1 15 (0.77 to 1 74) 

087 


10 

0.88 (0.51 to \S2) 
0.78(0.44 10 1.41) 
0.85(0.4210 1.72) 
1-5«(0a0IO 3.01) 

32 


lU 

114(0 8510 2.13) 
1.18(0.71 lot.as) 
1.21 (0 68 10 225) 
1 40(0.71 10 2.78) 

0.05 


10 

0.85(0.41 10 l.rb) 
0.86(0.41 to 1.83) 
1.31 (0.57 10 3 00) 
1 89 (0 79 to 4 51) 

0.03 


10 

1.91 (1.03 10 3 57) 
1.52(0.7810 3.05) 
l.oa (0*310 2.72) 
0.78 (0.23 lo 2 JO) 

047 


1 

0a4(0i31o1JS) 
0.4O (020 lo OJBl 
90 (0.43 kl 1.S6) 
81 (034 10 1.S2) 

0.48 



• CVD. candovascului (Joeaae; IHD, ischemic h«ar1 dseas^; TOTTEQ. todc equivalen 
] Numbers in parentheses. 95% conlKjencs IntarvaJ. 



i ol polychlonnated dbanzo-p-diaiu^a and 



TABLE 7. Cancer mortality In relaUon to quintlles (upper qulntlle divided into docilae) of TCOD' 
and TOTTEQ" levelt (ng/kg of blood fat) at the end of exposure, excluding pertons from the opiata 
department (chemical workeis only. i«o lowett qulnlilos at reterenes): Hamburg, Germany, 19S2-1992 



TCOO 
CDOcenLrallon 


Canav 


Toneo 

Gonceriration 


CarKsr 


0-I4.4 

14.5-19.2 

49.3-1567 

158.B-<M4.6 

344.7-3.890.2 

p for trend 


10 

1.20 (0.66 lo2.19)t 
1.33(0.73 lo 140) 
1.15 (057 lo 2.30) 
2.28 (1.UI0 <.£?:■ 

tO.Ol 


1.19-39.S 
39.6-93.9 
99.0-278.3 
278.6-S4S.2 
545.3-4.361.9 

p lor trend 


1.0 

0.90(0.4810 1.67) 
C.91 (0.48 to 1.73) 
0.99(0.46 to 2.13) 
1.73(0.81 10 3.66) 

0,06 



' TCDO, tstrachiorodibenjo-p-dioxln: TOTTEQ, lone aquivaleneies of polychlortnalfld dbonro-p-dieilnj and 
ans. 
t Numbers in parentheses. 95% conlltJonce Interval. 



mortality of the highest 1(JUD exposure increased lo 
2.28 CXS percent CI 1 .14 to 4 59), and the lest for trend 
wa;; .significant. 

DISCUSSION 

The results of analyses using an external referent 
group revealed trends of increasing risk for total mor- 
tality, cancer niortality. and isclieniic heart diseases 
mnilaltly with increasing estimated levels ot TCDf) 
and total toxic equivalencies. For cardlova.'icular dis- 
eases other than ischemic tieart diseases and fur nun 



cancei/noncardiovascular diseases taken together, no 
dose-related trend was observed. However, signifi- 
cantly elevatej risks were observed for these outcoincs 
in some exposure categories. Deviations ftom the 
trend for total monality. cancer, and ischemic heart 
diseases occurred, especially in the lowest TCDD and 
total toxic e^juivalcncies categories, thus complicating 
the evaluation of r)\t analyses using only the PCDD/F- 
exposed cohort. I'his comparison showed a similar 
pattern of effects .icross exposure categories, but 
the effects were lo'v-r .-nH rh.- ra-nrl'J '.u"-" n.".' as 



235 



11/29/95 14:48 ©607 770 8623 

1172 l^lcoch Janys et al. 



Schecter SUNY 



eiees' 



markcd as m tlic analysis using an unexposed refci- 
cnce colmn. 

Till; subaimlysis of cancer monality controllhig for 
i.ucApusuic Id i!iiin;iliyl sulfaic iniJiCJie.s rli.ll devia- 
lions from (lie trend may be due Ui exposure lo olhcr 
carcinogcn.t 

Intormacion was no( available Ui assess possible 
confounding taciors tor ischemic heart diseases in ihc 
workplace, such as sucss related lo shifl work or 
exposure to some solvents (37). However, even in the 
inlcrnal compari>;on. the higllc.^^ risk eslimates for 
cancel and isclicinic liciin t^ist:asc.< wer* consl.';ten(ly 
(ound in the highesi exposure groups, and Ihe lesls for 
(rend remained significant or of borderline signili- 
caiiLc I'lJi cancer and ischemic heart diseases. Fuiihcr- 
mnrc, the rclaiive risk tor cancer monality of 2.03 ia 
the highe.si 'IC'IJI.'' group was significant. No dosc- 
rclaled trend was observed for all other causes com- 
bined. This does not necessarily imply (he lack of an 
effect of TCDD .ind total toxic equivalencies on other 
causes of death For example, we reported an elevated 
standardized monality rado for suicide in (he clieiiiical 
worker cohon with respect to the German population 
(6). 

The major strength of the present study is the avail- 
ability of a quar.Iilalive measure of exposure, which 
allows a direct estimate of dose-iespoiise relations. 
The exposure indicator is based on the relation be- 
tween work histories and blood or adipose tissue levels 
of PCDD/F froin .?bi)ut 16 percent of (he cohon. 
However, there aie scveial pulcnlia! .sources of error 
and bia.s in (his nieasuie thai rt.ust 1 - considered. One 
possible source of bias is the lack of taiidom sampling 
of the subgroup with fCDlJ/l- assays Bias in the slope 
of tissue TCDD regressed on the duration of employ- 
nieiit 111 a particuUtr department could arise, for exam- 
ple, if worl-'crs with long durations and ''iw TCDD 
levels were systematically undcitepresenied in the val- 
idation study. In order for such bias to induce con- 
founding between exposure and monality outcomes, it 
would be necessary that any bias in the exposure 
measure he related (o disease status (or other risk 
factors for early (norlality), indirect evidence that such 
selection factors were either not operative or were 
consistent over time stems from the fact that the pat- 
tern of effects of different c(nploymcnl duralinns on 
PC[)D/F levels changed li(tle from the analysis of ihe 
first ')2 workers examined (30) to the analysis pre- 
sented here for 190 workers. 

A second source of uncenainty in the expo.sure 
measure follows from the fact that the estimates of 
rCDD/F l'!veis at (he end of exposure (when employ 
nicnt in a dcp.innient endi:d) w.-ic derivcil from blood 
nu.isiircmriil.-, \i-.irs filer Con.N-'oucnllv. rh.- assi:-Tr> 



lion of firsi-order kinelic elimination is a potential 
source ol bias. II the kinetics are nol firsi prder. or the 
csliiiiule ol liail-lifc is iiiaccuiate oi inappropriate, 
(hen eslimalcs of lissue l-'CUlJ/F levels during expo- 
sure could be biased for workers with greater lengths 
of lime bi'.iween exposure and PCDD/P assays. The 
half-lives used were trom our own study (31), and they 
me 111 good agreement with estimates from other stud- 
ies (.18-40), especially tor TCDD. In order to a.s.sess 
the impact on results of alternative assumptions about 
half-lives and kinetics, wc conducted some sensitivity 
.'uialyses (dala iiul siiL .u. ^Ve did not find suhstaniial 
deviations from the results presented here on relative 
nsk estimates. The possibility of confounding due to 
bias in estimated exposure cannot be eliminated. How- 
cvei, the magnitude ot the observed relative risks at 
higher levels of exposure could only he explained by 
even stronger associations between bias in measure- 
ment and mortality risks. 

Ihe relation ot the different mortality outcomes to 
tile higher chloanatc^ '"'■jxins and furans was assessed 
by expressing the latter in terms of TCDD (oxici(y by 
(oxic equivalency factors. These have been derived 
from aniinal studies addressing different toxic end- 
points (carcinogenic, reproductive, immunologic, ter- 
atogenic (41)). Use of these toxic equivalency factors 
in the calculation oi the exjiosure parameters in our 
cohon assumes that these factors reflect (he toxic 
potency of ihe different congeners in humans and wiih 
regard to the endpoints under smdy. The similanties of 
liiC obs.:-.V(;d dose-response paitems lor 'I'CDD and 
total toxic equivalencies are consisleni with this as- 
sumption 

The known risk factors for ihc different monality 
outcomes under consideration could not be assessed 
on an individual basis in our study Potential con- 
founding has to be taken int^i consideration. Wuh 
regatd lo smoking, we pointed out earlier that the 
avail.ibic data on a subgroup of the siudy cohort indi- 
cated comparable prevalences of smoking m ihe two 
cohorts (73 percent prevalence for self-reported smok- 
ers and cxsmokers among chemical workers. 76 per- 
cent prevalence among gas workers (6)). In addition, 
for (he 4S0 chemical workers wi(h known smoking 
hisiory, (he correladon between smoking status (ever 
vs. never) and estimated TCDD levels was r = 0.065 
(p > (1.10). This small association indicate-s that 
smoking is unlikely lo have seriously biased tlic esti- 
mate of the relation between PCDDiT exposure and 
iiionalilY. 

With regard to isctiiMiiic heart diseases, other estab- 
lished sisk iaciors (serum lipoproteini, blood picssur;. 
diabetes, and f'ody mass mde\) could tx confounder 



236 



11/29/95 14-49 0697 770 8623 



Schecter SUNY 121919 

Dtoxin. Cane*', a"'^ Iscncrmc Mean Uceaae 1173 



strongly associated with aisignmeni tii jobs wiih 
higher PCDD/P exposure. While such a job iis.sign- 
mcfit process seenis unlikely, there is evidence frimi 
epidemiologic findings and animal models stiggesiing 
lh■^:. 5ome ri^k r'-C'.;rs for these ischcnic heail diseitsts 
III ly be impacted by PCDD/F exposure. Such effeci.s 
would conslitute a caus.^l pathway by which an impact 
of PCDD/F exposure on ischemic heart diseases mor- 
tality might operate. In order for the observed associ- 
ations between PCDD/F exposure and mortality to he 
due to confoiMidiiig, there would have to have been a 
strong .<;electioti proce.ss operating in which workers 
wjili increased monality risk foi other reasons wcri 
placed in high PCDD/F exposure jobs. 

The statistical analyses were performed using an 
exiemal cohort and the two lowest PCDD/h cjuintile.'; 
of the culiuit of chemical workeis as reference cate- 
gories. The strength of the internal comparison is that 
possible differences between the study and reference 
groups that could have affected tiie mortality (socio- 
economic .status, medical selection at the time of entry 
into the plant, health care) are min:rTi:7,ed. Tlic internal 
comparison is critical in two additional respects. I) On 
the one hand, the available blood levels showed that 
the internal reference group was not at background 
exposure to PCDD/F and that the potential for 
PCDD/F e.xpo.sure itf.sclassification was larger in the 
lower dose ranges, indicated by the large confidence 
intervals of the department-dcpcaJent exposure esti- 
mates (table I). 2) On the oilier hand, this cornparison 
could be biased by exposure to other substances, es- 
pecially carcinogens or suspected carcinogens, thai 
were associated with lower PCDD/F exposure. One 
such substance was dimethyl sulfate exposure in the 
opiate department of the plant where, if at all, low 
exposure to PCDD/F had occurred. As outlined in the 
subaralysis excluding workers from this department, 
the dose-response cuive for cancer mortality became 
more pronounced. Oilier substances of interest might 
have been ben7xnc and the tlifferent isomers of hexa- 
chlorocyclohcxanc. Exposures to these were highest in 
the hexachlorocyclohexanc and lindane departmcnis. 
for which low PCDD/F exposure was estimated (see 
table 1). The advantage of the cxtemaj comparison is 
that the baseline category consists of a cohort with 
only background cxposuie to PCDD/F and, besides 
exposure to bcnj.ene in a subgroup, also to other 
carcinogens. 

TTic socioecunomjc siams of both cohort."; is com 
parable, and both come from the same region. There is 
i:o indic.iuon that coin.paiiy medical selection or health 
-are differed t<twceii the cohorts. The standaidi/.-.d 
mortality ratio for tnl.il mortality tor the refereno* 
•-ohoit in relation to tiie p-.^pulation of me i-edcr'.l 



Republic of (jennany was 0.80 (95 percent CI 0.75 10 
U.XA), indicating a healthy worker effect. However, the 
standardised mortality ratio for all cancers combmcd 
W.IS 0% (95 percent Ci 0.87 10 1.06) (34). Thus. 
especially with respect to cancer mortality, u is rea- 
sonable to assume that the observed elevated relative 
risks lor the chemical workers could not be attributed 
to unusually low mortality in the referent cohort 

Other monality studies in the context of PCDD/F 
exposure have shown no consistent pattern with re- 
spect to ischemic hean diseases monality However, 
these studies have not incJMdcd detailed exposure- 
response analyses. Z^ihcr et al. (5) observed a slight 
elevation of deaths due 10 cardiovascular diseases 
(ICD-9 codes 390-459) Based upon only 24 deaths, 
they found a standardized monality ratio of 1.21 (90 
percent CI 0.83 to 1.7). In a study with much more 
power, Fingeihut et al. (4) reported a standardized 
monality ratio of 0.96 (95 percent CI 0.87 to 1.06) 
based on 393 cases No detailed exposure-related anal- 
ysis for ischemic heart diseases was reported. A study 
from the NetherKinds (42) found eight deaths due to 
myocardial infarction in a group of 141 workers ex- 
posed in a TCDD accident in 1963. Seven of these 
workers suffered from severe chloracnc. Otlier occu- 
pational monality studies have shown slight nonsig- 
nificant elevated nsks for arteriosclerotic h-an dis- 
eases (43) or no effect (44, 45). 

In the Seveso mortality study (46), an elevated stan- 
dardised mortaJity ratio was observed for all cardio- 
va.scular diseases (standardized monality ratio = 1.75, 
95 percent CI 1.0 to 3.2) and for ischemic heart disease 
(standardized mortality ratio = 2.22, 95 percent CI 0.8 
10 5.9) in the population of the most coniaminited 
zone A. In light of our findings, the speculation of the 
authors that the increa.sed ischemic heart diseuse.s mor- 
tality in Seveso may have been due to tJie stress of the 
.iccident needs to he reconsidered. 

It IS difficult to draw conclusions on the reaction of 
the dose-response curve in the low- to mid-dose re- 
gion This dil'lkuliy arises from potential exposure to 
other carcinogens and potential increases in mea.sure- 
inent errors in these groups. Future work with these 
data will focus on these issues. However, visual in- 
spection indicates that both the ischcnuc heart dis&ascs 
and cancer curves showed a sublinear form. The tests 
for trend were significant, indicating the presence of 
dose-related effects. For ischemic hean diseases mor- 
tality in the external cornparison, a numerical but 
nonsignificant elevation in nsk was obsf.rvablc at the 
lowest dose (about 100 ngfki>, of total toxic cguiv.-leii- 
cies). The elevation of cncer mortality v/as signincant 
or of bord'iilinc siJiiiiicaiice Lhrou-'hout the wlwle 
dose ra!;;e. While i;;- .- ■' 1 .^■• ;.:-h.--,i i'.- ■■■■• .^is--i< •< 



237 



11/29/95 14^51 
1174 Hesch-Janys el al. 



©607 770 8623 



Schecter SUNY 



eieu 



arc consi.sicni with a threshold moJel, (hose on cancer 
do not suggcil a threshold. 

In summary, ihe resiilis of this cohort study support 
the hypothesis of a dose-rclaled effect of PCDD/F un 
cancer ;;r.d ischemic hM.rl diseases mottah'.v. 'n fl"; 
caie ol' ciiicc. . uiesc findings refine the strong existing 
evidence of a carcinogenic effect of PCDD/F in hu- 
mans. In the case of ischemic heart diseases, there is 
.■lome evidence from animal models that TCDD may 
promote alheroscltrosij. and this lends credibility to a 
causal mteipreiation of our findings. However, the 
inconsistency ot findings across epidemiologic studios 
indicates the need for further investigation. Future 
morbidity .studies should address this question in 
greater detail. 



ACKNOWLEDGMENTS 

This study w.is supported by the Federal Ministry of 
Research and Teclmnlogy (grant 0IHK233)-, Pt^chrr.gu 
Ingclhcim Company; Employment Accidcnl Insurance 
Fund (Berufsgenossenschaft) of the Chemical Industry, 
Germany; and Ministry of Work, Health, Duci ^v^-, ,.,.airs 
of tlie Frci: and Han.scatic City of Hamburg 



REFERENCES 

I. Zeisc L, Huff IE. .Salmon AU, et al. Human risks from 
2.3,7.8-ierracliIorcxiihenzo-/j-<lioxins and hex.ichlorodibento- 
/7-dioxins. Adv Mod Environ Toxicol 1990.17:29.V3'12. 

2 Kimmig J. Schul? KH Bcruflichc Akjic (.sog. Chlorakne) 
durch chlorieric arom.iuschc zyklischc AJitr. (In Germaji). 
Dcrmatologica 1957;1 15.540-6. 

3. Bauer H. Schuiz KH, Spiegclbcrg U. Bcnjpiche Vcrgifiungcn 
i ■■ tier Herstellung von ChJorphcnol-Verbuidungcn. (Ir\ Ger- 
man). Arch Gcwerbcpathol Gewcrbe Hygiene 1964 18- 
538-55 

4 Fingcrtiui MA, Halperin WE. Marlow DA, ci al. Cancer 
morulity in workers exposed to 2,3.7.g-lclrachlorodibcnw-i7- 
dioxin N Engl J M«i 1991;199:212-18. 

5, Zober A. Mcisercr P. HuSer p. Thmy-fuur year mortality 
follow-up of BaSP employees exposed to 2.3,7.8-TCDD aitcr 
the 1953 accidcnl. Int Arch Occup Environ Health I'/W 62 
139-57. 

6 .Manz A, Berger J, Du/yer JH, et al. Cancer iDorlality «niong 
workers in a chemical plant contaminated with dioxin. Lancet 
1991,338 959-64. 

7. Dwyer JH. Resch-Jany.s D, Berger J, el al. Duration of occu- 
parionaJ exposure to dioxin-coniaminateil substances and nsk 
of cancer morrjliry. (Abstract), .^jii 1 Epidenuol 1992 136 
1018 

5 Moses MR, Libs KD, Crow J, et al. Health sutas of workers 
with past exposure to 2.3,7,8.tetrachlorodihenzo-p-dioiin in 
the manufacture of 2.4,5-tnchlorophcnoiyacetic acid, com- 
parison of findings with and without chloriCDc. Am J Ind Med 
1984,5:161-82. 

9 Suskind RR. Hen/Si-rg vr:. Human hralih effecti of 2,4. 5-T 

and iLs toxic contattunanls lAMA 1984,751 2372-80 
10 Roegucr RH. Wolfe WH. Michalefc IE, =t al. Air Force Health 
Study An cpidcmiologic.il investigation of health cffi-xts in 
All Foice personnel followinu cxjiosurc to hcrbicidts. San 



Anlonio. TX Epidemiology Kesearch Division, Arnmrong 
t-aboraiory. Human .Sysieins Division. Bruuk.', Air I'orce Ba« 
1991, (hiial repon). 

. Zober A, Oil MG. Mcsscrcr P Mortidily follow up study of 
IJASF employers exposed to 2.3,7,a-tci/achlorodibcn7o-p-di- 
ouii nXOD) after a 1953 chemical reactor incident Occup 
F-nviron McJ I994;.5I 479-86 

:. Benncr A. Edict L. Mayer K. er aj, Untersuchungsprogramm 
"Dioxin" der Berufsgenossenschaft dcr chenii.scJicn Indujlric, 
CrgcbnislK-jiJil— Teil II (In Gemian) Arbeiisincdujn Sou- 
almcdizin tiniwelliiicji/.in I994;29 2-6 

i Manin JV. Lipid abnormaliuc. m workers exposed to dioxin 
Bt J Ind Med 1984,41 254-6 

- Jennings AM. Wild 0. Wai-d JD. et al. Immunological abnor- 
malilici 17 years alici atcidcnial exposure to 2,3,7,g.ieua- 
chlorodiben7.o-p-dioxin Br J Ind Med 1988.45:701-4. 

I- Jaiising PJ, Korff R. Dioxinhelasiung und GcsundJieits- 
sturuiigcn — eine Uniersuchung 2.3,7.8-TCDD-cxponJcrtcr 
A/beitjicliiiicr, (In German) Zent/albl Arbcitsaicd I99'2;42r 
-19'! 7. 

i. Calvert GM. Wille K. Sweeney M. zi al DviJuaiion of seiuiu 
Lpid euuccniraiions among (J S workers exposed to 2,3.7.8- 
teuachlorodibenio-p-dioxin. Presenterf al Ihe 13th Interna- 
tional Symposiuhi on Chlorinated Uioxins and Related Com- 
pounds (Dioxjn '93). Wien. Ausuia, .September 1993. 
Wolfe W, Michalck !, Miner /. et al Diabetes versus dioxin 
body burden in veterans of Opciauon Ranch Hand. Orgino- 
halogcn tJompounds 1992,10 279-82. 

. Sweeney MH, Homung RW. Wall DK. et al. 2.3.7.8-Tctra- 
chlorodibenzo-;).dioxio (TCDD). related increase in diabetes 
and scrum glucose levels in wor*.cr5 exposed to TCDD-con- 
uminalcd chemicals. Pcrscnted ar die 12th International Sym- 
posium on CliJonnatcd Dioxins and Related Compounds (Di- 
oxin '92), Tampere, Finland, August 1992. 

. Kociba R.I. '.'.cyis DO. Beyer TZ. .■: al Resuhs of a rwo-year 
cluoiue toxicity and oncogenicity snidy of 2.3.7.8-leliachloro- 
dibcn7o-p-dioxin in rats. Toxicol AppI Pharmacol 1978.46 
279-3U3 

Kociba RJ. Keyes DG. Beyer /E c: al, I^ng-term toxicologic 
smdics of 2.3.7. 8-teirachJorodibenzo-;7-dioxin (TCDD) in lab- 
oratory animals Ann N Y Aejd Sci l979;320:397-4Ot. 
Kelhng C^ . Nfenahan LA, Peictson RE, Effects of 2.3.7,8- 
teUachlorod;benzo-;3-dioxin treatment on chemical functjoa of 
the rat heart Tosicol AppI Phamijcol 1987.91:497-501. 

. Canga L. Rjfkind R. Heart as a Lugct organ in 2.3.7,8- 
tetrachlorodihen7o-p-dioxin toxiciry dcctcascd P-adi^enefgic 
responsiveness and evidence of increased intracellular cal- 
cium. Proc NaU Acad Set U .S A 1988.85 905-9. 

. Hcrmansky SJ. Holcslaw TL, Murray WJ. el al. Biochemical 
and functional effect of 2.3,7.8-tetiachIorodiberio-p-dioxin 
on the hcans of female rats. Toxicol AppI Pharmacol 1988; 
95 175-84 

. Brewster DW. Bombick DW, Matsuniura F. Rabbit serum 
hypertnglyce.-idemia a/lcr adirjr.istnlion of 2,3,7.8-tctracljlu- 
rodibeiizo-p-dioxin. I Toxicol Fnvi;-on Hcilth 1988;25- 
495-507. 

Swift LL, Gasicwicz TA, Dunn GD, et al. Characterization of 
tJic hypcrlipiucmia in guinea pigs induced by 2,3,7,8-ietra- 
chlorodibenio-p-dioxin. Toxicol AppI Pharmacol 1981:59: 
■)89-9-;, 

Schiller CM, Adcock CM. Moure Ra. ct al Effect of 2,3.7.8- 
tctrachlort>dibcti20-;3-dioxjn and fasung on body weight and 
lipid parameters in raLs. Toxicol AppI Pharmacol 1 985:81: 
356-fil 

Jovanovich L. Levin S. Khan M. Significance of tnircx-causod 
hypoglycemia and hyperllpidcmu in rats, J Biochem Toxicol 
1987.2:203-13 

Reich-Jaiiys D. Berger I. Maiiz A, ct ,il. EnrwickJung eincs 
quanuLiuvcn F.xposiuonsindikatcrs fur die Exposiuon gege- 
ntlbcr polychlomtcn Dibcnzo-Diox:r,cn und Furancn und 
Sch.lt'ung iler biolugischcn Haibxtrts;-eit in cincr epiderai- 
ulo.;i'.chcn B^riifskJ-bs siu.^ie (■ ■ G,-.rr-.r.i t '. ■-■■•'- "• 



238 



11/29/95 14:52 ©607 770 8623 



Schecter SUNY a 012 

Oioxin, Cancer, and Ischemic Heart Dis«ase 1 175 



umcuie Epidemiol I9M;25:20-3I. 

29. B«:k H. Eckan K. Malhar W, « al. Uveh of PCDD"s and 
PCDr'8 in adipose (issue or oeeupaliuitally ciuusoJ workers. 
Chemojpherc 1989;18:507-16. 

30. Flcsch-Janys D, Berget 1, Konieuko .' t al. Quanoficalion of 
exposure lo rlioz:n5 and furaju in a cohort of a herbicide 
f,.-,iu.,-.;ii plaiil in Hamburg. FRG. Chemosphere 1992;ZS: 
1021-8. 

31. Flcsch-Janys D. Gum P, Jung D, ei al. Firsl rcaulu of an 
inveiligation of Uic elimination of polychlorinalcd dibenzo-p- 
dioxins and dibenzofursns (PCDD/F) in occupaiionally ex- 
posed person.'!. Dioxin '94. Organohalogen Compounds 1994; 
21:9>-9. 

32. Papkc O, Ball M, Us A. PCDD/PCDF in humans. 1 1993 
'.:pd.ite of backgr-iind data. Cbejnojphere 1994:29:2355-60. 

33. Rat dcr Sachversiindigen fUr Umwcltfragen. Umwcll- 
gutachien 1987. (In Cennan). Stungarl: Verlag W, Kohiham- 
mer. 1988. 

34. Berger J. Majiz A. Cancer of the stomach and the colon- 
rccluni ajiioiig wuilier^ In a coke gas plant. Am J Ind Med 
1992;22;825-34. 

35. Rolhrnan KJ. Modem epidemiology. Boston: Little. Brown 
and Company. 1986. 

36. SAS Institulc, Inc. SaS software. Cary. NC: SAS In.stitute. 
Inc. 1994. 

37. Krislcasen T. Cardiovascular diseases and ihc work 
environment; a critical review of the epidemiologic literature 
on chemical factors. Scand J Work Environ Health I989;15: 
245-64. 

38. Ptrklc JL, Wol/c WH. Paltcrson DG. ct al. Estimate.^ of the 
half-life of 2.3.7.8-lctrachlorodibenxo-p-dioun in Vietnam 



veterans of Operation Ranch Hand I Toxicol linviron Health 
1989:27:155-71. 

39. Wolfe W, Michalck J, Miner 1. et al, Dioxin haU-Ufe in ■ 
veterans of Operation Ranch Hand. Organohaiogen Cocn* 
pounds 19'J2:10:239-')2. 

40. N.--';:5.i II. CJcrthoux PM. Pailcrsnn DG Jr. a al. Half.|,fe 
of 2,3.7.8-ie(tachiorodjb6rzo-p-dioxin in scrum of Seveso 
ndults. inlcriin report. Dioiir) '94, Orgjnohalogcn Compounds 
1994:21 Rl-S 

41. Ahlborg UG. Brower A, Fingethut MA, et al. Imp»a of 
polychlorinated dibcn7.o-p-<Jioxin.^. dibenzofurans. and byphc- 
nyls on human and environmental health, with special empha- 
si.s on appilcaiioii of the toxic equivalency factor coiicept. Bur 
J Pharmacol 1592;223:179-200. 

42. Daldctup I,M. Zcllcnraih D. Dioxin exposure: 20 year follow- 
up, (Letter) Lancet 1983:12:1134 

43. Zack JA. Gaffey WR. A mortality study of workers employed 
iit the Monsanto Company plant in Nirro. West Virgmia. In: 
Tuckes RJ;. Young AJ,. eds. Human and envitoomcDlal mSa 
of clilunnaled dioxins and related compounds. New York: 
Plenum Press. 1983:575-91. 

44. Ou MG, Ol.tnn RA. Cook RR, et al. Cohort monaTity study of 
chemical workers with potcotial exposure lo higher chlofi- 
nau!d dioxins. J (Dccup Med 1987;29:422-9. 

45. Bond GG, McLaren EA, Lipps TL. el al. Update of raottalily 
among chemical workers with potential exposure to higher 
chlorinated dioxins. J Occup Med 1989,31:121-3. 

46. Bertazzi PA, Zoccheni C. Pesaton AC. et al. Ten-year mor- 
tality -<:tudy of the population involved in the Seveto inindent 
in 1976. Am J Epidemiol 1989.129:1187-200 



239 



Dow Brand Dioxin: 

Dow Makes You Poison Great Things 



Edited by Jack Weinberg, 

Contributors include Joe Thornton, Charlie Cray and Bill Walsh 

Assisted bv Bonnie Rice and Katherine Schultz 



240 



— launched a new trade group, the Chlorine Chemistry Council, to handle public relations, 
political lobbying, and "scientific initiatives" on all issues for the chlorine industn,' From its origm, 
the CCC was a Dow-led effort The Council's first managing director was Brad Lienhardt. a 
career-long Dow employee 

According to Chemical and Engineering News, the CCC's estimated 1994 budget was SI2 
million In-kind contributions to the CCC-led effon from member companies was estimated at ten 
times that amount This put the estimated 1994 resources of the CCC at over SI 30 million [Hirl 
1994] 

The CCC made its muscle apparent it published a thousand-page "scientific" repon, 
prepared by consultants which rex'iewed the ioxicolog\' of a wide range of organochlorines and 
concluded that chlorinated organic chemicals can not be regulated as a class, and that as currentl\- 
used, they are safe for health and the environment Some consultants who helped prepare and 
review this report were respected academics who subsequently became vocal critics of 
environmental groups and agencies seeking to phase-out or restrict chlorinated chemicals 

The CCC contracted with public relations firms and hired its own public relations staff In 
1994, 11 got an opportunity lo flex political muscle when the Clinton White House proposed that 
EPA conduct a study of the environmental and health impacts of chlorinated organic chemicals 

The CCC immediately expressed "outrage" It generated, by its own estimate, a million 
letters to Congress CEO and other senior officials were instructed to contact a long list of 
representatives, cabinet members, and executive branch appointees The CCC sought to generate 
hysteria by mischaracterizing the proposed study as "EPA's Recommendation to Ban Chlorine " 
[Lienhardt 1994] 

Dow wrote to all its customers and requested that they and their employees write to the 
President and Congress and oppose an> stud)- of chlorine [Sosville 1994] Dow told the press and 
Its employees that EPA planned to "ban" chlorine and that Dow's Michigan division, "which 
employs about 3500 people, doesn't have replacement products in mind should chlorine be 
banned " [Henze 1994] 

Dow CEO frank I'opolTmischaractenzcd the proposed stud\' as "EPA is trying to ban an 
element on the periodic table " |Popnff I994| CMA ofllcials met with cabinet members and 
secured a "moderating statement " L'ltimatelN, Congress ancl EPA failcc' to act on the proposed 
.study 



4 4 The Dioxin Reassessment Undermining Science at EPA 

In 1994. EPA scientists released the long-awaited draft of their Dioxin Reassessment This 
document was prepared o\'ei the course of three vears b\ scientists at EP.'K. the National Institute 



241 



of Environmental Health Sciences, and other agencies, was reviewed by numerous expea panels 
durmg the drafting processes, and was aired in pre-draft form at public hearings in several cities 

The document concluded that dioxm was an extraordinarily potent environmental 
hormone, caused a wide variety of toxic effects, and that background exposures may already be in 
the range at which health effects can occur The authors of EPA's report also published the 
majority of their findings in peer-reviewed scientific journals and books 

Dow and the CCC moved immediately to undermine EPA's alarming findings CCC 
organized a public relations push, and EPA public hearings in Washington on the reassessment 
were dominated by the CCC's hired scientific consultants The main thrust of the Dow/CCC 
olfensive, howe\er. centered on the EP.\ Science Advisorv' Board, which was slated to review the 
draft reassessment 

The SAB held one meeting to receive public comment testimony consisted of a fifteen 
minute presentation by a single environmental group and thirteen presentations by industry and 
its consultants, for a total of 3 hours and 40 minutes The CCC and its consultants made several 
separate presentations at which EPA's conclusions were attacked in the most strident tone 

More significantly, the chemical industry's inftuence extended to members of the SAB 
panel, the group given the task of drafting the SAB's review of the Dioxin Reassessment's 
chapters covering health risks associated with dioxin in the environment. Two individuals stand 
out William Greenlee, a Scientist then at Purdue University, and John Graham of the Flarvard 
Center for Risk Analysis 

Observers close to the review process have identified Greenlee and Graham as the two 
members of the SAB health panel who most actively and consistently challenged the validity of 
the dioxin health risk conclusions contained in the EPA Report Greenlee and Graham were the 
pai'.c! members who pressed most vigorously and eftectively for an outright rejection of the risk 
characterization section of the report Were Greenlee and Graham truly objective reviewers'' 

Durmg an SAB meeting in .May. 1995, panel members were asked to disclose research 
grants in dioxm-relatcd fields The transcript shows that Greenlee stated 

I'm Bill (j/ccniec from Purdue ll/uvcrsiiy In addition lojundingjrom Mil. I 
haw rccciwd research \iraiiisfrom the American l-oresi Paper Association and (ieneral 
I'.leciric, and I've also received gi/ls /or research from ( liemical Manufacturers 
Association and Dow ( liemical. [ECR 1 995] 

The descriptive term "gifts tor research" is highly unusual. Why does Greenlee distinguish 
these from his "research grants " Records from the Purdue University School of Pharmacy and 
Pharmacal Sciences describe grants from Dow and CM.-\ to Greenlee as having been awarded for 
a "dioxin research program" for the period JuK I, 1994 through June 30, 1995 [Purdue, 1995] 



242 



These grants amounted to S45,000 from Dow and 575,000 from CMA Greenlee's 
"dioxin research program" also reportedly received 565,000 from the American Forest & Paper 
Association (AFPA) during the same period [Purdue, 1995] 

in addition, Greenlee received a 1993-9-'1 grant from the AFPA for 5973,800 to study 
"Development of a Biological Basis for Dioxin Risk in Humans [Purdue 1994] In a private 
conversation with editors of the newsletter "Waste Not," Greenlee confirmed he had administered 
grants to study dioxin for several million additional dollars from the AFPA prior to his tenure at 
Purdue 

AFPA is the industry organization serving as the primary representative of pulp and paper 
manufacturers opposing regulations and legislation to cunail dioxin emissions from mills that 
bleach with chlorine-based chemicals CMA (together with its subsidiary', the Chlorine-Chemistn,' 
Council) is the industry- organization serving as the primary representative of the 
chlorine-chemistr>' industry on dioxin-related matters Dow Chemical is probably the world's 
largest root source of dioxin Greenlee's history of service to these organizations helps explain a 
strangely candid comment in the transcript of the SAB panel's May meeting Commenting on 1 

"ver\' personal questions about our own biases," Greenlee said "Those of us for whom dioxin 1 1 
supports our family, sometimes we keep looking for problems that aren't necessarily there because | 
it puts food on the table " [ECR] 

John Graham serves as director of the Harvard Center for Risk Analysis In the month 
prior to the SAB meeting, Graham's Center organized a high-profile conference on drinking water 
u.iu health risks, "financed by a grant from the Chlorine Chemistry Council and the Chemical 
Manufacturers' Association " [CCC 1995] Graham's Center has also received unrestricted grants 
of flinds from Dow Chemical in the years 1 990, 1 99 1 , 1 992 & 1 993 In addition, his Center has 
received unrestricted grants of funds from several other companies with a strong interest in the 
outcome of EPA's Dioxin Reassessment including CIBA-GEIGY, DuPont, GE, Georgia-Pacific, 
Hoechsi-Celanese, ICl. Kodak, Monsanto and Olin 

Individuals like Greenlee and Graham, whose careers are enhanced b\' their ability to raise 
large sums from dioxin-interested corporations should not have agreed to participate on the health 
panel They should have recused themselves to avoid the perception of a conflict of interest 
Instead, both vigorousK' participated in the work of the panel intervening at e\'er\ occasion to 
challenge and downpla\' EPA's characterization of health risks associated with dioxin 

At the time of this writing, the S.AB panel's repon is not yet complete (though a final draft 
will likely be complete by time this report is released) The likely final product will be a consensus 
document that makes no one happy On the one hand, scientific evidence presented b\' EPA 
linking minute levels of dioxin in the environment to potentialpublic health injun,- is so 
strong it is unlikely effons by panel members such as Greenlee and Graham to uiterls discredit 
EPA conclusions will prevail On the other hand, by the nature of consensus, strong 



20 



243 



disagreements on the panel will likely be reflected in language that muddies the EPA's conclusions 
and helps lay the basis for further delays in taking action. 

As such, Dow and its chemical industry allies will have achieved another victon. Deiav 
and confusion have always been primarv' industry goals This is the third EPA dioxin 
reassessment in 10 years, and the existei.ee of an on-going reassessment has been used as an 
excuse for making no decisions in the interim Each new study has been undertaken at the urging 
of the chemical and paper industries 

The chemical industry made us "delay by studying" strategy clear at a CCC strategy 
session held in 1994 The newspaper In These Times obtained the notes of a guest at the 
meeting 

The speakers acknow/eJi^'ed iliul indiislry is vulnerable in heiiii^ re^ulaied because 
"Jioxin can go in any Jireciion " as a public relations issue. People don't have a had 
idea of chlorine, but they do about dioxin. We were cautioned to "downplay the 
connection. 

We were also warned that chlorine customers are very concerned about 
chlorinated hydrocarbons that contaminate the environment and act as estrogen 
mimickers that disrupt the body v glandular .system. We were advi.sed to respond to 
questions with long-term scientific predictions — 10 years in the future — that cannot be 
verified. They .said USA Today in particular cannot resist such predictions. And they 
advi.sed. "If you ever come acro.ss re.search that is negative, just talk about the need to do 
more research and study the i.s.sue. [Bleifuss 1995] 



244 

n Institute for Agriculture and Trade Policy ^§"612-379-5980 1^12/6/95 04:31PM Ql/ 



December 6, 199d 

Honorable Dana Rohrabacher 
House of Representatives 
Washington, DC. 20515 ■ 

Dear Mr. Rohrabacher, 

Regarding the December 13th hearing on EPA 's dioxin reassessment by the Subcommittee on 
Hnergy and Environment, we would like you to adrl :: ■ eral key witnesses (see attached list) to the 
Subcommittee's current witness list. 

As you know, dio.xin has become a major public health and environmental threat, for which the 
scientific evidence, including that presented in the form of EPA's rlio.an reassessment, is 
unassailable. For example, the revievv committee of the Science Advisory Board "signed off on 
the issues of greatest concern to the American people. The review committee agreed with the EPA 
that: 

• Dioxin is a probable human carcinogen. 

• Dioxin harms the reproductive and immune systems and impairs normal child development at 
extremely low levels of exposure. Dioxin exposure is associated with endometriosis, decreased 
testosterone levels and sperm counts, glucose intolerance, immune system suppression, infertility, 
birth defects and other serious health problems. 

• Dioxin is more toxic than virtually all other compounds the EPA has studied. The margin of 
safety between ex[ v>;"urc and health effects is smaller for dioxin than for other chemicals. 

• The American people are being exposed to dioxin through the lcKid we eat every day. The 
consumption of d^iiy products and meat contribute over ninety percent of the average daily intake. 

• Dioxin comes from human-made sources like incineration, paper and PVC manufacturing, and 

the production ol chlorinated pesticides and other chlorinated organic compounds. 

What is abundantly clear to those of us who have followed environmental health regulation over 
the last 20 years or so, is that if dioxin had been a product, it would have been banned years ago. 
However, because dioxin is an unwanted by-product of man\' chemical, industrial, and waste- 
disposal processes, doing anything meaningful about it requires taking on the huge lobbying 
power of those special interests. Thus, even though the pollutant is in our food, in our tissues, 
,tnd in mothers' breast milk at levels at which we should anticipate effects in animals, including 
primates, we see still more attempts to obfuscate the need for significant acti' n in this matter. It is 
highly regrettable that the legislati\e prcx-ess has been tainted by such blatant contlicLs ot interest. 

The Sul\;ommittee's current list of non-governmenud witnesses is composed exclusi\ely ot 
individuals whose scientific integrity is c..:ui^'."o,i!i,-;.:i! by the funding of lieir work by dioxin- 
polluting inilustnes such as incinerator, chemical and pulp and paper corporations. 

In this light, there is no defense of a hearing on this subject that does not adequately rellect the 
views of the v;tft majority of the scientific community and indiv idual citizens w ho li\ e in 
communities affected by dioxin 

Suiely the Subcommittee intends to present the best thinking of the scientific community on this 
important subject. .As currently structured, this hearing would serve the narrow interests ot certain 
corporate polluteis, to the tletriiiient of [lublic health and science itself Congress should not be 



245 



Institute for Agriculture and Trade Policy 



'gf 612-379-5980 



|j]12/G/95 04:31PM Q 2/5 



seen as staging "witch hunts" on behalf of its campaign financien; against the exhaustive science 
upon which EPA's reassessment is based. 

If any hearing is to be held, it should be on the protracted and unnecessary' delays that have 
plagued the completion of this reassessment, which was originally commissioned under the Bush 
Administration in 1991 and was scheduled to be completed by the fall of 1993. 

In an effort to bring this hearing more into balance, we have attached a list of many qualified 
experts who would make excellent witnesses on this issue. We would like to discuss this list with 
you and/or your staff, as soon as possible. 

Thank you for your most serious consideration of this matter. 

Sincerely, 



Rick Hind 
Greenpeace 
Washington, DC 



Jackie Hunt Christensen 

Institute for Agriculture & Trade Policy 

Minneapolis, MN 



Charlotte Brody Dr. Paul Connett 

Citizens Clearinghous for Hazardous Waste Professor of Chemistry 



Falls Church, VA 



Terri Swearingen 

'Iri-State Liivironmenlal Council 

Chester, WV 

Stormy Williams 

California Communities Against Toxics 

Rosamond, CA 

John Pruden 

National Citizens .Mliance 

Ossineke, MI 



Wendy Gordon 

Mothers & Others for a Livable Planet 

New ^'ork. N^' 

Peter Washburn 

Natural Resources Council of .Maine 

.•\ucusta, ME 

Joe Thornton 

Center for Environmental Re.<*arcii and 
Conscr\ aiion, Columbia University 
New ^'ork, NY 

Alicia Culver 

Government Purchasing Project 

Washington, DC 



St. Lawrence University 
Canton, N"\' 

Aionzo Spencer 
Save Our County 
East Liverpool, OH 

Keith .\shdown 

Cancer Prevention Coalition 

Chicago, IL 

Denise Lee 

Anson County Citizens Against Chemical 
Toxins & I'ndcrground ?;o;agc 
\\'adesboro. NC 

Fiances Dunham 

Citizens Against Toxic Exposure 

Pensacola, FL 

Br\ony Schwan 

Women's \ oices for the l-.arth 

Missoula, MT 

Theresa Mills 

Parkridge Area Residents Take Action 

Columbus, OH 



.\nn Hedges 

Montana Environmental Information Center 

Helena. MT 



246 



["3 Institute for Agriculture and Trade Policy ^^ 612-379-5980 



12/6/95 04:31 PM 



Daniel Rosenburg 

U.S. Public Interest Research Group 

Washington, DC 



Kim Phillips 

Midway High School Parent-Teacher 

Association 

McGregor, TX 



Lorrie Cotterill 

Groups Allied to Stop Pollution 

Wilmer, TX 



Ellen Connett 
Editor, Waste Not 
Canton, NY 



Nina LaBoy 

South Bronx Clean Ajr Coalition 

Bronx, m' 



Richard Schweiger 
Community Nutrition Institute 
Washington, DC 



Jane Williams 

Desert Citizens Against Pollution 

Rosamond, CA 



Elmer Savilla 

Partners in the Environment 

Mount Vernon, VA 



Marti Sinclair 

Adans tor a Clean Environment 

Ada, OK 



Corinne Whitehead 
Coalition tor Health Concerns 
Benton, KY 



Carol Dansereau, J.D. 
Washington Toxics Coalition 
Seattle, WA 



Barbara Mohon 

Gulf Coast Environmental Defense 

Gulf Breeze, FL 



Joan Garrett 

Lehigh Valley Coalition for a Safe 

Environment 

Nazareth, PA 



Craig Williams 

Chemical Weapons Working Group 

Berca, KY 



Liz Crowe 

Kentucky Environmental Foundation 

Berca, KY 

Sue Pope 

Downwindcrs At Risk 
Midlothian, TX 

Joanne Almond 

Stanly Citizens Opposed to Toxic Chemical: 

Albemarle, NC 

Michael Gregory 

Anzona Toxics Information 

Bisbee, .AZ 



Linda Lett 

Citizens United and Aware for a Safe 

Environment 

Midlothian. TX 

Bill Freese 

Huron Environmental Activist League 

.Alpena, MI 

Greg Karras 

Communities for a Better Environment 

San Francisco, CA 

Neil Carman, Ph.D. 

Lone Star Chapter of the Sierra Club 

Austin, TX 



Scott Scderst, im 
Great Lakes United 
Ann .Arbor, Ml 



?arah Barnard 

Montanans Against Toxic Burning 

Bozeman, MT 



LaNelle Anderson 
Channeh iew Citizens Against 
Environmental (Contamination 
Chann Kicw, TX 



Phyllis Glaser 

M(.)tlicrs Organized to Stop Environmental 

Sins 

Winona, T.X 



247 



^ Institute for Agriculture and Trade Policy ^^612-379-5980 1^12/6/95 04:31PM Q 4/S 



Alisa Gravitz 
Co-op America 
Washington, DC 



Beatrice Taggart 

Citizens Opposed to Polluting the 

Environment 

Holbrook, M\ 02343 



248 

[^ Institute for Agriculture and Trade Policy ^"612-379-5980 1^12/6/95 04:31PM 



Rolcn(iulJWitncss(-sJorDtctmhciJ.2ihJi«iuingj:>n_!!Sdi;aUfLi,Jnlegrilyjiiii^ 
Mandates: Ca s e Study 3 -- HPA's Dioxin Reassessment 

Dr. Linda Birnbaum, the EPA scientist most responsible for writing "Chapter 9" of the dioxin 
reassessment. 

Dr. Richard Clapp, Director of Center for Environment Health Studies at the Boston University 
School of Public Health and member of the S.A.B panel that recently evaluated the reassessment 
for the EPA. 

Dr. Arnold Schecter, of the State University of New York at Binghamton and the first scientist 
to document dioxin in human tissue and food, on whose work the reassessment is, in part, based. 

Dr. Paul Connetl, Professor of Chemistry at St. Lawrence University who has worldwide 
experience documenting the dioxin hazards posed by waste incineration. 

Dr. James Dnyer, of the University of Southern California, School of Medicine who has just 
coauthored an article in the America Journal of Epidemiology showing "a strong dosedependent 
relation between mortality due to cancer or ischemic heart diseases and exposure to polychlorinated 
dioxins and furans" based on a study of more than 1,100 chemical workers. 

(Ret.) Admiral Elmo Zum«alt,.Jr., former Chief of Naval Operations, a major participant in 
government efforts to study dioxin containing Agent Orange with additional expertise in 
selecting panels of scientists who are not funded by or agents of dioxin-producing companies. 

Lois Marie (Jibbs, a former resident of Love Canal, New 'I'ork who has just written a book 
Dying From Dioxin. and who also heads up the Citizens Clearing House for Hazardous Waste. 

II for some reason an> of liicsc people are not available on December 13th, we would be happy to 
recommend other equally qualified experts for this hearing. 



249 



THE VIAlL STRgET JQJJRHKL WBDNSSDAY, JULY 19. i<»S 



-■•^n:' 



Letters to the Editor ^^ 



EPA*s Dioxin Review 
ts ^cience, Not Policy . 

I inamccnied tboui (|i« portnytl M .■ 
BPA tcton UlKAllimi E. KcU/s Jtfw » 
.cdtteriahpt|« pUee 'OeanlRf Up E7A'f .. 

' nwuQMr'alniceuntcventonalvtat ' 
OwRUielciieeAdvlsbnrBotrdluiMid' ^ 
•taut JM MVKjr'f dnft 4talA rMHur -* 
' iDut nlatf tM poloL TTte tPA ««icon« - ' ,, 
(Ite i»d9Qi Rftew oT'lU tfteicta Rpoft u 

■ Mrt a( « conl(m4n{ cflort to bmln Om • 
lyil raace afideiitAc ofilnlon In reacMnf 
Hi ooadufldM. fiovrrcr. bi nqr viev, Kb-. 

' prRMtiitf far iiM wUnr to ratte mcb 
nufh feAetmaMt trtirn the baud lM> pot 
TOi, eooQiatod a (kttt of Us npoct ¥*^>^ ; 
In' crtttdxlac Qw raacscaaNQt-'i'tt. ■ 

. ftolty nAqr. lb. Kcilr ifaia teismlBbiiiji 
point-lMi ■ k id«sUac utoaMit.'M ■ ■'; 

' • ttfvhUityMfftiigiCSbeiMBi TtettnTM ''' 
Um nm batt ttw aUrUHi(K*ib»llwi / 
agtaer, amtv^og ttkiKf vUkfnc^i 

■ Mart aecWoBt. • • •-' "^ - -*-*:-••-- ■ 

CDqtrvjr to (tM uiUwr'f kiMrtiaa; r^ 

- search (km •! die SPA is idtntlQeiUy .' 

eraflbte,' R b Mbj«c(ed to' i ufle ptnd w . 

Ki«vle««iKlttIftn4ttMadesla(nnh 
r otiJedfVet. lO. Kdly tuentf tW 
becxae the BPA hu « rested bttCRSt Is"^ '. 
leetdtlinc^iggela^ tt bis eoatprooiind its 
■dadlOc Msfrny. nnt, ttie b wTMf to 
tsj tfait *iiiKab or BPA's flawed potUao 
oa dfonas has taeo bised on inteml re- 

~mrdL* WhBe dw Q>A hu beea u intar 
asdsosl lesder ia oertiln «reu o( dioKii) 
tesein^ ttielflOfryaf* aaalysii toduded 
peoifnflewed BUnbov from nwadt he - 
KotldiPKittof wnc&vuBotpcrfbmtdbj ! 

; llttKPA.tccgad,uy}ntorestede6i«vtr ' 
of BPA aeknee vigaid faww tlist Ibt peer 
revtew prooats he* befn Oie (ooK cf bh 
(erne KruOny bitenwitit ti the EPA ler 
U>e JM tiefet>iftar».Mdtb«tthe>fBety 
b'ltracljr veqistttod to utiRf pesfe 
riewed cdanoe, totb Ms mrn «J«1 fnm olh- ■ 
cts, la its «nt^n«i. TUrd. the dkola u- 
icsimcia has boan eiatiwlaiy of aa epen 

'fad paiticUalo^ cdentiQe proeeH, In- 

' vdlTWtlHDMccds of tdeitdsts trao Mdie 
of (he aeeqcjr. It has r(ce|T«d pnbe Horn 
mwr4UrtettnUiatr«f«rd;Iatttotato- - 
fcrro} Qoi all Qkm sdeoUsU <haif the 
•aimMasMdrtCttistocTottjMttvwT • * 

. : tb«)tTsa»«<^»ehBf«tabbtocn>- 
^«MI pardd^ko hr the 'tdetg nc' 
condMutt^ri tod^cadeot peer tertevoC * . 
'evvbtfewdtipcniaadcenUmiiBf pAite . 
tnvuifuuc&t lo 4|r pnocM i^eaeid thp.'.: . 
beat my cCdatot |b> aweiimeptt. Xnan: ■ 
ei^oos vfn «f»M that th« SPA'S deetr.^ ' 

imsiDp(o(a0t9i(taeJieal(liiiidUif|B4; ' 

• . . Ba8WJ.HlJXlW.P8i).' 
AssbtaM Adatabtnter . 
f^ Rcfearch and OcreicpaNat;.' 

.' En*lTonment«t Prnforilnn Arwrv 



250 
SAB Chair Response to Wall Street Journal Article on Oaain 

JuJy 6. 1995 

Mr. k^ed Ciabb 
Lett in to tbe Editor 
WaJ Street Journal 
200 Liberty Street 
Ne4york.NY 10281 

De^r Mr. Crabb: 

As Chair of tbe EPA Science Advisory Board (SAB) revie* commitcee for ffA's Dioxin 
Reassessment Review, I was disappointed at ihe nish-to-judgmcnt article that uppe^ad in the Wail 
Sin et Jouiual of June 29 under the byline of Kaihryn E, Kelly and headed ■CIcanin^Bp EPA's 
Die !un Mess.' Ms. Kelly's characterization of the SAB panel's assessment of tbe Eft document can 
on! I represent her owa speculation and preconceptioos, since the SAB Commiitce hs not yet come 
(o f nal consensus judgments. Also, ber cbaracchzauon of comments by iodi vidua! Konibers of the 
SAP panel are not consistent with those made during the panel's deliberations. 

While many of the oral comments of members of tbe SAB Comniiitee M the neeling and 
many of their written comments in the draft report, currently in preparaiion. ore crilkal of the EPA's 
rea ^sessment document, many othcn were quite complimentary of EPA's erforis to aake a full and 
bal inccd tepott. Furthermore, much of the new and valuable infomaiion has come bom EPA\ own 
res wch. EPA should be commended for the weil-targeted research th^t it has publiiked in (he peer- 
tty iewed scientific literature on this inoportant topic, and Ms. Kelly'» mischaractcrizabon of this 
research as policy or politically driven is misguided and misleading. 

The solution to the dilemmas arising from costly reguialioos in the absence of adequate 
sci^ntinc knowledge lies in more research of the kixxl Ms. Kelly attacts. not in le<ss. 

Finally, if EPA really wanted to iMih to regulate Dioxin sources in the ehv'uwuncni. it would 
noi have bared ita soul (and warts) before an SAB review panel in open session. Based upon my 
pa ;i experience in comparable reviews of documents on environmental tobacco smoke and criteria 
air pollutants. EPA will carefUIly consider the forthcoming SAB review conunentary and prepare an 
im proved dioxin reassessment that will provide it with a firmer busi.s for any regulatory decision.s 
thft it may eventually make. 

Very tivly yours, 

/signed/ 
Morton Lippmann. R».D. 
P.'ofessor 
New York University Medical Center 



251 

Appendix II — Correspondence 



^v^EDSr,, 



!> #^ \ UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

I ^^1/^ ? WASHINGTON, D.C. 20460 



MAR 2 T 1996 



OFFICE OF CONGRESSIONAL 
AND LEGISLATIVE AFFAIRS 



Honorable Dana Rohrabacher 

Chairman 

Subcommittee on Energy 

and Environment 
Committee on Science 
House of Representatives 
Washington, D. C. 20515-6301 

Dear Mr. Chairman: 

This is in response to your letter of February 14, 1996 to Dr. William H. Farland, Director 
of our National Center for Environmental Assessment, containing 1 5 questions concerning the 
Agency's mercury study. The questions appear to be based on the external review draft of the 
Mercury Study Report to the Congress made available in December 1994. 

The Report is now undergoing extensive interagency review under the auspices of the 
Office of Management and Budget. It is expected to be finalized in time to be made public on or 
about April 15, 1996, as required by court order. The comments of all interested Executive 
Branch agencies are being addressed and the Report being revised. Until this process is complete 
and the Report is final, we will not be in a position to respond to your questions. We will do so 
upon completion of the Report. 

In the meantime, if we can assist you in any way, including a briefing on the Report 
development process, we would be glad to do so. 

Sincerely, 

Ly^e M. Ross 

Director, Legislative Division 




252 



U.S. HOUSE OF REPRESENTATIVES 

COMMITTEE ON SCIENCE 

SUITE 2320 RAYBURN HOUSE OFFICE BUILDING 

WASHINGTON, DC 20515-6301 

(202)225-6371 

Imeinei SCIENCE@Mfl HOUSE GOV 



Febnaary 14, 1996 



Dr William H Farland 

Director for the National Center for Environmental Assessment 

Office of Research and Development 

U S Environmental Protection Agency 

401 M Street, SW 

Washington, DC 20460-1101 

Dear Dr Fariand 

Thank you for your excellent testimony before the Subcommittee on Energy and 
Environment on December 13, 1995 regarding EPA's reassessment of dioxin 

Enclosed are some additional questions submitted by Congresswoman Barbara Cubin 1 
would appreciate receiving your responses by Wednesday, February 28, 1996. The 
information will be included as part of the official printed record of the December 13 
hearing Please forward this information to the Subcommittee office, B-374 Rayburn 
House Office Building, Washington, DC 20515 to the attention of Ms. Jennifer Disharoon, 
Staff .Assistant 

Again, thank you for your valuable contribution to the hearing. 

Cordially, 



Dana Rohrabacher 

Chairman 

Energy and Environment Subcommittee 



DRjId 
Enclosure 



253 



Questions to William H. Farland, 

Director of Health and Environment Assessment 
US EPA 

During vour testimony on December 13, you indicated certain procedures would be followed to assure 
that fiiture studies submitted to Congress by EPA would be based on a process that would result in an 
"open, participatory environmental health assessment." 

The following questions concerning the EPA'a mercury report to Congress are submitted in view of 
this commitment. 

1.) The EPA computer air model used to predict the fate and transport of mercury in the 
atmosphere results in predictions that greatly overly exaggerate mercury deposited in the 
environment. EPA model results are high by a factor of 10 to 100 based on actual field 
observations. For example, EPA's predicted high-end range for mercury m fish due to 
atmospheric mercury is 14 times higher than the highest levels actually found m fish (26 ug/g 
versus 1.8 ug/g). In fact, levels of mercury m fish actually swimming in a concentrated 
discharge of mercury waste were lower than the levels of mercury predicted by EPA's model 
for fish generally. 

1 A.) How has EPA resolved the problems with these flawed computer models? 

IB.) How has EPA validated the fate and transport models for mercury emissions? 

2.) EPA's model is based on non-peer reviewed, multi-media modelmg, with seemingly no 
validation from field data. Industry would not be permitted to use the EPA model in 
submitting applications for permitting facilities, yet EPA uses the model indiscriminately 
EPA recently changed the air quality models from the model (ISC3). The ISC3 model 
continues to have some of the same problems in overly exaggerating deposition of mercury as 
COMPDEP. 

How has EPA resolved the problems regarding wet and dry deposition so that the 
computer model does not overly exaggerate mercury deposition concentrations? 

3.) There is a significant body of information on the actual mercury content offish, within 
EPA and at various agencies. It should be relatively easy task for EPA to validate its models 
by comparing the model results to real life EPA itself has acknowledge that the models used 
by the Agency overly predict concentrations actually found m fish swimming near sources of 
atmospheric mercury. 

Given EPA's admission that the models used are inaccurate, what steps are being taken 
to validate each model and each assumption used m the models? 

4.) EPA's modelmg of impacts of deposited mercury on surface water runoff carrymg this 
mercury into lakes and streams does not seem to mcorporale even the latest models used by 
EPA's own water quality staff 



23-557 0-96-9 



254 



What are the models used by the EPA's water quality staff and how do they differ from 
the models used in the Mercury Reports to Congress. Most important, why do they 
differ? 

5.) Do the FDA, NIEHS and the EPA agree on an ADI or RPD for methyl mercury where 
e?cposure is from consumption of ocean fish? 

6.) A respected scientist, Dennis Crump analyzed the data from the Iraqi incident used in the 
mercury report and concluded that it supported £m RED about eight times higher than that 
determined by EPA How do you account for such a significant difference in interpretation of 
the same data? 

7.) EPA's projection offish consumption rates is based on a three day dietary study which 
shows about 30 percent of the population eating fish in the three day span in which almost all 
data points represents a single meal. 

8.) What assumptions are made to e.Ktrapolate this mformation to a daily input over a long 
enough period to be relevant when comparing it to an RED which by definition pertains to 
lifetime exposure? 



9.) The NIEHS Report on Mercury (January, 1993) recommends a study is needed to confirm 
the mercury developmental toxicity threshold predicted from the fraq studies. NIEHS 
recommends the study confirm the mercury threshold for the U.S. population (or an analogous 
population) the consumes methylmercury in fish. Does EPA agree with this recommendation 
and, if not, why not? Do the Seychelles Island studies fulfill the NIEHS recommendation? 

10 ) EPA has based its assessment of the human and environmental effects of mercury on 
short term, massive exposures to mercury or methylmercury. How are studies such as the 
Seychelles Islands study of chronic, long term exposures to low levels of methylmercury 
through fish consumption consideration by the Agency? 

11.) EPA previously calculated reference doses for methylmercury chronic toxicity and for 
methylmercury developmental toxicity. These references doses are associated with woman of 
reproductive age and children and adults (other than woman of reproductive age). Does EPA 
intend to continue treating methylmercury toxicity in this way? If not, why not? 

12.) The draft Mercury Report to Congress presents only one calculated reference dose that is 
applied to the general U.S. population as well as sub-populations of potential special concern. 
This represents a change from previous EPA documents thai present two very different 
reference doses. How is this apparent change in assessing methylmercury toxicity justified? 

13.) In the June, 1994 EPA "Guidance for Assessing Chemical Contaminant Data for Use in 
Fish Advisories - Volume II Risk Assessment and Fish Consumption Limits" EPA states: 

"Although these are numerous developmental toxicity studies available, the 
doscresponse results are not consistent due, in part, to the variety of endpoints which 



255 



have been evaluated. Additional studies are needed to identif>' a NOAEL based upon 
sensitive developmental toxicity endpoints." 

What new studies did EPA identify in 1994 or 1995 that overcame the limitations of previous 
studies to allow the determination of a new NOAEL and reference dose? Why were these 
studies better than the previous work used in assessing methylmercury toxicity? 

14.) TTie 1993 NIEHS Report of Mercury points our problems in making accurate estimates 
of United States fish consumption with available sources offish consumption data giving 
inconsistent estimates. How did EPA estimate fish consumption by the general U.S. 
population and special sub-populations? How were the problems identified by NIEHS 
overcome? How do the estimates offish consumption used by EPA for the Mercury Report to 
Congress compare with other estimates if fish consumption? 

15.) Preliminary reports from the Seychelles Islands study indicated that there were no 
adverse health effects found relative to the maternal hair mercury levels that were found, how 
does this finding compare with the conclusions reached by EPA in the draft Mercury Report to 
Congress? How will EPA determine if the Seychelles Island and Faroe Islands studies justify 
a change in the conclusions reached in the draft Mercury Report to Congress? 



2S^ 



MIKE DOYLE 
COMMITTEE ON SCIENCE 



1218 LONGWOHTM Building 

Washington, DC 20515 

(2021 225-2135 

DISTRICT OFFICES 



Congress; of t\)t Winittti States 

i^ousc ot iRepreSEntatibes 



541 Fifth Avenue 

McKEESPOBT. PA 15132 

14121664-4049 



December 11, 1995 

Mr. Paul Sutton 

Chief, Homeless Veterans' Housing Programs 

Division of Veterans' Programs 

101 Eggerts Crossing Road 

CN340 

Trenton, New Jersey 08625-0340 

Dear Mr. Sutton: 



I understand that you have been in contact with the Democratic staff of the House Committee on 
Science with regard to the December 13 hearing on the U.S. Environmental Protection Agency's 
(EPA) Dioxin Reassessment, and that you intend to submit testimony on behalf of the Viemam 
Veterans of America (VVA). 

As the only Member of Congress to serve on both the Committee on Science and the Committee 
on Veterans' Affairs, I am especially concerned as to how this issue impacts our nation's veterans. 
I am anxious for the Science Committee to hear from the veterans' community in assessing the 
dioxm issue, and am hopeful that Admiral E. M. Zumwalt, Jr. will appear at the December 13 
hearing on behalf of the Agent Orange Coordinating Council. Knowing of your expertise and 
experience in this area, I think the Science Committee would benefit from your input as weli. In 
that regard, there are some points pertaining to the Dioxin Reassessment that I hope you would be 
able to address in your testimony. 

The VVA's interest in the relationship between Agent Orange and dioxin exposure with the health 
effects experienced by those who served in Vietnam is clearly understood and widely recognized 
by Members of Congress. I am confident that a majority of Members are supportive of both 
continued research on the health effects of Agent Orange exposure, and compensation for illnesses 
resulting from it. However, I think that there may exist some confusion about whether VVA and 
the Agent Orange Coordinating Council have an interest in the contemporary scientific and 
regulatory issues associated with dioxin. In order to clarify this issue, please respond as to 
whether your organization is involved in issues relating to dioxin exposure through incineration, 
pulp and paper production, and other industrial activities. 

I am aware that the VVA has been an advocate for research into the short-term and long-term 
health effects of Agent Orange exposure. Are there areas of research related to dioxin that VVA 
feels are important in understanding the contemporary issues associated with dioxin? If there are, 
how do you feel that the results of these studies were adequately addressed and incorporated into 
EPA's recent dioxin reassessment effort? 



257 



Mr. Paul Sutton 
December 11, 1995 
Page 2 



If you can provide a response prior to the start of business on December 13,1 would be pleased to 
present it at the hearing for inclusion in the official record of the hearing. The fax number for my 
Washington office is (202) 225-3084. 

I thank you m advance for your consideration and wish you and your family a happy holiday season. 
Sincerely, 




(a^ 



Mike Doyle 
Member of Congress 



MD:pmc 



258 




'12/95 TUE 15:04 FAI 809 561 7604 VETERANS' HAVEN 

Vietnam | Veterans of America 

1224 M Street. |jjW, Washington. DC 20005-'il83 

Tdf phiwc (202) 628-2700 • Gcnenil H«i (202) fi28-5»Kn • AUvnCilcy Hi (2( !) (i:«Ji'J<)7 - I 



@002 



Inc. 



^ Not-ForFrnfit Vfleranx Service Organization Ouiriercd by the United Statea Conifres^ 
I "WA, At Work in Your Community" 



12 December 1995 



SEM T VIA Ff A TO: rj >02l ajfi- 
TJ 

r 

w. 



You 
cor 



r letter 
jcrninq: 



Member of Congress 



The Honorable Mike Do^le, 

nited states House of Re resentatives 

218 Longworth Buildirg 
Washington, D. C. 20515-3 



3f 11 pedmber 1995; 

iearings - EPA Reassessment of Dioxin 



DJear Mr. Doyle: 



s positij 
issues 

WAV 
to our 



nuj erous 



ati 



Thank you for your letter and interest in VVA 
relative to contemporary scientific and regulatory 
associated with iioxin exposure. Let me assure you that 
position is ^at these issues are of great concern 
membership and tie leadership of WA because of 
environmental ha lards existent in American society 
membership and tie representatives of the National 
Coordinating I Cou tcil, on which I sit as a represen-. 
are unanimou^ in pppi^sing any dilution of the drafi 
of dioxin that has been circulated bji EPA over '^he 
years . 

■V^VA ijas ;been actively involved in contempoij-ari 
pnd regulatory issues such as opposition to the cor s 
municipal incinerators, incineration of dioxin cont a 
residues at Jacksonville, Arkansas, advocating for 
paper and has been (an active participant in the' Citizen's 
Conferences on Dioxin. The third such conference will convene 
Baton' Rouge, Louisiana in March 1996. 



today . Ot 
Agent Orange 
ive fo^ WA, 
reassessment 
past two (2) 



scientific i 
struct ion of' 

minat^ 
chloririe-free 

in 



sJe 



At our Seventh National Convention this past Aigust, WA 
created an 'Environmental Hazards Subcommittee to ad iress these 
contemporary matters. As art attachment, I am includ .ng copies of 
Resolutions enacted at that! convention which serve is policy 
statements for WA on this Issue. 

I 1 ^ 

Areas of research in wllich\ WA believes resources should be 

directed include dioxin disposal methods and manufacture of 
alternatives to dioxin that will alleviate the danger of exposure 
to living humans and to those as yet unborn to these toxic 
substances, thereby significantly reducing future birth defects 
commonly associated withithe parent's exposure to, dioxin. From 
the document^ provided by EjPA, it does not appear |that attention 



259 



12/12/95 TUfe 15^04 FAI 609 561 7604 | VETERANS' HAVEN 

The Honorable Mike Doyle, J^ember of Congress 
United States House of I|ppr,esentatives 
12 December 1995 
Page 



i]003 



was paj 
out ovei 



I 

id rto this sort of 
er Jthe past 15 - 20 



research, much of which has been carried 
years, both by industry and government . 



our 
concern 



Thank you for your interest in this issue and for asking for 
perspective on this matter which should be of paramount 
ern to all Americans, veteran and non-veteran cAike. 



Our best! wishes to you and yours in this Hoi id y Season 




LM 1351, Vice-Chair 
Orange/Dioxin Committee 



:PLS 

Attachments 

cc: George claxton. Chairman 

Catherine M. Greene, Vice-Chair 



Hary'j. Schoelen, National Qffifce Staff Liaison 



260 



12/12/95 TUE 15:05 FM 609 581 7604 
I 
WA 1995 Convention Resolutions - 



VETERANS.:. HAVEN . -_®-QP-'» 

Agent Orange/Dioxin Committee 

\ 

I I 



DIOXIN DISPOSAL METHODS 

AO-6-95 

Issue: 

Disposal and storage of dioxin-contamin^ed materials and sedimeints can have a direct health impact on 
all citizens of this country. 

Background: 

Ocean dumping of conjaminated materials can directly impact on the food chain, leading to ingestion of 
dioxin-laced fish, fowl, etc. In addition, unrestricted disposal of dioxin-contaminated materials in 
landfills can affect ground water reservoirs and aquifers. Incineration of these materials maw result in 
release into the atmosphere of potentially hazardous substances. Proper and safe disposal musjt be used 
in dealing with dioxins, WA must remain knowledgeable about sediments and related factors and 
support necessary research to guarantee minimal health risks to the community. 



This resolution reaffirms and updates 
P'osition: 



solution AO-9-93. 



\. 



Vietnam Veterans of America, Inc., at nation^ convention iryHouston, Texas, August 15-20, 1995, 
opposes ocean dumping of dioxin-contaminated materials and calls for immediate termin^on of this 
practice. WA supports research on existing methods of disposal or storage of dioxin-cJntaminated 
sediments and stands ready to work with all concerned scientific and ecological groups to ensure proper 
disposal or storage of these contaminated sediments. 



.KOSEAN-^'ET ERAf ' isI AGENT ORAfJGJE/IH OXIN 
HEALTH CARE AND COMPgNSATIOCL- -^ 



AO- 



Issue: 



American veterans wcre>exposed to A^nt Orange/dioxin while serving in the Republic of Korea and no 
action has been takcr^ by tm>lJ.S/govemment 

III 
Background: 



Veterans who servptfin Korea still feel t 
birth defects ipnheir offspring. The 
Orange/diojrin issue for aijy veterans. 
Orang^/^oduct Liability lawsikit, know I 



pffecis of exposure such a^ ( 
government has 
Korean veterans 
MDK38I, and plaint ff 



LTesolutTon reaffirms Resolution AG- 



cers, unexplained illnesses, anc 

;redibly dealt with the Agent 

not involved with the Agent 

vleterans did not agree with the 



261 



12'lJe/9^ TUE 15:05 FAI 609 56^ 76% 

VyA 1995 Convention Resolutions - 

I 

- — PotjBjbt"' 



VETERANS' HAVEN ' ®0°5 

' Agent Orange/Dioxin Committee 



. — O/irtji nm V' Llf JUlu^ ot A nienca 
- — -T^tTfiff^^—^'Vf cg g _ ^ - 
gov^nmeuHbr reseaj=eh^d com] 




ition in HougonJiiJmvAuewf ' TJ^?e7^i995r a^es 
najjinnal le aflffr5fiip"7irv VA W J|)))ly-prestnTE~fo all branches of 



It r^efyiffp-in-thgTt 



mY-Amencaijuvcterans^xposed lo Apent Q iange^di&x 
'iffn presumptive exposure. '^^^^ ~~ ~ 



)REN'S HEALTH CARE 
AO-«-95 



issue: 



There is no health care or compensation provided to veterans' chile 
birth defects, deficiencies, or other disabihties resulting from 
Orange/dioxin and other toxic chemicais while in military service. 

Background: 



ren pnd future generations who have 
their parents' exposure to Agent 



I While the healtn-car^ and compensation needs of some veterans affected by exposure jo Agent 
Orange/dioxin are beiiig met by the Department of Veterans Affairs (DVA) and through impleincntation 
of P.L. 1102-04, services for veterans' children bom with defects or learning disabilities associated with 
their pafents' cxposurq to such chemicals have been ignored by all segments of the governmei it. 

This resolution reaffin|is and updates Resolution AO-3-93. 



Position: 



Vietnam Veterans of America, Inc., at nati9nal convention in Houston, Texas, August 15-20, 1995, 
supports a comprehensive health-care and special-needs program to assist Vietnam veterans' children and 
subsequent genprations who have birth defects, deficiencies, or disabilities reasonably associated with 
parental exposure to Agent Orange/dioxin and other toxic chemicals while in military service. 

I L I __ I I 

» — -3teEf ¥- ORANGE/DltM Bffn'ffiTW6^r I 



Issue: 



Cl 




262 



12/12/95 TUE 15:06 FAX 809 561 7604 | 
' WA 1995 Convention I^csolutions — 



VETERANS' HAVEN 



Agent Orange/Dioxiii Committee ■ 




•pfiy^^f^ipnmrti ti HUH iMVff peti l ite uii t lu. luviuw |um.l who jia allcgpfljnki Ye 




T Aj-fpfi-|y prnnnnll^ ■Mv4-^.TjTTnT< l^f ^ geffl' OrgnEe/dtOMB-aettt glk. 



papermakingImanufacturing processes 



Issue: 



AO-10-95 



Promoting the elimination of dioxins intrc uced into the environment from papermaking manufacturinj 
processes should be an'objective of j/ietn: n Veterans of America, Inc 

Backgroimd: 



The use of chlorine in the papen 
which arc released into the envira 



pg industry's bleaching processes has been proven to create dioxin; 

Inment. In recent years, concerned with their role' and theii 
responsibility to help protect the entironment, a segment of the| papermaking industry has worked tc 
develop and market "chlorine-free" Ipap^r. The term "chlorine-free" is applicable to two different 
processes. Most widespread is theprocesscaJled "elemental chlorine-free" paper which does use chlorine 
in the process, but does not contribute to di )xins as a by-prodoct. Today, "elemental chlorine-free" paper 
comprises about 60-70% of the print paf ;r market. A small but growing segment of the industry has 
gone one step further. It has developed a id markets a "total chlorine-free" paper which is totally free 
of chlorine in the manufacturing process. Total chlorine-free" paper now makes up less than 1 % of the 



263 



12/12^95 TUE 15:08 FAI 809 581 7804 



WA 1595 IConvention ResoIutio||s - 



VETERANS' HAVEN 



Boo? 



Agent Orange/Dioxht Committee 



print paper market. Both types of *chlorine-ftee* paper arc available and cost about 10-25% moie than 
paper thai is not 'chIorine-&ee. ' 



Position: 



Vietnam Veterans of America, Inc., at national convention in Houston, Texas, August 15-20, 1995, 
commends those segments of the papermalnng industry who are engaged in research and developme nt 
of alternative manufacturing processes to eliminate the fiiither introduction if dioxins into tlie 
environment, especially those papermalcers who have gone 'the extra mile'yin developing aiid 
manufacniring "total chlorine-free" paperi and, in siq)port of attaining a dioxin free environment, WA 
shall take all necessary measures to maximize the use of paper products utilized and consumed by VV A 
that are manufacnired using the "chlorine-free" processes and WA encourages its State Coimdis aid 
Chapters to do likewise. . ' 

BAN THE MA>fUFACTURING, SALE, AND USE OF 2,4-D 



Issue: 



AOll-95 



) 



For at least SO years the Department of Del ense has intentionally exposed military persomie] to potential y 



During the war in Vietnam, when, herbicides were used 
iql were not aware of the toxicity of the chemicals used. 



dangerius substances, often in secret, 
d^foli^ dejise junglei our military pers( 

A^ a result of exposure to 2,4-D in vAnam, veterans are bemg diagnosed 20 years later with ra e 
cancers, sarcomas, immune defici^nciesnnd Central Nervous System disorders Children of exposi d 
veterans arc bomlwitt( learning disabilities, birth defects and deflcibncies 

Today, herbicide 2,4-D is being used for weed control across the United States; at National Cemeterie ; 
school yards, golf courses and hospitals. It is used by utility companies, die D^artment of 
Transportation and railroads. Additionally, 2,4-D is being used by farmers whic^ in turn is 
contaminating food crops, cattle, pigs, /chickens, etc. In addition, 2,4-D is being used to |eliminate the 
growth of plant life in our lakes, therepy contaminating our freshwater and saltwater fish. 

•iTo date, approximately 240,000 veteirans have died from diseases caused by exposiirc to Agent 
Orange/Dioxin and the number climbs e^ery day. The continued use of 2,4-D today further exposes our 
famines and chile^ren to the same fchcnwal our veterans were exposed to in Vietnam, llus exposure 
jeopardizes the health of our famil », (^ildrcn and future generations, making them susclptible to the 
same diseases our veterans are dyii g fr< 

Background: 

Vietnam Veterans are acutely aware oil the deadly consequences of exposure to 2,4-D. Health and 
Welfare Canada and the United States Environmental Protection Agency have identified at least four 
different isomers of dioxin as contaminants in 2,4-D. These dioxins include the 2,3,7t8-TCDD isomer, 
which is the most deadly poison knownilo man. j 

Dioxin is contaminaring the food chain of Vietnam veterans and compromising the immune systems of 
their children. Even more seriously, 2.4-D is being used at National Cemeteries, which shows the 
government s insensitivity to victims that have died of dioxin related cancers. 



264 



]2'12/95 TUE 15:07 FAI 609 581 7804 
WA 1995 Convention Resolutions > 

Position: 



VETERANS' HAVEN 



laoos 



Agent Orange/Dioxin Committee 



Vietnam Veterans of America, Inc., at natiooal convention in Houston Texas, August 15-20, 1995, will 
seek legislation ind administrative action to help ban the manufactuft, sale and use of 2,4-D worldwifle. 

1. WA will talce all steps necessary to promote legislation to carry out this action. 

2. WA encourages itis membership through chapters and state councils to work with representatives ilnd 
state I^islators to obtain their support to help ban the manufacture, sale and use of 2,4-D worldwide. 

-^ ffiUICAL fcUUiyiVlJi-lNI AND SUPPLIES FQRVIEmAW HOSPIT i ttS 




exLsts,A-fiLJl llEial rill imitloH Ljnedical equip ment and siipp1ii>.»; ^ttjl]" 
stem. 




265 



U.S. HOUSE OF REPRESENTATIVES 

COMMITTEE ON SCIENCE 

SUrrj 2320 RAYBURN HOUSE OPFICE BUILDING 

WASHINGTON. DC 20515-6301 

(2021225-6371 

Inisnw: SOCNCEOHR.HOUSE GOV 

Febaiary 16, 1996 






Dr Donald G Barnes 

Science Advisory Board 

US. Envirorunental Protection Agency 

401 MSt, SW 

1145 West Tower 

Washington, DC 20460 

Dear Dr Barnes 

On December 13, 1995, the Energy and Environment Subcommittee of the Committee on 
Science held a hearing on EPA's Dioxm Reassessment Report Dunng that hearing. Admiral 
Zumwalt asserted that several members of the Science Advisorv' Board's dioxin reassessment 
review committee may have had a conflict of interest because they or their organizations received 
research funds from industry sources with an economic interest in the outcome of dioxin 
regulations 

To assist the Members in evaluating these allegations. I request that you provide responses 
to the following items by February 23, 1996: 

1) Please describe the general process by which individuals are selected to serve as SAB 
Members, consultants, or federal experts on specific scientific review panels such as 
the dioxin review In particular, please describe the policy of the SAB with respect to 
participation in scientific reviews by individuals who may have financial or other 
conflicts of interest, and the process by which such potential conflicts of interest are 
identified and evaluated Please provide copies of any written guidehnes or 
procedures which the SAB may have regarding such pohcies and processes Are 
individuals being considered for appointment to specific scientific review panels 
required to disclose whether they have any financial or other ties to industries or other 
special interest groups that have an economic or other interest in the outcome of the 
subject under review'' Under what circumstances are individuals appointed to serve 
on special review panels if they could be considered to have such a conflict of interest? 



') 



266 



Dr Donald G Barnes 
Febniary 16, 1996 
Page 2 



Have Science Advisory Board Members ever recused themselves from participation in 
a specific review due to a real or perceived conflict of interest'' 

2) Please provide copies of any written materials relating to the review of potential 
conflicts of interest of any individuals appointed to, or considered for appointment to, 
the ad hoc Dioxin Reassessment Review Committee, including any disclosure 
statements provided by such individuals 

3) How does the Science Advisory Board ensure that its review is truly independent of 
the EPA office that prepared the matter under review'' Are appointments to specific 
scientific review committees made solely within the SAB'' What role or influence, if 
any, do EPA personnel outside of the SAB have in such appointments'' Did EPA 
personnel outside of the Science Advisory Board have ?jiy role or influence in making 
appointments to the ad hoc Dioxin Reassessment Review Committee'' 

If you have any questions regarding this request, please call either Mr Michael Rodemeyer (225- 
6375) or Dr. Jean Fruci at 225-81 15. I appreciate your assistance in providing this information 



Sincerely, 

George E Brown, Jr Q 

Ranking Minority Member 






267 



UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 



V<<f C:\acimin\browmein2.1et 



OFFICE OF THE ADMINISTRATOR 
SCIENCE ADVISORY BOARD 



February 23, 1996 

Congressman George Brown 
Committee on Science 
House of Representatives 
Washington, DC 20515-6301 

Dear Congressman Brown: 

I am writing in response to your February 16, 1996 letter 
asking for specific information regarding membership on the 
Science Advisory Board (SAB) . 

I recognize the important role that you have played in the 
creation and growth of the SAB over the years and appreciate your 
interest in making a good institution even better in the future. 

As background I have included the following: 

1. A brochure containing an overview of the Board's current 

structure and function (Attachment 1) and 

2. A copy of the most recent Annual Report of the SAB Staff that 

provides more detailed information of membership on the 
Board and its practices (Attachment 2). 

I have divided your three questions into smaller parts and 
have replied to them below. 



^JCy ntcycleamecycimit 

'^ '^ PrWad on paper IIWI 00«i 






268 



Qla. "Please describe the general process by which individuals 
are selected to serve as SAB members, consultants, or 
federal experts on specific scientific review panels, 
such as the dioxin review." 

Alaa: A succinct description of Members, Consultants and Federal 
Experts is found in "Types of Affiliation with the 
SAB", Appendix B2, FY94 Annual Staff Report, EPA-EC-95- 
001, p. B-10, October, 1994. [Attachment 2] 
In short, SAB Members are non-government scientists who 

1. Are qualified by education, training and experience 

to evaluate scientific and technical information 
on matters referred to the Board and 

2. Are appointed by the Administrator to serve two-year 

terms on the Board, working through one or more of 
the 11 Committees of the Board. 
SAB Consultants are similarly competent individuals who are 
appointed by the SAB Staff Director to a one-year term 
and are generally called upon to augment particular 
review panels when additional, specific expertise is 
needed. 
Federal Experts are Federal {other than EPA) employees who 

are invited by the SAB Staff Director to participate in 
particular SAB reviews meetings because of their 
peculiar experience and expertise. 
Alab: Information on the selection process for SAB Members and 
Consultants is found in the following 

1) "Guidelines for Service on the Science Advisory 

Board" Appendix Bl, FY94 Annual Staff Report, EPA- 
EC-95-001, pp. B-2 thru B-9, October, 1994 
[Attachment 2] 

2) "Selection of Consultants for Science Advisory 

Board", draft operations manual for SAB staff, 
January, 1995. [Attachment 3] 

3) "SAB Membership Search/Selection Process", draft 

document being prepared for consideration by the 
Membership Search Subcommittee of the SAB 
Executive Committee, February 18, 1996 
[Attachment 4] 
In short, the Member ship search and selection process is 
continually open so that nominations are accepted 
throughout the year. The process involves input from 

a) The SAB Staff 

The SAB Staff utilize formal and informal contacts 
inside and outside the Agency to generate the 
names of strong candidates. 

b) The public 

Suggestions from the public result from a 

generally biannual request for nominations 



269 



that IS published in the Federal Register, 
unsolicited nominations throughout the year, 
and/or specific inquiries to specific groups. 

c) The Agency 

Agency personnel, who have often been working a 

particular technical issue for many months or 
even years, are usually aware of most of the 
specialists in that field and make 
suggestions to the SAB Staff. The SAB Staff 
is aware that such Agency suggestions may 
reflect an inadvertent bias towards 
individuals who are favorably disposed toward 
the Agency's project. Therefore, these 
recommendations are examined with particular 
care, with an emphasis on assuring a balance 
of points of view on the Committee. 

d) The Board 

Current Members of the Board provide suggestions 

for candidates, based upon their professional 
knowledge and contacts. The Executive 
Committee has also established a Membership 
Search Subcommittee, whose responsibilities 
have included taking a global view of the 
list of candidates likely to be submitted to 
the Administrator, checking for diversity in 
terms of gender, "address" (e.g., academic, 
environmental community, industry, etc.), 
minority status, and geography. 
Historically, the selection process has consisted of 
the SAB Staff Director's presenting the Deputy 
Administrator with at least two names for every 
open slot on the Board's roster. In most cases, 
the Staff Director has recommended one of the two 
names and has included a justification for the 
recommendation. The final selection decisions are 
made by the Deputy Administrator. 
Selection of Consultants and Federal Experts is a 

similar process, except that the appointments are 
made by the Staff Director, generally acting on 
recommendations from the Staff and the Panel 
Chair. The Staff and Panel Chair are aware of 
both the particular technical needs for a 
thorough, credible review and the need for balance 
and objectivity in the Panel itself. 
NOTE: In the case of the dioxin reassessment, I recused 
myself from the traditional role of the Staff 
Director, due to my long history in working on 
Agency dioxin issues over the past 15 years. By 



270 



prearrangement, those Staff Director 
responsibilities were pass on to the Deputy Staff 
Director, Mr. A. Robert Flaak. Mr. Samuel 
Rondberg was the Designated Federal Official who 
carried out most of the Staff responsibilities for 
the review. 

Qlb: "In particular, please describe the policy of the SAB with 
respect to participation in scientific reviews by 
individuals who may have financial or other conflicts 
of interest, and the process by which such potential 
conflicts of interest are identified and evaluated. 
Please provide copies of any written guidelines or 
procedures which the SAB may have regarding such 
policies and processes." 

Alb: Regarding conflict of interest , under 18 U.S.C. Section 
208 (a) , Federal employees, including "special 
government employees" that serve on the Science 
Advisory Board, are barred from participating in any 
"particular matter" which affects their employers' 
financial interests. As defined in the Standards of 
Ethical Conduct for Employees of the Executive Branch, 
"The term particular matter encompasses only matters 
that involve deliberation, decisions, or action that is 
focused upon the interests of specific persons or a 
discrete and identifiable class of persons." 
Generally, the SAB doesn't deal with particular matters and, 
specifically, its consideration of dioxin is not a 
particular matter because dioxin is widespread in the 
environment and because the Agency's reassessment was 
aimed at dioxin wherever it is found and from whatever 
sources it might come--from food to incinerators, from 
volcanos to pulp and paper, from human milk to chemical 
companies, etc. 
Under 19 U.S.C. Section 208(b)(3) agencies are authorized to 
waive the 208 (a) restriction where "the need for the 
individual's services outweighs the potential for a 
conflict of interest [COI] created by the financial 
interest involved." 
Such waivers are often granted to SAB Panelists in cases in 
which the Board is making recom.mendations on general 
research directions (but not on specific grants and 
contracts, which would be "particular matters"), which 
could conceivably affect the financial interests of the 
Panelists' employer. For example, a university 
professor's recommendations to the Agency on research 
could affect the number and size of grants that the 
Agency supports in a given area. That research area 



271 



could be the professor's own or an area of research of 
some other professor at the same university. In the 
latter case, the professor could be totally ignorant of 
the fact, but it would still constitute a conflict. In 
such cases of research recommendations, the Agency 
generally issues a waiver; otherwise, the Agency would 
be excluding itself from the advice and insights of 
some of the most knowledgeable researchers in a given 
field. 

As a part of the process of assessing whether a legal COI 
exists or not, each member of an SAB Panel (i.e. 
Members and Consultants) must submit a Confidential 
Financial Disclosure Report (SF-450) (Attachment 5) . 
The information includes data on assets and income, 
liabilities, outside positions, agreements and 
arrangements, and gifts and travel reimbursements for 
the individual and members of his/her immediate family. 
The completed form is reviewed by SAB Staff, with legal 
counsel as needed, prior to the public review meeting 
and a judgment is made about whether there is a 
conflict-of-interest or not. By law, EPA cannot make 
this information available to the public. 

The Board is also concerned about appearance of conflicts of 
interest. To address this concern, it has become the 
practice to begin SAB public meetings with a period of 
voluntary disclosure. During the disclosure period, 
which was adapted from a practice used in National 
Research Council panels, SAB Panel members may share 
with one another and with the public information that 
will help others understand "where they are coming 
from" on the issues. The audience is free to use this 
information in evaluating the individual's comments on 
the subjects under discussion. The following factors 
are generally addressed during the disclosure: 

a. Research conducted on the matter. 

b. Previous pronouncements (e.g., court testimony) made 

on the matter. 

c. Interests of e.-r.ployer in the matter. 

d. A general description of any other financial 

interests in the matter. (Note that none of the 
financial interests would constitute a legal 
conflict-of-interest or else the person would not 
be on the Panel--unless a waiver had been 
granted. ) 

e. Other links; e.g., research grants from parties — 

including EP.n--that would be affected by the 
matter . 



272 



Recently, the Membership Search Subcommittee of the SAB 
Executive Committee has discussed approaches for 
improving the disclosure process. The Subcommittee 
will report on their discussions at the public 
Executive Committee on Feb. 28. 

More detailed information about the disclosure practice can 
be found in 

1) "Guidelines for Public Disclosure at SAB Meetings", 

Attachment to Appendix Bl, FY95 Annual Staff 
Report, EPA-EC-95-001, p. B-8 thru B-9, October, 
1994 [Attachment 2] 

2) "Policy for Public Disclosure at SAB Meetings" and 

the attached "Mock Disclosure: How to Implement 
the Policy of Public Disclosure at SAB Meetings", 
Latest revision: August 4, 1995. [Attachment 6] 

Qlc: "Are individuals [who are] being considered for appointment 
to specific scientific review panels required to 
disclose whether they have any financial or other ties 
to industries or other special interest groups that 
have an economic or other interest in the outcome of 
the subject under review?" 

Ale: As noted in Alb, the candidates for Panels are required to 
submit the Confidential Financial Disclosure Report 
(SF-450) . Legal counsel has advised us that this is 
the only requirement that we can legally make. The 
Board has embraced the practice of voluntary public 
disclosure as a means for permitting the sharing of 
additional information. 

Qld: "Under what circumstances are individuals appointed to serve 
on special review panels if they could be considered to 
have such a conflict of interest?" 

Aid: As noted above, under 18 U.S.C. Section 208(b)(3) agencies 

are authorized to waive the restriction where "the need 
for the individual's services outweighs the potential 
for a conflict of interest [COI] created by the 
financial interest involved." Waivers are often 
granted in matters of recommendations for directions of 
future research. 

Qle: Have Science Advisory Board Members ever recused themselves 
from participation in a specific review due to a real 
or perceived conflict of interest? 

Ale: Yes. In the case of dioxin, one Member chose not to 

participate due to an affiliation with one of the 
principal protagonists in the matter. A second Member 



273 



chose not to participate due to earlier public 
statements made on the matter. 



Q2 : "Please provide copies of any written materials relating to 
the review of potential conflicts of interest of any 
individuals appointed to, or considered for appointment 
to, the ad hoc Dioxin Reassessment Review Committee, 
including any disclosure statements provided by such 
individuals . " 

A2 : Each member of the Panel submitted a Confidential Financial 
Information form {SF-450) (Attachment 3) . The SAB 
Staff reviewed these submissions for possible legal 
conflicts of interest, conferring with the Office of 
General Council, as needed. As noted above, the SF-450 
documents are confidential, and the Agency cannot be 
released to the public. 
The disclosure statements of each of the Panel participants 
at the May, 1995 meeting were presented orally and are 
a part of the transcript of that meeting. (See pp. 1- 
25 of Attachment 1 : Transcript of the May 15-16, 1995 
meeting the Science Advisory Board's Panel on Dioxin 
Reassessment Review.) 

Q3a: "How does the Science Advisory Board ensure that its review 
IS truly independent of the EPA office that prepared 
the matter under review?" 

A3a: In short, we do the best we can in the face of competing, 
but equally worthy, considerations. There can be no 
assurance of absolute independence or absence of bias, 
but we do take steps to minimize its presence and 
impact as follows: 
Our first consideration is the technical qualifications of 
the candidates. Because of their technical expertise, 
many of these individuals will be known to the Agency 
and may, in fact, have interacted with the Agency on 
the issue before. This is particularly true for an 
issue like dioxin that has been attracted the Agency's 
and the nation's attention for more than two decades. 
We do make certain that none of the individuals has 
been directly involved in the production of the 
Agency's document under review, although, on occasion, 
we may include--and even seek out--individuals who have 
participated in earlier peer reviews of the document. 
The intention is to have a link to any earlier 
perspectives generated by other independent bodies. 
Our second consideration is the possibility of a legal 
conflict of interest, as discussed above. 



274 



Our third consideration is the formation of a balanced panel 
who collectively have the breadth of knowledge and 
experience to address all of the issues under 
discussion and who collectively represent a range of 
scientific points of view on the issues. Experience on 
the SAB and elsewhere has indicated that providing a 
balanced panel is an effective way to minimize the 
impact of subtle biases and predispositions. 

We also provide an opportunity for the voluntary, public 

sharing of information about the Panelists' backgrounds 
so that other Panelists and the public can evaluate for 
themselves how much those respective backgrounds might 
color the views expressed. 

Q3b: "Are appointments to specific scientific review committees 

made solely within the SAB? What role or influence, if 
any, do EPA personnel outside of the SAB have in such 
appointments?" 

A3b: As noted above, the actual appointment of Members to the SAB 
are made by the Deputy Administrator, through a process 
that is informed by input from the SAB Staff Director. 
In the case of Panelists appointments, also described above, 
the SAB Staff Director makes the decisions based on 
recommendations from the SAB Staff and the Panel Chair, 
informed by--but not determined by--input from the 
.A.gency . 

Q3c: "Did EPA personnel outside of the Science Advisory Board 
have any role or influence in making appointments to 
the ad hoc Dioxin Reassessment Review Committee?" 

A3c: The procedures followed in the case of the Dioxin Panel were 
consistent with the process described above. If 
anything, the SAB was more circumspect than usual about 
the participation of the Agency in selecting the Panel 
members, given the amount of the public interest in the 
issue . 
It was the judgment of the Executive Committee--the parent 

committee of the Dioxin Reassessment Review Panel--that 
the Panel should be structured around the existing 
Indoor Air Quality/Total Human Exposure Committee and 
the Environmental Health Committee. The SAB Staff and 
the SAB Chair determined who would chair the 
enterprise . 
In short, the Dioxin Reassessment Review Panel was a 

creature of the Board, by the Board, and for the Board. 



275 



A more detailed discussion of the Dioxm Panel Selection 

process is contained in "Panel Selection for SAB Review 
of EPA's Dioxin Reassessment", February, 1996. 
[Attachment 8] 

Finally, for your information, I am enclosing a copy of my 
reply to Admiral Zumwalt, who raised some of these same issues in 
a letter to the Administrator last month [Attachment 9] . 

If you have any questions about these answers, in 
particular, or more generally, about any other aspects of the 
SAB, please do not hesitate to contact me at TELE — 260-4126; 
FAX--260-9232; or INTERNET--barnes.don@epamail.epa.gov. 




Donald G. Barnes PhD 
Staff Director 
Science Advisory Board 



Attachment 1: "Science Advisory Board" (a brochure) 
Attachment 2: SAB FY94 Annual Staff Report: The Year of 

Reinvention, October, 1994 
Attachment 3: "Selection of Consultants for Science Advisory 

Board Panels", Drafted Jan., 1995 
Attachment 4: "SAB Membership Search/Selection Process", February 

16, 1996 
Attachment 5: Confidential Financial Information form (SF-450) 
.attachment 6: "Policy for Public disclosure at SAB Meetings" and 

attached "Mock Disclosure", August 4, 1996 

revision . 
Attachment 1 : Pages 1-25 of the transcript of the May 15-16, 1995 

meeting the Science Advisory Board's Panel on 

Dioxin Reassessment. 
.Attachment 3: "Panel Selection for SAB Review of EPA's Dioxin 

Reassessment", February, 1996 
Attachment 9: Barnes to Zumwalt reply to issues raised in the 

latter' s January 2, 1996 letter to the 

Administrator, February 22, 1996. 



276 






•u 


, 'p: 




-i-I ■« 












o o - 


1 C-£ 




S ^ E 














'd — ■ ^ 


'o ''=^"0 


i^ Sj ^ 



'"C fe ■£-■= °* ■ 



2:tt;K.igHic< 



E 

o -c o 






a> Is- 



fsS|:S 



,0 E "= 
£ S o 

i 3 2- -S 



E< 



1- 6 "I , 











fN 
















c 




-0 






<' 




NO 


Si 




,g 




r-) 


t^ 




't;^ 




NO 









c^ 














— 


-o 










-^ 




















r^ 


NO rrj 


c 




ils 


U 


-On 


g 


a 


d 


3§ 


i 





c 


a_» - — - 


,_o 


IE 




c 


Cl, ■ — " 


< 


"1 


« t^ — 
<: ^- 


^ 


l^ 




^ 




H u. 




ll^.s.i 



E -£ E E 

000c 



s: -^ .5 CJJ S 



o _£■ 

o M 
^ 2 



^ I 5 o- 



g P c 5 







' O ■= «i ° 



E E 






"'So 



g g :2 



277 




'±"i -s '^ "^ 



^ -^ ^ ^ 



pi 


3 


.0 


S 


cZ 


u 


I'l 


^r 





'- 


Mj 


rg 


hi 


_" 


&D 


■w 


E 


f 




a 


c 


'"3 


00 

.9 


.5 '^ 


c 






















> 


.0 


p». 


■5 


^ 


.y 


y s 


" 


i 


(S 




g 


=2 


"rt 


:§ 


.1 '5 


c 




• 


i 


< 




J 


• 


i-s 





1 




c 


^2 




a 




g 


-0 


« 



« t; o </> 
S £ S 2 



S " 2 _0 g S 3,T3 p g 

P j! H -c ■! S S 



-a c 

S .1 § 1 " 



S "O ■ 



bO-5 



E ' o 6 

~ -J£ .Ti -O 

c -a < 

_ i 






oh i2 ^2 •< 






Hi III 



o -s 

Hi 

s * c 



_^ G "i^ "^ "£ . 
o ^ E E"5 



S 5 M a!^ ^ 



E -3 



278 



Uncted States 
Environmentat 
Protection Agency 



Science Advisory Board 
1400 I 

Wathinglon, DC 



EPA-SAB-95-001 
OCTOBER 1994 



«»EPA SCIENCE ADVISORY BOARD 

FYI994 ANNUAL STAFF REPORT 

The Year of Reinvention 



Science Advisory Board 




ReeycM/Recyclablc Primed with Vegetable Oil Based Ms on 100% Recycled Paper (50% Postconsumer) • Please recyde as newsprint 



279 



aaeB-2 . ANNUAL REPORT 



gag 



APPENDIX B1 
GUIDELINES FOR SERVICE ON THE SCIENCE ADVISORY BOARD 

Background 

The Science Advisory Board (SAB) was established in 1974 by the Administrator. 
In 1978 the SAB received a Congressional mandate to serve as an independent source 
of scientific and engineering advice to the EPA Administrator. 

The SAB consists of approximately 100 Members, who are appointed by the 
Administrator. These members serve on specific standing committees. The Chairs of 
the Committees also serve as members of the Executive Committee, which oversees all 
of the activities of the Board. 

In many of its activities, the members of the Board are supplemented by 
Consultants, who are appointed by the SAB Staff Director after conferring with the Chair 
of the Committee on which the consultant is to serve. Also, on occasion, Panels will be 
supplemented by "liaison members" from other governmental agencies. These people 
are invited by the Staff Director to participate in an ad hoc manner in order to bring their 
particular expertise to bear on a matter before the Board. 

Both the Executive Committee and the permanent Committees may choose to 
conduct issue-specific business through Subcommittees that are chaired by SAB 
members. Reports from Subcommittees are reviewed by the respective permanent 
Committees. The Executive Committee reviews all reports, independent of their origin, 
prior to formal transmission to the Administrator. The sole exceptions are reports from 
the Clean Air Scientific Advisory Committee and the Clean Air Act Compliance Analysis 
Council, which are a separately chartered FACA committees operating within the SAB 
structure. 

Criteria for Selection of Members and Consultants 

The SAB is chartered as a Federal Advisory Committee, subject to the rules and 
regulations of the Federal Advisory Committee Act (FACA) (Public Law 92-463). The 
charter provides guidance and restrictions on selection of SAB members. The four 
most significant of which are; 



Report of the Science Advisory Board Staff 



280 



ANNUAL REPORT page B-3 

a) Members must be qualified by education, training and experience to 
evaluate scientific and technical information on matters referred to the 
Board. 

b) The composition of Board committees, subcommittees and panels must 
be "balanced", representing a range of legitimate technical opinion on the 
matter. 

c) No member of the Board may be a full-time government employee. 

d) Members are subject to conflict-of-interest regulations. 

The scientific and technical quality and the credibility of those selected is a 
paramount consideration. Secondary factors considered include the geographic, ethnic, 
gender, and academic/private sector balance of committees. Other factors that 
contribute to, but do not determine, the selection include demonstrated ability to w/ork 
well in a committee process, write well, and complete assignments punctually. 

Nominations for membership/consultantship on the Board are accepted at any 
time. On a biannual basis, the SAB Staff Office publishes a notice in the Federal 
Register formally soliciting the names of candidates for SAB activities. 

Terms of Appointment 

Members serve at the pleasure and by appointment of the Administrator. In 
order to provide suitable terms of service and to insure the infusion of new talent, the 
following guidelines are generally followed: 

Members are generally appointed in October for two-year terms which may be 
renewed for two additional consecutive terms. Chairs of the standing committees are ' 
also appointed for two-year terms which may be renewed for one additional term. If a 
member is appointed as Chair, this term of service (2-4 years) is added to whatever 
term of service he/she may accrue as a member. For example, 



Report of the Science Advisory Board Staff 



281 



page B-4 




. A 


NNUAL REPORT 


Years 
as member 


Followed by years 
as Chair 


Followed by years 
as member 


Total 
vears 


2 
2 
4 
6 



2 or 4 
2 or 4 
2 or 4 




0or2- 




2 

4-6 
6-8 
8-10 



Reappointment as a member is possible after a two-year hiatus from the SAB, during 
which time the individual may be called upon to serve as a consultant for a specific 
issue. 

Consultants are appointed to provide the necessary expertise for specific issues. 
Their terms of appointment are for one year, beginning at any time, and are renewable 
annually. Their formal appointments may be continued beyond completion of a given 
project so that their expertise can be quickly assessed in future with a minimum of 
paperwork. 

In general, interagency liaisons participate for the term of issue resolution only. 
Member and Consultant Selection Process 

Members are appointed by the Administrator based on nominations forwarded by 
the SAB Staff Director and the Chair of the Executive Committee. These nominations, 
in turn, are based on recommendations made by the Designated Federal Official (DFO- 
the member of the SAB Staff with principal responsibility for servicing standing 
Committees) and the Chairs of the standing Committees. The DFO has the 
responsibility for developing a list of candidates, utilizing all credible sources, including 
members of the SAB, other DFOs, EPA staff, staff at the National Academy of 
Sciences\National Research Council, trade groups, environmental groups, professional 
organizations, scientific societies, regulated industries, and the informed public. 

On occasion, an ad hoc Membership Subcommittee of the Executive Committee 
has been established to assist in the selection process. This group is consulted about 
possible names and used as a "sounding board" when decisions are being made about 
appointments. The Membership Subcommittee's principal role is to maintain the 
integrity of the process and to probe the extent to which objective selection criteria and 
procedures are being followed. They also raise questions about adherence to the 

Report of the Science Advisory Board Staff 



282 



ANNUAL REPORT . page B-5 

Statement of Intent on Women and Minorities, adopted by the Executive Committee in 
1 990, which was designed to increase the representation of these groups on the Board. 

Consultants are appointed by the Staff Director following a similar procedure. 
Panel Selection Process 

In general, once the Board and the Agency have agreed upon a topic for SAB 
review, the subject is assigned to one of the standing Committees. The Committee 
Chair and the DFO have primary responsibility for forming a review Panel (the full 
Committee or a Subcommittee, as the case may be.) The Panel will contain some or all 
members of the Committee. In many instances, consultants may also be added to the 
Panel in order to obtain specialized expertise on the particular issue under discussion. 

A key aspect in the Panel selection process is the "charge", the mutually agreed 
upon description of what the Agency would like the review to accomplish and/or what 
the SAB expects to focus upon. The most helpful charge is one that prescribes specific 
areas/questions that need attention and/or answers. At a minimum, the elements of the 
charge should be sufficiently precise that the SAB can determine what additional 
consultant expertise is needed to conduct the most helpful review. 

Often the DFO begins by soliciting ideas about potential members from the 
Agency staff who are intimately acquainted with the issue and will therefore are often 
aware of the most informed people. A conscious effort is made to avoid selecting 
individuals who have had a substantive hand in the development of the document to be 
reviewed. At the same time, experience has shown the utility of having some 
representation from individuals/groups who may have been involved in prior reviews of 
the issue or the document. The goal is to minimize the appearance or practice of an 
individual's reviewing his/her own work, while at the same time, maintaining an historical 
link to earlier deliberations surrounding the document/issue. Once the Agency staff has 
suggested nominees and provided background information on the individuals, their 
direct role in the panel selection process is complete. Agency staff, the requesting 
office, and others may be consulted at a later stage for information about nominees 
received from other sources. 

The goal is to gather a balanced group of experts who can provide an 
independent assessment of the technical matters before the Board. Discrete inquiries 

Report of the Science Advisory Board Staff 



283 



aoefi-6 ANNUAL REPORT 



Bsa: 



about the nominees are made with a number of different sources. This might include, 
for example, making inquiries with editors of newsletters, professional colleagues, and 
experts who are on "the other side" of the issue. As time and resources permit and 
controversy demands, names of nominees will be investigated via computer search of 
their publications and pronouncements in public meetings. 

Frequently, a determining factor for selection is the availability of the individual to 
participate in the public review. In the case of multiple-meeting reviews, the SAB may 
enlist the assistance of a particularly skilled consultant who cannot attend all meetings, 
but who is willing to do additional homework and/or participate via conference call. 

In some cases, the Panel Chair consults with key members of the Panel for their 
advice before completing the empaneling process. The final selections for consultants 
are compiled by the DFO in conjunction with the Chair of the Panel and are submitted to 
the SAB Staff Director for discussion and appointment. 

Conflict-of-interest and Public Disclosure 

The intent of FACA is to construct a panel of knowledgeable individuals who are 
free of conflicts-of-interest. In this regard, each Panel member must complete a 
confidential financial information form that is reviewed by the Deputy Ethics Officer to 
determine whether there are any obvious conflicts-of-interest. 

Legal conflict-of-interests generally arise in connection with "particular party 
matters." In general, the SAB (in contrast with the FIFRA Scientific Advisory Panel 
(SAP)) does not get involved in "particular party matters," hence, legal conflicts-of- 
interest are rare on the SAB. However, technical conflicts-of-interest can arise, 
particularly for participants from academic institutions, in connection with Panel 
recommendations for additional research studies. In most such cases, the DFO's work 
with the Panel members to apply for waivers from the conflict-of-interest concerns on 
this matter. The requests for waivers are evaluated on a case-by-case basis by EPA's 
Office of the General Council. (The Agency generally determines that the benefits to 
the country derived from these experts' recommendations for additional research, 
outweigh any technical conflict-of-interest that might be involved.) 

However, the Board is also concerned about "apparent conflicts-of-interest." 
Consequently, Members and Consultants to the Panel are generally selected from the 

Report of the Science Advisory Board Staff 



284 



aaeB-S ANNUAL REPORT 



SBg 



ATTACHMENT 
Guidelines for Public Disclosure at Sab Meetings 

Background 

Conflict-of-interest (CO!) statutes and regulations are aimed at preventing 
individuals from (knowingly or unknowingly) bringing inappropriate influence to bear on 
Agency decisions which might affect the financial interests of those individuals. The 
SAB contributes to the decision-making process of the Agency by evaluating the 
technical underpinnings upon which rules and regulations are built. SAB Members and 
consultants (M/Cs) carry our their duties as Special Government Employees (SGE's) 
and are subject to the CO! regulations. 

Therefore, in order to protect the integrity of the advisory process itself and the 
reputations of those involved, procedures have been established to prevent actual COI 
and minimize the possibility of perceived COI. These procedures include the following: 

a) Having M/C's file, at the time of appointment, Special Form 450, Confi- 
dential Statement of Employment and Financial Interest. This form is a 
legal requirement and is maintained by the Agency as a confidential 
document. 

b) Providing M/C's with written material; e.g., "Ethics in a Nutshell" and a 
copy of Ethics Advisory 92-1 1 . 

c. Delivering briefings to M/C's on COI issues on a regular basis. 

The following is a description of an additional voluntary ' procedure that is 
designed to allow both fellow M/Cs and the observing public to learn more about the 
backgrounds that M/C's bring to a discussion of a particular issue. In this way, all 
parties will gain a broader understanding of "where people are coming from" and 
provide additional insights to help observers and participants evaluate comments made 
during the discussion. 



' Note: The disclosure procedure is voluntary, and members/consultants are not obligated to reveal information contained In 
their Form 450 that would ovenwise remain confidential. 



Report of the Science Advisory Board Staff 



285 



ANNUAL REPORT ■ page B-7 

"broad middle° spectrum of opinion on the technical issue under discussion. Experience 
has shown that achieving balance through equal representation of extreme views 
reduces the chance of achieving a workable consensus-pro or con-that the Agency 
needs to more forward. 

The "public disclosure" (see Attached) process (a standard part of all SAB Panel 
meetings) is a mechanism aimed resolving the apparent conflicts-of-interest issues. 
This procedure involves an oral statement (sometimes Panel members supplement this 
with a written document) that lays out the individual's connection with the issue under 
discussion; e.g., his/her area of expertise, length of experience with the issue, sources 
of research grants, previous appearance in public forms where he/she might have 
expressed an opinion, etc. This recitation of prior and/or continuing contacts on the 
issue assists the public, the Agency, and fellow Panel members in assessing the 
background from which particular individual's comments spring, so that those comments 
can be evaluated accordingly. 

Conclusion 

These Guidelines are intended to assist the SAB in adhering to the mandates 
and spirit of the Federal Advisory Committee Act. By following these Guidelines the 
Board should be well-positioned to provide technically-sound, independent, balanced 
advice to the Agency. At the same time, they provide assurance that there will be 
adequate participation by and renewal with well-qualified experts from the various 
communities served by the Board. 



Prepared: Oct 14, 1991 
Revised: Nov 26. 1991 
Revised: Oct. 12. 1994 



ATTACHMENT 



Report of the Science Advisory Board Staff 



23-557 0-96-10 



286 



ANNUAL REPORT . page B-9 

Procedure 

When an agenda item is introduced that has the potential for COI-actual or 
perceived-the Designated Federal Official (DFO) will ask each M/C on the panel to 
speak for the record on his/her background, experience, and interests that relate to the 
issue at hand. The following items are examples of the type of material that is appropri- 
ate to mention in such a disclosure; 

a) Research conducted on the matter. 

b) Previous pronouncements made on the matter. 

c) Interests of employer in the matter. 

d) A general description of any other financial interests in the matter: e.g., 
having investments that might be directly affected by the matter. 

e) Other links: e.g., research grants from parties-including EPA-that would 
be affected by the matter. 

The DFO will also publicly refer to any waivers from the COI regulations which have 
been granted for the purposes of the meeting. 

The DFO will assure that the minutes of the meeting reflect that fact such disclosures 
were made and, if possible, the nature of the disclosures. In addition, the minutes 
should describe any situations in which, in the opinion of the DFO, an actual or per- 
ceived COI existed and how the issue was resolved. 



Report of the Science Advisory Board Staff 



Bsai 



287 



eB-10 . ANNUAL REPORT 



APPENDIX B2 
TYPES OF AFFILIATION WITH THE SAB 

Members are individuals who serve on the SAB and who are appointed by the 
EPA Administrator, normally for a two year term (renewable in two-year increments up 
to a total of six years). Members are either can be either SGEs or Representatives (see 
below), although the preference is that they serve as SGEs. They are compensated for 
their time unless they elect to serve without compensation (WOC). Their travel and per 
diem expenses are paid. They are subject to conflict of interest laws and fill out all 
personnel paperwork. Members can vote on issues, although most SAB business is 
conducted by consensus. 

Consultants are individuals vA\o serve on the SAB and who are appointed by the 
SAB Staff Director, normally for a one-year terms, renewable on an annual basis until 
either their expertise is no longer needed or they elect to stop serving. Consultants are 
either can be either SGEs or Representatives (see below), although the preference is 
that they serve as SGEs. They are compensated for their time unless they elect to 
serve without compensation (WOC). Their travel and per diem expenses are paid. 
They are subject to conflict of interest laws and fill out all personnel papenA^ork. 
Consultants cannot vote on issues, although most SAB business is conducted by 
consensus. 

Special Government Employees (SGEs) are individuals who are brought "on- 
board" using a personnel appointment involving a modest amount of 
paperwork. They are normally compensated for their time unless they 
elect to serve without compensation (WOC). Their travel and per diem 
expenses are paid. They are subject to conflict of interest laws and 
certain postemployment restrictions. 

Representatives are individuals who serve on the SAB, but whose economic 
interests cannot be fully separated from those of their employer. Repre- 
sentatives are chosen because a) the SAB would gain technical benefit 
from hearing the technical views of the employee and/or b) the employer 
would not allow their experts to participate in any other way; cf., in some 
instances, service as an SGE can limit subsequent activities of that expert 
in future dealing with the Agency on the matter. They do not fill out any 
personnel paperwork. They are not compensated for their time; travel and 

Report of the Science Advisory Board Staff 



288 



ANNUAL REPORT . page B-11 

per diem expenses maybe covered by either their employer or EPA. They 
are not subject to the financial disclosure or conflict of interest laws. 

Federal Experts are Federal (other than EPA) employees who participate in SAB 
reviews because of their peculiar experience and expertise. They speak for themselves 
as technical experts. They are not compensated for their time by the SAB; however, 
travel and per diem expenses may be paid. No paperwork other than a Travel Authori- 
zation is prepared, in cases in which EPA does the travel. They are subject to their own 
Agency's conflict of interest regulations, and they do not file an SF-450 (financial 
disclosure form) with the SAB. They are asked to participate in the formal conflict of 
interest disclosure at the beginning of SAB meetings, as appropriate. Federal Experts 
may contribute to the development of the Committee's report, but they do not vote. 

Other Terms: 

The Chair is the leader of an SAB Committee or Subcommittee. A Committee 
Chairs is an SAB member selected by the Administrator, informed by advice from the 
Staff Director. A Subcommittee Chair is usually an SAB member selected by the 
Committee Chair. Consultants and Representatives do not usually serve as Chairs. 

An Invited Expert is an individual with special expertise who is brought to a meeting 
at SAB expense, but who is not being brought on board as a Member or Consultant. 
The individual's involvement with the Committee is limited to presentations and discus- 
sion. He/she does not work on the report or vote on matters before the Committee. 
The Travel Authorization reads Invitational Travel. 

An Invited Participant is an individual who has been formally appointed as a Member 
or Consultant but whose paperwork has not been completed prior to the meeting. The 
person is reimbursed for travel expenses, but cannot receive salary prior to completion 
of the personnel action (SF-50). A completed SF-450 (financial disclosure form) is 
needed prior to formal participation on a Panel. The Travel Authorization reads 
Invitational Travel. He/she may contribute to the report and, in the case of someone 
invited to serve as a Member, may vote, if the occasion should arise. 



Report of the Science Advisory Board Staff 



289 



payi 



e B-12 



ANNUAL REPORT 



APPENDIX B3 
SAB MEMBERS FOR FY94 



LAST NAME 


FIRST 
NAME 


COM 


Abriola 


Linda 


EEC 


Ayres 


Stephen M. 


CASAC 


Bailey 


Paul 


lAQC 


BaJr 


William 


RAC 


Bean 


Judy 


owe 


Bockstael 


Nancy E. 


EEAC 


Brown 


Stephen L. 


RAC 


Buffler 


Patricia 


CASAC 


Bull 


Richard 


DWC 


Bunn 


William 


EHC 


Cams 


Keith E. 


DWC 


Clescerl 


Lenore 


DWC 


Conway 


Richard A. 


EEC 


Cooper 


Edwin 


EPEC 


Cooper 


William E. 


EPEC 


Crump 


Kenny 


EHC 


Cummlngs 


Ronald G. 


CAACAC 


Dalsey 


Joan M. 


lAQC/EC 


Dale 


Virginia 


EPEC 


Deisler 


Paul F. 


EC/RSAC 


Dickson 


Kenneth L. 


EPEC/EC 


Dudek 


Daniel J. 


CAACAC 


Fabryka-Martin 


Joan 


RAC 


Fan-Cheuk 


Anna 


DWC 


Ford 


Jean 


CASAC 


Freeman 


A. Myrick 


EEAC 


Gallo 


Michael 


EHC 


Gerba 


Charles P. 


DWC 


Gonzalez-Mendez 


Ricardo 


RAC 


Harwell 


Mark A. 


EPEC 


Hazen 


Robert 


lAQCC 


Henderson 


Rogene 


EHC 


Hoel 


David 


RAC 


Hoffman 


Owen 


RAC 


Huggett 


Robert 


EC/EPEC 



AFFILIATION CITY, STATE 

University of Michigan Ann Arbor, Ml 

Medical College of Virginia, VCU Richmond, VA 

Stoneybrook Laboratories Inc. Princeton NJ 

Battelle Pacific Northwest Labs Richland, WA 

University of Miami, Dept of Epidemiology Miami, FL 

University of Maryland College Park, MD 

Risks of Radiation Chemical Compounds Oakland, CA 

University of California Berkley, CA 

Washington State University Pullman, WA 

Mobil Corporation Princeton, NJ 

Washington University SL Louis, MO 

Rensselaer Polytechnic Institute Troy, NY 

Union Carbide Corporation Charleston, WV 

UCLA School of Medicine Los Angeles, CA 

Michigan State University East Lansing, Ml 

ICF Kaiser Ruston, LA 

Georgia State University, Policy Res. Center Atlanta, GA 

Lawrence Berkeley Laboratories Berkeley, CA 

Oak Ridge National Laboratory Oak Rkjge, TN 

Shell Oil Co. (Retired) Austin, TX 

University of North Texas Denton, TX 

Environmental Defense Fund New York, NY 

Los Alamos National Laboratory Los Alamos, NM 

California Environmental Protection Agency Berkley, CA 

Hariem Hospital New York NY 

Bowdoln College Brunswick, ME 

Robert Wood Johnson Medical School Piscataway, NJ 

University of Arizona Tucson, AZ 
University of Puerto Rico, School of Medicine San Juan, PR 

University of Miami Miami, FL 

NJ Dept. of Envir. Protection and Energy Trenton, NJ 
Lovelace Biomedi. & Env. Research Institute Albuquerque, K,A 

Medical University of South Carolina Charieston, SC 

SENES Oak Ridge, Inc. Oak RWge, TN 

College of William and Mary Gloucester, V.^ 



Report of the Science Advisory Board Staff 



290 



ANNUAL REPORT 



page B-13 



LAST NAME 


FIRST 
NAME 


COM 


Jackson 


Richard 


EHC 


Johnson 


Charles 


DWC 


Johnson 


James H. 


EEC 


Kachel 


Wayne M. 


EEC 


Kahn 


Bemd 


RAC 


Klaassen 


Curtis 


DWC 


Kneese 


Allan 


EEAC 


Kolstad 


Charles 


EEAC 


Kripke 


Margaret 


EC 


Larson 


Timothy V. 


lAQCC 


Leaderer 


Brian P. 


lAQCC 


Ughty 


JoAnn S. 


EEC 


Lioy 


Paul J. 


lAQC 


Lippmann 


Morton 


EC 


Uu 


Benjamin 


CASAC 


Loehr 


Raymond C. 


EC 


Maki 


Alan 


EPEC 


Makhijani 


Arjun 


RAC 


Matanoski 


Genevieve 


EC 


Mattison 


Donald 


EHC 


Mauderly 


Joe 


CASAC 


McClellan 


Roger 0. 


RSAC/EC 


McElroy 


Anne 


EPEC 


Mendelsohn 


Robert 


EEAC 


Mercer 


James W. 


EEC 


Middleton 


Paulette 


CASAC 


Monson 


Richard 


EHC 


Morandi 


Maria 


lAQCC 


Morse 


Roger 


lAQC 


Murarka 


Ishwar 


EEC/EC 


Norton 


Bryan 


EEAC 


Nordhaus 


William 


EEAC/ 
CAACAC 


Oates 


Wallace 


EEAC 


Pellizzari 


EdoD. 


DWC 


Perera 


Frederica 


EHC/EC 


Pfaender 


Frederic K. 


EPEC 


Pitot 


Henry C. 


EHC 


Pohland 


Frederick 


EEC 



AFFILIATION CITY, STATE 

Califomia St. Dept. of Health Berkely, CA 

Malcom-Pimie (Retired) Bethesda, MD 

Howard University Washington, DC 

Martin Marietta Corporation Oak Rkjge, TN 

Georgia Institute of Technology Atlanta, GA 

University of Kansas Medical Center Kansas City, KS 

Resources for the Future Washington, DC 

University of Illinois Urbana, IL 

M.D. Anderson Cancer Center, U of Texas Houston, TX 

University of Washington Seattle, WA 

John B. Pierce Lab, Yale School of Med New Haven, CT 

University of Utah Salt Lake City, UT 

Robert Wood Johnson Medical School Piscataway, NJ 

New York University Medical Center Tuxedo, NY 

University of Minnesota Minneapolis, MN 

University of Texas at Austin Austin, TX 

Exxon Company, USA Houston, TX 

Institute for Energy and Env. Research Takoma Park, MD 

Johns Hopkins University, Dept of Epidem. Baltimore, MD 

University of Pittsburgh Pittsburgh, PA 

Lovelace Biomedical & Env Institute Albuquerque, NM 

Chemical Industry Instutite of Toxicology RTP, NC 

State University of New York - Stony Brook Stony Brook, NY 

Yale University New Haven, CT 

GeoTrans, Incorporated Sterling, VA 
Univ. Cooperation for Atmospheric Research Boulder, CO 

Han/ard School of Public Health Boston, MA 

University of Texas, Health Science Center Houston, TX 

Environmental & Technical Services, Inc. Troy, NY 

Electric Power Research Institute Palo Alto, CA 

Georgia Institute of Technology Atlanta, GA 

Yale University New Haven, CT 

University of Maryland College Park, MD 

Research Triangle Institute RTP, NC 

Columbia University New York, NY 

University of North Carolina Chapel Hill, NC 

University of Wisconsin Madison, Wl 

University of Pittsburgh. Pittsburgh, PA 



Report of the Science Advisory Board Staff 



291 



page B-14 




ANNUAL REPORT 


LAST NAME 


FIRST 
NAME 


COMM 


AFFILIATION 


CITY, STATE 


Pojasek 


Robert B. 


EEC 


GEI Consultants, Inc. 


Winchester,MA 


Portney 


Paul 


EEAC/EC 


Resources for the Future 


Washington, DC 


Price 


James 


CASAC 


Texas Nat. Res. ConservatiOR Comm. 


Austin, TX 


Radike 


Martha J. 


EHC 


University of Cincinnati 


Cincinnati, OH 


Ray 


Verne A. 


DWC/EC 


Pfizer, Inc. 


Groton, CT 


Reitz 


Richard 


DWC 


Dov/ Chemical Co. 


Midland, Ml 


Repetto 


Robert 


EEAC 


World Resources Institute 


Washington, DC 


Samet 


Jonathan M. 


lAQCC 


Johns Hopkins University 


Baltimore, MD 


Schmalensee 


Richard 


CAACAC/EC 


Massachusetts Institute of Technology 


Cambridge, MA 


Seeker 


W. Randall 


EEC 


Energy & Environmental Research Corp. 


Irvine, CA 


Sextro 


Richard 


RAO 


Lav/rence Berkeley Laboratories 


Berkeley, CA 


Shaub 


Walter 


EEC 


Corp. on Res. Recovery & the Env., Inc. 


Washington, DC 


Silbergeld 


Ellen 


EC 


Environmental Defense Fund 


Washington, DC 


Smith 


V. Kerry 


EEAC 


Duke University 


Durham, NC 


Smith 


William H. 


EPEC 


Yale University 


New Haven, CT 


Snoeyink 


Vernon L. 


DWC 


University of Illinois 


Urbana, IL 


Stavins 


Robert 


EEAC 


Harvard University, JFK School of Govnt. 


Cambridge, MA 


Symons 


James M. 


DWC 


University of Houston 


Houston, TX 


Tietenberg 


Thomas 


EEAC 


Colby College 


Waterville, ME 


Upton 


Arthur C. 


EHC 


University of New Mexico 


Santa Fe, NM 


Viscusi 


W. Kip 


EEAC 


Duke University 


Durham, NC 


Watson 


James E. 


RAC/EC 


University of North Carolina 


Chapel Hill, NC 


Wegman 


David 


EHC 


University of Massachusetts 


Lowell, MA 


White 


Ronald 


lAQC 


American Lung Association 


Washington. DC 


Wolff 


George T. 


CASAC/EC 


General Motors Env. & Energy Staff 


Warren, Ml 


Yates 


Marilyn 


DWC 


University of California 


Riverside, CA 


Young 


Terry F. 


EPEC 


Environmental Defense Fund 


Oakland, CA 



Report of the Science Advisory Board Staff 



292 



ANNUAL REPORT 



page B-15 



APPENDIX B4 
SAB CONSULTANTS FOR FY94 



LAST NAME FIRST 


COMMITEE 


AFFILIATION 


CITY, STATE 




NAME 








Adams 


William 


EPEC 


ABC Laboratories 


Columbia, MO 


Ahmed 


Atxjul Karim 


EHC 


Committee for National Inst, for Envir. (NIE) 


Washington, DC 


Alexander 


Martin 


EPEC 


Cornell University 


Ithaca, NY 


Allen 


Herbert 


RSAC 


University of Delaware 


Nevrark, DE 


Aim 


AlvinL 


RSAC 


Science Applications International, Inc. 


McLean, VA 


Auerbach 


Stanley 


EPEC 


Oak Ridge National Laboratories 


Oak Ridge, TN 


Bartell 


Steven 


EPEC 


Oak Ridge National Laboratory 


Oak Rklge,TN 


Bates 


David 


RAC 


Univ of British Columbia 


Vancouver, BC 


Bauman 


Bruce J. 


EEC 


American Petroleum Institute 


Washington, DC 


Beck 


Barbara 


CASAC 


Gradient Corp. 


Cambrklge, MA 


Beckett 


William 


RSAC 


Yale University School of Medicine 


New Haven, CT 


Bedford 


Barbara 


EPEC 


Cornell University 


Ithaca, NY 


Benowitz 


Neal 


lAQCC 


University of California at San Francisco 


San Francisco, CA 


Berkowitz 


Joan B. 


EEC 


Farkas Berkowitz & Company 


Washington, DC 


Bishop 


Richard C. 


EEAC 


University of Wisconsin-Madison 


Madison, Wl 


Boesch 


Donald 


EPEC 


University of Maryland 


Cambridge, MD 


Bond 


James A. 


EHC 


Chemical Industries Inst, for Toxicology 


RTP, NC 


Boston 


Harry L. 


EPEC 


Oak Ridge National Laboratory 


Oak Ridge, TN 


Bostrom 


Anne 


RAC 


Georgia Institute of Technology 


Atlanta, GA 


Brierley 


Corale 


EPEC 


VistaTech Partnership, Ltd. 


Sandy, UT 


Buchsbaum 


Robert 


EPEC 


Massachusetts Audubon Society 


Wenham, MA 


Burks 


Sterling L. 


EPEC 


Oklahoma State University 


Stillwater, OK 


Burns 


David 


lAQC 


University of California at San Diego 


San Diego, CA 


Byus 


Craig 


RAC 


University of California at Riverside 


Riverskle, CA 


Carlson 


Gary P. 


EHC 


Purdue University 


West Lafayette, IN 


Carpenter 


George F. 


EEC 


Michigan Dept of Natural Resources 


Lansing, Ml 


Cartwright 


Keros 


EEC 


Illinois State Geological Survey 


Champaign, IL 


Charbeneau 


Randall J. 


RAC 


University of Texas at Austin 


Austin, TX 


Chien 


Calvin 


EEC 


E.I.DuPont deNemours Company 


Wilmington, DE 


Chlsolm 


J. Julian 


CASAC 


Kennedy Krieger Institute 


Baltimore, MD 


Clifton 


Kelly 


RAC 


University of Wisconsin-Madison 


Madison, Wl 


Coates 


Joseph 


RAC 


Coates & Jarratt, Inc. 


Washington, DC 


Colome 


Steven 


CASAC 


Integrated Environmental Sciences 


Irvine, CA 


Coppock 


Robert 


EEC 


World Resources Institute 


Washington, DC 


Cortese 


Anthony D. 


RSAC 


Tufts University 


Medford. MA 



Report of the Science Advisory Board Staff 



293 



page B-16 




. ANNUAL REPORT 


LAST NAME 


FIRST NAME 


COMMITEE 


AFFILIATION 


CITY, STATE 


Cory-Slechta 


Deborah 


EPEC 


University of Rochester 


Rochester, NY 


Costanza 


Robert 


EPEC 


University of Maryland/Cheasapeake 


Solomons Island, ^ 


Crapo 


James D. 


CASAC 


Duke University Medical Center 


Durham, NC 


Cropper 


Maureen L. 


EEAC 


The World Bank 


Washington, DC 


Cummins 


Kenneth 


EPEC 


S. Fla. Water Mgmt. District 


W. Palm Beach, R 


Cutshall 


Norman H. 


EC 


Martin Marietta Energy Systems, Inc. 


Oak Ridge, TN 


D'Elia 


Christopher 


EPEC 


University of Maryland 


College Park, MD 


Dabberdt 


Walter 


EPEC 


National Ctr for Atmospheric Research 


Boulder, CO 


Dagirmanjian 


Rose 


DWC 


University of Louisville 


Louisville, KY 


deFur 


Peter L. 


EPEC 


Environmental Defense Fund 


Washington, DC 


Denison 


Richard 


EEC 


Environmental Defense Fund 


Washington, DC 


Diamond 


GaryL. 


EHC 


Syracuse Research Corporation 


Syracuse, NY 


Dickinson 


Robert E. 


EPEC 


National Center for Atmospheric Research 


Boulder, CO 


DiGiovanni 


John 


RAC 


University of Texas 


Smithville, TX 


DiGiulio 


Richard 


EPEC 


Duke University 


Durham, NC 


Dockery 


Douglas W. 


CASAC 


Harvard School of Public Health 


Boston, MA 


Dorn 


Philip B. 


EPEC 


Shell Development Company 


Houston, TX 


Dysart 


Benjamin 


EEC 


Environmental Issues Management 


Atlanta, GA 


Eatough 


Delbert 


lAQC 


Brigham Young University 


Provo, UT 


Enslein 


Kurt 


EHC 


Health Designs, Inc. 


Rochester, NY 


Ensley 


Burt D. 


EPEC 


Envirogen, Inc. 


Lawrenceville, NJ 


Epstein ' 


Lois 


EEC 


Environmental Defense Fund 


Washington, DC 


Ewing 


BenB. 


EEC 


Consultant 


Lummi Island, WA 


Feero 


William 


RAC 


Electric Research and Management, Inc. 


State College, PA 


Fenters 


James 


CASAC 


ITT Research Institute 


Chicago, IL 


Finkel 


Adam M. 


EHC 


Resources for the Future 


Washington, DC 


Fisher 


Gerald 


CASAC 


Sandoz Research Institute 


E. Hanover, NJ 


Fishoff 


Baruch 


CASAC 


Carnegie Mellon University 


Pittsburgh, PA 


Ford 


Davis L. 


EEC 


Davis L. Ford & Associate 


Austin, TX 


Frank 


Nedd R. 


CASAC 


Johns Hopkins University 


Baltimore, MD 


Gallagher 


John 


EPEC 


University of Delaware 


Lewes, DE 


Gasiewicz 


Thomas A. 


EHC 


University of Rochester, School of Medicine 


Rochester, NY 


Gentile 


James M. 


DWC 


Hope College 


Holland, Ml 


Goldstein 


Bernard 


EHC 


UMDNJ-Robert Wood Johnson Medical School 


Piscataway, NJ 


Goldstein 


Robert A. 


CASAC 


Electric Pov^er Research Institute 


Palo Alto, CA 


Gordon 


Gilbert 


DWC 


Miami University 


Oxford, OH 


Gordon 


Theodore 


EEC 


Retired 


Vero Beach, FL 


Gosselink 


James G. 


EPEC 


Louisiana State University 


Rock Island, TN 


Goyer 


Robert 


EHC 


Consultant 


Chapel Hill, NC 


Grelecki 

1 ' 


Chester 


EEC 


Hazards Research Corporation 


Mount Arlington, i^J 



Report of the Science Advisory Board Staff 



294 



ANNUAL REPORT 



£a^ 



e B-17 



LAST NAME 


FIRST NAME 


COMMITEE 


Greer 


Unda 


NRDC 


Guilmette 


Raymond 


RAC 


Hammond 


Katharine S. 


lAQCC 


Hammond 


Paul B. 


CASAC 


Hansen 


Frederic J. 


EC 


Harbison 


Raymond 


EHC 


Harris 


Robert L. 


RAC 


Hartung 


Rolf 


EPEC 


Hawkins 


Charles 


EPEC 


Heath 


Clark 


RAC 


HIdy 


George M. 


EEC 


Hockman 


Edwin L. 


EEC 


Hopke 


Philip 


RAC 


Howard 


Walter 


EHC 


Inyang 


Hilary 


EEC 


Jacobson 


JayS. 


CASAC 


Jasanoff 


Sheila 


EC 


Jeffries 


Harvey E. 


CASAC 


Jenkins 


Kenneth 


EPEC 


Johnson 


E.Marshall 


EHC 


Johnson 


James D. 


DWC 


Johnston 


Carol A. 


EPEC 


Kabat 


Geoffrey C. 


lAQC 


Kalton 


G. Graham 


RAC 


Kasperson 


Roger E. 


EPEC 


Kaufman 


David G. 


DWC 


Kendall 


Ronald 


EPEC 


Khalil 


M. Aslam 


EEC 


Kim 


Nancy K, 


EHC 


Kimberle 


Richard A. 


EPEC 


Koenig 


JaneQ. 


CASAC 


Kreamer 


David K. 


RAC 


Kuschner 


Marvin 


EHC 


Laird 


NanM. 


RAC 


Lamb 


James C. 


RSAC 


Lebowitz 


Michael 


CASAC 


Lederman 


Peter B. 


EEC 


Lee 


Ramon 


DWC 


Legge 


Allan 


CASAC 


Longo 


Lawrence D 


CASAC 



AFFILIATION CITY, STATE 

Natural Resources Defense Council Washingtin, DC 

Inhalation Toxicology Research Institute Albuquerque, NM 

University of Massachusetts Medical Ctr Worcester, MA 

University of Cincinnati/Ketter Cincinnati, OH 
Oregon Department of Environmental Quality Portland, OR 

Univ. of Florida Alachua, FL 

University of North Carolina-Chapel Hill Chapel Hill, NC 

University of Michigan Ann Arbor, Ml 

Utah State University Logan, UT 

American Cancer Society Atlanta, GA 

Electric Power Research Inst. Palo Alto, CA 

Amoco Corporation Tulsa, OK 

Clarkson University Potsdam, NY 

Retired St. Louis, MO 

Geoenvironmental Design & Research, Inc. Fairfax, VA 

Boyce Thompson Institute at Cornell Univ Ithaca, NY 

Cornell University Ithaca, NY 

University of North Carolina Chapel Hill, NC 

California State University Long Beach, CA 

Jefferson Medical College Philadelphia, PA 

University of North Carolina Chapel Hill, NC 

Univ. of Minnesota Duluth, MN 

Yeshiva University Bronx, NY 

Westat Rockville, MD 

Clark University Worcester, MA 

University of North Carolina Chapel Hill, NC 

Clemson University Pendleton, SC 

Oregon Graduate Institute Beaverton, OR 

New York Department of Health Albany, NY 

Monsanto Company St. Louis, MO 

University of Washington Seattle, WA 

University of Las Vegas Las Vegas, NV 

State University of New York, Stony Brook Stony Brook, NY 

Harvard University Boston, MA 

Jellinek, Schwartz & Connolly, Inc. Ariington, VA 

University of Arizona, Tucson, AZ 

Roy F. Weston, Inc. Westchester, PA 

Illinois American Water Company Belleville, IL 

Biosphere Solutions Calgary, Alberta, 

Loma Linda University Loma Linda, CA 



Report of the Science Advisory Board Staff 



295 



re B-18 



ANNUAL REPORT 



LAST NAME 


FIRST NAME 


COMMtTEE 


AFFILIATION 


Cmr, STATE 


Lowndes 


Herbert E. 


EHC 


Rutgers University 


Piscataway, NJ 


Lue-Hing 


Cecil 


EEC 


Metro. Water Reclani. Dist of Gtr Chicago 


Chicago, IL 


Luthy 


Richard G. 


EEC 


Carnegie-Mellon University 


Pittsburgh, PA 


MacKay 


Donald 


EPEC 


University of Toronto 


Toronto, Ontario 


Mahoney 


James 


CASAC 


International Technology Corporation 


Torrance, CA 


Mailman 


Richard B. 


EHC 


University of North Carolina 


Chapel Hill, NC 


Mancini 


John 


EPEC 


John Mancini Consultants, Inc. 


Ariington, TX 


Manning 


William 


CASAC 


University of Massachusetts 


Amherst, MA 


Martin 


James 


RAC 


Univ of Michigan 


Ann Arbor, Ml 


Marty 


Melanie 


CASAC 


CA Office of Env Health Hazard Assessment 


Berkeley, CA 


Massmann 


Joel 


EEC 


University of Washington 


Seattle, WA 


McBee 


Karen 


EPEC 


Oklahoma State University 


Stillwater, OK 


McClelland 


GaryH. 


EEAC 


University of Colorado 


Boulder, CO 


McKinley 


Marvin D. 


EEC 


University of Alabama 


Tuscaloosa, AL 


McMichael 


Francis C. 


EEC 


Carnegie-Mellon University 


Pittsburgh, PA 


McMurry 


Peter H. 


CASAC 


University of Minnesota 


Minneapolis, MN 


Menzel 


Daniel B. 


EHC 


Duke University Medical Center 


Durham, NC 


Mercer 


Robert R. 


CASAC 


Duke University Medical Center 


Durham, NC 


Meyer 


H. Robert 


RAC 


Consultant 


Fort Collins, CO 


Michel 


Jacqueline 


RAC 


Research Planning Inc. 


Columbia, SC 


Miller 


Fred 


EHC 


Chemical Industry Institute of Toxicology 


RTP, NC 


Mitchell 


Robert C. 


EEAC 


Clark University 


Worcester, MA 


Moomaw 


William R 


EPEC 


Tufts University 


Medford, MA 


Morey 


Rexford 


EEC 


Moray Environmental Mgmt, Inc 


Hudson, NH 


Morgan 


M. Granger 


EEC 


Carnegie Mellon University 


Pittsburgh, PA 


Morrison 


Robert D. 


EC 


R. Morrison & Associates 


Valley Center, CA 


Mueller 


Peter K. 


CASAC 


Electric Power Research Institute 


Palo Alto, CA 


Mullins 


Judith 


EEC 


General Motors 


Detroit, Ml 


Mushak 


Paul 


CASAC 


PB Associates 


Durham, NC 


Napier 


Bruce A. 


RAC 


Battelle Pacific Northwest 


Richland, WA 


Nerode 


Anil 


RSAC 


Cornell University 


Ithaca, NY 


Neuhauser 


Edward 


EPEC 


Niagara Mohawk Power Corp 


Syracuse, NY. 


Neuhold 


John M. 


EPEC 


Utah State University 


Logan, UT 


Nielsen 


David M. 


EEC 


Nielsen Ground-Water Science, Inc. 


Galena, OH 


Nisbet 


lanC. 


EPEC 


I.e. T. Nisbet & Company, Inc. 


Lincoln, MA 


Nixon 


Scott 


EPEC 


University of Rhode Island 


Narragansett, Rl 


North 


D. Warner 


EHC 


Decision Focus, Inc. 


Los Alto, CA 


Nygaard 


Oddvar 


RAC 


Case Western Reserve University 


Cleveland, OH 


O'Connor 


Mary Ellen 


RAC 


University of Tulsa 


Tulsa, OK 


O'Melia 


Charles 


EEC 


Johns Hopkins University 


Baltimore, MD 



Report of the Science Advisory Board Staff 



296 



ANNUAL REPORT 



ie B-19 



LAST NAME 


FIRST NAME COMMITEE 


AFFIUATION 


CITY, STATE 


Oberdoerster 


Gunter 


EHC 


University of Rochester 


Rochester, NY 


Olsen 


Betty H. 


EPEC 


University of California, Irvine 


Irvine, CA 


Omenn 


Gilbert 


CASAC 


University of Washington 


Seattle, WA 


Oppenheimer 


Michael 


CASAC 


Environmental Defense Fund 


New York. NY 


Overcash 


Michael R. 


EEC 


North Carolina State University 


Raleigh, NC 


Pefley 


Richard 


CASAC 


Rebred 


Santa Clara, CA 


Peterson 


Richard 


EPEC 


University of Wisconsin 


Madison, Wl 


Pierce 


Donald 


RAC 


Oregon State University 


Corvallis, OR 


Poe 


Gregory L. 


EEAC 


Cornell University 


Ithaca, NY 


Preslo 


Lynne 


EEC 


ICF Kaiser Engineers 


Oakland, CA 


Rabinowitz 


Michael B. 


CASAC 


Marine Biological Laboratory 


Falmouth, MA 


Rail 


David 


EHC 


Consultant 


Washington, DC 


Regal 


Philip 


EPEC 


University of Minnesota 


Minneapolis, MN 


Reuhl 


Kenneth R. 


EHC 


Rutgers University 


Piscataway, NJ 


Riley 


Jesse 


RAC 


Consultant 


Charlotte, NC 


RIngen 


Knut 


EHC 


Center to Protect Workers Rights 


Washington, DC 


Ringer 


Robert K. 


EPEC 


Consultant 


Traverse City, Ml 


Risser 


Paul G . 


EPEC 


University of Newr Mexico 


Albuquerque, NM 


Roberts 


Donald W. 


EPEC 


University of Arizona 


Tucson, AZ 


Roberts 


Paul 


EEC 


Stanford University 


Palo Alto, CA 


Rockette 


Howard 


lAQC 


University of Pittsburgh 


Pittsburgh, PA 


Rodier 


Patricia 


DWC 


University of Rochester 


Rochester, NY 


Rodricks 


Joseph V. 


RAC 


Environ Corporation 


Arlington, VA 


Rose 


Joan B. 


EHC 


University of South Florida 


St. Petersburg, FL 


Ross 


Benjamin 


RAC 


Disposal Safety, Inc. 


Washington, DC 


Ross 


Stephen T. 


EPEC 


University of Southern Mississippi 


Hattiesburg, MS 


Roth 


Philip 


CASAC 


Envair 


San Anselmo, CA 


Rowe 


Robert D. 


CASAC 


RCG/Hagler, Bailly, Inc. 


Boulder, CO 


Rozman 


Karl K. 


EHC 


University of Kansas Medical Center 


Kansas City, KS 


Rundberg 


Robert S. 


RAC 


Los Alamos National Laboratory 


Los Alamos, NM 


Russell 


Clifford S. 


EEAC 


Vanderbilt University 


Nashville, TN 


Ryckman 


Devere 


EEC 


REACT 


St. Louis, MO. 


Safe 


Stephen H. 


EHC 


Texas A&M University 


College Station, TX 


Saum 


David • 


EEC 


Infiltec, Saum Enterprises, Inc. 


Falls Church, VA 


Schachter 


Edvirin Neil 


CASAC 


Mt. Sinai Medical Center 


New York, NY 


Schnoor 


Jerald 


EPEC 


University of Iowa 


Iowa City, lA 


Schreck 


Richard 


CASAC 


General Motors Research Laboratory 


Warren, Ml 


Schull 


William 


RAC 


University of Texas 


Houston, TX 


Sclalli 


Anthony 


EHC 


Georgetown University Medical School 


Washington, DC 


Segerson 


Kathleen 


CASAC 


Department of Economics 


Storrs, CT 



Report of the Science Advisory Board Staff 



297 



page 


B-20 




ANNUAL REPORT 


LAST NAME 


FIRST NAME 


COMMITEE 


AFFIUATION 


CtTY, STATE 


Shapiro 


Joseph 


EPEC 


University of Minnesota 


St. Paul, MN 


Shugart 


Herman H. 


EPEC 


University of Virginia 


Charlottesville, VA 


Shugart 


LeeR. 


EPEC 


Oak Ridge National Laboratory 


Oak RkJge, TN 


Sinclair 


Warren 


RAC 


National Council on Radiation Protection 


Bethesda, MD 


Small 


Mitchell 


EEC 


Carnegie Mellon University 


Pittsburgh, PA 


Smith 


Clifford V 


RAC 


GE Fund 


Fairfield. CT 


Sobsey. 


Mark D. 


DWC 


University of North Carolina 


Chapel Hill. NC 


Spade 


Anne 


EPEC 


Purdue University 


West Lafayette, IN 


Speizer 


Frank 


CASAC 


Harvard School of Public Health 


Boston. MA 


Spengler 


John D. 


CASAC 


Harvard University 


Boston, MA 


Stein ^ 


Michael 


EC 


University of Chicago 


Chicago, IL 


Stetter 


Joseph R. 


lAQCC 


Transducer Research, Inc. 


Naperville, IL 


Stolwijk 


Jan 


lAQCC 


Yale University 


New Haven. CT 


Stout 


Judy 


EPEC 


Dauphin Island Sea Lab 


Dauphin Island, AL 


Sunderman 


Frederick 


EHC 


University of Connecticut School of Medicine 


Farmlngton, CT 


Susskind 


Charles 


RAC 


University of California 


Berkeley, CA 


Suter 


Glenn 


CASAC 


Oak Ridge National Laboratory 


Oak Ridge. TN 


Swenberg 


James A. 


EHC 


University of North Carolina 


Chapel Hill, NC 


Taub 


Frieda B. 


EPEC 


University of Washington 


Seattle, WA 


Taylor 


George E. 


CASAC 


University of Nevada-Reno 


Reno, NV 


Templeton 


William L. 


RAC 


Battelle Pacific Northwest 


Richland, WA 


Tephly 


Thomas R. 


DWC 


University of Iowa 


Iowa City, lA 


Thein 


Myint 


EC 


Oak Ridge National Laboratory 


Oak Ridge, TN 


Tiedje 


James M. 


EPEC 


Michigan State University 


East Lansing, Ml 


Tikuisis 


Peter 


CASAC 


Defense Civil Inst of Env. Medicine 


North York, ONT 


Till 


John E. 


RAC 


Radiological Assessments Corp. 


Neeses, SC 


Travis 


Cheryl 


RSAC 


University of Tennessee 


Knoxville, TN 


Trehy 


Michael 


RSAC 


Monsanto Corporation 


St. Louis, MO 


Trussell 


R. Rhodes 


DWC 


Montgomery Watson Consulting Engineers 


Pasadena, CA 


Utell 


Mark 


CASAC 


Unlv of Rochester Medical Center 


Rochester, NY 


Valentine 


Jane 


EHC 


University of California at Los Angeles 


Los Angeles, CA 


Van 


Richard A. 


RAC 


Lawrence Livermore National Laboratory 


Livermore. CA 


Konynenburg 










Vlachos 


Evan 


EEC 


Colorado State University 


Fort Collins. CO 


Voilleque 


Paul 


RAC 


MJP Risk Assessment, Inc. 


Idaho Falls. ID 


von Lindem 


Ian 


CASAC 


TerraGraphlcs Environmental Engineering 


Moscow. ID 


Wallsten 


Thomas 


EHC 


University of North Carolina 


Chapel Hill. NC 


Walton 


Barbara 


EPEC 


Oak Ridge National Laboratories 


Oak RWge. TN 


Ward 


C. Herb 


EEC 


Rice University 


Houston. TX 


Ware 


James H. 


CASAC 


Harvard University 


Boston, MA 



Report of the Science Advisory Board Staff 



298 



ANNUAL REPORT 



£23; 



e B-21 



LAST NAME 


FIRST NAME 


COMMITEE 


Weiss 


Bernard 


EHC 


Weis 


Judith S. 


EPEC 


Weiss 


Scott T. 


lAQC 


Whicker 


Floyd W. 


RAC 


Whipple 


Christopher 


RAC 


White 


Warren H. 


CASAC 


Wiersma 


G. Bruce 


EPEC 


Williams 


Philip B. 


EHC 


Wilson 


John 


EEC 


Wilson 


Richard 


RAC 


Winner 


William 


EPEC 


Witschi 


Hanspeter 


RSAC 


Wood 


Ronald W. 


CASAC 


Woods 


James E. 


lAQC 


Wyzga 


Ronald 


EHC 


Yosie 


Terry F. 


EC 


Zeise 


Lauren 


EHC 



AFFIUATION CITY, STATE 

University of Rochester Rochester, NY 

Rutgers University Newark, NJ 

Harvard University Boston, MA 

Colorado State Universtiy Fort Collins, CO 

Clement International Oakland, CA 

Washington University St Louis, MO 

University of Maine Orono, ME 

Philip Williams & Associates, Ltd. San Francisco, CA 
New Mexico Institute of Mining and Technology Socorro, NM 

Harvard University Cambridge, MA 

Oregon State University Corvallis, OR 

University of California-Davis Davis, CA 

New York University Medical Center New York, NY 

Virginia Polytechnic Institute Blacksburg, VA 

Electric Power Research Institute Palo Alto, CA 

E. Bruce Harrison Company Washington, DC 

California Environmental Protection Agency Berkeley, CA 



Report of the Science Advisory Board Staff 



299 



February 22, 1996 F:\meinb\panel.sel 

Received from Bob Flaak, drafted in Jan., 1995 

SELECTION OF CONSULTANTS FOR SCIENCE ADVISORY BOARD PANELS 

Draft SOPS for SAB Staff 
Background 
1 

2 Under the provisions of the Federal Advisory Committee Act 

3 (FACA) , all Federal advisory committees, including the Science 

4 Advisory Board, are required to have balanced membership. 

5 Balance, in this context, refers to the breadth of technical 

6 viewpoints represented during the consideration of scientific, 

7 engineering and economic issues. The SAB is committed by both 

8 principal and law to convening panels that meet this requirement. 

9 In addition, to the extent practicable, the Board will broaden 

10 the concept of balance to include appropriate geographical and 

11 organizational representation. 
12 

13 The Charter of the Board states that the Board "...will 

14 consist of a body of independent scientists and engineers of 

15 sufficient size and diversity to provide a range of expertise 

16 required to assess the scientific and technical aspects of 

17 environmental issues." The Charter goes on to state that the 

18 Board is "...authorized to consitute such specialized committees 

19 and ad hoc investigative panels and subcommittees as the 

20 Administrator and the Board find necessary to carry out its 

21 responsibilities." 
22 

23 The Science Advisory Board consists of approximately 100 

24 members who are appointed by the EPA Administrator, and who serve 

25 on the ten standing committees and various ad hoc panels of the 

26 Board. The bulk of the reviews conducted by the Board are 

27 carried out by these standing committee. When additional 

28 expertise or balance is needed, these members are supplemented by 

29 consultants who are appointed by the SAB Staff Director. In 

30 certain cases, an ad hoc panel is created to review a specific 

31 issue. 
32 

33 Although every effort will be made to ensure that all SAB 

34 panels are balanced, clearly, issues that are more controversial, 

35 contentious or complicated will require a more concentrated 

36 effort by staff to ensure that the appropriate balance is 

37 achieved. During this process, consistency is maintained with 

38 the July 1994 EPA Peer Review Policy. The procedure outlined 

39 below identifies the primary steps in the process whereby the 

40 Board creates balanced panels and how the SAB Staff, and 

41 ultimately, the SAB Staff Director makes decisions concerning the 

42 selection of consultants. 
43 

44 



300 



45 Types of Review Panels 
46 

47 The Board conducts it operations using several types of 

48 review groups. These include the following: 
49 

50 a) Standing Committee - these are one of the ten committees 

51 that conduct the bulk of the scientific and technical reviews 

52 performed by the Board. These committees consist of between 

53 seven and fourteen members who are appointed by the EPA 

54 Administrator. Sometimes the committees are supplemented by 

55 consultants to the Board. The Committees report to the SAB 

56 Executive Committee. 
57 

58 b) Subcommittee - a group formed under one of the ten 

59 standing committees, chaired by a member of the Board (usually 

60 from that standing committee) and containing a number of members 

61 of that parent committee, other SAB members and consultants to 

62 the Board. Subcommittees report to its parent committee. 
63 

64 c) ad hoc Panel - a group formed by the Executive Committee, 

65 chaired by a member of the Board (usually from the Executive 

66 Committee) and containing a number of SAB members and consultants 

67 to the Board. Ad hoc panels report to the Executive Committee. 
68 

69 The term "Panel" will be used in this procedural document to 

70 include all of the above groups. 
71 

72 Types of Committee Review Operations 
73 

74 The Board conducts consultations , provides advisories and 

75 performs reviews . In addition, the Board may also offer 

76 unsolicited commentaries on issues of interest. These are 

77 defined elsewhere. For the purpose of this procedural document, 

78 the term "review" will be used to include all such operations. 
79 

80 Development of the Charge 
81 

82 In general, once the Board and the Agency have agreed upon a 

83 topic for SAB review, the subject is assigned to one of the 

84 standing committees or an Executive Committee ad hoc panel. The 

85 committee Chair and the Designated Federal Official (DFO) have 

86 primary responsibility for forming a balanced review panel. A 

87 key aspect in the panel selection process is the charge, the 

88 mutually agreed upon description of what the Agency would like 

89 the review to accomplish and/or what the SAB expects to focus 

90 upon. A well-characterized charge is essential to the panel 

91 selection process, for it identifies the critical expertise 

92 necessary for the review process. 
93 

94 



301 



95 Panel Selection Procedures 
96 

97 a) General - A conscious effort is made to avoid selecting 

98 individuals who have had a substantive hand in the development of 

99 the document to be reviewed. At the same time, however, 

100 experience has shown the utility of having some representation 

101 from individuals or groups who may have been involved in prior 

102 reviews of the same issue or document. The goal is to minimize 

103 the appearance or practice of an individual's reviewing his/her 

104 own work, while at the same time, maintaining an historical link 

105 to earlier deliberations surrounding the document or issue. 
106 

107 b) Specific Procedures - These are the usual steps taken by 

108 the DFO in the panel selection process. 
109 

110 1) Identify the critical issues and areas of expertise 

111 needed for the review. This information comes from the written 

112 charge, from conversations with EPA Program staff providing the 

113 review materials, and from a review of the documents that are the 

114 subject of the proposed review. 
115 

116 2) Identify the knowledgeable stakeholders. These include 

117 Agency program offices. Laboratories, Regional Offices and other 

118 Agency components, other Federal, state or local government 

119 organizations, environmental groups, industry or trade 

120 organizations, citizen groups or other interested parties. 
121 

122 3) Solicit candidates from appropriate stakeholders. By 

123 knowing the issues identified in the charge, these groups can 

124 provide the SAB with suggestions to improve the balance of the 

125 panel being formed. Candidates may also be obtained from the 

126 SAB'S periodic Federal register notice soliciting candidates for 

127 the Board. 
128 

129 4) The DFO will work with the panel Chair to identify 

130 critical needs and to determine which areas of expertise and what 

131 individuals will constitute a balanced panel. At this point, the 

132 DFO should involve the SAB Membership Subcommittee, soliciting 

133 their views on expertise or suggestions on candidates. 
134 

135 



302 



136 
137 
138 
139 

140 
141 

142 
143 
144 
145 
146 



147 
148 
149 
150 
151 
152 
153 
154 
155 
156 
157 
158 
159 

160 
161 
162 
163 
164 
165 
166 
167 
168 
169 
170 
171 
172 
173 
174 
175 
176 
177 
178 
179 



5) The DFO will usually develop a simple matrix to identify 
the expertise needed and the candidates considered. An example 
of each is given in the lower portion of the matrix: 



Charge 


Expertise 


Candidate 


Source of 


Address of 


Element 


Needed 




Candidate 


Candidate 


Identifies 


identifies 


name of 


who 


what 


the 


the needed 


individuals 


provided 


organizati 


specific 


discipline 


being 


the name of 


on is the 


element of 


or 


considered 


the 


candidate 


the Charge 


specialty 




candidate (s 


from 
(e.g. , 
industry, 


















etc) 


Review of 


Toxicology 


Dr. R. 


EPA/ORD 


U. 


the 




Smith 




Pittsburgh 


Adequacy 






Panel Chair 




of the 




Dr. S. 




U. Chicago 


Human 


Epidemiolog 


Jones 


FR Notice 




Health 


y 






NRDC 


Chapter 




Dr. L. 


Gen. Motors 




Carbon 




Brown 




Consultant 


Monoxide 






Gen. Motors 




Air 




Dr. D. 


and Panel 


Oak Ridge 


Quality 




Moran 


Chair 


NL 


Criteria 










Document 




Dr. J. 
Jackson 







6) Once primary candidates are identified, the DFO will 
consult with the Staff Director to identify any remaining issues 
and to finalize the panel selections. The Staff Director will 
approve the list of panelists to be recruited and/or to serve on 
the panel. 

7) The DFO will then contact prospective panelists to 
determine availability and interest, preparing the final roster 
of panelists. 

8) Once this has been completed, personnel paperwork will be 
initiated for any new consultants. A letter will be prepared 
inviting each panelist to serve on the panel for the stated 
purpose. This letter will be signed by the Staff Director. 

9) The DFO will prepare a brief summary for the permanent 
administrative record, including the matrix outlined in 5) 
above, to identify how balance was achieved for this particular 
panel . 



303 



February 16, 1996 F:\ineinb\ineinbproc.doc 

SAB MEMBERSHIP SEARCH/SELECTION PROCESS 

The Members (Ms) of the Science Advisory Board (SAB) are 
appointed by the Administrator. The Executive Committee of the 
SAB has adopted guidelines on service on the Board [Ref: Annual 
Report of the SAB Staff, Appendix Bl, "Guidelines for Service on 
the Science Advisory Board", EPA-SAB-EC-95-001] that have 
generally been followed by the Administrator, as well. 

Historically, the Administrator has made appointments from a 
list of candidates supplied by the Staff Director following an 
extensive search process, which is the subject of this document. 

The SAB Staff maintains "an open application" policy 
regarding nominations for membership on the Board. That is, 
names of potential candidates are accepted from any source at any 
time. 

The SAB Staff Director develops the list of candidates by 
drawing upon a) input from the SAB Staff, b) input from the public, 
c) input from the Board, and d) input from the Agency. 

Note that the Panel of' experts convened to examine a 
particular issue is usually composed of Members of the SAB and of 
Consultants to the SAB. Members are appointed by the 
Administrator to serve on any of 10 standing committees that will 
review a range of issues. Consultants are appointed by the Staff 
Director — upon the advice of the SAB Staff, generally with the 
concurrence of the Chair of the Panel — to participate most often 
in the review of a single issue. 

Additional details on different kinds of affiliations with 
the SAB can be found in the Annual Report [Ref: Annual Report of 
the SAB Staff, Appendix B2, "Types of Affiliation with the SAB", 
EPA-SAB-EC-95-001]. 

Input from the Staff 

The SAB Staff are responsible for tracking the membership 
rosters of their Committees and for planning changes in 
membership that are consistent with FACA, the guidelines, and the 
needs of the Committees to have relevant expertise available to 
address adequately the issues coming before the Committee. 

In carrying out this responsibility, the SAB Staff draw upon 
their professional knowledge and contacts. 

In some instances, the Staff have generalized the task by 
maintaining a graphical presentation of Committee membership, 
expertise, and terms of service, projected out over a 5-10 year 
period. (See attached.) The chart shows when a person with a 
certain expertise completes his/her term of service, thus 
necessitating a replacement. This assessment of needs focuses 
the membership search process. The intent is to apply this long- 
range planning strategy more uniformly across the Committees. 

The selection of SAB Consultants is separate from, but 
related to, the selection of SAB Members. The SAB Staff play a 
key role in identifying candidates to serve as Consultants to 



304 



participate in reviews of specific issues. The Staff comb a 
variety of sources in the public and private sectors to gather 
names of Consultant candidates. For particularly controversial 
issues, the list of candidates can approach or exceed 100 
individuals. 

Consultants often develop into good candidates for 
membership, since participation as a Consultant allows the 
individual and the Board to mutually assess the level of 
interest, availability, and effectiveness of the relationship. 

Input from the Public 

On a generally biannual basis the SAB Staff Director 
solicits the names of candidates for any and all of the SAB 
committees via a public notice in the Federal Register. The 
notice describes the Board, its structure and function, the 
necessary qualifications for members, and the process for 
submitting nominations. This solicitation usually results in the 
submission of the names of about 100 candidates. 

On occa.sion, the Staff will contact specific groups to call 
to their attention that nominations for SAB membership are being 
accepted. Such groups have included the American Industrial 
Health Council (AIHC) , the Association of Hispanic Colleges and 
Universities (AHCU) , the Environmental Defense Fund (EDF) , and 
Women in Engineering and Science (WISE) . Other groups who have 
expressed an interest in supplying nominations include the 
National Association of State Universities and Land-Grant 
Colleges (NASULGC) . 

There are plans to extend the solicitation for nominees 
through the SAB Home Page on the Internet, through news releases 
to newsletters and professional society publications, and through 
networking with other professional and advisory groups. 

Input from the Board 

Each year the SAB Staff work with the Committee Chairs to 
review the upcoming openings on the Board, to identify needed 
expertise for each of the Committees, and to suggest the names of 
candidates to submit to the Administrator. In many cases this 
process involves some or all of the Members of a given Committee. 

Some time ago the Executive Committee established a 
Membership Search Subcommittee, whose responsibilities have 
included taking a global view of the list of candidates likely to 
be submitted to the Administrator, checking for diversity in 
terms of gender, "address", minority status, and geography. In 
addition, the Subcommittee serves as a source of counsel to the 
Staff Director on issues related to membership. 

The Staff Director also keeps the SAB Chair informed of 
developments throughout the candidate selection process. 

Input from the Agency 

The Agency is also an important, initial source of names of 
candidates for SAB membership. In many instances the Program 
Offices have been working a particular technical issue for many 



305 



months or even years. Therefore, they have are generally aware 
of most of the specialists in that field. 

The SAB Staff is aware that such suggestions may reflect an 
inadvertent bias towards individuals who might be favorably 
disposed toward the Office's project. Therefore, these 
recommendations are examined with particular care, with an 
emphasis of assuring balance on the Committee. 

There are plans to formalize this process through a 
solicitation letter from the Deputy Administrator to the Agency 
asking for the names of candidates to serve on the Board. (A 
similar procedure is currently followed for obtaining Agency 
requests for projects that should be placed on the SAB ' s agenda.) 
The process would begin in the early spring and be designed to 
dove-tail with the public solicitation. 

The Final Selection 

As noted above, the appointment of SAB Members is within the 
purview of the Administrator, who generally delegates the actual 
selection to the Deputy Administrator. 

The Federal Advisory Committee Act (FACA) lays down the 
following general criteria for membership: 

a. Technically qualified individuals 

b. Non-Federal employees 

c. A "balanced" Board, which has been interpreted as 
meaning a range of legitimate scientific points of 
view. Experience has shown that the Board functions 
most effectively when its Members are selected from the 
"broad middle" of the spectrum of technical points of 
view, rather that from the "wings". 

Historically, the selection process has involved the SAB 
Staff Director's presenting the Deputy Administrator with at 
least two names for every open slot on the Board's roster. In 
most cases, the Staff Director has recommended one of the two 
names and has included a justification for the recommendation. 

In some instances, the Deputy Administrator has accepted the 
recommendations directly. In other cases, he/she has discussed 
the list with the Staff Director. On one occasion the Deputy 
Administrator conferred with scientifically oriented AAs before 
making the final selection, without the Staff Director being 
present. This year, the Staff Director was asked to confer with 
the AAs and to include their reaction to the list in his 
submission. 

Within the past decade, the Administrator has not appointed 
anyone to the SAB whose name has not passed through some version 
of the process described above. 



306 



Procedure 

At the beginning of an SAB meeting on a single issue or when an agenda item is 
introduced that has the potential for COI or other impartiality concerns, the DFO will 
ask each M/C on the panel to speak for the record on his/her background, experience, 
and interests that relate to the issues at hand. 

The following are examples of the type of material that is appropriate to mention 
in such a disclosure (please refer to Attachment A - Mock Disclosure which provides 
an example of how an individual can provide their disclosure at an SAB meeting): 

a) Research conducted on the matter by the individual or their employer. 

b) Previous public pronouncements (particularly those cases in which a 
specific position is taken), e.g., judicial proceedings such as serving as an 
expert witness or providing testimony, preparation of articles for general 
or scientific readership, media appearances (TV, radio, newspapers, etc.), 
etc. 

c) Interests of employer in the matter, and the specific role of the individual 
in that interest.. 

d) A general description of any other financial interests in the matter: e.g., 
having investments that might be directly affected by the matter. Note: 
Members/Consultants are not obligated to reveal information contained in 
their SF-450 that would otherwise remain confidential. 

e) Other links: e.g., research grants to the individual or their employer from 
parties-including EPA-that would be related to the matter. 

During this disclosure, the M/Cs should not refer to any of their activities as a 
"conflict of interest". If a real conflict did exist, the DFO would have made that 
judgment prior to the meeting. 

The DFO will also publicly refer to any individual waivers from the COI 
regulations which have been granted by EPA for the purposes of the meeting. The 
DFO will assure that the minutes of the meeting reflect the fact that such disclosures 
were made, and if possible, the nature of the disclosures. In addition, the minutes 
should describe any situations in which, in the opinion of the DFO, an actual or 
perceived COI existed and how the issue was addressed. 



G:\USER\SAB\POLICIES\DISCLOS.COI 
Last Revised: August 4, 1995 



307 






I Mi. -I 



^ o S E .;£ c 
o- E .2 E S i£ o 

- = s i = E S 



g >- * 5 E s i . 



V ~ S E - = -^ ■ 



1 a- o u. 1- a - 
■ S^^ = E „ 

•> I i - s- 

■ "~ £■ E g " §.• 
■ fl .^ M — .- 

• eII^I I. 



9--Sa- S.P^- 



ust di 
s of [ 
iaI in 
ental 
mmin 
mem 
rvicei 
ment 
rporat 


^111 = 


you m 
usines 
f i nanc 

incid 
ly swi 

aparti 
ool se 
: apart 
ily coi 


1 fund, pensic 
lUsl disclose 
sources of inc 
investment f 
, identify it b 


Thus, : 
de or b 
parate 
t solely 
ur fami 
ses an 
its p 
lose the 
he fam 


ysis. 
■y tra 
:ir se 
e no 
if yc 
urcha 
tion t 
disci 
1 to t 


3 ^ -o -a " 
1 S«H-" 



" " > I S § ' I £ s s * 



f I i-l-i 5 g. 



• E c E °- S I 






! E j; i; .9 
; > 3 ~ D. 

f = c" 5 , 

'o s; g,>, 

= ~ 9 

'^^ <= 

^. 3 ;c 



s si 



^ Si S - a 3 

= '' ^ ^ g _■ 

D. C T3 ■= f^ 

iE o ^ E - ^ 

" 1! a 3 3 -c 

c "S S BO 

aj w o ^ e tj 



•E * 
5 5 



.':i «i 5 .2 -o — u E w -^ - D. 
3;;-n_E — r-S-i — o. 

' 5 " I g -n g.H s ^.i; :e g- 

■Sisi.oS£E^.E2^ = 
> ~ ^ "^ ~ ^ .^ •- I' -5 CL_ .£ 
S §..2,- I -.S-5 E 1-5 

:;S"E'5S^-g_-S>'i^£ 



^OH-£''ES«ia, 



WT3i£.-04JJ = 

Is -g = ■£ o 5 
Ka"sSl!=E 
"Sii>s-3_og 



o s.a: 



a.-o 



E := ■ _ 

- E a -S E 5 o 



2.S i 0.0 o o S. 

^■^ i-s esl . 

>-S°2i~ cEc 
o g. u c § c I 

^c = E'^--^5 
_c---iM E°or03'' 

- '^I = - "^ I ■^l = 2 K 
i_u _ ™ o c ^ = u. .2 " 

-Ills 5=lll^" 









1 


^ 




B 



u 


& 


£ 


E 





V 


< 


B. 


£ 


E 


ss 


A 


£ 


B 


^ 


^ 


n 




3 


hi 

CO 


E 


(A 



V 


U 


ij 


> 

3 
u 


a 
SI 

E 


U 




w 







M 


u 




u 







<J e 
I I 



11 1:!- 



. E 
c j; 5 .c ■- oib 






i ^ c o fl « "o 

=* S C o. 2 5 = 

00— " >> ■/: 

g u § 2 a. W .Si > 

M > g M ,. „ 3 



111 Ji|^^ 

O„3uj0-O.2nlo 

£> Si-^SSiEcS 

— OCC— c>- 4>Q. 

■o£ = E2^-oS-Ou 

g := c e _ >- a E Q--D 



.2 § 



; g-.E ~ 3 E a o 



o = 



a., 

e-E 



1 I 



■8 .2 s ° > 



.- O S - M 






^^ i-J 



1 2 1 
«8 »? 12 



ftp 2 ^ c-s 






308 



« 4> t B ooj= G *i 1^ f^ 'Ji an 'fS u wtrT3 

B c ^ M-o : -g 2 fe i i c _ 1, .2 c S 

-I E °lS ^-"--S = ° I"^ 3 '^ = 

° - ° o ■- o f. a ■? o I u -= = -s SI 

3 „- 1 S g i C " S < = S 8 S.- - S I 



f'^? 



ii.2 o 
C 2 "" 2 " S 
£ 55 00 > " > 



.- Si c j:; 
B8 o o ^ 



.2 



OS !§ o 5 £ i 



o i ^ a. 0.!= n.E.Hg<:2.ii™S-a.E2 



oil ° 

^ « § 8 

" o3 3 

I is si 



5 °-£* 

_>i > S C fcj 

.•2 ^ g - 3 
^ o = § .a 

< ■£ O (0 M 



1 K 

2 
"S 3 



^ s 



- K - Ji r 

u 2 g = 6 

" S I = ^ 

g u 3 o o 

= ^ o >> = 

!S S. u =■ > 



< C Ci 



u 3; =■ i^' g ^ «■ u E 



If 



- - 1 SL S 2 i 
- - -5 ° §..2 r J E S 

2y-S-3i:5£_ic-2- 

' " € -d '^ g -' _ -5 
; I S I £ I g i i 



'S.-S, 



= o 



,£^S 



<=■;;; -^ 



2 mB'^'S e S a > i -o 



! I, 
ll 

c 
It 



3 - 






■s-'~~ 



S S^ S^S 



c S S S t! 

D. 3 — C -^n 
u O O « -S 



2 >■«= I 
8i E = S-g 
— -a >.-o C 



^1 



o -a -o 2"! g 
"= - 5 S "■ o. 

- 5 .2 J se _ 



i£ .= € S-'S S, 



B o 



.|| 



E 3 S -S 
S > o — 



'S.f 



i S Si s. = 

^ E S 2 = 

. I S £ I 

H = S- = 2 



' ii 



- = 5 c o g£ S g c^23 



iS-i 



= l|clii8 = 

I |5».= "l|^2<Sgg.-S 

3 •= § •? -o ^ -2 «..2 - s i- . a - 

^ > E 8 S:= o'3'3y=5 = u 



« « ^ -o "3 -o "3 

I 8 s ".i I s. 

- = .£ 5 s i " 

: 5 o J c 5 "o 



S E 



' » O >, M 



«. S = C = 3 

a|i.= iis- 
§ - e I " g £ 

g 8-" g -O'S 
" o o £ .2 < " o 

~ E g g — ;g c 



'= .2 



"5 « ^ c E jAC S 

.° g i ■§ 



s^ 



^ -a O o .2 ^ 

g "■- o.E i:it^ 

E ;^ o D-.E _ j: M 
OSOji-EE*! 

u 3 . ^•S^8•2 
■SS- = p*j>ts 



8^- 

E-f. 



_ oi tm **• »» 

I- S ll' 






« o = 
.2gE 






: or* g 



. 2 w .2 ' 



It 



o o •= o I i 






- 5 °a 



^ 5.2 2 

o = a ?i 

■a g 5 J2 

w ™ w ti; 

"2 -• - o a 

2 -o u — g 

^ .a s .^ — 



E3i,?i 
12.^ si 

i.E'«l5 



W "^ C 



309 





1 






- 1 










; 


£ 


1 

E 


1 




--'c 




i 


[I 


s 


i'l 


1 


K- 


= 1 




'i^ 


8. 


-S 






- ° 


< 


s s 


? ? 






'o 




C ^ 






c 


if 


IC 
















c 


1 






- 




£ 






* 














t 


o 






■5. 




k 






? 


1 


I 






1 


1 


e 






^ ^ 










^ "^ 


1 








2 £ 








4 


^ C 


■^ a 


V 


1 


1 


^ ^' 


:^ 


° 


' 


t 




- ' 


















\, \. 


c ^ ^ 


- 


















; i E 








E ^ 


S ». 1 


% 






^ "« 


c = -■- 


- 






-c ^ 


i'S.'^ 


^ 






- =J 


e |~, 


° 


1 






I=! 


I 


1 




^ u 


- t £. 


oe 






~ »; 


-o"*^ S 


= 












^ 




■s ; 


- ^ - 


- 


J 




~ 3 


O-H c 


£ 


1 




-c ^ 




< 


2 






■s 


o 












S 




^ t 






s- 


>■ 




£i 


a 


I 


u 


■- 3 




M 




< 




a/- 


^ 






5 
E 



l|n|i|||i;J}iij^Jjji|ipt □niijjll^ 

|!y:i 1 tiii^iii 
iflMg 1 =i!i|sl 



a s^£ »; 



I s :- 1 s I 



?l fltliiiHiNiii'lliMil 1 illitllltl 



" s i. i ^ - „ - ,= = 
I a " t 



310 



|_ 

i 

o 

fi_ 

I 
I 

1 

6 - .. - , , 



I 

i 



a 

a 



g □ i 

2f u 1 

p S' 

a. E s- 

u f ■ 

a £•■ 

3 I ' 

O 5. 



D 



D 



1 8^ = 1 1 

=• g I I t 5 






h 
n 






1' 



; ~ E , 



I li I 2i - ' 



311 
POLICY FOR PUBLIC DISCLOSURE AT SAB MEETINGS 



Background 

The Science Advisory Board (SAB) contributes to the decision-making process 
of the U.S. Environmental Protection Agency (EPA) by evaluating the technical 
underpinnings upon which rules and regulations are built. In conducting such 
evaluations, SAB members and consultants (M/Cs) carry out their duties as Special 
Government Employees (SGE's), and, as a result, are subject to the COI regulations. 
Conflict-of-interest (COI) statutes and regulations are aimed at preventing individuals 
from (knowingly or unknowingly) bringing inappropriate influence to bear on Agency 
decisions which might affect the financial interests of those individuals, their family 
members and/or the organizations which employ them. 

In order to 'protect the integrity of the SAB process itself and the reputations of 
those involved, procedures have been established to address conflict-of-interest and 
other concerns about members' and consultants' impartiality. These procedures 
include the following: 

a) Having SAB M/Cs file an SF-450, Confidential Financial Disclosure 
Report (with annual updates, as required); 

b) Providing SAB M/Cs with required annual training via written informational 
material; e.g., "Standards of Ethical Conduct for Employees of the 
Executive Branch" (5 CFR Part 2635), "Take the High Road," and EPA 
Ethics Advisories 92-1 1 and 94-18; 

c) Delivering briefings to M/Cs on COI issues on a regular basis. 

Through the above procedures and regular, informed contact with M/Cs, the 
Designated Federal Official (DFO) on the SAB Staff normally identifies actual, as well 
as perceived, COI issues long before a public meeting occurs. When an actual COI 
situation is determined to exist, appropriate steps are taken to protect the individual 
and the process (e.g., either the M/C will recuse him/herself from discussions of the 
issue, the DFO will seek another M/C to participate in the meeting in lieu of the recused 
M/C, etc.). 

The following is a description of the public disclosure policy, an additional 
procedure that is designed to allow both fellow SAB M/Cs and the observing public to 
learn more about the backgrounds that SAB M/Cs bring to a discussion of a particular 
issue. In this way, all parties will gain a broader understanding of "where people are 
coming from" and provide additional insights to help observers and participants 
evaluate comments made during the discussion. 



312 



MOCK DISCLOSURE 
Or, How to Implement the Policy for Public Disclosure at SAB Meetings 



Background 

For several years each SAB meeting has had a period of "disclosure", during 
which panelists orally and voluntarily state their previous involvement with the technical 
issues before the Board. Each panelist is provided with a copy of "Policy for Public 
Disclosure at SAB Meetings" as guidance on the type of information to include in the 
disclosure. 

The mock disclosure below is intended to provide further guidance on how the 
disclosure might proceed. It is assumed, for purposes of this illustration, that the panel 
is reviewing a risk assessment of buckminsterfullerenes. 

Issues and Mock Responses 

a) Research conducted on the matter. 

/ have conducted research and published results on the 
thermodynamics and kinetics of the fullerene formation In low temperature 
flames. In some of this work, I have speculated about the possible 
occurrence of fullerenes in the environment. This information is relevant 
to the exposure portion of the risk assessment before us. I have not done 
any work on the toxicity of fullerenes, although-since I work with these 
materials routinely-l have both a professional and personal interest in the 
topic! Consequently, I am aware of a good bit of the literature related to 
the toxicology of fullerenes. 

b) Previous pronouncements made on the matter 

In addition to my scientific publications and presentations at 
professional meetings, I have written one general article for Discover 
magazine and have appeared in a NOVA TV segment on fullerenes. In 
the Discover article I did express some caution that in the current 
somewhat frenetic drive to investigate these unique materials and their 
physical properties (e.g., superconductivity), it is important that we also 
investigate the health and environmental hsks possibly posed by these 
substances. I have not appeared in any judicial proceedings related to 
the risks of these materials. 



313 



c) Interests of employer on the matter 

My employer-Buckyballs, Inc-is deeply involved in the 
development and testing of fullerenes for commercial purposes. My 
responsibilities are limited to the basic science division of the company 
and have nothing to do directly with product development, marketing, or 
sales. 

After discussing my situation with the SAB Staff and the EPA's 
Office of General Counsel, it has been determined that I have a legal 
conflict-of-interest in this review. However, the Agency has determined 
that my technical contribution is of such importance in this case that the 
Agency has granted me a waiver which will allow me to participate in this 
review. The DFO has a copy of the waiver for anyone who would wish to 
see it. 

I want to assure everyone that I will be as professionally objective 
as I can be on this matter But I think it is important that you are all aware 
of the conditions under which my participation is taking place. 

d) A general description of any other financial interests in the matter 

The SAB Staff have reviewed my Confidential Financial Disclosure 
statement (Form SF-450) and have determined that, other than my 
relationship with my employer, I have no other legal conflict-of-interest. 

However, I want everyone to be aware that my son is doing PhD 
work at the University of Cincinnati and has chosen to work in the area of- 
-you guessed it— fullerenes; specifically chlorine derivatives of branched- 
chain derivatives of C^q fullerenes. My principal interest here is in not 
getting scooped by my own son! He is currently supported by a grant 
from the National Science Foundation, although his major professor has a 
grant from the US EPA which supports another graduate student's work 
on continuous emission monitohng systems (CEMS) for particulate matter 
in the 10-20 micron range. 

e) Other links; e.g., research grants 

Early in my career, 20 years ago, I benefitted from an EPA training 
grant given to the University of Pittsburgh where I took my PhD in 
synthetic organic chemistry. Before joining Buckyballs, Inc eight years 
ago, I was an associate professor in the chemistry department at Cornell 
University. Duhng that period I received grants from a number of 
governmental sources (not EPA), plus two multi-year grants from the 
National Alliance for Incineration (NAI), which funded my work in flame 
chemistry. My first published paper on fullerenes stemmed from work 
supported by the NAI. 

G:\USER\SAB\POLICIES\MOCKDISC.COI 



314 



UNITED STATES 
ENVIRONMENTAL PROTECTION AGENCY 



SCIENCE ADVISORY BOARD 



DIOXIN REASSESSMENT REVIEW 



Grand Ballroom B-C 
Herndon Renaissance Hotel 

13869 Park Center Road 
Herndon, Virginia 22071 

Monday and Tuesday, 
May 15 and 16, 1995 

9:00 a.m. and 3:45 p.m. 

APPEARANCES: 

Chair 

DR. MORTON LIPPMANN 
New York University Medical Center 
Institute of Environmental Medicine 
Tuxedo, New York 

Members 

DR. WILLIAM B. BUNN 

Mobile Administrative Services Company, Inc. 

Princeton, New Jersey 

DR. KENNY S. CRUMP 
K S Crump Division 
Ruston, Louisiana 

DR. ERNEST E. McCONNELL 
Raleigh, North Carolina 

DR. HENRY C. PITOT 

McArdle Laboratory for Cancer Research 

Madison, Wisconsin 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



315 



APPEARANCES: (Continued) 
Consultants 

DR. RICHARD W. CLAPP 

B.U. School of Public Health 

Boston, Massachusetts 

DR. JOHN DOULL 
University of Kansas 
Kansas City, Kansas 

DR. RONALD W. ESTABROOK 
The University of Texas 
Dallas, Texas 

DR. JOHN GRAHAM 

Harvard Center for Risk Analysis 

Boston, Massachusetts 

DR. WILLIAM GREENLEE 

Purdue University 

West Lafayette, Indiana 

DR. NORBERT KAMINSKI 
Mich-igan State University 
East Lansing, Michigan 

DR. THOMAS MACK 

University of Southern California 

Los Angeles, California 

DR. JOHN McLACHLAN 

Tulane University 

New Orleans, Louisiana 

DR. DAVID OZONOFF 

Boston University School of 

Public Health 
Boston, Massachusetts 

DR. GABRIEL PLAA 
Department of Pharmacology 
Montreal, Quebec, Canada 

DR. DONALD REED 

Oregon State University 

Corvallis, Oregon 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



316 



APPEARANCES: (Continued) 

Consultant s 

DR. KNUTE RINGEN 

Center to Protect Workers' Rights 

Washington, D.C. 

DR. ALAN SILVERSTONE 

SUNY Health Science Center 

Syracuse, New York 

DR. SIDNEY STOHS, Dean 
Creighton University 
Omaha, Nebraska 

DR. BERNARD WEISS 
University of Rochester 
Rochester, New York 

DR. HANSPETER WITSCHI 
University of California 
Davis, California 

DR. TIMOTHY ZACHAREWSKI 
University of Western Ontario 
London, Ontario, Canada 

Federal Experts 

DR. MICHAEL GOUGH 
U.S. Congress OTA 
Washington, D.C. 

DR. MICHAEL I. LUSTER 

NIEHS/NIH 

Research Triangle Park, North Carolina 

DR. THOMAS UMBREIT 
CDRH/FDA 
Rockville, Maryland 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



317 



APPEARANCES: (Continued) 

Exposure Pane l 

Chair 

DR. JOAN DAISEY 
Lawrence Berkeley Laboratory- 
Berkeley, California 

Members 

DR. PAUL BAILEY 

Mobil 

Princeton, New Jersey 

DR. ROBERT HAZEN 
Bureau of Risk Assessment 
State of New Jersey 
Trenton, New Jersey 

KAI-SHEN LIU 

California Department of Health Services 

Berkeley, California 

THOMAS E. McKONE, Ph.D. 
University of California 
Davis, California 

DR. MARIA MORANDI 
University of Texas Health 
Science Center at Houston 
Houston, Texas 

DR. JONATHAN M. SAMET 
Johns Hopkins University 
Baltimore, Maryland 

DR. WILLIAM RANDALL SEEKER 

Energy and Environmental Research Corporation 

Irvine, California 

RON WHITE 

American Lung Association 

Washington, D.C. 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



23-557 0-96-11 



318 



APPEARANCES: (Continued) 

Consultan ts 

DR. RONALD KITES 
Indiana University 
Bloomington, Indiana 

DR. NANCY KIM 

New York State Department of Health 

Albany, New York 

DR. DENNIS PAUSTENBACH 
McLaren/Hart/ ChemRisk 
Alameda, California 

DR. JOHN JAKE RYAN 
Bureau of Chemical Safety 
Ottawa, Ontario, Canada 

DR. VALERIE THOMAS 
Princeton University 
Princeton, New Jersey 

Designated Federal Officials 

SAMUEL RONDBERG 

Science Advisory Board (1400F) 

U.S. Environmental Protection Agency 

Washington, D.C. 20460 

A. ROBERT FLAAK 

Science Advisory Board (1400F) 

U.S. Environmental Protection Agency 

Washington, D.C. 20460 

Staff Secretary 

MARY L. WINSTON 

Science Advisory Board (1400F) 

U.S. Environmental Protection Agency 

Washington, D.C. 20460 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



319 



AGENDA 

AGENDA ITEM : PAGE ; 

Plenary Session 
Monday, May 15, 1995 

Opening Comments 8 

Dr. Lippmann, Mr. Rondberg 

Committee Introduction 9 

Committee 

Overview Briefing 26 

Dr. Far land and staff 

Public Comment 74 

Dr. Clay Frederick 74 

AIHC 

Michael Pompili 84 

Columbus, Ohio, Health Department 

Dr. Paul Koval 87 

Ohio EPA 

Greg Rigo 93 

Columbus Health Department 

Jeffrey Hahn 98 

Integrated Waste Services Association 

William Okleshen 109 

American Hospital Association 

Larry Dusay 109 

American Hospital Association 

Edwin Holstein 114 

American Hospital Association 

Joe Thornton 121 

Greenpeace/Dr . Barry Commoner 

Dr. John Moore 135 

Institute for Evaluating Health Risks 



EXECUTIVE COURT REPORTERS, INC, 
(301) 565-0064 



320 



AGENDA 

AGENDA ITEM : PAGE : 

Plenary Session 
Monday, May 15 , 1995 

William Carroll 141 

Vinyl Institute 

Public Comment 

Nate Karch 141 

Chlorine Chemistry Council 

Dr. Gary Kajanian 149 

Dr. Alan Okey 162 

Environ Corporation 

Plenary Session 
Tuesday, May 16, 1995 

Review of Conclusions 170 

Drs. Lippmann, Daisey and Committee 



EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



321 



1 PROCEEDINGS 

2 9: 00 a.m. 

3 Opening Cominents 

4 Monday, May 15, 1995 

5 DR. LIPPMANN: Good morning. 

6 We ask everybody to please take their seats. 

7 We do need to start on time. 

8 On behalf of the Science Advisory Board 

9 Committees arrayed around this table and their 

10 consultants, I'd like to welcome everybody in the 

11 audience to this meeting, to review the dioxin risk 

12 assessment documents prepared by the agency staff and 

13 their contractors. 

14 This is an extremely tight schedule, and a 

15 very, very large committee. I hope we can all be brief 

16 and to the point throughout this exercise; otherwise, 

17 we just can't possibly finish our — our review. 

18 This is a very important document, a very 

19 contentious document. You — most of all of you, 

20 certainly everybody on the panel, has seen all the 

21 documents, six volumes, plus all the material that was 

22 sent to you by the various interested parties. 

23 Clearly, we have our work cut out for us, and 

24 I don't want to take any more time in introduction. 

25 I'll turn — I'm Dr. Lippmann from New York University. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



322 



9 

1 I'll be chairing the Health Panel and working with my 

2 colleague, Dr. Daisy, who is chairing the Exposure 

3 Panel, and we will be responsible for the integration 

4 of the two documents at the end. 

5 I'll turn the microphone over to Sam 

6 Rondberg, Science Advisory Board DFO, who will be 

7 giving us his introductions and some of our marching 

8 orders about procedures we have to follow for this 

9 public meeting. 

10 Committee Introduction 

11 MR. RONDBERG: Thanks, Mark. 

12 Just for those of you who are not into the 

13 archei of the Federal Advisory Committee Act, DFO is 

14 designated federal official. By law, every government 

15 advisory committee has to have a federal staff person 

16 who makes sure that the rules and regulations 

17 concerning advisory committees are followed. That's 

18 the last I'll talk about that. 

19 I actually serve as executive secretary, is 

20 the real description of the function that I provide. 

21 Just a little bit of administrativia before 

22 we get to the substance of the day, primarily for 

23 members of the committees. 

24 We'll be having lunch in the rooms. The 

25 Exposure Panel will withdraw with their cigars and 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



323 



10 

1 brandy and so forth to the room next door, and the 

2 Health Panel will be dining in here. I'll need to get 

3 a count later of how many people from each group are 

4 choosing to buy lunch. It's going to cost you about 

5 $19, but it's a fairly nice buffet. Sorry about that. 

6 The restaurant here is just too small to be able to 

7 handle us and turn the group over in the time that we 

8 need to get back to work. So, we're dining in. 

9 Very briefly, if you take a look at the 

10 folders that were in front of your place at the table, 

11 there is a huge raft of paper in there, just in case 

12 that you were running short of paper from the stuff 

13 that you got in the mail. The usual things, like the 

14 agenda and the committee roster is in there. 

15 There is a piece of paper labeled "Procedures 

16 for Public Disclosure SAB Meetings", which you need to 

17 take a look at, and we'll be going over that in a 

18 minute. Robert Flack, who's the assistant staff 

19 director of the Science Advisory Board, and is serving 

20 as the executive secretary and DFO for the Exposure 

21 Panel for this, will be leading the group through that 

22 as, hopefully, quickly as possible. 

23 Of a more substantive nature, you will find 

24 some additional reading materials in there. A blue 

25 book that's produced by the Environ Corporation for the 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



324 



11 

1 American Paper Institute, and some plain white paper 

2 with some additional materials that have been submitted 

3 by the public since the last mailing. 

4 There is a submission from a Dr. Hardell in 

5 Sweden, who is taking issue with how some of his data 

6 has been used by other public commenters. Dave Bayliss 

7 has a submission, and I believe that's just those two 

8 are in there. 

9 One last administrativia. If any of you had 

10 any administrative problems concerning your travel or 

11 something, a bit later, we'll have two of the SAB 

12 administrative support staff sitting outside. They can 

13 change travel arrangements for you or if you have some 

14 other problem with your hotel accommodations, 

15 reservations or anything like that. I know some of you 

16 may have had to stay somewhere else. 

17 Barring -- and you also find the forms to 

18 fill out to get reimbursed for your travel and your 

19 other expenses. 

20 With that, let me turn it over -- unless 

21 someone has a question on procedure, turn it over to 

22 Bob Flaak to lead you through the disclosure part of 

23 the meeting. 

2 4 MR. FLAAK: Thank you, Sam. 

25 One thing I'd like to remind all of the panel 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



325 



12 

1 members, the court reporter has a very difficult task 

2 today to maintain track of who's speaking, and to keep 

3 track of everything that's being put into the 

4 transcript. 

5 So, as a reminder, and we'll remind you as we 

6 go through the course of the meeting, please be sure to 

7 speak at one of these microphones, and if one of them 

8 isn't immediately in front of you as you are about to 

9 make a comment, I ask that you either drag it over near 

10 you or have one of your colleagues near you bring it 

11 over closer to you, so the court reporter can pick up 

12 everything that you say. 

13 For members of the audience that have a 

14 comment to make, and once they get recognized by the 

15 Chair, I ask that you use the microphone that's 

16 standing up in the middle of the audience, the free- 

17 standing mike. Come up, state your name and whatever 

18 your comment might be, so again we can get that into 

19 the record. 

20 The podium that sits in the middle of the 

21 room, once we're through with the presentations and 

22 such, will be moved out of the way. So, those of you 

23 who are sitting somewhat behind it, we'll see if you're 

24 sleeping, and we'll move it out of the way. 

25 Okay. One thing I'd like to do now, I'd like 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



326 



13 

1 to start on our public disclosure process. This is 

2 something that we do at all of our SAB meetings, and 

3 it ' s a means whereby those of you in the audience and 

4 the other members around the table can determine 

5 something about the backgrounds of the other members of 

6 the panel, and the sorts of activities they might have 

7 been involved in with regard to the issue that we are 

8 looking at. 

9 Now, this is different than conflict of 

10 interest. Conflict of interest is something that we 

11 deal with long before this meeting comes to the public 

12 view, and that's something that Sam and I have a 

13 responsibility for and making sure that individuals who 

14 sit at the table are not in a conflict of interest 

15 situation, which creates severe problems for them as 

16 well as for the agency as we do this kind of a review. 

17 What I'm asking the panel members to do today 

18 is to go through a brief discussion of their activities 

19 that relate to certain areas, which I'll identify in 

20 just a moment. 

21 The way we normally do this is we go around 

22 the table and ask each individual to answer these five 

23 or six guestions. We found in the past with a panel 

24 about half this size it takes over an hour. So, we're 

25 going to shorten the process a little bit and do it a 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



327 



14 

1 little differently this morning, and instead of doing 

2 it that way, I'm going to go through the questions one 

3 at a time and canvas the panel as a group for each of 

4 these questions. 

5 Let me read the questions first, so you can 

6 understand what it is I'm talking about. We ask panel 

7 members whether they've done any research on this issue 

8 before, and I suspect that's probably going to be true 

9 for most of you. I'm not looking for a lengthy 

10 discourse on this. 

11 Any previous pronouncements you've made. In 

12 other words, have you been an expert -- prepared expert 

13 testimony. Have you been an expert witness on this 

14 issue before this agency or any other agency, in 

15 particular? Does your employer have particular 

16 interest in this matter? Any financial interests you 

17 have in this particular matter? For example, does a 

18 panel member own stock in a company that produces the 

19 issue that we're discussing? And other individual 

20 links you might have, research grants from EPA, for 

21 example, on issues related to dioxin. 

22 So, with that in mind, let me go through the 

23 questions first, one at a time, and ask the panel 

24 members, I'll just go around the room briefly, and ask 

25 if any of you have any specific areas where you might 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



328 



15 

1 have some disclosure you wish to make on these items, 

2 bearing in mind that we have looked at the confidential 

3 financial disclosure statements of every member of this 

4 panel and identified no such conflicts that exist with 

5 regard to the work that we are dealing with today. 

6 This is primarily a sense of where people are 

7 coming from. So, let me ask the first question. 

8 On research conducted on this matter, does 

9 anybody have anything they wish to raise? 

10 Let me start with Bob Hazen and around that 

11 end of the table. Bob, do you have anything in 

12 specific? 

13 DR. HAZEN: No, I don't believe there are any 

14 issues of concern for me. 

15 MR. FLAAK: All right. Coming down that side 

16 of the table, I don't necessarily need a negative from 

17 everybody, but coming down, does anyone on this side of 

18 the table have any research issues they wish to 

19 identify? If so, please raise your hand on this side 

20 of the table. On the far side of the table. On this 

21 side of the table. Okay. 

22 Has anyone made previous pronouncements on 

23 this matter? Have they been expert witnesses or 

24 provided testimony? Again, starting on your end. Bob. 

25 DR. HAZEN: No, I haven't. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



329 



1 MR. FLAAK: Okay. Are you speaking for 

2 everybody? Anybody on this side of the table? 
.3 DR. BAILEY: No, I haven't. 

4 MR. FLAAK: Down this end over here? 

5 DR. McKONE: I think I should point out — 

6 MR. FLAAK: Please identify yourself. 

7 DR. McKONE: Oh. Get the microphone to work. 

8 MR. FLAAK: Is it working? Okay. 

9 DR. McKONE: I was one of the reviewers of 

10 the first day's document. Tom McKone. 

11 MR. FLAAK: Anybody else on this side? Yes? 

12 DR. GOUGH: Yes. Do you include being an 

13 expert witness at a trial? 

14 MR. FLAAK: Right. 

15 DR. GOUGH: Okay. Michael Goagh. I was an 

16 expert witness in two trials concerning dioxin exposure 

17 in 1989 and '90, perhaps, when I was not a federal 

18 employee. 

19 MR. FLAAK: Okay. Anybody on this side? I'm 

20 sorry? 

21 DR. CRUMP: This is Kenny Crump. From the 

22 period of about 1980 to about 1995, I have testified in 

23 probably about a half a dozen trials involving dioxin, 

24 one of which is still active. 

25 DR. LUSTER: I testified many years ago for 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



330 



17 

1 the EPA on the EPA Dow hearings for dioxin. 

2 DR. OZONOFF: I'm Dave Ozonoff. I've 

3 testified in the Times Beech trial which involved 

4 dioxin exposures maybe seven-eight years ago. No 

5 active cases, though. 

6 DR. PAUSTENBACH: Yes. Dennis Paustenbach. 

7 I've been involved in two or three trials in recent 

8 times, and probably half a dozen depositions, and I 

9 don't have any pronouncements that I've made before the 

10 agency before, but I did serve in the last peer review, 

11 I think it was '87. 

12 DR. KIM: I'm Nancy Kim. I guess the only 

13 thing that's applicable to me is I served on the last 

14 peer review panel, too. 

15 MR. FLAAK: Anybody else on that side of the 

16 table? Yes? 

17 DR. PCAMINSKI: I'm Norv Karainski, and I served on 

18 the National Academy of Sciences committee to review 

19 the health effects of herbicides on Vietnam veterans. 

20 MR. FLAAK: Anybody at the front table? 

21 DR. CLAPP: I'm Richard Clapp, and I 

22 testified before the congressional committee of, I 

23 think it was. Veterans Affairs about health effects of 

24 Agent Orange, and I've also testified in two trials 

25 having to do with dioxin in St. Louis. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



331 



18 

1 MR. FLAAK: Anybody else at the front table? 

2 (No response) 

3 MR. FLAAK: Our third question deals with 

4 your — oh, I'm sorry, John. 

5 DR. DOULL: I've been involved in a couple of 

6 trials, also, now that I recall. 

7 MR. FLAAK: Anybody else? 

8 (No response) 

9 MR. FLAAK: All right. The third question 

10 deals with the interests of your employer in the 

11 matter. 

12 Does anybody's employer have a particular 

13 interest in this issue? 

14 Bob, again, let me start on your side. 

15 DR. HAZEN: Well, yes, I'd say the State of 

16 New Jersey has a particular interest in this issue. 

17 MR. FLAAK: Thank you. Bob. Anybody else on 

18 this side? Yes, sir? 

19 DR. UMBREIT: My employer has some interest 

20 in this, although not the particular center I work for. 

21 MR. FLAAK: Anybody else on this side? 

22 DR. UMBREIT: With the building trades, our 

23 members have interests in this. 

24 DR. WHITE: Ron White with the American Lung 

25 Association, and our organization has an interest in 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



332 



19 

1 this issue, also. 

2 DR. McKONE; Tom McKone , I believe the 

3 Lawrence Livermore Laboratory, who I work for, has been 

4 trying to build some sort of an incinerator. I've not 

5 been involved with that activity, but it is an issue 

6 there. 

7 MR. FLAAK: Anybody else on this side? 

8 (No response) 

9 MR. FLAAK: On the other side? Nancy? 

10 DR. KIM: I'm Nancy Kim. I work with New 

11 York State. New York State is interested in dioxin 

12 issues. I guess since I wasn't really sure what the 

13 research aim meant, I guess I should also say that we 

14 have been involved in looking at dioxin exposure in the 

15 state office building, in several landfills, and some 

16 fish and dairy issues, too. 

17 MR. FLAAK: Anybody else on that side of the 

18 table? 

19 DR. PAUSTENBACH: Yes, I'm with a consulting 

20 firm, and we -- people within the firm certainly do 

21 some dioxin consulting. I've tried to avoid it for 
2 2 awhile now. 

23 MR. FLAAK: Okay. 

24 DR. THOMAS: I'd like to go back to this 

25 issue of research and just point out that I have done 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



333 



20 

1 research on sources of dioxin and made my own admission 

2 inventory. 

3 MR. FLAAK: Valerie and any of the others, 

4 make sure to identify yourselves, so the court reporter 

5 catches who you are. Sometimes it's hard to catch the 

6 names. 

7 Anybody else on this side? 

8 DR. RYAN: My name is John Ryan from Canada, 

9 and our federal agency is in Canada, and we are 

10 involved in the regulation. 

11 MR. FLAAK: Anyone else on this side? Yes? 

12 DR. OZONOFF: I'm Dave Ozonoff. I also work 

13 for the Department of Veterans Affairs, and they 

14 certainly have an interest in this. 

15 MR. FLAAK: Anyone at the front table? 

16 DR. SILVERSTONE: Al Silverstone. I, like 

17 Nancy Kim, am an employee of the State of New York, 

18 . though in the university system, and our hospital, 

19 which is a state university hospital, is trying to get 

20 an incinerator approved. I also have research grants 

21 on the effects of dioxin on immune system development. 

22 DR. McCONNELL: Gene McConnell. I have 

23 designed or helped design and evaluate studies of PCBs, 

24 several types of PCBs. These studies are on-going at 

25 the present. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



334 



21 

1 DR. BUNN: I'm Bill Bunn. I'm with Mobil 

2 Corporation. We have the usual industrial interest in 

3 these and other related compounds, not felt to be 

4 different than general industry. 

5 MR. FLAAK: Anybody else on the front table? 

6 (No response) 

7 MR. FLAAK: Anybody else on this question? 

8 (No response) 

9 MR. FLAAK: All right. The next question 

10 deals with the general description of any financial 

11 interest you have in the matter. Much of these are 

12 covered. Those of you as you recall having filled out 

13 your confidential financial disclosure statements may 

14 have included some of these things in there. These are 

15 not things we're asking you to disclose. We're just 

16 asking for any general financial interest you might 

17 have in this matter. Chances are beyond what you had 

18 in that disclosure form, there may not be any others. 

19 Are there any financial interests in this 

20 particular issue? Anybody? 

21 (No response) 

22 MR. FLAAK: All right. The last question 

23 deals with research grants from parties, including EPA, 

24 that would be affected by this matter. 

25 Is anyone involved in research grants, 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



335 



22 

1 particularly from EPA, that might be affected by this 

2 matter? 

3 Take Bob's side again, for the start. 

4 Anybody over here? 

5 DR. McKONE: Tom McKone. I receive quite a 

6 bit of funding from the State of California, 

7 Environmental Protection Agency, to look at multi-media 

8 exposure modeling that's quite related to this, and 

9 some of that funding is actually — the state's grants 

10 come from the EPA through cooperative agreements. So, 

11 it's indirectly EPA-funded. 

12 DR. REED: I'm Donald Reed, Oregon State 

13 University, and I'm Director of the Environmental 

14 Health Sciences Center at Oregon State. Within that 

15 center, we have responsibility for a program grant that 

16 is on the toxicity of halo carbons, and members who 

17 participate in that research, some of them are doing 

18 research on dioxin. 

19 MR. FLAAK: Anybody else on this side? 

20 DR. SAMET: I'm Jon Samet. I have no direct 

21 funding from parties involved in this. I am Chair of 

22 the Department of Epidemiology at Johns Hopkins, which 

23 is — there is a large industry-funded study of paper 

24 workers in progress in my department. I have no direct 

25 involvement with that project. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



336 



23 

1 MR. FLAAK: Thanks. The other side? Anybody 

2 over here? 

3 DR. SEEKER: Yes. I'm Randy Seeker from EER 

4 Corporation. My company has a contract to help support 

5 the EPA in the development of their new max standards 

6 for hazardous waste incinerators. 

7 DR. KITES: Ron Kites from Indiana 

8 University. I have research grants from the National 
Science Foundation on dioxin and other pending 
applications to do research on dioxin. 

DR. KIM: Nancy Kim. There are several parts 
of the health department, the laboratories and research 
may have grants from EPA or other funded — funding 
groups, which I am not aware of. 

I also know that my part of the agency has 
applied for a grant with EPA to look at dioxin 
exposure. 

DR. OZONOFF: I'm Dave Ozonoff from Boston 
University, School of Public Kealth. I'm chair of the 
department that has grants from NIEHS, where the money 
actually comes from EPA, and I'm the Director of the 
Super Fund Basic Research Center, which has dioxin- 
related research in it. That center is funded by EPA 
money, although it is administered by NIEKS. 

MR. FLAAK: All right. Thank you. Anybody 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



337 



24 

1 else on this side? Yes? 

2 DR. GREENLEE: I'm Bill Greenlee from Purdue 

3 University. In addition to funding from NIH, I have 

4 received research grants from the Air.erican Forest Paper 

5 Association and General Electric, and I've also 

6 received gifts for research from Chemical Manufacturers 

7 Association and Dow Chemical. 

8 MR. FLAAK: Anybody else on this side? 

9 DR. KAMINSKI: Yes. My name is Norv Kaminski 

10 from Michigan State University. I have a research 

11 grant from the NIEHS to study the immunotoxicity by 

12 PCDD. 

13 I think I also should mention, I'm not sure 

14 which category this should fall under, but I have and 

15 continue to serve as a consultant for Dow-Corning 

16 pertaining to interactions between silicone products 

17 and the immune system. 

18 MR. FLAAK: Thank you. Anybody else on the 

19 head table here? On this end? Anybody down this end 

20 yet? 

21 DR. SILVERSTONE: Al Silverstone. I've 

22 been -- I'm listed as a consultant on an EPA contract 

23 with the Syracuse Research Corporation on toxic 

24 chemicals, although I've not been asked to do anything 

25 yet. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



338 



25 

DR. STOHS: Sid Stohs, Creighton University. 

We have funding from the Air Force Office of Scientific 

Research involving various halogenated pesticides, and 

there's some work that does relate to dioxins. 

DR. WEISS: Bernie Weiss from the University 

of Rochester. We have a grant from the International 

Life Sciences Institute to pursue questions about the 

developmental toxicity of PCDD. 

MR. FLAAK: Are there anybody — anyone else 

on the panel have anything else to say about this? 

(No response) 

MR. FLAAK: Okay. I think we're ready to 

start the presentations. I'm going to turn the mike 

back over to Mort Lippmann, the chair, so we can begin 

with the process of the meeting. 

Thank you. 

DR. LIPPMANN: Okay. Well, the chair is also 

not involved in any of these issues. I have EPA 

research money but nothing related at all to dioxin. 

We'll move on to the first set of public 

comments. We have public comments for the group as a 

whole, and we have other time for public comments on 

the health issues or the exposure issues separately. 

I will ask — oh, I'm sorry. We'll come back 

to the public comments momentarily. 

EXECUTIVE COURT REPORTERS, INC. 
(301) 565-0064 



339 



February 23, 1996 F:\proj\dioxpane.doc 

PANEL SELECTION FOR SAB REVIEW OF EPA'S DIOXIN REASSESSMENT 

Sam Rondberg's 2/20/96 

EPA released the final draft of the Dioxin Reassessment in 
mid-October, 1994; on December 20, 1994, CRD provided a draft 
Charge to the SAB Staff. 

Pursuant to earlier discussions by the SAB Executive 
Committee, Dr. Matanoski requested that the SAB Staff work with 
the Chairs of the lAQC (Dr. Daisey) and EHC (Dr. Perera) to 
negotiate a final Charge and organize a joint review of the 
reassessment document. Soon after receipt of the Charge, Dr. 
Perera decided that (because of her position on the NRDC Board of 
Directors) it would be inappropriate for her to Chair the EHC for 
this particular review, and recused herself from the activity. 
Soon afterward. Dr. Matanoski asked Dr. Morton Lippmann to assume 
the Health Panel Chair [in place of[ Dr. Perera and to lead the 
overall dioxin review activity. 

Once a draft Charge was in hand, the SAB Designated Federal 
Official for this project (Mr. Samuel Rondberg) began identifying 
possible candidates, based on recommendations from SAB Staff, the 
Chairs of the Health and Exposure Panels, ORD Staff, and on 
recommendations previously volunteered by several industry 
groups. During the process, SAB staff also queried the Audubon 
Society, Greenpeace, the National Resources Defense Council, and 
the Environmental Defense Fund for recommendations. Some of the 
individuals contacted as potential consultants also provided 
additional recommendations — typically co-workers, former 
students, etc. From the totality of the names assembled, the 
Chairs and SAB staff selected a "short-list" for the Health and 
Exposure Panels. Persons on the two lists were then contacted to 
determine their willingness to serve, and screened for overt 
conflict situations (such as participation in groups planning to 
present an advocacy position at the SAB meeting or having already 
taken a strong public position on the issues to be discussed) . 
Several potential candidates on the short-list were eliminated as 
a result of this screen. 

All persons willing to serve, and who passed the initial 
conflict "screen" were then provided with a copy of the draft 
Charge (for either Health or Exposure, as appropriate) and asked 
to identify (in rank order) the three issues they would prefer to 
work on if selected for the review. Although the specific 
discipline of each individual was already identified, it was felt 
that self-assignment to issue would yield the best possible 
match. At the same time, the process to enroll as Consultants 
those persons not already "on-board" as current SAB Members or 
Consultants was started. Each of these persons completed an SF 
450 (Financial Disclosure Statement) as part of this process. 
Review of the disclosure statements by the DFO and Assistant SAB 
Staff Director did not disclose any conflict situations, and none 



340 



of the selected panelists was disqualified from participating. 
One Consultant to the Exposure Panel was recused from commenting 
on the findings of the Health Panel because of prior activities 
of his employer concerning dioxin health effects. 

Once the self -assignments were completed, SAB Staff arrayed 
the selections against the 23 questions in the Health Charge and 
2 questions in the Exposure Charge and discussed the 
distribution with the Chairs. The resulting consensus was to 
invite all respondents for the Health Panel (save one, who was 
dropped to avoid having two individuals from the same university 
and department on the Health Panel) and for the Exposure Panel to 
participate, schedules allowing. The driving factor behind this 
decision was to have in-depth coverage for all 43 issues, as well 
as to have the Panels constitute a broad and balanced range of 
backgrounds and outlook. 

The individuals "surviving" this selection process were then 
queried as to availability during- the months of April and May, 
1995; May 15/16 were then selected as the two days with the 
greatest number of panelists available. Individuals who had 
listed those two days as "Not Available" were contacted, and in 
some cases, persuaded to revise their schedules in order to 
participate. This process ultimately resulted in 25 
Members/Consultants (M/C) for the Health panel and 14 for the 
Exposure Panel. Once Membership stabilized, the tentative 
assignments of M/Cs to specific issues was revised and "Leads" 
assigned for each issue. 

Table 1 lists the participants in the two panels, their 
affiliation, and SAB status. 

Table 1 — Affiliation of Panelists 



AFFILIATION 


Number 


HEALTH 

Percent 


EXPOSURE 
Number Percent 


ACADEMIC 


18 


72 


5 36 


INDUSTRY 


1 


4 


1 7 


CONSULTANT 


2 


8 


2 14 


FEDERAL GOVT. 


3 


12 


1*** 7 


STATE GOVT. 








3 22 


OTHER 


1 


4 


2 14 


TOTAL 


25* 


100 


14* 100** 



•Includes Chair 

•Actual total less due to rounding 

•Canadian Govt. 



>*^^°'^-^ 
^ ^ 



ISE 



341 



UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 2046^3 ^^d^ij,^^^^^^^. 5 -L^t 



OFFICE OF THE ADMINISTRATOR 
SCIENCE ADVISORY BOARD 



February 22, 1996 

E.R. Zumwalt, Jr. 

Admiral USN (Ret) 

Chairman, Agent Orange Coordinating Council 

1000 Wilson Blvd. Suite 3105 

Arlington, VA 22209-3901 

Dear Adm Zumwalt: 

I am responding to your January 2, 1996 letter to 
Administrator Browner requesting her to "administratively make 
the decision not to use "Corporate Docs" (scientists who receive 
grants, compensation, consulting fees, etc. from corporations who 
produce dioxin as a by-product of their manufacturing processes) 
on the Science Advisory Board." 

I want to provide you with some additional information about 
how your concerns are addressed in rules that govern the 
operations of advisory committees, such as the Science Advisory 
Board, and how they are implemented at the SAB. 

Regarding conflict of interest in general, under 18 U.S.C. 
Section 208(a), Federal employees, including "special government 
employees" that serve on the Science Advisory Board, are barred 
from participating in any "particular matter" which affects their 
employers' financial interests. However, under 18 U.S.C. Section 
208(b)(3) agencies are authorized to waive the restriction where 
"the need for the individual's services outweighs the potential 
for a conflict of interest [COI] created by the financial 
interest involved." 

Regarding these rules and the SAB, the SAB generally doesn't 
deal with particular matters and, specifically, dioxin is not a 
particular matter because it is widespread in the environment and 
because the Agency's reassessment was aimed at dioxin wherever it 
is found and from whatever sources it might come--from food to 
incinerators, from volcanoes to pulp and paper, from human milk 
to chemical companies. 



^^^y Recycled^ecyclable 

•^ ^^ Prt/Med on paper m«l oontait 
X 75% rscydad ftol 






342 



As a part of the process of assessing whether such a legal 
COI exists or not, each member of an SAB Panel (i.e.. Members and 
Consultants) must submit a financial disclosure report that is 
reviewed by staff, with legal counsel as needed, prior to the 
meeting. By law, EPA cannot make this information available to 
the public. 

As a Federal advisory committee, an SAB panel is required to 
include a balance of points of view on the technical issues it 
addresses. Achieving such a balance is a challenge, particularly 
in a case as enduring and controversial as dioxin. One method of 
seeking balance is to have a large and diverse group of 
participants, so that no one point of view dominates the 
proceedings. In the case of the dioxin review, we enlisted 39 
different scientists who were qualified to examine dioxin issues 
and who came from a wide spectrum of institutions and backgrounds 
from across the country. Some of these scientists may have 
received research support from corporations associated with 
dioxin-containing materials. We recognize that some observers 
may believe that this fact would affect the participants' views 
on the technical issues considered by the panel; however, we 
believe that the importance of hearing their technical input 
outweighs this concern. 

The SAB has also adopted a practice of voluntary "public 
disclosure" at the beginning of its meetings on specific issues. 
During the disclosure exercise, the panelists may share with 
their colleagues and members of the public information about 
their backgrounds that might be relevant to the issue at hand; 
this may include sources of funding. 

As you and I discussed at the Greenpeace offices late last 
year, the SAB is continually seeking to make improvements in our 
process, including the issue of perceived conflict of interest. 
An SAB subcommittee will present recommendations for such 
irSprovements at the public Executive Committee meeting on the 
afternoon of Feb. 28 to be held in the Administrator's Conference 
Room (Rm 1103, West Tower, Waterside Mall, 401 M St. SW, 
Washington, DC) . The intent is to have a process that is open, 
fair, and informed. 

In closing, I want to state that I do not agree with your 
general characterization of any scientist who might receive a 
grant from a particular industry as a "pseudo scientist" or a 
"Corporate Doc". Such a broad, prejudicial characterization is 
both unwarranted and unsubstantiated. The history of the SAB is 
replete with examples of men and women of science who have served 
the country well with the highest level of credibility, and 
professionalism, regardless of their professional backgrounds and 
current employment. Our system, however imperfect, is designed 
to solicit the views of a wide range of credible voices on 
technical issues, so that a consensus position can emerge in full 
view of the public. 



343 



I would be happy to discuss these matters further with you ' 
and explore suggestions for improving the process within the 
limits of the law. Thank you for your continuing interest in the 
Science Advisory Board. 



Sincerely, 




jonald G. Barnes, 
Staff Director 
Science Advisory Board 



PhD 



Administrator Carol Browner 
Deputy Administrator Fred Hansen 
SAB Executive Committee 



o 



23-557 (352) 



BOSTON PUBLIC LIBRARY 



3 9999 05984 240 9 



ISBN 0-16-052655-8 



9 780160"526558 



90000