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HERBICIDE BACKGROUND INFORMATION
o
VEGETATIVE MANAGEMENT ENVIRONMENTAL STATEMENT
Pacific Northwest Region, ,
U,S. Department of Agriculture - Forest Service
1974-1975
/
AD-33 Bookplate
(1-63)
NATIONAL
LIBRARY
REPORT
ON
BACKGROUND INFORMATION
FOR
AMITROLE
lie nFPT OF l\GR^CULTURAL
NMlONftL ftWKULTURft' LIBRW
AUG 9 19?9
CMMOGING = PREP-
COMMITTEE MEMBERS
D. A. Graham R-6
R. Romancier PNW
Peter Thiesen R-6
720674
BACKGROUND DOCUMENT ON AMITROLE
I. General information
References;
(1) Amchem Products, Inc.
1971. Memorandum on amitrole registration.
28 July 1971 (attached).
(2)
1972. Selected labels for Amchem Products, Inc.
herbicides containing amitrole (attached).
(3) Oregon Extension Service.
1970. Oregon weed control handbook. Oregon State
Univ. Coop. Ext. Serv., Corvallis, Oregon.
287 pp.
(4) Washington State University and Department of Agriculture.
1971. Washington pest control handbook. Washington
State Univ., Pullman, Washington. 569 pp.
(5) Weed Society of America.
1967. Herbicide handbook of the Weed Society of
America. W. F. Humphrey Press, Inc.,
Geneva, N. Y. 293 pp.
A. Common name; amitrole (5; 10)
B. Chemical name; 3-amino-l , 2 , 4-triazole (5; 10)
C. Registered uses; Registered for use on annual and perennial
grasses and broadleaf weeds, poison ivy, poison oak, and
eight species of woody plants (2) . Amitrole is registered
for use on industrial and other non-crop land (including
forest land and rights-of-way) only (1) .
D. Formulations manufactured
1. 50% active water-soluble powder; Amchem Weedazol,
2. 90% active water-soluble powder; Amchem Amizol and
American Cyanamid Amino Triazole Weed Killer,
3. amitrole + ammonium thiocyanate liquid; Amchem Amitrol-T
and American Cyanamid Cytrol Amitrol-T,
#
4. amitrole + simazine: Amchem Amizine (wettable powder)
and Amchem Liquid Amizine (liquid)
E. Dilutions of formulations for use: 5 to 15 gal water per
acre for aerial application and 20 to 300 gal water per
acre for ground application.
F. Rate and method of application
1. amitrole (Amizol and Amino Triazole Weed Killer):
2 to 10 lb ai/A ground application (2)
2. amitrole 4- ammonium thiocyanate (Amitrol-T and Cytrol
Amitrol-T) :
1- to 2-gal (1 gal contains 2 lb each amit-ole and
ammonium thiocyanate) in 20- to 100-gal water per acre
for ground application (2)
ig- to 10-gal in 5- to 15-gal water per acre for aerial
application (usual aerial spray rate to release conifers
from salmonberry in Pacific Northwest is 1 gal amitrole-T
in 9 gal water per acre) (2) .
G. Tolerances in food or feed and other safety limitations: FDA
has declined to set a tolerance for amitrole under terms of
FIFRA. Amitrole is an antithyroid agent (goitrogen) and
produced thyroid tumors in rats fed at 100 ppm for 68 weeks (1) .
Amitrole is nonvolatile and nonflammable (5) . It is mildly
corrosive to bare iron, aluminum, copper, and copper alloys (5).
Equipment should be flushed thoroughly with water after use
(4, 5).
H. Manufacturer or producer
Amchem Products, Inc. American Cyanamid Corporation
Ambler, Pennsylvania 19002 P. 0. Box 400
Princeton, New Jersey 08540
II. Toxicity data on formulation to be used
References :
(1) Amchem Products, Inc.
1959. Progress report on Amchem Amitrol-T.
Amchem Products, Inc. Tech. Data Sheet H-78.
7 pp. mimeo.
(2) Bond, C. E., R. H. Lewis, and J. L. Fryer.
1959. Toxicity of various herbicldal materials to
fishes. Biological problems in water
pollution, pp. 96-101. Trans. 1959 Seminar.
U.S.H.E.W.
-2-
e
(3) Carter, Mason C.
1969. Amitrole. Degradation of herbicides
(P. C. Kearney and D. D. Kaufman, ed.),
pp . 187-206. Marcel Dekker, Inc., N.Y.
Dunachie, J. F. and W. W. Fletcher.
1970. The toxicity of certain herbicides to hen's
eggs assessed by the egg-injection technique.
Ann. Appl. Biol. 66 ( 3) : 515-520 .
(5) Marston, R. B. , D. W. Schults, T. Shiroyama, and
L. V. Snyder.
1968. Amitrole concentrations in creek waters
downstream from an aerially sprayed water-
shed sub-basin. Pest. Monit. J. 2:123-128.
(6) Oregon Extension Service.
1970. Oregon weed control handbook. Oregon State
Univ. Coop. Ext. Serv. , Corvallis, Oregon.
287 pp.
(7) Washington State University and Department of Agriculture.
1971. Washington pest control handbook. Wash. State
Univ., Pullman, Washington. 569 pp .
(8) Weed Society of America.
1967. Herbicide handbook of the Weed Society of
America. W. F. Humphrey Press, Inc.,
Geneva, N.Y. 293 pp.
(9) Weir, R. J., 0. E. Paynter, and J. R. Elsea.
1958. Toxicology of 3-amino-l, 2,4-triazole.
Hormolog 2(1): 13-14.
Additional references:
general
American Cyanamid Company.
1956. Aminotriazole-acute and subacute toxicity.
American Cyanamid Company, Central Medical
Dept .
wildlife
Dewitt, J. B., W. H. Stickel, and P. F. Springer.
1963. Wildlife studies, Patuxent Wildlife Research
Center. USDI Fish and Wildlife Serv. Circ.
167:74-96.
Includes toxicity of amitrole to bobwhite
quail, ring-necked pheasants, and mallard
ducks .
-3-
aquatic life
Bond , C . E .
1960. Weed control in fish ponds. Oregon Weed
Conf. Proc . 9:29-32.
Hughes, J. S. and J. T. Davis.
1962. Toxicity of selected herbicides to bluegill
fish. La. Acad. Sci. Proc. 25:86-93.
Lhoste, J.
1959. Dangers to aquatic fauna in the use of
chemical herbicides. Phytoma 105:13-17.
bees
King, C. C.
1960. Effects of feeding herbicides to honey bees
(Abstr.). N. Central Weed Contr. Conf.
Proc. 17:105.
A. Safety data
1. Acute mammalian studies
a. Oral LD^q:
Amitrole Amitrole-T
(mg/kg) (mg/kg)
mice 14,700 (9)
rats 25,000 (7, 8, 9) 5,000 (6, 7)
Intravenous LD^q
mice 1600 no effect (9)
cat 1750 no effect (9)
dog 1200 no effect (9)
b. Dermal LD^q: ^ 10,000 mg/kg (rabbits) for Amizol (7)
c. Inhalation:
d. Eye and skin irritation:
2. Subacute studies
a. Oral: dietary levels of 1000 and 10,000 ppm
administered to rats for 63 days resulted in altered
body weight gain and fatty metamorphosis of liver
cells (9). After 68 weeks of a two-year feeding
trial on rats, levels up to 50 ppm have no effect.
-4-
#
At 50 ppm and above, amitrole acts as a goitrogen;
the effect is reversible within two weeks after
amitrole is withdrawn (9) .
b. Dermal
c. Inhalation
Note : poisoning symptoms have not been noted for pure
amitrole. In the event of ingestion of amitrole-T,
thiocyanate poisoning should be suspected. The
acute oral LD^q of NH^SCN is 750 mg/kg (rats) (8).
3. Other studies which may be required
a. Neurotoxicity
b. Teratogenicity: no teratogenic effects in hen's
eggs (4)
c. Effects on reproduction
d. Synergism: Experimental results indicate that
addition of ammonium thiocyanate to amitrole
(amitrole-T) increases degree of control of
quackgrass, Bermuda grass, and stolonif erous bent
grasses (1) . The effect of NH^SCN is synergistic
with the rate of NH^SCN being more important than
the rate of amitrole. Also see:
Boyd, P. G. 1965. Field observations with
thiocyanate activated amitrole. Pesticide
Progr. 3(6):139.
As noted earlier, the addition of NH^SCN reduces
the LD^q value over that of amitrole alone (25,000
mg/kg for amitrole and 5,000 mg/kg for amitrole-T
on rats) .
e. Potentiation
f. Metabolism
(1) in plants: Amitrole may combine with serine
in plants to form 3-(3-amino-l,2,4-triazole-l-
yl)-2-aminopropionic acid (3-ATAL) (3). The
formation of 3-ATAL apparently represents
detoxification, since the derivative is less
toxic and less mobile than amitrole. Ammonium
thiocyanate, which synergizes the action of
amitrole, inhibits the formation of 3-ATAL (3).
-5-
Two other unidentified metabolites have been
found in some plant species. One of these,
unknown III, probably is an artifact of the
isolation procedure (3). This compound was
five to eight times more active than amitrole
on tomato and lettuce roots.
(2) in animals: refer to--
Fang, S. C. , S. Khanna, and A. V. Rao.
1966. Further study on the metabolism
of labeled 3-amino- 1 , 2 , 4- triazole
and its plant metabolites in rats.
J. Agric. Food Chem. 14(3) : 262-265 .
g. Avian and fish toxicity: Amitrole was not toxic to
largemouth bass up to 1000 ppm in 48 hour median
tolerance tests; the LD50 for Coho salmon was
325 ppm for a 48 hour exposure (2). An aerial
application of 2 lb ai per acre of amitrole near
Astoria, Oregon resulted in such low levels of
amitrole that toxicity to warm-blooded animals was
unlikely (5). Sampled streams were not buffered
against direct herbicide application in this study.
h. Carcinogenicity: Amitrole is an antithyroid agent
and has been tested for controlling hyperthyroidism.
The stimulation of abnormal growth of the thyroid
gland after feeding high dosages of amitrole has
been construed as evidence of carcinogenicity. In
chronic feeding studies involving exaggerated rates
fed over a long period of time, thyroid tumors began
appearing in rats fed at 100 ppm for 68 weeks.
B. Physical-chemical properties
References:
( 'I Bailey, G. W. and J. L. White.
1965. Herbicides: a compilation of their
physical, chemical, and biological
properties. Residue Rev. 10:97-122.
(2) Weed Society of America.
1967. Herbicide handbook of the Weed Society
of America. W. F. Humphrey Press, Inc.
Geneva, N.Y. 293 pp.
1. Boiling point: see (1), melting point 159°C (1, 2)
2. Flash point: nonflammable (2)
3. Physical state: white crystalline powder (2)
-6-
4. Density: see (1), molecular weight 84.1 (2)
5.
Vapor pressure:
nonvolatile
6.
Solubility: (2)
Solvent
Temperature
Solubility
(°C)
(g/100 g)
Acetone
—
Insolub le
Diesel oil
—
Insoluble
Ethanol
75°
26
Ether
—
Insoluble
Kerosene
—
Insoluble
Water
25°
28
7. Stability: stable; no shelf life limitations (2).
III. Efficacy data under field and laboratory conditions
References ‘for effectiveness and phytotoxicity (parts A and B) :
(1) Amchem Products, Inc.
1960. Amitrol, b izac and combinations of both
for control of woody plants. Amchem Pro-
ducts, Inc. Tech. Serv. Data Sheet H-79.
5 pp. mimeo. (page 2 attached).
(2) Fechtig, A. D. and W. R. Furtick.
1964. Control of giant Himalaya blackberry
(Rubus procerus P. J. Muell) with organic
chemical compounds. West. Weed Contr. Conf.
Res. Prog. Rpt. 1964:40.
(3) Finnis, J. M.
1964. Chemical control of salmonberry. West.
Weed Contr. Conf. Res. Prog. Rpt. 1964:48.
(4) Krygier, James T. and Robert H. Ruth.
1961. Effect of herbicides on salmonberry and
on Sitka spruce and western hemlock
seedlings. Weeds 9 (3) : 416-422 .
(5) Leonard, 0. A. and W. A. Harvey.
1965. Chemical control of woody plants.
California Agric. Exp. Sta. Bull. 812.
26 pp.
(6) Newton, Michael.
1963. Some herbicide effects on potted Douglas-fir
and ponderosa pine seedlings. J. Forestry
61(9) :674-676.
#
-7-
(7) Newton, Michael.
1970. Herbicides in forestry. Oregon weed
control handbook. pp. 222-231. Oregon
State Univ. Coop. Ext. Serv. , Corvallis,
Oregon .
(8) Warren, Rex.
1970. Control of common weeds. Oregon weed
control handbook. pp. 247-265. Oregon
State Univ. Coop. Ext. Serv., Corvallis,
Oregon.
(9)
1970. Industrial weed control. ^ Oregon weed
control handbook. pp. 243-244. Oregon
State Univ. Coop. Ext. Serv., Corvallis,
Oregon .
(10)
1970. Weed and brush control along highways,
roadways and fence lines, ^n Oregon
weed control handbook. pp . 239-242.
Oregon State Univ. Coop. Ext. Serv.,
Corvallis, Oregon.
(11)
1970. Weed control along irrigation and drainage
canals. Oregon weed control handbook,
pp. 245-246. Oregon State Univ. Coop.
Ext. Serv., Corvallis, Oregon.
A. Effectiveness for intended purpose when used as directed
(see table on page 9)
B. Phytotoxicity (see table on page 9)
-8-
RELATIVE EFFECTIVENESS OF AMITROLE AND AMITROLE-
APPLIED AS FOLIAGE SPRAYS
FOR SPECIFIC SPECIES AND WEED CONTROL PROBLEMS
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-9-
C, Translocation in plant treated
References :
(1) Clor, M. A., A. S. Crafts, S . ^^amaguchi .
1964. Translocation of -labeled compounds
in cotton and oaks. Weeds 12(3): 194-
200.
(2) Crafts, A. S.
1961. The chemistry and mode of action of
herbicides. Interscience, N.Y. 269 pp.
(3) Forde, B. J.
1966. Translocation patterns of amitrole and
ammonium thiocyanate in quackgrass.
Weeds 14 (2) : 178-179 .
(4) Leonard, 0. A.
1963. Translocation of herbicides in woody
plants. Soc . Amer. Foresters Proc.
(5) Leonard, 0. A., D. E. Bayer, and R. K. Glenn.
1966. Translocation of herbicides and
assimilates in red maple and white
ash. Bot. Gazette 12 7 (4) : 193-201 .
Amitrole applied to either leaves or stems was absorbed and
transported throughout red maple and white ash trees (5).
Amitrole apparently moves both in the cell wall (apoplast)
and living protoplasm (symplast) of plants (4). Applications
to leaves move downward and throughout the plant; applications
to lower stems or roots apparently move upward in the
transpiration stream (2). Translocation of amitrole from the
leaf of quackgrass was retarded over 12 hours by ammonium
thiocyanate applied as a spray or as a spot (3) . When
amitrole was applied without NH^SCN, there was considerable
movement to immature leaves and roots. After 24 hours,
marked s3miplastic movement occurred; plants treated with
both chemicals showed the most movement (3).
D. Persistence in s^il, water, or plants
References :
(1) Carter, Mason.
1969. Amitrole. ^ Degradation of herbicides,
pp. 187-206. Marcel Dekker, N.Y.
-10-
(2)
Day, B. E. , L. S. Jordon, and R. T. Hendrixson.
1961. The decomposition of amitrole in
California soils. Weeds 9 (3) : 443-456 .
(3) Frear, D. E. H.
1964. Fate of 3-amino-l, 2 ,4-triazole in soils.
J. Sci. Food Agric. 15 (8) : II-85-5 .
(4) Freed, V. H. and W. R. Furtick.
1961. The persistence of amitrole in soil
when used for chemical fallow.
Hormolog 3(1).
(5) Ludzack, F. J. and J. W, Mandia.
1962. Behavior of amitrole in surface water
and sewage treatment. Proc. 16th
Ind. Waste Conf., Purdue Univ. Engng.
Ext. Serv. No. 109:540.
(6) Marston, Richard B. , Donald W. Schults, Tamotsu
Shiroyama, and Larry V. Snyder.
1968. Pesticides in water: amitrole concen-
trations in creek waters downstream
from an aerially sprayed watershed
sub-basin. Pest. Mont. J. 2 (3) : 123-128 .
(7) Norris, Logan A.
1967. Chemical brush control and herbicide
residues in the forest environment.
In Herbicides and vegetation management,
pp. 103-123. School of Forestry, Oregon
State Univ., Corvallis, Oregon.
(8)
1970. Degradation of herbicides in the forest
floor. Tree growth and forest soils
(Youngberg, C. T. and C. B. Davey, ed.)
pp. 397-411. Oregon State Univ. Press,
Corvallis, Oregon.
(9)
1970. The kinetics of adsorption and
desorption of 2,4-D, 2,4,5-T, picloram,
and amitrole on forest floor material.
West. Soc. Weed Sci. Res. Prog. Rpt.
1970:103-105.
(10) Norris, L. A., M. Newton, and J. Zavitkavoski.
1966. Stream contamination with amitrole
following brush control operations with
amitrole-T. West. Weed Contr. Conf.
Res. Prog. Rpt. 1966:20-22.
-11-
(11)
Norris, L. A., M. Newton, and J. Zavitkavoski .
1967. Stream contamination with amitrole
from forest spray operations. West.
Weed Contr. Conf. Res. Prog. Rpt.
1967:33-35.
(12) Sund, Kenneth A.
1956. Residual activity of 3-amino-l , 2 , 4-
triazole in soils. Agric. Food
Chem. 4(l):57-60.
1. Soil:
Amitrole residues could not be detected two months
after application of one- to two-pounds per acre on
three soil types in Oregon (4) . Amitrole was adsorbed
in red alder humus more rapidly than it was desorbed (9).
After 35 days, recovery of amitrole from red alder floor
material had dropped to 20 percent (8) . The presence
of 2,4-D or ammonium thiocyanate are not likely to
influence the persistence of amitrole in the field
(8:407). Degradation of amitrole proceeded at a near
normal rate in steam-sterilized forest floor material
despite nearly complete absence of biological activity
(8:408). Amitrole appears to become tightly adsorbed
to soil particles and can complex metals (12). It
may also act in the soil’s base exchange system (11).
Amitrole disappears rapidly from soils. Disappearance
has been attributed to adsorption, microbial degradation,
and nonbiological destruction (1). Evidence indicates
that nonbiological destruction is the most important
cause of amitrole disappearance in soils (1).
2. Water:
Amitrole was not degraded by biologic action in river
water, sewage, activated sludge, or anaerobic digestion
tests (5). Amitrole Interfered with nitrification in
river water and activated sludge. Clorination degraded
amitrole to unidentified compounds. Studies of amitrole
contamination in streams following aerial applications
indicate that maximum residues occur immediately after
spraying and decline rapidly (6, 7, 10, 11). Maximum
concentration of 155 ppb at the downstream edge of a
100-acre unit treated at two pounds per acre was attained
30 minutes after application began (6). It decreased
to 26 ppb by the end of the two hour application and to
non-detectable amounts six days after spraying. No
amitrole was detected at any time 1.8 miles below the
sprayed area. In another study, maximum concentration
immediately downstream from the sprayed area was 422 ppb
-12-
0.17 hours after spraying and dropped to 6 ppb 8 hours
after spraying (7). Residues did not persist into the
next year and heavy rains six months after application
did not introduce measurable amounts of amitrole into
the same stream (11).
3. Plants:
The s-triazole nucleus is highly stable and few workers
have reported evidence of ring cleavage under physiological
conditions (1). The half-life of amitrole in corn was
about 8 days. Disappearance in soybeans was much slower.
Amitrole could not be detected in cotton after 4 days but
large quantities of metabolic products were present. Ring
cleavage has been observed in oats and barley but not in
beans and tomatoes. Photodecomposition in the presence
of riboflavin has also been reported. Amitrole
degradation in plants seems to involve conjugation between
amitrole and endogenous plant constituents. These
products contain the intact triazole nucleus which often
can be regenerated by chemical treatment. The principal
detoxification product seems to be 3-(3-amino-l, 2 ,4-
triazole - 1 -yl) -2-aminopropionic acid (3-ATAL) .
E. Compatibility with other chemicals
Amitrole and amitrole-T are compatible with many other
herbicides, but other pesticides and fertilizers should
be used with caution. All amitrole formulations can be
mixed with 2,4-D, 2,4, 5-T, simazine (and other S-triazines) ,
bromacil, and diuron.
IV. Environmental impact
A. Effects of pesticide on non-target organisms.
B. Residues in or on food or feed.
Reference: (1) Ecological effects of pesticides on non-
target species. 1971. 220 pp. U. S. Government Printing
Office S/N 4106 - 0029. (Listed in Selected U.S. Govern.
Publ. 1(3)--1972).
The U.S. Government publication (1) contains pertinent
information for each pesticide discussed concerning non-
target mammals, birds, fishes, amphibians, mollusks, arthropods,
annellids, plants, and microorganisms. It also presents
information on biological concentration in food, chains and
persistence for each pesticide.
-13-
(2) Norris, Logan A.
1971. Chemical brush control: assessing the
hazard. J. Forestry 69(10) : 715-720.
Logan Norris (2) concludes that the relatively
large doses of amitrole required to produce acutely
toxic responses in most non-target organisms are
not likely to occur from normal chemical brush control
operations on forest lands. The short persistence,
lack of biomagnification in food chains, and the rapid
excretion by animals preclude chronic exposure and,
therefore, chronic toxicity.
-14-
REPORT
ON
BACKGROUND INFORMATION
FOR
ATRAZINE
\ ■
i ; >5:
‘■'ft-
7
B
t
Assignment:
Pesticide; Atrazine (AAtrex)
Use; Herbicide
Priority; 1
Team; M, Weiss (R-3) (For F, Yasinski (R-3) )
W. Davis (R-4)
H, Pangman (R-4)
c
I. GENERAL INFORMATION
Coirenon Namc„ ALrazinci
1/
B . Chcirn'cal Name. 2- ch loro -'A-e thy lami no-6 - isopropyl amino - s-
triazino (Anon., 1971a)
C. R c y, i s t c r e cl U s e s . AAtrcx 80W is registered for season-long
vveed control in corn and sorgiium and for weed control in certain
other crops; in non-crop areas; and industrial sites (Anon., 1971b)-—'
AAtrex BOW is registered for use in forest and Ch.ristmas tree planta-
tions of Douglas-fir, grmid fir, noble fir, v.Tiite fir, lodgepole pine,
ponderosa pine, and Scotch pine (The registration for AAtrex BOW limits
its use in forest and Christmas tree plantations to the Pacific North-
west, west of the Cascades.) (Anon., 1971b)
D. Fonnulat ions Manufactured . A_Atrex BOW, a wcttable powder
containing 807o active ingredient (Anon., 1971a). 2l!
E„ Dilution of Formulation to Use.
of
AAtrex
1. Forest and Christinas Tree Plantations (Anon., 1971b)
For annual broadleaf and grass weed control - 2^-5 pounds
BOW is diluted in 20-40 gallons of water per acre.
For
in 20-40 gallons
quackgrass control
of water per acre.
5 pounds of AAtrex BOW is diluted
2. Nonselectivo Weed Control on Non-Crop Land (Anon. , 1971b)
least
1
Use sufficient
gallon of water for
water to assure thorough
each pound of AAtrex BOW
coverage
more if
Use at
practical.
F , Tolerances in Food or Feed and Other Safety Limitations
Tolerances for Residues of Atrazine (Anon, , 1971b)
Tolerances for residues of atrazine on certain raw agri-
cultural coirunodit ies have been set as follows;
15.00 ppm In or on corn forage or fodder (including
field corn, sweet corn and popcorn), perennial
ryegrass, sorghum fodder and forage.
1/ Trademark: A\trex, Gesaprim
ll AAtrex 4L, a liquified formulation containing 4 lbs. of technical
atrazine per gallon, is registered for season-long weed control in corn
and sorghum (Anon, , 1971c)
2
10.
o
o
ppm
In
or
on
p ineapple
fodder
and
forage.
5.
o
o
ppm
In
or
on
wh c a t
fodd
er and
s t r aw .
0.
,25
ppm
In
or
on
fresh
corn
inc lud
ing
sweet c
(kernels jilus cobs husks removed) corn
grain (includes popcorn), macadamia nuts, pine-
apples, sorghum grain, sugarcane, sugarcane fod-
der and forage, wheat grain.
0.02 ppm In eggs, milk, meat, fat and meat by-
products of cattle, goats, hogs, horses, poul-
try and sheep.
2 o Other Safety Limitations
a. "Care should be taken to avoid using AAtre>; where
adjacent desirable trees, shrubs, or plants might be injured" (Anon. , 1971b) .
b. Forest and Christmas Tree Plantations (Anon. , 1971b)
"Do not graze treated areas. Do not apply to seedbeds.
Do not make more than one application per year,"
c . Nonsclect ive Weed Control on Non-Crop Land .
(See Supplemental page 1)
G . Rate and Method of Application
1. Forest and Christmas Tree Plantations (Anon., 1971b).
For annual broad leaf and grass weed control, AAtrex is
applied broadcast at rates of 2 to 4 pounds active ingredient per acre.
It is applied "between fall and early spring while trees are dormant or
soon after transplanting and before weeds are ll^ inches high." For band
application, the rate is reduced in proportion to the area treated.
For quackgrass control, AAtrex is applied broadcast at rates
of 4 pounds active ingredient per acre. It is applied "in fall or early
spring while trees are dormant and before weed seedlings are more than
1^ inches high."
2. Nonselect ive Weed Control on Non-Crop Land (Anon. , 1971b)
/vAtrex 80W is applied "before or soon after v;eeds begin
growth . "
To control most annual broadleaf and grass weeds (such as
barnyardgrass , cheatgrass, crabgrass, lambsquarters , foxtail, ragv;ecd,
3
puncturcv inc , and turkey mullein), AAtrex 80W is applied broadcast at
rate of 4.8 to 10 pounds active ingredient per acre.
To control hard-to-kill annual and many perennial broad-
leaf and grass weeds (sucli as blucgrass, burdock, Canada tliistle, dog-
fennel, orchardgrass , plantain, quackgrass, purple top, redtop, and
smooth brome) , ^VAtrex 80W is appJ ied broadcast at rates of 10 to 20
pounds active ingredient per acre.
To control hard-to-kill biennial and perennial v^7eeds (such
as bull thistle and sowthistle), AAtrex SOW is applied broadcast at rates
of 20 to 40 pounds active ingredient per acre.
For longer residual control in regions of high rainfall
and a long growing season, /uAtrex SOW is applied broadcast at rates of
20 to 40 pounds active ingredient per acre.
the lov7er
matter; the
organic matter”
H. Manufacturer or Producer
Geigy Agricultural Chemicals
Division of CIBA-GEIGY Corporation
Ardsley, New York 10502
II. TOXICITY DATA ON FORMULATION TO BE USED
3. "In each case where a range of rates is given,
rate should be used on light soils and soils low in organic
higher rate should be used on heavy soils and soils high in
(Alien., 1971b)
A. Safety Data
1. Acute Mammalian Studies
a. Oral
Species
Formulation Dosage LD5Q
Albino rats
Ailbino mice
Albino rats
Technical 3,080 mg/kg (Anon,, 1971a)
Technical 1,750 mg/kg (Anon., 1971a)
SOW 5.1 + 0.4 g/kg (Anon., 1971a)
Palmer and Radeleff (19G9) studied the toxicity of atrazine
and other herbicides to cattle, sheep, and ch.ickens. For atrazine , "Cat t le
and sheep were dosed by eitlier drench or capsule, cliickens by capsule. The;
toxic dosage for cattle was 25 mg/kg after 8 doses by drench and 2 by cap-
sule. The toxic dosage for slieep was 5 mg/kg.” '^lov/ever, one sheep received
199 consecutive doses at 50 mg/kg before it was poisoned and died. Chickens
4
given 10 at 50 mg/kg had a significant reduction in weight gains."
(Sec Supplemental pages 1 and 2)
b. Dermal
Species Formulation Dosage LD5Q
Albino rabbits SOW 9.3 + 0.9 g/kg (Anon., 1971a)
c. Inhalation. "there has been no evidence of toxicity in
rats subjected to aerosol dust containing the equivalent of 1.6 mg/litcr
of technical grade atrazine." (Anon., 1971a)
d . Eye and Skin Irritation
2. Subacute Studies
a. Oral
"No observable ill effects have been detected in cattle,
dogs, horses, or rats fed a diet which included more thari 25 ppm atrazine
over extended periods." (Anon., 1971a)
"Administration of daily dosages of 100 ppm of an 807.
wettable powder formulation of atrazine to cov/s for 21 days or feeding
30 ppm of this formulation i'n grain to cattle for four weeks resulted in
no observable effect." (Anon,, 1971a)
3 , 0th or Studies i-Th ich M ay Be Required
a. Teratogenicity and Carcinogenicity. "Long term studies
in rats and mice have revealed no carcinogenic or teratogenic effects
either in the parents or progeny following long term administration of
atrazine." (Anon,, 1971a)
The Technical Panel on Carcinogenesis of the Secretary's
Commission on Pesticides and Their Relationship to Fnvironraental Health
(Anon. , 1969) examined the available reports on tests of tumorigenicity
conducted on about 100 pesticidal chemicals and assigned each of the
pesticides to one of four groups: A, B, C, or D. Atrazine was placed
in the group containing those pesticides for which the available evidence
was considered insufficient for judgement (Group C). Atrazine was further
pla ced in Priority Group C4 , one of four priority groups in Croup C.
Priority Group C4 was characterized by "Tumor incidence not elevated in
adequate studies conducted in one species fniousc^ only but current guide-
lines require negative results in tv;o animal species for judgements of
negativity."
Chapter 8 of the Report of the Secretary's Commission on
5
Pesticides and Their Relationship to Environiriental Health (Anon. 1969)
contains information on tests run by the Bionctics Research Laboratories
of Litton Industries with various pesticides and related compounds for
teratogenic effects. "The Bionetics data were reanalyzed statistically
to account for litter effects." Ihe data for atrazine was placed in
Table 3, the table containing data on "Tests which showed no significant
increase of anomalies (v/ith particular doses, solvents, or test strains)."
The data for atrazine from table 3 was as follows:
Compound
Strains
Solvent
Dose per kg.
body wt.
Increased
mortality
(C57BL/6)
Total
number
of litters
Atrazine
C3H
DMSO
46.4 mg.
6
Do
C57
DMSO
46.4 mg.
13
Do
AKR
DMSO
46.4 mg.
15
^ * M^ifagenicity
Table 3, page of the Report of the Secretary's Commission
on Pesticides and Their Relationship to Environmental Health (Anon,, 1969)
contains a "List of various pesticides (1000 ppm, 12 hrs.) known to pro-
duce mutations in barley and relative efficiency of each to control and
to 5,300 R of X rays (Wuu and Grant, lll)."i./ Atrazine is listed as having
a relative efficiency of 10, X rays a relative efficiency of 32, and
control a relative efficiency of 1,
Page 639 of the Report of the Secretary's Commission on Pesticides
and Their Relat i.onship to Environmental Health (Anon., 1969) contains data
collated from files of the Environmental Mutagen Information Center. Data
on atrazine ■was presented as follows:
Pesticide
Organism
in which
tested
Assay
system
Biological
Dose effect
MG
registry
No.
Atrazine
Barley
Anther
1000 ppm- Soaked Slight effect
70 2/
on meiosis (Cx)
Slight effect
70 2/
on meiosis (C'l)
!_/ The paper cited (Wuu and Grant, 111) w^as Wuu, K. D. and W. F. Grant.
Morphological and somatic chromosomal aberrations induced by pesticides
in barley (Hordium vulgare). Can. J, Genet, cytol, 8: 481-501, 1966
_2/ EMIG registry No. 70 is for the following paper: Wuu, K. D, and
W, F. Grant. Ciiromosomal Aberrations Induced by Pesticides in Meiotic
Cells of Barley. Cytologia 32: 31-41., 1967.
Avian and Fish Toxicity
6
Route Dosage
Species
Formulation
Administered
LD50-
LC50
(Anon,
1971a)
liallard duck
Technical
5-day feeding
19,560
ppm
(Anon. ,
1971a)
Bobv/hite quail
Technical
7-day feeding
5 , 760
ppm
(Anon. ,
1971a)
Rainbow trout
Technical
96-hr. exposure
4.5
ppm
(Anon. ,
1971a)
Bluegill sunfish
Technical
96-hr. exposure
24
ppm
(Anon. ,
1971a)
Gold fish
Technical
96-hr. exposure
60
ppm
(Anon. ,
1971a)
LD50
Species
Formulation
Sex Age (957o
Conf. lim.)
mg /kg
Mallards
807o Wettable
Female 6 mos.
^2000
Tucker and
powder Crabtree (1970)
B . Physical- Chemical Properties
1. Physical State. IVhite, crystalline substance which is
non- combustible and non-corrosive. (Anon., 1971a)
_7
2. Vapor Pressure. At 20° C: 3.0 X 10 mm of Hg (Anon,, 1971a).
3. Solubility at 27° C. (Anon., 1971a)
Solvent
22m
Water
33
n-Pentane
360
Diethylether
12,000
Methanol
18,000
Ethyl acetate
28,000
Chloroform
52,000
Dimethyl sulfoxide
183,000
Stability. (See Supplemental page 3)
"Atrazine is stable in neutral, slightly acid, or basic
media. It sublimes at high temperatures and when heated, especially at
high temperatures in acid or basic media, hydrolyzes to 2-hydroxy-
4-ethylamirio-6-isopropylamino-s-triazine wliich has no herbicidal activity,"
(Anon., 1971a)
"Shelf life of the formulated SOW product in unopened paper
or polyethylene bags is more than five years." (Anon., 1971a)
7
#
III. EFFICACY DATA UNDER FIELD AND LABORATORY CONDITIONS
A • Effectiveness for Intended Purpose Wlien Used as Directed
Bickford ct al. (1965) found that atrazine improves survival of
Douglas- fir seedlings and ponderosa pine seed spots. Atrazine was applied
in March at 5, 3 1/3, and 1 2/3 pounds per acre of 807o active material to
plots near Corvallis, Oregon. Seedlings were planted on five dates from
Novemiber to March and spots were seeded in April. Survival of seedlings
was 'doubled on the plots where 12/3 pounds an acre was applied, and in-
creased to nearly five times the survival obtained on untreated plots,
in situations where 3 1/3 pounds were applied. There was little differ-
ence in survival betv;een plots with 3 1/3 pounds an acre and plots with
5 pounds an acre." "Response from seeded plots indicated comparable weed-
control requirements for planted Douglas- fir and seeded ponderosa pine."
Newton (1964) tested atrazine; Amitrcl, Simazine, at a 1:3
mixture; Simazine; and Isocil for weed control in planted Douglas-fir.
On treated plots, half of the seedlings were planted before treatment
and half v/ere planted after treatment. Spring treatments with atrazine
at 5 pounds active ingredient per acre gave complete weed control with
no conifer damage. "Fall treatmeiits produced poorer weed control and
possibly some conifer damage." Newton "concluded that spring applications
of herbicides are generally superior to fall treatments in this region of
low summer precipitation and wet winters, and that it is wise to avoid
chemicals which either allow rapid regrovTth of weeds, or damage seedlings
through their o\m toxicity. These results suggest atrazine as the most
promising chemical for this type of treatment under local conditions, and
rates of roughly four pounds active material in spring applications."
Gratkowski (1971) tested atrazine and several other chemicals for
grass and forb control in Douglas-fir plantations at four locations in
southwestern Oregon, Two of the locations were on the wet coastal slope
of the coast range and two were in the dry interior valleys. "Terbacil
proved most promising in these tests." In discussing the reasons for his
tests, Gratkowski states that "Atrazine is widely used for grass control
in plantations, but it is relatively ineffective on broadleaf v;eeds."
Newton and Webb (1970) in the summary of their paper state that
"llie limited information available suggests that herbicides applied success
fully in regeneration of Douglas-fir may largely be considered effective
and safe for ponderosa pine. With atrazine or dalapon, or both ,lierbaceous
weed control should be sufficient to establish pine in most areas. 'two,
4-D and other foliage - active compounds may be applied, but v;ith full
consideration of the hazards involved. Ponderosa pine is resistant to
atrazine, but the threshold of resistance is probably lower in coarse -
textured soils. Resistance of weeds to atrazine will be comparably lower
in the coarse- textured soils, however, and less material is needed to
accomplish the same job of v/ced control with the same degree of safety.
On. some soils, largely rocky and coarse textured or gravelly, vegetation
is not responsible for rapid drying. On such sites, good control of
weeds alone is not sufficient to guarantee survival."
B. Pliytotoxicity (See Supplemental page 4)
"Plant species such as corn and sorghum have the ability to
readily metabolize atrazine into nonphytotoxic compounds, therefore, they
are resistant to rates of atrazine commonly used for weed control. Other
plant species differ in their abilities to metabolize atrazine so various
degrees of susceptibility can be seen." (Anon., 1971a)
Kozlowski and Kuntz (1963) studied the effects of atrazine and
other herbicides on red pine (Finns resinosa Ait ♦ ) and vmite pine (Pinus
strobus L. ) seedlings. They found that applying simazine, atrazine or
propazine as a pre-emergence spray or directly to recently germinated
seedlings caused severe damage. As a pre-emergence treatment, atrazine
was applied immediately after planting at rates of 1, 2, and 4 pounds per
acre. Atrazine did not affect seed germination. However, "atrazine ad-
versely affected seedling growth and caused varying degrees of mortality.
Within seven days after emergence, a slight needle curling was observed.
Chlorosis developed and grov;th was visibly depressed. Adverse effects
increased wi.th time." "One m.onth after germination, approximately 10 per-
cent of the seedlings had died in flats treated vrLth 4 pounds atrazine
per acre."
As a post-emergence treatment, atrazine was applied 3 weeks after
seeding, "Seed germination and emergence of ^diite pine continued over a
3 week period." Atrazine was sprayed at rates of 1, 2, and 4 pounds per
acre. One month after treatment all red pine seedlings were dead on both
soil and sand at all rates. "Tlie following percentages of \diite pine seed-
lings were killed on treated soil and treated sand, respectively, at the
indicated rates (per acre): 4 pounds, 82 and 90 percent; 2 pounds, 67 and
91 percent; and 1 pound, 55 and 33 percent." "In general, the seedlings
which had emerged prior to treatment suffered somewhat less injury and mort-
ality than did the seedlings which emerged after treatment."
"Simazine, atrazine, and propazine did not leach readily from the
surface inch of Plainfield sand wlien 2, 4, or 8 surface inches of water
were applied. Some atrazine, however, moved do\imward from the first inch
more readily than did simazine or propazine." "No injury occurred to 2-0
red pine when simazine was applied to the soil surface at 4 or 8 pounds
per acre or when simazine was applied to the foliage only. Uhen, however,
amounts of simazine equivalent to 4 or 8 pounds per acre (soil-surface
basis)were incorporated into the soil, especially in the root zone, severe
injury resulted and seedlings eventually were killed." "These experiments
emphasized that wliereas young seedlings arc killed by triazine herbicides,
9
older seedlings are not, because the roots of the older seedlings normally
are below the layers of soil which contain ph.ytotoxic amounts of these
chemicals « *'
Kozlowski and Torrie (1965) studied the effect of soil incor-
poration of atrazine and other herbicides on germination and develop-
ment of very young red pine (Finns resinosa Ait , ) seedlings. Atrazine
was sprayed at rates of 2, 4, 8, and 16 pounds per acre to the surface
of^ flats containing Plainfield sand. Tlie following day the soil was mixed
and pine seeds were planted. "Soil-incorporated atrazine was exceedingly
toxic to the seedlings at all dosages." With the exception of ipazinc up
to 4 pounds per acre, the soil-iiicorporated triazine herbicides were gen-
erally very toxic to young pine seedlings. "'flie toxicity varied greatly
in the following decreasing order: atrazine, simazine, prometryne, propazine,
ipazine," "Certain triazines exhibited greatly delayed toxicity. For
example, more seedlings died in the last 20 days of the experiment than
in the first 90 days ..." "Seed gerraination was influenced only ver}^
slightly or not at all, by a variety of soil- incorporated herbicides.
In contrast, all but one of the soil-incorporated herbicides caused seed-
ling mortality and decreased dry-weight production of seedlings in vary-
ing amounts," "llie toxicit}^ of soil-incorporated herbicides was generally
much greater than when the same herbicides were applied to the soil
surface, "
Walker (1964) tested atrazine and other s-triazine compounds
as aquatic herbicides, Atrazine was applied in the field in open plots,
whole ponds, and to plastic enclosures. Atrazine was applied at rates
of 0.2 to 6.0 ppmw to 11 submerged plant species and 4 kinds of filamen-
tous algae. "Eradication was most consistent in water treated in total
volume dosages. Weeds were controlled in ponds or plastic enclosures
while poor results were obtained in partial treatments of open plots.
Atrazine concentrations of 0.5 to 1.0 ppmw effectively controlled most
filamentous algae and pondweeds in pond applications. Spray applications
of wettable powder generally were more effective than broadcasting gran-
ular atrazine. The duration of phytotoxity varied from seasonal control
or growth inliibition achieved at the lower concentration (0.5 ppmw) to
complete eradication ^^?hich exceeded a year's length as the result of
higher rates (1.0 ppnw) . Emergent grasses and herbaceous plants also
were affected in a manner similar to simazine applications." "Simazine
and atrazine were slow to give results in the aquatic environment, A
two- to six-week lapse was required before phytotoxity symptoms v/ere
noted. Tlie characteristic herbicidal effect of simazine, atrazine, and
propazine was a chlorotic appearance along with progressive decomposition
of affected plant parts. Inhibition of plant growth often was accompanied
by spotty eradication of rooted aquatic plants and filamentous algae.
Phytoplanl^ton tubidity was curtailed temporarily following the herbicide
applications. On<'.e the higher plants decayed, zooplankton also became
abundant." "Tl^e ecological sequence of the secondary succession was
noted following the eradication of aquatic vegetation. The use of
plastic enclosures allowed critical comparison of the ecological changes
10
produced by various rates and plant conditions." "Algae rarely were
controlled for more than one season. Inhibition of phytoplankton was
temporary, lasting less than 2-3 months in most applications."
C . Translocation with Plant Treated
"Atrazinc enters plants primarily through the root system.
Inside the plant it crosses cortical tissue to the xylem. Tlie xylem
appears to be the principal tissue by which atrazine is translocated.
Atrazine is translocated upward in plants and upon accumulating in
photosynthetic tissues (i.e, chloroplasts) , the plants die. Atrazine
is also absorbed to some extent through the foliage." (Anon., 1971a)
D. Persistence in Soil, Water, or Plants (See Supplemental page 5)
Kearney (1970) refers to an extensive review of the literature
by himself and others^' on the persistence of 11 major classes of pest-
icides in soils, llie triazine herbicides were grouped with the urea
and picloram herbicides. For the group, the time required for loss of
75 to 100 percent activity is 18 months.
Kozlov^ski and Kuntz (1963) found that "when Plainfield sand to
V7hich atrazine, simazine, or propazine was surface - applied and leached,
most of the herbicide remained in the first inch of soil regardless of
whether 2, 4, or 8 inches of water were used in leaching. However, some
herbicide, especially atrazine, moved doT^mward to a 6-inch depth. With
increased amount of leaching more herbicide v;as translocated out of the
first inch of atrazine- treated soil. Such an effect was not as apparent
v/ith simazine - or propazine - treated soil. The greater leachability of
atrazine was probably related to its greater solubility." "Tliis study,
which dem.onstrates the difficulty of removing triazine herbicides from
upper soil levels even with large amounts of water, emphasizes the dangers
of possible persistence and accumulation of triazine herbicides in forest
nurseries, even in light sandy soils."
E. Compatibility with Other Cltemicals
"When weeds are resistant to AAtrex, combinations of AAtrex
with sodium chlorate formulations, dalapon, TCA, amitrole, simazine
(Princep), and other compounds be used to broaden the spectrumi of
weed control." (Anon., 1971al
Kearney, P. C. , R. G. Nash, and A. R. Iscnsee, 1969. Persistence of
pesticide residues in soils, Chapter 3, p.p. 54-67. In M. W. Miller and
G, C. Berg (eds . ) „ Chemical fallout: Current research on persistent
pesticides, Springfield, 111, 'iliomas .
11
IV. ENVIRONMENT IMPACT
A. Effects of PcsticidG on Non-Tarp,et Organisms
Walker (1964) studied atrazine and other s-triazine compounds
as aquatic herbicides. Atrazine was applied at rates of 0.2 to 6.0 ppmw
to 11 submerged species and 4 kinds of filajnentous algae. Samples of
bottom fauna organisms were taken from plastic enclosures used in the
study. "Determination of acute toxicity to organisms was based upon
comparison of samples obtained from the treated area and untreated control
up to six v/eeks following the application. Clironic toxicity was measured
by comparative production three months to a year following the application."
"The herbicidal destruction of plant cover in fish habitat exposes smaller
forage fishes to predation by larger sport fishes. No toxicity to fishes
was demonstrated by the application of the s-triazine compounds under
field conditions." "In contrast to simazine, atrazine was somev;hat toxic
to bottom fauna. Among the most sensitive organisms v;ere mayflies
(Ephemeroptera ) , caddis flies (Tricoptera) , leeches (Hirudinea) , £ind
gastropods (Musculium) . The most significant reduction in bottom fauna
was observed during the period immediately following the application.
Bottom fauna appeared to recover according to observations made four to
six months following the treatment in the simazine tests."
B o Residues
St. John et al. (1964) studied the fate of atrazine and other
chemicals in the dairy cow. "Four holstein cows were catheterised and
each was fed one of the herbicides at the 5 ppm level (based on a daily
ration of 50 lb.) for four days. llie pure herbicides in absolute ethyl
alcohol (except atrazine, which was dissolved in acetone) were mixed with
the grain. Morning and evening subsaraples of the total mixed milk were
taken one day prior to feeding (control sample), daily throughout the
feeding period, and for two days thereafter. Tlie total daily urine sample
was similarly collected, weighed, mixed, and subsampled over the same
test period." "A colorimetric method and isolation procedure was developed
for atrazine in milk and urine based on the Zincke reaction with active
halogen compounds ..." "The residue determined represented intact
atrazine, since the Zincke reaction is applicable only to compounds con-
taining active halogens, Atrazine may have been largely converted to
hydroxy atrazine and excreted in the urine as a water-soluble conjugate
of this compound." "No residues of these herbicides were found in the
milk. About 2% of intact atrazine was eliminated in the urine."
Norris et al. (1967) "made a preliminary survey of atrazine
residues in deer harvested from forest lands treated with this herbicide
for grass control. Deer were harvested at various intervals after appli-
cation of the herbicide [^17 days, 26 days, and 44 days^, and various
organs and body tissues v»erc removed, placed in plastic bags, and frozen
12
<
as quickly as possible, 'flie analytical procedure was essentially that
outlined in Geigy Analytical Bulletin Number 7 with the exception that
the herbicide was determined with a gas chromatograph, " "Unfortunately,
a control animal was not available; so there is no indication whether or
not deer normally carry atrazine residues, however this possibly appears
quite unlikely. On the basis of our analysis using two different columns
and a halogen specific detection system there is little question that the
chemical measured is in fact atrazine." "We found no atrazine residue
greater than 76 ppb in portions of these animals which might normally be
used for human consumption. In one animal, not listed above, residues
of 326 ppb atrazine were found in the thyroid and 498 ppb in the lymph
glands. Another animal yielded a fat sample v;hich contained 688 ppl)
atrazine. "
'‘Iti general this survey indicates that atrazine applied for grass
control on forest lands of southern Oregon will enter several tissues and
organs of deer. The length of persistence of the chemical in these tis-
sues is not clear from this study. Tlie likelyhood (sic.) of encountering
dangerous residues of atrazine in tissues of Jmportance for human con-
sumption appears low,"
I
CITED REFERENCES
Anon, 1969. Report of the Secretary’s Commission on Pesticides and
Tlieir Relationsb.ip to Environmental Health, Parts I and II, U, S.
Department of Health, Education and Welfare. 677 p.
Anon. 1971a. AAtrex herbicide technical bulletin. Geigy Agricultural
Chemicals, GAG 700-564. 8 p.
Anon. 1971b. AAtrex SOW herbicide sample label. Geigy Agricultural
Cliemicals. GAC 130-069. 8 p.
Anon. 1971c, A/^trex 4L herbicide sample label. Geigy Agricultural
Chemicals. GAC 130-070. 4 p.
Bickford, M, L., J. Zavitkovski, and M. Newton, 1965. Atrazine improves
survival of Douglas-fir seedlings and ponderosa pine seed spots.
Research Progress Report. Research Committee Western Weed Control
Conference. 48-49.
Gratkowski, H. 1971. Grass and forb control in Douglas-fir plantations.
Research Progress Repo7.*t, Research Committee Western Society of Weed
Science, 31.
Kearney, P, C, 1970. Summary and conclusions, in Residue Reviews.
Vol. 32. Single Pesticide Volume: Hie Triazine Herbicides. 391-399.
Kozlowski, T. T. and J. E. Kuntz. 1963. Effects of simazine, atrazine,
propazine, and eptam on pine seedlings. Soil Sci. 95: 164-174.
Kozlowski, T. T. and J. H. Torrie. 1965. Effect of soil incorporation
of herbicides on seed germination and growth of pine seedlings.
Soil Sci. 100(2): 139-146.
Newton, Michael. 1964. Chemical weed control in conifer plantations.
Research Progress Report. Research Committee Western Weed Control
Conference, 42-43,
Newton, Michael, and W. L. Webb. 1970. Herbicides and the management
of young pine. Symposium Proceedings: Regeneration of Ponderosa Pine.
School of Forestry. Oregon State University, Corvallis. 94-99.
Norris, Logan A., M. Newton, and J. Zavitkovski. 1967. Atrazine residues
in d eer. Research Progress Report, Research Committee Western Weed
Control Conference. 30-31,
Palmer, J. S., and R. D. Radclcff. 1969. llie loxicity of some organic
herbicides to cattle, sheep, and chickens. U. S. D. A. A. R. S.
Production Research Report No. 105. 26 p.
St. John, Lo E., D. G. Wagner, arid D. J, Lish. 1964. Fate of atrazine
kuron, silvex, and 2,4,5-T in the dairy cow. J. Dairy Sci. 47(11):
1267-1270.
Tucker, R. K. and D. Glen Crabtree. 1970. Handbook of Toxicity of
Pesticides to Wildlife. U. S. D. I, Fish and Wildlife Service.
Bureau of Sport Fisheries and Wildlife. Resource Publication No. 84.
131 p.
Walker, Charles R. 1964. Simazine and other s-triazine compounds as
aquatic herbicides in fish habitats. Weeds 12(2): 134-139.
Supplemental page 1
Additional Information
I. GENERAL INFORMATION
F , Tolerances in Food or Feed and Other Safety Limitations
2 . Other Safety Limitations
c . Nonselcctive Weed Control on Non- Crop Land
*'Do not contaminate domestic or irrigation water
supplies, or lakes, streams or ponds." (Anon., 1971. AAtrex SOW
herbicide sample label, Geigy Agricultural Cliemicals. GAG 130-069.
8 p.)
II. TOXICITY DATA ON FORMULATION TO BE USED
A, Safety Data
1. Acute Mammalian Studies
a. Oral
Palmer and Radeleff studied the toxicit}^ of atrazine
and several other herbicides to cattle, sheep, and chickens. For
atrazine tests, "cattle and sheep were dosed b}’' eitlier drench or cap-
sule, chickens by capsule. The toxic dosage for cattle v?as 25 mg. /kg.
after 8 doses by drench and 2 by capsule. Tlie toxic dosage for sheep
was 5 mg, /kg. No lesser dosage was tried. However, one sheep received
199 consecutive doses at 50 mg. /kg. before it was poisoned and died.
Chickens given 10 at 50 mg. /kg. had a significant reduction in weight
gains . "
"To relate the toxic dosages found for cattle, sheep,
and chickens to the application rates recommended for each herbicide,"
the authors "calculated the probable amounts that could be consumed
daily from recently sprayed fields or pastures. In these calculations,
we considered neither the influence of environmental factors such as
soil type, temperature, and rainfall, nor the decomposition rates of
the herbicides being studied.
'"The U.S.D.A. Summary of Registered Agricultural Pest-
icide Chemical Uses' was utilized for the application rates!/. An
1^/ U. S. Department of Agriculture. 1966. U. S. D. A. Summary of Re-
gistered Agricultural Pesticide Clicmical Uses. Ed. 2, Sup. Ill, 836 pp.
(See also subsequent preliminary notices of U. S. D. A. pesticide sum-
mary entry to Dec. 15, 1967.)
Supplemental page 2
arbitrary, although realistic, yield of 0.1 pound of air-dry forage
per square foot of area was selected, which is equivalei^t to approx-
imately 2 tons per acre. Tliis would represent a high-quality, improved
pasture. Tlie reader must, of course, make adjustments for local con-
ditions. A sparse cover of vegetation would allow more of tlie herbicide
to reach the ground and be unavailable to animals, whereas a more lush
vegetative cover would tend to hold more of the material available. In
the latter case, however, less of the total forage of the area v/ould be
consumed in any one day.
"Further assumptions were; (1) that an animal X'/ould con-
sume, as forage, 3 percent of its body XN^eight each day; and (2) that all
the chemical formulation applied would adhere to the vegetation. Although
this latter is never actually the case, this assumption gives the maximum
exposure to be expected.
"An application of 1 pound of chemical to 1 acre of land
provides 10.4 milligrams for each square foot. We may simplify the whole
calculation to a single statement that 1 pound actual of herbicide per
acre provides a 7-milligram per kilogram (mg. /kg.) dosage to the animal
under the conditions here assumed to exist. Each 2.2 pounds of animal
x^eight equals 1 kilogram or 1,000 grams. In turn, 1 pound equals 454
grams. The equivalent of 1,000 mg. /kg. is 454 milligram per pound
(mg. /lb.)."
"Application rates for atrazine range from 0.4 to 6.4
pounds actual per acre. Rates of less than 1 pound x/ould be hazardous
for sheep. Rates of 3 pounds actual per acre x^ould be hazardous for
cattle. Tlie 6.4 pound rate would be hazardous for chickens." (Palmer, J.
and R. D. Radeleff. 1969. Tlie toxicity of some organic herbicides to
cattle, sheep, and chickens. U. S. D. A. A. R. S. Production Research
Report No. 106, 26 p.)
I
I
Supplemental page 3
5 . Stability
a. Atrazine is a relatively stable compound, but is
subject to decomposition by ultraviolet irradiation. However, under
normal field conditions this effect would be small.
b. Microbial action probably accounts for the major
breakdowi of atrazine in the. soil.. A range of soil micro-organisms
can utilize it as a source of energy and nitrogen. Tlie effects of
atrazine on these and other organisms appear to be small.
References
1, Bryant, J. B, 1963. Bacterial decomposition of some
aromatic and aliphatic herbicides, Ph.D. Tl^esis
Pennsylvania State University, University Park.
2. Volk, G. M. and C. F. Eno. 1962. The effect of sima-
zine and atrazine on certain of the soil microflora
and their metabolic processes. Florida Soils and Crop
Sci, Soc, 22: 49-56.
c. The significance of photodecomposition and/or volatil-
ization of atrazine from soil is not fully understood. Available data
indicate that both occur to some extent if high temperatures and pro-
longed sunlight follow application before precipitation, but that these
factors are of little direct importance in atrazine dissipation under
most field conditions. Atrazine is m.ore subject to UV and volatility
losses than simazine, but probably about equal or less subject to these
losses compared to the commercial methylmercapto- or methoxytriazines .
References
1, Foy, Co L. 1964. Volatility and tracer studies with
alky-lamino-s- triazines . Weeds 12: 103- 108,
2o Jordan, L« S,, B. E. Day and W. A. Clerex. 1964. Photo
decomposition of triazines. Weeds 12: 5-6.
3, Kearney, P. S., J, T. Sheets, and J. W. Smith. 1964.
Volatility of seven s- triazines. Weeds 12: 83-87.
d. Atrazine is very stable over several years of shelf
life, with only slight sensitivity to natural light and extreme temp-
eratures which would occur normally.
Supplemental page 4
B PhytotoxicitY> Translocation, and Persistence In Plants
1. Atrazine is absorbed through both roots and foliage, al-
thougli foliar absorbtion is often small in most plants under field
conditions, depending on species, environmental conditions, ct cetera.
The herbicide can be washed off plant foliage by rain.
Following absorption through roots and foliage, it is translocated
acropctally in the xylem and accumulates in the apical meristems. It
acts as a photos^aithetic inlil.bitor , but may have additional effects.
Atrazine is readily metabolized by tolerant plants to
hydroxy-atrazine, which in turn is further degraded to CO2 and other
metabolities . l*his non-enzymatic alteration of atrazine is a major
protective mechanism in most crops where it is used. Soil placement
selectivity is also important in the case of some deep rooted perennial
crops. Atrazine accumulates in sensitive plants, causing chlorosis
and death.
Limited studies have shovm some minor fungicidal and
nematocidal activity but no insecticidal activity.
References
1. Funderburk, H. H. and D, E. Davis, 1963. The m.etabolism.
of C 14 chain-and ring- labeled simazine by corn and
the effect of atrazine on plant respiratory systems.
Weeds 11; 101-104.
2. Gysin, H. and E. Knusli. 1960. Cnemistry and herbicidal
properties of triazine derivatives. Advance. Pest.
Control Res. 3: 289-358.
3. Hilton, J. L., L. L. Jansen, and H. M. Hull. 1963.
Mechanisms of herbicidal action. Ann. Rev. Plant
Physiol. 14: 353-384.
4. Montgomery, M. and V. H. Freed. 1964. Metabolism of
triazine herbicides by plants. J. Agr, Food Cl\em.
12: 11-14.
Supplemental page 5
C. Persistance In Soils
1 , Adsorption and T.eachlng Characteristics In Basic Soil Types
a. Atrazine is more readily adsorbed on muck or clay
soils than on soils of lov^/ clay and organic matter content. 'fhe down-
ward movement or leaching is limited by its adsorption to certain soil
constituents. Adsorption is not irreversible and desorption often
occurs readily, depending on temperature, moisture, pM, etc. Atrazine
is not normally found below the upper foot of soil in detectable quant-
ities, even after years of continuous use.
The residual activity of atrazine in soil at selective
rates for specific soil types is such that most rotational crops can be
planted one year after applications, except under an arid or semiarid
climate. Atrazine will persist longer under dry and cold conditions or
conditions not conducive to maximum chemical or biological activity.
Broadcast rates needed in some of the heavier organic matter soils of
the North Central states result in enough residue carry over, under some
conditions, to injure small grains, alfalfa, and soybeans planted 12
months later. Plant removal and chemical alteration are also factors
in dissipation.
References
1, Ashton, F. M, 1961, Movement of herbicides in
soils with sim.ulated furrow irrigation. Weeds 9:
612-619
2e Talbert, R. E. and 0. H. Fletchall. 1964. Inact-
ivation of simazine and atrazine in the field.
Weeds 13: 33-38
3, 1965. Tlie adsorption of some s-triazines
in soils. Weeds 13: 46-52
4« Gysin, H. and E. Knusll. . 1960. Cliemistry and herb
icidal properties of triazine derivatives. Advance
Pest. Control Res. 3: 289-358.
REPORT
ON
BACKGROUND INFORMATION
FOR
CACODYLIC ACID
I. GENERAL INFORMATION
A. Common Name . Cacodylic acid.
B. Chemical Name. Dimethylarsinic acid.
C . Registered Uses.
1. For post-emergent weed control.
2. For conifer and hardwood control.
3. For bark beetle suppression and prevention. This use is
registered only for application by professional foresters in forestry
management programs in the Rocky Mountains of South Dakota, Colorado,
Arizona, and New Mexico.
D. Formulation Manufactured. Silvisar 510 Tree Killer--a solution
containing 6.0 lbs. of dimethylarsinic acid equivalent per gallon.
(See Table 1 for materials used for post-emergent weed control.)
E. Dilution of Formulation for Use. Silvisar 510 is entirely
soluble in water and can be mixed with water to form diluted solutions.
Half-strength Silvisar 510--full strength Silvisar 510 mixed with
an equal amount of water--has proven effective in bark beetle suppression
and prevention.
F . Rates and Methods of Application.
1. Conifer and Hardwood Control (Silvicide). Full- strength
Silvisar 510 is injected into undesirable trees by two methods:
a. Ansul "Hypo-Hatchet" Injection. This hatchet-like
unit cuts and injects in one operation. The injector works by
inertia and is calibrated to inject at least one milliliter of
chemical per stroke. Rates for this method are:
(1) Conifers and Hardwood - Growing Season. For
trees below 8 inches diameter at breast height (d.b.h.), make one
cut per 2 inches of d.b.h. (4^" spacing between cut edges) at waist
height or below. For trees 8 inches d.b.h. and larger, make one
cut per 1 inch d.b.h. (1%” spacing between cut edges).
(2) Conifers - Dormant Season. Make one cut per 1
inch of d.b.h. (1%" spacing between cut edges) at waist height or
below.
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(3) Hardwoods - Dormant Season, Make a complete frill
at v/aist height or below.
b. Spaced-Cut Application. A hatchet or similar cutting
tool can be used to make the cut and Gilvisar 510 added to the cut
v;ith a plastic squeeze bottle or pump-tj'pe oil can other than those
made of zinc, tin, or aluminum. Rates for this method are:
(1) Conifers and ilar dwoods - Growing Season . For
trees below 8 inches d.b.h., apply 1 milliliter of oilvisar 510 per
cut per 2 inches of d.b.h, (6" spacing between cut centerlines) at
vra,ist height or below. For trees 8 Inches d.b.h. and larger, use
1 to 2 milliliters per cut per 1 inch d.b.h. (3" spacing between
cut centerlines') .
(2) Conifers - Doimiant Season. Apply 1 milliliter
of Silvisau' 510 per cut per 1 inch of d.b.h. ("3” spacing between
cut centerlines),
(3) Hardwoods - Dormant Season. Apply 1 milliliter
of Silvisar 5IO per cut in a complete xirill at wa,ist height or below.
Bark Beetle Prevention and Suppression. A complete,
trough-like frill is made around the entire tree within I8 inches
of the ground using a hand hatchet or small ax. A plastic squeeze
bottle is used to apply 1 milliliter of chemical evenly in the friLl
for each inch of tree circumference.
a. Pre-Flight Trea.traent - Dendroctonus ruf ipennis Only.
(1) Fall Treatment. Trees ai'e frilled and treated
with half-strength or full-strength Silvisar 510 in October and
felled 4 weeks a,fter treating.
(2) Spring Treatment. Trees are frilled and treated
with half- strength Silvisar 5IO 4-8 weeks before peak beetle emergence
and felled 2-4 weeks after treating.
b. Pre-Harvest lYeventive Treatment - D. rufipenni s , D.
ponderosae , D. pseudotsugae . D. a,d;iunctu3 , Ips ..lecontei , I. pini ,
and 1, confusus . Trees ai'e i’rilled and treated with Itill- strength
Silv'j.sau' 510 at least 4 weeks befoi-e cutting. A minimum of 4 v/eeks
should be aiLlowed betv/een treating and felling.
c. Post-Flight Treatment. - D. rufipennis, 1). ponderosa,
D. pseudotusgae , D. ad;'junctus , I_. lecontel , ])ini , and confasus
Trees are I'rJ.lJed and treated v/itii full-strcngUi Silvisar 5I0 v/ithin
2-3 weeks after beetle atta.ck.
“3-
G . Tolerancer; in Food or Feed and Other Safety T;iinito.tions . The
following tolerances have been granted for cacodylic acid oqiressed
as AS2O3:
2.8 ppm in cotton seed
1.4 ppm in kidneys and livers of cattle
0.7 ppm in meat, fats, meat by-products except kidney and liver
Silvisar 5IO forms arsine gas when it comes in contact with
zinc, tin, or aluminum; therefore, this material should not be stored
or applied in containers made of these metals. Silvisar 51O is
moderately corrosive; therefore, injection equipment should be
thoroughly rinsed with water immediately after use.
H. Manufacturer or Producer
TTie Ansul Company
Marinette, Wisconsin 54l43
II . TOXICITY DATA ON FORIiULATION TO BE USED
A. Safety Datajv^
1. Acute Mammalian Studies
a. Oral
(1) Estimated Acute LD50
^ (a) Technical Gra.de Cacodylic Acid. 77 /b cacodylic
acid (CA); 0.7 g per kg (adult male albino rats); V/ARF Institute
(Wisconsin Alumaii Research Foundation Laboratories. Madison, V/iscensin).
(b ) Technical Gra de Sodium Cacodylate ( NaCA) .
30}o CA equivalent; 4.3 g (ilaCA) per kg (adult male albino rats'): WARE
Institute.
(c) Ansar I60. Sodium cacodylate 24.78*'^; CA
equivalent 30*13'^; sodium chloride~8.707o; 3*2 cc per kg (adult albino
rats); WARF Institute.
(d) Phy^tar ^6o. 23.4'}^ CA eowivalent; 254.0
I’lg/kg (Holstein dair;;," calves); E. S. Erv;in & Associates, Phoenix,
Arizona.
Excey;t whei'e othem..ase noted, toxicity do,ta was summarized from a
report by 'fl-ie Ansul Company, Marinette, Wifjconsin, entitled "Toxicological
Data - Methanea.rsoni c Acid and Dimethylarsinic Acid," June 5? lS^7j v/ith
an addenduia dated October 10. 19^9*
S.
-U-
(e) Ansar l60. 24.78/y sodium cacodylate;
8.76 CA; 30* CA equivalent; 200.0 mg/kg (Holstein dairy calves);
E. S. Erv/in & Associates, Phoenix, Arizona.
(2) Acute Oral LD50
(a) Technical Grade Cacodylic Acid. 6l.3^ CA;
i.4o g per kg (young male albino rats); 1.28 g per kg (young female
albino rats); Industrial Bio-Test Laboratories, Northbrook, Illinois.
(b) Phytar ^60. 23.4^ CA eqiiivalent; 2.6 g
(560) per kg (young male and female albino rats); Industrial Bio-Test
Laboratories .
(c) Silvisar ^10. 56.0^ CA; 1.8 g per kg
(young male albino rats); 1.0 g per kg (young female albino rats);
Industrial Bio- Test Laboratories.
(3) Acute Oral LDpoo
(a) Technical Grade Sodium Cacodylate. 1.23 g
per kg (dairy calves); E. S. Ei'V';in & Associates.
(b) Phytar ^6o. 2.0 g per kg (dairy calves);
E. S. Erwin & Associates.
b. Eye and Skin Irritation
(1) Dermal Irritation
(a) Ansar 160. 24.78*^ sodium cacodylate; 8.76']^
CA; 30 • 13*5^ equivalent; non- irritating to the skin in 72-hour exposure
(albino rabbits); V/ARF Institute.
(b) Technical Grade Cacodylic Acid. -Non-irritating
to the skin in 24-hour exposure (albino rabbits); WARF Institute.
(2) Eye Irritation - Technical Grade Cacodylic Acid.
Non- irritating to the eyes in 2-4 sec. exposure (adult albino rabbits);
VARF Institute.
2. Subacute Studies
a. Oral
(1) Technical Grade Cacodylic Acid. Technical grade
cacodylic acid v/as fed to v;eanling male rats at 700, l400, and 2800
ppm in the hartal ration daily for 3 veekn. Substantial drop in food
consumption and v/cif/ht gain at 2800 ppm. LVidence of reduced activity
of spermatogonia cells vith some" atrophic changes of the seminiferous
cells at 2OOO j'ijmi. One ajiiiial shov;ed some early degeneration of the
hepatic cells. No sucli findings at 700 end l400 pjmi. WARF Institute.
(2) Phytar ’^60. ^60 was fed at 200, 400, and 1200
mg per kg in 8 ])ounds of supj)lemental cottonseed meal to each of two
Holstein calves at each level, each day for 1 v;eek. 200 mg per kg -
calves quit feeding on 7th day: UOO mg per kg - calves quit feeding
on 6th day; 1200 mg ]>er kg - one calf quit feeding on 5th day; 1200
mg per kg - one caJ.f died on 3rd day. Only one calf of six showed
diai'rhea. Remaining five calves recovered completely on normal ration
for 7 days, E. S. Eiv/in & Associates.
(3) Ansar I38. A 60-day feeding test on the
metabolism of cacodylic acid (Ansar I38) in dairy cows was conducted.
Tv7o Holstein miik cow's were fed a. diet of ground barley, wheat brs,n,
and cottonseed meal containing 10 ppm of cacodylic acid. This
resulted in a dai.Ly intake of 2U.5 rng/kg/cov7. In another group
of cows, an equal v/eight of arsenic acid vzas fed to cows. The
milk from both gronps of these cows was analyzed and found to
contain no arsenic during the entire test period. The excretion
of arsenic is priirarily by \;ay of the urine, and a balance betw'een
intake and output is present after 30 days of feeding. At the end
of the experiment, the cows -were sacrificed and 10 tissues and bone
were analysed for iU'senic. It was concluded that no tissues stored
arsenic compounds on a cumulative basis, even though fractional parts
per million of ai'scnic were detected in the liver, spleen, and pancreas.
The differences in arsenic content of the organs from .the cows fed
cacodylic acid :md tliose fed arsenic acid w^ere insignificant (Peoples
1964).
(4 ) Pure Cacodylic Acid. Cacodylic acid was fed
at 3j 15 j s,nd 30 to dogs, and at 3? 15? srid 100 ppm to rats, in
the basal ration for 90 days. No-effect level for dogs - 30 ppm.
No-effect level for rats - 100 ppm. WARF Institute.
t>. Perimil - Technical Grade Cacodylic Acid. Technical
grade cacocpy'lic acid, in the form of an aqueous suspension, was applied
by rubbing to the clipped (area of about 4x6 iqches) trunks of
adult mule albino rabbits, at levels of 1.0, 1.6, 2.5, 3.9, 6.0, and
9.4 g per kilogi'cun. ivo rabbits v;ere used at each level, with the
skin abraded on one imiinal and intact on the other. A rubber sleeve
was ])laced over i,’r.e treated area. Exposure v;as for 12 hours overnight,
after whicli the sleeve was removed, the animul wiped clean and returned
to its cage. Treatment v/as for 5 days per w^eek for 3 weeks, followed
-6
by a 2-week post- treatment observation period. Dermal LDpoo " S
per kg for abraded animals; Dcriinl LDioo - 2.5 g per kg for intact
animals; Derma.l LDq - 1.6 g per kg for intact animals. WAI^F Institute.
3. Other Studies
a. Carcinogenicity. Arsenic has only been associated
with poisoning and was indicated quite early as a carcinogen. More
evaluations suggest that the early -tests reporting arsenic- induced
carcinoma were inadequate. Frost (l970) cites numerous studies v/hich
attempted but failed to -demonstrate arsenic- induced carcinoma.
Cacodylic acid was place . in group c4 by the Secretary’s Commission
on Pesticides and their relationship to environmental health (Mrak
1969) • Ihis group contains pesticides vehich were judged not positive
for carinogenicity in one species (mouse), but current guidelines
require negativity in two species. The commission gave this group
a moderate priority for testing, but felt no changes in practices in
the field w'ere warranted.
S. S. Pinto and B. M. Bennett (19^3 ) believe that
it is a mistake to malce blardcet condemnations of the use of arsenic
without first looking at the data. He has review^ed the early
literature on human tumors from arsenic and also the recent opinions
and interpretations of these early papers, Tliere is reason to believe
that the "arsenic tumors" observed in l820 may have been due to other
causes such a.s selenium poisoning. He reviewed the medical histories
and causes of dea,th of the long-term employees of a copper smelting
company producing arsenic trioxide. He shouted that the workers do
excrete higli levels of a.rsenic, but that their incidence of cancer
is no greater than for other persons in the State of Washington.
He concluded that there is no evidence that exposure of these workers
to arsenic trioxide is a cause of systemic cancer in humans. In a
sense, this amounts to the use of human guinea pigs for establishing
the lack of carcinogenicity of arsenic trioxide.
b. Mu tagenicity. Cacodylic acid is a mitotic poison in
imammalian organisms. King and Ludford (i960) found that injections in
mice produced "jjrofound disturbances of cell division" and it "stimulated
mitosis in cells of the crypts of Lieberkuehn" and of transplanted
tumors. liie significance of this finding in terms of e>qDosure to
cacodylic acid in the field is not kno\-m.
c. Teratogenicity. Cacodylic acid is considered to be
a teratogenic o.gent, pi-oducing abnormalities during eiiibryonic development.
TlTere are several rel’erences to this type of action, although only tv/o
excunples are quoted, Calzgeber (i-955) obscra^ed teratogenic effects
in 10-day chick eiibryo genital organs cultured in vitro and has reported
J
-7-
that the greatest damage is to the cortical region. Rostand (195O)
has treated tadpoles of Ran a temporia v;ith solution.s of cacodylic
acid for 3 v/eeks vhen the hind legs were in the process of development,
and abnormalities were observed at 0,01% of sodium cacodylate. (This
concentration is 100 ppm and is equivalent to 2?0 Ib/acre ft of water.)
Additional testing, using the techniques reported
by Mrak (l970), is needed. Relation of these i-eports of teratogenic
potential and field use of the chemical require further investigation.
d. Fish Toxicity
(1) Sodiiun Ca-codylate (liaCA). 30^ CA equivalent;
TLm (median tolerance limit) at 9^hours -- 750 ppm (bluegill sunfish).
Louisiana Wildlife & Fisheries Commission.
(2) Phytar ^60. 23.1^ CA equivalent; TLm at 9^
hours -- 80 ppm (bluegill sunfish), Louisiana Wildlife & Fisheries
Commission,
(3) Other Studies. K. H. Oliver (1966) exposed
Gacibusia addinis (mosquito fish ) , Notropis rnaculatus (tail-light
shiner y, and Micropterus salmoides (largemouth black bass) to
concentrations ranging ilrom 100 to 10,000 ppm of ca.codylic acid for
periods up to 72 hours. All three species of fish survived the 100
ppm level for this period. Although there were some deaths of the
Gaiobusia. at lower doses, 12 out of 20 survived 63I ppm for 72 hours.
Five out of 10 of the Notropis survived exposure to 63I ppm for 72
hours. In a similar experiment with tadpoles, it was sho>m tadpoles
(Bufo terrestyis ) survived the 100 ppm level for ^1-8 hours, and all died
a.t this time period at 1,000 ppm. The Bureau of Commercial Fisheries
(1966) shoi/ed that cacodylic acid at 40 ppm has no effect in 48 hours
on pink shrimp (Penaeus duorarimn ) , eastern oyster (Crassostrea
virginica) , or longnose killifish ( Fundul.us similis)^
e. Game Bird Toxicity. Mallard, ducks and chuliar
partridge were dosed at levels of Silvisar 5i0 (50% CA) up to 2000
All birds survived, but some showed s;ymptorns of intoxication
at higher dosages. U.S, Depai'tment of interior, P'ish and Wildlife
Service. 2/
f. Chicken Feeding Studies. Itire cacodylic acid was
fed at 0.6, 6.0, and 60 ppm in the basal ration of 7 female and 3 male
leghorn chickens at each level, for 10 weeks. No significfint arsenic
residues in eggs, lean meat, liver, and kidneys at 0.6 and 6,0 ppm.
No I'esidues in fat at all levels. Some sioall but definite arsenic
2/^ Memo from Jack F. Welch, Director, Bureau of Sj)orts Fisheries and
Wildlife, Fish and Wildlife Service, U.S. Dept, of Interior, Denver,
Colorado, to B'. leroy Bond, Assistart Regional B'orester, USDA Bkrest
Sei'vice, Albuquerque, New Mexico, dated Marcli 20, 1970.
-8-
residues in ecgs, lean meat, liver, and kidneys at 60 ppm. One week
post-feedin{^ on basal ration only removed residues in liver and
kidneys, and reduced level in lean :neat, for 60 ppm level. WARF
Institute.
B, Physical- Chemical Properties
1. Boiling point - -t-110*^ C.
2. Flash point - none
3. Physical state - crystalline
I4. Density - 1.U4 grara/ml.
5. Vapor pressure - same as water
6. Solubility - 200 g/lOO g vrater; 2o g/lOO g alcohol.
Insoluble in ether.
7. Stability soinev/hat hygroscopic. Stable to fuming nitric
acid, aqua regia, hot Kl>In04 sol.
8. Melting point - 195-196® C.
Ill . EFFICACY DATA liTTDER KEEL'D AilD TV\B0MT0RY COriDITTONS
A. Effectiveness for Intended Purpose When Used as Directed
1. As a Systemic Insecticide for Bark Beetle Suppression
and Prevention
a. Post-Flight Treatment. Chansler and Pierce (1966)
pioneered the investigations into the use of cacodylic acid treatment
for bark beetle suppression. They injected undiluted Ansar 16O
lierbicide (a solution manufactured by The Ansul Company containing
the equivalent of 3*25 lbs. of cacodylic acid per gallon) and Silvisar
510 Tree Killei' directly into the sap streams of individual ponderosa
pine infested with Dendroctonus adjunct us and D. ponderosae , Douglas-
fir infested with D. pscudotsugae , and Engelirann spruce infested v/ith
D. rufipennis , soon after attack. Population reductions from this
treatmicnt ranged from 84-99 percent. Chansler et al. (1970 ) treated
^ Data obtained from TSI Cor.Tpany, Flanders, Nev; Jersey.
-9-
ponderosa pine with undiluted Silvisar ^10 vitliin 2 weeks after they {
had "been infested by D. ponderosap and obtained almost complete beetle
reduction. D. ruf ijieniiis broods v;ere significantly reduced when newly
infested trees were treated v;ith undiluted Silvisar 5IO (Buffam 1969a.).
Buffam and FlaJvc (1971 ) obtained 100 percent mortality of D. adjunctus
broods v/hen recently infested ponderosa pines were treated v;ith undiluted
Silvisar ^10. Ollieu (1969) obtained percent reduction of D. frontalis
brood v/hen pines were treated with Silvisar 510 at 1-2 days after attack.
Brood reduction was only 59 percent v;hen trees were treated 3-^ days
after attack.
b. Pre-Attack Treatment. Several studies have been
made to determine the effectiveness of cacodylic acid-treated trees
as lethal traps. lecontei was attracted to ponderosa pine treated
with Silvisar 510 and felled 4 weeks later (Buffa,m 1969b). However,
significantly more attacks were found in non-treated, felled trees.
Beetle mortality in treated trees averaged percent, while that in
non-treated -'.ms i.ess than 1 percent. Stelzer (1970 ) found that density
of attack and subsequent mortality of brood and attacking adults of
I. lecontei vanied considerably with the time of year the trees were
treated. D. ponderosae attracted to ponderosa pine treated with
undiluted Silvisar 5IO prior to the attack period were unable to
produce brood (Chansler et al. 1970). Very few D. rufipennis brood
\:ere produced in iingelmann spriuce trees treated with undiluted Silvisar
510 at least 4 weeks before felling (Buffan and Yasi.nski 1971)- Frye
and VJygant (1971 ) treated Erigelmajrm spruce with undiluted Silvisar 5IO
and felled the trees 9-1^ days later. D. rufipennis brood development
was prevented in the treated trees. Buffam (1971) tested different
treatment times and dosage rates to determine the most effective
combination against D. ruf inennis . Hs.lf- strength Silvi-sar 5IO was
as effective as full-strength in reducing brood development. Engelmann
spruce treated in raid-J'une and felled 2 weeks later were as effective
in attracting D. rufipennis as non-treated trees. Fev; survivors were
found in treated trees, whereas significant numbers were found in
non-treated trees.
Williamson (1970) obtained decreased brood survival
in pines treated with cacodylic • acid before attack by the southern
pine beet-le. Uillia^nson (1971) suggests a pest management system for
the southern pine beet.le in which the synthetdc attractant ihrontalure
is used to attract beetles to cacodylic acid-treated trees. Ibis
method has also been suggested for surroression of the spruce beetle
(Anonymous 1971b). The Frontalure-cacodylic acid treatment v/as tested
in loblolly pine stands in Virginia in 1971 for control of the southern
pine beet]e (Morris and Capony 1971). lliis method resulted in a 62
percent reduction in beetle populations.
-10-
h
\
McGbchey and Nagel (1967) cliccked vestern hemlock
trees killed vith a 90 percent solution of Silvisar ^10 during thinning
operations. Tney found that neither Ps cud ol wl e s i. nus grand is or P.
tsugae suiuAived in treated trees. Oliver (l9'^ found that D. brevicomis
broods suin'-ived in injected trees, and attacked and killed six leave
trees. Neud^on and Holt (1971 ) found that brood of D. ponder c-sae and
1. pini were not able to survive applications of cacocf;>^lic acid,
monosodium methanearsonate (MSM\), and a mixture of cacodylic acid
and MSMA during pre commercial thinning operations in ponderosa pine.
c. General. Little is knovai of the mode of action of
cacodylic acid in killing bark beetles. Chansler and Pierce (1966)
postulated that treatment may kill the cambium layer and make the
habitat unfavorable for the insect, or this material may have’ direct
insecticidal properties. A study reported by the Southern Forest
Research Institute (Anonymous 1971a-) showed that cacodylic acid was
not toxic to adult southern pine beetles when applied topically in
concentrated form. Newdon and Holt (1971 ) report that reduction of
organic arsenicals to a.rsines is a possible explanation for mortality.
Frye (1970) added Silvisar 5IO to groimd phloem and then planed this
in test tubes along with D. rufipernis males and fema-les. Beetle
morta.lity ranged from 16 percent with the 0,06 percent solution to
100 percent at the 0.5> and 10 percent solutions PvPter 10 days of
exposure. Frye €uid Wygant (l9'ri) speculated that cacodylic acid
treatm.ent mdght break down the carbohydrate food source and alter
phloem pH, thus making an unfavorable environment for the sprace
beetle.
Bark beetles often carry blue stain Fungus into
attacked trees. The sapwood of infested trees normally becomes
colonized by this staJ.n within 1 or 2 years. Fr^^e and Wygant (1971 )
found that blue stain was very light in treated trees and heavy in
untreated trees. Hinds and Buffan (l97l) fouiid that stain ha,d
penetrated the sapw^ood of untreated trees, but was negligible in
treated trees 1 year after treatmient.
Associated insects ai'e often not affected by cacodylic
acid treatment. I'’rj'"e and VJygant (1971 ) noticed that egg gallery
cons truction by the ambrosia beetle, Tr^podendron linea,tum, was not
impaired in tree.ted Engekiminn spinice. Hinds and Buff am (l97l) also
found aaabrosia beetle galleries to be conrtnon in treated Engelimnn
spruce. Flatheaded borer lar^/ae were fo’ond in ponderosa pine treated
with MSMA, cp.codylic acid, and a mixture of botli (Nev/ton and Holt 1971).
McGhehey and Nagel (1967) felt that t?ie cacodylic acid treatment in
hemlock had no adverse effect on parasites and predators because larvae
of the f].y, Medctcra aldri chii , were found in lar^/al mines and adults
of the v.'asp, Ceciriostiba ^uta, energed from treated trees.
-11
2, As a Silvicide
Experiments with cacodylic acid for thinning began in
1963 in Nev/ Zealand (llarrison-Smith I963). Cacodylic acid was added
to holes made by a boring macliine to thin stands of Monterey pine,
Hedderv.’ick (1966) treated stems of Finns rad i at a and P. patula in New
Zealand v/ith cacody^lic acid. He concluded that cacodylic acid v;as a
comparatively safe and effective substitute for sodium arsenite when
used in solution at high concentrations. At lov; concentrations ,
cacodylic acid was little m.ore efficient than ammonium sulphamate
and \7&s nine times more expensive. Day (1965) injected cacodylic acid
into red iriaple, aspen, paper birch, sugar maple, ironv/ood, serviceberi’y,
and jack pine, and concluded that this material has considerable potential
as a silvicide. Smith (1966) reported results of studies in 1964 and
1965 vrhere cacodylic acid was tested against jack pine and red pine.
Almost complete cro^■/n-kill was obtained w/ith this material. Smath
(1966) also reported results of a study by VJelton and Theiler, Bureau
of Indian Affairs, Ixime Deer, Montana. In this study, almost complete
crowni-kill of ponderosa pine was obtained with injection of a 30 percent
solution of cacodylic acid. Smith (1965) said that 90-100 percent crown-
kills and defoliation of red maple, hickories, aspen, paper birch,
hawthorn, pin cherries, American beech, red oak, a,nd other hardwoods
occurred from frill injections of Ansar 160. Bore-hole injections of
Ansar I60 into quaking aspen, red maple, j;aper birch, and red oak resulted
in excellent results, except w'ith red oalc. Smith (1965) concluded that
Americsn elm, American bassw^ood, and Eastern hop hornbean can be crown-
killed by a oneshot injection of Ansar I60 during the growing season
as a result of a test by the PCimberly- Clark Corporation.
^Injection of a 25 percent aqueous solution of cacodylic
acid gave 100 percent kwill of Douglas-fir, cherry, willow, and hawthorne,
cUid relatively poor control of bigleaf maple in studies by Nev/ton (1964).
Injector treatments of Tordon, 2,4-D, cacodylic amid, and a mn>rfcu.re of
2,4-D, 2,4,5-T, and TBA wnre tested by Ne\rton (1965). Tordon gave the
best kill of Douglas-fir, followed by cacodylic acid. Cacodylic acid
tended to concentrate in terminal wAorls of branches, thus killing
tops but not the entire trees in many cases. Newton and Holt (1967b)
injected cacodylic acid into ponderosa pine at four different seasons
and at three dosage rates. lAe response to treatments in September
and December wns much less than that to trea-tments in March and June.
"Virtually any treatment during spring months apx>ea.red to produce good
results." Newton and Holt (1967c) injected undiluted endothall, an
endothall and Silvex mixture, and cacodylic acid into Oregon oak,
bigleaf marJ-e, and red alder. "None of tiiese materials were com])letely
effective on a.11 species, al.thcugh. cacodylic acid ai)y)eared to be the
best general defoliant." Nevrton tuid Holt (1967a) cilso tested cacodylic
acid against lodgcpole pine at different seasons and with tiiree dosage
-12-
rates. "Generally, lodge])ole pine ajjpcars to be veiy sensitive to
cacodo>’'lic acid. Limits of effectiveness appear to be imposed by
lateral translocation restrictions, since all tissue within the
apparent range of herbicide movement was badly damaged, regardless
of dosage." Newton (1967) injected Douglas-fir trees with several
herbicides at several dosage rates--cut spacings--and found that
picloram, Tordon, ond cacodylic acid gave the best results. Newton
and Webb (19?0) state that cacodylic acid and are effective in
killing young ponderosa pines any season of the year. They also state
that of the two herbicides, MSMA is cheaper and more effective.
Ne^-rton (1968) simmiarized the work with cacodylic acid.
Injections of this material gave excellent results against bitter
cherry; good res'olts against alder, Douglas-fir, grand fir, lodgepole
pine, Oregon white oak, and ponderosa pine; fair to good results
against v/estern heralock. When mixed v;ith MSi-IA, the results were
excellent against Douglas-fir, and good against lodgepole pine and
ponderosa pine. Top-kill of Sitka spruce was obtained with cacod;>"lic
acid. Oliver (197O) reported that injections of cacodylic acid into
ponderosa pine, Douglas-fir, red fir, and white fir resulted in
inadequate thinning in two of the three test stands.
B, Persistence in Soil, Water, or Plants. See Section IV3.
C, Compatibility with Other Cliemicals. Ca.codylic acid is
compatible v/ith MStlA.
IV. ENVIEONiENTAL BIPACT
A. Effects on Non-Target Organisms. Sollioan (1950 ) describes
cacodylic acid as a material v/hich has medicinal properties similar
to those of inorganic arsenic "to which it is partly reduced in the
body." Since the reduction is slov? the toxicity is reduced in the
body." Preliminary experiments by Peoples (l9o^i ) are contradictory
and indicate that no reduction to trivalent arsenic occurs since
administralion of cacodylic acid to cov/s, followed by analysis of
tissues, shov/ed only the pentavalent arsenic to be present. Cacodylic
acid, especial] y ^/hen gi.ven by mouth, imparts a, garlic odor to the
breath, sweat, and urine. The dosages vdiich have been given to hiomans
as pills or as hypodermic injections var;^'" from 0.025 to O.I5 g/day;
Sollman (l950) adds, however, that cacodylat-e is not effective in
the chemotherapy of syphilis, bacterial, or parasitic infections.
Peoples (196^1)5 working with pentavalent inorganic arsenic
a.cid, found 76-98 percent of daily dose excreted in urine by cows
during a 7-veek feeding study. Similarly, little to no arsenic was
recovered from various anknal tissues.
-13-
Tarrant and Allard (l972) (aee Norris ISATl) studied the
excretion of arsenic in U3.\ine from forest workers using cacodylic
acid as a silvicide. Significant quojitities of arsenic in urine
from certain individuals suggests uptaJ<:e of this chemical through
the skin occurs a,nd dermal exposure should be avoided.
The toxicity of cacodylic acid in humans is not knovm, but
v/orkers in The AnsuJL Chemical Company plant have had repeated exposiires
over long periods of time. Trie Ansul Company says that their e>qierience
confirms the observations on rats that the toxici ■ty of these compounds
is "relatively low" (Stevens 1966). Norris (l97l) concluded the safe
use of organic arsenicals depends on minimizirog exposure of applicators
and animals in treated areas.
Morton at al. (1972) fed herbicides to the honeybee, Apis
mellifera, in 60 percent sucrose syrup at concentrations of 0, 10,
100, and 3.000 parts per m.illion by weight. Canodylic acid was
extremely toxic at 100 and 1000 ppim-r and moderately toxic at 10 ppim'7.
B . Residues in or on Food or Feed or Entering into Food Chain
via. Air, V/a.ter, Soil, Plants, or /mirnals. Ca,cod;y'lic acid, methanearsonic
a,cid, and their salts are contact-type, post-emergence herbicides.
Elirnan (1965) ha.s reported that w’-heri pasture lands are treated with
5 lbs. of Ccicodylic acid, ajid planted to alfalfa and rye grass vrithin
3 days after treatment, grovdih was not inhibited and cuttings from
these two crops did not show arsenic residues.
Eliman (1965) found that when a combination of 10 13:)/acre of
cacodylic acid and 10 lbs. of DSMA viere used in grapefruit orchards,
no residues could be found in the fruit. In soil build-up tes'ts,
utilizing 15j 22, 4l, and 79 Ib/acre of DSMA, nb arsenic residues
v;ere found in -graiDe fruit.
Ehman and Birdsall (1963) reported on a study that involved
the resjdual effects of cacodylic acid on beans, potatoes, carrots,
cabbage, corn, and soybeans. The test plots v/ere sprayed with 1
gal. of a cacodylic acid solution. The tree.tment was equivalent to
5 Ib/acre of pure cacodylic acid. The plots ’..■ere pla.nted 5 days
later. 0\''er a period of 1 month, 8.9 inches of rai.nfall v;ere
applied. The increase in soil arsenic by analysis was 3 at a
3“inch depth. T3ie authors stated, "There wds no significant pickup
of arsenic by edible crops in the treated plots." Unfortunately,
no data for control plots -were presented.
Nevrton (see Norris 1971) treated conifers with organic
arsenicals in a thinning st\idy in November. Foliage samples
contained 13.0 ppm, 139 Ppm, and yO ppm tlie following Aj)ril, June,
and August, respectively. Allard (see Norris 1971) measured
-Ih-
Il6 ppm As in dead pine needles ojid 2.5 ppm As in green needles from
a treated tree, liiese data indicate needle fall from treated trees
is a significant source of arsenic v;hich will enter the forest floor.
Norris (personal conmnmi cation ) finds MSMA and cacodylic acid are
leached fairly quickly through 3" inch columns of chopped ponderosa
pine, Douglas-fir, or mixed true fir- larch needles. In soil, he finds
MSMA is quite resistant to leaching. Cacodj'-lic acid is more mobile,
but not to the extent that contamination of ground water is a problem.
Newton (l9?l) has reviewed the metabolism of the organic
arsenicals and suggests that arsine or all<:yl arsine are logical
products of the microbial metabolism of MSIiA and cacodylic acid.
VAiile the arsines are fairly toxic, they are also gases and would
be expected to leave treatment areas in low concentrations in mass
air movement. Tire production of arsine analogs under field conditions
has not been demonstrated.
A nutriber of studies have examined the soil behavior of MSMA
and cacodylic acid. Dickens and Hiltbold (1967) shov/ed DSMA was
extensively adsorbed by various soils from water solutions of the
herbicide. Soils V7ith higher clay content adsorbed, more DSMi-A. No
DSMA leached through a 10-inch column of clay soil with 20 inches
of water, while 52 percent of applied DSMiA leached through a 10- inch
column of laam. The reminder of the herbicide appeared to be tightly
bound to the soil. Dickens and Hiltbold (1967) also demonstrated up
to 16 percent dimethylation of DSMA in soil in 30 days. VJoolson
et 8,1. (1969) reports organic and inorganic arsenic behavior similarly
in soil. They find soils high in aluminum and iron bind arsenic
tight.ly and reduce its availability, in a sense, detoxifying the
arsenic. Tney show for instance the water soluble (available)
ai'senic level in a clay loam is decrea,sed by 90+ percent in 4 v/eeks
after application.
Ehraan and Birdsall (1963) studied the adsorj>tion of cacodylic
acid on pasture sod. THey sprayed the sod (4 ft. x 4 ft. x 10 in.)
with 3 *81 g of Ansul’s Ansar 138> containing 65 percent cacodylic
acid, and O.85 g of Drralphor 620 surfactant. The sods v/ere watered
with about y inch of rainfall at 1, 2, and 4 v;eeks. Some of the sod
clay samples leached arsenic in the first 24 hours. In general, the
cacodylic acid was strongly bound to the clay, silt loam, and sand
sods. After 1 v;eek, the cacodylic acid becane evenly distributed
throughout a 10- inch depth.
Elunan (1965) found tliat when an cunount of disodium methanearsonate
(DSMA) equivalent to 28 .lb/ acre v/as applied to the top of a soil coluiiai
v/hich v:as j.eaclied v/ith 60 indies of water, less than 10 percent of the
applied DSMA shov/ed up in the leaciiate. VIhen sandy loam v;as used in-
-15-
the soil column, the figure vas less than 6 percent. In a similar
experiment performed with V) Ib/acre of cacodylic acid, and using
an extrapolation to 60 inches of leaching water, about 9 percent
leached through the sand column and 6 percent for the sandy loam.
It is evident that jDSM and cacodylic acid are largely inactivated by
the soil.
LITER'\TUKE CITED
Anonymous. 19?Ia. Means to suppress brood development of the southern
pine beetle in trees baited v/ith Frontalure. Progress Report -
Southern Forest Res. Institute. Mar. -Apr. : 7.
Anonymous. 1971h. Spruce beetle attacks trees baited with frontalin.
Progress Report - Southern Forest Res. Institute. Jul.-Aug. : l6.
Buffam, P. E. 1969a. Final Report - Pre- and post-flight treatments
with cacodylic acid for control of the Engelmann spruce beetle on
Mt. Taylor in I967. Office Report, USDA, Forest Service, South-
western Region. 4 p.
Buffam, P. E. 1969^:). Results of an Ips lecontei- cacodylic acid
study at Prescott, Arizona, in l^H^. Office Report, USDA, Forest
Service, Southwestern Region. 4 p.
Buffam, P. E. 1971. Spruce beetle suppression in trap trees treated
with cacodylic acid. J. Econ. Entomol. 64(4): 958-60.
Buffam, P. E. , and H. U. Fla,ke, Jr. 1971. Roundheaded pine beetle
mortality in cacodylic acid-treated trees. J. Econ. Entomol.
64(4): 969-70.
Buffam, P. E. , and F. M. Yasinski. 1971. Spruce beetle hazard
reduction wdth cacodylic acid. J. Econ. Entomol. 64(3): 751-2.
Bureau of Commercial Fisheries. I966. Bioassay screening test on
cacodylic acid. Gulf Breeze Lab., Fla.
Chansler, J.-F., D. B. Cahill, and R. E. Stevens. 1970. Cacodylic
acid field tested for control of mountain pine beetles in ponderosa
pine. USDA Forest Service Res. Note PuM-l6l. 3 p.
Chansler, J. F. , and D. A. Pierce. I966. Bark beetle m.ortality
in trees injected with cacodylic acid (herbicide). J. Econ.
Entomol. 59(6): 1357--9.
Day, M. U. 1965* Cacodylic acid as a silvicide. Michigan Quart.
Bull. 47(3): 383-386.
Dickens, R. , and A. E. HUtbold. 1967- Movement and persistence of
methanearsonates in soil. Weeds 15: 299- 304.
Ehman, P. J. I965. liie effect of arsenical buildup in the coil
on subsequent grov/th and residue content of cro])S, Southern
V/eed Control Conf. Proc. 18.
Ehman, P. J. , and J. J. Birdj:all. 19^3. Fate of cacodylic acid in
soil and plants. Dept, of Anny Contract DA-18-064~IjML-2826 (A) .
U.S. /Crniy Biol. Ijab,, Fort -Detrick, Md.
iYost, D. V. 1970. Tolerances for arsenic and selenivuii: A psychodynainic
problem. World Rev. of Pest Contr. Spring 197, 9(l): 6-27.
FryCj R. H. 1970. Spruce beetle mortality v;ith cacodylic acid in
Engelraann spruce trap trees. Master’s thesis, Colorado State
University, Fort Collins, Colo. 96 p.
f'rye, R. H. , and N. D. Wygant. 1971. Spruce beetle mortality in
cacodylic acid-treated spruce trap trees. J. Econ. Entomol.
64(4): 911-16..
Harrison-Smith, J. L. I963. Progress in poison thinning. New Zealand
Timber J. Oct. I963: 25~27.
Heddein-7ick, G. W. I966. Cacod^v'-lic acid as an arborcide. New Zealand
Pest Contr. Conf. Proc., l^th Conf: l65"l69.
Hinds, T. E., and P. E. Buffam. 1971. Blue stain in Engelrriann
spruce trap trees treated v/ith cacodylic acid. USDA Forest
Sei^vice Res. Note Fd-1-201. 4 p.
King, H. , a.nd R. J. Ludford. i960. The relation betv;een constitution
of arsenicals and thin action on cell division. J. Chem. Soc.
2086-2088.
McGhehey, J. H. , and W. P. Nagel. I967. Bark beetle m.ortalfty in
precoiranercial herbicide thinning of westeihi hemlock. J. Econ.
Entomol.- 60(6): 1572-4.
Morris, C. L. , and J. A. Copony. 1971. Fi'ontalure- cacodylic' acid
tested for control of southern pine beetle on the eastern shore
of Virginia. Progress Report - Southern Forest Res. Institute.
Sep. -Oct. : 20.
Morton, H, L. , J. 0, Moffett, and R. H. MacDonald. 1972. Toxicity
of herbicides to newly emerged honey bees. Environ. Entomol.
1(1): 102-104.
Mrak, Knil M. I969. Repoi't of the Secretary's Commission on pesticides
and their relationship to environmental health. U.S. Dept, IDE-/.
Nev.-ton, M. 1964. Chemical control of conifers for pre-commercial
tlilnning. V/estein V/eed Contr. Coni'. Res. Progr. Rep. 43-44.
4
-18-
Newton, M. 19^5« Injectoi- treatincnts for pre-coinmcrcial thinning
of Douglas-fir. V/estern V/eed Contr, Conf, Res. Progr. Rep. 42-43.
Nev/ton, M. I967 . InfD.uence of season and dosage on effectiveness
of injections for control of Doug],as-fir . Western V/eed Contr.
Conf. Res. Progr. Rep. 262.
Newton, M. I968. Chemical silviculture. S;;>Tnpos ium : Management of
young growth Douglas-fir and western hemJ.ock. Oregon State
University, Corvallis, Ore. 21-29.
Nev7ton, M. 1971. Organic arsenicals: Breakdoim in forest trees
and in media containing energy sources- -a progress report to
Environmental Protection Agency, Aug. 26, 1971. Oregon State
University, Corvallis, Ore.
Newton j M. , and H. A. Holt. 1967a. Response of lodgepole pine to
injections of cacodylic acid. V/estern V/eed Contr. Conf. Res.
Progr . Rep . 268 .
Newton, M. , and }I. A. Holt. 196715. Response of ponderosa pine to
injections of cacodylic acid. V/estern V/eed Contr. Conf. Res.
Progr. Rep. 267.
Nevrton, M. , and H. A. liolt. 1967c. Tests of herbicides for multiple
species control by injection. Western V/eed Contr. Conf. Res.
Progr. Rep. 270.
Nevrton, M. , and H. A. Holt. 1971. Scolytid and buprestid mortality
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Entomol". 64(4): 952-8,
Newton, M. , and W. L. V/ebb. 1970. Herbicides and management of
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1969. 9^-99.
Norris, L. A. 1971. Studies of the safety of organic arsenical
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Precommercial thirming in the Pacific Northwest. V/ashington
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distribution of arsenic in soil. A:ii. Chem. Soc. Mtg., N.Y., N.Y.
-20-
ENVIRONMENTAL STATEMENTS
BACKGROUND DOCUMENT
PESTICIDES
DICAMBA
JULY 1972
F. W. Pond (R-1) , Leader
R. Dalen (R-5)
H. Williston (SA)
DICAMBA
General Information
A. Common name
Dicamba, Banvel, Banvel D
B . Chemical name
3,6-dichloro-o-anisic acid
(2-methoxy-3,6-dichlorobenzoic acid)
C. Registered uses
Postemergence weed control in field corn, wheat, oats, barley,
sorghum, pasture/rangeland, perennial grass grown for seed, turf-
grass, industrial brush control, and for noncropland areas such
as fencerows, roadways, and wastelands.
D. Formulations manufactured
1. Banvel Herbicide - U.S.D.A. Reg. No. 876-25
Active ingredients
Dlmethylamine salt of 3 ,6-dichloro-o-an-'‘ =:ic acid 49.0%
Dimethylamlne salts of related acids 7.9%
Inert ingredients
Water 43.1%
2. Banvel Brush Killer (oil soluble)
Active Ingredients
3 , 6-dichloro-o-anisic acid 44 . 5%
Related acids 6.6%
Inert ingredients 48.9%
3. Banvel 5G Granules - U.S.D.A. Reg. No. 876-103
Active Ingredients
3,6-dichloro-o-anisic acid 5.0%
Related acids .9%
Inert ingredients
Attapulgite clay 94.1%
4. Banvel lOG Granules
Active ingredients
3,6-dichloro-o-anisic acid 10.0%
Related acids 1.8%
Inert ingredients
Attapulgite clay 88.2%
2.
0
E and F. Dilution of formulations for use and rate and method of
application
There are several dilutions of formulations recommended for use.
Many of these dilutions are in combination with other chemicals
(2 ,4-dlchlorophenoxy acetic acid or 2 ,4 ,5-trichlorophenoxy acetic
acid). These dilutions, mixtures, recommended target species,
rates, and methods of application for each of the four formula-
tions manufactured are listed in the Appendix.
II. Toxicity data on all formulations (Velsicol Chemical Corporation
Bulletin 521-2)
A. Safety data
1. Acute mammalian studies
a. Oral
Oral LD^q (acid) - rats: 2900 + 800 mg/kg
Oral LD^q (DMA) - on the following:
Rat
Guinea pig
Rabbit
1028 mg/kg
566 mg/kg
566 mg/kg
b . Dermal
The dimethylamlne salt of dicamba administered undiluted
to the skin of rabbits and rats produced a very mild
irritation when administered dally for 2 weeks. When
diluted 1:40 in water, no irritation was observed even
after 30 days. There was no evidence of systemic toxicity
from percutaneous absorbtion.
c. Inhalation
No evidence of toxicity due to inhalation has been noted.
Proper care should be used when applying the herbicide,
especially when using a granular form.
d. Eye and skin Irritation
Mild irritation was produced on the skin of rats and
rabbits if dicamba was applied daily in undiluted strength
for 2 weeks. A 0.1 ml. aqueous solution of the DMA salt
of dicamba produced no Injury when applied undiluted to
3.
the cornea or iris; there was only a iow grade irritation
which disappeared rapidly. The compound caused no
irritation or injury when administered to eyes as a
2 percent or a .2 percent aqueous solution, either as
single doses or as repeated doses over a period of a week.
2. Subacute studies
a. Oral
Dicamba was fed for 13 weeks to male and female rats at
the rate of 100, 500, 800, and 1000 ppm of the diet.
Food consumption and growth rate remained normal, no
deaths occurred, and pathology at the end of 7 weeks was
negative. At the end of 13 weeks, there was some liver
and kidney pathology at the 800 and 1000 ppm level, but
none at or below the 500 ppm levels.
Rats, fed at 5, 50, 100, 250, and 500 ppm of diet and
dogs, fed at 5, 25, and 50 ppm of diet, showed no apparent
effects after 2 years of continuous feeding.
Lactating dairy cattle were fed dicamba at the rate of
10, 25, and 50 ppm of diet. The milk showed no residue
of the chemical. When the dosage was raised to 80 and
400 ppm of the diet, residues not exceeding .15 ppm
were detected after 9 days of continuous feeding.
b . Dermal
The dimethylamine salt of dicamba administered undiluted
to the skin of rabbits and rats produced a very mild
irritation when administered daily for 2 weeks. When
diluted 1:40 in water, no irritation was observed even
after 30 days. There was no evidence of systemic toxicity
from percutaneous absorbtion.
c. Inhalation
No evidence of toxicity due to inhalation has been noted.
Proper care should be used when applying the herbicide,
especially when using a granular form.
3. Other studies which may be required
s
a. Neurotoxicity
There were no S5nnptoms of neurotoxicity in any studies.
4.
b. Teratogenicity
Rats on a diet containing 500 ppm dicamba for 3 or 4 months
did not produce evidence of teratology over a three genera-
tion study.
c. Effects on reproduction
Rats on a diet containing 500 ppm dicamba for 3 or 4 months
did not show change in reproductive capacity in either
parents or offspring.
d. Synergism
There were no synergistic effects in the studies of rats
feeding on a diet of 500 ppm dicamba.
e. Potentiation
No evidence of potentiation in any studies of dicamba.
f. Metabolism
Metabolism of rats was not affected by diets of 5, 50,
100, 250, or 500 ppm dicamba over a 2-year period. Dogs
on diets of 5, 25, and 50 ppm dicamba showed no effects
after 2 years on the diet.
g. Avian and fish toxicity
LD50 toxicity of dicamba is set at 673 mg/kg for domestic
hens and at 800 rag/kg for pheasants.
LC50 toxicity of dicamba on rainbow trout at 24 and 48 hours
was 35,000; and at 96 hours, 28,000 micrograms per liter
of water. For bluegills at 24 hours, the LC^q was
130,000 micrograms; and at 96 hours, 23,000 micrograms per
liter. Thus, the concentration which would kill 50 percent
of the fish of both species at 96 hours ranges between
23 and 130 ppm of dicamba.
A study on small carp showed that at 24 hours, the LC30
for the DMA salt formulation was 659 ppm and at 48 hours,
465 ppm.
The median tolerance limits for juvenile coho salmon
exposed to dicamba were 151 and 121 ppm active ingredient
for 24 and 48 hours, respectively.
C
5.
B. Physical-chemical properties
1. Boiling point
The melting point for dlcamba is 114 to 116°C.
2. Flash point
Nonflammable
3. Physical state
a. Reference grade - White crystalline solid.
b. Technical -grade - Brown crystalline solid.
4. Density
Mollecular weight - 221.05
5. Vapor pressure
3.75 X 10"^mm. Hq. at 100°C.
6. Solubility
Solvent
(at 25°C.)
Water
HAN
Xylene
Ethanol
7. Stability
Stable toward oxidation and hydrolysis under conditions of
normal use. Resistant to acid and strong alkali.
III. Efficacy data under field and laboratory conditions. (Velsicol
Chemical Corporation newsletter Vol. 1, #2, and Velsicol Chemical
Corporation Bull. 521.2.)
Dicamba
gm/lOQ ml
DMA salt of dicamba
(gm acid equivalent
per 100 ml)
0.45
5.2
7.8
92.2
72
A. Effectiveness for Intended purposes when used as directed. Dicamba
is apparently effective when used as directed on certain plant
species. (See I - E and F.) The effectiveness may be less than
with other herbicides and is affected by variations in soil,
climate, and other variables. Potential users should check with
local Agricultural Experiment Stations concerning individual species
and/or soils. If local information is not available, a small field
6 .
c
trial may be advisable before investing large sums of money in
treatment (Brady, Peevy, and Prine and Starr).
B. Phytotoxicity
Dicamba is readily absorbed through both roots and leaves. Although
the mode of action of growth regulator-type compounds has not been
fully elucidated, death of susceptible plants treated with dicamba
is probably influenced by disruption of normal metabolic and
growth activities.
Chlorobenzoic acids as a group have the ability to modify the
transport of lAA (Brian) . Foy and Penner found that dicamba
inhibited the tricarboxylic acid cycle substrate oxidation by
mitochondrial fractions isolated from etiolated cucumber cotyledons.
Phloem, cambium, and associated parenchyma near the nodes of
alligatorweed (Alternanthera sp.) plants were disrupted by treat-
ment with dicamba. Van Overbeek has stated that chlorinated
benzoic acids, which have auxin activity, act fundamentally in
the same manner as 2,4-D.
C. Translocation with plant or animal treated
Dicamba is absorbed by both roots and leaves. Once inside the
plant, the material is translocated in both the xylem and phloem
(Cain, Hurtt and Foy, Linder et.al. , Leonard et .al . , Chang and
Vanden Born, and Hall and Brady).
When ingested by dogs, dicamba was rapidly excreted in the urine.
About 12 percent of the dose was excreted in conjunction with
glycine and the remainder excreted unchanged.
D. Persistence in soil, water, or plants
Harris, Boppart, Markland, Freisen, and Weber and Best have all
shown that dicamba is relatively easy to leach from surface layers
of soil. Comparltively , dicamba is considered one of the most
mobile of the herbicides after it enters the soil.
Sheets et.al. . Burnside and Lavy, Chirchrillo, and Velsicol
Chemical Corporation have studied degradation of dicamba in the
soil. They found that degradation by chemical and/or microbial
action was most rapid when soils were at or near 80 percent field
capacity and at 25° to 35°C. Under these conditions, breakdown of
the chemical was complete within a time frame of 1 to 2 months.
The rate of biodegradation increases with temperature; reaching
maximum at about 28° to 35°C. At somewhere near 50 percent
moisture (by weight) , biodegradation reaches maximum and then
declines with increasing moisture. These temperatures and moisture
contents are conducive to bacterial action. Audus and Cain found
7.
that Bacillus cereus var. mycoides was capable of decarboxylating
dicamba and stated that this bacterium is a common organism,
found widely distributed in the soils. Studies by Velsicol
Chemical Corporation found that dicamba rapidly was broken down
or leached from the deeper layers of soil. Within 10 months
after application, dicamba applied at up to 6 pounds per acre
had disappeared from both the 0-12" and 12-24" depths. Thirty-
two inches of rain had fallen during the 10-month period.
There is some evidence that dicamba may be broken down by photo-
decomposition CVelsicol Development Newsletter Vol. 1, //2) .
Since the dimethylamine salt of the acid is quite soluble in
water, photo-decomposition might be one of the few ways breakdown
occurs in water. Uptake by stream or pond vegetation and ultimate
metabolism by the plants would also contribute to clearing water
of the chemical. Precautions should be taken to avoid contamina-
tion of waterways, ponds, or lakes.
Dicamba is not too persistent in plant tissues. Dissipation can
occur by metabolism within the plant; exudation from the roots;
and loss from the leaf surface by washing, photo-decomposition,
or chemical decomposition (Velsicol Development Newsletter Vol. 1,
#2). Malina found that dicamba and its metabolites (5-hydroxy-2
methoxy-3,6-dichlorobenzolc acid and 3 ,6-dichlorosalicylic acid)
were dissipated rapidly from bluegrass and burmudagrass as shown
in the following:
Period
after
5-hydroxy-2 methoxy- 3,6dichloro-
3,6-dichlorobenzoic salicylic
treatment Dicamba (ppm) acid (ppm) acid (ppm)
(days)
2 lb.
5 lb.
10 lb.
2 lb.
5 lb.
10 lb.
7
51.1
86.2
250.0
33.6
19.3
135.0
negligible (less
14
24.4
51.8
96.0
14.5
34.7
33.6
than 0.05 ppm)
30
6.7
15.9
21.7
11.9
32.0
42.2
amounts in all
60
4.0
4.5
12.5
9.7
11.9
25.3
cases
Morton et .al. found similar dissipation patterns from green tissues
of silver beardgrass, little bluestem, dallisgrass, and sideoats
grama. It should be noted that both metabolites of dicamba are
of low order toxicity. Both metabolites are also herbicldally
inactive.
E. Compatibility with other chemicals
The DMA salt of dicamba is compatible with most common organic
pesticides as well as nitrogen containing fertilizer solutions
8.
(Velsicol Chemical Corporation Bull. 07-151-501). Precipitation
of the free acid from water may occur when this formulation is
combined with lime-sulfur, heavy metal salts, or strongly acidic
solutions or materials. Compatible salt formulations containing
3.0 pounds dicamba acid equivalent per gallon plus 3.0 pounds
2,4-D acid equivalent per gallon can be diluted in relatively
hard water without formation of sediments or precipitates.
Compatibility with salt formulations of MCPA is also excellent.
Like most auxin related herbicides, dicamba has a detrimental
effect on plants. Sensitivity of plants varies considerably.
Patric and Campbell categorized plants in West Virginia into three
susceptibility classes as follows:
IV. Environmental impact
A. Effects of pesticide on non-target organisms
Least Susceptible
American beech
Fern
Hickory
Striped maple
White ash
Chestnut oak
Grasses
Sedge
Sugar maple
Witch hazel
Intermediate in Susceptibility
Blackberry
Black cherry
Chestnut
Deertongue grass
Fireweed
Loosestrife
Red oak
Serviceberry
Violet
Black birch
Black gum
Cucumber tree
Dock
Flowering dogwood
Red maple
Sassafras
Sourwood
Most Susceptible
American elder
Azalea
Black locust
May apple
Nettle
Pokeweed
Sheep sorrel
Staghorn sumac
Twisted stalk
Bindweed
Blueberry
Mulkin
Pin cherry
Puckley ash
Smar tweed
Teaberry
They also found that plants were less responsive to pelleted
(granules) formulations than to liquid formulations sprayed
directly on the foliage. Application of the pelleted formula-
tions were most effective when applied during rapid growth (high
moisture content) of the plants.
The effect dicamba might have on beneficial insects or aquatic
insects is not documented. However, the chemical's relatively
high LD50 for several animal species (Section II-A) indicates
that mortality due to the chemical should be low or non-
existent providing adequate care is taken in application. If
the Insect is feeding on the more susceptible plants of the area,
its food supply would be limited by the plant kill. The insect
would then have to move out of the treated area or adjust to
some other source of food.
The direct effects of dicamba on fish, birds, wildlife, humans,
and domestic animals are shown in Section II-A. Providing ade-
quate controls are maintained, there should be small chance for
animals to receive a lethal dose due to treatment. However, the
food supply of many wildlife species may be restricted following
an application of the herbicide. Animals dependent on the more
susceptible species will be forced to leave the area.
The LD^q levels for the various animals, fowl, and fish, were
established by feeding trials which lasted up to 2 years (see
Section II-A) .
Residues
Studies of the dissipation of dicamba in grass and small grains
showed that disruption within living plant tissue was generally
logarithmic with time (Velsicol Chemical Corporation Bull.
07-151-501). Application of .5 lb. /acre dicamba on wheat (5 leaf
stage) showed that residues declined from 63 ppm on day of applica-
tion to zero 28 days after treatment. In corn, no dicamba
residues were detected at ensilage stage when 1 Ib/acre was
applied preemergence. Postemergence, .25 lb. /acre applied up
to the time corn was 36 inches tall yielded no residues at
ensilage time. The method used on residue analysis was the
electron capture gas chromotographic method described by Smith et.al.
Dicamba is evidently excreted rapidly from mammals which may have
ingested the chemical. There is no evidence that the chemical
is stored and retained by specific organs. Being highly water
soluble (in the DMA formulation) , the chemical would tend to
move through the body rapidly. This proved to be true in a
feeding study on dogs (Velsicol Chemical Corporation Bulletin
07-151-501). Dicamba was rapidly excreted in the urine. About
12 percent was excreted in conjugation with glycine and the
remainder was unchaged.
Dicamba tends not to remain as a residue in either plants, soil,
or water (See III-D) .
11.
APPENDIX
This information is taken directly from Velsicol Chemical Corporation
Bulletin 07-001-501 and Velsicol Chemical Corporation Pamphlet "Banvel
Industrial Herbicides."
1. Banvel Herbicide (Water Soluble) - U.S.D.A. Reg. No. 876-25
FIELD CORN POST-EMERGENCE
USE
WEED
DOSAGE/ACRE
APPLICATION
Field Corn
Smart weed
Broadcast
BANVFI, may be applied over the top
(not reRistered
('anada thistle
.26 to 50 Pint (2-4
of fiebi corn until corn is 36 inches tall
for use on
Cocklebur
07. dicamha acid
or until 1.5 days before tas.sel cmer
sweetcorn or
Pigweeds
equivalent) 1 gallon
gem'e, whichever occurs first Do not
popcorn)
Lambsquarter
Ragweed
treats 16 to 32 acres.
apply BANVEL after this height or
growth stage. It is not necessary to use
Mustard
Band
drop nozzles when applying BANVEL
Sunflower
12" band in 40" row
alone Banvel at Vi pint (2 oz dicamha
Velvetleaf
.075 to .150 Pint
acid equivalent) may be tank mixed
Pepperweed
(.6-1.2 oz. dicamba
with 4 to 8 oz. active ingredient of
Waterhemp
acid equivalent)
2,4-D amine for broader spectrum
Common morning glory
1 gallon treats 53.3
weed control. When 2,4-D is tank
Spanish nettle
Poorjoe
to 106.7 acres.
mixed with Banvel. drop nozzles are
to be used to direct spray to base of
Prostrate Spurge
12" band in 30" row
com plant after com is 8 inches tall
Annual Clover
.1 to .2 Pint (.8 to
Do not make over one post-emergence
and any other
annual broadleaf weeds
1.6 oz. dicamba acid
equivalent) 1 gallon
treats 40 to 80 acres.
12" band in 20" row
.16 to .30 Pint (1.2
to 2.4 oz. dicamba
acid equivalent)
1 gallon treats
26.7 to 63.3 acres.
application per season.
RATE TO USE
Weeds are easier to kill when they are small and it is suggested that the lower rate of BANVEL be used when weeds are
less than 2 inches tail, and the higher rate be used when weeds are over 12 inches tali. Some older weeds are harder to
kill and will be suppressed with BANVEL.
12.
FIELD CORN POST-EMERGENCE
BANVEL AND ATRAZINE TANK MIX
CROP
USE
DOSAGE/ACRE
USE DIRECTIONS FOR
BANVEL + ATRAZINE TANK MIX
Field Corn
OroM
Foxtail (giant yellow,
green)
Crabgraaa
BamyardgraM
and other annual
graas weeds
Broodcatt
Smartweed
Canada Thistle
Pigweed
Lambsquarter
Ragweed
(common, giant)
Mustard
Velvetleaf
Pepperweed
Morning glory,
common
Spanish Nettle
Poorjoe
Spurge, prostrate
CHove/, annual
Sowthistle
Horsenettle
Horseweed
and other annual
broadleaf weeds
Broadcast
0.5 pint
BANVEL (4 oz. dicamha
acid equivalent)
plus
1.26 to 2 0 lbs.
Atrazine 80 W
(1.0 to 1.5 Ibe.
active ingredient)
1 gallon treats
16 acres
Band
12" band in 40" row
0.15 pint BANVEL
plus
.4 to .6 lbs.
Atrazine 80 W
1 gallon BANVEL
treats 53 acres
12" band in 30" row
0.2 pint BANVEL
plus
.5 to .8 lbs.
Atrazine 80 W
1 gallon BANVEL
treats 40 acres
12" bond in 20" row
0.3 pint BANVEL
plus
0.7 to 1.2 lbs.
Atrazine 80 W
1 gallon treats
27 acres
For control of grass and broadleaf
weeds, tank mix BANVEL plus Atra-
zine and nr\ake application up to 3
weeks after planting and before grass
reaches I'/i inches tall. It may be nec-
essary to cultivate at lay by time to
remove surviving weeds or to give soil
aeration. Consult the Atrazine 80 W
label concerning instruction on method
of application and use precautions fur
Atrazine.
13.
SMALL GRAINS (not underseeded to legumes)
USE
WEED
DOSAGE/ACRE
APPLICATION
.Spring SiMshsI
Wheat and Oats
Wild iHirkwheat
Sm.artwcMsI
25 I'int
(2 oz. dicamha
acid c(|uivalent)
A|)ply at 2 to .5 leaf stage of wheal or
oats May be tank mixed with 4 li 0/
p<T acre of M('PA or 2.4 I)
.Spring .S<sshsl
Barley (Montana
and North Dakota
Only)
Wihl buckwheat
Smartweed
19 Pint
( 1 ,r> 02. dii-amba
acirl equivalent
/'opiy at 2 to .'1 h‘af stage of harley
May hi' tank mixed with 4 (> <>/ iht
acre of M(T’A at the 2-3 leaf stage of
barley or with 4 02, per acre of 2,4-D
at the 5 leaf stage. Apply only one
application per sea.son and do not use
higher rate than recommenderl
l•^■lll .Se«sle<l
B.irley. Oats
and Wheat
Dog fennels
(mayweed an<l
com chamomile)
Corn cockle
(k)W cockle
Knawel (German moss)
.25 to .5 Pint
(2 to 4 02. dicamba
acid equivalent)
For the su|)pression or control of
weeds, make application immeiliately
after winter dormancy and before
grain begins to joint May be tank
mixerl with 4-6 oz |>er acre of MCPA
or 2.4 D
h’all See<le<l Wheat
Fidrlleneck
Gromwells
.25 to .5 Pint
(2 to 4 02. dicamba
acid equivalent)
plus
.5 to .75 lbs. active
ingredient 2,4-D
LV ester |
Make application immediately after
winter riormancy anri before wheat
beings to join. BANVEL and 2.4-D
LV ester to be tank mixed
GRAIN SORGHUM — POST-EMERGENCE
SorKhum (Grain)
C’arelessweerl (pi»fweed)
Sunflower
Lamhsquarter
Puralane
Cocklebur
Annual Morning Glory
and other annual
Broadleaf Weerls
Broadcast
,5 Pint (4 02.
dicamba acid
equivalent) 1 gallon
treats 16 acres
Band
20 Inch Band in
40 Inch Row .25 Pint
(2 02. dicamba acid
equivalent) I gallon
treats 32 acres
16 Inch Band in 40 Inch
Row .2 Pint (1.6 02.
dicamba acirl equivalent)
1 gallon treats 40 acres
12 Inch Band in 40 Inch
Row .14 Pint (1.2 01.
dicamba acid treatment)
I gallon treats 56 acres
BANVEL is to be applied as a post
emergence treatment. For most e(Te<'
tive weed control, apply when weeds
are small. As weeds become larger
they are harder to kill but will be sup-
presse<l with BANVEL
BANVEL is to be applied from 10
days after emergence of the grain sor
ghum from the ground until 25 days
after emergence from the ground Do
not apply later than 25 days after
emergence of the sorghum from the
ground.
BANVEL may be applied over the top
of sorghum or as a directed applies
tion BANVEL may be used on both
irrigated and non irrigated grain sor
ghum Make no more than one appli
ration per season Mix proper amount
of ihemical with 10 to 25 gallons of
water per acre Do not apply BAN
VEL to sorghum grown for seed pro
duction Under certain conditions, sor
ghum ma> show temporary edects
from treatment such as onion leaflng
or flattening of the plants, but within
10 to 14 days affected plants will re
cover See IMPORTANT gra2ing
statement (Page 1) for limitations on
grazing and feeding of treated sor
ghum
14.
GRAIN SORGHUM— HARVEST AID TREATMENT
USE
WEED
DOSAOE/ACRE
APPLICATION
SorKhum,
Carelea^weed (pigweed)
Broadcast
Harvest-aid treatment is limited to
Grain
f>amhe(|uarter
50 Pint BANVEL
Texas and Oklahoma and is limited lo
Kochia
(4 oz. dicamba
fi single api>lioatinn per crop season.
Sunflower
acid equivalent)
Do not use BANVEL for harvest-aid
Cocklebur
1 gallon BANVEL
treatment if BANVEL has been ap-
Morning glory, annual
and other annual
treats 16 acres
plied earlier that season
broadleaf weeds
For suppression and retardation of
susceptible weed, make application
from the soft dough stage of the sor-
ghum until 30 days prior to harvest
BANVEL may be applied over the top
of sorghum or as a directed applies
tion.
BANVEL may be used on both irri-
gated and non-irrigated sorghum. Mix
proper amount of chemical with 10 to
25 gallons of water per acre.
GRASS SEED PRODUCTION
For establishment
of perennial grasses
including bluegrass,
lawn-type fescues
and other special
grasses
or
Established
perennial grasses
grown for seed.
Sheep sorrel (red sorrel)
.5 to 1 Pint
(4 to 8 oz. dicamba
acid equivalent)
For established perennial grasses make
application between November 15 and
April 1 or prior to boot stage. For new
seeding make application to foliage in
spring after the seed crop has 3 to 5
leaves. Use sufficient water to give
complete coverage (3 to 40 gallons per
acre).
Nightflowering catchfly
White cockle
Alfalfa
.5 to 1 Pint
(4 to 8 oz. dicamba
acid equivalent)
For established perennial grasses make
application to foliage in spring when
seed crop is 2 to 4 inches high. For
new seeding see sheep sorrell control
directions above.
Bladder campion
duckweeds
(common, mouseear)
Stitchwort
dover
Curly dock
Cow cockle
Dog fennels
(mayweed and
com chamomile)
Knotweed
Top growth control of
field bindweed,
Russian knapweed
and Canada thistle
Ettablithad OraM
1 to 2 Pints
(.5 to 1.0 lb. dicamba
acid equivalent)
N«w Soadlng
.5 to 1 Pint
(4 to 8 OZ. dicamba
acid equivalent)
For established perennial grasses make
application to foliage in spring. For
new seeding see sheep sorrell control
directions above.
Downy bromegrass
(cbeatgrass)
Rattail fescue
Ripgut brome
2 to 4 quarts
(2 to 4 lbs. dicamba
acid equivalent)
Make application in fall after harvest
and burning and within 3 to 14 days
after first irrigation and before weed
has more than two leaves.
15.
SPOT APPLICATIONS ONLY OF PERENNIAL BROADLEAF
WEEDS IN CROPLAND ROTATED TO WHEAT
LOCATION
WEED
DOSAGE/ACRE
APPUCATION
Idaho
Montana
Nevada
Oregon
Utah
Washington
Canada thistle,
Field bindweed
(momingglory),
Russian knapweed.
Leafy spurge.
Tansy ragwort.
Black knapweed.
Curly dock.
Bitter dock
4-6 quarts per
acre (4-6 lbs.
dicamba acid
equivalent)
Spot application may be made to fal-
low land, wheat stubble, or land to be
rotated to wheat. Application can be
made in raid-summer to fall of year
when weeds are actively growing.
WHEAT may be planted one month
after application. BANVEL applied at
rates of 6 lbs. per acre (dicamba acid
equivalent) may cause some wheat in-
jury. See note below.*
Colorado
Kansas
Nebraska
North Dakota
South Dakota
Wyoming
Canada thistle.
Field bindweed.
Russian knapweed
Leafy spurge
1-2 quarts per
acre (1-2 lbs.
dicamba acid
equivalent)
Spot application may be made to fal-
low land, wheat stubble or land to be
rotated to WHEAT. Application
should be made in fall of year when
weeds are actively growing. Treatment
can be made within 90 days prior to
planting or after planting, but before
wheat emerges. See note below. *
*Note: In most cases these above treatments will not kill perennial weed seedlings which germinate from seed one or two
years after treatment. Once the effect of the chemical has been lost, a follow-up program for seedling control or oti<er cul-
tural practices should be instituted.
16.
PASTURE AND RANGELAND GRASSES AND NON-CROPLAND
USE
PaHture an<l
RanKeland flrajme*
im<l Non-cropland
areaa such as
fencerows, road-
ways, wasteland
and similar areas
WEED
DOSAGE/ACRE
Blood weed
.5 Pint (4 os.
Wild buckwheat
dicamha acid
Annual clover
equivalent)
Hubam clover
Cowcockle
For spot treatment
Com cockle
mix 0.3 teaspoon
Cocklebur
BANVEL* Herbicide
Dogfennels (mayweed.
with 1 gallon water to
com chamomile)
! treat 1 square rod
Knawel (German moes)
1 ( 272 square feet)
Knotweed
i
Larabequarter
j
Mustard
Field pennycress
Redroot pigweed
Tumble pigweed
Poorjoe
Common ragweed
Rabbit brush
Sheep sorrel (red sorrel)
Smart weed
Spanish nettle
Spikeweed
Prostrate spurge
Sunflower
Waterhemp
Bladder campitm
1 Pint (8 oz. dicamba
Buffalobur
acid equivalent)
Burclover
duckweed
Chicory
Croton (goatweed)
For spot treatment
Chirly dock
mix 0.6 teaspoon
Kochia
BANVEL* Herbicide
Annual morning-glory
with 1 gallon water to
Punctu revine
treat 1 square rod
Tansy ragwort
(272 square feet)
(rosette stage)
Giant ragweed
Rattlebush
Sesbania
Shepherdspurae
Teasel
VehreUeaf
Wormwood
APPUCATION
For control or suppression of listed
weerls, apply BANVEL*' when w«ksIs
are actively growing
For ground equipment use 10 to 20
gallons of water per acre when treat
ing annual broadleaf weeds and for
top growth control of perennial broad
leaf weeds. For maximum control of
perennial broadleaf weeds use up to
100 gallons or more of water per acre
Rates of BANVEL* in excess of 4
pounds per acre dicamba acid equiva
lent may cause temporary injury to
sensitive graas species.
For waiting period between treatment
and grazing or harvest of treated grass
see IMPORTANT section.
PASTURE AND RANGELAND GRASSES AND NON-CROPLAND (coni.)
USE
WEED
DOSAGE/ACRE
APPUCATION
Pasture and
Top Growth Control:
1 Pint (8 oz.
Rates of BANVEL* in excess of 4
Rangeland Grasaes
Canada thistle
dicamba acid
pounds per acre dicamba acid equiva
and Non-cropland
Russian thistle
equivalent)
lent may cause temporary injury tn
areas such as
Field bindweed
sensitive grass sp>ecie8
fencerows, road-
Black knapweed
For spot treatment
ways, wasteland
Leafy spurge
mix 0.6 teaspoon
For waiting period between treatment
and similar areas
Perennial sow thistle
BANVEL* Herbicide
and grazing or harvest of treated grass
and other perennial
with 1 gallon water to
see IMPORTANT section
broadleaf weeds
treat 1 square rod
(272 square feet)
Spiny aster
1 Quart (1 pound
Slender aster
dicamba acid
Balloon vine
Clover
equivalent)
Dwarf mallow
For spot treatment
Wild garlic
mix 12 teaspoons
Goldenrod
BANVEL* Herbicide
Diffuse knapweed
with 1 gallon water to
Spotted knapweed
treat 1 square rod
Wild onion
Povertyweed
Perennial ragweed
Small leaf sida
Rough sump weed
Tarbuah
Sowthistle
Tievine
Water primrose
(272 square feet)
Blueweed
2 Quarts (2 pounds
Rates of BANVEL* in excess of 4
Buckrush
dicamba acid
pounds per acre dicamba acid equiva
Wild carrot
equivalent)
lent may cause temporary injury to
Cottonwood (seedlings)
Creoeotebush
For spot treatment
sensitive grass species.
Evening primrose
mix .75 tablespoon
For waiting period between treatment
Groundsel
BANVEL* Herbicide
and grazing or harvest of treated grass
Spotted knapweed
with 1 gallon water to
see IMPORTANT section
Lote
treat 1 square rod
Mesquite
Western whorled milkweed
Climbing milkweed
Stinging nettle
Silverleaf nightshade
Pepperweed (tall whitetop)
Pingue
Poison ivy
Bur ragweed
Tansy ragwort
(mature stage)
Redvine
Sagebrush
Perennial smartweed
Snakeweed
Wood sorrel
Musk thistle
Trumpet creeper
Yarrow
Yaupon
(272 square feet)
18.
PASTURE AND RANGELAND GRASSES AND NON-CROPLAND (cont.)
USE
WEED
DOSAGE/ACRE
APPUCATION
Pasture and
Rangeland Grasses
and Non-Cropland
areas such as
fencerows, road-
ways, wasteland
and similar areas
Bedstraw
Field bindweed
Blackberry
Bluebell
Bracken fem
Prickly pear (cactus)
Hop clover
Dewberry
Grape
Carolina geranium
Wild honeysuckle
Horsemint
Horseweed
Huisache
Russian knapweed
Kudzu
Bull nettle
Poison oak
Running live plantain
(turbinella)
Pokeweed
Leafy spurge
Sumac
Canada thistle
Sowthistle
Delmation toadflex
Vetch
White lupine
Wild plum
Waterhemlock
Willow
Yucca
1 to 2 gallons
(4 to 8 pounds
dicamba acid
equivalent)
For spot treatment
mix 1 .5 to 3 table-
s|xx>ns BANVEL*
Herbicide with
1 gallon water to
treat 1 square rod
(272 square feet)
Rates of BANVEL® in excess of 4
|K>und8 |)er acre dicamba acid equiva-
lent may cause temporary injury to
sensitive grass species.
For waiting jreriod between treatment
and grazing or harvest of treatinl gras.s
see IMPORTANT section.
Bracken fem
1 to 2 gallons (4 to
8 pounds dicamba
acid equivalent)
Apply as a pre-emergerue application
before emergence of the fronds
Eastern persimmon
1 to 2 gallons in 100
gallons water (4 to
8 pounds dicamba
acid equivalent)
Apply to ground under tree as basal
treatment using .13 to 25 pint of
spray solution per inch diameter of
the plant. May also he used as a stem
foliage treatment with sufficient water
to give good coverage
NON-CROPLAND — BRUSH CONTROL
USE
WEED
DOSAGE/ACRE
APPLICATION
Foncerows,
Roadways, Utility
RiKhts-ofWay,
Wasteland and
Similar Non-
Cropland
Mixed brush including both
deciduous (hardwood) and
evergreen species. A partial
list of trees controlled by
BANVEL 4 2.4-D or 2,4,5-T
is as follows:
ash persinrunon
aspen pine
basswood poplar
cedar sassafras
cherry service berry
chinquapin spicebush
cucumber-tree sour wood
gum sumac
dogwood sycamore
elm thomapple
hickory thornberry
hornbeam willow
locust witch hazel
maples yaupon
oak and others
1.25 Quarts
1 25 Lbs. dicamba
acid equivalent), per
100 gallons water
plus
2.5 Lbs. active
ingredient 2,4-D or
2,4,5-T (amine or
L.V. ester) per 100
gallons of water
For broarl spectrum brush control,
tank mix BANVEL with 2.4 D or
i 2,4 , 5. T.
Treat all stems and foliage with spe
cial emphasis on covering the root
crown. For best results apply at the
rate of 200 to 300 gallons of pater per
acre. Lesser amounts of water may be
used but maintain minimum of 25
quarts of BANVEL per acre when
tank mixed with 2,4-D or 2,4,5 T.
Make repeat application when needed
Eastern persimmon
1 to 2 gallons in
100 gallons water
(4 to 8 lbs. dicamba
acid equivalent)
Apply to ground under trees as basal
treatment using 13 to 25 pint of spray
solution per inch diameter of the
plant. May also be used as a stem
foliage treatment with sufficient water
to give good coverage.
TREE INJECTION
Tree kill by
injection
Alder (Red)
Ash (White)
Aspen
Basswood
Beech
Birch (Yellow, Paper)
Dogwood
Gum (Sweet, Black)
Hickory
Huckleberry
Maple (Red, Sugar)
Oak (Blackjack, Post)
Persimmon Pine (White)
Mix 1 part BANVEL
Herbicide to 1 part
water or use
BANVEL Herbicide
undiluted
Apply 5 to 1.0
milliliter (ml.) per
injection.
Overlap cuts or
space cuts up to 2
inches apart from
edge to edge
May be applied anytime during the
year. To obtain satisfactory kill the
cut must penetrate the bark and the
cambium layer (sapwood). Applica-
tion may be made by special designed
injector that meters out desired qu^m-
tity of chemical or cuts may be made
with an axe and chemical applied with
an oil can or other suitable applica-
tor Symptoms of injury will be noted
within a few weeks but kill may take
several months.
Oak (Black, Chestnut,
Red, White)
Pine (Shortleaf)
Mix 1 part BANVEL
to 4 parts water.
Apply .5 to 1.0
milliliter (ml.) of
mix per injection
Space cuts up to 3
inches apart from
edge to edge
20.
BANVEL INDUSTRIAL BRUSH AND WEED
CONTROL LABEL REGISTRATIONS
USE
WEED/BRUSH
DOSAGE/ACRE
1 APPLICATION
Righte-of-Way
(utility, railroad,
highway, pipeline).
Non-selective foreat
brush control, fence-
rows, drainage ditch
banks, wasteland and
similar non-cropland.
Unwanted woody brush
including both hardwood
and evergreen spiecies.
A partial list of trees
controlled by BANVEL
+ 2,4D- is as follows:
Alder
Ash
Aspen
Basswood
Cedar
Cherry
Chinquopin
Cucumber tree
Gum
Guava
Dogwood
Elm
Hemlock
Hickory
Hombean
Locust
Maple
Oak
Persimmon
Pine
Poplar
Sassafras
Schinus
( Ch ristm as berry )
Service berry
Spicebush
Spruce
Sycamore
Thomapple
Thomberry
Willow
Yaupon
1 quart BANVEL
( 1 .0 lb. dicamba
acid equivalent)
per 100 gallons water
plus
2.0 lbs. active ingre-
dient 2,4-D (amine or
L.V. ester) per 100
gallons water
I Hydraulic Spray Application
. Stem Foliage — High Water Volume
i
Tank mix BANVEL with 2,4 D and
make application after leaves are fully
developed until three weeks before
frost.
Treat all stem and foliage to run-off
with special emphasis on covermg the
root crown.
Depending upon height and density of
the brush, apply 200 to 3(X) gallons of
spray mix per acre.
2V* gallons BANVEL
(9.0 lbs. dicamba acid
equivalent) per 100
gallons of water
plus
18.0 lbs active ingre-
dient 2,4-D (amine or
L.V. ester) per 100
gallons water
Back Pack Mitt Blowor Application
Basal Stem Foliage — Low Water
Application
Tank mix BANVEL with 2,4-D and
make application after leaves are fully
developed. Treatment may be made
up to three weeks of frost Treat all
stem and root crown to run-off Use
mist blower application on brush 6
feet tall or less at the rate of 30 to
35 gallons total spray mix per acre
6.0 gallons BANVEL
(24 lbs. dicamba acid
equivalent)
plus
12 gallons (4 lbs. active
ingredient/gallon) 2,4-D
(amine or L.V. ester) in
82 gallons water (total
100 gallons spray mix)
Aerial Application — 12 Gallons
Spray Mix Par Acre
Temk mix BANVEL + 2,4-D at the
given rate when applying 12 gallons
of total spray mix per atre.
Treatment may be made from the
time the leaves are fully developed
until 3 weeks before frost.
Mesquite
Sumac
Wild plum
Witch Hazel
and many other
woody plant species
2.5 gallons BANVEL
(10 lbs. dicamba acid
equivalent)
plus
5.0 gallons (4 lbs. active
ingredient/gallon) 2,4-D
(amine or L.V. ester) in
92.5 gallons water
Aeriol Application — 30 Gallons
Spray Mix Per Acre
Tank mix BANVEL + 2,4-D at the
given rate when applying 30 gallons of
total spray mix per acre.
21.
BANVEL INDUSTRIAL BRUSH AND WEED
CONTROL LABEL REGISTRATIONS (cont.)
USE
WEED/BRUSH
DOSAGE/ ACRE
APPUCATION
Riphta-of-Way
(Utility, railroad,
highway, pipeline).
Non -selective
forest brush control,
fencerows, drainage
ditch banks, wasteland
and similar non-
cropland.
For control of annual and
deep rooted perennial
broadleaf weeds. A partial
list of weeds controlled by
BANVEL and BANVEL
+ 2,4-D mixtures is as
follows:
Curly dock
Field bindweed
(morning glory)
Leafy spurge
Russian Knapweed
Canada Thistle
Tansey Ragwort
Puncture Vine
Pereiuiial Ragweed
Tievine
Milkweed
Red vine
Dalmatian toadflax
and many other
perennial broadleaf
weeds
Annual Broodlaof Wood*
Wild buckwheat
Smartweed
Pigweed
Lambsquarter
Ragweed
Mustard
Velvetleaf
(]!hickweeds
Dogfennels
Clover
Sheep sorrel
Henbit
English daisy
Purslane
Carpetweed
Cocklebur
Knawel
1.0 pint BANVEL
(0.5 lb. dicamba acid
equivalent)
plus
1.0 to 2.0 lbs. active
ingredient 2,4-D (amine
or L.V. ester) per
100 gallons water.
For effective broad spectrum control
of annual and perennial broadleaf
weeds tank mix BANVEL + 2,4-D as
directed under rate of application.
Make application when weeds are
actively growing.
Apply at the rate of 100 to 200 gallons
of spray mix per acre. If lower vol-
umes of water are used then irtcrease
the amount of chemical per 100 gal-
lons of water accordingly.
If perennial broadleaf weeds are the
predominant weed problem, then use
the higher spray rate.
Bracken fern
1 to 2 gallons (4 to
8 lbs. dicamba acid
equivalent) per acre
Apply as a pre-emergence application
before emergence of the fronds in suf-
ficient water to ghre good coverage.
#
22.
2. Banvel Brush Killer (Oil Soluble)
BANVElf- IfO.S. is to be tank-mixed with 2,4-D or 2,4»5-T ester which is soluble in oil. This
combination is to be used with diesel oil or fuel oil. DO NOT USR] WITH WATPHt.
IJs(‘ HANVEL"" ^-O.S. plus 2,4-1) or 2,4,5-T ester to control unwanted woody plants along
utility, railroad, highway and pipeline rights-of-way; for nonselective forest brush control; and
brush control in wasteland and similar noncropland areas.
BANVEL^ 4.-0.S. plus 2,4-D or 2,4,5-T ester controls both hardwood and evergreen species,
such as alder, apple, ash, beech, birch, cascara, cedar, cherry, dogwood, elderberry, elm, fir,
grape, hemlock, hickory, hornbeam, locust, maple, oak, pine, poplar, sassafras, spruce, sumac,
walnut, willow and other woody plant species.
DORMANT STEM BROADCAST
Treat any time brush is dormant and most of
the foliage has dropped off. Thoroughly wet
the entire brush or tree to runoff. For root-
sucking species, put special emphasis on cov-
ering the root crown.
GROUND APPLICATION
For hydraulic spray application — tank-mix 1-
3 quarts (T-3 lbs. dicamba acid equivalent) of
BANVEL" 4-0. S. with 2-6 lbs. acid equiva-
lent of 2,4-D or 2,4,5-T oil soluble ester in
sufficient oil to make 100 gallons of spray
mixture. Apply at the rate of 100 gallons of
spray mix per acre.
For back-pack mist blower application, tank-
mix 2-4 gallons (8-16 pounds dicamba acid
equivalent) of BANVEL® 4-0. S. with 16-32
pounds acid equivalent of either 2,4-D or
2,4,5-T oil soluble ester in sufficient oil to
make 100 gallons of spray mixture. Apply at
the rate of 30 gallons of spray mixture per acre.
AERIAL APPLICATION
(Western Oregon and Washington only)
Tank-mix 1 quart (1 lb. dicamba acid equiva-
lent) of BANVEL® 4-O.S. with 4 lbs. acid
equivalent of 2,4-D or 2 lbs. acid equivalent
of 2,4,5-T oil soluble ester in sufficient oil to
make 10-20 gallons of solution. Apply at the
rate of 10-20 gallons per acre.
BASAL BARK TREATMENT
Spray the basal parts of the brush and tree
trunk from the ground line up to a height of
lyz to 2 feet. Spray until runoff with special
emphasis on covering the root crown. Thor-
ough wetting of the indicated area is needed
to achieve good control. Treatment may be
made at any time during the year, including
the winter (except when snow or water pre-
vents spraying to the ground line).
For hydraulic spray application, tank-mix 1-3
quarts (1-3 lbs. dicamba acid equivalent) of
BANVEL® 4-O.S. with 2-6 lbs. acid equivalent
of either 2,4-D or 2,4,5-T oil soluble ester in
sufficient oil to make 100 gallons of spray mix-
ture. Use 100 gallons of spray mixture per acre.
For back-pack mist blower application, tank-
mix 2-4 gallons (8-16 lbs. dicamba acid equiv-
alent) of BANVEL® 4-O.S. with 16-32 ll)s. of
either 2,4-D or 2,4,5-T oil soluble ester in
sufficient oil to make 100 gallons of spray mix-
ture. Apply at the rate of 30 gallons of spray
mixture per acre.
1
23.
3. Banvel 5G Granules - U.S.D.A. Reg. No. 876-103
USE
WEED/BRUSH
DOSAGE
APPLICATION
Pasture, rangeland,
and non cropland
areas such as
fencerows, road-
ways, wasteland
and similar areas
Eastern Persimmon
Use 2 level teaspoonsful
of BANVEL 5% Granules
per inch diameter of the
trunk of the plant
(Example; Use 6 tea-
spoonsful for a tree with
a trunk 3 inches in
diameter)
Scatter the granules evenly on the
ground within 6 inches of the trunk
Apply BANVEL granules any time
after buds start to open and before the
leaves and branches stop growing in
the summer.
Creosotebush
Tarbush
Use 2 heaping table-
spoonsful of BANVEL
5% Granules per 4 feet
diameter of canopy
Make application just prior to or in
the early part of the rainy season
Scatter the granules uniformly under
the canopy of the shrub
Salt Cedar
Use 1(X) to 200 pounds
of BANVEL 5% Granules
per acre (5 to 10 Ibe.
dicamba add equivalent)
Make application just prior to or in
the early part of the rainy season. Ap-
ply BANVEL granules uniformly over
the area to be treated.
Canada Thistle
Field Bindweed
(Morning glory)
Russian knapweed
Leafy spurge
Bur ragweed
Skeleton weed
Apply at the rate of 80
to 160 lbs. BANVEL
5% Granules (4 to 8
lbs. dicamba acid equiva-
lent) per acre. For spot
treatment apply 0.6 to
1.0 lbs. BANVEL 6%
Granules per sq. rod
(272 sq. ft)
For best results, apply BANVEL
granules uniformly when plants are
actively growing. This would normally
be in the spring or fall when plants
are putting out new growth
Bracken fern
Apply at the rate of
120 to 160 lbs. BANVEL
6% Granules (6 to 8
lbs. dicamba add equiva-
lent) per acre. For
spot treatment apply
.76 to 1.0 lb. BANVEL
6% Granules per sq. rod
(272 sq. a)
Apply granules uniformly as a pre-
emergence application before emer-
gence of the fronds.
Artichoke thistle
Apply at the rate of
20 to 40 lbs. BANVEL
5% Granules (1 to 2
lbs. dicamba add equiva-
lent) per acre. For
spot treahnent apply 2
to 4 os. BANVEL 6%
Granules per sq. rod
(272 sq. a)
Make uniform application of BAN-
VEL granules when plants are actively
growing.
s
24.
4. Banvel lOG Granules contain twice the active ingredient as Banvel
5G Granules. Target species for both formulations are the same
but the lOG Granules are especially useful for spot treatment of
areas where low densities of target species occur. This formulation
is especially useful on eastern persimmon, creosotebush , tarbush,
and salt cedar. One-half the suggested dosage for 5G Granules
should be sufficient.
25.
LITERATURE
Audus , L. J. 1964. The physiology and biochemistry of herbicides.
Academic Press, pp. 104-206.
Boppart, E. A. 1966. Chemical leaching and bioassay of Banvel D granules.
Biological Research Section, Herbicide Report 47-H-66. Velsicol
Chemical Report.
Brady, Homer A. 1971. Other brush-control sprays compared to 2,4,5-T
ester. Southern Weed Science Society. Proc. of. 24:251-254.
Brian, R. D. 1964. The classification of herbicides and type of toxicity.
In: The physiology and biochemistry of herbicides. Edited by: L. J.
Audus. Academic Press. 555 pp.
Broadhurst, N. A., M. L. Montgomery and V. H. Freed. 1966. Metabolism
of 2-methoxy-3,6-dichlorobenzoic acid (dicamba) by wheat and bluegrass
plants. J. Agr. Food Chem. 14:585-588.
Burnside, 0. C. and T. L. Lavy. 1966. Dissipation of dicamba. Weeds.
14:211-214.
Cain, P. S. 1966. An investigation of the herbicidal activity of
2-methoxy-3 ,6-dichlorobenzoic acid. Thesis, Ph.D. U. of 111.,
Agronomy, 131 pp.
Chang, F. Y. and W. H. Vanden Born. 1968. Translocation of dicamba in
Canada thistle. Weeds. 16:176-181.
Chirchrillo, M. T. 1968. Biodegradation of Banvel D under varying condi-
tions of temperature and moisture. Microbiology Lab. Report No. 15.
Velsicol Chemical Corp. (Unpublished).
Corbin, F. T. 1967. Influence of pH on the detoxification of herbicides
in soil. Southern Weed Conference. Proc. of. 20:394.
Corbin, F. T. and R. P. Upchurch. 1967. Influence of pH on detoxification
of herbicides In soil. Weeds. 15:370-377.
Friesen, H. A. 1965. The movement and persistence of dicamba in soil.
Weeds. 13:30-33.
Foy, D. L. and D. Penner. 1965. Effect of inhibitors and herbicides on
tricarboxycylic acid cycle substrate oxidation by isolated cucumber
mitochondria. Weeds. 13:226-231.
Hall, Oscar and Homer A. Brady. 1971. Mixing herbicides alters their
behavior in woody plants. Southern Weed Science Society. Proc. of.
24:255-262.
26.
Harris, C. I. 1963. Movement of dicamba and diphenamld in soils. Weeds.
12:112-115.
Harris, C. I. 1967. Movement of herbicides in soil. Weeds. 15:21^-216.
Hurtt, W. and C. L. Foy. 1965. Some factors affecting the excretion of
foliarly applied dicamba and picloram from roots of Black Valentine
beans. Plant Physiology, Supplement. 40:48.
Leonard, 0. A., L. A. Lider and R. K. Glenn. 1966. Absorbtion and
translocation of herbicides by Thompson Seedless (Sultanina) Grape,
Vitps vinifera L. Weed Res. 637-49.
Linder, P. J. , J. W. Mitchell and G. D. Freeman. 1964. Persistence and
translocation of exogenous regulating compounds that exude from roots.
J. Agr. Food Chem. 12:437-438.
Markland, F. E. 1968. Evaluation of encapsulated granules of Banvel D
for leaching characteristics. Biological Res. Section, Herbicide
Report 31-H-68. Velsicol Chemical Corp.
Morton, H. L. , E. D. Robison and R. E. Meyer. 1967. Persistence of 2,4-D,
2,4,5-T, and dicamba in range forage grasses. Weeds. 15:268-271.
Pate, D. A., H. H. Funderburk, Jr., J. M. Lawrence, and D. E. Davis. 1965.
The effect of dichlobenil and dicamba on nodal tissues of alligatorweed.
Weeds. 13:208-210.
Patric, James H. and John Campbell. 1970. Some experiences with dacamba
in controlling revegetation of deforested land in West Virginia. NE
Weed Control Conf. Proc. Vol. 24:61-68.
1969. A substitute for 2,4,5-T in eastern hardwood sprout and
brush control. NE Weed Control Conf. Proc. Vol. 23:320-328.
Peevy, Fred A. 1971. Wide-spaced injections of herblcldal mixtures for
controlling weed trees. Southern Weed Science Society. Proc. of.
24:263-267.
Prlne, E. Lynn and John W. Starr. 1971. Herbicide control of Japenese
honeysuckle in forest stands. Southern Weed Science Society. Proc. of.
24:298-300.
Reinhart, K. G. 1965. Herbicide treatment of watersheds to increase
water yield. NE Weed Control Conf. Proc. Vol. 19:546-551.
Sheets, T. J., C. I. Harris, D. D. Kaufman and P. C. Kearney. 1964. Fate
of herbicides in soils. NE Weed Control Conf. Proc. Vol. 18:21-31.
27.
Smith, M. , H. Suzuki and M. Malina. 1965. Analysis of dicamba in crops
and milk, including a rapid cleanup method. Jour. Assn. Official
Agr. Chemists. 48:1164.
Technical Services Request F-31. 1965. Soil dissipation study, Banvel D
residues. Velsicol Chemical Corp.
Technical Services Request F-59. 1965. Banvel D residues. Velsicol
Chemical Corp.
Van Overbeek, J. 1964. Survey of mechanisms in herbicide action. In:
The physiology and biochemistry of herbicides. Edllfed by: L. J.
Audus, Academic Press. 555 pp.
Velsicol Chemical Corp. 1971. Banvel herbicides general bulletin. Velsicol
Chemical Corp. Bull. 07-151-501:4 pp.
Velsicol Chemical Corp. 1971. Banvel federal label registrations. Velsicol
Chemical Corp. Bull. 07-001-501:15 pp.
Velsicol Chemical Corp. 1971. Banvel herbicides for brush and broadleaf
weed control. Velsicol Chemical Corp. unnumbered pamphlet. 7 pp.
Wart, D. J. 1964. Effect of herbicides on plant composition and metabolism.
In: The physiology and biochemistry of herbicides. Edited by: L. J.
Audus, Academic Press. 555 pp.
Weber, J. B. and J. A. Best. 1971. Activity and movement of 13 soil-
applied herbicides as influenced by soil reaction. Southern Weed Science
Society. Proc. of. 24:403-413.
Weed Science Society of America. 1970. Herbicide handbook of the Weed
Science Society of America. WSSA Monograph //3: 136-139.
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REPORT
ON
BACKGROUND INFORMATION
FOR
MSMA
9
I. GENERA.L INF0K4ATI0N
A. Coinmon Name. MSMA.
B. Chemical Name. Monosodium acid methanearsonate or monosodiiam
methanearsonate .
C. Registered Uses. For post-emergent weed control and as a
silvicide for control of undesirable conifers and big leaf maple.
D. Formulations Manufactured. (See Table 1 for materials other
than silvicides.
1. Silvisar 550 Tree Killer. 6.0 lbs. MSMA per gallon. USDA
Reg. No. 6308-58.
2. Vichem 120 Arsonate Silvicide. 6.66 lbs. MSMA per gallon.
USDA Reg. No. 2853-39.
3. Glowon Tree Killer. 5*5 lbs. MSMA per gallon. USDA
Reg. No. 10592-1.
E. Dilution of Formulation for Use. Use in undiluted form as
a silvicide.
F. Rate and Method of Application
1. Silvisar 550 Tree Killer
a. Spaced-Cut Injection with Ansul "Hypo-Hatchet" Irijector.
This hatcheb-like unit cuts and injects in one operation. The injector
works by inertia and is calibrated to inject at least one milliliter
of chemical per stroke. Rates for this method are:
(1) Conifers and Big Leaf Maple (Growing Season). For
trees below 8 inches diameter at breast height (d.b .h. ) , make one
cut per 2 inches of d.b.h. (4y” spacing between cut edges) at waist
height or below. For trees 8 inches d.b.h. and larger, malce one cut
per 1 inch d.b.h. (l-g-" spacing between cut edges).
(2) Conifers (Dormant Season). Make one cut per
1 inch of d.b.h. (if" spacing between cut edges) at waist height
or below.
(3) Big Leaf Maple (Dormant Season). MaJte a complete
frill at waist height or below (cuts need not be overlapping).
#
Tatle 1. — Solutions containing monosodium methanearsonate that are registered for uses other
than as a silvicide.
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4
b. Spaced- Cut Application. A hatchet or similar cutting
tool can be used to make the cut, and the MSMA added to the cut with
a pump-type oil can, plastic squeeze bottle, or other suitable
dispenser. Rates for this method are:
(1) Confers and Big Leaf Maple (Growing Season). For
trees below 8 inches d.b.h., apply 1 to 2 milliliters of Silvisar 550
Tree Killer per cut per 2 inches of d.b.h. (6" spacing between cut
centerlines) at waist height or below. For trees 8 inches d.b.h.
and larger, use 1 or 2 milliliters per cut per 1 inch d.b.h. (3"
spacing between centerlines ) .
(2) Conifers (Dormant Season). Apply 1 to 2 milliliters
of Silvisar 550 Tree Killer per cut per 1 inch of d.b.h. (3" spacing
between cut centerlines ) .
(3) Big Leaf Maple (Dormant Season). Apply 1 to 2
milliliters of Silvisar 550 Tree Killer per cut in a conq)lete frill
at waist height or below. (Cuts need not be overlapping.)
2. Vichem 120 Arsonate Silvicide - Conifers Only. Cut-frills
are made with an ax.
a. Growing Season. For control of conifers under 7"
d.b.h. with a live crown of less than one-half the total tree height,
apply Vichem 120 Silvicide at 1 milliliter (ml) per frill and cut
a frill for every 2 inches of tree d.b.h. For larger diameter trees
or trees with a full live crown, apply Vichem 120 Silvicide at 1 ml
per frill and cut a frill for every 1 inch of tree d.b.h.
b. Dormant Season. For control of conifers under 7”
d.b.h. with a live crown of less than one-half the total tree height,
apply Vichem 120 Silvicide at 1 ml per frill and cut a frill for
every 2 inches of tree d.b.h. For larger diameter trees or trees
with a full live crown, apply Vichem 120 Silvicide at 1 to 2 ml per
frill and cut almost overlapping frills completely around the
circumference of the tree, especially on larger trees.
3. Glowon Tree Killer. Effective on conifers but not on
most hardwoods. Apply undiluted into horizontal ax frills cut on
the trunk usually at waist height or below. ' Use the same dosage in
dormant season as during growing season. For control of young conifers,
less than 6" d.b.h., with a full crown, apply Glowon Tree Killer at
1 ml per frill and cut a frill for every inch of tree d.b.h. For
control of young conifers, less than 6" d.b.h., with only half or
less of a complete crown, apply Glowon Tree Killer at 1 ml per frill
and cut a frill for every 2 inches of tree d.b.h. Large trees with
-3-
full crowns require almost overlapping frills for effective control.
Do not store in or place in contact with alimiimm, copper, or
galvanized metal containers.
G. Tolerances in Food or Feed and Other Safety
1. Tolerance as .A.S2O3, 0.7 Ppm in cottonseed, and 0.9 in
cottonseed hulls.
2. Safety Limitations
a. Cotton. Do not graze or feed forage from treated
areas to livestock.
h. Drainage Ditch Banks. Do not graze treated areas.
Do not contaminate waters used for domestic consumption, or hy animals,
wildlife, and aquatic life, or for irrigation purposes.
H. Manufacturers or Producers
1. The Ansul Company, Marinette, Wisconsin.
2. Vineland Chemical Company, Vineland, New Jersey.
3. Key Chemicals, Inc., Anacortes, Washington.
II. TOXICITY DATA ON MSMAI/
A. Safety Data
1. Acute Mammalian Studies
a. Oral
(1) Acute Oral LD50
(a) Technical Grade Methanearsonic Acid. 92.8*^
methanearsonic acid; 1.4 g per kg (adult meAe alhino rats); WARN Institute
(Wisconsin Alumni Research Foundation, Madison, Wisconsin).
(h) Ansar I70» 51*3?^ MSMA; 1„8 g per kg (young
male and female alhino rats ) ; Industrial Bio-Test ’Lahoratories,
Northbrook, Illinois.
Except where noted, toxicity data was summarized from a report by
The Ansul Company, Marinette, Wisconsin, entitled "Toxicological
Data - Methanearsonic Acid and Dimethylarsinic Acid," June 5? 19o7j
with an addendum dated October 10, 1989«
_4-
(c) Ansar ^29. 34.8fo MSMA; 1.8 g per kg (young
male and female albino rats); Industrial Bio- Test Laboratories.
(2) Acute Oral LDpoo
(a) Ansar 170» 325 mg per kg (dairy calves);
E. S. Erwin & Associates, Phoenix, Arizona.
(b) Ansar 529« 400 mg per kg (dairy calves);
E. S. Erwin & Associates.
(3) Other Acute Oral Studies
(a) Rodents . Meliere (1969) has measured the
acute oral toxicity of me thane ar sonic acid in male mice and has found
that the LDpo is 185 mg/kg. He found the LD50 of* ii^e di sodium
methanearsonic acid to be greater than 245 mg/kg. In data supplied
by the manufacturers and listed in the Suggested Guide for Weed Control
(USDA Agricultural Handbook 332, 1967)5 the acute oral toxicity for
rats of the monosodium and the disodium methanearsonic acids is 7OO
mg/kg for MSMA and 8OO to 2,800 for DSMA. These figures are slightly
at variance with the toxicity data supplied by The Ansul Chemical
Company. It is clear that methanearsonic acid and its salts MSMA
and DSMA have about the same acute oral toxicity in rats as cacodylic
acid and are less toxic to rats and mice than is sodium arsenite.
It also appears that the disodium methanearsonate (DSMA) is much less
than the parent acid and the difference is greater than might be
predicted on the basis of their arsenic content.
(b) Steers. Dickenson (see Norris 1971) fed
a commercial formulation of MSMA to steers. He found lethal effects
. after 10 mg/kg/day for 10 days. Additional work remains to be
completed in Dickenson’s study.
b. Estimated Acute Dermal LD^q - Ansar 529* 2-4 g per
kg (adult male rabbits ) . The skin irritation tests with methanearsonic
acid were conducted in the usual manjier using the intact skin of three
rabbits and the abraded skin of. three rabbits. After 24- and 72-ho'ur
exposure to this herbicide, it was found to produce a slight edema
amd to be mildly irritating. The reactions obseived in the highest
doses prior to death included general inactivity, _loss of appetite,
mild sedation, dyspnea, and muscular weakness. At 1,400 rng/kg, the
animals which succumbed lived about 24 hours following administration.
WARE Institute.
c. Acute Inhalation - An.sar 529 « Non- irritating to the
respiratory tract (albino rats); WARE Institute.
d. Eye Irritation - Ansar ^29. Non- irritating to the
eye (adult albino rabbits); WARB’’ Institute.
2, Subacute Studies
a. Oral
(l) Twenty-Four- (24) Hour Foraging on Treated
Johnson Grass by Dairy Calves
(a) Ansar 170. Four calves were pastured for
24 hours on 20- by 30“foot (l/70th acre) plots of thick Johnson grass
3 to 4 feet high, previously sprayed to run-off with Ansar 170 at a
rate of 1.05 gallons per acre in 70 gallons of water. There was no
evidence of imp alat ability due to the herbicide. All calves showed
a mild diarrhea, which disappeared 48 hours after removal from the
plots. No other symptoms appeared for 2 weeks post-treatment. E. S.
Erwin & Associates.
(b) Ansar 529« Same test and results as above,
but sprayed with Ansar 529 at a rate of 1.75 gallons per acre in 70
gallons of water. E. S. Ervrin & Associates.
(2) One-Week Feeding to Dairy Calves - Ansar 529»
529 was fed at 4o, 80, and 240 mg/kg, in 8 pounds of supplemental
cottonseed meal, to each of two Holstein calves at each level, each
day for 1 week. 4o mg/kg - meal consumption dropped to about 4
pounds after 1 day: 80 mg/kg - calves quit feeding on 4th day;
24o rag/kg - calves quit feeding on 3rd day. None of the calves
developed diarrhea. All calves recovered rapidly when returned to
normal ratloq at the end of 7 days. E. S. Erwin-& Assdciates.
(3) Lactating Cattle Feeding Study - Pure
Methanearsonic Acid. Methanearsonic acid was fed at 0.3? 3.0, and
30 ppm in 5*5 pounds' of supplemental cottonseed meal, to each of
three lactating cows at each level, daily for 9 weeks. No significant
residues in milk and edible tissues. Methanearsonic acid is poorly
absorbed in intestinal tract and rapidly excreted in the urine. Dr.
S. A. Peoples, Department of Physiological Sciences, University of
California, Davis, California.
(4) Ninety- (90) Day Feeding Study in Rats and
Dogs - Pure Methanearsonic Acid. liethanearsonic acid was fed at 3?
15 j and 30 ppifi to dogs, and a,t 3? 15? 30? s^d 100 ppm to rats, in
the basal ration for 90 days. No-effect level for dogs - 30 ppm;
no-effect level fo2' rats - 100 ppm. WARE Institute.
-6-
I
b. Dermal. Considered mildly irritating to the skin
(albino rabbits). WARF Institute.
3. Other Studies
a. Carcinogenicity. Arsenic has only been associated
with poisoning and was indicated quite early as a carcinogen. More .
evaluations suggest that the early tests reporting arsenic-induced
carcinoma were inadequate. Frost (l970) cites numerous studies which
attempted but failed to demonstrate arsenic-induced carcinoma.
Cacodylic acid was placed in group c4 by the Secretary's Commission
on Pesticides and their relationship to environmental health (lirak
1969) • This group contains pesticides which was judged not positive
for carinogenicity in one species (mouse), but current guidelines
require negativity in two species. The commission gave this group
a moderate priority for testing, but felt no changes in practices
in the field were warranted. The similarities in chemical and physical
properties of MSMA and cacodylic acid justify extrapolation of data
between these two compounds.
S. S. Pinto and B. M. Bennett (1963) believe that
it is a mistake to make blanket condeimations of the use of arsenic
without first looking at the data. He has reviewed the early
literature on human tumors from arsenic and also the recent opinions
and interpretations of these early papers. There is reason to believe
that the "arsenic tumors" observed in I82O may have been due to other
causes such as selenium poisoning. He reviewed the medical histories
and causes of death of the long-term en5)loyees of a copper smelting
company producing arsenic trioxide. He showed that the workers do
excrete high levels of arsenic, but that their incidence of cancer
is no greater- than for other persons in the State of Washington. He
concluded that there is no evidence that exposure of these workers
to ai'senic trioxide is a cause of systemic cancer in humans. In a
sense, this amounts to the use of human guinea pigs for establishing
the lack of carcinogenicity of arsenic trioxide.
b. Mutagenicity. Cacodylic acid is a mitotic poison
in mammalian organisms. King and Ludford (i960) found that injections
in mice produced "profound disturbances of cell division" and it
"stimulated mitosis in cells of the crypts of Lieberkuehn'' and of
transplanted turaors . The significance of this finding in terms of
exposure to MSMA and cacodylic acid in the field is not kno™.
c. Teratogenicity. Cacodylic acid is considered to
be a teratogenic agent, producing abnormalities during embry-onic
development. There are several references to this type of action,
although only two exai^roles are quoted. Salzgeber (1955) obsem/ed
I
-7-
(
teratogenic effects in 10-day chick embryo genital organs cultirred
in vitro and has reported that the greatest damage is to the cortical
region. Rostand (1950 ) -las treated tadpoles of Rana temporie. with
solutions of cacodylic acid for 3 weeks when the hind legs were in
the process of development^ and abnormalities were observed at 0.10
percent of sodiura cacodylate. (This concentration is 100 ppm and is
equivalent to 270 Ib/acre ft. of water.)
Additional testing, using the techniques reported by
Mrak (19?0), is needed. Relation of these reports of teratogenic
potential and field use of the chemical require farther investigation.
d. Avian Toxicity - Chicken Feeding Study - Pure
Methanea^rsonic Acid. Methanearsonic acid was fed at 0.03? 0.3? and
3.0 ppm in basal ration to each of nine leghorn hens at each level,
daily for 4 weeks. No arsenic residues in meat at all levels.
Slight arsenic residues in eggs at 3»0 ppm. No pathological evidence
of toxicity at any level. Dr. S. A. Peoples.
e. Fish Toxicity
(1) Pare MSMA (no surfactant present). 48-houi-
LC90 '■ above 1000 ppm (bluegill sunfish). Louisiana Wildlife &
pjsheries Commission.
(2) Ansar 529 (surfactant present). 96-hour LCgQ -
31.1 ppm (goldfish); 9^-hour LC50 - 13*4 ppm (fathead minnows).
Bureau of Sport Fisheries & Wildlife.
(3) Ansar 529 (surfactant present). ^96-hour TLm
(median tolei*ance limit )" 300 ppm (bluegill sunfish). Louisiana.
Wildlife Sc Fisheries Commission.
B . Pliysical- Chemical Propertie
1. Boiling point - none
2. Flash point - none
3. Physical state - white crystalline solid
4. Density - 1.5 g/iAL
5. Vapor press'ore - insignificant
2/ Data obtained from The Ansu.1 Company, Biological Research Center,
Weslaco, Te xas .
-a
n
6. Solubility - in H2O at 20° C. = 25.6^ or 25 g/lOO inl
7. Stability - stable
8. Melting point - 132-139° C. (pure hexahydrate )
III. EFFICACY DATA UNDER FIELD Am LABORATORY CONDITIONS
A. Effectiveness for Intended Purpose. Newton (1968) reported
that results with injections of MSMA were excellent aga.inst Douglas-fir,
western hemlock, and ponderosa pine; good against bigleaf maple, grand
fir, lodgepole pine, and Sitka spruce; and, when mixed with cacodylic
acid, excellent against Douglas- fir and good against lodgepole pine and
ponderosa pine. Newton and Holt (1968) reported that MSMA is quite
efficient against bigleaf m^ple, but does not grea.tly affect Oregon-
white oak. They also stated that MSMA treatments in all seasons provide
80 percent or better control of Douglas-fir and ponderosa pine, although
insect acti.vity is least with fall and early winter treatments for
the latter species. Spring and fall treatments provide the best control
of bigleaf maple. New’ton and Webb (1970) stated that MSMA and cacodylic
acid are effective in killing young ponderosa pines any season of the
yea-r, and tha.t MSMA is cheaper and more effective than cacodylic acid.
Lower seolytid attack levels occurred in trees treated with MSMA.,
cacodylic acid, and a mixture of MSMA and cacodylic acid than in
untreated, felled trees (New’ton and Hold 1971). Flatheaded borers
were common in trees treated with MSMA. Little hatching of Dendroctonus
ponderosae occurred in trees treated with FEMA. Flatheaded borer larvae
and ambrosia beetles survived all treatments.
Newton and Smith (197^) summarized herbicide injection tests
in Vermont from I966-7I. Beech, red maple, and hard m-aple were injected
with Silviser 5IO (cacodylic acid) and Silvisar 590 (MSMA) during August
of these years. "All species were readily killed by both Silvisar
formula.tions " Red maple and hard maple were quite sensitive to
Si.l-^/is8.r 590, while beech wa,s the most resistant species. Some recovery
of tree health occurred with Sil^risar 510, while damage continued in-
trees treated vMth Silvisar 590. Newton and Smith (.1971) also stated
that I'ecent studies in Tennessee indicate that spaced injections with
a Hypo-Hatchet of Silvisar 510 and Silvisar 590 were effective on
hardwoods in the fall, but results for the same treatments in winter
and spring were less impressive.
B. Persistence in Soil, Water, or Plaints. See Section WB.
C. Compatibility with Other Chemicals. MSMA is compatible with
cacodylic acid aad 2,4-D.
-9-
IV. ENVIRONl^NTAL IMPACT
A, Effects on Non-Taxget Organisms. Evans and Allard (see Norris
19^fl) determined that the LD^q ^ commercial formulation of MSMA
to snowshoe hares is 173 Kig/kg.
Norris (1971 ) related an incident of snowshoe hare mortality
in connection with the use of MSMA as a silvicide. Seven dead animals
were found around areas which were used for cleaning application
equipment. High arsenic residues were found in soil and vegetation
samples from the area. Caid.es s handling of MSMA may present a hazard
to both the applicator and animals.
Morton et al. (1972) fed herbicides to the honeybee, Apis
mellifera, in 60 percent sucrose syrup at concentrations of 0, 10,
100, and 1000 parts per million by weight. MSMA. was extremely toxic
at 100 and 1000 ppmw.
B . Residues in or on Food or Feed or Entering into Food Chain
via Air, Water, Soil, plants, or AnimaAs. Ehman (1965) reported on
the effect of high levels of DSMA ( di s odium methanearsonate) appli-
cations to soil on cotton, soybeans, sorgh'ara, and peanuts. The DSMA
was applied at ra.tes of 9»5? 31*55 and 63 Ib/acre (equivalent to 2,
75 and l4 years of use in cotton, two applications of 2.25 Ib/acre/year) .
Wlien cotton, soybeans, sorghum, and peanuts were plarited on the day
of treatment, only the peanuts had to be replanted. The second planting
of peanuts and the original planting of cotton, soybeans, and sorghum
all developed normally. There was some slight stunting at the 63
Ib/acre level in the early stages of gro^-Tth. A.11 high samples showed
arsenic residue from 0.29 lo 3-64 ppm for treated samp3>es (controls
0.10 to 0.18 ppm). Peanuts and sorghum grain contained low residues
at the 9*5 Ib/acre rate. At the high rates, residues varied from
0.52 to 3*12 ppmi. Cotton seed contained residues at the 31*5 83
Ib/acre rates. There was no arsenic residues in the soybeans from
any of the plots.
Ehman (I965) found that when a combination of 10 Ib/acre of
cacodylic acid and 10 lb. of DSKA. v^ere used, in grapefruit orchards,
no residues could be fo^und in the fru.it. In sod.] build-up tests,
utilizing I5, 22, 4l, and 79 Ib/acre of DSidA, no arsenic residues
were found in grapefruit.
A few studies have been conducted on organic arsenic residues
in grasses (Long et al. 19^2; Lucas 1964). A wide raige in a.rsenic
residue on coasta.l Bermuda grass has been found (Searcy and Pa,tterson
1964; McBee et al. 1967). When calcium acid methanearsonate (CAM.)
-10-
r
was applied at the rate of 5 It. of arsenic per acre, the arsenic
content went from ll4 ppm at 5 days to 5 PP^ at 33 days . In
comparison, monosodium acid methanearsonate (IVISMA.), at the same
application level, fell from 1921 ppm at 7 days to 38.9 at
36 days. Disodiijm methanearsonate (DSMA.) (4 lb. of arsenic per
acre) was more persistent. The amount of arsenic fell from 475.2
ppm at 5 days to 101.8 at 33 days.
Johnson and Kiltbold (1969) found concentrations of As in
several crop plants ranging from 1.6 ppm to 5.2 ppm in soils receiving
MSMA, DSMA, or JiAIiA at rates ranging to 8 pounds per acre, DSMA was
absorbed by foliage of Bermuda grass and translocated towards leaf
tips and roots*. Uptake from soil was much less. Arsenic residues
declined from 100 ppm to 35 PP^^-. in 30 days in Beimuda grass treated
with 2 Ib/acre DSMA.. Arsenic residues in roots increased to 80 ppm
in the same period (Duble et al. I969).
Newton (see Norris 1971) trea,ted conifers with organic
arsenicals in a thinning study in November. Foliage samples con-
tained 110 ppm, 139 PPBij and 58 ppm the following April, June, and
August, respectively. Allard (see Norris 1971) measured II6 ppm As
in dead pine needles and 2.5 PPm As in green needles from a treated
tree. These data Indicate needle fall from treated trees is a
significant source of arsenic which will enter the forest floor.
Norris (personal communication) finds MSMA and cacodylic acid are
leached fairly quickly through 3-inch colimmsof chopped ponderosa,
pine, Douglas-fir, or mixed true fir-larch needles. In soil, he
finds MS14A is quite resistant to leaching. Cacodylic acid is more
mobile, but not to the extent that contamination of groTind water
is a problem. Canutt and Norris (see Norris 1971) hava not found
detectable quantities of As in streams flowing from areas thinned
■vd-th MSMA.
Von Endt et al. (1968) incubated labeled MSI4A in foui-
soil types and found 1.7 to 10 percent degradation of the J4SMA in
60 da;ys. The probable degradation product of this reaction is an
inorganic arsenate which is inherently more toxic than MSMA; however,
inorganic arsenic coiTpcunds are much less available for uptake by
plants or soil microorganisms and may, j.n fact, represent less hazard
than the MSMA.
Newton (1971 ) has reviewed the metabolism’ of the organic
arsenicals and suggests that arsine or alkyl arsine are logical product
of the microbial metabolism of MSMA and cacodylic aci.d. /Jhile the
a,rsines are fairly toxic, they are also gases and would be expected
to leave treatment areas in low concentrations in mans air movement.
The production ojI carsine -analogs under field conditions he,s not been
dem.onstra.ted.
11-
A nimiber of studies have examined the soil behavior of MSMA
and cacodylic acid. Dickens and Hiltbold (1967) showed DSilA was
extensively adsorbed by various soils from water solutions of the
herbicide. Soils with higher clay content adsorbed more DSMA. No
DSMA leached through a 10-inch column of clay soil with 20 inches
of mter, while 52 percent of applied DSMA leached through a 10- inch
column of loam. Ttie remainder of the herbicide appeared to be tightly
bound to the soil. Dickens and Hiltbold (1967) also demonstrated up
to 16 percent dimethylation of DSMA in soil in 30 days. Woolson
et al. (1969) reports organic and inorganic arsenic behavior similai-ly
in soil, liiey find soils high in almiiinim and iron bind arsenic
tightly and reduce its availability, in a sense, detoxifying the
arsenic. They show, for instance, the water soluble (available)
ai'senic level in a clay loam is decreased by 90+ percent in 4 weeks
after application.
Ehman (1965) found that when an amount of disodium m.ethanearsonate
(DSMA) equivalent to 28 Ib/acre was applied to the top of a soil column
which was leached with 60 inches of water, less than 10 percent of
the applied DSfiA showed up in the leachate. T^en sandy loam was used
in the soil column, the figure was less than 6 percent. In a similar
experln'ient performed with I5 Ib/acre of cacodylic acid, and using
an extrapolation to 60 inches of leaching water, about 9 percent
leached through the sand colum and 6 percent for the sandy loam.
It is evident that DSIVLA. and cacodylic acid are largely inactivated
by the soil.
-12-
LITERATURE CITED
Dickens, R., and A. E. Hiltbold. 196?. Movement and persistence
of inethanearsonates in soil. Weeds 15: 299-304.
Duble, R. L. , E. C. Hold, and G. G. McBee, 1969« Translocation
and breakdown of DSMA in coastal bermudagrass . J. Agr. Food
Chera. 17: 1247-1250.
Ehman, P. J. 1965* effect of ai'senical bnildup in the soil on
subseauent grovrth and residue content of crops. Southern Weed
Contr. Conf. Proc. I8.
Frost, D. V. 1970. Tolerances for arsenic and seleniura: A psychodynamic
problem. World Rev, of Pest Contr. Spring 1970, 9(l): 6-27.
Johnson, L. R. , and A. E. Hiltbold. I969. Arsenic content of soil
and crops following use of methanearsonate herbicides. Soil
Sci. Soc.Amer. Proc. 33: 279-282.
King, H. , and R. J. Ludford. i960, niie relation between constitution
of arsenicals and thin action on cell division. J. Chem. Soc.
2086-2088.
Long, J. A., W. W. Allen, and E. C. Holt. I962. Control of nutsedge
in bermudagrass tui-f. Weeds 10: 285-287.
Lucas, R. E. 1964. Ansar l84 disodium methyl- arson ate and related
compounds as selective johnsongrass herbicides in cotton. Southern
Weed Contr. Conf. 17: 62-66.
McBee, G. G. , P. R. Johnson, and E. C. Holt. I967. Ai-senic residue
studies on coastal bermudagrass. Weeds 15: 77-79-
Meliere, K. A. 1959- Cacodylic acid. U.S. Arm^f Engineering Commiand,
Array Chemical Center. ECNR No. 34, June 1959} AD 318626.
Morton, H. L., J. 0. Moffett, and R. H. MacDonald. 1972. Toxicity
of herbicides to newly emerged honey bees. Environ. Entomol.
1(1): 102-104.
Mrak, E. M. I969. Report of the Secretary's Commission on pesticides
and their relationshj.p to environmentaJ. health. U.S. Dept. HEW.
Newton, M. I968. Chemical Silviculture. SA/rnposiura: Management of
young grow'th Douglas-fir and western hemlock. Oregon State
University, Corvallis, Ore. 21-29.
13-
Nevrt.on, M. 1971. Organic arsenicals: Breakdown in forest trees
and in media containing energy sources — a progress report to
Environmental Protection Agency, Aug. 26, 1971. Oregon State
University, Corvallis, Ore.
Newton, M. , and H. A. Holt. I968. Hatchet-’injection of phenoxys,
picloram and arsenicals for control of some hardwoods and
conifers. Proc. of the Western Soc. of Weed Sci. 22:20-21.
Newton, M. , and H. A. Holt. 1971. Scolytid and huprestid mortality
in ponderosa pines injected with organic arsenicals. J. Scon.
Entomol. 64(4): 952-8.
Newton, M. , and P. W. Smith. 1971. Chem.ical silviculture in northern
hardwoods: A summary of herbicide treatments on the Shatterack
Forests Property involving injection and aerial spraying. Office
Report, Oregon State University, Corvallis, Ore. 5 P.
Newton, M. , and W. L. Webb. 1970. Herbicides and management of
young pine. From symposium on regeneration of ponderosa pine
held at Oregon State University, Corvallis, Ore, Sep. 11-12,
1969. 94-99.
Norris, L. A. 1971. Studies of the safety of organic arsenical
herbicides as precoramercial thinning agents: A progress report,
Precoramercial thinning in the Pacific Northwest. Washington
State University, Pullman, Wash. p. 63-74.
Pinto, S. S., and B, M. Bennett. I963. Effect of arsenic trioxide
exposure on mortality. Arch, of Environ. Health 1: 583-591*
Rostand, J. 1950. Chemical teratogenesis in anurian batrachians.
Conpt. Rend. Soc. Biol. l44: 915-917.
Salzgeber, B. 1955. Modification obsem/ed in chick embryo genital
organs inplanted iu vitro after treatment with different
teratogenic substances. Compt. Rend. Soc. Biol. l49: I9O-I92.
Searcy, V. S., and R. M. Patterson. 1964. Weed control in
establishjnent of coastal bermudagrass . Southern Weed Contr.
Conf. Proc. 17: IO6.
USDA. 1967. Agr. Handbook No. 332. ARS,
Von Endt, D. W. , P. C. Kearney, and D. D. Kaufman. 1968. Degradation
of M3MA by soil microorganisms. J. Agr. Food Chem. I6: 17-20.
Woolson, E. A., D. C. Kearney, and J. H. Axley. 1969* Chemical
distribution of arsenic in soil. Am. Chem. Soc. Mtg., N.Y., N.Y.
REPORT
ON
BACKGROUND INFORMATION
FOR
PICLORAM
FTCLOrj\M - BACKGROUND INTOrJIATION STATETffiNT
Prepared by Robert F. Buttery, Timothy R. Plumb and Kenneth D. Weyers
. General Information
A. Common name(s) - Piclorain, Tordou, ATCP
3. Chemical name - 4-amiao-3, 5 ,G-tricliloropicolinic acid
C. Registered uses - Control of annual and deep rooted perennial v/eeds
in non crop land.
D. Formulation (s) manufactured -
1. Tordon 101 mixture
Active Ingredients:
4-araino-3 ,5 ,6-tricliloropi colinic acid as the
triisopropanolamine salt -------------- 10.2%
2 . 4- dlciiloroph('no;;yacetic acid as the
triisopropanolamine salt -------------- 39.6%
Inert Ingredients -------------------50,2
Acid Equivalents;
4-amino-3 ,5 ,6 trichloropicolinic acid -------- 5.7%
2 .4- dichlorop't'.enoxyacctic acid - -- -- -- -- -- - 21.2%
U.S.D.A. Registration No. - 464-306
2. Tordon ICK Pellets
Active Ingredients:
4- am ino- 3 , 5 , 6 - 1 r i ch lo rop i cc 1 in i c acid
as the potassium salt --------------- 11.6%
Inert Ingredients: 88.4%
Avci >1 Eq ui valent :
4-amli)o-3,5,6-tric’’.loro)ij colinic acid - -- -- -- - 10%
U.S.D.A. Registration Mo. - -- 464-320
3. Tordon 22K Uecd ITillcr
Active Ingredient:
4-amino-3,5 , A-trichloropicolinic acid as the
potassium salt ------------------- 24.9%
Inert Ingredients ----------- — ------ 75.3%
Acid Eq ui va I e n t s :
4“amino-3 ,5 >6- trichloropicolinic acid
(2 lbs. /gal.) 21.5%
U.S.D.A. Registration Mo. - - 464-323
4. Tordon Beads
Active Ingredients:
4-amino-3,5 ,6-trichloropicolinic acid as the
potassium salt 2,3%
Disodiun tetraborate pentaliydrote - - -- -- -- -- - 79,2%
Disodium tetraborate decahydrate ----------- 16,5%
Iincrt Ingredients: - -- -- -- -- -- -- -- -- 2.0%
y\cid Equivalents:
4-amino-3 ,5 ,6-trichloropicolinic acid -------- 2.0%
Boron Trioxide 43,3%
U.S.D.A. Registration No. - - 464-333
5. Tordon 212 Mixture
Active Ingredients:
4 - amino - 3,5,6 - trichloropicolinic acid as
the triisopropanolamine salt ------------ 18.1%
2 ,A-dichlorophenoxyacetic acid as the
triisopropanolamine salt -------------- 37.7%
Inert Ingredients -------------------44.2%
Acid Equivalents:
4 - amino - 3,5,6 - trichloropicolinic acid - - - 10.1%-1 lb. /gal.
2,4 dlchlorophenoxy acetic acid --------- 20.2%-2 lb. /gal.
U.S.D.A. Registration No. - - 464-361
6. Tordon 155 Mixture
Active Ingredients:
4 - amino - 3,5,6 - trichloropicolinic acid as the
isooctyl ester ------------------- 15.1%
2 ,4 ,5-trichlorophenoxyacetic acid as the
propylene glycol butyl ether esters --------- 63.4%
Inert Ingredients 21.5%
Acid Equivalents:
4 - amino - 3,5,6 - trichloropicolinic acid - - - 10.3%-1 lb. /gal.
2,4,5 - trichlophenoxyacetic acid -------- 41.3%-4 lbs, /gal.
U.S.D.A. Registration No. 464-364
E. Dilution of formulations and rate and method of application.
1. Tordon 101 Mixture:
Use Tordon 101 Mixture at rates of 1/2 to 3 gallons per acre to
control broadleaved weeds and at rates of 1 to 4 gallons per acre
to control woody plants and vines. In all cases use the amounts
specified in enough water to give thorough and uniform coverage
of the plants to be controlled. NOTE: Tordon 101 Mixture docs
not mix readily with oil.
For best results applications should be made when weeds and brush
are actively growing. Applications in late summer when the plants
are mature or during period of drought may result in less effec-
tive control. Treatment will not cause permanent, if any, damage
to common established grasses.
High Volume Leaf-Steam Treatment: Use Tordon 101 Mixture at
the rate of 1 gallon in water to make 100 gallons of spray to
control broadleaved weeds, vines and other woody plants. Apply
after the foliage is well developed and in a manner to give
thorough spray coveraj^^e. For woody plants, up to 6 to 8 feet
tall, use a drenching spray and wet all leaves, stems, ai\d root
collars. For hard to kill species such as ash and oak soak the
soil around the root collar. NOTE: Do not allovj the spray to
contact desirable plants, and do not soak the soil over roots
of such plants.
-9-
o
Low Volume Ground or Aerial Foliage Treatment.: For these uses
the required amount of Tordon 101 Mixture should be applied in a
total spray volume of 10 to 25 gallons per acre, depending upon
the plant species, height and density of growth. The preferred
volume range is 15 to 25 gallons per acre. For these Low Volume
uses, Tordon 101 Mixture should be used only in thickened (high
viscosity) spray mixtures. Such mixtures should be prepared
using NORBAK particul ating agent as directed in a separate pub-
lication "INSTRUCTION >h\NUAL FOR NORBAK PARTICULATING AGENT V7ITH
HERBICIDES" (available from the Dow Chemical Company) and in the
accompanying "GUIDE TO INGREDIENT NEEDS AND PROCEDUTJ-:S TO FOLLOW
FOR MIXING SPRAYS CONTAINING TORDON xOl MIXTURE PLUS NORBAK PAR-
TICULATING AGENT." Thickened sprays prepared by using high
viscosity invert emulsions or other drift reducing systems may be
utilized if they are made as drift-free as are mixtures contain-
ing NORBAK particulating agent mixed according to manufacturer's
directions .
r>roadleaved Annual and Perennial VJeed and Woody Vine Control:
Use Tordon 101 Mixture at rates of 2 quarts to 3 gallons per acre
in 15 to 25 gallons of a water spray mixture containing the amount
of NORBAK particulating agent required to provide the recommended
thickness. Apply to problem weeds and vines any time after grov.'tb.
begins in the spring and before the ground freezes in the fall.
For seasonal control of vigorously growing stands of field bind-
weed, Canada thistle or mixtures of these with susceptible
annua], weeds such as ragweed, daiidelion, pjantain, clovers and
dock use 2 to 3 quarts of Tordon 101 Mixture per acre in 15 to
25 gallons of water spray containing NOPvBAK particulating agent.
In arid areas and for control of more resistant perennial weeds
use 1 to 3 gallons of Tordon 101 Mixture per acre in 15 to 25
gallons of spray containing KORBAIC particulating agent. Use 1
to 1.5 gallons per acre to control species such as Canada thistle,
field bindv;eed and milkv;eed. The higher rates should be used
under drought stress conditions and for the ?iore resistant species
such as bouncingbet, leafy spurge, toadflax and v;oody vines.
Woody Plant Control: Use Tordon 101 Mixture at the rate of 1 to
A gallons per acre in 15 to 25 gallons of a water spray mixture
containing NORBAK particulating agent. For susceptible seedling
stages of species such as aspen, cherry and sumac use 1 to 1.5
gallons of Tordon 101 Mixture per acre in 15 to 25 gallons of
a water spray mixture containing NORBAK particulating agent.
For more m.ature and/or less susceptible species such as willow,
buttonbush, black locust, sassafras, sumac, tulip poplar and
cherry growing in sandy loan soil, use 2 to 2.5 gallons of Tordon
101 Mixture per acre in 15 to 25 gallons of a water spray m.ix-
ture containing NORBAK particulating agent.
-3-
For rfKjre resistant brush such as naple, pine, sourwood, black-
gum, cedar and oak where growing on heavy clay soils or on rocky
terrain, use 3 to 4 gallons of Tordon 101 Mixture per acre in 15
to 25 gallons cf a water spray mixture containing NORBAK partic-
ulatlng agent. Use the higher rate and volume where the foliage
of more difficult to kill brush is covered with dense vine growth.
NOTE: For best results under conditions of drought stress use
the higher rates recommended. Even these rates under such con-
ditions may not be as effective as the lower rates under good
growing conditions.
Cut Surface Treatments: In forest and other non-crop areas to
kill unwanted trees of hardwood species such as eim, maple, oak
and conifers such as pine apply Tordon 101 Mixture, either vin-
diluted or diluted in a 1 to 1 ratio with water, as directed
below.
With Tree injector Method: Application should be made by inject-
ing 1/2 milliliter of undiluted Tordon 101 Mixture or 1 milliliter
of the diluted solution through the bark at intervals of 3 inches
bet\'7een edges of the injector wound. The injections should com-
pletely surround the tree at any convenient height.
With Frill or Girdle Method: Make a single girdle through the
bark completely around the tree at a convenient height. Wet the
cut surface with tlie diluted solution.
Both above methods may be used successfully at any season except
during periods of heavy sap flox7 of certain species - for example
maples .
2. Tordon lOK Pellets:
Tordon lOK Pellets may be applied at any time soil is free from
frost, llox-rever, best results are obtained from applications In
the spring before growth begins or during periods of vigorous
growth and when abundant rainfall can be expected. Distribute
Tordon lOK Pellets uniformly as spot or broadcast treatment to
the soil over the roots of x^7oody plants to be controlled.
Broadcast application is the preferred method of treatment for
dense stands of brush. Use Tordon lOK Pellets at the rate of
60 to 85 })ounds per acre (approximately 1-1/2 to 2 lbs. per 1000
sq . ft.) and distribute evenly over the entire area where brush
is to be controlled.
To control solid stands of very susceptible species such as
maple, conifers, locust", aspen and wild rose use Tordon lOK
Pellets at the rate of 60 lbs. per acre.
-4-
€
To control brush of mixed species use Tordon lOK Pellets at
the rate of 75 lbs. per acre.
To control solid stands of hard to kill species such as black-
gum, oak and ash use Tordon lOK Pellets at the rate of 85 lbs.
per acre. Re-treatment of ash may be necessary the following
year.
Spot application is generally the preferred method of treatment
for scattered or sparse stands of brush. Spread Tordon lOK Pellets
evenly on the soil over the entire root system (around the main
stem) and outward to 1 foot beyond the branch tips (drip-line) .
Use at the rate of 1 to 2 tablespoonfuls (1 to 2 ounces) per 30
square feet of soil surface.
Use the higher dosage al?^ to control brush on very sandy, gravelly
or rocky soils and in areas where heavy rainfall can be anticipated
3. Tordon 22K Weed Killer:
Mix with water and apply as a coarse, low pressure spray (20 to
40 lbs. per sq. in.). Apply anytime during the growing season
(when frost leaves soil in spring until ground froe;:es in fall) ,
and preferably when rainfall can be expected soon after application
For General Use on Perennial Weeds on Non-cropland, use 1 to
1-1/2 gallons of Tordon 22K Weed Killer per acre in 50 to 100
gallons of v/ater and spray to v;et weed foliage and soil. NOTE:
T^ocal conditions may affect the use of herbiciiles . State agri-
cultural experiment stations or extension service weed specialists
in many states issue recommendations to fit local conditions. Be
sure that use of this product conforms to all applicable regulation
For Use as a Spot Treatment on Perennial Weeds, Mix at the rate
of 1 gallon of Tordon 22K per 100 gallons of water. Apply at the
rate of 100 gallons of spray mixture per acre. This will provide
a rate of 2 pounds of Tordon herbicide per acre. For small amounts
us 2-1/2 fluid ounces Tordon 22K per 2 gallons of water. For round
patches apply as indicated in the table.
Feet across Round Patch
to be* treated (weed area
plus 10 foot border;)
Gallons
of spray mixture
to apply
25
50
75
100
1.0
4.5
10.0
18.0
235 or (1 acre)
100.0
-5-
A. Tordon Beads:
Tordon Beads herbicide applied to the soil over plant roots is
highly effective for the control of broadleaved perennial and
annual weeds and undesirable v;oody plants on utility, highway
and other right-of-ways, fence rows, headlands around farm and
industrial buildings and storage sites.
For Control of Broadleaved Perennial and Annual Weeds: Apply
Tordon Beads uniformly anytime during the normal growing season
where sufficient moisture is available to carry the herbicide
into the soil. In areas where little or no summer rainfalJ.
occurs, application should be made in late summer or early fall.
Maximum effects of the treatment do not become apparent until the
chemical has been
Weeds Controlled*
carried by moisture into the soil.
APPLICATION PJ\.TES
Tordon Beads
Amount to Apply , Remarks
Docks
Larkspur
50 to 100 lb. per
r
j
acre
j Use lower rates in lov;
Pigweed
19 to 37 oz. per
rainfall areas in the
1000 sq. ft.
northern states such os
Povertywecd
Idaho, Montana, North
Sowtlilstle
5 to 10 02. per
Dakota, Oregon, South
(perennial)
sq. rod
Dakota, Wyoming and Wash-
Sunflower
ington . Higher rates
Tansy
should l?e used where rain-
Thistle
fall is greater or in
(plumeicss)
southern states such as
Toadflax
Arizona, Arkansas, Kansas
(dalmation)
Missouri, New Mexico,
Bindweed (field)
Oklahoma and Texas .
Bursage (bur-raweed
100 to 150 lb.
per acre
v/oolyleaf povertyx/eed) 37 to 56 oz. per
Knapv;eed
1000 sq . ft.
10 to 16 oz per
(Russian)
feo . rod
Milkx^eed
Spurge (leafy)
TliisLle (Canada)
i
1
*These are types or examples of v;ecds controlled
-6-
C
Tordon Beads herbicide is effective against a wide range of weeds.
Local conditions nay affect the use of herbicides. Consult your
State Agricultural Experiment Station or Extension Service weed
specialists for local recommendations. Be sure that the use of
this product conforms to all applicable regulations.
For Control of Woody Plants such as maple, locust, aspen, conifers,
other v;oody trees, slu*ubs, v;lld rose, brambles, wild grapes and
other vines, apply Tordon Beads uniformly to the soil over the
root zone. Apply anytime during the normal growing season where
sufficient moisture is available to carry the herbicide into the
soil in areas where little or no summer rainfall occurs application
should be made a;l. "bud break" in late winter or early spring.
Use at the rate of 300 to AOO pounds per acre (equivalent to ap-
proximately 7-1/2 to 10 lb. per 1000 square feet, 2 to 2-1/2 lb.
per sq. rod, or 1/A to 1 lb per 100 sq . ft.) Maximum effects of the
treatment do not become apparent until the. chemical has been
carried by moisture into the soil in the root zone of the plants.
5. Tordon 212 Mixture
Mix with water and apply as a coarse, low, pressure spray (20 to
50 lbs. per sq . in.). Apply anytime when fully developed green
leaves are present.
For General Use: The rate of Tordon 212 Mixture required varies
according to \7eed species and geographical location. The follow-
ing table sliov/s the amount of Tordon 212 Mixture that should be
mixed in v;ater to make 100 gallons of spray. Apply uniformly to
wet the X7eeds withoixt run-off. This will usually require about
100 gallons per acre.
Tordon 212 Mixture
Some of the Weeds to use in 100
to be Controlled gal, spray Remarks
Dock, Larkspur
Use lower rates in low
Pigweed
rainfall areas in the
Sowthistle
northern states such as
Sunflower (v.d.ld)
Idaho, Montana, North
Thistle (Canada) 1/2 to 2 gallons
Dakota, Oregon, South
Thistle (Musk)
Dakota, Washington and
Toadflax (Dalmation)
Wyoming. Higher rates
VJonnv.'ood (American)
should be used in southern
Bindweed (field)
states or v;here rainfall
Horsenettle (x^hite)
is greater such as Arizona,
Knapv/eed (Russian)
Arkansas, Kansas, Missouri, ^
Milkweed 1 to 3 gal.
New Mexico, Oklahoma, and |
Ragweed (bur)
Spurge (leafy)
Texas , j
Toadflax (yellow)
For Use on Round Patches of Weeds: Apply the required spray mix-
ture at the amount indicated in the following table.
Feet across Round Patch to be treated
(weed area plus 10 foot border)
Gallons of spray mixture
to apply
25
1.0
50
4.5
75
10.0
100
18.0
235 (or 1 acre)
100.0
NOTE: For small amounts of spray use Tordon 212 Mixture at rate of
1-1/4 to 2-1/2 fluid ounces in each gallon of water.
6. Tordon 135 Mixture:
Basal Bark Treatment: Use 1 to 3 gallons of Tordon 155 Mixture
in enough diesel oil, No. 1 or No. 2 fuel oil or kerosene to make
100 gallons of spray mixture. Apply with knapsack sprayer or pov;er
spraying equipment using low pressures (20-40 psi) . Spray the basal
parts of brush and tree trunks to a height of 12 to 15 inches from
the ground. Thorough wetting of the indicated area is necessary
for good control. Spray until run-off at the ground line is notice-
able. Old or rough bark requires more spray than smooth young
bark. Apply at any time, including the v.tLnter months, except when
snow or water prevent spraying to the ground line.
DORMANT STEM BROADCAST: Mix 3 to 6 quarts of Tordon 155 Mixture
brush killer in enough oil to make 100 gallons of spray. Apply
with knapsack or power spraying equipment, using low pressure
(20-40 psi) . Treat any time when brush is dormant and most of
the foliage has dropped. Thoroughly wet the upper parts of the
stems and use the remainder needed to wet the lower 12 to 15 inches
above the ground to the point of run-off. For root suckeri ug species
such as sumac, persimmon, sassafras and locust, also spray the
ground under the plants to cover small root suckers vjhich may not
be visible above the soil surface. Brush of average density and
4 to 6 feet high may take up to 150 gallons of spray mixture per
acre.
-8-
Tolerances in food or feed and other safety limitations.
Food or Feed Item
Tolerance (parts /million)
Forage grass
Kidney
Liver
Meat fat and byproducts
80
5
Milk
0.5
0.2
0.5
Safety limitations for the different Picloram are as follows:
1. Tordon 101 Mixture:
Do Not Allow Spray Drift: Tordon 101 Mixture is highly active
against most broadleaved plants. Tiny amounts may cause injury
to such plants if applied during either growing or dormant periods.
Do not use high pressure sprays. Do not apply or otherwise permit
Tordon 101 Mixture or sprays containing it to contact desirable
plants such as flowers, otlier ornamental plants, vegetables, grapes,
fruit trees, cotton, tobacco, tomatoes, potatoes, beans of all
types including soybeans, and other valuable broadleaved plants,
nor the soil containing roots of such valuable plants. Apply
Tordon 101 Mixture only when there is little or no wind and no
hazard from drift. Coarse sprays are least likely to drift.
Do Not Contaminate VJater: To avoid injury to crops or other
desirable plants, do not treat or allow spray drift to fall onto
inner banks or bottom of irrigation ditches.
Other Precautions: Do not store near food, feedstuff, fertilizer,
seeds, insecticides, fungicides or other pesticides. To avoid
injury to desirable plants, containers and sprayers used for Tordon
101 Mixture should not be reused to contain or apply other materials.
Rinse equipment and containers thoroughly with water and dispose
of wastes by burying in non-croplands av/ay from water supplies.
Containers should be disposed of by punching holes in them and
burying with v;aste.
CAUTION; KEEP OUT OF REACH OF CHILDREN. HAPdlFUL IF SWALLOWED.
CAUSES EYE INJURY. KW CAUSE SKIN IRRITATION. Avoid Contact with
Eyes, Skin and Clothing, Wash Well After Handling or Use. Keep
Container Closed. Keen Av;ay from Heat and Open Flame.
When handling concentrate wear suitable eye protection. In case
of eye contact, promptly flush X'/ith plenty of Xi7ater, and get medical
attention. Remove contaminated clothing and v/ash before reuse.
COMBUSTIBLE LIQCID.
-9-
2. Tordon lOK Pellets;
Apply only as recomnendecl to avoid injury to desirable plants.
Avoid application during v;indy periods when the product may be
blown from area to be treated.
Do not clean containers or application equipment over or near
areas where roots of desirable trees and other desirable plants
may extend into the soil where the chemical may be washed or other-
wise moved into contact with the roots.
Do not permit any of the product to be blown onto any parts of
desirable plants.
Do not allow the material to contaminate water used for irrigation,
drinking or other domestic purposes.
Do not store near food, feedstuff, fertilizers, seeds, insect-
icides, fungicides or other pesticides.
Equipment used for applying Tordon lOK Pellets should not be used
for applying other materials to desirable plants. Shipping con-
tainers should not be re-used for other materials wliich may be
applied to desirable plants. Dispose of empty containers by burn-
ing or burying in non-croplands av’ay from desirable plants and
v;ater supplies.
NOTE: Be sure that all use of Tordon lOK Pellets conforms to
local regulations.
CATUION; Keep out of Reach of Children.
3. Tordon 22K Weed Killer
Do Not Allow Spray Drift. Tordoi. herbicide is highly potent.
Tiny amounts may cause damage to plants if applied during either
growing or dormant periods. Do not use high pressure sprays.
Do not apply by aerial equipment. Do not apply or othen-7ise
permit Tordon 22K or sp»rays containing it to coptact desirable
plants such as vegetables, flowers, grapes, fruit trees, orna-
mentals, cotton, tobacco, tomatoes, potatoes, beans of all types
including soybeans, and other valuable broadlcaved plants, nor
the soil containing roots of nearby valuable plants. Apply Tordon
22K only when there is little or no wind or no hazard from spray
drift. Coarse sprays are least likely to drift.
Do Not Contaminate Water. To avoid crop or other plant injury,
do not treat or allow spray drift to fall onto inner banks or
bottom of irrigation and drainage ditches. Dike around and do
-10-
not Irrigate through treated areas. Do not contaminate water
used for drinking or other domestic purposes.
Do Not Move Treated Soil. Do not go over treated areas t-rlth land
levelers, cultivation or harvesting equipment, or move the soil
by any other means. Mark off treated areas v/ith stakes, posts
or fencing.
Do Not Graze Or Use Treated Areas for Crop Production.
Do Not Mix With Other Weedkillers or Other Pesticides.
Other Precautions: Do not store near food, feedstuff, fertilizers,
seeds, insecticides, fungicides or other pesticides. To avoid
injury to desirable plants, containers and sprayers used for
Tordon 22K should not be reused to contain or apply other mate-
rials. Be sure that all use of Tordon 22K conforms to local
regulations .
CAUTION - R\Y CAUSE IRRITATION - COMBUSTIBLE. Avoid Contact with
Skin and Eyes. Avoid Breathing Spray Mist. Keep Container Closed,
Keep Away from Heat and Open Flame. Keep Out of tlie Reach of
Children .
4. Tordon Beads:
USE PRECAUTIONS:
Avoid Improper Application: Tordon herbicide is highly active
against most broadleaved plants. Small quantities nay cause
damage to plants whether applied during the growing or dormant
season. Do not apply or othert^ise permit Tordon Beads to contact
desirable plants such as vegetables, flowers, grapes, fruit trees,
ornamentals, cotton, beans, soybeans and other valuable broad-
leaved plants nor the soil containing roots of such plants grow-
ing thereon or nearby or where such plants are to be grown.
Avoid Water Contamination: To avoid crop or other plant injury,
do not treat inner banks or bottom of irrigation and drainage
ditches. Do not contaminate water to be used for drinking or
other domestic purposes.
Avoid Movement of Treated Soil: Avoid the movement of treated
soil into untreated areas.
Other Precautions: Do not store near food, feedstuffs, fertilizer,
seeds, insecticides, fungicides or other pesticides. To avoid
Injury to desirable plants, containers and equipment used for
Tordon Beads should not be re-used to contain or apply other
materials .
f
-11-
Dispose of empty containers: Burn or bur};^ in non-cropland away
from desirable plants and water supplies .
CAUTION: DUST CAUSES IRRITATION. MAY BE HARIIEUL IF SWALLOWED.
KEEP OUT OF REACH OF CHILDREN. Avoid Skin and Eye Contact. Wash
After Handling.
5. Tordon 212 Mixture:
Do Not Allow Spray Drift. Tordon and 2,4-D herbicides are highly
potent. Tiny amounts may cause damage to plants if applied dur-
ing either growing or dormant periods. Do not use high pressure
sprays. Do not apply or otlierwise permit Tordon 212 Mixture or
sprays containing it to contact desirable plants such as vege-
tables, flox\’ers, grapes, fruit trees, ornamentals, cotton, tobacco,
tomatoes, potatoes, beans of all types including soybeans, and
other valuable broadleaved plants, nor soils containing roots of
nearby valuable plants. Apply Tordon 212 Mixture only when there
is little or no iiazard from spray drift. Coarse sprays are least
likely to drift. Do not apply by air, as this increases drift
hazard.
Do Mot Contaminate Water. To avoid crop or other plant injury,
do not treat or allow spray drift to fall onto inner banks or
bottom of irrigation and drainage ditches. Dike around and do not
irrigate through treated areas. Do not contaminate water used for
drinking or other domestic purposes.
Do Not Move Treated Soil. Do not go over treated areas with land
levelers, cultivation or harvesting equipment or move soil from
treated areas by any other means.
Do Not Treat Areas Intended to be used for desirable plants or
Food Crops, It usually requires up to 3 years for Tordon herbi-
cide to be deactivated by the soil.
Do Not Mix in the Sprayer with Other Weedkillers or Other
Pesticides .
Other Precautions: Do not store near food, feedstuff, fertilizer,
seeds, insecticides, fungicides or other pesticides. To avoid
injury to desirable plants, containers and sprayers used for Tordon
212 Mixture should not be reused to contain or apply other mate-
rials. Rinse equipment and containers thoroughly with water and
dispose of wastes by burying in non-crcplands away from v;ater
supplies. Containers should be disposed of by punching holes in
them and burying with v/aste.
CAUTION. KEEP CUT OF REACH OF CHILDREN. HARMFUL IF SWALLOWED.
CAUSES EYE INJURY. MAY CAUSE SKIM IRRITATION. Avoid Contact
with Eves, Skin and Clothing. Avoid Breathing Sprav Mists.
Wash Well After Handling or Use. Keep Container Closed \Tacn Not
Using. In case of contact, flush eyes writh plenty of water; and
get medical attention. Remove grossly contaminated clothing and
wash before reuse.
-12-
6, Tordon 155 Mixture:
Do Not Use Tordon 155 Mixture With Water. Tordon and 2,4,5-T
herbicides are highly potent and even minute quantities may
damage plants during both the growing and dormant periods. There-
fore, do not apply or otherwise permit Tordon 155 Mixture or spray
mist containing it to contaminate soil used to grow desirable
susceptible plants nor to contact susceptible plants such as
vegetables, flowers, grapes, fruit trees, ornamentals, cotton,
beans of all types including soybeans and other desirable broad-
leaved plants. Applications should be made only when there is no
hazard from spray drift. Coarse sprays are less likely to drift.
Do not allow the material to contaminate water used for irrigation,
drinking or other domestic purposes. Do not store near food, feed-
stuff, fertilizer, seeds, insecticides, fungicides or other pesti-
cides. Because of the difficulty of thoroughly cleaning sprayers
such equipment should not be used for applying other materials
to desirable plants. Shipping containers should not be re-used
for otlier materials v;hich may be applied to desirable plants.
This product is toxic to fish. Keep out of lakes, streams or
ponds .
Rinse equipment and containers thoroughly with X'/ater and dispose
of vjastes by burying in non-cropland axi/ay from \i7ater supplies.
Containers shou] d be disposed of by punching holes in them and
burying with waste.
NOTE: Be sure that all use of Tordon 155 Mixture conforms to
local regulations.
CAUTION. KEEP OUT OF THE REACH OF CHILDREN. HARflFUL IF SWALLOWED.
MAY CAUSE IRRITATION. Avoid Contact with Eyes, Skin and Clothing.
In case of contact wash x;ith plenty of water.
G. • Manufacturer or producer:
The Dow Chemical Company
Midland, llichigan 48640
II. Toxicity Data on Formulation to Be Used
A . Safety data
Based on numerous tests, the recommended use of picloram containing
herbicides should present no safety hazard to humans, liv^estock, or
x;ildlife (143) . McCollester and Leng also report tliat no alarming
pharmacological or toxicological properties x;ere found in investiga-
tions in animals, fish, and aquatic organisms. Formulations con-
taining phenoxy derivatives appear to be more toxic than picloram
alone .
V
-13-
Acute Tnammalian studies.
a. Oral . The acute oral toxicity of picloram to various animals
in terms of LD^q (lethal, dose to kill 50 percent of the
animals) values ran^e from 2,000 mg of picloram/kg of body
weight in nice and rabbits to 8,200 mg/kg in rats. The
LD50 value for cattle and sheep are greater than 750 and
1,000 mg/kg respectively (230). A single dose of up to 500
tig/kg gave no evidence of toxicity in calves, and the
value for chicks is approximately 600 mg/kg. Lynn (13A)
reported that sheep shov/ed no ill effect from the acid form
of picloram at rates up to 650 mg/kg and the K-salt formu-
lation (25 percent active ingredient) up to 4,650 mg/kg.
Hov/ever, the Tordon 101 formulation (10.7 percent picloram
and 39.6 percent 2,4-D as triisopropanolamlne salts) pro-
duced toxic effects at 2,530 mg/kg and subsequent death in
3 days. Cattle v;ere more sensitive in shov;ing toxic effects,
but not deatli, at a rate of Tordon 101 of 1,900 mg/kg; no
death was reported at a rate greater than 3,000 mg/kg.
Bovey and Seif res (36) noted that there are no Imov/n reports
of liUiTian sickness resulting from the handling or application
of picloram.
b. Dermal . Skin irritation is minim.al, and picloram is not
likely to be absorbed through 'the skin. The LD^q value for
rabbits is greater than 4,000 mg/kg, the highf^^^'t value tested
(230). In a similar test, Tordon 22K at 2,000 mg/kg Cciused
no observable effect while a similar rate of Tordon 101 caused
slight hyperemia and slight necrosis (134) .
c. Inhalation . Picloram dusts may be somewhat irritating, but
they are not likely to cause illness (230) . Inhalation of
air for 7 hours bubbled through a solution of Tordon 22K
produced no observable adverse effects during or within 2
weeks after exposure (134) .
d. Eye and skin irritation. Picloram may cause mild Irritation
to the eyes which heals readily and no corneal injur>’ is
likely (230) . Undiluted picloram applied directly to the
conjunctival sac of white rabbits produced slight redness
and slight comeal cloudiness both of which disappeared in
1 to 2 days (134) . The Tordon 101 mixture v;as slightly more
irritating.
Subacute studies.
a. Oral . Feeding studies for 90 days in rats showed no adverse
effects from dietary levels as high as 0.1 percent (1,000
ppm) of picloram (143). The only effect noted at 0.3 percent
picloram in the diet was an increase in liver/body weight
-14-
ratios of the females. Only slight to moderate pathological
changes were observed in the liver and kidneys on a diet
containing 1 percent (1,000 ppm) picloram. No adverse effects
were noted in any animals fed a 0.3 percent triisppropanolamine
salt picloram diet.
In long-term feedings, albino rats and beagle dogs x^7ere fed
picloram at a rate of 15 to 150 mg/kg of body weight for 2
years. No observable adverse effects were noted in either
species as measured by body weight, food consumption, be-
havior, mortality, hematological and clinical blood chemistry
studies, and urine analyses. Also, no pathological differences
were found between the incidence or kind of tumors in control
and treated animals. No adverse effects were found in sheep
or cattle fed picloram at 73 mg/kg/day for 30 days.
b. Dermal . Continued exposure for 9 days of the skin of rabbits
to the undiluted acid form of picloram caused only slight
exfoliation and hyperemia (134) . Other tests where the skin
of rabbits was exposed for several days to various concentra-
tions of picloram showed no severe or prolonged effects.
Exposuie of the skin of human subjects to a 10 percent solution
of picloram caused no skin irritation- (the duration of the
test was not reported) .
c. Inhalation. No information available.
3. Other toxicity studies which may be required.
a. Neurotoxicity . No information available.
b. Teratogenicity . Only one brief reference; see section "C"
below.
c. Effects on reproduction. No adverse effects were found in
albino rats fed picloram at various levels in the diet up to
3,000 ppm. through three generations (two litters per genera-
tion) in terms of fertility, gestation, viability, and
lactation by body weight records and by teratological exam-
ination of the fetuses (143). Mice fed 0.01 percent picloram
in their diet for 4 days before mating and 14 days after mat-
ing produced the same number of offspring before and after the
test.
d. Synergism. No information available.
e. Potentiation. No information available.
f. Metabolism. McCollester and Leng (143) reported that dogs
fed on a diet containing 97 ppm picloram (carboxyl- ^*C-
-15-
labeled) excreted 90 percent of the dose unchanged in the
urine within A8 hours after feeding, Picloram apparently
did not accumulate in the tissue of the animals and neither (
was it decarboxylated vivo . Based on work by other inves-
tigators (e.g. Fisher et al . 1965), McCollester and Leng con-
cluded that mammals were found to eliminate 93 percent of the
picloram from the bloodstream and kidneys as an unchanged
compound in the urine before the liver had an opportunity to
act on it. Menzie (145) referring to Redemann et al. (179)
noted that picloram. remained mainly unchanged in spring v;heat
groxv/n on treated soil; liowever, metabolites in low levels
were found including 4-amino-6-hydroxy-3,5-dichloropicolinic
acid, oxalic acid, lipid conjugates, and 4-ainino-3,5,6
trichloropyridine .
g. Avian and fish toxicity. Kenaga (118) reported that all der-
ivatives- of picloram exhibit lo\; acute toxicity to birds and
fish. If the recommended use directions are followed, there
is low potential h.azard , if any, to fish, from terrestrial
runoff water or from direct accidental contamination of water
and there is no hazard to birds.
Japanese iind Bobv/hite quail (Coturnix couturr.ix j aponica and
Colinus virginianus respectively) and mallard ducks (Anas
platyrhynchos) fed picloram ar rates up to 1,000 ppm or more
did not receive the kOrQ (median i.ethal concentration) values.
Bobx^hite quail and mallard ducks had a calculated dosage
of 23,000 and 385,000 ppm respectively. Japanese quail v.^ere
fed up to 1,000 ppm of picloram in their diet for each of
three successive generations v.’itliout effect on mortality,
egg jiroduction, and fertility.
Kenaga (118) also reported on the effect of nicloram on 15
species of fish including rainbow trout (Salmo gairdnerii
Richardson) and channel catfish (ictalurus me las Rafinesque) .
Picloram forr.iulations as acids, salts, and esters were gen-
erally low in toxicity to fish (LC^q ^ 1.0 ppm). Assuming
that all material was completely dissolved, a 3 pound appli-
cation of picloram to an acre of xjatcr 3 inches deep x/ould
result in a maximum concentration of 4.5 ppm. This is less
than the RC^q values of the picloram salt fomulations to
the fish studied. However, the isooctyl ester x;ould be toxic
to the most sensi/tivc species which had an value around
1 ppm. Kenaga noted that picloram herbicides are not recom-
mended for aquatic uses. Land ap])lications of 3 pounds a.e.
per acre would not likely result in concentrations as high
as 1 ppm in X\^ater Xv’hetlier by accidental application or by
runoff because of the dilution, sorption, anfl degradation
that occurs.
-16-
Referring to other work, Kenaga noted that a 90-day exposure
of bluegill (Leponis r.acrochlrus Rafinesque) to 5 to 8 ppm
of picloram resulted in a 30 percent kill and some loss of
weight in tlie survivors. Hardy (lOA) studied the effect of
the K-salt of picloram on the biological food chain of algae-
daphriia-fish . The presence of 1 ppm of picloram did not retard
algae grov/th. Daphnia which were maintained in 1 ppm a.e,
of picloram for 10 weeks developed and reproduced normally
with no build-up of herbicide in their tissue. Guppies
kept in v/ater at 1 ppm a.e. of picloram and fed a diet of
daphnia reared in a similar picloram solution appeared normal
in development, behavior, and reproduction.
h. Carcinogenicity. No information available.
B. Physical-chemical properties of the pure chemical (4-amino-3,5 ,6-
trichJ.orcpi colinic acid).
1. Boiling point: Decomposes at approximately 215 C.
2. Flash point:
a. Pure chemical — ?
b. Tordon 101 Mixture — 35 C TOC
c. Tordon lOK Pellets — Nonflammable.
d. Tordon 22K Weed Killer — Combustible (flashpoint unkno’.'m) .
e. Tordon Beads — Nonflammable
f. Tordon 212 Mixture — Nonflammable
g. Tordon 155 Mixture--140 C COC.
3,. Physical state; White powder with a chlorine-like odor.
4. Density: No information.
5. Vapor pressure:
a. 6.16 X 10“7 Hg at 35 C
b. 1.07 X 10"^ m Hg at 45 C
6. Solubility: At 25 C
Solvent
g/100 Ml Solvent
££m
Acetone
Acetonitrile
Benzene
Carbon disulfide less than
Diethyl ether
Ethanol (2B absolute)
Isopropanol
Kerosene
Metliylene chloride
Water
1.98
0.16
0.02
0.005
0.12
1.05
0.55
0.001
0.06
0.043
Less than 10
19,800
1,600
200
Less than 50
1,200
10,500
5,500
600
430
7. Stability: No Information
-17“
III. Efficacy data under field and laboratory tests
A. Effectiveness for intended puiT?ose
Picloram alone (Tordon 22K) or mixtures with phenoxy herbicides
(Tordon 212 and 225) have been the only effective treatment for
the control of Gamble oak (Quercus gambellii Nut. ) in southwest
Colorado. Rates of Tordon 22K up to 2 pounds have given up to
80 percent stem kill and it is the only single treatment giving
comparable results to Tordon 22K plus silvex (Kuron) (139)*
Gantz and Warren (8o) found that picloram plus 2,i4-D, at 1/1+ plus
oz. per acre respectively, gave satisfactory control of wild
buckwheat (Pojygonum convolvulas ) in spring wheat, barley, and
winter wheat with adequate crop safety. Picloram at rates of 3
eind 1+ pounds per acre killed almost all plants of bi'ush species
in Texas except Texas persimmon; lower rates were effective on
honey mesquite, pricklypeaj:, and whitebrush (?li). In California,
a single broadcast application of 2 pounds a.e. per acre of
picloram gave approximately 85 percent kill of chamise
(Adenostoma fasciculatum) (172); while in other work three annual
broadcast applications of 6 pounds a.e. per acre of picloram
gave less than 50 percent plant kill of scrub oak (Quercus
dumps a) (173).
Soil application of Tordon to control woody plants should be
made prior to or during early spring growth and when rain is
expected afterward. Treatment at other times may be effective,
but higher dosages may be required.
Many annual broadleaf weeds can be killed with foliar
applications of Tordon at rates as low as 1/^ to 1/2 ounce per
acre.
Most established perennial grasses are not affected by rates of
1 to 2 pounds per acre. A large number of deep-rooted
perennial broadleaves such as Canada thistle, bindweed,
leafy spurge and larkspur eire readily controlled with 2 pounds
per acre. White top (Lepedium sp.), peppercress and related
species generally require 3 pounds per acre for good kills.
Among woody plants, maple, cherry, aspen, cottonwood, birch,
locxist, rose, poison oak, and most conifers eire quite
susceptible to Tordon. Oak generally requires higher dosages
for good kills and sojne species such as ash or toy on all
show some resistance.
18
Phytotoxicity
Lee (129) reported that picloram adversely affected seed
production in a number of grasses (e.g. Colonial bent grass) in
Oregon at rates of 1.0 to 1.5 pound per acre; however, none of
treatments affected seedling development. Wheat (Triticum acstivum L.)
was most susceptible to herbicide damage at the late tiller
stage when 0.5 oz. of picloram per acre significantly reduced
kernel yield (163). Both monocots in the seedling stage and
dicots at all stages of development are adversely affected
by low to moderate rates of picloram. However, at very low
rates (e.g. 5 >; 10-5 M) picloram promoted growth in soybeans.
Baur et al . (18) reported that solutions of picloram at
0.25 to 0.50 ppb stimulated a significant increase in the
fresh weight of com, soybeans, cotton, cowpeas, and sorghum
and v;heat at 100 ppb. Picloram at 100 ppb caused a reduction in
tlie fresh and dry weight of dicot species while a decrease was
found in com, wheat, and sorghum at 1,000 ppb. Rice v;as
not affected at 1,000 ppb. Grover (92) reported that the
effective dose (ED^q) v^hich affected 50 percent of sunflov/er
plants was not correlated to clay content v;hen soil
applications were used, but it was significantly related to
soil organic matter. High ED50 values were required v;hen
pH was lowered or raised above 6.5. The lowest concentrations
of picloram in ppm giving detectable symptoms in some of the more
sensitive plants are as follows: pinto beans 0.02, pole beans,
soybeans, safflower, and sunflower at 0.001 ppm (2^0).
Relatively low rates of Tordon may affect desirable plants,
thus care in application should be exercised to avoid spray
drift or contaniinatlon of Irrigation water.
At equivalent rates of application, the phytotoxic effect
of picloram may last longer than that of urea and triazine
herbicides when crops sensitive to picloram are planted
after its application. Included among the more sensitive
crops are legumes, tomato, cucumber, potato, cotton, safflower,
sunflovrer, lettuce, bucla<;heat, sugar beets, tobacco and
soybeans. However, the phytotoxic action may not persist as
long as for urea and triazine herbicides when lower rates
of picloram are used, or when crops tolerant to* picloram are
planted after application of the herbicide.
C. Translocation
Evidence indicates that picloram is readily translocated
throughout a plant and it is picked up both by the foliage
and the roots. Sharma et al. (201) reported that Canadian
thistle (Cirsium arrense (L) Scop.) readily adsorbed picloram
and translocated it in botVi the phloem and the xyleia. It
19
tended to accumulate in young growing leaves where a
substantial portion of it was retained. Small amounts of
picloram were exuded by the roots into the soil. Isensee
et al. (116) found that picloram was rapidly absorbed by
oats and soybeans, with substantial redistribution in the
plant and some exudation from the roots back into the culture
medium. Picloram uptake decreased with an increase in
pH from 3.5 to A. 5, but pH had little effect from A. 5 to 9.5.
Low concentrations of metabolic inhibitors (e.g. 2,A-dinitro-
phenol, sodium arsenite) stimulated picloram translocation
and high concentrations depressed it.
Tordon herbicide is absorbed and translocated readily by
both roots and tops of most plants. It is moved to all
parts of plants readily. In rapidly growing susceptible
plants, symptoms of leaf and stem tvjisting may be visible
in 1 to several hours after exposure. Later symptoms
include leaf cupping, pointed leaves and fruit and epinasty
similar to other growth regulator herbicides.
Tordon herbicide may be applied to plants as foliar sprays,
soil treatments or trunk injections. Best results on deep
rooted perennial broadlcaf v;eeds are obtained when sprays
are applied to the foliage before bloom and rain falls soon
aften^ard. Applications can be made at any tiiae of the year
v;hen action tli rough soil is expected. Kills will not be
effected, however, until the chemical is taken into the
root zone. Spot treatments with Tordon in cropland are
possible but food or feed crops should not be haT^/ested from
the treated area until residue tolerances have been established
for this use.
D. Persistence in soil, v;ater, or plants
In a review article on the movement and degradation of picloram,
Goring and Hamaker (239) noted that it is broken dovm in
plants, in the soil, and by pure cultures of microorganisms,
and it can be degradated by sunlight. There is evidence the
decomposition is most rapid in slightly acid soil. Leaching
through the soil accounts for loss of a major amount of
the picloram, especially in sandy soils in areas- of lilgh
rainfall. However, it may not be readily leached out of the
Lop A feet of heavy soils. Because of its low vapor pressure,
loss by volatilization is negligible. There is evidence that
only a small amount of picloram will be removed from an area
ill runoff water. Studies indicate that all of the picloram
applied to soils cannot be accounted for, and further studies
are needed to determine the fate of picloram in the environment (29).
20
r
1. Solis , Hamaker et al. (102) found chat the percent of
piclorani decomposition v;as generally greater at loxi/er
Initial concentrations. For practical purposes, half-order
kinetics were more useful and almost as accurate as
Michaelis-Menten kinetics for predicting the rate
of picloram decomposition in soils. Half-order kinetics
provide a useful relationship betX'/een the rate of
decomposition and concentration. Results also suggest
some correlation between soil organic matter content and
the rate of herbicide decomposition. This is not surprising
since other studies indicate that the maximum rate of
decomposition is related to the activity of the microbial
population which is in turn related to the amount of
organic matter present (239) . The proportion of ionized
to non-ionized picloram decreases with decreasing soil pH.
There is an increase in soil adsorption with decreasing
pH and increasing organic matter content (92) . Minimum
adsorption occurs in neutral or alkaline sandy soils
low in organic matter, and it increases with higher
amounts of hydrated iron and aluminum oxides (100) .
Hamaker et al. (241) estimated the rate of picloram
breakdown in different climatic regions in the U.S.A.
and determined that the half-order constants, Ki/2, vary
from fibout 0.2 in colder, dryer areas to 1.0 in hotter,
wetter areas. With initial rates of 1 oz. and 2 pounds
a.e. per acre, the time for decomposition to concentration
of 0.01 oz. per acre would take from 4.5 months to 4.6
years respectively, where the ^\f2 ^.2 and from 0.9
to 11.0 months where the is 1.0. These predicted
values were found to have good correlation with field data.
Based on plots in California, South Dakota, Kansas, and
Minnesota, the disappearance of picloram applied at rates
of 1.4 to 4.2 pounds per acre ranged from 58 to 90 percent
the first year and 78 to 100 percent the second year.
The estimated half-life of picloram ranged from 1 to
13 months.
Bovey and Scifres (36) reviewed the literature concerning
the residual characteristics of picloram in a grassland
ecosystem and noted that most investigators
agree that dissipation was accelerated at higher
temperatures. Picloram was least persistent in sandy
soils and loss is probably due to leaching. The soil
pH and percent clay content did not affect the rate of
decomposition v:hi?Le percent organic matter and moisture
content and temperature were important.
21
Bovey and Scifres described the novement and loss of
picloran through soil profiles in subhumid, tropical,
and seniarid sites. In vegetated, subhunid areas, picloram
at 2 pounds per acre disappeared from the top 2 feet of soil
within 12 v;eeks and an 8-pound rate v;as not detectable
in the top 2 feet a year after application. Only 10 to
25 percent of the applied picloran actually reached the soil
surface. In another test, usually less than 2 ppb of
picloram v;ere found at all levels down to 8 feet one
year after a 1-pound per acre application of tb»e K-salt. On
fallowed areas, soil texture, herbicide rate, and rainfall
governed the degree and rate of vertical picloran movement.
On vegetated tropical sites, only 5 ppb were detected
one year after treatment witli 9 pounds a.e. per acre.
On all such locations there was rapid rovement from the
top 12 inches of soil and leaching was the most important
means of picloram dissipation. The probability of
sufficient rainfall for leaching in a serdarid site is
obviously less than in a liumid one; here photodecomposition
is probably important. On slopes exceeding 3 to 4 percent,
lateral leacliing may be more important than available
information indicates, especially following lieav^' rainfall.
The leaching pattern of picloram esters and salts are
similar (56). vrnerc esters v/ere used, the uniiy Jrolyzed
esters were found in the top 5 cm of soil; only the acid
form was found below 5 cm. It was not possible to
distinguish between the acid and. salt formulations.
The salt form v;as not affected by temperature and it v.’as
loss subject to photodecomposition than tlie ester forri\.
Merkle et al. (146) found 15 to 25 percent of the picloram
still present in soils even after applications as low
as 0.5 pound per acre. The original soil moisture content
did not affect the depth of leaching.
Bovey and Scifre.s (3G) reported that little data is available
to substantiate microbial breakdov.Ti of picloram In soils.
Tliey suggested that resistance to microbial degradation
may account for its long persistence. Youngson ct al. (239)
studied the effect of 19 microorganism.s on the decomposition
of 1 ppm of picloran in nutrient cultures. Decomposition
was small, ranging from 0.2 to 1.2 percent and picloram
was not a preferred energy source by any of the test
microorganisms. Approximatelv 10,000 to 100,000
pounds of organic matter would be broken dovm to each pound
of picloram.
22
Markle ct al. (1A6) found that the effectiveness of
soil applications of picloram was reduced if extended
periods of hot, sunny weather follox'/ed which suggested that
photodecomposition might result in a loss of picloram
activity. Hall et al. (98) found that UV light caused
a 20 percent degradation- of picloram for each A8 hours of
exposure. Decarboxylation did not appear to be a major
pathway in photodecomposition. The possibility that
degradation v;as by a free radical mechanism v/as
considered plus the possibility of using inhibitors of
free radical reactions to prevent photodecompositiou.
Merkle et al . (1A6) found tliat photodecomposition of
picloram in petri dishes by UV light greatly exceeded
that which occurred in the field, which vjere 90 and 15
percent respectively.
h^J^ter. Norris (165) reported on the presence of residues of
summer-applied picloram in stream vjater in Oregon after the
first fall storms. In an area where 67 percent of a watershed
was sprayed in August, residues up to a maximum of 78 ppb
were detected after the initial 1 inch storm and they
decreased thereafter. No residues V7ere found after late
October or where only a small portion of a watershed was
treated. In a chaparral area in southern California after an
August application of 1, 2, and A pounds a.e. per acre of
picloriira, the first runoff water contained 0.1, 0.5,
and more than 0.5 ijpm of picloram respectively (90).
After ]-5 inches of rain, residues had dropped to 0.01, 0.03,
and 0.03 ppm of picloram.
Haas et al. (97) reported that water that collected in
ponds adjacent to treated areas contained picloram up
to 18A ppb v/hen runoff occurred within 2 v;ee]:s after
application. Maximum picloram concentration v;as onl}’
28 ppb if the first runoff did not occur until 6 v;eehs .
Picloram concentration in pond water decreased rapidly
the first 100 days down to a relatively stable concentration
of ca. 5 ppb. It was not found in detectable concentration
0 or 0.5 miles doimstream from an 80 acre area 5 months
after an application of ca. 1 pound a.e. per acre,
although the first runoff water contained up to 29 ppb.
No picloram contamination was found in well water up to
2 years after adjacent areas were treated \vlth ca. 1
pound a.e. per acre.
%
23
V60*iou3 studies cited by Bovey and Seif res C36)
indicated that water that runs off a treated area a
few days after picloram treatment contained up to l8U ppb
of picloram, but no residues were detected 6 months to
1 year later. However, the authors refer to a report
(53) where a maximum of 370 ppb of picloram in water from
an area treated 7 days before with 9 pounds per acre of
picloram. Since there was a possible 22-fold dilution
of picloram concentration in this test, the authors
warned that crop damage could result from irrigation
with water from treated watersheds. Picloram was present
only in trace amounts in 3 months and it was undetectable
within a year. Vegetative grow'th of sensitive crops
would probably not be reduced by single irrigation
with water containing 1 to U ppb of picloram, but a
concentration of 10 ppb or more could severely affect
some sensitive crop seedlings (36), Schneider et al. (192)
reported that a sand aquifer accidentally contaminated by
picloram would not be a hazard if the well was pumped soon
after contamination, but if primping was delayed several
weeks, herbicide recovery would no longer be practical.
3. Plants . Interception of picloram sprays by vegetation
would reduce the amount of picloram residue in the soil;
a dense stand of oak might intercept up to 90 percent of
the amount of picloram applied (1U7). The residual
level of picloram in or on grass rapidly decreased after
the initial deposit of liquid spray which amounted to
a maximum of up to 200 ppm for each pound applied per
acre (81). This decreased to less than 50 ppm in 2 weeks.
An average of 9I percent of the picloram wats gone by the
next growing season and ranged from 60 percent in
Montana to 100 percent in Georgia, Oklahana, and Texas.
Grass in the spring the following year after application
showed no residue to a maximum of 12 ppm/pound/acre.
No nonextractable residues (by normal extraction
procedure) were found. Plant residues from granular
formulations increased to a maximum at about 8 weeks after
application, and they were generally lower than those
found after foliar applications.
Baur and Bovey (15) found that grasses treated with
picloram up to 2 j>ounds per* acre contained an average of
2,650 ppb of fresh weiglit 1 month after treatment which
dropped to 10 ppb in 6 months. Bovey and Scifres (36)
referred to work in semiarid areas which indicated a
90 percent dissipation of picloram from grass 30 days
after treatment. However, root uptake accounted for a
delayed increase in picloram residue concentration.
Accumulations like this were not found in the more humid
areas where picloram was rapidly leached to the lover
part of the soil profile.
r
24
Residues of picloraa in voody plants in tropical areas
ranged from 31 to 6^k ppm immediately -after spraying
2 pounds a.e. per acre of pi dor am to less than 1 ppm
a month later (36). Live oak plants in suhhumid areas
dissipated 99 percent of the amount detected at 1 month,
6 months later. In semiarid areas (e.g. northwest Texas)
picloram was reduced by 99 percent within 30 days after
application to broadleaved species (199)« Leaves from
treated mesquite and chinnery oak increased the picloram
content of the surface litter at 60 days compared to
that 30 days after treatment.
E, Compatibility
Picloram has been formulated in various combinations with
several of the phenoxy herbicides (see section I-E). Alley (5)
reported that 2,U-D used in combination with low rates of picloram
gave better control of deep-rooted perennial weeds with lower
rates of picloram than when it waa used alone. Interactions of
picloram and phenoxy herbicides may be either additive or
competitive based on plant response, but a certain amount of
picloram was replaceable by phenoxies without reducing
phytotoxicity (122). Meyer and Riley (150) found that mixing
picloram with phenoxy herbicides , diesel oil, or ammonium
thiocyannate did not increase whitebush control.
IV. Environmental impact
Some reference to the effect of picloram on plants and animals are
made in previous sections.
A. Effects on nontarget organisms
In a review article, Bovey and Scifres (36) concluded that
picloram residues do not appear harmful to mammals, fish,
birds, or insects which inhabit the ecosystem. Picloram passes
rapidly, intact through mammalian systems without apparent
detrimental effects even at relatively high concentrations.
Biological significance is related primarily to plant life.
Goring et €l1. (88) reported on the effect of picloran on
microorganisms. Tests were run ^ vitro in both liquid and agar
mediums which contained concentrations of picloram from 0 to
1,000 ppm. After 2 to 3 days growth and numbers were compared
visually. Tests were als^o r\in in vivo on 50-gr. quantities of
air dry soil treated with picloram at 0 to 1,000 ppm and incubated
for 1 day to 1 month. Colonies were counted after 4 days and
compared to those in soil to which only water was added. The
results of studies with 46 different soil microorganisms
indicated that concentrations up to 1,000 ppm did not retard the
growth and development of any of the organisms except Thiobacillus
thlooxidans . Nitrification of ammonium to nitrite while
25
partially inhibited at 1,000 ppm a.e, was not inhibited at
100 ppm; nitrification of nitrite to nitrate in v'joil was not
inhibited at 1,000 ppm. Tu end Bollen (220) studied the effect
of picloram on microorganisms in three Oregon soils and they
also found that picloram had little obvious effect at concentrations
up to 1,000 ppm on armionification, nitrification, sulfur
oxidation, and organic matter decomposition.
Eeference to the effect of picloram on fish, birds, and other
animals was made in section '’ill- A'*. McCollester and Leng (1^3)
estimated the acceptable daily intake of picloram for man, based
on extrapolation of long and short-term toxicity studies in
laboratory animals.. Based on the procedures established by
the Joint FAO/WHO Expert Committee on Food Additives and employing
a 100-fold safety margin, the acceptable daily intake of picloram
for man is calculated to be 1.5 mg/kg of body weight per day.
Assuming that a person is in the top 10 percent of consumers
whose food consumption is 1.5 to 3.5 times the mean for broad
groups in the United States, a person would consume only 0.1 mg
per day from meat of animals grazed continuously on grasses
containing 200 to ^400 ppm of picloram. This is only a fraction of
the 90 mg/day that a 130 pound man could safely consvime, and it
represents a safety margin of 90,000 to 1 compared to the no ill
effect level demonstrated in laboratory animals.
B. Residues in or on food or feed or entering the food chain
Reference to residues and persistence of picloram in soil, water,
and plants was made in section "III-D". MacLean and Davidson
( ) who referred to the toxi logical work by Palmer and Radeleff
(167) noted that assuming a given amount of . forage yield, forage
consumption, and that all chemical applied sticks to the vegetation,
a maximum dosage possible would be 7 mg/kg for each pound per
acre of herbicide applied. Therefore, the maximum dosage that
cattle might ingest if fed on vegetation immediately after
spraying 4 pounds per acre of picloram would be 28 mg/kg.
Work by Kutschinski (12^*) on residues in milk from cows fed daily
rations containing picloram at rates up to 1,000 ppm, equivalent
to 18 mg/kg/day for 2 weeks, showed residues from 0.05 to 2.0 ppm.
The residue levels dropped to less than 0.02 ppm within 2 to 3
days after withdrawal. In a similar test, tissue of steers fed
up to 1,600 ppm in their total diet (equivalent to 23 mg/kg/day)
reached a maximum in the blood after 3 days of feeding and
rapidlj' declined after withdrawal (125). During this time, the
residues were ^ess than 0.05 to 5.0 ppm in muscle and fat, 0.1
to 2.0 ppm in blood and liver, and 2 to I8 ppm in kidney. They
decreased to less than 0.1 in kidney and less than 0.05 ppm in
other tissue 3 days after withdrawal. Concentrations of 200 to
^00 ppm of 'picloram were required in the diet of cattle to
produce residues of 0.05 to 1.0 ppm in edible tissue such as fat
and muscle.
26
BIBLIOGRAPHY OF PICLORAM REFERENCES
(Most Weed Society Proceedings and governmental publications have not been included)
1. Agbakoba, Chuma S.O. and J.R. Goodin. 1969. Effect of stage of growth
of field bindweed on absorption and translocation of ^^C-labeled 2,4-D
and picloram. Weed Sci. 17(4); 436-438.
2. Agbakoba, Chuma S.O. and J.R. Goodin. 1970. Absorption and trems location
of 2^C-labeled 2,4-D and picloram in field bindweed. Weed Science
18(1); 168-170.
3. Agbakoba, Chuma S.O. and J.R. Goodin. 1970. Picloram enhances
2,4-D movement in field bindweed. Weed Science l8(l): 19-21.
4. Alley, H.P. 1965* A promising future for the control of perennial
weeds. Down to Earth 21 (1-2); 8-10.
5. Alley, H.P. 1967. Some observations on tordon-2,4-D herbicide
combinations. Down to Efirth 23(l): 2, 35-36.
6. Alley, H.P. and G.A. Lee. 1966. Crop tolerance to picloram residuel.
West. Weed Contr. Conf. Res. Rep. p. 102
7. Aly, O.M. and S.D. Faust. 1964. Studies on the fate of 2,4-D and
ester derivatives in natviral surface water. J. Agr. Food Chem.
12; 541-546.
8. Ai’nold, W.R., P. W, Santelmann, and J.Q. Lynd. 1966. Picloram and
2,4-D effects with Aspergillus niger proliferation. Weeds l4; 89-90.
9. Arvik, J.H., D.L. Willson, and L.C. Darlington. 1971* Response of
soil algae to picloram - 2,4-D mixtures. Weed Science 3.9(3): 276-278.
10. Ashton, F.M. , D. Penner, and S. Hoffman. 1968. Effect of several
herbicides on proteolytic activity of squash seedlings. Weed Sci.
16(2): 169-171
11. Bachelard, E.P. and R.D. Ayling. 1971. The effect of picloram and
2,4-D on plant cell membranes. Weed Res. ll(l): 31-36.
12. Bachelard, E.P. and V.H. Boughton. 1967. The effect of weedicides
on growth of radiata pine seedlings. Aust. Forest 31(3): 211-220.
13. Bachelard, E.P. and R. Sands. I966. Effect of weedicides on starch
content and coppicing of cut stumps of manna gum. Aust. Forest 32(l): 49-54.
14. Balayannis, P.G. , M.S. Smith, and R.L. Wain, 1965* Studies on plant
growth regulating substances. 30C. The metabolism of V-(2,4,5-trichloro-
phenoxy) butyric acid in what and pea stem tissues. Annals of
Applied Biology 55: 261-265 .
27
15. Baur, J.R. and R,W, Bovey. 1969. Distribution of root-absorbed
picloram. Wed Sci. ITC^i): 52^528.
16. Bavir, J.R. and R.W, Bovey. 1970, The uptake of picloram by potato
tuber tissue. Weed Science l8(l); 22-2U, A
17. Baur, J.R., R.W. Bovey, R.D. Baker, and I, Riley. 1971. Absorption
end penetration of picloram and 2,l4,5-T into detached live oak leaves.
Weed Science 19(2); 138-l4l,
18. Baur, J.R., R.W. Bovey, and C.R. Benedict, 1970. Effect of picloram on
growth and protein levels in herbaceous plants. Agron. J. 62:627-630.
19. Baur, J.R., R.W. Bovey, and J.D. Smith. 1969. Herbicide concentrations
in live oadc treated with mixtures of picloram and 2,U,5-T. Weed Sci,
17(^); 567-570.
20. Baur, J.R. and P.W. Morgan. I969 Effects of picloram and ethylene
on leaf movement in Huisache and Mesquite seedlings. Plant Physiol.
41i(6): 831-838.
21. Beger, H.W. 1970. Treatment of bloodwood (Fucalypus dichromophloia)
with piclor am/2, and the pentrant dimethyl sulphoxide. Queens J. Agar.
Aaim. Sci. 27(l): 17-20.
22. Biswas, P.K, and R.L. Haynes. 1970. Herbicidal effects on water
uptake of seeds of selected weed species. Physiol. Plant 23(3); 5^'3-590.
23. Bjerke, E.L. , A.H, Kutschinski, and J. C. Ramsey. 1967. Determination
of residues of U-amino-3 , 5 ,6-trichloropicolinic acid in cereal
grains by gas chromatography. J. Agr. Food Chem. 15: U69-^73.
2^, Bovey, R.W. I969. Effects of foliar ly applied desiccants on selected
species under tropical environment. Weed Sci. 17(l): 79-83.,
25. Bovey, R.W. , J. R. Baur, and H.L. Morton. 1970. Control of huisache and
associated woody species in South Texas. J. Range Menage. 23:^7-50.
26. Bovey, R.W. , F.S. Davis, and M.G. Merkle. 1967. Distribution of
picloram in Huisache after foliar and soil applications. Weeds
15(3): 245-21+9 .
27. Bovey, R.W. and J. D. Diaz-Colon. I969. Effect of simulated rainfall
on herbicide performance. Weed Sci. 17(2); I5U-I57.
28. Bovey, R.W. , C.C. Dowler, and J, C. Diaz-Colon. I969. Response of
tropical vegetation to herbicides. Weed Sci. 17(3): 285-290,
29. Bovey, R.W. , C.C. Dowler, and M.G. Merkle. 1969. The persistence
and movement of picloram in Texas and Puerto Rican soils. Pest.
Monit. J. 3:177-181.
28
4
^0. Bovey, R.W. , M.L. Ketchersid, and M.G. Merkle, 1970, Ccmparison of
salt and ester formulations of picloram. Weed Science l8(^); UU7-H51.
31. Bovey, R.W. , R.E. Meyer, F.S. Davis, M.G. Merkle, ‘and H.L. Morton,
1967. Control of woody and herbaceous vegetation with soil sterilanta.
Weeds 15(i*); 327-330.
32. Bovey, R.W. and F.R. Miller. I969. Effect of activated carbon on
the phytotoxicity of herbicides in a tropical soil. Weed Sci.
17(2): 189-192.
33. Bovey, R.W. , F.R. Miller, and J. Diaz-Colon. I968. Growth of crops
in soils after herbicidal treatments for binish control in the tropics.
Agron. J. 60:678-679.
3k. Bovey, R.W. , H.L. Morton, and J.R. Baur. 1969. Control of live oak
by herbicides applied at various rates and dates. Weed Sci.
17(3): 373-376.
35. Bovey, R.W. H.L. Morton, J.R. Baur, J.D. Diaz-Colon, C.C. Dowler,
and S.K. Lehman. 1969 . Granular herbicides for woody plant control.
Weed Sci. 17(4); 538-5^1.
36. Bovey, R.W. and C.J. Scifres. 1971. Residual characteristics of
picloram in grassland ecosystems. Tex. Agr. Exp. Sta. B-1111. 2k p.
37. Brender, E.V. and E.L. Moyer. I965. Further progress in the control
of Kudzu. Down to Earch 20(4): 16-I7.
33. Burnside, O.C. , G.A. Wicks, and C.R. Fenster. 1971. Dissipation of
dicamba, picloram, and 2,3,6-TBA across Nebraska. Weed Science
19 (i+): 323-325.
39. Butts, J.S. and S.C. Fang. 1956. Tracer studies on the mechanism
of action of hormonal herbicides. U.S. Atomic Energy Rpt. TID 7512,
p. 209-214.
40. Byrd, B.C. and F.A. Nyman, Jr. I966. Progress report on highway
vegetation control experiments using tordon 101 mixture and norbak
particulating agent. Down to Earth 22(l): 28-31.
41. Ceirvell, K.L. 1968. Tordon effective in red maple tree injection
studies. Down to Earth 24(3): 17-18.
42. Chang, In-Kook and C.L. Foy. 1971. Effects of picloram on
germination and seedling development of four species. Weed Science
19(1): 58-64.
43. Cheing, In-Kook and C.L. Foy. 1971. Effects of picloram on mitochondrial
swelling and ATPase. Weed Science 19(l): 5^ — 57.
44. Cheng, H.H. I969. Extraction and colorimetric determination of
picloram in soil. J. Agr. Food Chem. 17(6): 1174-1177.
29
45. Coble, H.D. , R.P. Upchurch, and J,A. Keaton, 1969. Influence of
time and method of application on turkey oak response to picloram
plus 2,4-D, Weed Sci. 17(l): 67-91.
46. Coble, H.D. , R.P. Upchurch, and J.A. Keaton. 1969. Response of
voody species to 2,4-D, 2,4, 5-T, and picloram as a fiinction of treatment
method. Weed Sci. 17(l); 40-46.
47. Corbin, F.T. and R.P. Upchurch. 1967. Influence of pH on detoxication
of herbicides in soil. Weeds 15(4); 370-377.
48. Corbin, F.T. , R.P. Upchurch, and F.L. Selman. 1971. Influence of pH
on the phytotoxicity of herbicides in soil. Weed Science 19(3): 233-239*
49. Corns, W.G. I967. Effects of added surfactant on toxicity of picloram,
2,4-D and 2,4,5-T to Pomlus tremuloides Michx, eind P. balsamifera L. saplings.
Can. J. Plant Sci. 47(6): 711-712.
50. Couch, R.W. and D.E. Davis. 19 66. Kudzu control with tor don. Down
to Earth 22(3) : 2.
51. Cozeirt, E.R. I965. Reclamation of Macartney rose infested fence rows
with tordon herbicide. Down to Earch 21 (1-2): 15-18.
52. Dana, M.N. I967. Brush control in sphagnum moss bogs. Weeds 15(4); 38O-381.
53. Davis, E.A., P.A. Ingebo and C.P. Pase. I968. Effect of a watershed
treatment with picloram on water quality. USDA, Forest Service
Research Note RM-100. p.4.
54. Davis, F.S., R.W. Bovey, and M.G. Merkle. I968. The role of light,
concentration, and species in foliai* uptake of herbicides in woody
plants. Forest Sci. l4: 16 4-169.
55. Dexter, A.G. , F.W. Slife, and H.S. Butler. 1971. Detoxification of
2,4-D by several plant species. Weed Science 19(6): 721-726.
56. Dickens, R. and G.A. Buchanan. 1971. Influence of time of herbicide
application on control of kudzu. Weed Science 19(6): 669-671.
57. Dos Santos, C.A. Lobato, and N. Grassl. 1970. Extermination of
"lieteiro" (Tabernaemontana fuchslaef olia D.C.) with herbicides.
Biologico (Sao Paulo) 36(10); 280-283.
58. Dowler, C.C. I969. A cucumber bioassay test for the soil residues of
certain herbicides. Weed Sci. 17(3): 309-310.
/
59. Dovrler, C.C., W. Forestier, and F.H. Tschirley. 1963. Effect and
persistence of herbicides applied to soil in Puerto Rican forests.
Weed Sci. l6(l): 45-50.
30
oO. 2owler» C,C. euad FtH. Tschirley. 1970, Evaluation of herbicides
applied to foliage of four tropical woody species. J, Agr,
Univ. P.R. 5^(^): 676-682,
61. Dowler, C.C. , F.H. Tschirley, R.W. Bovey, and H.L, Morton, 1970,
Effect of aerially- applied herbicides on Texas and Puerto Rico
forests. Weed Science l8(l): l64-l68,
62. Dubey, H.D. 1969. Effect of picloram, diuron, ametryne, and prometryne
on nitrification in some tropical soils. Soil Sci, Soc, American
Proc. 33(6): 893-896.
63. Edmond, D.B. and E.M. Wright. 196U. The effect of U-amino-3,5.6-
trichloropicolinic acid on ryegrass-white clover pastures. New Zeal.
J. Agr. Res. 7(i^): 770-773.
6ii. Egley, G.H. and J.E. Dale. 1970. Ethylene, 2-chloroethylphosphonic
acid and witchweed germination. Weed Science 18(5): 586-589«
65. Eisinger, W, and D.J. Moore. 19 65. Tordon a new synthetic growth
regulator. Proc. Indiana Acad. Sci. 75: 63 (Abstract only),
66. Elsinger, W.R. and D.J. Morre. 1971* Growth regulating properties
of picloram 4-amino-3,5»6-trichloropicolinic acid. Can. J. Bot.
U9(6); 889-897.
67. E*singer, W., D.J. Morx'e, and C.E. Hess. 1966. Promotion of plant
growth by tordon herbicide. Down to Earth 2l(U): 8-10.
68. Elwell, H.M. 1968. Winger elm control with picloram and 2,U,5“T with
and without additives. Weed Sci. l6(2): 131-133.
69. Fenster, C.R. , O.C. Burnside, and G.A. Wicks. I966. Comparison
of the residual effects of dicamba, picloram, and 2,3,6-TBA with
field beans (Phaseolus vulgaris L.). Proc. North Cent. Weed Cont.
Conf. 20:20
70. Ferguson, R.H. I965. Tordon controls range brush in New Zealand and
Australia. Down to Earth 2l(3): 18-21.
71. Finnis, J.M. 1967. The effect of tordon on vine maple. Down to Earth
22(U): 22-23.
72. Finnis, J.M. and J.D. Sund. 1970. Planting of Douglas-fir seedlings
following aerial application pf tordon 101 mixture herbicide. Down
to Earth 26(1): 10-11.
73. Fisher, D.A. , D.E. Bayer, and T.E. Weier. I968. Morphological
and anatomical effects of picloram on Ph^eolus vulgaris. Bot, Gaz.
129(1); 67-70.
31
7^. Fisher, C.E. S»D. Robison, G.O. Hoffman, C.H. Meadors, and B,T. Cross,
1970. Aerial application of chemicals for control of brush on
rangeland. Brush Research in Texas/1970, Texas ASsM Univ. , Texe^
Agr. Exp. Sta. , College Station, p. 5-H* PR-2801.
75. Fisher, D.E. , L.E. St. John, Jr., W.H. Gutermann, D.G. Wagner,
and D.J. Lisk. (Pesticide Residue Lab., Cornell Univ,, Ithaca, N.X., USA)
Fate of Banvel T, loxynii, tordon, and trifluorilin in the dairy cow.
J. Dairy Sci. 48(12): 1711-1715.
76. Fletcher, J.T. I968. The (pbytotoxic) effect of picloram on tomatoes
and cuciimbers. Weed Res. 8(2): 153-155.
77. Foote, L.E., D.L. Kill, and C. S. Williams. 1970. Canada thistle
control on roadsides. Down to Earch 26(2): 22-26.
78. Friesen, G. I965. Wild buckwheat control with tordon, Down to
Earch 20(4); 9-10.
79. Friesen, H.A., and D.A. Dew. 1966, (Exp. Farm, Can. Dep, Agr.,
Lacombe, Alberta Can.) The influence of temperature and soil
moistiire on the phytotoxicity of dicaroba, picloram, bromoxynil,
and 2,4-D ester. Can. J. Plant Sci. 46(6): 653-660,
80. Gantz, R.L. and L.E. Warren. I966. Wild buckwheat control in small
grain crops with tordon herbicide. Down to Earth 22(l): 13-15.
81. Getzenduner, M.E. , J.L. Herman, and Bart VanGlessen. I969. Residues
of 4-amino-3,5»6-trichloropicolinic acid in grass from application
of Tordon herbicides. Agr. and Food Chem, 17(6): 1251-1256.
82. Gibs On, J.W. I969. Weed control with repeated applications of tordon
herbicides. Down to Earch 25(3): 12-14.
83. Gibson, J. W. and J.B. Grumbles. 1970. Aerial application of herbicides
for control of whitebrush and associated species. Down to Earth
26(2): 1-4.
84. Goldschmidt, E.E. and B. Leshem. 1971. Style abscission in the
citron (Citrus medica L. ) and other citrus species: Morphology,
physiology and chemical control v^th picloram. Amer. J. Bot. 58(1): 14-23.
85. Goodin, J.R. and F.L.A. Becher. 1967. Picloram as an auxin
substitute in tissue culture. Plant Physiol. 42:523.
86. Goodin, J.R. and Wei-Chin Chang. 1969. A new selective bioassay
for tordon in water, Down to Earth 24(4): 4-5.
87. Goodin, J.R. L.S. Jordan, and W.H. Isom. 1967. Low rates of tordon
for field bindweed control, Down to Earth 22(4): 6-7.
88. Goring, C.A.I., J.D. Griffith, F.C. O'Melia, H.H. Scott, and C.R. Youngson.
1967. The effect of tordon on microorganisms and- soil hiological.
processes. Down to Earth 22ih): l4-17.
89. Goring, C.A.I., C.R. Youngson, and J.W. Hamaker. I965. Tordon
herbicide. . .disappearance from soils. Down to Earth 20(U): 3-5«
90. Green, Lisle R. 1970. Effect of picloram aind phenoxy herbicides in
small chaparral watersheds. Res. Progress Rpt., Western Soc, of
Weed Science, Sacramento, p. 2U-25.
91. Grover, R. I967. Studies on the degradation of l*-amino-3,5,6-
trichloropicolinic acid in soil. Weed Res. 7:8l-67«
92. Grover, R. 1968. Influence of soil properties on phytotoxicity
of 4-amino-3 ,5»6-trichloropicolinic acid (picloram). Weed Res. 8:226-232.
93. Grover, Rj-970. Influence of soil-moisture content on the bioactivity
of picloram. Weed Science l8(l); 110-111
9^. Grover, R. 1971 • Adsorption of picloram by soil colloids and various
other adsorbents. Weed Science 19(^+): 4l7-^l8.
95. Guazzelli, R.J. and G.P. Rios. I966. Herbicide test on Mata-Barata
(Andira sp.). Pesquis Agropecuar, Brasil 1: 329-332.
96. Haagsma, T. and E.E. Wiffen. 1966. Farm evaluation of tordon plus
phenoxy herbicide combination for weed control In spring wheat in
western Canada— 1965. Down to Earth 2l(i<); 22-23.
97* Haas, R.H. , C.J. Scifres , M.G. Merkle, R.R. Hahn, and G.O. Hoffman.
1971. Occurrence and persistence of picloram in natural water
resources. Weed Res. 11:54-62.
98. Hall, R.C., C.S. Giam, and M.G. Merkle. 1968. The photolytic
degradation of picloram. Weed Res. 8:292-297*
99. Hall, R.C., C.S. Giam, and M.G. Merkle. 1970. A new technique for
the determination of picloram and other herbicides containing
carboxylic acid and ester groups. Analytical Chem. 42: 423-425*
100. Hamaker, J.W., C.A.I. Goring, and C.R. Youngson. I966. Sorption
and leaching of 4-amino-3 ,5 ,6-trichloropicolinic acid in soils.
Adv. Chem. Ser. , 60:23-27.
101. Hamaker, J.W., H. Johnston, rIt. Martin, and C.T. Redemann. 1963.
A picolinic acid derivative: A plant growth regulator. Science,
M.Y. , 141-363.
102. Hamaker, J.W., C.R. Youngson, and C.A.I. Goring. 1968. Rate of
detoxification of 4-amino-3,5 »6-trichloropicolinic acid in soil.
Weed Res. 8:46-57*
33
103* Hauce, R.J. 1969« Further observations of the decomposition of
herbicides in soil. J. Sci. Food Agr, 20(3); lUU-145.
104, Hardy, J.L. I966. Effect of tordon herbicides on aquatic chain
organisms. Down to Earth 22(2): 11-13.
105» Harrigan, G. 1970. Chemicals answer northern Australian challenge.
Down to Earth 26(3): 16-I8.
106. Hart, G.L. I966. Control of poison oak on military reservations with
tordon. Down to Earth 22(3): 6-7.
107. Heikes, E.E. 1964. Tordon and other herbicides .. .field testing for
the control of deep-rooted perennial weeds in Colorado. Down to
Earth 20(3): 9-12.
108. Helling, C.S., D.D. Kaufman, and C.T. Dieter. 1971. Algae
bioassay detection of pesticide mobility in soils. Weed Science
19(6): 685-690.
109. Hemphill, D.D. I968. Perfonnance of vegetable crops on en area
treated with tordon herbicide. Down to Earth 24(l): 2, 24,
110. Herr, D.E., E.W. Stroube, and D.A. Ray, 1966. Effect of tordon
residues on agronomic crops, Down to Earth 21(4): 17-18,
111. Herr, D.E. , E.W. Stroube, and D.A. Ray. 1966. The movement and
persistence of picloram in soil. Weeds l4(3): 248-250.
112. Hoffman, G.O. I967. Controlling prickl^^pear in Texas. Down to
Earth 23(l): 9-12.
113. Hoffman, G.O. 1971. Practical use of tordon 225 mixture herbicide
on Texas rangelands. Down to Earth 27(2): 17-21.
114. Horton, R.F. and R.A. Fletcher. I968. Transport of auxin,
picloram, through petioles of bean and coleus and stem sections of
pea. Plant Physiol. 43(12): 2045-20 48.
115. Hixll, H.M. and H.L. Morton. 1971. Morphological response of two
mesquite varieties to 2,4, 5-T and picloram. Weed Science 19(6); 712-716.
116. Isensee, A.R. , G.E. Jones, and B.C. Turner. 1971. Root adsorption
and translocation of picloram by oats and soybeans. Weed Science 19(6): 727-731
117. Kef ford, N.P. and 0. H. Caso. I966. A potent auxin with unique
chemical structure — 4-amino-3,5»6-trichloropicolinic acid. Bot. Gaz,
127:159-163.
34
Il8, Kenaga, E.E. 1969« Tordon herbicides — evaluation oX safety to fish
and birds. Down to Earth 25(1): 5-9 •
^ 119. Klingman, G.C. and H. Guedez. 19^7 « Picloraa and its effect on
field-grown tobacco. Weeds 15(2): lU2-1^6.
120. Kozlowski, T.T. and Sasaki. 1968, Germination and morphology
of red pine seeds and seedlings in contact viT,n EPTC, EDEC, CDAA,
2,i*-D and picloram. Proc. Amer. Soc. Hort. Sci. 93:655-662.
121. Kozlowski, T.T. , S. Sasaki, and J.H. Torrie. 196?. Effects of
temperatiire on phytotoxicity of monuron, picloram, CDEC, EPTC, CDAA,
and sesone to young pine seedlings. Silva Fenn. l(3): 13-28.
122. Krawiec, S. and D.J. Morre. 1968. Interactions of tordon
herbicide applied in combinations. Down to Earth 2^(3); 7-10.
123. Kreps, L.B. and H.P. Alley. 1967. Histological abnormalities
induced by picloram on Canada thistle roots. Weeds 15(l): 56-59.
12k, Kutschinski, A.H. I969. Residues in milk from cows fed l4-amino-3,5»6-
trichloropicolinic acid. J. Agr. Food Chem. 17:288-290.
125. Kutschinski., A.H. and Van Riley. 1969. Residues in various tissues
of steers fed 4-amino-3,5,6-trichloropicolinic acid. J. Agr.
Food Chem. 17:263-287.
126. Laning, E.R., Jr. 1963. Tordon... for the control of deep-rooted
X>erennial herbaceious weeds in the Western States. Down to Earth
19(1): 3-5.
127. Lawson, H.M. 1965 . Chemical control of bracken fern in the British
Isles with tordon. Down to Earth 20(U): 13-15.
128. Lee, G.A. , A.K. Dobrenz, and H.P. Alley. 1967. Preliminauy
investigations of the effect of tordon and 2,^i-D on leaf and root
tissue of Canada thistle. Down to Earth 23(2): 21-23.
129. Lee, W.O. 1970. Effect of picloram on production and quality of
seed in several grasses. Weed Science l8(l); 171-173.
130. Leiderman, L. and N. Grassl. 1970. Chemical control of the equatic
plant aquape (water hyacinth) in the Rio Preto, municipality of Peruibe,
Sao PauJ.o. Biologico (Sao PaAlo) 36(6): 157-159.
131. Leonard, O.A. , C.E. Carlson, and D.E. Bayer. 1965* Studies on
the cut surface method. 11. Control of blue oak and madrone. Weeds
13(i*): 352-356.
132. Leonard, O.A. , R.K. Glenn, and D.E. Bayer. 1965. Studies on the
cut-surface method. I. Translocation in blue oak and madrone.
Weeds 13(U): 3^6-351.
♦
35
Ij3. Leonard, O.A., R.J. Weaver, and R.K. Glen, I967. Effect of 2,l4-D
and picloram on translocation of ^^C-assimilates in Vitis yinifera
L. Weed Res. 7(3); 208-219.
I3H. Lynn, G.E. I965. A review of toxicological information on tordon
herbicides. Down to Earth 20(4): 6-8.
135. MacRae, I.C. and M. Alexander. 1965- Microbial degradation of
selected herbicides in soil. J. Agr. Food Chem. 13:72-76.
136. Malhotra, S.S. 1966. Aberrations of the nucleic acid metabolism
of plants induced by 4-aniino-3,5»6-trichloropicolinic acid. Ph.D.
Diss., University of Illinois, Urbana, Illinois.
137* Malhotra, S.S. and J. B. Hanson. 1970. Picloram sensitivity and
nucleic acids in plants. Weed Science l8(l) : 1-4.
138. Mann, J.D. and M. Pu. 1968. Inhibition of lipid synthesis by
certain herbicides. Weed Sci. l6(2): 197-198.
139* Marquiss, R.Vf. 1971. Gambel oak control studies. Down to Earth
27(2): 22-24.
140. Martin, S.C., S.J. Shellhorn, and H.M. Hull. 1970. Emergence
of fourwing saltbush after spraying shrubs with picloram. Weed Science
18(3); 389^392.
141. McCarty, M.K. and C.J. Scifres. I968. Smooth bromegrass response
to herbicides as affected by time of application in relation to
nitrogen fertilization. Weed Sci. l6(4): 443-446.
142. McCai’ty, M.K. and C.J. Scifres. 1969. Herbicidal control of
western ironweed. Weed Sci, 17(l): 77-79-
143. McCollister, D.D. and M.L.Leng. I969. Toxicology of picloram
and safety evaluation of tordon herbicides. Down to Eai*th 25(2); 5-10.
144. Meikle, R.W. , E.A. Williams, and C.T. Redemann. 1965- The synthesis
of 4-amino-3,5»6-trichloropicolonic-carboxy C"^^ acid and its use in a
study of the metabolism of tordon herbicide in carbon dioxide
evolution from treated soil. l49th Amer. Chemical Soc. Mtg.,
Abstracts, Detroit, Mich. April 4-9, p. 19A.
145. Menzie, C.M. I966. Metabolism of pesticides. U.S. Fish and Wildlife
Service. Special Scientific Rpt. — ^Wildlife No. 96. Patuxent V/ildlife
Res. Center, Laurei, Maryland. 274 p.
146. iMerkle, M.G., R.W. Bovey , and F.S. Davis. 1967. Factors affecting
the persistence of picloram in soil. Agron. J. 59;4l3-4l4,
147. Merkle, M.G., R.W. Bovey, and R. Hall. I966. The determination
of picloram residues in soil using gas chromatography. Weeds l4(2); l6l~l64.
36
l48. M<rkle, M. G. and F. S. Davis. 1967. Effect of noisture stress on
absorption and movement of picloram and 2,U,5-T in beans. Weeds 15(l): 10-12.
1^9. Meyer, R.E. 1970. Picloram and 2,U,5-T influence on honey mesquite
morphology. Weed Science l8CU); 525-531.
150. Meyer, R.E. and T.E. Riley. 1969. Influence of picloram granules
and sprays on whitebrush. Weed Sci. 17(3): 293-295«
151. Mitich, L. W. 1966, Leafy spurge — a problem weed controlled by
tordon. Down to Earth 2l(U): 11-13.
152. Mitich. L.W. 1967. Control of leafy spurge, field bindweed and
western snowberry with tordon herbicide. Down to Eeirth 23(3): 8-11.
153. Moffat, R.W. 1968. Some factors affecting the disappearance of
tordon in soil. Down to Earth 23(4); 6-10.
154. Molberg, E.S. 1965 . Experiments with tordon for weed control in flax.
Down to Earth 20(4); 11-12.
155. Montaldi, E.R. 1970. Cynodon dactylon ; A possible cause of its
diageotropism. Rev invest agropecusir. Scr 2 Biol. Prod. Veg. 7(2); 67-87.
156. Moreland, D.E. , S.S. Malhotra, R.D. Gruenhagen, and E.H. Shokraii.
1969. Effects of herbicides on RNA and protein. Weed Sci. 17(4): 556-563.
157. Morgan, P.W. and J.R. Baur. 1970. Involvement of ethylene in
pi dor am-induced leaf movement responses. Plant Physiol. 46(5): 655-659
158. Morgan, P.W. , R.E. Meyer, and M.G. Merkle. I969. Chemical
stimulation of ethylene evolution and bud growth. Weed Sci.
17(3): 355-355.
159. Moseman, R.F. and W.A. Aue. 1970. Novel determination of picloram
by gas-liquid chromatography. Chromatogr. 49(3): 432-441.
160. Motooka, P.S., D.F. Saiki, D.L. Plucknett, O.R. Younge, and
R.E. Daehler. I967. Control of Hawaiian Jungle with aerially
applied herbicide. Down to Earth 23(l): 18-22.
161. Mounat, A., P. Schiltz, and F. Casamajour. I968. Effects of
picloram on tobacco. Seita Serv. Exploin Ind. Tabaca Allumettes
Ann. Dir. Etud. Equip. Sect. 2 5; 67-74.
162. Nalewaja, J.D. 1970. Reaction of wheat to picloram. Weed Science
18(2); 276-278.
163. Nalewaja, J.D. and R. E. Bothun. 1969* Response of flax to
postemergence herbicides. Crop Sci. 9(2); I6O-I62.
37
ib4. Nation, H,A. I96T. Report on tree control via injection with
tordon 101 mixture. Down to Earth 23(2); 24-27.
165. Norris, L.A. I969, herbicide runoff from forest lands sprayed in
summer. Res. Progress Rpt., Western Soc. of Weed Science, Las Vegas
p 24-26.
166. Norris, L.A. 1969. Degradation of several herbicides in red alder
forest floor material. Res. Progress Rpt., Western Soc. of Weed
Science, Las Vegas, p. 21-22
167. Palmer, J.S. and R.D. Radeleff. I969. The toxicity of some organic
herbicides to cattle, sheep, and chickens. USDA Prod, Res. Rpt. No. I06.
168. Perala, D.A. and C.S. Williams. 1970. Site preparation for conifers,
using herbicides and subsequent burning in a northern Minnesota
hardwood stand. Down to Earth 26(3); 5-8 •
169. Perry, P. W. and R. P. Upchurch. 1968. Growth analysis of red
maple and white ash seedlings treated with eight herbicides.
Weed Sci. l6(l): 32-37.
170. Peters, E.J. and S.A. Lowance. 199. Gains in Timothy forage from
goldenrod control with 2,4-D, 2,4-DB, and picloram. Weed Sci.
17(4): 476-474
171. Peters, E.J. and J.F. Stritzke. 1970. Control of persimmon with
various herbicides and methods of application. Weed Science l8(5): 572-575*
172. Plumb, T.R. 1968. Control of birush regrowth in southern California
with tordon and phenoxy herbicides. Down to Earth 24(3): 19-22.
173. Pliuab, T.R. 1971. Broadcast applications of herbicides to control
scrub oak regrowth. USDA, Forest Serv. Pacific Southwest Forest Sc Range
Experiment Sta. , Berkeley, Calif. Res. Note PSW-261, 4 p. , illus.
174. Pridham, A.M.S. and R.A. Schwartzbeck. I965. Tordon herbicide
for control of Japanese bamboo in the northeastern United States.
Down to Earth 2l(l-2); 21-22.
175. Rahman, A. and W.G. Corns. 1970. Response of winter rye to
applications of 2,4-D and picloram at various growth stages. Can.
J. Plant Sci. 50(5): 600-602.
176. Reber, L.J. , R.K. Miller, J.A. Tweedy, end J.D. Butler. 1971.
Berbicidal effects <^of picloram on bermudagrass . Weed Science 19(5): 521-524.
177. Redemann, C.T. 19^5. Fate of 4-amino-3,5»6-trichloropicolinic
enid in the rat. 150th Meeting, ACS, Atlantic City, Sept.
178. Redemann, C.T. I965. Fate of 4-amino-3,5 »6-trichloropicolinic
acid in the dog. 150th. Meeting, ACS, Atlantic City, Sept.
38
179. -Rederaonn, C.T., P.H. Hamilton, and C,R. Younger, 1965. The fate of
U-Miino-3 ,5 ,6-trichloropyridine-2 ,3 ,5 ,6-Cl^_2-carboxy-C^^ acid
in spring wheat. Abstjracts of the ll+9th Amer, Chemical Soc, Mtg.,
Detroit, Mich., April 4.-9: 20A-21A.
180. Redemann, C.T., R.W. Meikle, P. Hamilton, V.S. Banks, and C.R. Yovingson.
1968. The fate of ii-amino-3,5,6-trichloropicolinic acid in spring
wheat and soil. Bull. Env. Contamination and Toxicology 3(2): 80-82.
181. Reid, C.P.P. and W. Hurtt. I969. A rapid bioassay for stimultaneous
identification and quantitation of picloram in aqueous solution.
Weed Res. 9(2): 136-l4l.
182. Reid, C.P.P. and W. Hurtt. 1969 . Translocation and distribution of
picloram in bean plants associated with nastic movements. Plant Physiol.
4U(10): 1393-1396.
183. Reid, C.P.P. and W. Hurtt. 1970. Root permeability as affected by
picloram and other chemicals. Physiol. Plant 23(l): 12li-130.
I8U. Reimer, C.A., B.C. Byrd, and J.H. Davidson. 1966. An improved
helicopter system for the aerial application of sprays containing
tordon 101 mixture particulated with Morbedt. Down to Earth 22(l): 3-6,
185. Renney, A.J. and E.C. Hughes. 1969. Control of knapweed, Centaarea
species, in British Columbia with tordon herbicide. Down to Earth
2h{k): 6-8.
186. Robison, E.D. I967. Response of mesquite to 2,^,5-T, picloram, and
2,U,5-T picloram conbinations . Proc. So. Weed Sci. Soc. 20:199.
187. Saha, J.G. end L.A. Gadallah, 1967. Determination of the herbicide
tordon (4-amino-^ ,5 »6-trichloropicolinic acid) in soil by electron
capture gas chromatography. Ass. Office Anal. Chem. J. 50(3): 637-641.
188. Sargent, J.A. and G.E. Blackman. 1970. Studies on foliar penetration.
VI. Factors controlling the penetration of U-amino-3,5,6-trichloropicolinic
acid (picloram) into the leaves of Phaseolus vulgaris. J. Exp. Bot.
21(66): 219-227.
189. Sawamura, S. and W.T. Jackson. I968, Cytological studies in vivo
of picloram, pyriclor, trifluralin, 2,3,6-TBA, 2,3,5,6-TBA, and
nitretlin. Cytologia (Tokyo) 33(3/4): 545-554 (rec'd 1969).
190. Schiltz, P. 1969. » Effects of picloram on the organogenesis of some
Hicotianae. Seita Serv. Exploit Ind. Tabaes Allumettes Ann Dir Etud
Quip Sect. 2 6: I89-I98.
191. Schmutz, E.M. and D.E. Little. 1970. Effects of 2,4, 5-T and
picloram on broom snakeweed in Arizona. J. Range Manage. 23(5): 354-357.
39
Iy2. Schneider, A.D. , A.F. Wiese, 0,R. Jones, and A.C, Mathers. (1971).
Determining the fate of herbicides in the Ogallala Aquifer. Texas
Agr. Exp. Sta. B-1112, 15 p.
193. Schrank, A.R. I968. Growth and geotropic responses of Arena
coleoptiles to i*-amino-3 ,5 »6~trichloropicolinic acid. Physiol. Plant
21(2); 311+-322.
19^. Scifres, C. J. and R.W. Bovey. 1970. Differential responses of
sorghum varieties to picloram. Agron. J. 62:775-777.
195. Scifres, C.J., R.W, Bovey, and M.G. Merkle. 1972. Variation in
bioassay attributes as quantitative indicies of picloram in soils.
Weed Res. (In Press).
196. Scifres, C. J, , O.C. Burnside, and M.K. McCarty. 1969. Movement
and persistence of picloram in peisture soils of Nebraska, Weed Sci.
17(1*); 1*86-488.
197. Scifres, C. J. , R.R. Hahn, and J. H. Brock. 1971. Chemical control
as related to phenology of common broomweed. J. Range Manage
2^:370-373.
198. Scifres, C.J., R.R. Hahn, J. Diaz-Colon, and M.G. Merkle. 1971.
Picloram persistence in semiarid rangeland soils and water.
Weed Science 19(4); 381-384.
199. Scifres, C.J., R.R. Hahn, and M.G. Merkle, 1971. Dissipation of
picloram from vegetation of semi-arid rangelands. Weed Science
19(4); 329-331.
200. Scott, P.C. and R.O. Morris. 1970. Quantitative distribution and
metabolism of auxin herbicides in roots. Plant Physiol. 46(5) J 680-684.
201. Sharma, M.P. , F.Y. Chang, and W. H. Vander Born, 1971. Penetration
and translocation of picloram in Canada thistle. Weed Science
19(4): 349-355.
202. Sharma, M.P, and W,H, Vanden Bom, 1970, Foliar penetration of
picloram and 2,4-D in aspen and balsam poplar. Weed Science l8(l); 57-63.
203. Sharma, M.P, and W. H. Vanden Born. 1971. Effect of picloram on 1^
C02-fixation and translocation of 1^0 assimilates in Canada thistle,
soj'^bean and corn. Can, J. Bot. 49(l): 69-74.
204. Shellhorn, S.J. and H. M. Hull. 1971, A carrier for some water-soluble
herbicides. Weed Science 19(l): 102-106.
40
205. Shipman, R.D. 1971. Soil applied herbicides in the control of
temperate zone grasses, broadleaf veeds and woody plants. Final Report.
The Pennsylvania State University, University Park, Pennsylvania l6802.
Contract No. DAAA13-69-C-0035 with Fort Detrick, Frederick,
Maryland 21701. lUo p.
206. Sterrett, J.P, 1968. Response of oak and red maple to herbicides
applied with an injector. Weed Sci. 16(2): 159-l6o.
207. Sterrett, J.P, I969. Injection of red maple and hickory with
picloram, 2,4,-D and 2,i*,5-T. Down to Earth 25(2): 18-20.
208. Sterrett, J.P. I969. Injection of hardwoods with dlcamba, picloram,
and 2,U-D. J. Forest, 67(11): 820-821.
209. Swanson, C.R. and J.R, Baur. I969. Absorption and penetration
of picloram in potato tuber discs. Weed Sci, 17(3): 311-31U.
210. Swezey, A.W. and A. Montano. I968. Chemical brush control and
grass improvement in pastures in Central America. Down to Earth 24(l): 6-9.
211. The Dow Chemical Company. I966. Determination of residues of tordon
acid in wheat grain by gas chromatography. ACR 65. 3R. 11 p, illus. Feb. I4.
212. The Dow Chemical Company. 1966. Determination of residues of tordon
acid in wheat straw by gsn chromatography. ACR 66.5. 12p. illus. Maj*- 6.
213. The Dow Chemical Company. I967. Determination of residues of tordon
acid in bovine tissues by gas chromatography. ACR 67.2. 17 p illus. June 21,
21U, The Dow Chemical Company. 1967. Determination of residues of tordon
acid in milk by gas chromatograpny. ACR 67.3. 11 p. illus. June 22.
215. The Dow Chemical Company. 1968. Determination of ij-amino-3 ,5»6-
trichloropicolinic acid in water. ACR 68.II1. l6p. illus. Sept. 26.
216. The Dow Chemical Company. 1968. Residue determination method—
Gas chromatographic determination of residues of 4-amino-3 ,5*6-
trichloropicolinic acid in soil treated with tordon herbicide.
ACR 68.7. 13 p. illus. June 7*
217. Trichell, D.W. , H.L. iMorton, and M.G. Merkel. I968. Loss of herbicides
in rxinoff water. V7eed Sci. l6(4): UU7-47i9.
218 Tsay, Ruey-chyong, and F.M. Ashton . 1971. Effect of several
herbicides on dipeptidase activity of squeish cotyledons . Weed
Science 19(6): 682-684.
219. Tschirley, F.H. I967. Problems in woody plant control evaluation
in the tropics. Weeds 15(3): 233-237.
I
41
220. Tu, C.M. and W.B. Bollen. 1969. Effect of tordon herbicides on
microbial activities in three Willamette Valley soils. Down to Eeirth
25(2); 15-17.
221. Tueller, P. T. and R.A. Evans, 1969* Control of green rabbitbmsh
and big sagebrush with 2,^-D and picloram. Weed Sci. 17(2): 233-235.
222. Upchurch, R.P. , H.D. Coble, and J.A. Keaton. 1969. Rainfall
effects following herbicidal treatment of woody plants. Weed Sci,
17(1): 9M8.
223. Valentine, K,A, 1970, Creosotebush control with phenoxy herbicides,
picloram, and fuel oil in Southern New Mexico, N, Mex. Agr. Exp.
Sta. Bull 3-12.
224. Vonden Born, W.H. I965. The effect of dicamba and picloram on
quackgrass, bromegrass , and Kentucky bluegrass. Weeds 13(4): 309-312,
225. Van Schreven, D.A. , D. J. Linderbergh, and A. Koridon, 1970,
Effect of several herbicides on bacteria populations and activity
and the persistence of these herbicides in soil. Plant Soil 33(3): 513-532.
226. Vernie, F. , J. Lhoste, and A. Casanova. I966. (France). Trial
results with picloram for weed control in winter \fheat. Weed Res.
6(4) i 322-331.
227. Victoria, J,, A. Sanchez, and R. Barriga. 1970. Eradication of coconut
palms affected with red ring disease (Rhadinaphelenchus cocophilus
Cobb 1919 Goodey i960, Nematoda: Aphelenchoididae) , by tne use of
chemical substances. Rev inst. Colomb. Agropecuar 5(3): 185-197.
228. Warden, R.L. 1964. Tordon.., for the control of field bindweed and
Canada thistle in the North Central United States. Down to Earth
20(2): 6-10.
Watson, A.J. and M.G. Wiltse. 1963. Tordon... for brush control on
utility rights-of-way in the Eastern United States. Down to Earth
19(1): 11-14.
229. Wax, L.M. L.A. Knuth, and F.V/. Slife. 1969. Response of soybesms
to 2,4-D, dicamba and picloram. Weed Sci. 19(3): 388-393.
230. Weed Sci. Soc. Amer. 1967. Herbicides Handbook. W.F. Hiimphrey
Press, Inc,, Geneva, N.Y. 293 p.
231. Whipple, S.D. and K.P. Moeck. I968, Potential uses of Tordon
lOK pellets in forest management. Down to Earth 24(1); 13-17.
232. Whiting, F.L, and J, M. Lyons. 1971. A versatile tr act or -mounted
research spray system. Weed Science 19(6)): 743-745.
233. i/icks, G.A. , C.R. Fenster, and O.C, Burnside. 1969. Selective
control of plains priiikljipeGr in rangeland with herbicides ,
Weed Sci. 17C^): i^oS-Ull.
234. Wiese, A.F., J. Gibson^ and D. Lavake. I967. Controlling large
field bindweed infestations with repeated applications of tordon.
Down to Earth 23(2): 2, 37-39.
235. Wilson, J.H. I967. A bio-assay of Tordon solutions. Rhodesia
Zambia Malawi J. Agi . Res. 5(3): 307-308.
236. Wilson, J.H. 1967. The effects of basal injections of Tordon on
some central African indigenous trees. Rhodesia Zambia Malawi
J. Agr. Res. 5(3): 301-303.
237. Woolson, E.A. and C.I. Harris. 1967. Methylation of herbicides
for gas chromatographic determination. Weeds 15(2): 168-170.
238. Young, N.D. 1968. Tordon for eucalyptus control — a tool for laud
development in Australia. Down to Earth 2i*(3): 2-6.
239. Youngson, C.R., C.A. I. Goring, R.W. Meikle, K.H. Scott, and J. D.
Griffith. 1967. Factors influencing the decomposition of tordon
herbicide in soils. Down to Earth 23(2): 3-11.
2U0. Goring, C.A. I. and J.W. Hamsiker. 1971. A Reviev;. . .The degradation
and movement of picloram in soil and water. Down to Earth 27(l): 12-15.
24l. Hamaker, J.W., C.R. Youngson, and C.A. I. Goring. 1967. Prediction
of the persistence and activity of Tordon herbicide in soils under
field conditions. Down to Earth 23(2): 30-36.
43
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REPORT
ON
BACKGROUND INFORMATION
FOR
THE PHENOXY HERBICIDES
2,A-D - 2,A.5-T - 2»A.5-TP
COMMITTEE MEMBERS;
Dr. L. A. Norris
P.N.W.
Dr. H. Gratkowski
P.N.W.
C. Graham
P.N.W.
W. F. Currier,
R-3
Chairman
TABLE OF CONTENTS
Page
Section I General Information 1
Common Names
Chemical Names
Registered Uses
Formulations and Manufacturers 3
Dilutions and Formulations 8
Rates and Methods of Application 10
Tolerance and Safety 14
References for Section I 16
Section II Toxicity Data and Physical Properties 19
Acute Toxicity 19
Chronic Toxicity 23
Teratogens 26
Mutagens 26
Carcinogens 26
Physical Properties 31
References to Section II 34
Section III Metabolism 38
Metabolism of 2,4-D 38
Metabolism of 2,4,5-T 44
Metabolism of 2,4,5-TP 45
References to Section III 48
Section IV Efficacy Data Under Field and Laboratory
Conditions 63
Effectiveness for Intended Purpose 53
Phytotoxicity 64
Translocation with Plants Treated 78
Compatibility 81
References for Section IV 83
Section V Residues ; 85
In Soil 85
In Water 89
In Plants 93
In Air 100
In Animals 102
In Food 106
References to Section V HO
TABLE OF CONTENTS
(Continued)
Section VI Environmental Impacts of the Phenoxy
Compounds 2.4-D, 2,4,5-T, and 2,4,5-TP 120
Hazards to Man 120
Hazards to Animals (Domestic and Laboratory) 127
Hazards to Vegetation (Indirect Effects) 137
Hazards to Insects 142
Hazards to Soil Fauna 144
Hazards to Aquatic Organisms 145
Hazards to Wildlife 154
RReferences to Section VI 156
FOREWORD
The task of gathering and assembling background information on the three
phenoxy herbicides (2,A-D, 2,4,5-T and 2,4,5-TP) becomes rather formidable.
This group of herbicides have been successfully used over a wide spectrum
since the late 1940' s. There is probably more knovm and more been written
about this group of compounds than any other group.
For these reasons, the Committee established some ground rules:
1. Only the formulations which are recommended for range and forestry
use were considered. There are hundreds of formulations which could be
listed but would serve no useful purpose in the work of the Forest Service.
2. The three phenoxys 2,4-D, 2,4,5-T and 2,4,5-TP are included in
one report. The three compounds are so similar in many respects and most
of the literature refers to two and sometimes all three in regard to
environmental impacts and residues. Much duplication was avoided in the
approach the committee followed.
When necessary, detailed information is included on each herbicide.
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PHENOXY HERBICIDES
Section I
I. General Information
The phenoxy herbicides 2,4-D 2,4-dichlorophenoxyacetic acid; 2,4,5-T,
2,4 ,5-trichlorophenoxyacetic acid; silvex, 2-(2,4,5 trichlorophenoxy)
propionic acid are registered by the Environmental Protection Agency
for use on forest and range land and on utility right-of-ways. 2,4-D
is most widely used to control herbaceous weeds on agriculture crop
land, and is registered for use on orchards, vegetable fields, berries,
vineyards, grain and hay crops, fallow land and pastures. 2,4-D
along with 2,4,5-T and Silvex, is also a valuable herbicide for
controlling many woody plants on forest and rangeland. The label
details all the registered uses. If a use is not on the label, it
is not registered for that use.
At the present time the pure acid of the phenoxys are almost never
used as herbicides. In the past they found limited use when formulated
as an emulsifiable acid. The earliest widespread use of these chemicals
was an inorganic salts of the acids. These formulations proved to be
of limited value and have generally gone out of use, although some
sodium salt of 2,4-D is still used in general agriculture on certain
crops .
-1-
The water soluble and soil soluble amine sales account for less than
10 percent of total use of Phenoxy herbicides for forestry and range
purposes. Amines are. less volatile than the ester forms of these
herbicides and are used where the vapors of the esters could cause
damage to nearby susceptible species. Water-soluble amines are
usually used for cut surface or injection into individual stems.
This treatment is highly selective and safe, but is expensive in
time and labor. However, the method is justified where values are
high and there are relatively few (not more than 200) stems per acre.
If the number of stems is high, an oil-soluble ester can be used in
011 and is applied as a basal spray without bark incision. This
method is less effective and usually gives unsatisfactory control
except upon highly susceptible thin-barked plants especially during
the growing season. The oil-soluble esters are usually more satis-
factorily used as basal sprays. Oil-soluble amines can be used as
foliage sprays upon susceptible species where the volatile vapors
of even low volatile esters of 2,A-D may be a hazard to nearby
susceptible crops or plants.
Esters of the phenoxy herbicides may be either high volatile or
low volatile depending upon the length of the carbon chain of the
alcohol used to formulate the herbicide. Low volatile esters are
usually used in foliage sprays and provide satisfactory results
on a wide spectrum of species. High volatile esters are not
recommended for use on forest and rangeland because volatile
vapors may damage nearby non-target species.
-2-
At the present time, low volatile esters are used on at least 80
to 90 percent of all forest and range Improvement spray projects.
Formulations
The following list contains formulations which are recommended
for use on range and timber areas. The label of any chemical
container should be studied carefully, and the Information relied
upon and adhered to. This Information Is derived from much
research and Is part of the labeling and registration process
for herbicides which Is carefully regulated by federal and state
agencies. Some typical forms of phenoxy herbicides are:
A. Esters
1. Low volatile
a. Propylene glycol butyl ether
b. Butoxy ethauol
c. Isooctyl
2. High volatile
a. Isopropyl
b. Butyl, n-Butly and Isobutyl
c. Ethyl
B. Amines
1. Water soluble
a. Dimethyl amine
b. Trlethanol amine
c. Trllsoproponol amine
-3-
2. Oil soluble
a. Dodecyl amine
b . Tetradecyl amine
c. N-oley 1-1, 3, -propylene diamine
C. Parent Acid
D. Inorganic salts
1. Sodium
2. Potassium
3. Lithium
4 . Ammonium
-4-
Table 1 Trade names, chemical formulations, and manufacturers of products containing two or more
pounds of acid equivalent (a.e.) per gallon of product.
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-5-
Table II, Trade names, chemical formulations and manufacturers of
products containing two or more pounds acid equivalent
(a.e.) per gallon of product.
2,4.5-TP (Silvex)
MANUFACTURER TRADE NAME FORMULATION STRENGTH
Diamond Shamrock
Crop Rider
Isooctyl ester
A
lbs.
a.e. /Gal.
Dow
Kuron
Propylene glycol
butyl ester
A
lbs.
a.e. /Gal
Hercules
Silvl Rhap
2 Ethylhexyl ester
A
lbs.
a.e. /Gal .
Afflchem
Veedone
Butoxyethanol ester
A
lbs.
a.e. /Gal.
Rhodia
Chipman
Low volatile ester
A
lbs.
a.e. /Gal.
Miller
Sllvlcide
Potassium Salt
A
lbs.
a.e. /Gal.
-6-
(
Table III. Trade names, chemical formulations and manufacture of
products containing two or more pounds acid equivalent
(a.e.) per gallon of product.
2,4,D (Low Volatile)
MANUFACTURER
TRADE NAME
FORMULATION
STRENGTH
Diamond
Crop Rider
Isooctyl ester
4-6 lbs. a.e. /Gal.
Monsanto
Field Clean
Isooctyl ester
6 lbs. a.e. /Gal.
Chevron Chem.
Ortho
Isooctyl ester
4 lbs. a.e. /Gal.
Stauffer
Stauffer 2,4-D
Isooctyl ester
4 lbs. a.e. /Gal.
Rhodla
Chipman
Isooctyl ester
4-6 lbs. a.e. /Gal.
Dow
Esteron 99
Propylene glycol
butyl ester
4-6 lbs. a.e. /Gal.
Hercules
Weed Rhap
Ethylhexyl ester
4 lbs. a.e. /Gal.
Monsanto
Amine Weed Killer
Dimethyl amine
4 lbs. a.e. /Gal.
Miller Chem.
Hormotox
Dimethyl amine
4 lbs. a.e. /Gal.
Diamond
Crop Rider
Dimethyl amine
4-6 lbs. a.e. /Gal.
Chipman
Chipman
Amine No. 4 —
Amine No . 6
Dimethyl amine
If If
4-6 lbs. a.e. /Gal.
Chevron Chem.
Ortho
Dimethyl amine
4 lbs. a.e. /Gal.
Stauffer
—
Dimethyl amine
4 lbs. a.e. /Gal.
Diamond
Dacamine
N-oley 1-1 , 3-propylen-
diamine 4-6 lbs. a.e. /Gal.
Dilutions of Formulation for Use
Hormone type herbicides are highly active in a biological sense, there-
fore very small amounts are required to obtain desired results. For this
reason they are always diluted with a carrier to obtain the desired
distribution over the sprayed area and coverage of the spray droplets
over the leaf and stem surfaces. An equal volume of large droplets
cannot be substituted for the same volume composed of a large number of
small droplets. For example, 100 small droplets on a leaf may be equal
to 1/lOth the total volume of one large droplet. The combined effect of
the small droplets, although containing only 1/lOth as much spray, may
be many times more than the effect of the one large droplet. About 75
droplets per square inch, regardless of their size, are required for
a satisfactory effect of phenoxy hormone type herbicides (Behrens 1957).
Droplets should not be reduced in size too much however, since the
probability of drift Increases with decreasing droplet size. About 200-
300 microns volume mean diameter (VMD) is about the smallest droplet
that can be used without excessive drift hazard (Akesson, Wllce, and
Tates 1971). Their recommendation is 450 micron VMD for aircraft spraying.
Total gallonage per acre must be Increased to maintain the necessary
number of droplets per square inch if droplet sizes exceed 800 microns
VMD.
Individual stem treatments can be made with the undiluted concentrate,
however, they are usueilly diluted with water or diesel oil to reduce
the amount of chemical used. Carriers or dilutents are usually used
u
-8-
for foliar and other broadcast applications. The most common carriers
for foliar applications are diesel oil, diesel oil-water emulsions,
and water. Manufacturer's labels list recommended carriers and specific
mixing directions and should always be read carefully and followed.
Water is used with water-soluble amines and with emulsifiable acids
and esters to form emulsions. Water carriers are usually used early
in the season before leaf cuticles thicken. Older plants with thin
cuticles may also be sprayed with water dilutents.
Oil-water emulsions (1/2 to 1 gpa of oil) are usually considered to be
better than a straight water carrier, and are as effective and are
usually cheaper than a straight oil carrier. If large amounts of
clean water have to be transported long distances, they sometimes can
become more expensive than lesser amounts of diesel oil. Lower volumes
of sprays using diesel oil dilutents can often be used with equal
satisfaction as higher volumes of water-oil emulsion sprays. Oil
dilutents have lower surface tensions than water and therefore
dispurse and spread better which tends to make them more effective
carriers than water. Caution should be used when exceeding 5 gallons
of diesel oil per acre, for the oil itself is somewhat phytotoxic and
may kill and dessicate tissue of the leaves, thus cutting down or
eliminating herbicide absorption.
-9-
Rate and Method of Application
There are two basic methods of herbicide application. (1) Broadcast and
(2) individual plant treatment. These may be further divided as follows:
A. Broadcast spraying
1. Aerial spraying
a. Helicopter
b. Fixed wing aircraft
2. Ground rig spraying
a. Boom spraying
b. Broadjet
c. Mist blower
d. High volume-hand gun
B. Individual plant treatment
1. Foliage spraying
a . Hand gun
(1) Power sprayer (may be high volume or low volume per
acre depending upon plant numbers and volume needed
for adequate coverage)
(2) Backpack sprayer (low volume per acre, few small plants)
b. Backpack mist blower - may be broadcast spraying if plant
numbers are high.
-10-
2.
Stem treatments
a. Injections
b. Frills
c. Stem sprays
3. Stump treatments.
Broadcast spraying is aimed at covering the foliage of all the plants
on the target area with an adequate amount of herbicide to bring about
the desired results. Broadcast spraying is usually done at rather low
volumes of 3 to 20 gallons of carrier per acre. High volume ground
sprays, 100 to 200 gpa with a truck-mounted power sprayer and hand
gun are usually restricted to roadsides or to other rights-of-way and
industrial sites. From 1/2 to 4 pounds a.e. of herbicide per acre are
usually applied in broadcast sprays. The most common rate is about
2 pounds per acre. High volume sprays usually contain about four
pounds a.e. herbicide per 100 gallons of spray solution.
When doing individual plant foliage spraying, spray solutions are
usually mixed the same as for high volume spraying at two to six
pounds per acre per hundred gallons (AHG) . The foliage of each
plant is sprayed until wet to runoff. When there are high nximbers
of plants per acre, these treatments may exceed 200 or more gpa.
For this reason, if plant numbers to be sprayed exceed 100 to 150
per acre, it is usually cheaper to broadcast spray. Of course, if
there are certain susceptible plants on the area which must be saved,
broadcast spraying cannot be used.
-11-
Stem treatments are widely used to remove undesirable plants from a
stand. Again, this is a highly selective but costly method if large
numbers of plants are to be treated. The following are the most commonly
used mixes for these treatments.
Pounds of Herbicide (a.e./lOO gal.)
Range
Most Common
Injection
10 - 30
20
Basal or stump spray
16 - 20
16
Frill 1/
4-20
8
V Sometimes the pure amine formulation is used without dilution.
Stump treatments may be either sprayed to wet the freshly cut
top and sides or the chemical can be painted on liberally with
a paint brush. The spray mix is usually about the same as used
for a basal stem spray.
Inverted or thickened emulsions can be used to create larger spray
droplets and to help avoid drift. There are several thickening agents
which can be added to spray solutions. Also, small amounts of water
in large amounts of oil will create an inverted emulsion. These
thickened sprays have a larger average droplet size which reduces,
but seldom eliminates, spray drift hazard. Thickened or invert
sprays still have a large range of droplet sizes. The smaller
-12-
droplets are subject to drift and the large drops may not give adequate
coverage of droplets per square inch. When using thickened sprays, it
may be necessary to increase the gallons per acre to maintain the
coverage necessary for the spray to be effective. In general, the
inverted or thickened sprays have not given as good results as normal
spray emulsions.
Thickening agents and inverts offer considerable promise for safe
application of herbicides. Each of the materials have certain
advantages and limitations. Successful use requires a knowledge
of its specific characteristics. Drift control is accomplished
by a reduction in percentage of small drift susceptible droplets
in the spray. Nozzle tip design and orientation, solution, viscosity,
air speed and sprayer pressure appear to be important factors factors
in determining the success of thickened sprays.
Regulating droplet breakup holds promise in controlling drift.
The Micro Foil Boom used with a helicopter, provides a spray having
a minimum of large and small droplets. Good coverage is obtained with
moderate volumes of carrier. Special care is required to maintain
the system free of foreign matter which would plug the small orifices.
The system has not been evaluated with fixed-wing aircraft. Further
evaluation is necessary to determine the potential of this equipment for
controlling drift of herbicide sprays applied in rangeland brush and weed
control. Additional research is needed to develop methods of regulating
spray breakup with fixed-wing aircraft application.
Tolerances and Safety
Tolerances have been established for 2,A,-D in food and feeds. It is
expected that these petitions will be sufficient for fruits and vege-
table crops. New data on residue standards are being developed for
grass with respect to pasture and range usage.
Amendments to the petitions for tolerances for 2,4-D, Silvex, and
2,4,5-T have been submitted to the appropriate agency for inclusion
in uses for pasture and rangeland tolerances. At present, tolerances
for 2,4-D residues in feed and grains is 0.5 ppm; for forages it is
20 ppm. Some official tolerances have not been established yet, and
it should be understood that the tolerances listed do not necessarily
represent the potential hazard, but rather represent the amount
expected with good operational practices. In no case can the
tolerance be greater than the established safety threshhold, and in
most instances it is considerably lower. Wliere more than one
herbicide is involved, such as in brushkiller formulations, the total
residue for all herbicides cannot exceed the lowest established
tolerance threshhold for any one of the herbicides in the mixture.
In brushkiller for example, the established tolerance for either
2,4-D or 2,4,5-T whichever is the lowest for that crop would apply.
-14-
Hormone type herbicides degrade quite rapidly and will under most
conditions be well within the tolerance levels if time intervals,
dosages, and other directions specified on the label are followed
carefully. 2,4-D, 2,4,5-T and Silvex have a low direct toxicity to
man. However, some persons may be allergic to the chemicals or to
the oil used in the herbicidal mixtures, so skin contact should be
avoided. Gloves, goggles, and protective clothing should be avail-
able and when there is spray mist in the air, a respirator is also
a desirable piece of safety equipment. If any nausea or skin rash
is observed, directions in the Forest Service Health and Safety code
should be followed. If a doctor is consulted, information about the
chemical and mixtures being used should be made available to him.
-15-
REFERENCES FOR I - GENERAL INFORMATION
1. Akesson, Norman B. , Stephen E. Wilce, and Wesley E. Yates. 1971.
Confining aerial applications to treated fields — a realistic
goal. Agrichemical Age. December 1971, p. 11-14.
2. Akesson, Norman B., Wesley E. Yates, and Stephen E. Wilce. 1970.
Controlling spray atomization. Agrichemical Age. December 1970,
p. 10-17.
3. Agricultural Extension Service. 1967. Proceedings - aerial applicator's
short courses. University of California.
4. Bailey, J. Blair and John E. Swift. 1968. Pesticide information
and safety manual. Univ, of Calif. Agric. Extension Service.
Agricultural Experiment Station.
5. Behrens, Richard. 1957. Influence of Various Compounds on the
Effectiveness of 2,4,5-T Sprays. Weeds, 5:183-186.
6. Bentley, Jay R. and Kenneth M. Estes. 1965. Use of herbicides on
timber plantations. California Region and Pacific Southwest
Forest and Range Experiment Sta., San Francisco, California
7. Bentley, Jay R. 1967. Conversion of chaparral areas to grassland —
techniques used in California. Agriculture Handbook No. 328.
U. S. Dept, of Agriculture, Forest Service.
-16-
8, Butler, B. J. , N. B. Akesson, and W. E. Yates. 1969. Use of spray
adjuvants to reduce drift - transactions of the ASAE, Vol. 12(2)
182-186.
9. Dunham, R. S. 1965. Herbicide manual for noncropland weeds.
Agriculture Handbook No, 269, Agricultural Research Service.
10, Hayes, Wayland J. , Jr. 1963. Clinical handbook on economic poisons.
U, S. Dept, of Health, Education, and Welfare, Public Health
Service, Communicable Disease Center, Atlanta, Georgia.
11, Hoffman, Garlyn 0. and Robert H. Haas. Controlling Drift of Herbicides
Fact sheet, L848. Texas A&M University, College Station, Texas.
12, Kaupke, C. R. and W. E. Yates. 1966. Physical properties and drift
characteristics of viscosity-modified agricultural sprays.
Transactions of the ASAE, Vol. 9(6) : 797-799; 802.
13, Leonard, 0. A. and W. A. Harvey. 1965, Chemical control of woody
plants. California Agricultural Experiment Sta, Bulletin 812.
14, Montgomery, Marvin L. and Logan A, Norris. 1970. A preliminary
evaluation of the hazards of 2,4,5-T in the forest environment
U.S.D.A, Forest Service, Pacific Northwest Forest and Range
Expt. Sta. Research Note PNW-116.
-17-
15. Norris, Logan A. 1971. Chemical Brush control: assessing the hazard.
Jour. Forestry, October 1971 p. 715-720.
16. Romancier, Robert M. 1965. 2,A-D, 2,4,5-T, and related chemicals for
woody plant control in the southeastern United States. Georgia
Forest Research Council, Macon, Georgia, Report No. 16.
17. Weed Society of America. 1967. Herbicide Handbook of the Weed
Society of America. First Edition. W. F. Humphrey Press
Inc . , Geneva , New York .
18. Whitworth, J. W. and W. P. Anderson. 1969. Accurately predicting
a herbicide's potential. Weed Sci. Vol. 17 (3) :290-293 .
-18-
Section IX
ACUTE TOXICITY OF 2,4-D
Formulation
Organism
Dose
Effect
Reference
Butoxyethanol ester
Oyster
3.75 ppm(96hrs)
50% decrease
Butler
(1965)
in shell growth
Butoxyethanol ester
Shrimp
1 ppm (48 hrs)
No effect
Butler
(1965)
Butoxyethanol ester
Fish (Salt water)5 ppm
48 hr TLm
Butler
(1965)
Butoxyethanol ester
Phytoplankton
1 ppm
16% decrease
Butler
(1965)
in CO2 fixation
Dime thy lamine
Oyster
2 ppm (96 hrs)
No effect on
shell growth
Butler
(1965)
Dimethylamine
Shrimp
2 ppm (48 hrs)
10% mortality
or paralysis
Butler
(1965)
Dime thy lamine
Fish (salt water)
15 ppm (48 hrs)
No effect
Butler
(1965)
Dimethylamine
Phytoplankton
1 ppm (4 hrs)
No effect on
Butler
(1965)
CO2 fixation
Ethylhexyl ester
Oyster
5 ppm (96 hrs)
38% decrease
Butler
(1965)
in shell growth
Ehtylhexyl ester
Shrimp
2 ppm (48 hrs)
10% mortality
Butler
(1965)
or paralysis
Ethylhexyl ester
Fish (salt water
10 ppm(48 hrs)
No effect
Butler
(1965)
Ethylhexyl ester
Phytoplankton
1 ppm (4 hrs)
49% decrease
Butler
(1965)
in CO2 fixation
PGBE 1/ester
Oyster
1 ppm (96 hrs)
39% decrease
Butler
(1965)
in shell growth
PGBE 1/ester
Shrimp
1 ppm (48 hrs)
No effect
Butler
(1965)
PGBE 1/ester
Fish(salt water)
4.5 ppm
48 hr TLm
Butler
(1965)
PGBE 1/ester
Phytoplankton
1 ppm (4 hrs)
44% decrease
Butler
(1965)
in CO2 fixation
_!/ PGBE is propylene glycol butyl ether
I
-19-
Formulation
Organism
Dose
Effect
Reference
Alkanolamine
Chick
380-765 mg/kg
LD
50
Rowe, et al.(1954
Isopropyl ester
Rat
700 mg/kg
LD
50
Rowe, et al.(1954
Isopropyl ester
Chicks
1420 mg/kg
LD
50
Rowe, et al.(1954
Isopropyl ester
Guinea pig
550 mg/kg
LD
50
Rowe, et al.(1954
Butyl ester
Rat
620 mg/kg
LD
50
Rowe, et al.(195A
Butyl ester
Guinea pig
848 mg/kg
LD
50
Rowe, et al.(1954
Butyl ester
Chicks
2000 mg/kg
LD
50
Rowe, et al. (1954
PGBE
Rat
570 mg/kg
LD
50
Rowe, et al.(1954
Acid
Dog
100 mg/kg
LD
50
Rowe , et al . (1954
Acid
Chick
541 mg/kg
LD
50
Rowe, et al.(1954
Dimethylamine
Bluegill
166 ppm
48
hr TLm
Lawrence (1966)
Alkanolamine
Bluegill
435 ppm
48
hr TLm
Lawrence (1966)
Isooctyl ester
Bluegill
9 ppm
48
hr TLm
Lawrence (1966)
Butyl ester
Bluegill
1 ppm
48
hr TLm
Lawrence (1966)
Isopropyl ester
Bluegill
1 ppm
48
hr TLm
Lawrence (1966)
PGBE
Bluegill
3 ppm
48
hr TLm
Hughes&Davis (196
Triethanolamine
Swine
50 mg/kg
No
effect
Bjorklund & Erne
(1966)
Triethanolamine
Swine
500 mg/kg
Lethal
Bjorklund 6 Erne
(1966)
Butyl ester
Swine
100 mg/kg
No
effect
Bjorklund & Erne
(1966)
Triethanolamine
Chicken
300 mg/kg
No
effect
Bjorklund & Erne
(1966)
Butyl ester
Rat
620 mg/kg
LD
50
Edson et al.(1964
Isopropyl ester
Rat
700 mg/kg
LD
50
Hayes, (1963)
Unspecified amine
Mallard duck
2000 mg/kg
LD
50
Tucker & Crabtree
(1970)
Acid
Pheasant
472 mg/kg
LD
50
Tucker & Crabtree
(1970)
Acid
Mule deer
400-800 mg/kg
LD
50
Tucker & Crabtree
(1970)
*Footnote : dermal 300-1500 mg/kg various formulations
ACUTE TOXICITY OF 2,4,5-T
Oral
Formulation
Organism
Dose
Effect
Reference
Acid
Rat
500 mg/kg
“50
Rowe & Hymas
(1954)
Isopropyl ester
Mice
551 mg/kg
“ 50
Rowe & Hymas
(1954)
Butyl ester
Mice
940 mg/kg
LD 50
Rowe & Hymas
(1954)
Amyl ester
Rat
750 mg/kg
LD 50
Rowe & Hymas
(1954)
Isooctyl esters Bluegill
(From 3 manufacturers)
10-31 ppm
48 TLm
Hughes & Davis
(1963)
PGBE ester
Bluegill
17 ppm
48 TLm
Hughes & Davis
(1963)
Butoxyethanol ester
Bluegill
1.4 ppm
48 TLm
Hughes & Davis
(1963)
Triethanolamine
Swine
100 mg/kg
Locomotory disturb-
ance
Bjorklund &
Erne (1966)
PGBE ester
Oyster
0.14(96 hrs)
50% decrease in
shell growth
Butler (1965)
PGBE ester
Shrimp
1 ppm(48 hrs)
20% mortality
or paralysis
Butler (1965)
PGBE ester
Fish(salt water) 0.32 ppm
48 hr TLm
Butler (1965)
PGBE ester
Phytoplankton
1 ppm(4 hrs)
89% decrease in
CO2 fixation
Butler (1965)
Veon 2,4,5
Oyster
1 ppm (96 hrs)
No effect
Butler (1965)
Shrimp
1 ppm(48 hrs)
No effect
Butler (1965)
Fish(Salt water)l ppm(48 hrs) No effect Butler (1965)
Phytoplankton 1 ppm(4 hrs) No effect on
CO2 fixation
Butler (1965)
ACUTE TOXICITY OF 2, A, 5 -TP
Oral
Formulation
Organism
Dose
Effect
Reference
PGBE ester
Rat
650 mg/kg
LD 5Q
Bailey &
Swift (1968)
PGBE ester
Rat
1070 mg/kg
LD 50
Mullison(1966)
PGBE ester
Guinea pig
850 mg/kg
LD 50
Mullison(1966)
PGBE ester
Rabbit
850 mg/kg
LD 50
Mullison(1966)
P'CBE ester
Mouse
2140 mg/kg
LD 30
Mullison(1966)
PGBE ester
Chicken
2000 mg/kg
LD 30
Mullison(1966)
Acid
Mallard Duck
500 mg/kg
Minor symptoms
Tucker & Crab-
tree (1970)
Acid
Mallard Duck
2000 mg/kg
LD 30
Tucker & Crab-
tree (1970)
Isooctyl ester
Bluegill
5 ppm
48 hr TLm
Hughes &Davis
(1966)
PGBE ester
Bluegill
25 ppm
48 hr TLm
Hughes&Davis
(1966)
Butoxyethanol ester
Bluegill
2 ppm
48 hr TLm
Hughes&Davis
(1966)
Triethylamine
Bluegill
20 ppm
48 hr TLm
Hughes &Davis
(1966)
PGBE ester
Oyster
1
ppm for 96 hrs
23% decrease Butler (1965)
in shell growth
PGBE ester
Shrimp
0,
.24 ppm(48 hrs)
50% mortality
or paralysis
Butler (1965)
PGBE ester
Fish (Salt water)
0.36 ppm
48 hr TLm
Butler (1965)
PGBE ester
Phytoplankton
1 ppm (4 hrs)
94% decrease
C02 fixation
Butler (1965)
Acid
Rat
650 mg/kg
LD 30
Rowe & Hymas
(1954)
Butyl ester
Rat
600 mg/kg
“ 50
Rowe & Hymas
(1954)
PGBE ester
Rat
621 mg/kg
LD 30
Rowe & Hymas
(1954)
PGBE ester
Guinea pig
1250 mg/kg
LD 50
Rowe & Hymas
(1954)
PGBE ester
Rabbit
819 mg/kg
“ 50
Rowe & Hymas
(1954)
PGBE ester
Chick
1190 mg/kg
“ 50
Rowe & Hymas
(1954)
-22-
CHRONIC TOXICITY OF 2,4-D
%
Formulation
Organism
Dose
Duration
Effect
Reference
Triethanolamine
Swine
50/mg/kg/day
3 doses
None
Bjorklund &
Erne (1966)
Triethanolamine
Swine
50/mg/kg/day
8-10 doses
Minor trans-
ient effects
Bjorklund &
Erne (1966)
Butyl ester
Swine
50/mg/kg/day
<5 doses
None
Bjorklund &
Erne (1966)
Triethanolamine
Swine
500 ppm in feed.
1 month
Some locomo- Bjorklund &
tory distur- Erne (1966)
bance, depressed
growth rate, no
gross pathology
Triethanolamine
Rats
1000 ppm in water 10 mos.
Depressed growth Bjorklund &
rate, no gross Erne (1966)
pathology
Triethanolamine
Chicken
1000 ppm in water Daily Egg size normal, Bjorklund &
from hatch- production Erne (1966
ing through reduced 30%
first 2 mos.
of egg production
Alkanolamine
Sheep
100 /mg/kg/ day
481 days
No effect
Palmer & Rade
leff (1964)
Alkanolamine
Cattle
50/mg/kg/day
112 days
No effect
Palmer & Rade
leff (1964)
PGBE ester
Sheep
100/mg/kg/day
481 days
No effect
Palmer & Rade
leff (1964)
Ethylhexyl ester
Cattle
250/mg/kg/day
14 days
111 in 3 days , Hunt , et . al .
survive & re- (1970)
cover from 9
doses. 14 doses
lethal .
EthyJhexyl ester Sheep
250/mg/kg/day
17 days
Ill in 3 days Hunt, et. al.
17 doses lethal (1970)
Ethylhexyl ester
Sheep &
Cattle
100/mg/kg/day
10 days
None to minor
effects
Hunt, et. al.
(1970)
Not specified
Dog
500 ppm in feed
2 years
None
House et. al.
(1967)
-23-
Formulation
Organism
Dose
Duration
Effect
Reference
Not specified
Rat
1250 ppm in feed
2 years
No effects on House, et. al
growth, survival (1967)
hermatology or
tumor incidence.
Not specified
Rat
500 ppm in feed
2 years
No effects in
reproduction
studies .
House, et . al
(1967)
Alkanolamine
Chicken
100 mg/kg/day
10 days
No effect on
weight gain
Palmer &
Radeleff (196^
PGBE ester
Chicken
50 mg/kg/day
10 days
No effect on
weight gain
Palmer &
Radeleff (196‘
PGBE ester
Cattle
100 mg/kg/day
10 days
No effect
Palmer &
Radeleff (196‘
Acid
Mule deer
80 and 240
mg/kg/day
30 days
Minor symptoms
no weight loss
Tucker and
Crabtree(1970
CHRONIC TOXICITY OF
' 2,4,5-T
Formulation
Organism
Dose
IXiration
Effect
Reference
Not specified
Dog
10 mg/kg/day
5 days per wk. Minor weight Drill &
for 90 days loss, no other Hiratzka
effects. (1953)
Not specified
Dog
20 mg/kg/day
5 days per wk. Lethal between Drill &
for 90 days 11 and 75 days Hiratzka
(1953)
PGBE ester
Cattle
100 mg/kg/day
10 days
None
Palmer &
Radeleff (1969^
PGBE ester
Sheep
50 mg/kg/day
10 days
None
Palmer &
Radeleff (1969]
PGBE ester
Sheep
100 mg/kg/day
369 days
(dosed by cap-
sule) 111 at
367 doses,
lethal at 369
Palmer &
Radeleff (1969)
•
PGBE ester
Chicken
100 mg/kg/day
10 days
No effect on
weight gain
Palmer &
Radeleff (1969)
Triethylamine
Sheep
100 mg/kg/day
481 days
No effect
Palmer 4
Radeleff (1964)
Not specified
Mice
21 mg/kg/day
600 ppm in
4 weeks No mortality
18 months
Inues, et . al*
(1969)
diet. r"
-24-
%
CHRONIC TOXICITY OF 2, 4, 5 -TP
Formulation
Organism
Dose
Duration
Effect
Reference
Butoxyethanol
ester
Quail
5000 ppm in
feed
10 days
LD CQ
9350 mg/kg
House, et. al .
(1967)
Butoxyethanol
ester
Mallard Duck
2500 ppm in
feed
13 days
LD 50
33700 mg/kg
House, et. al.
(1967)
Butoxyethanol
ester
Pheasants
5000 ppm in
feed
<100 days
LD 50
9240 mg/kg
House, et. al.
(1967)
PGBE ester
Rat
30 mg/kg
90 days
No effect
House, et. al.
(1967)
Not specified
Rat
100 ppm feed
2 years
No effect
House, et. al.
(1967)
Not specified
Dog
190 ppm feed
2 years
No effect
House, et. al.
(1967)
PGBE ester
Sheep
100 mg/kg
11 doses
Lethal
Palmer &
Radeleff (1964)
PGBE ester
Cow
50 mg/kg
73
No effect
Palmer &
Radeleff (1964)
PGBE ester
Cow
100 mg/kg
29
Lethal
Palmer &
Radeleff (1964)
PGBE ester
Cow
50 mg/kg
8
No effect
Palmer, et. al
(1964)
PGBE ester
Cow
25 mg/kg
20
No effect
Palmer, et. al
(1964)
PGBE ester
Sheep
25 mg/kg
10
No effect
Palmer &
Radeleff (1969)
PGBE ester
Chicken
100 mg/kg
10
Small weight
loss
Palmer &
Radeleff (1969)
PGBE ester
Chicken
250 mg/kg
10
Greater
weight loss
Palmer &
Radeleff (1969)
-25-
PHENOXY HERBICIDES AS TERATOGENS, MUTAGENS
CARCINOGENS AND COMMENTS ON DIOXIN
(
Specific tests to determine the biological potential of chemicals as
teratogens, mutagens on carcinogens are outlined by Mrak (1969). The
techniques employed frequently involve high doses, extended periods of
e. posure, force feeding, subcutaneious injection, exotic solvents and
inbred strains of laboratory animals. Such techniques bear little
resemblance to the exposure non-target organisms encounter due to field
use of chemicals. These tests only establish that chemicals may or may
not have the biological potential to induce these effects. Careful
interpretation of data is necessary to determine the probability that
such effects are likely to occur in the field.
Carcinogenicity
Innes, et al (1969) reports 2,4-D isopropyl ester and 2,4,5-TP yielded
an increased tumor incidence in comparison to negative controls but the
level of significance was less than 0.02. Mrak (1969) suggests these
compounds need more testing but the priority for testing is not high in
comparison with some other pesticide.
2,4-D acid, butyl ester, isooctyl ester and 2,4,5-T acid were not tumor-
genic in mice (Innis et al. 1969). Miak (1969) did not find sufficient
information on other phenoxy herbicide formulations to make a judgement.
-26-
(r
Mutagenicity
2,A-D and 2,4,5-T have mutagenic potential as demonstrated In tests with
several plant systems (Mrak, 1969). Unrau and Larter (1952), Unrau (1953,
1954) found "highly significant" abnormalities of chromosome behavior In
rapidly dividing cells of wheat and barley sprayed with 2,4-D ethyl ester.
Muhllng et al (1960) also found chromosomal effects In peas treated with
2,4-D. Anderson (1967) on the other hand used a histidine deficient
mutant of Salmonella to look for mutagenic effects of many chemicals.
While several known mutagens Induced mutations In his test , none of 120
herbicides tested did so. Similar results were found In tests with other
organisms using a similar strategy (Anderson, 1967). The likelihood of
significant mutagenesis occurring from normal use of phenoxy herbicides Is
small.
Terratogenlclty
Mrak (1969) summarized the Blonetlcs research data on terratogenlclty of
herbicides.
2,4-D Isoctyl ester, 2,4-D butyl ester and 2,4-D Isopropyl ester produced
statistically significantly higher Incidences of congenital malformations
In mice or rats. 2,4-5-T was Intensively examined In the Blonetlcs study
because It proved highly teratogenic. Mrak (1969) also details test
results from Blonetlcs which show many of these same formulations are not
teratogenic In other strains of mice or rats or when other means of
exposure are used. Macleod et. al. (1971) questions the adequacy of the
Blonetlcs data because known teratogens and embryo toxins failed to
-27-
produce significant effects in these tests. The contamination of the
Bionetics 2,4,5-T with high levels of 2, 3, 7, 8- tetrachlorodibenzo-p-
Dioxin (dioxin) further invalidates the data for 2,4,5-T.
Verrett (1970) reported 2,4-D, 2,4,5-T and 2,4,5-TP all produced terrata
and chick edema syndrome following injection into the yolk sac of fertile
chicken eggs. This is an extremely sensitive test and the degree to which
it can be extrapolated to field exposure is limited, Johnson (1971)
summarized a variety of tests for teratogenicity of the phenoxy herbicides.
The studies with presently available commercial formulations of 2,4,5-T and
2,4-D show no teratogenic effects in rats at rates up to 50 mg/kg/day and
87.5 mg/kg/day respectively. Some fetal resorptions appear at higher
levels. Tests with silvex (up to 100 mg/kg/day) showed no effects in rats.
Higher ratio caused fetel resorptions or maternal toxicity.
Sparschu, Dunn, and Rowe (1971) determined the teratogenic properties of
dioxin. Their findings suggest the earlier findings of 2,4,5-T teratogen-
icity may be attributed to dioxin contamination of 2,4,5-T.
The National Academy of Sciences Advisory Committee on 2,4,5-T wrote the
following in their report to the Environmental Protection Agency.
"Much of the general toxicity attributed to 2,4,5-T in the past
now appears to have been caused by the contaminant TCDD (dioxin) .
The herbicide when essentially free of this contaminant, e.g. 1 ppm,
has relatively low toxicity for all animal forms in which it has
been tested.
-28-
"Particular attention was given to the teratogenic potential of
both 2,4,5-T and TCDD. Acceptable data are now available on the
embryotoxicity of 2,4,5-T in 6 mammalian species, mouse, rat,
hamster, rabbit, sheep and rhesus monkey. None of these showed
adverse effects at dosage of 40 mg/kg/day of maternal weight.
The mouse appears to be more sensitive than the other forms
studied in that it shows a low level of teratogenicity (cleft
palate) at 100 mg/kg/day given throughout organogenesis, whereas
hamster and rat required higher dosage to obtain comparable effects.
It is likely that all species could be caused to show some
embryotoxicity if 2,4,5-T dosage were raised high enough, a fact
already known for many prevalent environmental chemicals such
as aspirin, caffein, nicotine and organic mercury.
The dioxin contaminant TCDD also has been shown to have a low
teratogenic potential at doses in excess of 0.001 mg/kg, but this
dosage level is virtually impossible with currently produced 2,4,5-T.
No evidence has been found of significant potentiative interaction
between 2,4,5-T and TCDD."
The dioxin content of phenoxy herbicides is important. Dichlorodibenzo-p-
dioxin would be the major species of dioxin in 2,4-D. The tetrachloro-
dibenzo-p-dioxin would be the major species of dioxin in both 2,4,5-T and
2»4,5-TP. Johnson (1971) reports eight lots of silvex from production run
-29-
material (1967, 1968, and 1969 lots) did not contain detectable quantities
of dioxine. Current 2,4,5-T contains less than 0.5 ppm dioxin. Dichloro-
dibenzo-p-dioxin is not formed in the manufacture of 2,4-D. Kearney et
al (1970) analyzed 129 samples of 18 chlorophenol based pesticides for
dioxin. Only occasional samples of 2,4,5-T contained more than 0.5 ppm
dioxin. No samples collected after June 1970 contained more than 0.5
ppm dioxin.
Kearney et al (1970) reported the behavior of dioxin in the environment.
They found no uptake of dioxin from soil by plants and no translocation
of dioxin from treated foliage. Dioxin residues may be subject to
weathering. Dioxin is persistent in soil but does not leach in the soil
profile. It is probably tightly bound by soil components. Dioxin is
subject to photodecomposition but the significance of this in the field
is questionable.
Johnson (1970) reports dioxin is not likely to concentrate in fats like
DDT. When 2,4,5-T treated paper or foliage is burned, no dioxin was
detected in the vapor phase.
-30-
Physical Properties
2,^-D Acid
References
Bailey and White
(1965)
specific gravity
1.57
II
II
melting point
139°C
II
It
solubility in H^O
725 ppm @25°C
II
II
structure :
^0 - C - C ^ ®
/\
H ^ Cl
1
II
II
1
H
Cl
boiling point l60°C
SO. 4mm Hg
Melnikov
1971
melting points and
solubilities of several salts of
2,4-D and melting and boiling points of several
esters of 2,4-D are
given by Melnikov (1971).
vapor pressure of 2
,4-D esters is difficult to
measure and there is little agreement on values.
ester
Vapor pressure (mm Hg S25*^C)
References
Isopropyl
4.6 X 10 " ^
Flint et
al (1968)
Isopropyl
10.5 X 10 ■ ^
Warren &
Gillis(l952)
Butyl
8.9 X 10 " ^
Hamaker & Kerlinger
(1969)
Isooctyl
2 X 10 “ ^
“31-
ester
Vapor pressure (mm hg <S29 C)
References
- 6
Flint et al
(1968)
Ethlhexyl
2 X 10
- 6
It It
It
PGBE
3 X 10
. - 6
tl ft
tl
Butoxyethanol
^.5 X 10
specific gravity
melting point
solubility in H^O
1.80
15^
280 ppm <§25° C
Bailey & White(l9o5)
II II II
It II I'
II II I)
The melting points and water solubilities of several salts and
melting and boiling points of some esters of 2,4,5-T are given
by Melnikov (1971)» Vapor pressures of 2,4,5~T esters will be
similiar to vapor pressure of corresponding ester of 2,4-D.
Generally speaking, ethyl, propyl, isopropyl, butyl and
isobutyl esters are high volatile, whereas heavier esters such
as PGBE, ethylhexyl, isooctyl, or butoxyethanol are low volatile.
-32-
structure :
Re ferences
Bailey & White
(1965)
Melting point l80°C
140 ppm @25°C
See comments on 2,4,5-T. Same
remarks apply to 2,4,5-TP.
Solubility in H^O
LITERATURE CITED
V
1. Anderson, K. J. 1967. (personal conramnication) See House, et. al, 1967.
2. Bailey, J. B. and John E. Swift. 1968. Pesticide information and
safety manual. Univ. of Calif. Ag. Ext. Service. Berkeley, Calif.
3. Bailey, G. W. and J. L. V/hite. 1965. HERBICIDES; A compilation of their
physical, chemical, and biological properties. Residue Reviews
10:97-124.
4. Bjorklund, Nils-Erik and Kurt Erne. 1966. Toxicological studies of
phenoxyacetic herbicides in animals. Acta. Vet. Scand. 7:364-390.
5. Butler, P. A. 1965. Effects of herbicides on estuarine fauna.
Southern Weed Cont. Conf. Proc. 18:567.
6. Drill, V. A. and T. Hiratzka. 1953. Toxicity of 2,4-D and 2,4,5-T acid.
A report on their acute and chronic toxicity in dogs. AMA Arch.
Indust. Hyg. Occup. Med. 7:61-7.
7. Edson, E. F., D. N. Sanderson and D. N. Nookes. 1964. Acute Toxicity
Data for Pesticides. World Review of Pest Control 4(1) Spring 1965.
8. Flint, G. W. , J. J. Alexander and 0. P. Funderburk. 1968. Vapor
pressures of low volatile esters of 2,4-D. Weed Sci. 16:541-4.
9. Hamaker, J, W. and H. 0. Kerlinger. 1969. Vapor pressure of pesticides.
In: Pesticide formulation research. Adv. in Chem. Series No. 86.
Pages 39-54,
10. Hayes, Way land J. J, 1963. Clinical handbook on economic poisons.
U. S. Dept. Health, Education and Welfare.
-34-
11. House, W. B, et, al. 1967, Assessment of ecological effects of
extensive or repeated use of herbicides . Final report on
Midwest Research Institute Project 3103-B under Dept, of
Amy Contract DAHC15-68-C-0119 .
12. Hughes, J, S, and J, T. Davis, 1963. Variations in toxicity to
bluegill sunfish of phenoxy herbicide weeds 11:50-3.
13. Hughe®, J, S. and J. T. Davis. 1966. Toxicity of pesticides to
bluegill sunfish tested during 1961-1966. Report to
Louisiana Wildlife and Fisheries Commission, Monroe, Louisiana.
lA, Hunt, T,, M. , B. N. Gilbert and J. S. Palmer. 1970. Effects of a
herbicide, 2~ethylhexyl ester of 2,4-D on magnesium: calcium
ratios and blood urea nitrogen levels in sheep and cattle. Bull.
Environ. Contamination and Toxicol, 5:54-60.
15, Innes , J, R. M. et. al. 1969. Bioassay of pesticides and industrial
chemicals for tumorigenicity in mice: A preliminary note. J.
National Cancer Inst. 42:1101-14,
16, Johnson, J. E. 1971. The public health implications of widespread
use of the phenoxy herbicides and picloram. Biosci. 21:899-905.
17, Kearney, P. C, et, al. 1970, Report of research on dioxin. ARS, USDA,
and P?D to EPA, Beltsville, Maryland.
18, Lawrence, J. N. 1964, Aquatic herbicide data. USDA. ARS, Agricultural
Handbook 231.
19, Maclaod, C. M, et. al, 1971. Report on 2,4,5-T. A report of the
Panel on herbicides of the President's Science Advisory Committee.
Office of Science and Technology, Executive Office of the President
March 1971.
-35
20. Melnikov, N. N. 1971. Chemistry of pesticides. Residue Reviews.
36:1-480.
21. Mrak, Emil. 1969. Report of the Secretary's Commission on pesticides
and their relationship to environmental health. U.S. Dept. HEW.
December 1969.
22. Muhling, G. N. , J. Van'T Hof, G. B. Wilson and B. H. Grisby. Cytological
effects of herbicidal substituted phenols. Weeds. 8:173-181.
23. Mullison, W. R. 1966. Some toxicological aspects of silvex.
Southern Weed Cont. Conf. Proc. 19:420-35.
24. Palmer, J. S., D. E. Clark and L. M. Hurt. 1964. Toxicologic effects
of silvex on yearling cattle. Am. Vet. Med. Assoc. J. 144:750-755.
25. Palmer, J. S. and R. D. Radeletf. 1964. The toxicologic effects of
certain fungicides and herbicides on sheep and cattle. Ann.
N.Y. Acad. Sci. 111:729-36.
26. Palmer, J. S. and R. D. Radeleff. 1969. The toxicity of some organic
herbicides to cattle, sheep and chickens. Production Research
Report No. 106. ARS, USDA.
27. Rowe, V. K. and T. A. Hymas. 1954. Summary of toxicological information
on 2,4-D and 2,4,5-T type herbicides and an evaluation of the
hazards to livestock associated with their use. Am. J. Vet.
Res. 15:622-29.
28. Tucker, R. K. and D. G. Crabtree. 1970. Handbook of toxicity of
pesticides to wildlife. Resource Publication No. 84. Bureau
of Sport Fisheries and Wildlife. U.S. Dept, of the Interior.
29. Unrau, J. 1953. Cytogenic effects of 2,4-D on cereals. Canadian
Seed Growers Assoc. Ann. Report, pages 37-39.
-36-
30.
Unrau, J. 1954. Cytogenic effects of 2,4-D on cereals. Canadian
#
Seed Growers Assoc. Ann. Report, pages 25-28.
31. Unrau, J. and E. N. Larter. 1952. Cytogenical responses of cereals
to 2,4-D Canadian J. Bot. 30:22-27.
32. Verrett, J. 1970. Testimony before the U.S. Senate Committee on
Commerce, Sub-Committee on Energy, Water, Natural Resources
and the Environment. 15 April 1970. Serial 91-60. Pages 190-203.
33. Warren, J. C. R. and A. Gillies. 1952. Proc. 6th Meeting Eastern
Soc., National Weed Committee, page 98.
-37-
Section III
METABOLISM OF 2.A-D, 2,4, 5-T, and 2,4,5-TP 1/
4
2»4~D [2,4-Dichlorophenoxyacetic acid]
In feeding studies of 2,4-D with dairy cows and steers, (12, 13, 48,
49, 65) 2,4-D was found unchanged in the urine only. No evidence of
betaoxldation was found. Similar findings were obtained with sheep.
Ninety-six percent of an orally administered dose of 2,4-D-C- to a
sheet was excreted unchanged in the urine in 72 hours and slightly
less than 1,4% in the feces. Very little residual radioactivity was
found in edible tissue (28) .
In rats receiving 1 to 10 mg of 2,4-D, there was almost complete
excretion of the herbicide in the urine and feces in 48 hours. At
higher dosage levels, some accumulation in tissues occurred. Analyses
also indicated that traces of an unidentified metabolite appeared in
the urine (60).
After exposure of bean plants (Phaseolus) , sun flowers (Helianthus
annus) , maize (Zea mays) or barley (Hordeum) to 2,4-D, 2,4-dichloro-
phenol was observed (111) .
Hydrolysis of esters (30, 75) and decarboxylation (14, 33, 81) of
2,4-D by plants has also been shown. The free acid has been demon-
strated on bean plants, corn plants and forage after treatment with
2,4-D butoxyethanol, propylene glycol butyl, butyl and 2-ethylhexyl
-38-
»
esters (39, 51, 53, 63). Treatment of lemons with labeled 2,4-D
Isopropylester indicated that the ester was hydrolyzed and that part
of the 2,4-D then reacted with some plant constituent to form an ester-
like complex. Ester-like residues were also found after treatment with
the sodium, diethanolamine, or triethanolamine salts (34, 35). Samples
of fresh citrus peel were prepared by compositing peel samples obtained
from oranges from trees sprayed with 2,4-D isopropyl ester. In addition
to free acid and ester, a conjugate was also found. The latter became
available for extraction only after heat treatment. Preliminary
investigations indicated that 2,4-D was conjugated with pectin (73).
On cotton, cucumbers, beans, and grain sorghum, labeled 2,4-D gave
rise to C^*‘02 (56, 106, 109). Pea and tomato plants have also been
studied (38). In young leaves and bolls of cotton, material chroma-
tographically different from 2,4-D was formed. Sorghum converted
2,4-D to a complex different than that found in cotton (74, 77, 90,
104, 105, 106, 107, 108, 109).
Amino acids have been implicated in the formation of some compounds,
as in the case of 2,4-dichlorophenoxyacetylaspartic acid (3, 11).
Evidence indicated that 2,4-D moved through plants as a protein complex,
which could be recovered after aqueous extraction and NaOH hydrolysis,
into the roots where most of the degradation occurred (22). Resistant
plants were grown in water cultures treated with 2,4-D. Leaves were
homogenized and a protein fraction was obtained that contained 2,4-D
0 \J The numbers in parenthesis refer to references at the end of the
metabolism section.
-39-
OCH,
2,5-Dlchloro-4-hydroxy- 2 , 3-Dlchloro-
phenoxyace tic Acid 4-hydroxyphenoxy-
acetic Acid
(As Glucosides)
*^^haseolus
\vulgaris
Achromobacter
Plants, Silage
Decomposition
Aspergillus nir|er 9 a n
4-(2,4-DB) ^ °
2,4-Dlchloroanisole
r n
-Cl
r M
1
+
1
Cl-J
Cl
2,4-Dichloro-5- 2,5-Dlchloro-4-
hydroxyphenoxyacetic hydroxyphenoxy-
Acid acetic Acid
+ An Unchlorinated Phenol
+ 3 Unidentified Compounds
3- Chi orocatechol
3,5-Dichlorocatechol
g°5:-?-CH-CH.CH-c4°jj_^ Metabolized-
a-Chloromuconic Acid Chloride released
P -Chloromuconic
Acid
-40-
in a bound forrA not further identified (24) . In big leaf maple (Acer
H.^crcphyiriii7B T-arsh) ^ 2,4'"D was converted into two metabolites. One of
those was the same compound characterized previously (18) as a 2,4-D
protein cor.plex which yielded 2,4-D and 12 amino acids on acid hydrolysis
(80).
Glucose esters were suggested (31, 61, 62) and studies have shown that
glitcosidc complexes were formed- From stem tissues of oats (Avena
sativa) , l-0~(2,4-dichlorophenoxyacetyl) -B-D-glucose was Isolated (97),
and from stems of the kidney bean (Phaseolus vulgaris) , the 2,5- and 2,3-
dlchlorcphanoxyacetic acid glucosides have been obtained (96) .
From comparative studies with sensitive and insensitive plants, two
metabolic paths were proposed involving initial glucose ester formation
and oxidation ring cleavage of the aromatic ring in yield monochloroacetic
acid (100) . The latter has been detected in plants prior to the onset of
treatment symptoms; and it has been suggested that the effect of 2,4-D
resulted from the action of monochloroacetate arising from 2,4-D degradation
aoo, 112).
Plants are capable of hydroxy lating phenoxyacetlc acids (95, 110). When
bean plants were treated with 2,4-D, three compounds were found (31). One
corresponded roughly to that of 2,4-dichloranisole; one was water-soluble,
ether-insoluble ester derivative; and the third, an ether-soluble compound
with a basic structural change. The methyl derivative was less volatile
than 2,A-D methyl ester, but more volatile than the 4-hydroxy-2 ,4-D methyl
-41-
ester. It might be one of the other two hydroxy derivatives; however, 6-
hydroxy-2,4-D was not detected (10, 37, 55, 57, 58).
The bio transformation of 2, A-dichlorophenoxyalkanoic acids and related
compounds by soil microflora has been extensively studied (4, 5, 6, 7,
9, 15, 19, 20, 21, 29, 36, 37. 40, 43, 54, 59, 78, 91, 101, 102, 103).
Phenoxyalkanoic acids with an even number of carbons in the fatty acid
were converted by B-oxidation to products with an even number of carbons
(47, 50, 64, 101, 102, 103). A second mechanism involved cleavage of
the ether linkage (8, 17, 22, 70, 71, 72).
Evidence has been obtained that 2,4~D is dissimilated by a variety of
microorganisms (1, 82) through a 2,4-dichlorophenol and 4-chlorocatechol
(7). A product from the degradation of 2,4-D by bacteria of the genus
Pseudomonas has been identified as B-chloromuconic acid. A second species
of Pseudomonas gave rise to a-chloromuconic acid (44). In other studies,
6-hydroxy-2,4-D was reported (67). Pure cultures of a Nocard ia species
and an Achromobacter strain of bacteria rapidly degraded 2,4-D and the
presence of 2,4-dichlorophenol, chlorohydroquinone, a monochlorophenol ,
an unchlorinated phenol and three other unidentified compounds have been
demonstrated (6, 15, 16, 40, 78, 92, 93, 94). The main product of 2,4-D
metabolism by the mold Asperiglllus niger van Tlegh was 2 ,4-dlchloro-5-
hydroxyphenoxyacetic acid. By means of infrared and mixed melting points,
a second metabolite was identified as the 2,4-dichloro-4-hydroxyphenoxy-
acetic acid — the first time such a rearrangement was reported. Another
unidentified acid, not the 3- or 6- hydroxyacid, was also found (41, 42).
-42-
rnoto Decomposition
-A3-
Arthrobacter sp. degraded 2,A-D via 2, A-dichlorophenol and 2,3-dichloroanisole
(68, 69). In excess of 80% of the chloride was released in a 3 hour
Incubation period with crude extracts or the soluble fraction (67) . A
Corynebacterium species also degraded 2,A-D with quantitative release of
chloride. In natural surface waters, 2,A-D isopropyl and butyl esters
were hydrolyzed to 2,A-D and their respective alcohols (2) . When
triethanolamine salts of C^‘*-carboxy labeled 2,A-D were applied in water
to forest litter, liberation of C^**02 was rapid (79).
In the presence of water and ultraviolet light, 2,A-D decomposed rapidly
with formation of 2, A-dichlorophenol. This underwent further decomposition
to A-chlorocatechol , polymeric humic acids and chloride. Some 2-hydroxy-
A-chlorophenoxyacetic acid and a very small amount of 2-chloro-A-hydrcxy
phenoxyacetic acid were present (32, 52, 98, 99). In the presence of
riboflavin, compounds containing more than one aromatic nucleus were
probably also formed in addition to 2, A-dichlorophenol. Products differed
according to the original pH and concentration of the treated solution
(52).
2,A ,5-T [2,A, 5-Trichlorophenoxyacetic Acid]
Cows fed 2,A,5-T excreted it as a soluble salt in their urine (83).
When Wlnesap and Staymen Winesap cultlvars were exposed to 2,A,5-T
some decarboxylation occurred (81) . Bean plants (Phaseolus) , sun
flowers (Helianthus annus) and barley (Hordeum) converted 2,A,5-T to
its phenol (111). 2,A,5-T was also decarboxylated by woody plants (lA).
-44-
From comparative studies with sensitive and Insensitive plants, two
paths were proposed, Involving Initial glucose ester formation and
oxidative ring cleavage to yield monochloroacetate. The latter was
detected In treated plants prior to the onset of treatment symptoms
(100).
Sweetgum (Llquldambar styraclf lua L.) and southern red oak (Quercus
falcata Mlchx.) were sprayed with an aqueous homogenate of 2,4,5-T
n-butyl ester. After one month, leaves were collected and assayed
using gas chromatography to detect residues. 2,4 ,5-Trlchlorophenol
was observed but no evidence was found to Indicate formation of
2.4. 5- Trlchloranlsol (45, 46). After application to Blgleaf maple
(Acer Macrophyllum Pursh) and mesqulte seedlings, 2,4,5-T was metabolized
but the products were not Identified (76, 80) .
Triethanolamine salts of C^**-carboxy labeled 2,4,5-T were applied In
water to the surface of some collected forest litter. Liberation of C^'*0
was slow but increased with time (79) .
2.4.5- TP (Silvex) [ 2-( 2, 4, 5-Trlchlorophenoxy) propionic Acid]
When fed to cows, silvex was excreted as a soluble salt in the urine.
Kuron, the propylene glycol butyl ether ester of silvex, was hydrolyzed
prior to elimination (83) .
Samples of fresh citrus peel were prepared by compositing peel samples
obtained from oranges from trees sprayed with 2,4,5-TP propylene glycol
butyl ether ester. In addition to free acid and ester, a conjugate was
found. The latter became available for extraction only after heat treat-
ment. Preliminary investigations indicated that 2,4,5-TP was conjugated
with pectin (73). Decarboxylation of 2,4,5-TP by prickly pear (Opuntla
spp.) was 1/2 to 1/3 of that by soybean. In addition to unaltered
2,4,5-TP, at least four labeled metabolites were observed after application
of sllvex-l-C^ ** was applied to prickly pear (26, 27).
When the propylene glycol ether ester was applied to water overlying
various soil types, the herbicide was hydrolyzed almost totally to the
acid in about two weeks. Absorption of the acid by the soils was also
indicated (116) .
-46-
pear (Opuntla spp.) was 1/2 to 1/3 of that by soybean. In addition to
Unaltered 2,A,5-TP, at least four labeled metabolites were observed
after application of silvex-l-C^** was applied to prickly pear (26, 27),
V/hen the propylene glycol butyl ether ester was applied to water
overlying various soil types, the herbicide was hydrolyzed almost totally
to the acid in about two weeks. Adsorption of the acid by the soils was
also indicated (116).
monochloroacetate
REFERENCES TO METABOLISM OF
2.A-D, 2,4,5"T, 2,4,5-TP
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structure on microbial decomposition of aromatic herbicides.
Journal of Agriculture and Food Chemistry, vol. 9, p. 44-47.
2. Aly, Osman M. and Samuel D. Faust, 1964. Studies on the fate of
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of Agriculture and Food Chemistry, vol. 12, p. 541-546.
3. Andreae, W. A. and N. E. Good, 1957. Studies on 3-indole acetic
acid metabolism. IV. Conjugation with aspartic acld*and
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Plant Physiology, vol. 32, p. 566-572.
4. Audus, L. J., 1949. Biological detoxification of 2,4-dichloro-
phenoxyacetic acid in soil. Plant and soil, vol. 2, p. 31-36.
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phenoxyacetic acid in soils: isolation of an effective
organism. Nature, vol. 166, p. 356.
6. Audus, L. J., 1951. The biological detoxification of hormone
herbicides in soil, vol. 3, p. 170-192.
7. Audus, L. J., 1952. The decomposition of 2,4-dichlorophenoxyacetic
acid and 2-methyl-4-chlorophenoxyacetic acid in the soil.
Journal of the Science of Food and Agriculture, vol. 3, p. 268-274.
8. Audus, L. J., (Editor), 1964. The herbicide behavior. the
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-48-
9.
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14.
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from bean stems. Plant Physiology, vol. 36, p. 558-565.
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labeled 2,4-dichlorophenoxyacetic acid by bean stems:
heterogeneity of ehtanolsoluble, ether-soluble products.
Nature, volume 189, p. 763,
Bache, C. A., D, D, Hardee, R. F. Holland, and D. J. Llsk, 1964.
Absence of phenoxyacid herbicide residues in the milk of
dairy cows at high feeding levels. Journal of Dairy
Science, vol. 47, p. 298-299.
Bache, C. A., D. J. Lisk, D. G. Wagner, and R. G. Wagner, 1964.
Elimination of 2-methyl-4-chlorophenoxyacetic acid and
4-(2-methyl-4-chlorophenoxybutyric) acid in the urine from
cows. Journal of Dairy Science, vol. 47, p. 93-95.
Basler, E. , 1964. The decarboxylation of phenoxyacetic acid
herbicides by excised leaves of woody plants. Weeds, vol.
12, p. 14-16.
15. Bell, G. R,, 1957. Some morphological and biochemical characteristics
of a soil bacterium which decomposes 2,4-dichlorophenoxyacetic
acid. Canadian Journal of Microbiology vol. 3, p. 821-840.
16. Bell, G, R., 1960. Studies on a soil achromobacter which degrades
2,4-dlchlorophenoxyacetlc acid. Canadian Journal of Micro-
biology, vol. 6, p. 325-337.
t
-49-
17* Bocks, S. M. , J. R. L. Smith, and R. 0. C. Normal, 1964.
Hydroxylation of phenoxyacetic acid and anisole by
Aspergillus niger. (van Tiegh) . Nature, vol. 201, p. 398.
18. Butts, J. S., and S. C. Fang, 1956. Tracer studies on the mechanisms
of action of hormonal herbicides. U.S. Atomic Energy Report
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19. Byrde, R. J. W. , F. Harris, and D. Woodcock, 1956. The metabolism
of w- (2-nap thyloxy) -n-alkyl-carboxylic acids by Aspergillus
nlger. Biochemical Journal, vol. 64, p. 154-160.
20. Byrde, R. J. W. , D. Woodcock, 1957. 2. The metabolism of some
phenoxy-n-alkyl-carboxylic acids by Aspergillus niger .
Biochemical Journal, vol. 65, p. 682-686.
21. Byrde, R. J. W., and D. Woodcock, 1958. 3. The metabolism of
w-(2-napthyloxy) -n-alkyl-acrboxylic acids by Sclerotinia
laxa. Biochemical Journal, vol. 69, p. 19-21.
22. Canny, M. J., and K. Markus, 1960. The breakdown of 2,4-dichloro-
phenoxyacetic acid in shoots and roots. Australian Journal
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23. Castlefranco, Paul A. Oppenheim, and Shogo Yamaguchl, 1963.
Riboflavin mediated photodecomposition of amitrole in
relation to chlorosis. Weeds, vol. 11, p. 111-115.
24. Chkanikov, D. I. and N. N. Pavlova, 1966. Proteins responsible
for 2,4-D detoxication in resistant plants. Agrokhlmiya,
No. 5, p. 115-119.
-50-
25. Chow, P. N., 1966. Absorption, Translocation and Metabolism
of 2-(2,4,5-Trichlorophenoxy) propionic Acid-l-C^** in
Opuntia spp. Dissertation Abstracts, vol. 26, p. 4152.
26. Chow, P. N., 0. C. Burnside, T. L. Lavy, and H. W. Knoche, 1966.
Absorption, Translocation and Metabolism of Silvex in
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27. Clark, D. E,, J. E. Young, R. L. Younger, L. M. Hunt, and
J. K, McLaren, 1964. The fate of 2,4-dichlorophenoxyacetic
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29. Crafts, A, S., 1960. Evidence for hydrolysis of 2,4-D during
absorption by plants. Weeds, vol. 8, p. 19-25.
30. Crosby, D. G., 1964. Metabolites of 2,4-dichlorophenoxyacetic
acid (2,4-D) in bean plants. Journal of Agriculture and
Food Chemistry, vol. 12, p. 3-6.
31. Crosby, D. G., and Helmut 0. Tutass, 1966. Photodecomposition
of 2,4-Dichlorophenoxyacetic acid. Journal of Agriculture
and Food Chemistry, vol, 14, p. 596-599.
32. Edgerton, L. J. and M. B. Hoffman, 1961. Fluorine substitution
affects decarboxylation of 2,4-dichlorophenoxyacetic acid
la apple. Science, vol. 134, p. 341.
f'
-51-
33. Erickson, L. C., B. L. Brannaman, and Charles W. Coggins, Jr., 1963.
Residues in stored lemons treated with various formulations
of 2,4-D. Journal of Agriculture and Food Chemistry, vol. 11,
p. 437-440.
34. Erickson, L. C., and Henry Z. Nield, 1962. Determination of
2.4- dichlorophenoxyacetic acid in citrus fruit. Journal
of Agriculture and Food Chemistry, vol. 10, p. 204-207.
35. Evans, W. C., and P. Moss, 1957. The metabolism of the herbicide
p-chlorophenoxyacetic acid by a soil microorganism - the
formation of a B-chloro-muconic acid on ring fission.
Biochemical Journal, vol. 65, p. 8P.
36. Evans, U. C., and B. S. W. Smith, 1954. The photochemical
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37. Fang, S. C. , 1958. Absorption, translocation, and metabolism of
2.4- D-l-C^'* in pea and tomato plants. Weeds, vol. 6, p. 179-186.
38. Fang, S. C., E. G. Jaworski, A. V. Logan, V. H. Freed, and
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Aspergillus niger . Journal of the Chemical Society (London)
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40. Faulkner, J. K. and D. Woodcock, 1964. Metabolism of 2,4-
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van Tiegh. Nature, vol. 203, p. 865.
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Al. Faulkner, J. K. and D, Woodcock, 1965. Fungal detoxication.
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42. Fawcett, C. H. , J. M. A. Ingram, and R. L. Wain, 1954. The
B-oxidation of w-phenoxyalkylcarboxylic acids in the
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Degradation of 2,4 ,5-Trichlorophenoxyacetic acid in woody
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46. Gutenmann, W. H., 1964. Conversion of 4-(2,4-DB) to 2,4-dlchloro-
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48. Gutenmann, W. U., D. D. Hardee, R. F. Holland, and D. J. Llsk, ^
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for the demonstration of a pathway of phenoxy herbicide
degradation. Agronomy Journal, vol. 56, p. 91-92 .
71. MacRae, I. C., M. Alexander, and A. D. Rovira, 1963. The decomposition
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72. Meagher, W. R. , 1966. A Heat-Labile Insoluble Conjugated form of
2,4-Dichlorophenoxyacetic acid and 2-(2,4 ,5-Trichlorophenoxy)
propionic acid in citrus peel. Journal of Agricultural and
Food Chemistry, vol. 14, p. 599-601
73. Morgan, Page W., and Wayne C. Hall, 1963. Metabolism of 2,4-D
by cotton and grain sorghum. Weeds, vol. 11, p. 130-135.
74. Morre, D. James, and B. J. Rogers, 1960. The fate of long chain
esters of 2,4-D in plants. Weeds, vol. 8, p. 436-447.
75. Morton, H. L., and R. E. Meyer, 1962. Absorption, translocation
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78. Norris, L, A,, 1966. Degradation of 2,4-D and 2,4,5-T In Forest
litter. Journal of Forestry, vol. 64, p. 475-476.
79. Norris, L. A. and V. H. Freed, 1966. The metabolism of a series
of chlorophenoxyalkyl acid herbicides In blgleaf maple,
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labeled growth regulators of the phenoxy and naphthalenlc
types in apple tissue. Dissertation abstracts, vol. 28B ,
p. 415.
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Fate of atrazine, kuron, silvex, and 2,4,5-T in the
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90. Slife, F. W., J. L. Key, S. Yamaguchi, and A. S. Crafts, 1962.
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% 107 .
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#
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114.
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-62-
Section IV
Efficacy Data Under Field and Laboratory Conditions
A. Effectiveness for Intended Purpose When Used as Directed:
Three decades of intensive research has shown that 2,4-D and 2,4,5-T
are still our two most useful herbicides for controlling undesirable
woody plants on forest lands. Both chemicals are of approximately
equal value due to variation in susceptibility of our native shrubs
and tree species. Silvex (2,4,5-TP) is not generally as effective
as either 2,4-D or 2,4,5-T, and much smaller amounts of Silvex are
used on forest lands. Many species, like vine maple (Acer c ire ina turn)
in the Pacific Northwest respond only to 2,4,5-T. These three
herbicides are by far the most extensively used chemicals for woody
plant control on forest land throughout the Nation. After 30 years
of research, phenoxy herbicide. e not only the most effective
herbicides on woody plants on forest lands, but also the least
expensive, the least persistent, and the most selective for control
of undesirable woody species on forest land.
Substituting less effective herbicides would only Increase contamination
of the forest environment. Increased amounts of herbicide and additional
applications of these herbicides would be required to achieve similar
silvicultural results. It should also be noted at this time that the
phenoxy herbicides 2,4-D, 2,4,5-T, and 2,4,5-TP are biodegradable
and do not persist in the forest environment. Although this will be
-63-
stressed later, it should be noted at this time that by replacing
these compounds, we may inadvertently select and use chemicals that
are more damaging and persistent in the environment. We now have 20
years of accumulated knowledge concerning effects of 2,4,5-T on forest
vegetation without visible evidence of adverse effect on humans,
desirable vegetation, or wildlife. It is readily conceivable that new
chemicals may prove even less acceptable after a similar period of
use and study.
B, Phytotoxicity; (See tables)
It would be literally impossible to list the relative effectiveness
of 2,4-D, Silvex, and 2,4,5-T on the multitude of plants treated with
these herbicides in all parts of the Nation. Furthermore, the chemicals
are applied as aerial sprays, basal sprays, stem sprays, and with powered
ground apparatus in many different carriers. As stated earlier, there
are also a host of different types of formulations available as commercial
products containing acids, esters, amines, inorganic salts, etc. Therefore,
the following pages simply show the relative effectiveness of low volatile
esters of these three phenoxy herbicides when applied as aerial budbreak
or foliar sprays. In general, their relative effectiveness when used
in this fashion, is indicative of their relative effectiveness on the
same species when applied in other ways. Although the list of species
contains only a small percentage of those plants treated with 2,4-D,
Silvex, and 2,4,5-T, the fact that this lengthy list is so incomplete
-64-
serves to stress the relative importance of the three chemicals In
forests, on rlghts-of-way , range lands and pasture lands. If their
safe agricultural uses were also listed, the size of the document would
be overwhelming.
Table 1 RELATIVE EFFECTIVENESS OF 2,4-D, SILVER, AND 2,4,5-T
APPLIED AS AERIAL BUD-BREAK OR FOLIAR SPRAYS 1/
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Pinus Taeda 2,A,5-T 2 Emulsion LF I Amchem Prod. Inc
Problem Pounds ai
Area 2J Plant Chemical^/ per acreV DiluentV Season^ Results?^/ References
sf
00
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CM
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o o o
3: O
69
Xj See footnotes at end of tables
Problem Pounds ai
Area _2/ Plant Chemical^/ per acreV DiluentV Season^/ Results?^/ References
O
o
o
m
ir>
m
ON
CJN
C3\
rM
tH
1—4
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61
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cn
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ca
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70
Problem Pounds ai
Area Ij Plant ChemlcalV per acreA_/ Diluent V Season^/ Results?^/ References
o
ON
iH
fH
€S
>-i
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sr
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s
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Pinyons - Pinus edulis; - _ _ > Phenoxys
Pinus monophy ILa ; Pinus not effective
cembroides
%
M-l
6
c
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Area IJ Plant Chemical^/ per acre^/ Diluent V Season^/ Results^./ References
76
Footnotes for Table
a
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77
resistant; usually requires more than two treatments and may still show some
C. Translocation with plant treated:
\
Translocation of phenoxy herbicides is closely associated with movement
of organic foods from regions where sugars are synthesized to regions
where food is being utilized in growth and storage (28, 33, and 36).
Foliar applied herbicides move through the leaf cuticle into the
living cells and are then rapidly translocated through living tissues
(symplast) such as the lumina of sieve tubes in the phloem (29, 34).
Translocation is to areas where food is being used or stored at the
moment. For example, from leaves of young seedlings, movement is
into the roots, resulting in excellent plant kill. From later leaves,
foods and herbicides are moved into both roots and shoots; giving some
of the best kills on older plants. Movement from mature upper leaves
is largely into growing shoots, flowers, and fruits (29). In this
season, herbicides may begin to decrease somewhat in effectiveness.
In the process, appreciable amounts of the herbicide may be lost.
Some of this is absorbed on plant surfaces, other portions may not
be able to penetrate the plant cuticle and are leached from the
surface by rain, some of that which is absorbed into the plant may
be immobilized in the treated tissue by absorption to or conjugation
with cell constituents, additional portions may accumulate in vacuoles
of parenchyma, and finally, additional portions may be degraded by
enzyme systems within the plant.
-78-
Under any circumstances, movement of phenoxy herbicides in woody
plants varies considerably depending upon species, season, and
formulation of herbicide. Leonard and Crafts (33) tested several
herbicides on seven different species of shrubs in California.
All species showed different patterns of upward and downward movement
during various seasons of the year. Coyote bush absorbed and trans-
located radioactive 2,4-D only slightly in February, intensely in
April, and not at all in July. In February and March, movement was
downward from treated leaves; in April almost entirely upward. In
manzanita, 2,A-D was absorbed and translocated throughout May, but
most of the movement was downward. On live oak (Quercus wlsllzenll)
2,4-D was actively translocated from February through September:
in February, movement was entirely downward, some upward after new
growth started in March, but then largely downward throughout the
rest of the season. Presence of adequate soil moisture for food
manufacture and movement was important in activity of the herbicides
as well. Their study also showed that too quick a leaf kill
nullifies the effect of the herbicides. An early browning of leaves,
reduces absorption and translocation of the herbicides and results
In an ineffective treatment. This stresses the fact that different
species require different treatments both in rate of herbicide and
time of application. In evergreen species, chemicals may move up
and down the stems for many months; the period of movement may be
very short for deciduous species. Others (28) learned that trans-
location of phenoxy herbicides is much slower in woody seedlings
-79-
than in herbaceous seedlings (1) and that high humidity increases
uptake by oak seedlings. Yamaguchi (37) learned that 2,A-D and
probably the other phenoxy herbicides as well, translocate much
less readily than amitrole. He also found that 2,4-D moves into
plant leaves better from acidic solutions than from an alkaline
medium. Approximately ten times as much, 2,4-D was absorbed from
a medium of pH 3 then from one with a pH 11.
In basal sprays, low volatile esters dissolved in oil are heavily
applied to the lower 18 Inches of stems of shrubs and weed trees.
Such treatments are usually most effective during the growing
season, but are usually no better than foliar sprays on most
species. In basal bark applications, the herbicides move upward
through the xylem with the transpiration stream. From there,
there is increasing evidence that such material may move into
living tissues such as the phloem and be translocated to other
parts of the plant. On thin-barked species, there is evidence
that 2,4,5-T may be picked up as readily through the thin bark
as through the foliage (34). In this experiment, 2,4,5-T was
tested in three different formulations: an ester, an amine, and
an acid. In all cases, the ester form was picked up best.
Two additional points deserve mention. Freed and Morris (30)
have pointed out that ecotypic variation within species can
account for successful effects on a species in one area, while
the same treatment falls on the same species in another area.
-80-
4
This was first observed some years ago. The second point is
that phenoxy compounds, like other herbicides, may leak from
roots into soil, where they may affect soil microflora and
microfauna. This could have some hidden and unforseen effects
in silviculture. Such effects, however, may be counteracted to
some extent by Increased soil temperature and moisture that produce
increased amounts and activity of soil microflora and microfauna (31) .
D. Compatability
The phenoxy herbicides are compatible with each other and with
most other herbicides, but this compatibility is dependent to
a great degree on the particular formulation of- 2,A-D silvex,
or 2,A,5-T used. Phenoxy herbicides formulated for use only in
oil carriers should never be mixed with wettable powders like
atrazlne or other materials formulated only for use in water
carriers. Water soluble formulations such as amines or Inorganic
salts can be safely mixed with other water soluble herbicides
or wettable powders. Most phenoxy esters, however, are formulated
for use in either water, oil, or oil-in-water emulsions. Such
formulations can be mixed and applied simultaneously with oil-
soluble or water-soluble materials or with wettable powders such
as atrazine, terbacil, and dalapon.
-81-
Phenoxy herbicides are also sometimes considered for mixture and
application with fertilizers. When considered for simultaneous
application with phenoxy herbicides, however, the fertilizer must
be either water soluble or in liquid form. Recent research also
indicates that ammonia and urea fertilizers have different effects
on action of phenoxy herbicides. This should be considered before
making a choice of fertilizers.
-82-
REFERENCES
1. 1972. Specimen labels useful as references for these herbicides
may be obtained from:
Amchem Products, Inc.
Chipman Chemical Company, Inc.
Diamond Alkali Company
The Dow Chemical Company
Monsanto Chemical Company
Stauffer Chemical Company
Thompson-Hayward Chemical Company
2. Oregon Extension Service. 1970. Oregon weed control handbook.
Oregon Univ., Coop. Ext. Serv., Corvallis, Oregon 287 pp.
3. National Academy of Sciences, 1957. Principles of weed control,
Vol. 2, Weed Control, 471 pp.
4. Washington State University and Department of Agriculture, 1971.
Washington pest control handbook. Washington State Univ.,
Pullman, Washington, 569 pp.
5. Weed Society of America, 1967. Herbicide handbook of the Weed
Society of America. W. F, Humphrey Press, Inc., Geneva,
N.Y., 293 pp.
6. Anonymous, 1961. Herbicides and their use in forestry. Symp.
Proc., School of Forestry, Oreg. State Univ., Corvallis,
Oregon, 122 pp.
7. Arend, John L., and Eugene I. Roe, 1961. Releasing conifers
in the Lake States with chemicals. USDA, Agric. Handbook
No. 185, 22 pp.
-83-
8, Bentley, Jay R. , and Kenneth M. Estes, 1965. Use of herbicides
on timber plantations in California. California Region USES
and Pacific SW Forest and Range Experiment Station, US) A, A7 pp.
9. Brady, Homer, Fred A. Peev, and Paul Y. Burns, 1969. Erratic
results from aerial spraying of mid south hardwoods. Journal
of Forestry 67(6): 393-396.
10. Burns, Paul Y. (Ed.), 1958. Chemical pine release symposium, Proc.
The Dow Chemical Co., Louisiana State Univ. 67 pp.
11. Dahms, Walter G., 1961. Chemical control of brush in ponderosa
pine forests of Central Oregon. US Forest Service, Res. Pap.
39, 17 pp, Pacific Northwest Forest and Range Exp. Sta.,
Portland, Oregon.
12. Gratkowski, H., 1959. Effects of herbicides on some important
brush species in southwestern Oregon. U.S. Forest Service
Res. Pap. 31, 33 pp.. Pacific Northwest Forest and Range
Experiment Station, Portland, Oregon,
13. 1961, Toxicity of herbicides on three northwestern conifers.
U.S, Forest Service Res. Pap. 42, 24 pp.. Pacific Northwest
Forest and Range Experiment Station, Portland, Oregon.
14. 1961, Use of herbicides on forest lands in southwestern Oregon,
U.S, Forest Serv, Res. Note No. 217. 18 pp. Pacific Northwest
Forest and Range Experiment Station, Portland, Oregon.
15. Gratkowski, H. J. and J. R. Philbrick, 1965. Repeated aerial
spraying and burning to control sclerophyllous brush. Jour.
Forestry, 63(12) : 919-923.
-84-
16. Gratkowski, H., 1968. Repeated spraying to control southwest
Oregon brush species. U.S. Forest Serv. Res. Pap. PNW-
59. 6 pp. Pacific Northwest Forest and Range Experiment
Station, Portland, Oregon.
17. Leonard, 0. A. (Ed.) 1961. Tables on reaction of woody plants
to herbicides. Western Weed Control Conf. Res. Prog. Rpt.
pp. 27-37.
18. Leonard, Oliver A., and W. A. Harvey, 1965. Chemical control of
woody plants. Calif. Agric. Exp. Sta., Davis, Calif. Bull.
812, 26 pp.
19. Lindmark, Ronald D. , 1965. Removing undesirable trees from hardwood
stands. Central States Forest Experiment Station, U.S. Forest
Service, USDA, 23 pp.
20. McQuilkin, W. E., 1957. Frill treatment with 2,4,5-T and 2,A-D
effective for killing northern hardwoods. Northeastern For.
Exp. Sta., Station Paper No. 97, 18 pp.
21. Newton, Michael (Ed.) 1967. Vegetation management — system of
operation. Symp. Proc. : Herbicides and Vegetation Management
in Forests, Ranges, and Noncrop Lands. Oregon State University,
Corvallis, Oregon, pp. 8-11.
22, Romancler, Robert M. , 1965. 2,4-D, 2,4,5-T, and related chemicals
for woody plant control in the southeastern United States.
Georgia Forest Research Council Report No. 16. 46 pp.
Southeastern Forest Exp. Sta., US Forest Service, USDA.
-84a-
23. Rudolf, Paul 0,, and Richard F. Watt, 1956. Chemical control of
brush and trees in the Lake States. Station Paper No. 41,
58 pps. Lake States Forest Exp. Sta., US Forest Service, USDA.
24. Schubert, Gilbert H., 1962. Chemicals for brush control in Calif-
ornia reforestation. US Forest Service Misc. Pap. 73, 14 pp.
Pacific Southwest Forest and Range Experiment Station, USDA.
25. Sutton, R. F. , 1958. Chemical herbicides and their uses in the
silviculture of forests of eastern Canada. Forest Research
Branch Technical Note No. 68, 56 pp. Canada Dept, of Agri.
26. Tschirley, Fred H. (Ed.) 1968. Research report .. .response of
tropical and subtropical woody plants to chemical treatments.
Dept, of Agric. CR-13-67 , 197 pp. Agric. Res. Serv., Washing-
ton, D. C.
27. Walker, Laurence C. , 1956. Controlling undesirable hardwoods.
Georgia Forest Research Council Rep. No. 3, 24 pp. School
of Forestry, University of Georgia, Athens, Georgia.
28. Clor, M. A., A. S. Crafts, and S. Yamaguchi, 1964. Translocation
of C^**-labeled compounds in cotton and oaks. Weeds 12(3):
194-200.
29. Crafts, A. S., 1961. The chemistry and mode of action of herbicides.
Interscience Publ. N.Y. , 269 pp.
30. Freed, V. H., and R. 0. Morris, 1967. Environmental and other
factors in the response of plants to herbicides. Agric.
Experiment Sta. Tech. Bull. 100. 128 pp, Oregon State
University, Corvallis, Oregon.
/
-84b-
4
31
. Gratkowski, H., 1967. Ecological considerations in brush control.
In herbicides and vegetation management, Symp. Proc., Oregon
State Univ., Corvallis, Oregon, pp. 124-140.
32. Leonard, 0. A., 1963. Translocation of herbicides in woody plants.
Soc. of American Foresters Proc.
33. Leonard, 0. A., and Alden S. Crafts, 1956. Uptake and distribution
of radioactive 2,4-D by brush species. Calif. Agric. Exp. Sta.
University of California, Berkeley, California, Hllgardla 26(6)
366-415.
34. Leonard, 0. A., D. E. Bayer, and R. K. Glenn, 1966. Translocation
of herbicides and assimilates in red maple and white ash.
Bot. Gaz. 127(4) : 193-201.
35. Shaw, U. C. , J. L. Hilton, D. E. Moreland, and L. L. Jansen, 1960.
Herbicides in plants. Symp. Proc., The nature and fate of
chemicals applied to soils, plants, and animals, pp. 119-133.
Agric. Res. Serv., U.S. Dept. Agric. Beltsvllle, Maryland.
36. Woods, Frank W., 1955. Control of woody weeds. U.S. Forest
Serv. Occ. Pap. 143. 50 pp.. Southern Forest Experiment
Station, New Orleans, Louisiana.
37. Yamaguchi, Shogo, 1965. Analysis of 2,4-D transport. Div. of
Agric. Sci., Univ. of California, Berkeley, California,
Hilgardia 36(9) :349-377 .
-84c-
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Section V
Residues
A. Residues In Soli
The forest floor is a major receptor of phenoxy herbicides whether
applied from aircraft or by ground spray systems. There it may be
absorbed on soil colloids or absorbed in organic matter, degraded
chemically or biologically, volatilize and move to other areas,
or leach to depths or locations where it cannot be absorbed by
plant roots (11, 13). Once in the soil, however, the phenoxy
herbicides are not persistent (9, 11, 13, 14). 2,4-D is much
more rapidly degraded than 2,4,5-T or silvex, but even 2,4,5-T
will not usually remain in the forest floor from one year to the
next. Fairly rapid degradation of phenoxy herbicides in soil has
been shown in several studies (9, 10, 11, and 14). Generally,
these studies indicate that 85 to 90 percent of 2,4-D will be
degraded in about 15 days, but 2,4,5-T is more persistent. In
one study, 23 percent of 2,4,5-T was still present in soil after
13 days; this had decreased to 13 percent after 120 days.
The concensus is almost unanimous that degradation of phenoxy
herbicides in soil is microbial (4, 5, 7, 11, 14, and 15).
Steenson (16) believed that bacterial decomposition is aerobic.
Norris' (11) data indicates that soil microorganisms adapt more
readily to use 2,4-D than 2,4,5-T as a substrate, and that it
is for this reason that 2,4-D is degraded more quickly than 2,4,5-T
-85-
and possibly silvex (7). Repeated applications are more rapidly
decomposed by microbes than are the initial sprays (9, 10). This
would indicate that once adapted to use these materials as a substrate
soil microorganisms begin decomposition more quickly or their numbers
increase more rapidly when phenoxy herbicides once again appear in
their soil environment.
Finally, different formulations show different rates of degradation.
Pure 2,4-D acid degraded more quickly than either the solubilized acid
or the isooctyl ester (12) . Both acid and ester forms are leachable
from soil. Leaching and movement into streams does not usually become
a problem however, since the herbicides are rapidly decomposed in the
soil (10) .
Recent studies show that 2,4,5-T is extensively adsorbed by forest
floor material. About 60 percent of the 2,4,5-T in solution was
adsorbed at equilibrium (30°C) which was attained in a few hours
(14). The extensive interaction of 2,4,5-T with the forest floor
suggests only limited leaching should occur. In an agricultural
soil, 2,4,5-T remained in the upper six inches even after applica-
tion of 4.5 inches of water over a short period of time (17). A
lack of 2,4,5-T residues in streams flowing from treated areas (13)
suggests that a combination of rapid degradation and resistance to
leaching prevents stream contamination. (8)
f
-86-
Greenhouse tests using beans as the more, and tomatoes as the less,
sensitive indicator crop on several typical agricultural soil types
in Hawaii showed that 2,4-D applied as dust at 10 Ib/acre was dis-
sipated from the soil in 2-14 weeks, the rapidity of inactivation
depending on the higher temperatures and pH values of the soil. A
change of pH also was not correlated with organic-matter content,
fertilizers or adsorption capacity. The number of aerobic bacteria
appeared to be negatively correlated with 2,4-D persistence in the
soil (1).
After leaching a 25 cm-high soil column to which 2,4-D had been
applied superficially, almost the entire application was found in
the top 5 cm. At recognized application rates, and under favorable
conditions of moisture and temperature for soil microorganisms,
2,4-D was inactivated in a maximum period of six weeks. In a
forest clearing on relatively "inactive" acid soil, a heavy appli-
cation of 2,4-D was rendered 90% inactive in 15 weeks, but in
sterilized soil no decomposition of the substance was observed.
Its inhibiting action on germination was markedly stronger in sandy
than in loamy soils. Nitrification in nutrient solutions was con-
siderably checked at the normal application rate of 2,4-D, but
addition of soil almost completely counteracted this effect. (3)
The presence of Tordon 50 D (picloram tri-isopropanolamine 2,4-D
in the proportions 1:4) and 2,4,5-T in soil reduced the emergence
-87-
and survival of Pinus radiata seedlings, the major effect being on
survival. Effects of 2,A,5-T disappeared rapidly (within two months
of application) , whereas some effects of Tordon 50 D persisted for
at least six months. Sterilization of the soil by autoclaving did
not delay breakdown of the herbicide, nor did leaching of the soil
hasten the decline of its activity. The herbicides affected initial
growth of seedlings, but older seedlings would suffer little or no
damage if planted on sites treated with these herbicides a few months
previously (2).
The repeated applications of 2,4-D to soils resulted in a buildup
of organisms which rapidly decompose the hormone. Two bacterial
species were isolated from such treated soils; these were demon-
strated to be capable of inactivating 2,4-D added to the soil.
These were identified as Flavovacterium aquatile and a Coryne-
bacterium-like organism. Approximately ten times as much 2,4-D
as dinitro-o-cresol was required to inhibit the growth of the
following soil organisms; Rhizobium meliloti, R. trifoli, R.
lebuminosarum, R. lupini. Agrobacterium radiobacter, Azotobacter
chroococcum. A, beijerinckii, Nitrosomonas europaea. Bacillus
subtilis, B. mycoides, Escherichia coli. Bacterium aerogenes,
B. prodigiosum, Pseudomonas pyocyanea, Cellvibrio sp.,
Sytophaga sp., Mycobacterium phlei, Nocardia corallina,
Streptomyces griseus, and Micromonospora sp . It is considered
unlikely that the repeated applications of 2,4-D to soils would
-88-
seriously inhibit the beneficial bacterial flora. It is suggested
that there is a possibility that the repeated applications might
result in an excessive increase in the bacterial flora which would
inactivate the hormone and thus result in a decrease in the
effectiveness of the herbicide (6).
B. Residues in Water
All available information indicates that although some phenoxy
herbicides may enter streams flowing through or adjacent to areas
being sprayed, the levels in the streams will be very low. In 6
years of monitoring spray operations in western Oregon, scientists
have never found phenoxy residues exceeding 0.1 ppm in western
Oregon stre^lms (29, 31). Even this can be reduced or eliminated
by leaving untreated buffer strips between the sprayed area and
running streams. Such short-term initial low-level contamination
by 2,A,5-T is regarded as no hazard to fish or animals. Long-term
low-level pollution is only found where phenoxy herbicides are
applied directly on marshy areas.
In their report to Administrator W. D. Ruckelshaous of the
Environmental Protection Agency, the Advisory Committee of
Scientists on 2,A,5-T stated that all available data indicates
that the amount of 2,A,5-T entering water is small and doesn’t
stay long. It is adsorbed on clay or absorbed by viota within
-89-
days (36) . Phenoxy chemicals entering water may be lost by
volatilization, adsorption on sediments, absorption by biota,
by degradation, and by dilution as additional stream water
passes through the site. This latter function is by far the
most important. Almost all authorities agree that there is
adsorption on bottom sediments (18, 22) . This contamination of
bottom sediments, however, does not appear to last long. Concen-
trations of low volatile esters of silvex in water after application
on the surface of three ponds decreased to 0 by the end of three
weeks (18). Rapid degradation of phenoxy herbicides in water
appears to be the rule, especially in bodies of water with histories
of repeated applications of phenoxy herbicides. Several studies
indicate further that persistence of 2,A-D and 2,4,5-T in fresh
water ponds can be drastically decreased by adding small amounts
of soil previously treated with phenoxy herbicides (32) . Rapid
degradation of 2,A-D was also observed in water samples collected
from areas with a history of repeated 2,A-D applications (23) .
As stated earlier, most phenoxy herbicides enter aquatic environ-
ments during the actual period of spraying. There appears to be
little chance that additional amounts will be added to the water
with the passage of time. At normal application rates, approximately
100 to 300 ppm of herbicide will be found in vegetation shortly after
application. This will decline to low levels in a few weeks (31) .
-90-
r
Only small amounts of herbicide will enter streams by washing action
of rain from overhanging treated vegetation above a stream or from
leaves falling into water (29). Furthermore, repeated observation
indicates that heavy fall rains will not leach phenoxy herbicides
through the soil into streams if the herbicides have been applied
during the spring or very early summer. The phenoxy herbicides move
through the soil only in very small amounts and for very short
distances. There seems very little chance of stream pollution from
this source (30) . Although small amounts of phenoxy herbicides
are exuded from roots of treated plants, this also is a negligible
source of contamination. The amounts exuded are small and only
roots in the stream or in the hydrosoil would provide a source for
such contamination (29) . Such exhudation seems to occur most from
plants that are photosynthesizing most rapidly (25) .
In conclusion, it appears that it would be quite safe to continue
use of the phenoxy herbicides on forest lands. Where these chemicals
are used at rates up to 4 lbs. ae per acre and are properly applied,
there should be little or no danger to aquatic environments in the
treated areas or to nontarget organisms on the sprayed sites.
Since October 1965, samples of a water-suspended sediment mixture
from 11 streams in the Western United States have been analyzed
monthly for 12 pesticides including the herbicides 2,4-D, 2,4,5-T,
and silvex. No herbicide was found at any station during the first
year of the sampling program. (19)
-91-
Concentrations of (2,4-dichlorophenoxy) acetic acid (2,4-D) were
determined in irrigation water following bank applications for
weed control. Applications of 1.9 to 3 Ib/A of 2,4-D produced
maximum concentrations of 25 to 61 ppb. Reduction of herbicide
levels appeared to be due to dilution as the water flowed down-
stream. Rates of reduction in herbicide levels showed that
negligible concentrations would remain after the water traveled
a distance of 20 to 25 miles. The low concentrations of herbicides
observed in the irrigation water likely would not be hazardous to
crops or animals. (21)
In studies of the persistence of silvex in a closed artificial
aquatic environment in the laboratory, mean concentrations ranged
from 820 ppb immediately after application to 46 ppb after 19
weeks (Cochrane et al., 1965) (21). The ester of silvex was rapidly
hydrolyzed to the free acid. The authors speculated that, in
addition to loss through adsorption on hydrosoil or absorption by
aquatic vegetation, degradation also occurred (21).
A field study of silvex persistence was carried out in a creek
having very little water movement (Cochrane et al, 1965 (21) and
Nicholson, unpublished data) . After the first application,
concentrations ranged from 83 ppb one day after spraying to 1.1
ppb after 21 days. Silvex was not detectable after 35 days. After
the second application, concentrations ranged from 19 ppb one day
-92-
after spraying to 0.A8 ppb after 70 days. Following the third
application, concentrations decreased from 73 ppb immediately after
spraying to 2 ppb after A8 days, and to 0.1 ppb after 6 months.
Silvex could not be detected one year after application. Another
field test was carried out in a fast-flowing stream which provided
maximal opportunity for dilution and interchange of water. Residues
of silvex were not detected except during the first few hours following
treatment. The maximum level found in this study was 0.05 P.P.M (21).
C. Residues in Plants
Few studies have been conducted on herbicide residues in woody
plants, and even some of this limited information is questionable
or contradictory. Even less work has been done on the multitude
of possible metabolites and their incorporation into or conjugation
with plant constituents.
Persistence of 2,A-D, silvex, and 2,A,5-T in plants, is initially
dependent upon the amount of herbicide that actually reaches the
plant surface, and the percentage of this herbicide that is
absorbed by the plant. In aerial application, the percentage
reaching vegetation may be small. Interception disks at vegetation
level on one area in the Oregon Coast Range indicated that only
about one third of the herbicide applied was reaching the vegetation
(A8) . Once within the plant, the herbicides are rapidly absorbed
into the symplast and moved through the vascular channels along
0
-93-
L
with assimilates toward sinks where foods are being used. Enroute
their concentration may be further reduced by accumulation in
vacuoles of living parenchuma cells of phloem, cortex, xylem, and
pith (39) . Additional amounts may be metabolized through degradation
of the acetic acid side chain, hydroxylation of the aromatic ring,
or conjugation with a plant constituent (44) . Some herbicide may
even be immobilized by adsorption to cells or cell constituents
at any point along this route (50). As a result, because of
degradation, growth dilution, and other factors, residues of the
phenoxy herbicide in plants will probably be markedly reduced
within a few weeks after application (47) .
A review of the literature indicates the concensus that phenoxy
herbicides are among the least persistent herbicides in plants.
Most investigations indicate metabolism of 2,4-D and 2,4,5-T in
plants is similar, although their rate of degradation may vary
considerably even within a given species or genus. Metabolism
is much slower in dormant than in active tissues. Easier et al
(38) found that excised blackjack oak leaves broke down 59% of
2,4,5-T into three major unidentified metabolites in 24 hours, and
Morton (45) reported that 80% of 2,4,5-T applied to mesquite was
metabolized in 24 hours. The environment of mesquite prior to
treatment also affects the amount of phenoxyacetic herbicides
metabolized. 2,4,5-T metabolism was greatest in the range from 70®
to 8 ®F., less at 100®F., and completely inhibited at 50®F. In
(
-94-
another study, Morton et al (46 found that initial concentrations of
100 ppm of 2,4-d' or 2,4,5-T in grasses were decreased to 1 ppm and 2 ppm,
respectively, after 16 weeks. They concluded that the half life of
2,4,5-T esters in green grass tissues ranged from 1.6 to 2.9 weeks.
Only a small percentage of the numerous metabolites of the phenoxy
herbicides in plants have been identified. In sweet gum and southern
red oak, 2,4 ,5-trichlorophenol was identified as a common metabolic
product (40) . It is conceivable that other metabolic by-products
of the herbicides are utilized as constituents of the numerous
carbohydrates, amino acids, and the numerous proteins in plants.
In their report to the Administrator of the Environmental Protection
Agency, Wilson et al (52) concluded that 2,4,5-T doesn't accumulate
in plants or in any other compartment of the biosphere and that risk
of human exposure to 2,4,5-T in food, air, or water is negligible.
They stated that in 10,000 food and feed samples from 1964 through
1969, only 25 contained trace amounts of 2,4,5-T (less than 0.1 ppm).
As Norris (49) points out, these reports and the extensive healthy
resprouting of brush which commonly occur a year following spraying
on forest lands, suggests that high residues of 2,4-D, silvex, and
2,4,5-T do not persist for long periods in forest vegetation. Since
degradation processes in both soil and vegetation are quite similar,
and the phenoxy herbicides do not persist from year to year in soil,
it is also improbable that they would persist from one year to another
in vegetation.
U-
Other mechanisms also affect herbicides that are intercepted by
foliage. Herbicides adsorbed on the surface of leaves will be
washed off by winter rains, subjected to photodecomposition, and
degraded by microbes. That portion that is leached from the surface
will enter the forest floor and be degraded as described earlier.
It has been determined that bacterial degradation products of
phenoxy herbicides are carbon dioxide, inorganic chloride ions,
and water. Since all of these materials are normal parts of our
environment, such decomposition products are readily recycled
and used by forest vegetation.
Much of the furor concerning teratogenic effects of 2,A,5-T
centered on its contamination with TCDD (2 ,3 ,7 ,8-tetrachloro-
dibenzo-p~dioxin) . A slight change in the manufacturing process
and strict quality control now ensure that commercial herbicidal
products contain less than 0.1 ppm of TCDD — a level that poses
no hazard when the products are used at recommended rates.
Recent studies by scientists of the U.S. Department of Agriculture
should ease the minds of those concerned about possible effects of
TCDD in the environment (42) . Their research shows that TCDD is
not biosynthesized from chlorophenols , in soils, is not a photo
product of 2,4,5-trichlorophenol, and does not leach into the soil
profile. Further, TCDD is not absorbed into or translocated within
-96-
the plant from foliar applications, and is not taken up by plants
from the minute residues that might be present in soils. To be
absolutely sure, Kearney and his associates treated the soil in
this experiment with a concentration of TCDD approximately AO, 000
times greater than the amount that would be deposited in soil from
a 2-pound-per-acre application of 2,A,5-T contaminated with 1 ppm
of TCDD. This was incorporated in the top 1/3-inch of the soil
surface. About half of the TCDD applied to foliage could be washed
from the leaves by simulated rainfall 2 hours after application.
Finally, TCDD could not be detected even at a level of 0.5 ppm in
tissue extracts from 22 bald eagle carcasses. The scientists
concluded that contamination by chlorodioxin in 2,A,5-T has
produced no measurable effects on the environment.
It is evident from the way 2,A,5-T is used and its behavior in the
forest environment that the primary exposure of animals to this
chemical will be through consumption of treated vegetation. Let
us consider the amounts of 2,A,5-T which might be ingested from
the highest residues found (300 ppm) in the study by Morton et al.
(1967) (47). A high milk-producing animal might consume up to
10 percent of its body weight in green forage per day. A 1,000
pound animal consuming 100 pounds of forage containing 300 ppm
of 2,A,5-T would ingest 30 milligrams of 2,4,5-T per kilogram of
body weight, well below the toxic level.
-97-
This Is a maximum exposure and would be received only when ingesting
forage grasses shortly after treatment. If residue levels drop to
less than 10 ppm a few weeks after treatment (Morton et al. 1967)(A7),
the ingestion level of 2,4,5-T will be no more than 1 mg/kg.
Low-volatile and high-volatile esters of 2, A-dichloro-phenoxyacetic
acid (2,4-D) were sprayed on separate pastures at about double the
usual rate (43) . Milk from cows grazing these pastures contained
from 0.01 to 0.09 ppm 2,4-D during the first 2 days after spraying
and lower amounts thereafter. Residues in milk from cows put into
the pastures 4 days after spraying were below 0.01 ppm, the practical
limit of precision of the method used. Residues of 2,4-D, in or on
forage, declined rapidly during the experiment. Almost all the 2,4-D
in or on forage was hydrolyzed to the acid form in samples of forage
taken within one-half hour after spraying with the butyl ester of
2»4-D, and about 75% after applying the 2-ethylhexyl ester.
The herbicides 2, 4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-
trichlorophenoxyacetic acid (2,4,5-T), each labeled in the carboxyl
position were sprayed on a pasture consisting of a mixture of silver
beardgrass (Andropogon saccharoides Swartz.), little bluestem (A.
scoparius Michx.) , and dallisgrass (Paspalum dilatatum Poir.) and
a sideoats grama (Bouteloua curtipendula (Michx. Torr)) pasture over
a 3-year period (47) . Plant samples were harvested at intervals
between 1 hour and 16 weeks after treatment and residues determined
-98-
by radio assay. No important differences were found in the persis-
tence of herbicides or of different formulations of the same herbicide.
Rainfall was the most important factor influencing the persistence
of the herbicides. The little bluestem-silver beardgrass-dallisgrass
samples harvested 1 hour after treatment with the butoxyethyl ester
of 2,4,5-T contained both this ester and the acid of 2,4,5-T. One
week after treatment, the acid of 2,4,5-T and unknown metabolites
were found but no ester (47) .
Two chemicals were tested. One, an ester of 2,4,5-T, was considered
a representative formulation of the commercially available herbicides.
The other was 2,4,5-T in the form of an emulsifiable acid (51). Her-
bicides were applied to all streambank vegetation by the same operator.
Since there was interest in detecting maximum contamination, the
herbicides were applied during a low streamflow period. Flow in all
streams was less than 0.1 cubic foot per second (45 gpm) .
Water samples were taken periodically after treatment at various
locations up and down stream. The first samples were collected
immediately after spraying following by a second group of samples
four hours later. Thereafter, samples were collected daily during
the first week and twice a week during the next three weeks.
Additional samples were collected after each rainstorm.
/
-99-
Streamflow samples collected were tested for contamination by a
calibrated three-member odor panel (Figure 2) . The testing pro-
cedure used was that approved by the American Society for Testing
and Materials Results indicate that during the three weeks following
treatment, contamination of streamflow occurred only immediately after
spraying and after the first large storm. In addition, contamination
was detectable only within the treated reach of stream and no con-
tamination was ever found in a downstream sample. Downstream samples
were collected approximately one mile away from the treated areas and
In both locations below the junction of the two treated streams.
D. Residues in Air
A certain portion of the spray material is dispersed by the wind
as fine droplets. Additional amounts of chemical may be lost
through volatilization of spray materials falling through the
air or from intercepting surfaces. Most of the herbicide not
lost through drift or volatilization is intercepted by the
vegetation or the forest floor. Additional small amounts fall
directly on surface water (56) .
The actual amount of "drift" and volatilization is dependent on a
number of physical, chemical and environmental factors, some of
which can be controlled or avoided by the applicator. Among the
physical variables are the pressure of application, height and
-100-
speed of delivery, nozzle design and the like. Chemical factors
include the properties of the carrier and the herbicide.
Environmental factors include temperature, relative humidity
and wind (56) .
Losses of aerially applied chemicals by drift and volatilization
should be avoided. First there is the obligation to hold
environmental contamination to a minimum. Secondly, the more
chemical which reaches the target the greater the efficiency
of the operation (56).
The distribution of two pounds per acre 2,4,5-T applied as a
mixture of low volatile esters in diesel oil was determined
in the coast range near Eddyville, Oregon. Treatment was by
fixed wing aircraft in the early spring. Analysis of inter-
ception disks show an approximate 60 percent to 75 percent loss
of herbicide (57) .
In a survey in the State of Washington, 2,4,5-T was detected 9
days out of 99 at Pullman, in average concentration in positive
samples of 0.045 ug/m^. At Kinnewick it was found 14 days out
of 102 at average concentration in positive samples of 0.012 ug/m^
(53). In Cincinnati, Ohio, 0.04 ppm was found adsorbed on dust in
a trace of rain persumably from applications in Texas (55) . Photo
0 chemical degradation would be expected to occur in the air, partic
-101-
ularly at high altitudes and in dry climates where ultraviolet
radiation is highest. Kearney et al (54) report that exposure of
5 and 10 ppm water solutions of 2,4,5-T to ultraviolet light from
a 450 watt Hanovia lamp greatly reduced the 2,4,5-T present within
5 minutes. It is not possible to extrapolate accurately from these
data to the rate of decomposition in sunlight, but it is obvious
that photochemical degradation could play a significant role.
Probably most of the 2,4,5-T that gets into the air very soon
either settles out or is washed out by rain and thereby is returned
to soil and water (58) .
There is no evidence to suggest that 2,4,5-T remains in the air
for more than a few weeks after insertion (58).
E. Residues in Animals
Feeding studies with various animals have shown that the phenoxy
herbicides are rapidly excreted. Erne (1966) (60) reported the
major route of elimination of 2,4,5-T from pigs, calves, and rats
dosed with 100 mg/kg. was in the urine. Repeated doses did not
result in retention or accumulation of herbicide. A cow which
received 5 ppm 2,4,5-T in its feed eliminated essentially all
of the chemical within two days following exposure, and no 2,4,5-T
was found in the milk (62). Mice injected wih 100 mg/kg 2,4,5-T
eliminated approximately 70 percent within 24 hours (63).
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Evaluation of animal exposure to 2,4,5-T leads to the following
conclusions: (26)
1. Dairy and beef animals allowed to forage on treated grasses
will ingest highest concentrations of 2,4,5-T shortly after
application.
2. Because of degradation, growth dilution, and other factors,
residues of 2,4,5-T will be markedly reduced a few weeks
after application.
3. The herbicide is rapidly excreted; there is no accumulation
in animal tissues.
4. There is no detectable residue in milk; therefore, man will
not be exposed to 2,4,5-T through consumption of milk or meat
from animals foraging on treated grasses.
5. Long-term chronic exposure of wildlife should not occur since
2,4,5-T does not persist for long periods in the forest, and
repeated applications are rare.
The distribution and elimination of two phenoxyacetic acids, 2,4-D
and 2,4,5-T were studied with a chemical method in rats, pigs,
calves and chickens (60).
When administered orally as amine or alkali salts, the compounds
were readily absorbed and distributed over the organism in all
species studied. The absorption of 2,4-D in the form of an ester
-103-
was incomplete, however, the ensuing plasma and tissue levels of
2,A-D being only low, (Intact ester could not be detected in
plasma) (60)
The highest tissue levels of 2,A-D and 2,4,5-T were found in liver,
kidney, lung and spleen, the levels sometimes exceeding the plasma
level. In blood cells, 10-20% of the plasma level was found.
Penetration of 2,4-D into adipose tissue and into the central
nervous system was restricted, whereas a ready placental transfer
was demonstrated in swine. The distribution pattern did not show
any significant species or — in rats — sex differences. (60)
Elimination of the compounds was rapid, the plasma half-life
being about three hours in rats, about eight hours in calves
and chickens and about 12 hours in pigs. The tissue half-life
values ranged between five and 30 hours, the lower values being
found in rats. No retention in tissues was noted, nor was
accumulation seen on repeated administration (60) .
In pigs and chickens an increased elimination rate was observed
after repeated administration. (60)
The major excretory route seemed to be via the kidneys in all
species studied. Hens excreted small amounts of 2,4-D with the
eggs. (60)
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A gas chromatographic method for the determination of residues of
2,A ,5-trichlorophenoxyacetic acid and its propylene glycol butyl
ether esters in tissues and fluids is described (59) . Both
compounds were converted to the methyl ester of 2,4,5-T and
analyzed by microcoulometric gas chromatography using a column
of 15% Dow 710 on Chroraport XXX. Average recoveries of 2,4,5-T
added to fat, lean tissue, urine, and blood levels from 0.05
ppm to 20 ppm were 89.3, 89.6, 93.0, and 93.6%, respectively.
Corrected recovery of unraetabolized ester added to fat, lean
tissue, urine, and blood at levels from 0.5 ppm to 20 ppm averaged
77.9, 70.5, 94.2, and 92.5%, respectively.
Herbicide residues in blacktail deer was studied by Newton and
Norris (61). Their report summarizes an exploratory study
designed to gain some order-of -magnitude estimates of herbicide
residues in various organs of blacktail deer whose habitat was
entirely treated either with 2,4,5-T or atrizine. 2,4,5-T was
applied at the rate of two pounds per acre acid equivalent as
the isooctyl ester, with a small amount of 2,4-D in mixture, in
ten gallons fuel oil. Essentially no rain fell during the sampling
period.
Several deer were killed in each area at irregular intervals after
treatment in hopes of obtaining an estimate of cumulative effects,
elimination patterns and reduction of intake with time after treat-
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ment. From each deer were taken samples of tissue from brain,
thyroid, mesentery lymph nodes, spleen, heart, lung, liver, kidneys,
blood, muscle, urine, feces and stomach contents. Mammary glands
were sampled on pregnant does. Most of the deer were not fat enough
to provide samples of adipose tissue.
It is clear that deer do not accumulate large amounts of either
herbicide when exposed to maximum dosages throughout their habitats.
Intestinal contents provide abundant evidence of present or past
exposure, but low levels of herbicides in most body tissues is
evidence of breakdown within the animal, perhaps within some
endocrine glands, or passage through the digestive system.
These results are definitely not conclusive. They provide frag-
mentary evidence that (1) deer do not leave areas thus treated,
(2) safe limits for wildlife were apparently observed in these
operations, (3) deer do not accumulate 2,4,5-T and atrazine to an
appreciable degree, (4) that concentrations in flesh rarely reach
detectable levels, particularly in the case of 2,4,5-T, and (5)
this ruminant is able to degrade these herbicides almost com-
pletely soon after ingestion.
F. Residues in Food
Faust (1964) (69) in a survey of water pollution hazards to man
from organic pesticides, came to the conclusion that there did
not appear to be danger to health at the present time from the
-106-
4
background concentration of pesticides believed to be in ground
and surface water. However, 2,4-D could persist in lake water
and bottom mud for long periods under certain environmental
conditions. Work in Russia, quoted by Faust, suggested that
the threshold taste and odour concentrations auxin compounds
especially of phenolic derivatives such as 2,4-D, that would
prove unacceptable to the consumer were very considerably below
the threshold concentrations for toxic effects. A particular
risk might be supposed to lie in contaminated milk drawn from
cows feeding in treated pasture, but no residues of either
2,4-DB or 2,4-D were found in the milk of cows that had been
fed these compounds (72).
Authorization to use 2,4,5-T on food crops depends on demonstrating
that no residue exists in the edible product at harvest (58). The
following studies illustrate the amounts of 2,4,5-T that may
persist in food crops at various intervals after treatment.
When 2,4,5-T was applied to apples as a spray concentration of
40 ppm, residue in the fruit had fallen to 0.004 ppm in 22 days.
(68) The application of 2,4,5-T to blueberries at 1 pound per
acre resulted in a concentration in the fruit of 0.05 to 0.33 ppm
44 days after application although none was found 733 days after
application (71). No detectable 2,4,5-T (sensitivity = 0.01 ppm)
was found in rough rice 50 days after applying 2.25 pounds per acre
of 2,4,5-T (70). The rice straw contained 0.18 to 1.04 ppm 2,4,5-T
50 days after but not 84 days after application.
-107-
Further evidence that very little 2,A,5-T gets into food is seen in
results of assays of raw agriculture products and in the Market
Basket Survey samples. From about 10,000 food and feed samples
examined from 1964 through 1969 only 25 contained trace amounts
of 2,4,5-T (1 ess than 0.1 ppm) and only two contained measurable
amounts, 0.19 ppm in a sample of milk in 1965 and 0.29 ppm in a
sample of sugar beets in 1966 (65). Furthermore, of the 134 total
diet samples involving 1600 food composites (Market Basket Survey)
analyzed from 1964 through April 1969, only three contained 2,4,5-T.
Two were dairy products containing eight to 13% fat with 0.008 and
0.19 ppm in the fat. A single meat, fish and poultry composite
from Boston consisting of 17 to 23% of fat was found to contain
0.003 ppm 2,4,5-T on a fat basis (65, 64, 66).
It is concluded from the foregoing that: (1) the herbicide 2,4,5-T
does not accumulate in any compartment of the biosphere. (2) The
risk of human exposure to 2,4,5-T in food, air or water is
negligible (58) .
From the very nature of their use, it is unlikely that auzin
herbicides will appear as significant residues in food crops. Williams
(1964) (73) was unable to detect any residues of auxin herbicides
in a number of total diet samples down to the limit of sensitivity
(0.01 ppm) of his analytical techniques. Duggan and Weatherwax (1967)
-108-
(67) calculated pesticide chemical residues in "total diet" samples
collected on 46 days in 25 American cities during a 699 day period
from June 1964 to April 1966. Each sample represented the total
amount of food and drink consumed by one person over a two-week
period. The total samples represented in all a food and drink
supply sufficient for 644 days. Herbicide chemicals were found
infrequently and averaged about 0.01 mg/day of which one third
was 2,4-D and half was MCPA and pentachlorphenol (POP) combined
2,4-D was found in oils and fats (0.001 mg in 1964/1965) and sugars
and sugar products (0.004 mg. in 1964/1965) , (0. 002 mg. in 1965/1966),
while MCPA was found in grain and cereals (0.002 mg. in 1964/1965),
in dairy products (0.003 mg in 1965/1966), and in leafy vegetables
(0.001 mg. in 1965/1966). These amounts are substantially below the
limits set for acceptable daily intake by the World Health Organization
and United Nations committees. It seems probable, therefore, that
toxic hazards from auxin herbicide residues in food are very small (72) .
-109-
REFERENCES
A. References: Residues in Soil
1. Akamine, E. K., 1951. Persistence of 2,4-D toxicity in
Hawaiian soils. Bot. Gas. 112, pp. 312-319
2. Backelard E. P., 1971. A study of the persistence of
herbicides in soil. Weed Abstracts 20(1): 59
3. Flieg, 0.; Pfaff C., 1951. Movement and decomposition
of 2,4-D in the soil, also it's influence on
microbiological transformations. Lands Forsch 3,
pp. 113-122
A. Freed, V, H., and M. L. Montgomery, 1963. The metabolism
of herbicides by plants and soils. In Residue Rev.
3:1-18.
5. Hernandez, T. P. and G. F. Warren, 1950. Some factors
affecting the rate of inactivation and leaching of
2,A-D in different soils
6. Jensen, H. L. and H. I. Peterson, 1952. Decomposition of
hormone herbicides by bacteria. Acta. Agric. Scand.
2, 215-231.
7. Loos, M. A., 1969. Phenoxyalkanoic acids. In degradation
of herbicides, Kearney, P. C., and D. D. Kaufman (Ed.)
Marcel Dekker, New York. pp. 1-A9.
-110-
8. Montgomery, M. L. and L. A. Norris, 1970. A preliminary
evaluation of the hazards of 2,4,5-T in the forest
environment. USDA Forest Service Research Note PNW
116.
9. Newman, A. S., and J. R. Thomas, 1950. Decomposition
of 2, A“dichlorophenoxyacetic acid in soil and liquid
media. Soil Sci. Soc. Amer. Proc. 14:160.
10. Norman, A. G., and A. S. Newman, 1950. The persistence
of herbicides in soils. Proc. Northeast Weed
Control Conf. 4:7.
11. Norris, Logan A., 1966. Degradation of 2,4-D and 2,4,5-T
in forest litter. J. Forestry 64(7) :475-476.
12. Norris, Logan A., and D. Greiner, 1967. The degradation
of 2,4-D in forest litter. Bull. Environ. Cont. &
Tox. 2:65-74.
13. Norris, L. A., 1967. Chemical brush control and herbicide
residues in the forest environment. In herbicides
and vegetation management, pp. 103-123. School of
Forestry, Oregon State Univ., Corvallis, Oregon.
14. Norris, Logan A., 1970. Degradation of herbicides in the
forest floor. In tree growth and forest soils, pp.
397-411. Oregon State Univ. Press, Corvallis, Oregon.
15. Norris, Logan A., 1971. The behavior of herbicides in the
forest. Mimeo, U.S. Forest Serv., Pacific N.W. Forest
and Range Experiment Station, Mimeo, 24 pp.
-Ill-
16. Steenson, T. I. and N. Walker, 1956. Observations in
bacterial oxidation of chlorophenoxyacetic acids
Plant and Soil 8:17.
17. Wiese, A. F., and R. G. Davis, 1964. Herbicide movement
in soil with various amounts of water. Weeds 12:101-103
Illus.
B. References; Residues in Water
18. Bailey, G. W., A. D. Thurston, Jr., J. D. Pope, Jr., and
D. R. Cochrane, 1970. The degradation kinetics of
an ester of silvex and the persistence of silvex in
water and sediment. Weeds 18(3) : 413-418 .
19. Brown, E., Nishioka, Y. A., 1967, Pesticides in selected
western streams — A contribution to the national program.
Pesticides monitoring J. l(2):38-46.
20. Cochrane, D. R. , J. D. Pope, Jr., H. P. Nicholson and G. W.
Bailey, The persistence of silvex in water and hydro-
soil. Water resources Res. 3:517-523. 1967.
21. Frank, P. A., R, J. Demint, R. D. Comes, 1970. Herbicides
in irrigation water following canal-bank treatment for
weed control. Weed science 18(6) : 687-692 .
22. Frank, P. A., and R. D, Comes, 1967. Herbicidal residues
in pond water and hydrosoil. Weeds 15:210-213.
-112-
23. Goerlitz, Donald F. , and William L. Lamar, 1967. Deter-
mination of phenoxy acid herbicides in water by
electron capture and microcoulometric gas chromalo-
graphy. U.S. Geol. Surv., Water Supply Pap. 1817-C.
21 pp.
24. Krammes, Jay S., and David B. Willets, 1964. Effect of 2,4-D
and 2,4,5-T on water quality after a spraying treatment.
U.S. Forest Service, Pacific SW Forest and Range Exp.
Station Res. Note PSW-52. 4 pp.
25. Lee, G. A., and H. P. Alley, 1970. Exhudation of picloram
and 2,4-D from Canada thistle roots. 1970 Res. Prog.
Report West. Soc. Weed Sci. pp. 101-102.
26. Montgomery, Marvin L., and Logan A. Norris, 1970. A
preliminary evaluation of the hazards of 2,4,5-T
in the forest environment. U.S. Forest Serv.,
Pacific NW Forest and Range Exp. Sta. Res. Note
PNW-116. 11 pp.
27. Norris, Logan A., 1967. Chemical brush control and
herbicide residues in the forest environment. In
herbicides and vegetation management, pp. 103-123.
Oregon State University, Corvallis, Oregon.
28. Norris, Logan A., 1968. Stream contamination by
herbicides after fall rains on forest lands.
Res. Prog. Report, West. Soc. Weed Sci., pp. 33-34.
-113-
29. Norris, Logan, A., and Duane G. Moore, 1970. The entry
and fate of forest chemicals in streams. Symp.
Proc., Forest Land Uses and Stream Environment,
pp. 138-158. School of Forestry and Dept.
Fisheries and Wildlife, Oregon State University
Corvallis, Oregon.
30. Norris, Logan A., 1971. The behavior of herbicides in
the forest. U.S, Forest Service, Pacific NW Forest
and Range Exp. Sta. 24 pp. mimeo.
31. Norris, Logan A., 1971. Chemical brush control: assessing
the hazard. J. Forestry 69(10) : 7 15-7 20.
32. Robson, T. 0., 1968. Some studies of the persistence of
2,4-D in natural surface waters. Proc. 9th Brit.
Weed Contr. Conf. pp. 404-408.
33. Smith, G. E., and D. G. Ison, 1967. Investigation of
effects of large-scale applications on aquatic
fauna and water quality. Pestic. Monit. J. 1(3):16-21.
34. Sooper, W. E. , I. C. Relgnor, and R. R. Johnson, 1966.
Effect of phenoxy herbicides on riparian vegetation
and water quality. Weeds, trees and turf, January 1966.
pp. 8-10.
35. Thomas, Richard E., Jesse M. Cohen, and Thomas W. Bendixen,
1964. Pesticides in soil and water, an annotated
bibliography. U.S. Dept. Health, Education and Welfare,
PHS Publ. No. 999-WP-17. 90 pp.
-114-
36. Wilson, James G. (Chnun.) , 1971. Report of the advisory
committee to the Administrator of the Environmental
Protection Agency. 75 pp., mimeo.
C. References; Residues in Plants.
37. Audus , L. J., 196A. The physiology and biochemistry of
herbicides. Acad. Press, New York, 555 pp.
38. Easier, E. , 1964. The decarboxylation of phenoxyacetic
acids by excised leaves of woody plants. Weed Sci.
12:14-16.
39. Crafts, A. S., 1961. The chemistry and mode of action of
herbicides. Interscience Publ. New York 269 pp.
40. Fitzgerald, C. H., C. L. Brown, and E. G. Beck, 1967.
Degradation of 2,4,5-trichlorophenoxyacetic acid
in woody plants. Plant Physiol. 42:459-460.
41. House, William B., et al., 1967. Assessment of ecological
effects of extensive or repeated use of herbicides.
Midwest Res. Instit., Kansas City Missouri 369 pp.
42. Kearney, P. C., A. I. Ivensee, C. S. Helling, E. A. Woolson,
and J. R. Plimmer, 1972. Environmental significance
of the chlorodioxins . Abstracts, Weed Sci. Soc. Amer.
p. 14.
-115-
A3. Klingman, D. L. , et al., 1966. Residues in the forage and
in the milk from cows grazing on forage treated with
esters of 2,A-D. Weeds 14:164-167.
44. Loos, M. A., 1969. Phenoxyalkanoic acids. In degradation
of herbicides, pp. 1-49, Kearney, P. C. and D. D.
Kaufman (Ed.). Marcel Dekker, Inc. New York.
45. Morton, H. L., 1966. Influence of temperature and humidity
on foliar absorption, translocation, and metabolism
of 2,4,5-T by mesquite seedlings. Weeds 14:136-140.
46. Morton, Howard L. , E. D. Robison, and Robert E. Moyer, 1967.
Persistence of 2,4-D, 2,4,5-T and dicamba in range
forage grasses. Weeds 15:268-271.
47. Montgomery, Marvin L., and Logan A. Norris, 1970. A
preliminary evaluation of the hazards of 2,4,5-T in
the forest environment. U.S. Forest Serv., Pacific
NW Forest and Range Exp. Sta. Res. Note PNW-116. 10 pp.
48. Norris, L. A., 1967. Chemical brush control of herbicide
residues in the forest environment. In herbicides and
vegetation management, pp. 103-123.
49. Norris, Logan A., 1971. Chemical brush control: assessing
the hazard. J. Forestry 69(10) :715-120.
50. Shaw, W C. , J. L. Hilton, D. E. Moreland, and L. L. Jansen,
1960. The fate of herbicides in plants. In the nature
and fate of chemicals applied to soils, plants, and
animals, pp. 119-133, Symp. Proc., USDA, Agric. Res.
Serv., Beltsvllle, Md.
-116-
51. Sopper, W. E. et al. , 1966. Effect on phenoxy herbicides
on riparian vegetation and water quality. Weeds, Trees
and Turf.
52. Wilson, James G. (Chmn) , 1971. Report of the Advisory
Committee on 2,4,5-T to the Administrator of the
Environmental Protection Agency. 75 pp . , mimeo.
D. References: Residues in Air
53. Courtney, K. D. and J. A. Moore, 1971. Teratology studies
with 2,4,5-T and tetrachlorodioxin . Submitted to
Toxic. Appl. Pharmacol.
54. Khera, K. S., B. L. Huston and W. P. McKinley, 1971. Pre-
and posnatal studies on 2,4,5-T, 2,4-D and derivatives
in Wistar rats. Toxic. Appl. Pharmacol., in press.
55. Moore, J. A. and K. D. Courtney, 1971. Teratology studies
with the trichlorophenoxyacld herbicides 2,4,5-T and
Silvex. Teratology in press.
56. Norris, L. A., 1967. Chemical brush control and herbicide
residues in the forest environment. In herbicides and
vegetation management in forest ranges and noncrop
lands, pp. 103-123. Oreg. State Univ., Corvallis.
57. Norris, L. A., and J. Zavitkovski. Unpublished data,
School of Forestry, Oregon State University.
58. Report of the Advisory Committee on 2,4,5-T to the
Administrator of Environmental Protection Agency.
-117-
L
E. References: Residues in Animals
59. Clark, D. E., 1969. Butyl ether esters in animal tissue
blood, and urine. J. Agr. Food Chem. 17 (6) : 1168-1170.
60. Erne, K. , 1966. Distribution and elimination of chlorinated
phenoxyacetic acid in animals. Acta. Vet. Scand:7:240.
61. Newton, Michael and L. A. Norris, 1968. Herbicide residues
in blacktail deer. From Forests treated with 2,4,5-T
and atrizine.
62. St, John, L. E., Wagner, D. G. , and Lisk, D. J. 1964. Fate
of atrizine, kuron, silvex, and 2,4,5-T in the dairy
cow. J. Dairy Sci. 47:1267-1270.
63. Zielinski, Walter L., and Fishbein, Lawrence, 1967. Gas
chromatrographic measurement of disappearance rates
of 2,4-D and 2,4,5-T acids and 2,4-D esters in mice
J. Agr. Food Chem. 15:841-844, illus.
F. References: Residues in Food
64. Corneliussen, P, E. , 1969. Pesticide residues in total
diet samples. Pesticide Monit. J., 2:140-152.
65. Duggan, R. E., 1971. Memorandum to Wayland J. Hayes,
Unpublished, March 12, 1971.
66. Duggan, R. E., H. C. Barry, and L. Y. Johnson, 1967.
Pesticide residues in total diet samples. Pesticide
Monit. J., 1:2-12.
-118-
67. Duggan, R. E. and J. R. Weatherwax. Dietary intake of
pesticide chemicals. Science 157, 1006 (1967)
68. Edgerton, L. J. and D. I. Lesk, 1963. Determination of
residues of 2 ,4 , 5-trichlorphenoxyacetic acid in
apples by radioiostopes and gas chromatographic
methods. Proc. Am. Soc. Hort. Sci., 83:120-125.
69. Faust, S. D. Pollution of the water environment by
organic pesticides. Clin. Pharmacol. Therap.
5, 677 (1964).
70. Syracuse University Research Corporation, 1970. 2,4,5-T
residues in rough rice and straw. Unpublished data.
Cited in Dow communication dated Jan. 19, 1971.
71. Trevett, M. F., 1964. A request for approval of a contact
method of applying 2,4-D and 2,4,5-T for control of
woody weeds in Maine lowbush blueberry fields. Un-
published data. Cited in Dow communication dated
Jan. 19, 1971.
72. Way, J. M, 1969. Toxicity and hazards to man, domestic
animals and wildlife. From Some Connomly Used
Auxin Herbicides. Residue Reviews, Vol. 26.
73. Williams, S. Pesticide residues in total diet samples.
J. Assoc. Office. Agri. Chemists 47, 815 (1964)
-119-
Section VI
ENVIRONMENTAL IMPACTS OF THE PHENOXY COMPOUNDS
2,4-D, 2,A,5-T, and 2,4,5-TP
A. Hazards to Man
There is no evidence of harmful effects on man being caused by any
of the three phenoxy compounds when used properly and in the manner
prescribed on forest and range vegetation. Human exposure to an
environmental chemical such as 2,4,5-T depends on (1) pattern of
usage, i.e., how widely and frequently applied and in what amounts
and, (2) its fate in the environment, i.e., does it accumulate or
is it degraded as fast as applied. These herbicides offer minimal
hazard to man and his environment under forest and range use, because
large and prolonged doses required to cause significant biological
effects do not occur.
The principal routes of toxicity to man are either orally or by
inhalation; there appears to be little hazard of transport through
the skin although individual allergies can develop leading to
dermatitis (Vallet 1965) (A6) . Eyes may be directly but are usually
only temporarily affected. Hazards to man may occur from the con-
centrated chemical before dilution, from inhalation of spray or
dust during application, or from ingestion of the chemicals in
food or in water. Because the greatest hazards are from the
concentrated chemical and because man is handling the chemicals
-120-
4
in this form at all stages from manufacture to dilution, it follows
that he is at greater potential risk than any other organism. How-
ever, there are very few reports in the literature of tests or
incidents of poisoning of man by these compounds, the majority of
these reports refer to accidental poisoning of children. As a
result it is now generally accepted that auxin-type 1/ herbicides
do not present a direct toxicity hazard to man (Barnes 1965)(A1)
when correctly handled or used for weed control.
Kraus in 19A5 (in Kephart, 1945) (A7) reported that he had taken
0.5 g. of 2,4-D per diem for 21 days with no demonstrable ill
effects. A clinical study was made in Denmark by Nielsen et al.
(1965) (A5) on a 23-year old man who had committed suicide by
apparently drinking 125 ml. of 50 percent w/v 2,4-D dimethy famine
salt. The total weight of 2,4-D in his body was calculated as
being not less than six g. (the equivalent of 80 mg. /kg.), about
10 percent of the total weight of active material ingested. The
principal damage appeared to be to nerve tissues and the central
nervous system (A) .
Edwards and Ripper (1953) (A2) have discussed the hazard to operators
from inhalation of sprays and aerosols during application of herbi-
cides with particular reference to methods of protection. Monarca
)J Auxin. Any group of substances which promote plant growth by
cell elongation, bring about root formation or cause bud
inhibition or other effects. 2,4-D, 2,4,5-T and 2,4,5-TP are
compounds of this group.
-121-
and Dr, Vito (1961) (A4) have described a clinical study of an acute
case of accidental poisoning of a man in Italy. In this instance
a farmer became ill after applying a 40 percent aqueous solution of
2,4-D by handpump against the wind. He was admitted to hospital,
suffered a relapse after 18 days, and recovered sufficiently to be
discharged after 40 days. Initial symptoms of muscular weakness,
vomiting, perspiring freely, and oliguria were noted in the field
while a diagnosis of bradycardia, respiratory difficulties, and
urinary abnormalities was made after admission to hospital. How-
ever, the authors report that the case was exceptional (A) . Fetisov
(1966) (A3) has reported similar field symptoms in Russian workers
engaged in field applications of 2,4-D. This author concluded that
a range of formulations of 2,4-D was "highly toxic to animals in
different ways of introduction." While reports of minor discomfort
following exposure to auxin sprays during field application are
rarely reported in scientific literature, there is no doubt that a
proportion of workers so exposed do suffer a degree of transitory
discomfort. Whether this is of any significance as long-term toxic
hazard has not been determined for man (A) .
There has been some alarm (perhaps unjustified) about the human
toxicity resulting from the use of 2,4-D and its derivatives.
Some of the case histories of persons contracting neuropathy as
a result of 2,4-D treatment are presented here to permit the reader
-122-
to form his own opinion about the magnitude of the hazard associated
with the use of 2,4-D compounds. (B) Goldstein et. al. (1959) (B) in
their report on peripheral neuropathy after skin exposure to an ester
of 2,4-D state that three individual patients, two farmers and a
female bookkeeper, suffered the disorder some hours after exposure
to the 2,4-D formulation while attempting to kill weeds. The
symptoms progressed through a period of days until pain, paresthe-
sias and parlysis were severe. Diability was protracted and recovery
was incomplete even after a lapse of years. They concluded that there
was little doubt that the symptoms resulted from the percutaneous
absorption of the 2,4-D. The electromyographic examinations supported
the diagnosis of peripheral neuropathy. Berkley and Magee (1963) (B)
report a similar case of neuropathy in a 39 year old farmer four days
after exposure to 2,4-D dimethylamine salt; the symptoms included
numbness and incoordination of the hand and finger muscles and a
slow recovery. These authors conclude that persons who get peripheral
neuropathy from exposure to 2,4-D are very rare compared to the number
of exposures there must be. They state that some individuals may have
a predisposition to neuropathy and suggest that all users of these
herbicides use protective clothing and wash immediately with soap and
water in case of accidental exposure.
Mitchell (1946) quotes the experimental work of E. J. Kraus concerning
the ingestion of 500 mg of purified 2,4-D/day by a man over a period
of 21 days without ill effect. Seabury (1963) reports on the adminis-
tration of the sodium salt of 2,4-D to two patients suffering from
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coccidioidomycosis. The first patient received an intramuscular
injection of 2,0 g without any toxic reactions. The second patient
received 3.6 g by parenteral injection; there were severe toxic
reactions including coma, fibrillary twitching of some muscles,
hyporeflexia and urinary incontinence. Recovery from the toxic
effects of the injections were complete in A8 hours but the
patient died of his disease 17 days after the injection (B) .
According to DiPalma (1965) (B), a man committed suicide by con-
suming about 6.5 g of 2,A-D; from this and the other information,
it appears that the lethal dose for a human lies in the range of
50 to 100 mg/kg (B) .
The Dow Chemical Co. (Cl) has prepared an extensive health inventory
of 126 manufacturing personnel in an effort to identify adverse
effects of inhaled 2,A,5-T. The inhalation rate of the agent was
estimated to be 1.6 to 8.1 mg/day per worker, depending on the work
assignment, for periods of up to three years and at total career
exposures in excess of 10,000 mg. The survey indicates that no
illness was associated with 2,A,5-T intake. Specifically there
was no increase in skin ailments or of alkaline phosphatase or
SGPT levels as compared with controls having no exposure to 2,A,5-T.
The result was entirely different in a plant where the 2,A,5-T
produced contained a high proportion of dioxin (TCDD) . The latter
plant was studied by Bleibert in 196A (C2) and again six years
-12A-
later by Poland et. al, (C3) who also reviewed earlier studies in
factories in other countries where TCDD had been a problem, Poland
and associates reported on 73 employees whose health was found to
be improved compared to that of workers in the plant six years
earlier. Eighteen percent of the men had suffered moderate to
severe chloracne, the intensity of which correlated significantly
with the presence of residual hyperpigraentation , hirsutism, and
eye irritation and with a high score on a test indicating a manic
reaction. The chloracne did not correlate with job location or
duration of employment at the plant or with coproporphrin excretion.
One of the men had uroporphyrinuria but, unlike the situation six
years earlier, no porphyria could be found. Systemic illness such
as may be produced by TCDD was markedly less than that reported in
previous studies of 2,4,5-T plants and probably no greater than
expected in unexposed men of the same age, (C)
As far as occupational exposure is concerned it is clear that any
danger of 2,4,5-T formulations residues in their TCDD content. The
primary manifestation of industrial TCDD intoxication is chloracne,
an easily detected, in fact highly disfiguring, dermatitis. It is
significant that this condition has not been a problem in factories
producing 2,4,5-T with a low content of TCDD, nor among persons who
apply the herbicide as a part of their regular occupation. It is
therefore highly unlikely that exposure to traces of TCDD will have
any effect on persons who use 2,4,5-T formulations occasionally or
who merely encounter possible traces of it in the environment . (C)
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Data are too limited for a firm conclusion but there is no evidence
to suggest that TCDD as a contaminant in 2,A,5-T is likely to be
encountered by animal or man in sufficient dosage to cause toxic
reactions.
No proven instance of toxicity associate^d with 2,4,5-T intake in
man has been found in industrial or agricultural workers known to
have had repeated, relatively high levels of exposure to 2,4,5-T
of low dioxin content; and the safety factor for the general popu-
lation is estimated to be several orders of magnitude greater than
that of 2,4,5-T factory workers (C) .
The very small number of cases in which human ingestion of 2,4,5-T
led to clinical illness offer no information on the minimal dosage
of the compound that is toxic to man. In animals, however, the
toxicity of 2,4,5-T is similar to that of 2,4-D, consequently some
information on 2,4-D is of interest. When 2,4-D was investigated
as a possible treatment for disseminated coccidiodomycosis , the
patient had no side-effects from 18 intravenous doses during 33
days; each of the last 12 doses in this series was 800 mg (about
15 mg/kg) or more, the last being 2000 mg (about 37 mg/kg) . A
19th and final dose of 3600 mg (67 mg/kg) produced mild symptoms . (C4)
Suicidal ingestion of a quantity of 2,4-D as a single dose known to
be greater than 6500 mg (in excess of 90 mg/kg) was fatal (C5) .
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The acid of silvex is appreciably irritating to the eyes and skin,
paricularly in high concentrations. The undiluted esters may cause
painful but temporary injury to the eyes. Skin irritation may occur
from repeated or extended contact vd.th the skin but there is no
evidence of toxicity resulting from skin absorption. There was no
sign of allergic response to the application of a 1% solution of a
commercial formulation of silvex to the skin of 50 human test
subjects (B) .
B. Hazards to Animals (Domestic and Laboratory)
The toxicity of agricultural chemicals to land fauna is normally
quoted in terms of the dose that kills 50 percent of a population
of test animals (LD50) . While this figure gives a useful indication
of the comparative toxicities of different compounds to a given
test species, the figures obtained in different tests may be
influenced by a number of factors. Thus the age and sex of the
test animal, method of dosing, and general conditions of the test
may have an important bearing on the susceptibility of the animals
to the compound being studied (A) . The formulation of the active
compound has a considerable influence: for instance, 2,A-D acid
has an to rats of 375 mg. /kg. but the sodium salt has an LD^q
of 805 mg. /kg., the propylene glycol butyl ether ester of 570 mg. /kg.
and the isopropyl ester of 700 mg. /kg. (Rowe and Hymas 1954) (A20) . It
should be noted, however, that Bjorklund and Erne (1966) do not regard
these differences as being appreciable. • In addition, the for
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different test species may vary quite widely: for example, 2,4-D
acid has an LD^q of 375 mg. /kg. for rats, of 100 mg. /kg. for dogs,
469 mg. /kg. for guinea pigs, and 541 mg. /kg. for chicks (Rowe and
Hymas 1954) (A20) .
Erne (1966) (A13) studied the distribution and elimination of 2,4-D
and 2,4,5-T in these animals. Amine and alkali salts of both compounds
were readily absorbed and completely distributed in the body, but 2,4-D
ester was incompletely absorbed and reached only a low level in the
plasma and tissues. The highest tissue levels of the two compounds
were found in liver, kidney, spleen, and lungs and the levels found
in these organs sometimes exceeded the level found in the plasma.
In blood cells some 10 to 20 percent of the plasma level was found.
Penetration of 2,4-D into placental tissue of pigs was recorded
but there was little or no evidence of penetration into adipose
tissue or the central nervous system. Elimination of the compounds
was rapid, the plasma half-life being about three hours in rats,
eight in calves and chickens and 12 in pigs. The tissue half-life
values ranged between five and 30 hours. No retention of the com-
pounds was noted in the tissues. There was no accumulation after
repeated dosing and in pigs there was an increase in the rate of
elimination after repeated administration. In all species, the
main excretory route was via the kidneys. Khanna and Fang (1966) (A16)
traced the metabolism of C^** labeled 2,4-D in rats dosed at rates
from one to 100 mg. /animal. Radioactivity was found in all the organs
studied together with some accumulation as early as one hour after
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dosing. At the one mg. dose rate a concentration peak of radioactivity
was demonstrated after six to eight hours but decreased thereafter and
was non-detec table by 24 hours. At the 80 mg. dose the peak occurred
at eight hours and persisted for 17 hours. Extracts of the tissues
were shown to contain mainly unchanged 2,4-D residues. No radioactivity
was found in the expired carbon dioxide, but elimination in urine and
faeces was dose dependent. At the one to 10 mg. doses 93 to 96 percent
of the ingested 2,4-D was excreted unchanged in the urine in the first
24 hours. At the 20 to 100 mg. doses greater amounts of 2,4-D were
found in the second 24 hour period after dosing, with a linear decrease
in percentage recovery with increase in dose. In experiments with
cattle Gutenmann et. al (1963) (A15) were unable to detect any residues
of 2,4-DB or 2,4-D in milk or faeces of cows fed five p.p.m. of either
compound in a 50 pound daily ration. In these experiments there was
no evidence of beta-oxidation of 2,4-DB to 2,4-D. Disappearance of
2,4-D was thought to occur as a result of dilution in the rumen,
soma absorption on the gut wall, and by decomposition. In subsequent
experiments Bache et. al. (1964) (A23) and St. John et. al. (1964) (D)
studied the fate of MCPA, MCPB , 2,4,5-T, and a number of other
herbicides in cattle. All the MCPA fed to a single steer (113.5
mg. single dose based on five p.p.m. of a 50 pound daily ration)
was accounted for in its urine over the four days after administration.
These authors discussed the significance of biological active residues
of auxin compounds in animal excreta that might become incorporated
in manure or straw. It was shown that 2,3,6-TBA residues in particular
could remain active for a period of months and affect susceptible
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crops to which the contaminated manure was applied. The same hazard
does not normally exist with the phenoxyacetic acid derivatives,
where the compounds are broken down and become biologically inactive
in a relativaly short period of time. However, Lisk (1966) (A17) has
pointed out that the excretion of 2,A-D in the urine of cows does
present the admittedly remote possibility of active 2,4-D being
transferred from a treated pasture to a susceptible crop.
Mitchell (in Kephart 19A5)(A7), Dalgaard-Mikkelsen et. al. (1959)(A10)
and Goldstein and Long (1960) (AlA) all reported that there were no
apparent ill-effects in cattle, sheep, or horses from grazing pasture
sprayed at herbicidal or two times herbicidal rates of 2,4-D or MCPA.
Grigsby and Farwell (1950) (In Springer 1957) (A22) reported that there
was no significant difference in the amount of feeding of horses,
cows, sheep, and pigs in untreated plots or plots sprayed with the
sodium salt or the isopropyl ester of 2,4-D or the isopropyl ester
of 2,4,5-T. However, there did appear to be less feeding in plots
sprayed with the alkanolamine salt of 2,4-D. There was no effect
on milk production of cows feeding on sprayed vegetation. Goldstein
and Long (1960) (A14) found no ill-effects on two cattle from adding
0.25 pints of a 1,5 percent w/v 2,4-D/2,4,5-T mixture to every five
gallons of their drinking water for 41 days. These authors also
reported spraying the skins of a calf, of a cow, of sheep, and of
pigs with doses ranging from 0.002 to 0.008 pounds of 2,4-D or 2,4-D/
2,4,5-T mixture, with no ill-effects. These dose rates would be of
the order of those that might occur in an instance of spray drift.
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Dobson (1954) (All) sprayed 2,4-D, or 2,4,5-T on grassed chicken
runs dally for 14 days at normal and ten times normal dose rates .
2,4,5-T significantly reduced egg production and the weight of the
birds; 2,4-D affected egg production, mainly in the second week
of spraying or during the week after spraying had stopped. In
all instances there was no effect on the fertility of the eggs
and all the progeny reared well, although the dose rates and
frequency of application in this trial were much more severe
than are likely to be found in practice. Erne (1966) (A13) showed
that some of the 2,4-D fed to hens could be excreted in their
eggs. Dunachie and Fletcher (1967) (A12) injected hen's eggs with
2,4-D, MCPB, 2,4-DB, and 2,3,6-TBA amongst a range of other
herbicides. Dose rates were 10, 100, and 200 p.p.m. equivalent
to 0.5, 5, and 10 mg. /egg. The percentage hatch was recorded.
At the lowest dose there was 90 percent from the TBA-treated
eggs, and 80 percent from the 2,4-D treated eggs. At the highest
dose there was 50 percent hatch from 2,4-D and TBA. None of the
chicks that hatched were deformed although some feather blanching
was noted from the 2,4-DB treatments. Roberts and Rogers (1957) (A19)
reported on various feeding experiments on turkeys with alfalfa
sprayed with a low volatile ester of 2,4,5-T at herbicidal rates.
No deleterious effects were noted. Calculations were quoted to
show that for a one kg. chicken to acquire a lethal dose of 2,4-D
from an application rate of one pound/acre, the bird would have to
consume in two days all the 2,4-D applied to the vegetation over an
area of 72 square feet.
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Accounts are given of direct oral dosing or dermal applications of
auxin herbicides to a variety of domestic animals by Kephart (1945) (A7)
(cow), Rowe and Hymas (1954) (A20) (laboratory animals and cattle),
Dalgaard-Mikkelsen et. al. (1959) (AlO) (heifers), Palmer (1963) (A18)
(cattle), Clarke et. al. (1964) (A9) (sheep), and Strach and Bohosiewicz.
(1964) (A21) (pigs) . Palmer (1963) (A18) gave daily oral doses of 2,4-D
alkanolamine salt to steers for five days in every seven. He recorded
signs of poisoning in animals dosed at 250 mg. /kg. after 15 administra-
tions as opposed to 86 administrations of 100 rag. /kg.; at 50 mg. /kg.
no ill-effects were recorded over a period of 112 administrations.
From these results he concluded that although animals could probably
ingest enough 2,4-D from concentrated solutions at any one time to
produce illness or death, the chronic toxicity of the compound was
sufficiently low to make it unlikely that an animal would pick enough
of it over a period time to cause any serious ill-effects. Further
work by Palmer and Radeleff (1964) (B) using single animals gave the
following results:
1. Sheep tolerated 481 daily doses of 100 mg. /kg. of the alkanolamine
or propylene glycol butyl ether ester of 2,4-D.
2. Cattle suffered from chronic typanites after 88 daily doses of
100 mg. /kg. of the alkanolcimine salt of 2,4-D. One animal died
after 34 daily doses of 200 mg. /kg.
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^ 4
3. Sheep tolerated A81 daily doses of 100 mg. /kg. of the triethy la-
mine salt of 2,4,5-T but succumbed to 369 doses of 100 mg. /kg.
of the propylene glycol butyl ether ester.
A, Sheep were killed by 383 daily doses of 100 mg. /kg. of MCPA amine.
Strach and Bohosiewicz (1964) (A21) reported that no abnormal behavior
in pigs had been noted following 40 daily doses of 15 to 100 mg. /kg.
of 2,4-D, nor from single doses of 2,4-D of 200 to 800 mg. /kg.
In short term trials by Bjorklund and Erne (1966) (A8), calves and
pigs showed definite though reversible symptoms of poisoning after
single doses of 2,4-D of 200 and 100 mg. /kg. respectively. Rats
and fowls did not show any sign of distress after single doses of
100 and 300 mg. /kg., respectively, and fowls tolerated daily doses
of 300 mg. /kg. daily in their feed for several weeks without visible
effects. Repeated daily doses of 50 mg. /kg., however, led to toxic
symptoms in some pigs. In longer term studies (Erne 1966) (A13) , five
young pigs were fed 500 p.p.m. of 2,4-D for up to 12 months but,
although various toxic effects were noted and their growth rate was
affected, none of the animals died. When 2,4-D was fed to a sow
throughout gestation and for a further six weeks, 10 of the 15
underdeveloped and apathetic piglets she produced died within 24
hours and the mother subsequently had to be slaughtered because
of abnormalities that developed in her spine. Heavy dosing of
pregnant rats, however, with 1000 p.p.m. of 2,4-D in their drinking
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water over 10 months and of their off-spring for up to two years,
while leading to retarded growth and increased mortality, did not
produce unequivocal signs of toxicity. Continued administration
of 500 p.p.m, of 2,4-D in feed or 1,000 p.p.m. in the drinking water
of fowls led to reduced egg production and kidney abnormalities.
These results led the authors to conclude that the chronic toxicity
of 2,A-D to the species studied was moderate. They were, however,
concerned about the mortality of new-born piglets, with evidence
of movement of 2,4-D through the placental tissues, and the reduced
egg production in fowls which they thought might indicate a possible
interference with reproductive processes.
In general the findings of other workers support these conclusions
on acute and chronic toxicity. In all the work quoted the amounts
administered to the test animals for effect, have been well in excess
of the amounts they might be expected to pick up from a treated
pasture, or in feed derived from crops that had at some time been
treated with auxin herbicides at normal dose rates. (A).
Dr. 0. G. Fitzhugh (1967), Toxicological Advisor, Division of
Toxicological Evaluation, Food and Drug Administration, writes
that the FDA laboratories have conducted a three generation, six
litter reproduction test in rats: (B)
1. In the two-year feeding test on dogs there were three male
and three female dogs in each group. The levels of 2,4-D in
the diets were 0, 10, 50, and 500 ppm 2,4-D. There were no
i
k
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gross or microscopic findings related to 2,4-D. There was no
dose-related clinical or hematologic effect. The "no effect"
level was greater than 500 ppm (i.e., not determined).
2, In the two-year rat feeding study there were 25 male and 25
female rats per group. The diets of the various groups contained
0, 5, 25, 125, 625, or 1,250 ppm of 2,A-D. There was no effect
on growth, survival, organ weights, hematologic values or
occurrence of tumors. Neither gross nor microscopic changes
were noted. No "no effect" level was found (i.e., greater
than 1,250 ppm).
3. In the rat reproduction studies 20 males and 20 females were used
(i.e., where there were enough survivors) and they were fed 0, 100,
500, or 1,500 ppm of 2,4-D in their diets. No effect was observed
at the 100 or 500 ppm levels. At the 1,500 ppm level, there was
no effect on fertility nor on the average number of pups/litter.
There were, however, significant effects on the average number
(%) weaned and also on the weights of the weanlings (i.e., average
weight of survivors) . No histopathology was done and the "no
effect" level is at least 500 ppm but less than 1,500 ppm of
2,4-D in the diet.
Palmer (1963) (Bl) conducted a chronic toxicity test with yearling
steers using an alkanolamine salt of 2,4-D (2,4-D Dow Weed Killer
-135-
Formula 40). He found that 112 daily doses of 50 mg. /kg. of this
2,4-D salt had no deleterious effect on the steer and concluded
that it was not accumulated in the steer since doses of 100 and
250 mg, /kg. had produced toxic symptoms. Clark (1964) (B2) confirmed
this observation by a study on the fate of 2,4-D in sheep using
labeled 2,4-D. He showed that 96% of the 2,4-D was excreted unchanged
in the urine in 72 hours. About 1.4% of the radioactivitiy was found
in the feces during this same period. A similar study was reported by
Khanna and Fang (1966) (B3) in which they fed labeled 2,4-D to
rats; they found that the time required for elimination was dependent
upon the dose. For example, a 1 to 20 mg. /rat dose was 88.8 to 95.6%
eliminated in 24 hours. At a dose of 100 mg. /rat, 144 hours was
required for 75.5% recovery of the radioactivity.
Grigsby and Farwell (1950) (B) sprayed alfalfa and brome grass with
two to four times the usual quantities of 2,4-D (sodium salt,
alkanolamine salt and isopropyl esters used in separate experiments)
and then fed it to sheep, chickens, swine, dairy cows and steers.
They concluded that these 2,4-D compounds were not injurious to
livestock under these conditions. They did, however, note an off-
flavor in the milk. Buck et. al. (1961) (B4) fed herbicide-treated
plants in an effort to determine whether the spraying of toxic weeds
would make them more palatable to cattle and it did not. There is,
however, an authenticated case in which sugar beot leaves accidentally
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sprayed with 2,A-D accumulated enough nitrate to become toxic (Stabler
and Whitehead, 1950) (B5) . This does not seem to be a severe practical
problem since sugar beets are very sensitive to 2,4-D, and are not
normally sprayed. Some early reports on the increase in HCN content
in wild cherry after spraying have not been disproved; instead the
level of HCN decreases steadily for 15 days (Lynn and Barrons, 1952) (B6)
after application of the 2,A-D.
\trazine (2-chloro-isopropylamino~6-ethylamino-s-triazine) , kuron
(propylene glycol butyl ether ester of 2-(2,4,5-trichlorophenoxy)
propionic acid) , silvex (2-(2,4,5-trichlorophenoxy) propionic acid) ,
and 2,4,5-T (2,4 ,5-trichlorophenoxyacetic acid) are often used for
weed and brush control in the vicinity of forage crops. The reality
of contamination of forage by drift or uptake prompted the study of
the fate of these herbicides in the dairy cow (D) .
No residues of these herbicides were found in the milk. About 2%
of intact atrazine was eliminated in the urine. About 67% of the
kuron was hydrolyzed and eliminated as silvex (sodium salt) in the
urine. Within experimental error, silvex and 2,4,5-T appeared to
be totally eliminated in the urine as salts (D) .
C. Hazards on Vegetation - Indirect Effects
Indirect effects of herbicides on grazing animals have been associated
with increased toxicity of toxic plants, increased palatability of
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normally non-palatable toxic plants (e.g., ragwort, Senecio jacobaea)
and induced toxicity in normally nontoxic plants (e.g., temporary
increases in nitrate content) (Willard 1950) (A40) . However, Fertig
(1953) (A29) claimed that, up to 1953 in America, in all cases where
poisoning of livestock from herbicides had been reported, the effects
noted could be attributed to some other cause.
Examples have been given by Willard (1950) (A40) of cattle eating
wild cherry (Prunus serotina) , of pigs eating Cocklebur (Xanthium
sp.), and of lambs eating thistles after herbicidal treatment with
auxins. Instances have been reported of ragwort becoming "sweeter"
for two or three days after application and being preferentially
grazed by cattle for a short period. Grigsby and Ball (1952) (A31)
and Lynn and Barrons (1952) (A3 ) investigated the hydrocyanic acid
(HCN) content of the leaves of wild cherry from untreated trees
and trees treated with 2,4,5-T. Their conclusions were that the
foliage was no more toxic to cattle after treatment and that there
might even be less HCN in the leaves of the treated trees than in
those of the untreated ones. Buck et. al. (1961) (A26) fed the
alkaloid-containing plants Delphinium barbeyl (tall larkspur)
and Helenium hoopseii (sneezeweed) , after treatment with 2,4-D
ester or 2,4,5-T ester, to calves and ewes. No increased toxicity
of the plants attributable to application of the herbicides was
noted. Williams and Cronin (1963) (A41) analyzed D. Berbeyi, treated
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with 2,A,5-T amine at various growth stages, and showed that the
alkaloid content of the plants was increased for several weeks after
treatment at the vegetative and early bud stages. It was noted, how-
ever, that the bitter taste of the alkaloids might make the treated
plants even less palatable to animals than untreated ones.
Swanson and Shaw (1954) (A38) showed that 2,4-D affected the HCN
content of Sudan grass (Sorghum vulgare ssp. sudanense) . Initially
there was a decrease in the content of HCN for four days after
treatment there was an increase over the controls which was maintained
for a further 12 days. Similar effects were shown to occur with the
nitrate content of leaves. Buck et. al. (A26) thought that there might
be a relationship between HCN and nitrate metabolism in Sudan grass,
an increase in one leading to a decrease in the other.
The clinical aspects of nitrate poisoning in stock, conditions under
which nitrates are likely to accumulate in the leaves of certain
plants, and lists of these plants have been reported by Bradley et. al
(1940) (A42), Davidson et. al. (1941) (A28), Gilbert et. al. (1946) (A32),
Case (1957) (A27) , and Sund et. al. (1960) (A37). The toxic effects of
nitrate are caused by a reduction of nitrate to nitrate and the con-
version by nitrite of haemoglobin in the blood to methoglobin: the
animal dies from asphyxia. Intravenous injection of methylene blue
in doses of two g./500 pounds of body weight gives Immediate relief.
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Nitrate in plants is generally present in the form of potassium nitrate
and increases in nitrate content have been associated with drought condi-
tions and high soil nitrogen (Gilbert et. al. 1946, (A32) , Case 1957(A27)).
Sund et. al. (1960(A37) noted a high nitrate content in Urtica spp.
and Rubus spp. after heavy rains, follov/ed by preferential grazing
of these and other weed species by cattle. A number of abortions
in these cattle was correlated with occurrence of high nitrate rather
than grazing of the weed species per se. Recent increases in vitamin
A deficiency i"' North American ruminants has been associated with
ingestion of nitrates occurring in herbicide treated plants by
Phillips (1964) (A34).
The accumulation of nitrates in the leaves of treated sugar beets
is well known (e.g.. Savage 1949)(A35). Increased levels of nitrate
in the leaves of this crop as a result of herbicide application have
been reported by Willard (1930) (A40), Stabler and Whitehead (1950) (A36)
and Whitehead et. al, (1956) (A39). Isolated incidents have been
reported of nitrate poisoning of cattle in America as a result of
feeding on sugar beet that had previously been sprayed. In one
incident in N. Dakota, the nitrate content of sugar beet leaves
after spraying was found to vary from 1.81 to 8.77 percent of the
dry weight, as against 0.22 percent for untreated plants and a
toxic level of 1.5 percent (Stabler and Whitehead 1950) (A36) .
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Cell-free extracts of maize and cucumber from plants that had been
previously sprayed with 10 and 100 p.p.m. of 2,4-D were investigated
by Beevers and Hageman (1962) (A24). The level of nitrate reductase
was increased in maize but reduced in cucumber. Studies on the
formation and breakdown of nitrates in plants (Fertig 1952) (A29)
Whitehead et. al. 1956 (A39) have shown that 2,4-D causes more
rapid increases in nitrate content than MCPA, that levels rise
to a peak soon after spraying and subsequently decrease with time,
and that increases in light intensity hasten decreases in nitrate
content .
Studies on forage crops (Berg and McElroy 1953) (A25) and on a
range of weed species (Frank and Grigsby 1957) (A30) have shown
which of these may contain high levels of nitrates after auxin
application. They also list a large number of plants in which
the levels of nitrate do not increase after auxin application.
It is clear from these reports that nitrate poisoning in stock
does occur from time to time and that it is possible for the
hazard to be increased by application of auxin herbicides to
nitrate-accumulating plants.
Livestock managers should make provisions to exclude cattle from
sprayed areas for short periods following treatment when the
probability of nitrate poisoning exist.
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D. Hazards on Insects
Herbicides affect bees (Apis mellifera) and other insects if they
kill the plants on which the insects feed (A). In addition, Wahlin
(1950) (A53) has reported that 2,4-D and MCPA were toxic to bees,
not only from visiting the flowers but also as a result of drinking
contaminated water trapped on treated plants. Other workers have
reported effects on bees after application of auxin herbicides to
plants in flower but not at other times (Haragsimova 1962, A54,
Palmer-Jones 1964, A51) . Palmer-Jones (1964) (A51) and Antoine
(1966) (A44) have suggested that 2,4-D might have some effect on
nectar which made it toxic to bees. King (1960a) (A49) has shown
that radioactive 2,4-D can be translocated to the nectar of
Poinsetta and red clover plants and may be detectable there for
two to three days after treatment. Feeding trials of auxin
herbicides to been have been reported by Glynne Jones and Connell
(1954) (A46) , Palmer-Jones (1960) (A51), King ( 1960b) (A49) , and
Byrdy (1962) (A45). Palmer-Jones (1964) (A51) found no effect on
bees that had been directly dusted with 2,4-D or when they were
made to crawl through 2,4-D dust in order to enter the hive.
Glynne Jones and Connell (1954) (A46) classed 2,4-D and MCPA as
stomach/contact poisons of low toxicity to bees, with LD50 values
of 0.015 mg. compared to insecticides in the range 0.00004 to 0.002
mg. Byrdy (1962)(A45), on the other hand, reported total mortality
of bees within four days of feeding 30 ug. of 2,4-D and 10 percent
mortality within three days rising to 20 percent in five days of
-142-
feeding 20 ug. Johansen (1959) (AA8) reported that 2,A-D and related
compounds were not toxic to bees, except when formulated as the
alkanolamine salt or the isopropyl ester.
Occasional observations on other insects have been reported. Maxwell
and Harwood (1960) (A50) treated broad bean (Vicia faba) plants with
sublethaldoses of 2,4-D and recorded a marked increase in the repro-
duction of the pea aphid (Macrosiphum pisi) feeding on them. The
longevity of adult aphids was unaffected. Robinson (1959) (A52) also
recorded increased fecundity in another pea aphid (Acyr thosiphon
pisum) after caging on broad bean plants treated with 2,4-D. Adams
(1960) (A43) and Adams and Drew (1965) (A43) showed that the application
of 2,4-D amine could enhance aphid infestation in New Brunswick grain
fields, probably as a result of depressing the activities of
coccinellid beetles predating on the aphids. In laboratory
experiments with coccinellid larvae treated with 2,4-D amine,
there was a fourfold increase in mortality and an increase in
time to pupation. There was little mortality amongst the adult
beetles, which usually recovered after a few hours inactivity.
Ishii and Hiran (1963) (A47) concluded that increases in the
growth rate of the larvae of the rice stem berer (Chilo suppressalis)
feeding on 2,4-D treated rice plants, was a consequence of increased
nitrogen content of the plants rather than a direct effect of the
chemical itself.
-143-
It appears that there may be some effects to bees from application
of auxin herbicides to plants in flower. These effects may be
negated by timing of application, size of treatment units and
method of application. Otherwise there would seem to be little
hazard to insects from direct toxicity of the compounds at normal
herbicidal rates of application.
E. Hazard to Soil Fauna
Bollen (1961) (A56) concluded that auxin herbicides, based on
phenoxyacetic and propionic acid, were the most susceptible
to breakdown by microorganisms of the many pesticides applied
to the soil. The importance of soil microorganisms in the
breakdown of these herbicides is well known from the work of
Audus (1964) (A55) and others. Webster (1967) (A57) has briefly
reviewed the literature on the influence of plant growth-regulator
auxin herbicides on the host/parasite relationships of nemotodes,
in which 2,4-D has been shown to increase nematode reproduction
in plant callus cultures. In addition, plant cell hypertrophy
and proliferation, which is a common effect of 2,4-D in many
plants, provides highly suitable conditions for development of
nematodes. In this way, susceptibility of a normally nematode-
resistant variety of oats could be induced, although there did not
appear to be any greater susceptibility of a non-resistant variety.
-144-
In conclusion, the work of Bollen (1961) and many others suggest
no significant impact on soil microbes at rates of application
used in forest or range spraying.
F. Hazards to Fish and Aquatic Organisms
Under field conditions the toxicity of a pesticide in water is
affected by a number of factors in addition to those that affect
its performance on land. Thus acidity, hardness of the water,
and the sorbent qualities of suspended organic matter in the
water may directly effect the toxicity. The trophic nature of
the ecosystem, the oxygen status of the water in respect of
both producers and demand, and the amount of movement of water
both within the system and in terms of flow will affect the
concentration of the chemical, its persistence and its possible
toxic side effects. Because of these, and many other interacting
factors, the toxicity of a given formulation of a given chemical
compound to an individual species will vary under field conditions
depending upon the nature of the water body and the immediate
environment. For this reason, toxicities to fish and aquatic
organisms are usually estimated in terms of median tolerance
limit for exposure to a given concentration of the pesticide,
for a given length of time (TLmx) (A) .
In addition to direct or indirect toxicity, the effects on
aquatic organisms of the removal of the substrate that gives
-1A5-
I
them food and shelter must also be considered. For instance,
in one of the Tennessee Valley Authority's reservoirs two
applications of 2,4-D controlled considerable acreages of
Eurasian water milfoil (Myriophyllum spicatum) . The eradication
of the plant eliminated the substrate that might have been
colonized by large populations of epiphytic insects such as the
larvae of midges, mayflies, and dragonflies (Smith and Isom 1967)
(A69) . It has also to be recognized that very heavy infestations
of submerged or floating aquatic plants may interfere with the
passage of nutrients and considerably reduce the temperatures
and dissolved oxygen values of the water (Fish 1966) (A64) . Thus,
any possible hazards from the use of a herbicide may be out-
weighed by the advantages gained from the removal of the vegetation.
Reviews of toxicity hazards to fish of a range of pesticides,
including auxin herbicides, have been made by Bauer (1961)(A60),
Bandt et, al. (1962) (A59), and Cope (1965 and 1966) (A61) . Cope
(1966) (A61) noted that variations in formulation gave rise to
greater differences in toxicity than the differences in toxicity
between the basic compounds. Ester formulations were often more
toxic than amine or metallic salt formulations. Similar observa-
tions were made by Lhoste (1959) (A67) who reviewed effects on a
number of crustaceans, aquatic Insects, and molluscs.
-146-
Trout (Salmo trutta) are normally regarded as being amongst the
most sensitive fish to water pollution. Alabaster (1958) (A58)
has given median tolerance limits for 24 and 48 hour (TLm24 and
TLm 48) exposures of trout to 2,4-D or 2,4,5-T, or to mixtures
of these two compounds, of 9.5 to 250 p.p.m., depending on
formulation, compared to 1,150 to 2,000 p.p.m. for sodium
chlorate or 0.005 p.p.m. for phenyl mercuric acetate. Holden
(1964) (A65) devised a formula for comparing the likely toxic
hazards to trout from a number of pesticides applied at
agricultural rates. The following comparative estimates of
hazard were given: aldrin = 70, POP = 7, MCPA = 1.5, 2,4-D = 1,
2,4,5-T = 0.5, paraquat = 1/12, simazine = 1/27, diquat = 1/40,
dalapon = 1/46, TCA = 1/120, and aminotriazole = 1/150.
Perch (Perea fluviatilis) and roach (Rutilus rutilus) are unlikely
to be affected by 2,4-D, or 2,4,5-T (Bandt 1957) (A59) at rates of
application used for aquatic weed control. In later trials Bandt
et. al. (1962) (A59) found threshold values for toxicity to perch
and roach of 2,4-D of 75 p.p.m. of 2,4,5-T of 55 to 60 mg/litre
and of 2,4-D + 2,4,5-T mixtures of 5 to 12 mg. /litre. Davis and
Hardcastle (1959) (A68) established median tolerance limits over
a 24 hour period (TLm24) for bluegill sunfish (Lepomis macrochirus)
to a number of herbicides. Values obtained when the compounds were
added to relatively pure water were 2,4-D = 39 p.p.m., MCPA = 20 p.p.m.
2,4-DB = 20 p.p.m., and 2,3,6-TBA = 1,800 p.p.m. Cope (1966) (A61)
-147-
noted delays in spawning of bluegill sunfish of up to two weeks
after treatment of water with the propylene glycol butyl ether
ester of 2,A-D at five and 10 p.p.m. However, no other effects
were noted on reproduction or on survival of fry. In pond experi-
ments, death of some fish as a result of 2,4-D treatment led to
increased size in the survivors, probably as a result of the
greater food supply available to the individual fish. In further
trials with bluegill sunfish, Hughes and Davis (1963) (A66) and Davis
and Hughes (1963) (A66) reported on effects of different formulations
of 2,4-D and other auxins. Their tests showed 2,4-D and 2,4,5-T
esters to have TLm24 ranging from 1.8 to 10 p.p.m. depending on the
ester used. Dimethylamine salts of 2,4-D and 2,4,5-T had TLm24 of
162 to 542 p.p.m. and 144 p.p.m., respectively, compared to the
alkyl amine salt of MCPA of 163.5 p.p.m. and of 2,4-D acid of 8.0
p.p.m. This work (which is referred to in Cope 1966 (A61) , see above)
shows the wide differences in toxicity that can occur in different
formulations and the care which must therefore be taken in assessing
the toxicity of an individual product before recommending it for use
as an aquatic herbicide.
In addition to work on fish. Walker (1962) (A70) has reported effects
on a variety of bottom-feeding fish food organisms following application
of 2,4-D to plastic enclosures at 1.0 to 4.0 p.p.m. Lhoste (1959) (A67)
has reported that ester formulations of 2,4-D or mixtures of 2,4-D and
2,4,5-T affected crustaceans, aquatic insects, and mollus s in the
range of 0.1 to 3.3 p.p.m.
-148-
The results of these various investigations suggest that at herbicidal
rates of application of auxins the hazards from acute or chronic
toxicities to aquatic organisms are low (B) . Nevertheless in some
instances the dose rates required for effective herbicidal action
for example in estuaries or where the chemical is likely to be
rapidly dispersed, may give rise to local and perhaps short term
concentrations not far removed from those required for toxic effects
on some organisms at susceptible stages of their life history. In
such cases, design the application of the phenoxy herbicide to
minimize the probability of entry of the chemical to the water.
As may be seen from Table I, it does make a difference which 2,4-D
compound is used in aquatic weed control. It is readily apparent
that the amine salts are less toxic to these fish than the esters.
The effect of 2,4-D on fish-food organisms is shown in Table VI-7.
It appears that 1 ppmw of 2,4-D gives about 43% reduction in weight
of fish food in one week and about 90% in one year; it should be
borne in mind that these data were collected in plastic enclosures
and the data may not be strictly comparable to the results expected
in field use of this herbicide. Table II presents some data on
the effect of herbicides on estuarine organisms including specifically
oysters, shrimp, juvenile fish and phytoplankton. This table shows
the activities of some other herbicides of interest to this particular
report (B) . Rawles (1965) (A68) also studies the effect of the 2,4-D
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herbicides on caged blue crabs (Callinectes sapidus) , eastern oysters
%
(Crassostrea vlrginica) , soft shell clams (Mya arenaria) , and various
species of fish. Under conditions used to control Eurasian milfoil
(Myriophyllum spicatum) only 2,4-D acetamide at 20 Ib/acre (ae) was
toxic to the test animals; the butyl and isooctyl esters were
effective and nontoxic.
TABLE I - EFFECT OF VARIOUS 2,4-D COMPOUNDS ON FISH
Compound of 2,4-D
(after J.
Cone, (pp
M. Lawrence, 1966)
m) Species Time(Hr.)
Remarks
Alkanolamine salt
435-840
Bluegill
48
LD
50
Dimethylamine salt
166-458
Bluegill
48
LD
50
Isooctyl ester
8.8-59.7
Bluegill
48
LD
50
Dimethylamine salt
10
Fathead Minnow
96
LD
50
Acetamide
5
Fathead Minnow
96
LD
50
Oil soluble amine salt 2
Bluegill, Fat-
head Minnow
4
(Mo)
LD
10
Propylene glycol butyl
Bluegill, Fat-
ether ester
2
head Minnow
4
(Mo)
LD
10
Butoxyethyl ester
2
Bluegill 4 Fathead
72
LD
70-100
Butyl and isopropyl
esters, mixed
1.5-1. 7
Bluegill
48
LD
50
N,N-Dimethyl coco-
amine salt
1.5
Bluegill
48
LD
50
Ethyl ester
1.4
Bluegill
48
LD
50
Butyl ester
1.3
Bluegill
48
LD
50
Isopropyl ester
1.1
Bluegill
48
LD
50
Duomeen-O-amine salt
0.5
Fathead Minnow
Bluegill
4
(Mo)
“
-150-
I
TABLE II AVERAGE NUMBERS OF BOTTOM ORGANISMS PER SQUARE FOOT FOLLOWING
APPLICATION OF
2.4-D RANGING
FROM ONE TO
FOUR PPMIV IN
SIX
PLASTIC ENCLOSURES, 1958
-1959
Taxonomic Group
Control
One Week
Six Weeks
12 Months
Mayfly nymphs
4.00
0.17
0.17
—
Horsefly larvae
12.44
4.50
4.50
3.67
Common midges
17.11
4.50
1.50
0.33
Mosquitoes
0.44
0.33
—
—
Phantom midges
3.00
1.00
3.33
0.33
Biting midges
1.22
0.33
0.50
—
Caddis fly larvae
2.78
1.33
0.17
0.33
Damselfly nymphs
0.22
0.17
—
0.67
Water beetles
0.02
—
0.17
3.33
Aquatic worms
24.11
10.00
4.50
1.67
Leeches
0.11
—
—
—
Clams
5.44
—
—
—
Snails
5.67
0.50
—
—
Total numbers
76.56
22.83
14.83
10.33
Total weight
1.299
0.733
0.175
0.127
Source: C. A. Walker,
Toxicological
effects of
herbicide on
the fish
environment, Missouri University Engineering Extension series 2.
Proceedings of the 8th Annual Air and Water Pollution Conference
1962, pp. 17-34.
-151-
Studies on the toxicity of 2,4,5-T to fish have been reported by a
number of investigators. Hughes and Davis (1963) (A66) have compared
the 48-hour median tolerance limit (TLm) of bluegill sunfish to one
; and five ester products
of 2,4,5-T:
Compound 2,4,5-T
48-hr TL
(ppm, ae"':
Dimethylamine salt
144.0
Isooctyl ester, supplier
A
31.0
Isooctyl ester, supplier
A
26.0
Isooctyl ester, supplier
B
10.4
Propylene glycol butyl ether ester
17.0
Butoxy ethanol ester
1.4
They concluded that 2,4,5-T compounds were in general more toxic
than the corresponding 2,4-D products but they were unable to explain
the difference observed in the toxicities of the isooctyl esters of
2,4,5-T from different suppliers.
Fish are more susceptible than birds to the butoxyethyl ester of
silvex. However, the potassium salt of silvex appears to be less
toxic to fish than the ester formulations. No attempt will be made
to present all of the fish toxicity data and the reader is referred
to the Pesticide Wildlife studies (1963, 1964). Some fish such as
the rainbow trout appear at times to be highly resistant to silvex
(Cope reports the LD 50 for a 96-hour exposure to be 1,300 ppm)
while at other times they appear to be fairly sensitive to silvex
-152-
(fish and wildlife report a 96-hour LD 50 of 1A.8 ppm). Five out
of five fathead minnows were able to survive a 72-hour exposure to
150 ppm of the potassium salt of silvex but other experiments indicate
that the safe limit for fathead minnows is between 1 and 3 ppm of the
butoxyethanol ester of silvex. Experience with silvex in treated
ponds confirms the observation that levels of 3 ppm and above produced
liver degeneration lesions, testicular degenerative lesions, atrophy
of the spermatic tubules and abnormal spermatozoa on redear sunfish.
No comparable changes were seen in the ovaries.
The possible hazard of aquatic weed control procedures to water fowl
was considered and analysis of the levels of silvex in the tissues of
four ring-necked ducks, six coots, one lesser scaup, one green-winged
teal and one gadwall showed low or no detectable residues. (B)
The effect of silvex to possible fish foods has shown that the n3rmphs
of the stonefly (Pteronarcys) could tolerate 5.6 ppm for 24 hours but
only 0.32 ppm for 96 hours. Half of the Daphnia magna exposed to
100 ppm of the potassium salt of silvex for 26 hours were immobilized;
this is a sign of toxicity but the level is far above the usual 2
ppm used for aquatic weed control. (B)
In summary, the toxicity of silvex is not great to animals, birds
and other wildlife; however, there is much variability in the
response of fish to silvex and some species may be injured or
-153-
killed at levels normally used for aquatic weed control. The
potassium salt appears less hazardous to the fish than the
butoxyethyl ester. (B)
G. Hazards to Wildlife
Hazards to wildlife from auxin herbicides have been reviewed by
Rudd and Genelly (1956) (A72), Springer (1957) (A22), and Mellanby
(1967) (A71) .
With any material having biological activity a risk of acute or
chronic toxicity is always present; however, authenticated incidents
of widescale poisoning of wild animals by these herbicides have not
been reported.
The real problem from the use of auxin herbicides in regard to
wildlife is ecological and not toxicological. The altering of
habitat can be a hazard to all forms of wildlife. The size of
treatment areas and the intensity of use (frequent applications)
become important considerations. Intensity of treatment (repeated
applications) is generally associated with agriculture land. This
rarely becomes a problem on forest or range lands. The size and
location of treatment areas on forest and range land is of utmost
importance in considering the effect of spraying on wildlife.
Spray areas must be designed to leave sufficient "reservoirs" of
habitat .
♦
-154-
Fortunately, today there are application techniques and adequate
spray equipment at our disposal to leave untreated areas in about
any design that is desired.
-155-
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A2 Edwards, C. J., and W. E. Ripper, Droplet size, rates of applica-
tion and the avoidance of spray drift. Proc. 1st Brit. Weed
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A3 Fetisov, M. E. , Problems of occupational hygiene in work with
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A5 Nielsen, K, B. Kaempe, and J. Jensen-Holm, Fatal poisoning
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A6 Vallet, G. , Les intoxications par les herbicides recents. Concours
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A7 Kephart, L. W., Moderator of session. Proc. 2nd N. Central
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A8 Bjorklund, N. E. , and K. Erne. Toxicological studies of
phenoxyacetic herbicides in animals. Acta Vet. Scand. 7,364 (1966)
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A15 Gutenmann, W. H. and D. J. Lisk. Conversion of 4-(2,4-DB) herbicide
to 2,4-D by bluegills. N.Y. Fish Game J. 12, 108 (1965)
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A17 Lisk, D J. How now brown cow? Farm Research 32, 15 (1966)
A18 Palmer, J. S. Chronic toxicity of 2,4-D alkanolamine salts to
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A48 Johansen, C. Bee poisoning. A hazard of applying agricultural
chemicals. Wash. State Coll. Agr. Expt. Sta. Circ. No. 356 (1959)
A49 King, C. C. Translocation of C^‘*-2,4-D and **-amitrole or their
metabolites to nectar in plants. Research Kept. 17th N. Central
Weed Control Conf. p. 105 (1960a)
A50 Maxwell, R. C., and R. F. Harwood. Increased reproduction of pea
aphids on broad beans treated with 2,4-D. Ann. Entomol. Soc.
Amer. 53, 199 (1960)
A51 Palmer-Jones , T. Effect on honey-bees of some chemical weedkillers.
New Zealand J. Agr. Research 3, 485 (1960)
A52 Robinson, A. G. Note on fecundity of the pea aphid Acrythosiphon
pisum caged on plants of broad bean vicia faba L. , treated with
various plant growth-regulators. Can. Entomologist 91, 527 (1959)
A53 Wahlin, B. Bina och hormonderivaten. Vaxtskyddsnotiser , Stockholm
14, 45 (1950)
A54 Haragsimova, L. Einfluss der in der Tschechoslowakei im Pf lanzenschutz
gebrauchlichen chemischen Mittel auf die Honigbiene (Apis mellifera L.)
Tagungsbericht 2. Inter. Arbeitstagung der Arbeitsgemeinschaf t .
Toxicologie von Pflanzensch, Mitt. Berlin 54, 35 (1962)
-161-
A55 Audus, L, J. Herbicide behavior in the soil. In: The Physiology
and biochemistry of herbicides (Ed., L. J. Audus). London-New York
(
Academic Press (1964)
A56 Bollen W. B. Interactions between pesticides and soil micro-
organisms. Ann. Rev, Microbiol. 15, 69 (1961)
A57 Webster, J. M. Some effects of 2 ,4-dichlorophenoxyacetic acid
herbicides on nematode-infested cereals. Plant Pathol. 16, 23 (1967)
A58 Alabaster, J. S. Toxicity of weedkillers, algicides and fungicides
to trout. Proc, 4th Brit. Weed Control Conf . , p. 84 (1958)
A59 Bandt, H. J. Uber die Giftwirkund von Herbiziden auf Fische.
Z. Fischerei 6, 121 (1957)
A60 Bauer, K. Studren uber Nebenwirkungen von Pf lanzenschutzmitteln
auf Fische und Fischnahrtiere. Mitt. biol. Bundesanstalt Land u
Forstwirtsch, Berlin-Dahlem 105, 5 (1961)
A61 Cope, 0. B. Some responses of fresh-water fish to herbicides.
Proc. 18th S. Weed Control Conf. p. 439 (1965)
A62 Davis, B. N. K. The immediate and long-term effects of the herbicide
MCPA on soil arthropods. Bull. Entomol. Research 56, 357 (1965)
A63 Davis, J. T. , and W. S. Hardcastle. Biological assay of herbicides
for fish toxicity. Weeds 7, 397 (1959)
A64 Fish, G. R. Some effects of the destruction of aquatic weeds
in Lake Rotoiti, New Zealand. Weed Research 6, 350 (1966)
A65 Holden, A. V. The possible effects on fish of chemicals used
in Agriculture. J. Inst. Sewage Purif. 4, 361 (1964)
A 66 Hughes, J. S., and J. T. Davis. Variations in toxicity to
bluegill sunfish of phenoxy herbicides. Weeds 11, 50 (1963)
-162-
A67 Lhoste, J. Les repercussions de I'emploi des desherbants
chimiques sur la faune aquatique C. r. Reun. Tech. d'Athenes
de I'UICN A, 253 (1959)
A68 Rawls, C. K. Field tests of herbicide toxicity to certain
estuarine animals. Chesapeake Sci. 6, 150 (1965)
A69 Smith, G. E. , and B. G. Isom. Investigation of effects of
large-scale applications of 2,A-D on aquatic fauna and water
quality. Pesticides Monitoring J. 1, 16 (1967)
A70 Walker, C. R. Toxicological effects of herbicides on the fish
environment. Proc. 8th Air Water Pollution Abatement Conf .
p. 17, (1962)
A71 Mellanby, K. Pesticides and pollution. New Naturalist No. 50
London-Glasgow. Collins (1967)
A72 Rudd, R. L., and R. E. Genelly. Pesticides. Their use and
toxicity in relation to wildlife. Calif. Fish Game Bull. No. 7
(1956)
B. House W. B., L. H. Goodson, H. M. Gadberry and K. W. Docktur, 1967.
Assessment of ecological effects of extensive or repeated use of
herbicides. Midwest Res. Inst. Proj . 3103-B. Adv. Res. Pro j .
Agency order 1086 Dept, of Def. Contract No. DAHC15-68-C-0119, 369 p.
B1 Palmer, J. S. Chronic toxicity of 2,A-D alkanolamine salts to
cattle. J. Amer. Vet. Med. Assoc. 1963.
-163-
B2 Clark, D. E., J. E. Young, R. L. Younger, L. M. Hunt, and J. K.
McLaren, 1964. The fate of 2,4-dichlorophenoxyacetic acid in
sheep, J. Agr, Food Chem. 12: 43-45.
B3 Khanna, Suchitra, and S. C. Fang. 1966. Metabolism of C^**-labeled
2,4-dichlorophenoxyacetic acid in rats. J. Agr. Food Chem. 14:
500-503
B4 Buck, W. B. et. al. 1961. Results of feeding herbicide treated
plants to calves and sheep. J. Amer. Vet. Med. Assoc. 138, 320
B5 Stabler, L. M. and E. I. Whitehead, 1950. The effect of 2,4-D
on potassium nitrate levels in leaves of sugar beets. Science
112, 749.
B6 Lynn, G. E. and K. C. Barrens, 1952. The hydrocyanic (HCN) content
of wild cherry leaves sprayed with a brush killer containing low
volatile esters of 2,4-D and 2,4,5-T. Proc. 6th NE Weed Control
Conf. p. 331.
C. Report of the Advisory Committee on 2,4,5-T. 1971. To the administrator
of the Environment Protection Agency.
Cl Sparschu, G. L., F. L. Dunn, R. W. Lisowe and V. K. Rowe, 1971.
Study of the effects of high levels of 2,4 ,5-Trichlorophenoxy-
acetic acid (2,4,5-T) on rat fetal development. Unpublished study.
C2 Johnson, J. E. 1970. The public health implications of widespread
use of the phenoxy herbicides and picloram. Presented at the
Symposium on Possible Public Health Implications of widespread
use of pesticides, American Institute of Biological Sciences,
Bloomington, Indiana, August 26, 1970.
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C3 King. C. T. G., 1971. Teratogenicity studies of 2,4,5-T and 2,A-D
Unpublished report, February 25, 1971.
C4 Tschirley, F. H., 1971. Report on status of knowledge regarding
2,4,5-T. Submitted by the USDA to the EPA, March 5, 1971. 2,4,5-T
Advisory Committee AE-20
C5 2,4,5-T Advisory Conunittee Exhibits I-13a, 1-14, and 1-15
D. St. John, L. E. and D. J. Llsk, 1964. Fate of atrazlne, kuron, sllvex,
and 2,4,5-T in the dairy cow. Journal of Dairy Sciences. November 1964.
Vol. XLVII. No. 11, pp. 1267-1270
-165-
REPORT
ON
BACKGROUND INFORMATION
FOR
SIMAZINE
2-23-72
Lisle R. Green
An Outline of Background Information
for the Herbicide SIMAZINE
1. General Information
A. Common name
1 . Si maz i ne
B, Chemical name
1 . 2-chl oro-^ , 6- bis (ethyl ami no )-s-triazine
C. Registered uses—^
1. As a selective herbicide to control the germinating seedlings
of most annual broadleaf and grassy weeds in:
a. Field and forage crops
(1)
A1 fa 1 f a—
(2)
Forage bermudagrasses— ^
(3)
Corn
W
Suga rcane
(5)
Grasses grown for seed (Pacific Northwest on
various perennial grasses used for lawns and
ly);
turf .
~ Special precautionary recommendations and statements warning of isolated
effects or special problems which may be encountered are published in
the sample label and general information brochure published by Gelgy
Agricultural Chemicals.
2/
— Don't graze livestock (sheep, dairy, or beef cattle) for 30 days
following a 1 to 3 lb. application, or 60 days following k lbs. Don't
cut for hay for 60 days following a 1 to 3 lb. per acre application, or
90 days following ^ lbs.
2
b . Fruit and nut crops
(1) Fruit crops“-appl es , pears, peaches, grapes,
cherries, plums, avocados
(2) Nut crops--wal nuts , filberts (in Washington and
Oregon)
(3) Bush f rui ts--blackberr ies , boysenberr i es , logan-
berries, blueberries
(4) Citrus f ru i ts--oranges , lemons, grapefruit
c . Nurseries, Christmas trees, plantings and shelterbelts
(1) Species
American elm
Austrian pine
Arborv i tae
Ba 1 sam f i r
Barberry
Blue spruce
Boxel der
Bush honeysuckle
Caragana
Cotoneaster
Dogwood
Doug 1 as-f i r
F raser f i r
Hemlock
Honey locust
Jun i per
Mugho pine
Norway spruce
Oregon grape (Mahon i a spp.)
Red cedar
Red oak
Red pine (Norway pine)
Red spruce
Russian olive
Scotch pine
Siberian elm
Wh i te cedar
White pine
Wh i te spruce
Yew (Taxus spp.)
d . Turf grasses for sod
(1) Species
St. Augustine
Cent i pede
Zoysia grass
Perennial ryegrass
Bentgrasses
Orchardgrass
Tall fescue
Fine fescues
e. Vegetable crops
Asparagus (established)
Art i chokes
3
f . Hard-tp-kill perennial weeds such as bull thistle,
bindweed, and perennial grasses.
2. Nonselective weed control for noncrop land.
a. At higher rates, simazine is used as a sterilant to
remove most or all vegetation from industrial sites,
fence rows, railroads, around utility poles, and along
roads .
3. Aquatic plants.
An experimental label has been granted for use in aquatic
environments for weed and algae control.
D. Formulations manufactured
1. A wettable powder containing 80 percent active ingredient,
marketed as Princep 8OW.
2. A granular form containing k percent active ingredient,
marketed as Princep-^G.
E . Dilutions of formulations for use in :
1. Use enough water with the wettable powder to assure thorough,
uniform coverage on the soil surface.
a . Ground applications
(1) 20 to 100 gallons of water per acre.
b. Broadcast aerial applications
(1) A minimum of 1 gallon of water for each 1 lb. of
simazine to be applied per acre for preemergence
applications, up to 15 gallons per acre.
1.
r
F. Rate and method of application
1. Rate of application.
a. Selective weed control to eliminate annual grasses and
broadleaf annual weeds from perennial vegetation.
(1)
Sand & loamy sand, low OM
Do
not use
(2)
Fine sand S sandy loam
1
to 2
1/2 lb. /acre
(3)
Loam 6 clay loam, low OM
2
1/2
to 3 lb. /acre
(h)
Clay, or other soils high
in OM
3
to k
1 b . /acre
(5)
High organic clays
k
to 5
lb./ acre
b. Nonselective weed control on noncropland.
(1) Most annual and many perennial
broadleaf and grass weeds 12 1/2 to 25 lb. /acre
(2) For "sterilant" effect of about
3 to 4 years, depending on rainfall. 25 to 50 lb. /acre
c. Water
plants.
(1)
Submerged, in ponds
0.5 to 2
ppmw
(2)
Sensitive emergent
[bu 1 rush (Sc i rpus ) ] ,
Carex, Polygonum,
Needlerush (E 1 eochar i s ) ,
arrowhead (Sagg i ttar ia) ,
willow (Sal i>T) [WaTker 1964]
10 to 20
lb ./acre
5
(F. - d. Discussion)
There are numerous reports in the literature which indicate that soil
organic matter is the most active soil component in adsorbing simazine,
thus reducing its phytotoxicity and requiring larger applications to do
the same weed control job. Many of these references are included in a
review article by Hayes (1970). There are also numerous references in
(1970)
Residue Reviews ^/which indicate that clay content of soil is also
important, and some where clay content didn't seem important. Type of
clay is important--montmor i 1 Ion i te being more active than kaolinite, for
example (Weber 1970). Perhaps an "average" of the clay-organic matter
situation was obtained by results of Nearpass (1965) who found adsorption
of simazine to be significantly correlated with percent of clay and highly
significantly correlated with organic matter and titratable acidity in
18 soils.
Evans et al. (19^9) found control of downy brome with simazine at
1 pound per acre averaged about 73 percent. There was good broadleaf
weed control but no control of Russian thistle. Green and Benedict
(unpublished manuscript) controlled downy brome and other annuals with
simazine at 1 1/2 to 3 pounds per acre on sandy loam soils.
Simazine at 2 pounds per acre controlled hoary alyssum (Ber teroa
1 ncana (L.) D.C.), a perennial weed, in alfalfa (Kust 1969)* Simazine
at 1 1/2 pounds per acre controlled annuals for one year in pecan orchards
and at ^ pounds, gave nearly complete control of all weeds, including
6
nutsedge and bermudagrass . The soil was a loamy fine sand (Norton and
Storey 1970). Simazine at 10 pounds per acre caused visible foliar
injury but no height or weight loss to young Japanese maple trees, and
there was no injury to yew (Danielson and May 1969)* There is lots of
experience which demonstrates the safety of older trees when simazine
is applied at 1 to A pounds per acre. There is some indication that
toxicity of simazine has decreased as soil moisture decreased (Grover
1966, Buchholtz 1965, and Evans et al . 19^9). "Holdover" effects are
generally small at less than 2 pounds of simazine per acre, but sensitive
plants are damaged at 2 pounds or more. At 10 pounds or more, residual
effects can be expected for at least three years. Most residual simazine
is in the surface few inches of soil.
Leaching has occurred to greater depths with A pounds than with 2
pounds, and deeper when rainfall was concentrated rather than spread
over several smaller storms (Rodgers 19^8).
(
7
2. Method of application
a. Ground sprayers--Most low pressure (25 to 40 1b,
pressure) sprayers can be used. Teejet 8003 or 8004
fan-type nozzles or equivalent. Tank must have
mechanical or bypass agitation.
b. Aerial spray.
c. Broadcasting of pellets.
(1)
Cyclone type hand spreaders
(2)
Field spreaders
(3)
Aerial
General
a. Application of either spray or granules should be made
prior to weed emergence, and certainly before weeds
are more than an inch or so tall. If taller than this,
amitrole or other herbicide that works through the
foliage should be applied with simazine.
b. Simazine has little orno foliar activity, and requires
rain or irrigation to take it into the root zone for
absorpt i on .
G . Tolerances in food or feed and other safety limitations
1. The Federal Food and Drug Administration has set tolerances
for residues and simazine on certain raw agricultural
commodities as follows:
a •
15.00
ppm
i n
or
on
alfalfa, bermudag rass , other grass
b.
10.00
ppm
i p
or
on
asparagus .
c.
o
vn
O
ppm
i n
or
on
art I chokes .
8
f
d. 0.25 ppm in or on almonds (hulls and nuts), apples,
avocados, blackberries, blueberries, boysenberr i es ,
cherries, fresh corn including sweet corn (kernels plus
cobs with husks removed), corn grain (including popcorn),
corn forage or fodder (including field corn, sweet corn,
and popcorn), cranberries, currants, dewberries, grape-
fruit, grapes, lemons, loganberries, macadamia nuts,
olives, oranges, peaches, pears, plums, raspberries,
strawberries, walnuts.
0.02 ppm (negligible residue) in eggs, milk, meat, fat,
and meat by-products of cattle, goats, hogs, horses,
poultry, and sheep.
2. Consult the Federal Food and Drug Administration for changes
and additions. These will also be reflected in the most
recently issued Geigy Agricultural Chemical Company technical
bulletin or labels covering simazine.
3. The marketing of raw agricultural commodities having residues
in excess of their permitted tolerances, or marketing those
for which no tolerances have been set and bearing residues,
will violate Federal Law when shipped in interstate commerce
and may violate State Law.
H. Manufacturer
1. Geigy Agricultural Chemicals
Saw Mill River Road
Ardsley, New York 10702
(
9
II. Toxicity data on formulation to be used
A. Safety data
1. Acute mammalian studies
a. Ora 1
Available evidence and experience indicates that
simazine has low toxicity to animals, and most likely
to man also. The acute oral toxicity (LD^q) of
simazine to rats, mice, rabbits, chickens, and pigeons
is in excess of 5,000 mg (5g)/ki logram (kg) of body
weight (Geigy Agricultural Chemical Co. 1970).
Cattle fed 250 mg of simazine/kg of body weight as a
drench showed poisoning symptoms after one dose, but
survived 3 doses with 11 percent weight loss (Palmer
and Radel iff 1 9^9) •
No cases of poisoning in man have been reported from
ingestion of simazine.
b. Dermal
The acute dermal LD^q of simazine to albino rabbits is
greater than lOg/kg. In a 21-day repeated dermal study
on albino rabbits, the LD50 was 2g/kg (Geigy Agricultural
Chemi cal Co. 1 970) .
No substantial skin irritation has been reported from
either experimental or commercial use.
c. I nhal at i on
No deaths or signs of toxicological or pharmacological
effects resulted from exposing groups of rats for one
hour to a dust aerosol of simazine 8OW. Aerosol con-
centrations ranged from 1.8 to A. 9 mg/1 of atmosphere.
d . Eye and skin irritation
No serious skin or eye irritation has been reported for
experimental or commercial use.
10
2. Subacute studies
a. Oral, b. Dermal, c. Inhalation
Two year chronic oral feeding studies, in which male and female
rats were given daily dosages at various rates as high as
100 ppm of simazine SOW in the diet, resulted in no gross or
microscopic signs of systematic toxicity due to ingestion
(Geigy Agricultural Chemical Co. 1970).
Two yearling cattle showed visible poisoning symptoms after
3 and 10 doses of 25 mg/kg. There were no symptoms at 10
mg/kg. One sheep was poisoned at 50 mg/kg after 17 doses,
and died after 31 doses, whereas another was poisoned with
10 doses but survived. Chickens dosed at 50 mg simazine/kg
showed reduced weight gain. Application rates in excess of
3 pounds per acre would be hazardous for grazing cattle and
in excess of 5 pounds for sheep. The 9*6-pound rate would be
hazardous for chickens (Palmer and Radeliff Sheep fed
up to 25 mg/kg for 5 weeks remained normal (Geigy Agricultural
Chemical Co. 1970).
3. Other studies which may be required
a . Neurotoxi ci ty
b . Teratogen i c i ty
c. Effects on reproduction
d . Synerg i sm
e . Potent i at ion
f . Metabolism and mode of action
Simazine enters weeds mainly through the roots. Its most
efficient use requires application before weeds germinate,
and rainfall sufficient to carry it to the root zone. It
is translated through the xylem to the leaves where it
disrupts the photosynthetic process (Geigy Agricultural
Chemical Co. 1970). Simazine at 0.12 to 1 ppmw inhibited
oxygen production through reduction of photosynthesis of
aquatic plants (Sutton et a1. 1969). It was noted during
another study that chlorophyll and cell chloroplast protein
was reduced in oat plants subjected to simazine at 1 ppm
for 6 days.
g • Avian and fish toxicity
11
(1) Fish toxicity
Simazine at 3 ppmw was reported to be nontoxic to
fish (Flanagan, Proc. NE Weed Control Conf. 1^:
502“505)» although in another situation, simazine
at 2 ppmw killed adult, but not young, redear
sunfish in one pond and not in a second (Snow,
Proc. So. V/eed Control Conf. 16: 329"335)* Green
sunfish were exposed to simazine by feeding of 3 to
10 mg/kg and by water bath (l and 3 Ppm) from which
they absorbed simazine in direct proportion to its
concentration in the water. No simazine residue
was detected 7 days after either treatment and there
appeared to be no damage to the fish (Rodgers 1970).
In another study, simazine at 2 ppmw controlled 80
percent of water plants while giving a safety factor
for aquatic life. The LD^q toxic dose to bottom
dwelling organisms was 28 ppmw. LD]q values for
three sunfish species were 20 ppmw and LD^q about
35 (Walker I96M.
(2) Av i an tox i c i ty
h. Carcinogenicity
12
B. Physical -chemical properties
1. Melting point
a. 225-227° C (^37-^41° F)
2. Flash point
3. Physical state and color
a. A noncombustible, white crystalline
commercial product is prepared as a
granules .
substance,
powder or as
Dens i ty
a. Molecular weight
is 201.7
Vapor pressure
a. Temp° C
MM Hg.
10
9.2 X 10"’°
20
6.1 X 10"5
30
3.6 X 10"^
50
9.0 X lo"'^
Sol ub i 1 i ty
Sol ub i 1
a. Solvent
Temp° C
ppm
Water
0
2.0
Water
20 (68° F)
5.0
Wa ter
85
8A.0
Methanol
20
^00.0
Petroleum ether
20
2.0
i
13
5. Stabi 1 i ty
Simazine has practically unlimited stability at room
temperature within a pH range of 3 to 10 (Gelgy
Agricultural Chemical Co. 1970).
Several workers have demonstrated photodecomposition in the
laboratory after exposure to ultraviolet light, and also
under sunlight when simazine was exposed on the soil surface
during the summer. In one case, this amounted to 25 percent
of its phototoxic effect in 25 days (Jordan et al. 1970).
Volatilization is most likely a source of loss from the soil
under conditions of high soil temperature, although simazine
is less volatile than most other s-triazines (Kearney et al.
196^) with virtually no volatility of simazine between 25 to
A5° C (77 “ 112° F). Several investigators have shown simazine
losses by volatilization at temperatures from 112° to 212° F
(Jordan et al . 1970). Loss from this source is probably very
smal 1 .
inactivation of simazine in the field was shown by Talbert
and Fletchall (190^) to be greatest when environment was most
favorable for growth of microorganisms. The available evidence
indicates that slow microbiological decomposition Is the
principle process Involved In dissipation of simazine
(Burnside et al . 19^1, Ragab and McCollum 19^1, Weed Research
1: 131"l^lj and Proc. , British Weed Control Conf. 5: 91“97).
The degradation processes are reviewed by Kaufman and Kearney
(1970).
14
111. Efficacy data under field and laboratory conditions
A. Effectiveness for intended purpose when used as directed
Simazine when used at prescribed rates for prescribed crops and
conditions seems to perform as advertised. It is registered for
and used as a selective herbicide on many perennial crops. It
is also registered for nonselective weed control on noncroplands.
B. Phy totox i c i ty
Simazine is toxic to a wide variety of grassy and broadleaf weeds.
It can be used as a selective herbicide because it is relatively
resistant to leaching (Ashton 1961, Montgomery and Freed 1959,
Roadhouse and Birk 1961, and Rogers 1962), and can readily be
placed in the root zone of recently germinated plants. Higher
rates have tended to leach deeper than low rates, and leaching
is deeper in sandy soil of low organic content than in organic
or clay soils, hence deeper rooted perennial plants can be
damaged by high rates, or if growing in sandy soils, or if heavy
precipitation carries the herbicide into their root zone.
There is variable tolerance among plants to simazine. Corn
evidently converts simazine to nontoxic materials (Montgomery
and Freed 1961). Western wheatgrass, crested wheatgrass, blue
grama, and sedge were less tolerant to s-triazines (simazine)
than needle- and - thread and sand dropseed in western Nebraska
(Wi cks et a 1 . 1 965) •
C. Translocation
Simazine is absorbed through plant roots with little or no foliar
penetration. It is translocated through the xylem, and accumulates
in the apical meristems and leaves.
15
D. Persistence in soil, water, or plants
1. Persistence in soil
Simazine will tend to persist longer in fine textured than
in sandy soils, in arid more than moist situations, in cold
more than warm soils, and in situations otherwise not
conducive to chemical and microorganism action.
The residual activity of simazine in soil at selective rates
for the specific soil types is such that many rotational
crops can be planted one year after application. However,
there is frequently some simazine residue that may affect
sensitive crops (Herbicide Handbook 1967, Lewis and Lilly
1966, Buchholtz 1965, and Burnside et al. 1965)*
Under arid conditions persisting near Reno, Nevada, simazine
at 1 pound per acre controlled annual weeds if rainfall was
normal, and perennial grasses could be planted a year after
the simazine treatment (Evans et al. 1969). Green and
Benedict (unpublished manuscript) found simazine at 3 pounds
per acre restricting downy brome growth for a year, with
partial downy brome recovery in two years.
E. Compatibility with other chemicals
Simazine is compatible with most other herbicides and fertilizers
at normal rates. It is frequently used with amitrole or other
foliar absorbed herbicide if weeds are already growing actively.
IV. Environmental impact
A. Effects on non-target organisms
These are believed to be small.
B.
16
i
Literature Cited
Ashton, F. M. 1961. Movement of herbicides in soil with simulated
furrow irrigation. Weeds 9: 612-619*
Buchholtz, K. P. 1965. Factors influencing oat injury from triazine
residues in soil. Weeds 13(^): 362-367*
Burnside, 0. C. , E. L. Schmidt, and R. Behrens. I96I. Dissipation of
simazine from the soil. Weeds 9(3): ^77“^84.
Burnside, 0. C. , G. A. Wicks, and C. R. Fenster. 1965* Herbicide
longevity in Nebraska soils. Weeds 13(3): 277"278.
Danielson, L. L. and C. May. 1989. Effects of several herbicides on
yews and Japanese maples. Weed Science 17(2):
Evans, R. A., R. E. Eckert, Jr., B. L. Kay, and J. A. Young. 1969*
Downy brome control by soil-active herbicides for revegetation of
rangelands. Weed Science 17(2): I66-I69.
Flanagan. Proc. NE Weed Control Conf. 14: 502-505.
Geigy Agricultural Chemicals. 1970. Princep herbicide. Tech. Bull.
Geigy Chemical Corp. , Ardsley, New York. 8 p.
Green, L. R. and E. W. Benedict. Soil sterilants to control herbaceous
vegetation on Intermountain fuel-breaks (unpublished manuscript).
Grover, R. I966. Influence of organic matter, texture, and available
water on the toxicity of simazine in soil. Weeds 14(2): 148-151*
Gunther, F. A. and J. D, Gunther. (Editors). 1970. Residue Reviews,
Vol. 32. The Triazine Herbicides. Spr i nger-Ver 1 ag , New York. 413 P*
Hayes, M. H. B. 1970. Adsorption of triazine herbicides on soil organic
matter, including a short review on soil organic matter chemistry. j_n
Residue Reviews 32: 131" 174.
Jordan, L. S. , W. J. Farmer, J. R. Goodin, and B. E. Day. 1970. Non-
biological detoxication of the s-triazine herbicides. j_n_ Residue
Reviews 32: 267~286.
17
Kaufman, D. D. and P. C. Kearney. 1970. Microbial degradation of s-
triazine herbicides. J_n Residue Reviews 32: 235“265.
Kearney, P. C. , T. J. Sheets, and J. W. Smith. 1964. Volatility of
seven s-triazines. Weeds 12(2): 83~87.
Kust , C. A. 1969* Selective control of hoary alyssum in alfalfa. Weed
Science 17(1): 99" 101.
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