Scientific criteria document for the development of a provincial water quality objective for cobalt (stable isotope) : report

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SCIENTIFIC CRITERIA DOCUMENT
FOR THE DEVELOPMENT OF
A PROVINCIAL WATER QUALITY
OBJECTIVE FOR COBALT
(STABLE ISOTOPE)

OCTOBER 1996

Ministry of

Ontario '"^'°"'""

and Energy

ISBN 0-7778-4673-X

SCIENTIFIC ClUTERIA DOCUMENT

FOR THE DEVELOPMEN I OF

A PROVINCIAL WATER QUALITY OBJECTIVE

FOR COBALT

(STABLE ISOTOPE)

OCTOBER 1996

®

Cade publication tcchniciuc
n"est disponible qucii anglais.

Copyriglil; Queen's Printer for Ontario. 1996

Ttiis publication may be reproduced for non-commercial purpo.ses

with appropriate attribution.

PIBS 336 IE

SCIENTIFIC CRITERIA DOCUMENT

FOR THE DEVELOPMENT OF

A PROVINCIAL WATER QL AUTY OBJECITVE

FOR COBALT

(STABLE ISOTOPE)

Report prepared by:
T. Flelcher'. G.L. Stephenson-, J. Wang- and CD. Wren-

' Standards Development Branch
Ontario Ministry of Environment and Energy

-Ecological Services for Planning Ltd.

361 Southgate Drive

Giicipli, Ontario

K I G 3M5

PREFACE

The Ontario Ministry of Environment and Energy develops Provincial Water Quality
Objectives, or Interim Objectives, for tliose substances deemed to be of greatest
environmental concern in Ontario. These as determined through a screening process
which considers persistence, potential to bioaccumulate, acute and chronic toxicity and
potential presence in the aquatic environment. Alternatively, Ministry staff who have a
direct responsibility for managing possible effects of these chemicals may request an
evaluation.

Provincial Water Quality Objectives and Interim Objectives (PWQO/IOs) are numeric or
narrative criteria intended to protect all life stages of aquatic organisms for indefinite
exposures and/or to protect recreational uses of water. PWQO/IOs for recreational uses,
including swimming, are currently based on microbiological and aesthetic considerations.
The potential for harmful effects from exposure to chemical substances during recreational
uses is unknown at present, but will be considered when scientific information becomes
available. Ontario Drinking Water Objectives and sport fish consumption guidelines are
also considered in protection of human health. PWQO/IOs represent a desirable water
quality for the protection of designated uses of surface waters in Ontario. PWQO/IOs do
not take into account analytical detection or quantification limits, treatability or removal
potential, socio-economic factors, natural background concentrations, or potential transport
of contaminants among air, water and soil. These factors are considered in policies and
procedures which govern the uses of PWQO/IOs, contained in the booklet. Water
Management: Policies, Guidelines and Provincial Water Quality Objectives of the Ministry
of Environment and Energy (OMOEE 1994a), which deals with all aspects of Ontario's
water management policy.

The process for deriving these criteria is detailed in Ontario's Water Quality Objective
Development Process (OMOE 1992a). The toxicology literature is reviewed for all of the
following areas: aquatic toxicity, bioaccumulation, mutagenicity, and aesthetic
considerations. The final Objective/Interim Objective is based on the lowest effect

concentration reported for any of tfiese factors on aquatic organisnns as well as taste and
odour considerations of the water. Where there are reliable and adequate data, an
Objective is developed using a safety factor. Where there are fewer data, an interim
Objective is developed using an "uncertainty factor". The size of the uncertainty factor
reflects the availability of appropriate data and the potential of the material to
bioaccumulate. Interim Objectives can be promoted to Objectives when sufficient reliable
data become available.

PWQO/IOs are used to designate surface waters of the Province which should not be
further degraded. They are also used in receiving water discharge assessments and may
be included in Certificates of Approval which are issued to regulate effluent discharges.
Where better water quality is required to protect other beneficial uses of the environment in
a given location, appropriate criteria and factors, including public health considerations, are
taken into account.

ACKNOWLEDGEMENTS

The authors would like to thank members of the MOEE Aquatic Criteria Development
Committee, and specifically Gary Westlake, Dave Rokosh, and Mike Salamone, from
Standards Development Branch, for the review of the first draft of this document.

The authors would especially like to thank the peer reviewers from outside of Standards
Development Branch. Thanks go to W. Frais (Bayer Rubber Inc.), W. Ng (Regional
Operations Division, MOEE), J. Hawley (MISA - MOEE), D. Skingsley (York University,
UK). R. Playle (Wilfred Laurier University), N. Nagpal (B.C. Environment), J. Johnston
(Lakefield Research), K.J. Buhl (U.S. Department of Interior, National Biological Service),
and from Environment Canada, S. Teed, C. Jefferson, D. Andersen, C. Dumaresq, A.
Pawlisz and S. Munger,

IV

SUMMARY

A Provincial Water Quality Objective (PWQO) was developed for cobalt for the protection
of aquatic life. Available information on the physical-chemical properties, aquatic toxicity,
bioaccumulation potential, taste and odour characteristics and genotoxicity potential of
cobalt were considered in developing the Objective.

Cobalt is an element which occurs naturally in the earth's crust. Approximately 10% of the
world's total production of cobalt comes from Canada. Cobalt is used in various alloys, as
a catalyzing agent, fertilizer and as a colouring agent in glass and ceramics. It is also
used in the medical field and as a farm feed additive.

Cobalt is found in trace amounts in surface waters of Ontario. In the Great Lakes, total
cobalt concentrations rarely exceed the detection limit of 1 |jg/L, however concentrations
as high as 80 pg/L have been reported in surface water near mine tailings.

Cobalt exists in surface waters mainly as the divalent and trivalent forms. Cobalt is
strongly adsorbed on suspended solids and sediments, Therefore very low concentrations
are found in the dissolved state. In most ecosystems, the sediment is the primary sink for
cobalt.

Compared to other metals, cobalt is slightly to moderately toxic. The literature indicates
that acute effects for a variety of aquatic lile occur between 1 mg/L and 450 mg/L.
Chronic effects range from 0.009 mg/L to 2 500 mg/L. Cobalt does not appear to
bioaccumulate to any significant degree in fish.

There was sufficient aquatic toxicity data available to derive a Provincial Water Quality
Objective. The recommended PWQO for cobalt is 0.0009 mg/L (0.9 pg/L) derived by
dividing the lowest acceptable effect concentration of 0.009 mg/L (28d reproduction
impairment and reduced survival of Daphnia magna) by an safety factor of 10.

The PWQO is above the OMOEE laboratory detection limit, however due to difficulties in
analysis, often the detection limit may be higher than the PWQO. This value should be
protective of effects due to aquatic toxicity, bioaccumulation, taste and odour effects.
There are indications that exposure to cobalt may cause mutagenicity. However insufficient
information was available to assess these effects on aquatic organisms.

Note: Concentrations in this document are expressed in a number of different units
commonly used in scientific papers. The conversion factors are:

1 gram per litre (g/L) = 1000 milligrams per litre (mg/L)

1 milligram per litre (mg/L) = 1000 micrograms per litre (pg/L)

TABLE OF CONTENTS

PREFACE ii

ACKNOWLEDGEMENTS iv

SUMMARY V

TABLE OF CONTENTS vi

1 0 INTRODUCTION 1

1.1 PRODUCTION AND USES 1

1.2 AQUATIC SOURCES AND FATE 2

1.3 AMBIENT CONCENTRATIONS IN ONTARIO WATERS 3

1 .4 AQUATIC CHEMISTRY 6

2.0 TOXICITY TO AQUATIC ORGANISMS 7

2.1 ACUTE TOXICITY 8

2.1 .1 Vertebrates 8

2.1 .2 Invertebrates 9

2.2 CHRONIC TOXICITY 11

2.2.1 Vertebrates 11

2.2.2 Invertebrates 12

2.2.3 Ottier Organisms (Algae. Prolists etc.) 14

2.3 SUMMARY OF TOXICITY DATA 15

2.4 EFFECTS OF WATER QUALITY PARAMETERS ON TOXICITY 17

3.0 BIOACCUMULATION 18

4.0 IMPACT ON TASTE AND ODOUR OF WATER AND FISH TAINTING 19

5.0 MUTAGENICITY 19

6.0 DERIVATION OF THE PROVINCIAL WATER QUALITY OBJECTIVE 21

6.1 Toxicological data 21

6.2 Bioaccumulation 22

6.3 Mutagenicity : 22

6.4 Taste and Odour 22

6.5 Other Effects 22

6.6 Dermal Effects 23

6.7 OMOEE Laboratory Detection Limits 23

6.8 Conclusion 23

7.0 RESEARCH NEEDS 24

8.0 OBJECTIVES OF OTHER AGENCIES 25

VI

9.0 REFERENCES '. 26

List of Tables

Table 1. Toxicity Ranking of Cobalt Compared to Other Metals 17

Table 2. Aquatic Toxicity Data Table for Cobalt 35

Table 3. Data Requirements for Provincial Water Quality Objectives .... 40

LIST OF FIGURES

Figure 1a. Objective Derivation Graph - Acute 43

Figure lb. Objective Derivation Graph - Chronic 44

VII

1.0 INTRODUCTION

Cobalt (Co) is a silver-grey, hard, magnetic, ductile, and somewhat malleable metal similar
to nickel and iron in appearance (Sax and Lewis 1989; Weast et al. 1987: Windholz et al.
1983). It is the 30th most abundant element on earth and comprises approximately
0.0025% of the earth's crust (Kirk et al. 1979). ASTDR (1991) reports that cobalt
frequently occurs in nature in association with nickel, and often with arsenic. In Cobalt,
Ontario, deposits of cobalt occur with silver (Hawley, Pers. comm). Cobalt is found in
various rock types present in Ontario, namely granite, basalt, shale, limestone, and
sandstone. Common ores may contain the minerals cobaltite (CoS^.CoASj), linnaeite
(C03SJ, carrollite, safflorite, skutterudite, smaltite (CoASj), and erythrite
(3CoO.AS2O5.8H2O) (Shamberger 1979; Windholz et al. 1983). The average total cobalt
concentration in Ontario soils is 4.4 mg/kg (Young 1979), while that in tailings deposits is
83 mg/kg (Hawley, 1980).

Cobalt is an essential nutrient required for vitamin B,2 metabolism. In mammals, Co
deficiency and low levels of vitamin B.j result in pernicious anemia, whereas excess results
in polycythemia (Martell 1975).

1.1 PRODUCTION AND USES

Cobalt was used as a colouring agent as far back as 2000 BC by the Egyptians, and later
by the Assyrians, Greeks, Romans, and Chinese (Kirk et al. 1979). By the 17th century,
Europeans had discovered methods of mining cobalt and used it to colour glass and
pottery. In 1914, the first cobalt produced commercially in the world was manufactured at
Deloro, Ontario. The plant at Deloro was closed down in 1961 due to the slumping
demand for cobalt (Azcue and Nriagu 1993). Today there are numerous uses for cobalt,
including uses in the industrial, agricultural and medical sectors.

Important cobalt deposits occur in Zaire, Morocco, Australia, and Canada (Weast et al.
1987). The reserves of Canada and Australia comprise about one quarter of the world

1

supply (Kirk et al. 1979). Emsley (1991) reports that 1984 world production of cobalt was
19 000 tonnes. In Canada, cobalt is produced mainly in Ontario and Manitoba (CCREM
1987) as a by-product of nickel-copper production.

Giancola (1994) reports that in 1993 there were nine mines in Ontario which produce
cobalt. All were in the Sudbury area. Cobalt is only incidently mined from these deposits,
primary ores are nickel, silver and copper (Hawiey, Pers. comm). In 1993 the cobalt
content of metal concentrates produced in Canada was 2 370 tonnes, of which
approximately 2 000 tonnes were produced in Ontario (NRC 1994, OMNDM 1994).
Ontario ranked fourth in world cobalt production, accounting for 1 1% of the worid total
(OMNDM 1994). Zambia was the world's largest producer in 1993 accounting for 25% of
total production.

Cobalt is used in various alloys including super-alloys, magnetic alloys (for the
manufacturing of jet and gas turbines, and stainless steels), dental and surgical alloys
(CCREM 1987; Shamberger 1979). Cobalt and its salts are also used in cemented
tungsten carbides, glass and ceramic paints, hygrometers, as catalysts tor organic
reactions, in electroplating, fertilizers, and as a foam stabilizer in beer (Shamberger 1979;
Sittig 1985: Windholz et al. 1983). Therapeutically, cobalt or cobalamin (vitamin B12) is
used in the treatment of cyanide poisoning and as a feed additive to correct deficiency
symptoms such as anaemia and retarded growth (Bellies 1979).

Radioactive cobalt-60 is used as an anti-neoplastic gamma ray source. However cobalt-59
has been found to be a possible (experimental) neoplastlgen and tumorlgen (Sax and
Lewis 1989; Sittig 1985; Windholz et al. 1983). Radioactive properties of cobalt will not be
further addressed.

1.2 AQUATIC SOURCES AND FATE

Cobalt residence time in the atmosphere is quite short. It is more likely to be found in
sediments, soils and water. It is estimated that weathering of rock and soils contributes

between 17 and 20% of the natural global emissions for cobalt, whereas biological action
by plants contributes 60% (Merian 1984).

Coal contains on average about 1 mg/kg cobalt, but concentrations can range up to 40
mg/kg. Combustion of coal is a major anthropogenic source of cobalt to the environment
{Merian 1984). Other anthropogenic sources include acid coal mine drainage, smeiter
emissions, raw and treated sewage (0.002-0.04 mg/kg and 0.001 and 0.03 mg/kg,
respectively), and application and losses of cobaltous sulphate-containing fertilizers (Smith
and Carson 1981).

Recent effluent discharge data are available from Ontario's Municipal/Industrial Strategy for
Abatement (f\/llSA) monitoring reports. Ten sectors (iron and steel, organic chemical
manufacturing, pulp and paper, metal mining, metal casting, industrial minerals, inorganic
chemicals, petroleum, waste water treatment plants and hydro-electric generation) were
required to monitor effluent quality for a one year period (OMOE 1988, 1990, 1991a-f,
1992b, 1993), Quantification of the total mass (effluent flow X effluent concentration) of
cobalt discharged to Ontario's surface waters could not be determined reliably because
many of the data were at or below the regulatory method detection limit (20 pg'L). The
data suggest that these industries contribute approximately 36 kg of cobalt per day to
Ontario watersheds. However, intake data suggest that 50-90% of cobalt in the discharge
was merely entrained by the industry. Significant dischargers of cobalt are the Mining
Sector and the Municipal Sewage Treatment plants, each contributing approximately 1/3
of the total discharge. However, recent closures of uranium mines in Ontario have
reduced mining sector discharge of cobalt by about 25% (Hawley, Pers. comm).

1.3 AMBIENT CONCENTRATIONS IN ONTARIO WATERS

Boomer (pers. comm.) reports that the routine OMOEE laboratory detection limit for cobalt
in surface water is currently 0.5 pg/L using pre-concentrated samples and ICP/MS
technology. However, there are problems when using this technique with samples
containing high concentrations of iron. Iron emits photons at a wavelength similar to that

of cobalt, resulting in interference. This may result in a detection limit 2-3 orders of
magnitude higher for samples containing high concentrations of iron. In general, OMOEE
data such as the Provincial Water Quality Monitoring Network (PWQMN) data or the Great
Lakes Surveillance Data report a detection limit of 1 pg/L. The MISA Regulatory Detection
Limit (RMDL) for cobalt was 20 pg/L.

Cobalt concentrations in oxygenated surface waters in Canada range from 1 to 47 pg/L
(NAQUADAT 1985, as cited in CCREM 1987) and are generally below 20 mg/kg in
freshwater sediments (Smith and Carson 1981). Background concentrations of cobalt
were higher in Lake Erie water than in Lake Ontario water, and were the lowest in Lake
Superior waters. Median values of dissolved, particulate, and total cobalt were 0.089,
0.005, and 0.096 pg/L, respectively, for Lake Erie; and 0.021, 0.0037, and 0.025 pg/L,
respectively for Lake Ontario (Rossmann and Barres 1988).

Monitoring data from the Ontario Ministry of Environment and Energy (OMOEE 1994b)
suggest that cobalt concentrations are generally beiow the detection limit of 1 pg/L in the
Great Lakes. For some areas, in particular the St. Clair River, concentrations as high as
10 pg/L have been reported, but it is unknown whether this is due to natural or
anthropogenic sources. While effluent data collected under the MISA program from
organic chemical manufacturing industries along the St. Lawrence River suggest that
cobalt may be being discharged, OMOEE data (OMOEE 1994b) report all values were
below 1 pg/L at seven ambient stations along the river.

Data were also available for Ontario inland waters collected under the Provincial Water
Quality Monitoring Network (OMOEE 1994c). Most areas monitored had cobalt
concentrations below the detection limit (1 pg/L), however there are areas that are
significantly contaminated with cobalt. These areas are generally downstream of mining
sites, particularly abandoned uranium mines. Waterbodies around Bancroft (NE Ontario),
including Farrell Creek, Paudash Lake, Deer Creek and Centre Lake contain cobalt
concentrations of 30 to 50 pg/L. Surface water around Cobalt, Ontario contain similar
concentrations of cobalt. The Trent River, near Peterborough, had concentrations of 30-40

pg/L cobalt, although there are no mines in the area. Tailings ponds and waterbodies
downstream of Bicroft Mine (also in the Bancroft area) contained concentrations ranging
from 25 to 60 |jg/L, while areas around Balmer Creek (NW Ontario near Red Lal<e) had
concentrations as high as 80 ng/L.

The Bicroft mine, and many of the others in the Bancroft area have been abandoned for
more than 20 years (Hawley, pers. comm.). However PWQMN data suggests that
leaching from the tailings is still of concern. It should be noted that the highest
concentrations were found directly in tailings ponds, and waterborne concentrations of
cobalt decreased steadily downstream due to dilution and/or sorption to sediments.

Ambient cobalt concentrations in the suspended solids of the Niagara River and the
sediments of Lake Ontario (Niagara Basin) were 0.021 and 0.017 mg/kg. respectively
(Thomas 1983).

Deloro, in southwestern Ontario (about 60 km NE of Peterborough) is the site of an
abandoned gold mining and refining site, which has a long history of metal contamination
(Azcue and Nriagu 1993). Cobalt, mined in Cobalt. ON or imported from outside the
province, was brought to the site for refining. Tailings contained high concentrations of
cobalt which leach into the Moira River. Although the refinery was closed in the 1960's,
and a tailings treatment plant has been built on-site, elevated concentrations of cobalt are
still detected in the Moira River. Just downstream of the Deloro site, levels of cobalt
ranging from 1 to 20 pg/L were detected. Cobalt concentrations in samples collected
further downstream ranged from 1 to 10 ^ig/L, while at the mouth of the river (near
Belleville) levels were below the detection limit (OMOEE 1994c). Mudroch and
Capobianco (1979) correlated cobalt concentrations in surface sediments to those in
submerged macrophytes of the Moira River drainage basin. For samples collected at the
same site, cobalt concentrations in surface sediments and in the macrophytes
Myriophyllum verticillatum and Elodea canadensis were 864, 262.5 and 10 pg/g dry weight,
respectively (Mudroch and Capobianco 1979).

1.4 AQUATIC CHEMISTRY

Cobalt metal (molecular weight 58.9) has a melting point of 1 493 °C and a boiling point of
3 100 °C, and is stable in air and water at standard temperatures (Sax and Lewis 1989;
Windholz et al. 1983). There are six oxidation states for cobalt -1, 0, +1, +2, +3, and +4.
In general the common valence of cobalt is +2 (cobaltous ion), except in coordination
complexes where the +3 (cobaltic ion) predominates (Shamberger 1979).

In aqueous solution the cobaltous ion (Co II) is stable but the uncomplexed cobaltic ion
(Co III) is a strong oxidizing agent (Trisdan et al. 1981). Based on simulations using the
MINEQL-1 model, cobalt metal should exist mainly as aquo ions (i.e. as an ion containing
water molecules) over a pH range of 4 to 7 (Campbell et al. 1982; Campbell and Stokes
1985).

ASTDR (1991) reports that in most freshwaters, less than 2% of cobalt species are present
in the dissolved state, most cobalt is precipitated or adsorbed on suspended solids or
sediments. However, the data from Rossmann and Barres (1988) Lakes Erie and Ontario
does not indicate the same ratio, with cobalt existing almost entirely in the dissolved state
in Lake Erie and existing in about equal proportions in Lake Ontario. Nriagu and Coker
(1980) determined that only 2-5% of cobalt was associated with humic acids in Lake
Ontario sediments. Illite clay suspensions (1 g/L), adsorbed 95% of cobalt at pH 8 and
40% at pH 4 at concentrations from 50 to 200 pg/L (O'Connor and Kester 1 975 as cited in
CCREM 1987). Adsorption of cobalt to clay minerals was found to increase with increasing
pH (Carson 1981; Murray and Murray 1973). In most waiers, the sediment is the primary
repository site of cobalt. Some mobilization may occur in acidic waters, in the presence of
excess chloride ions or chelating agents. Chelation of cobalt with ligands such as EDTA,
increases its solubility and mobility in the aquatic environment (CCREM 1987).

2.0 TOXICITY TO AQUATIC ORGANISMS

All candidate toxicological information is screened for acceptability. All information that
meets the following requirements is considered primary data:

• Toxicity tests must employ accepted laboratory practices of exposure and
environmental controls. While all tests must be evaluated on a case by case basis,
those tests following published protocols of government agencies or standard
setting associations are generally acceptable.

• Any tests may be acceptable, including static tests if it can be shown \ha\ con-
centrations of the toxicant are not changing (significantly) throughout the test and
adequate environmental conditions for the test species are maintained with respect
to such factors as dissolved oxygen and removal of metabolic wastes. Generally,
continuous flow exposures, and renewal tests (i e. static tests with replacement) are
acceptable if appropriate rates of renewal of toxicant are maintained. Static tests
are acceptable if concentrations of the toxicant are measured in the exposure
vessel at the beginning and end of the test and no more than 10% of the toxicant is
lost during the test. The use of chemical carriers is acceptable as long as the
concentration of the toxicant does not exceed water solubility in the absence of the
carrier. Appropriate chemical carrier controls must also be included.

• Dissolved concentrations of toxicant in the exposure vessels must be constant and
verified by measurements rather than calculated or measured only in stock
solutions. Tests will generally be considered unacceptable if more than 10% of the
toxicant is lost during the test.

• Test end points and lengths of exposure must be appropriate to the life stage of the
species tested and the characteristics of the substance. Although the definitive
bench mark for chronic toxicity is a whole life cycle test, partial life cycle and short
term or early life stage tests are acceptable as chronic data.

• Relevant environmental parameters such as temperature, pH and hardness must
have been recorded.

• Responses and survival of controls must be appropriate tor the species and test
used.

Data on vertebrates and invertebrates not meeting all of the above are denoted as
secondary in objective development documents. Secondary data are inadmissible in the
derivation of an Objective but are admissible in deriving an Interim Objective. Most tests
using aquatic plants w/ill also be classified as secondary due to the frequent use of artificial
media or a lacl< of standardized protocols; however, plant data may be used as the critical
endpoint for Objective development subject to best scientific judgement.

Toxicity data, current to February 1995, are summarized in Table 2. These data were
critically reviewed and classified as primary, secondary or ancillary data based on the
laboratory practices of the researchers. A more detailed explanation of the classification
procedure is outlined in "Ontario's Objective Development Process" {OMOE 1992a).

2.1 ACUTE TOXICITY

2.1.1 Vertebrates

There were two primary studies with vertebrates, both using fathead minnows {Pimephales
promelas). Additionally, there were four secondary studies on two fish species and one
frog species.

Diamond et al. (1992) reported hardness-dependent 48h-NOECs (No Observable Effect
Concentrations) for fathead minnows of 1.2, 7.3, 13.7 and 6.2 mg/L for hardnesses of 50,
200, 400 and 800 mg/l CaCOg, respectively. These tests were done under static
conditions with daily renewals. The authors reported that LC50 values for fathead minnow
tests could not be calculated due to the unexpectedly low sensitivity of this species to high
cobalt concentrations (^ 5 mg/L) over the 48h exposure period. Kimball (undated MS),

8

however, reported a 96h-LC50 of 3.61 mg/L, also using fathead minnows These tests
were done under flow-through conditions with a 5.8h turn-over time. It is unknown why
Kimball (undated MS) was able to derive a result with concentrations less than 5 mg/L,
while Diamond et al. (1992) was not. The longer exposure time may be the main reason,
since Kimball (undated MS) also reported a 192h-LC50 of 2.74 mg/L under the same
conditions, suggesting exposure periods have a significant effect on toxicity. These data
were considered primary as they employed good laboratory practices using measured
toxicant concentrations.

Secondary acute toxicity data were available for giant gouramis (Colisa fasciatus), fathead
minnows, and african clawed frogs (Xenopus laevis). 96h-LC50 values ranged from 22 to
13 500 mg/L (Srivastava and Agrawal 1979; Ewell ef al. 1986; Curtis and Ward 1981;
Sunderman 1992). Frogs exposed to a cobalt concentration of 5.453 mg/L exhibited
decreased growth and an exposure to a concentration of 0.325 mg/L resulted in 50%
embryo abnormalities after 96h, suggesting that sub-lethal effects may result at lower
concentrations than those needed for lethal effects (Sunderman 1992). The original paper
for this study could not be obtained, thus it was ranked as secondary.

Srivastava and Agrawal (1979) reported a 96-h LC50 of 225 mg/L of cobalt chloride for the
freshwater teleost, Colisa fasciatus. Although the LC50 was based on the salt, they did
not state whether it was anhydrous or hexahydrate. The conversions of the LC50,
assuming the salt used to be anhydrous or hexahydrate, results in 96h-LC50 values of

102.1 mg Co^VL or 55.7 mg Co'VL respectively. In addition to the 96-h LC50, Srivastava
and Agrawal (1979) reported that a 90-h exposure of the fish to a sublethal concentration
of 195 mg/L cobalt chloride salt caused a decrease in blood clotting time, an increase in
circulating thrombocytes, and leucopenia.

2.1.2 Invertebrates

There were three primary studies with three species of freshwater invertebrates (two
crayfish species and one daphnid). Secondary data were available for eleven species.

9

Most data were EC50s with exposure times varying from 24 to 96h. Acute toxicity values
ranged from about 1 mg/L to 500 mg/L. Daphnids appear the most sensitive invertebrate
to cobalt, while Tubifex appear to be the most tolerant.

Biesinger and Christensen (1972) reported 48-h EC50 values for Daphnia magna of 1.62
mg/L and 1.11 mg/L, with and without food, respectively. It appears that either the toxicity
of cobaitous chloride hexahydrate was reduced in the presence of added food, or toxicity
was enhanced in unfed organisms due to the stress of starvation. Khangarot et al. (1987)
reported two 24-h EC50s and two 48-h EC50s by applying different statistical methods to
the same raw data for Daphnia magna. The 24-h EC50s were 2.11 mg/L and 2.61 mg/L
with cobaitous chloride hexahydrate as the toxicant. The 48-h EC50s were 1 .52 mg/L and
1.49 mg/L (Khangarot et al. 1987). Baudouin and Scoppa (1974) reported a 48-h EC50
value of 1 .32 mg/L for D. hyalina using hexahydrated cobaitous chloride salt as the
toxicant.

Kimball (undated MS) conducted replicated acute tests with D. magna. Tests used
neonates <24-h old and were static, lasting either 48 h with and without feeding, or 96 h
only if fed This experiment involved measured toxicant conditions and was considered
primary. Feeding decreased the toxicity of cobalt at 48h. The 48h-EC50s of cobalt were
7.37 and 5.99 mg/L for daphnids that were fed and not fed, respectively. It is not clear
however if the effect was due to increased stamina of the Daphnia or interference with the
toxic action.

Diamond et al. (1992) reported 48h-EC50s for D. magna at four water hardness levels.
Reported values were 2.3, 4.6, 4.2 and >5.3 mg/L at hardness values of approximately 55,
255, 475, and 880 mg/L as CaC03, respectively. This experiment was considered primary.
The data suggests that toxicity is inversely proportional to water hardness.

Boutet and Chaisemartin (1973) reported 96h-LC50s of 8.8 mg/L and 10.2 mg/L. for two
species of crayfish, Austropotamobius pallipes paliipes and Orconectes limosus,
respectively. Both of these studies used measured toxicant concentrations and were

10

considered primary. In most cases, invertebrate studies lasting more than 48h are
considered chronic. However, crayfish life cycles tend to be longer in duration and a single
life stage may last for longer than 96h. Thus, these 96h experiments were considered to
be acute.

2.2 CHRONIC TOXICITY

2.2.1 Vertebrates

Three primary chronic studies using four species of vertebrates were found (Birge 1978,
Kimball undated f^S, Diamond et al. 1992). In addition, two studies were classified as
secondary. Toxicity values for cobalt ranged from 0.05 mg/L for a 7d-LC50 for the
narrowmouth toad (Gastrophryne carolinensis) to 15 mg/L resulting in haematological
changes in tilapia {Sarotheradon mossambicus).

BIrge (1978) obtained a 28-d LC50 of 0.47 mg/L for rainbow trout embryos. For goldfish
{Carassius auratus) and the narrow mouthed toad, the 7-d LC50 values were 0.81 mg/L
and 0.05 mg/L, respectively (Birge 1978).

Chronic toxicity of cobalt to fathead minnows was tested by Kimball (undated MS) starting
with eggs <40-h old and lasting until 28 days post hatch. At 1.61 mg/L there was a small
decrease in hatch success, however all fry were reported to have developmental
abnormalities. Only 23% of fathead minnows survived for 28d at 1.61 mg/L. Weight gain
was a more sensitive endpoint however, and fish exposed to 0.81 mg/L gained significantly
less weight than controls. Kimball (undated MS) reported that cobalt ranked fourth of
seven metals tested on fathead minnows for growth inhibition.

Jones (1939a) reported a 10-d NOEC of 10 mg/L for the stickleback Gasterosteus
aculeatus with cobaltous nitrate as the toxicant. The author observed that cobaltous
nitrate and several other salts of metals such as silver, precipitated with the mucus
secreted by the fish. Noticing an increase in the frequency and amplitude of respiratory
movements. Jones (1939a) postulated that this compensatory reaction was not adequate

11

to overcome impairment ot respiratory function due to the physical clogging of the gill
filaments by the precipitates, thus resulting in death by asphyxiation.

Diamond et al. (1992) examined the effects of hardness on survival and growth of fathead
minnows over seven days. While the data suggest that increasing hardness may decrease
chronic cobalt toxicity, the authors felt that there were too few chronic data available to
determine a definite relationship between cobalt toxicity and water hardness.

2.2.2 Invertebrates

Four primary chronic studies with three species of invertebrates were found. An additional
twelve secondary chronic studies were also identified. Toxicity values of cobalt ranged
from a low of 0.00016 mg/L causing terata in snail embryos to 139,32 mg/L for a 96h-LC50
for tubificids. Chronic studies investigate many types of toxic effects, both lethal and
sublethal, over a wide range of exposure times and it is not surprising that there is such a
large range of toxicity values.

Diamond et al. (1992) examined the effects of hardness on D. magna using 7-d sun/ival
and reproduction expehments. The auttiors reported that a number of experimental
problems caused difficulty in analyzing the results, and they reported that NOECs could
only be calculated for one hardness level (400 mg/L as CaC03) which was reported as <50
|jg/L. The authors do report, however, that their experiments suggest a hardness
dependant relationship for cobalt toxicity.

Boutet and Chaisemartin (1973) determined the 30-d LC50 for two species of crayfish, with
and without food. For A. pallipes pallipes the 30-d LC50 was 0.77 mg/L with food, and
0.79 mg/L without food. Similarly, the 30-d LC50 for O. limosus was 0.79 mg/L with food,
and 0.88 mg/L without. Thus, the addition of food had little effect on the toxicity of cobalt
as cobaltous chloride hexahydrate.

12

Biesinger and Christensen (1972) exposed D. magna to cobalt chloride hexahydrate for 3
weeks and reported the LC50 and sublethal effects. The 21 -d LC50 was 0.021 mg/L,
while a concentration of 0.024 mg/L caused a 15% reduction in weight as well as 12% and
45% increases in protein and glutannic oxalacetic transanninase (GOT), respectively.
These physiological responses occurred at Co^' levels greater than the LC50.
Reproduction was impaired by 16% and 50% at cobalt concentrations of 0.010 mg/L and
0.012 mg/L, respectively (Biesinger and Christensen 1972). Kaiser (1980) was able to
accurately predict the 16% reproductive impairment concentration given by Biesinger and
Christensen (1972), using an equation that incorporated ion-specific physical-chemical
properties {e.g., ionization potential and oxidation state).

Chronic toxicity of cobalt to D. magna was tested by Kimball (undated MS). Tests were
static with replacement and measured survival and several indices of reproductive success.
The 28-d LC50 was 0.027 mg/L Co, almost identical to that of Biesinger and Christensen
(1972). Kimball (undated f\/IS) reported that tests using Daphnia reproduction as the
endpoint were much more sensitive than those using lethality. The lowest concentration of
cobalt which significantly decreased reproduction (as mean young per female) was 0.009
mg/L. Kimball (undated MS) also compared the sensitivity of Daphnia and fathead
minnows to nine metals (V, Be, Tl, Co, Sb, Mn, Al, Mo and Be). For most metals, the
toxicity was similar for both organisms although the order of sensitivity changed somewhat.
In the case of cobalt however, Daphnia were nearly 60 times more sensitive than fathead
minnow. Compared to the toxicity of other metals, cobalt ranked fifth of the nine metals
tested on daphnids.

Sodergren (1976) reported a 96-h LC50 of 33 mg/L for the nymph of damselflies
{Ephemerella mucronata) exposed to cobalt nitrate. Cobalt toxicity was tested on E. ignita
nymphs in the presence of a food source Fontinalis dalecarlica. A four week exposure to
0.0326 mg/L of cobalt nitrate resulted in reduced growth (Sodergren 1976). A possible
explanation for the higher toxicity to E. ignita. presented by Sodergren (1976), is that the
nymphs received a greater dose of cobalt by consuming F. dalecarlica, which accumulates

13

cobalt. However, the observed toxicity may simply be a function of the longer exposure
period. These data were considered secondary.

A solution of cobaltous chloride at 10 mg/L of Co^*. was found to completely inhibit nuclear
expansion in the chloragocytes of Tubifex tubifex under hypoxic conditions (Fischer et al.
1980). Under aerobic conditions cobalt had neither a stimulatory nor an inhibitory effect on
nuclear expansion. The authors surmise that since cobalt is an effective inhibitor of haem
synthesis and possibly an inhibitor of globin synthesis, the depression of nuclear expansion
may be the result of cobalt's inhibitory effect on haemoprotein synthesis.

The probit-derived 96-h EC50 estimate for the rotifer, Phllodina acuticornis, exposed to
cobalt chloride was 27.8 mg/L with an endpoint criterion of no visible internal or external
motion (Buikema et al. 1974). Hardness of the water had little effect on cobalt toxicity in
this study.

Solski and Piontek (1987, in AQUIRE) reports planaria exposed to 0.002 to 0.028 mg/L
cobalt for 10 days showed a change in the ability to regenerate. This paper could not be
obtained and critically reviewed, and thus could not be used for criteria development.

Based on 96h-EC50 studies with T. tubifex, Khangarot (1991) found that cobalt ranked
24th of 32 elements tested. Cobalt was found to be twice as toxic to Tubifex than
magnesium, calcium and sodium, but at concentrations significantly less toxic than metals
such as lead, mercury or cadmium.

2.2.3 Other Organisms (Algae. Protists etc.l

According to the Objective Development Process (Of^OE 1992a), tests employing algae
are always classified as secondary data due to inherent difficulties in performing algal
expenments.

14

Toxicity studies were available for seven species of algae and two protists. Toxicity values
ranged from 0.1 mg/L to 50 mg/L for algae, while 3h-HTC (highest concentration where
protists were still observed alive after three hours) ranged from 1 000 to 2 500 mg/L.

Cobalt toxicity to algae was in the same order of magnitude as that of copper and nickel
(den Dooren de Jong 1965). For Chlorella vulgaris, the growth inhibition NOEC and LOEC
(lowest observed effect concentration) values were 0.226 mg/L and 0.442 mg/L Co'* as
cobalt chloride hexahydrate, respectively (den Dooren de Jong 1965). Hutchinson (1973)
reported 99% growth inhibition of this same species at 1.0 mg/L. For the more tolerant
species Haematococcus capensis, growth was inhibited by 80% at 5.0 mg/L (Hutchinson
1973). A more sensitive species was Chlamydomonas eugametos. which had 100%
growth inhibition at 0.5 mg/L (Hutchinson 1973). Other toxicity tests with algae showed
that concentrations of cobalt chloride between 2 and 9 mg/L Co^' were toxic to Anabaena
variabilis, whereas, concentrations between 20 and 50 mg/L were toxic to C. vulgaris
(Ahluwalia and Kaur 1988). Stokes (1981) reported EC50 values of 0.25 mg/L for
Scenedesmus acutiformis f. alternans and 0.1 mg/L for S. acuminatus. Sharma et al.
(1987) found Spirulina plater)Sls to be less sensitive to cobalt than other algae, with a 96-h
EC50 of 23.8 mg/L. The endpoint cnterion in this study was dry weight biomass as a
function of optical density at 490 nm and sublethal concentrations (0.1 and 0.5 mg/L)
resulted in an increase in biomass, which was ascribed to a hermetic effect.

2.3 SUMMARY OF TOXICITY DATA

Insufficient data prohibits comparison of the relative toxicities of the various forms of cobalt
to aquatic biota.

In general, acutely toxic concentrations from primary references indicated effects in the 1
to 10 mg/L range, except when organisms are exposed in very hard water, while
secondary values were as high as 450 mg/L. Toxicity values fall within the same range for
both vertebrates and invertebrates, however there are too few acute vertebrate studies for
accurate comparison. Chronic toxic concentrations of cobalt from primary references

15

suggest that effects are likely to occur in the range of 0.009 to 2 mg/L, while secondary
studies ranged from 0.0016 to 2 500 mg/L. In general, chronic data tend to vary more
widely than acute data due to the wide range of exposure times and types of endpoints
examined. Primary data suggest that invertebrates may be more sensitive to cobalt than
vertebrates under chronic exposures. Kimball (undated MS) reported that Daphnia are
more sensitive to cobalt than fathead minnows when exposed for 96h, however the extent
of the difference is not very large. Data compahng growth of fathead embryos and
Daphnia survival and reproduction suggested that Daphnia were approximately 60 times
more sensitive to cobalt than are fathead minnows (Kimball undated MS).

Khangarot and Ray (1989) summarized how cobalt toxicity compared to the toxicity of
other metals tested on various aquatic species (Table 1). Cobalt tends to be slightly to
moderately toxic, however some species appear to be especially sensitive. Kimball
(undated MS) found that Daphnia magna were more sensitive to cobalt than many other
minor inorganics {e.g.. beryllium, selenium, thallium etc.). However, this study did not
expose organisms to metals such as mercury, cadmium or lead, that other experiments
have shown to be much more toxic. For example, Khangarot and Ray (1989) found that
cobalt was approximately 1000 times less toxic than mercury. Birge (1978) ranked cobalt
in an arbitrarily determined, Toxicity Group 1 , based on toxicity studies with toads, goldfish
and rainbow trout. This category included more toxic metals such as silver, mercury, and
cadmium.

16

Tabic I: Toxicily ranking cil aibalt coinparcd lo oihcr metals (modified from Khangarnt ami Ray 1989)

.Species Tested

Eiidpoint

Cobalt

Ranking

# of Metals
Tested

Reference

Clitorclla viili;ans

l:C50

8

y

Sakaguchi ei at. (1977)

Paramecium

I.C50

7

9

Shaw (19.'i4)

Folyccin nigra

LC50

7

16

Jones (1939b)

Daphniu maiina

48liT,(:S0

5

23

Khangaroi k Ray (1989)

Dapknia magna

481vLC50

5

9

Kimball (undated MS)

Duphiiia magna

2Sd LC5()

1

9

Kimball (undateii MS)

Daplmia magna

28d-repi()diicIi(Tn

1

9

Kimball (undated MS)

Daphnia magna

6)liT-C50

8

19

Anderson (1948)

Daphnia magna

48h-EC.50

fi

15

Biesinger and Christensen
(1972)

Daphnia hyalina

48hT;C?()

-J
/

12

Badouin and Scoppa (1974)

Cyclops ahyssfriim
prealpins

4Sh [■rso

K

12

[ladoijiii and Scop[)a (1974)

Tiihijex luhiJL'x

WhT-X'.'SO

24

32

Khangaroi (1991)

Cypris siibgUihnsa

48h-IZC5()

II

28

Khangarot and Ray
(unpublished 1

Li'hisU's reliciilalti^

LDSO

s

9

Shaw and Grushkin (1957)

Gasierosteiis aculcatu},

1 C'SO

1 1

18

Jones (1939a)

runephak'.i promclas

i'J2iiTx:'.'s()

4

8

Kimball (undated MS)

Pimephaies pramelas

2Kd-survival

4

7

Kimball (undated MS)

Guitruphrynt' curolinensis

7d-LC5()

II

■)->

Birgc (1978)

Rana hcxaJaccyia

')()hT_C?()

7

9

Khangaroi et at. ( 1982)

Bufa vallireps

LD50

7

9

Shaw and Gnishkin (1957)

2.4 EFFECTS OF WATER QUAUTY PARAMETERS ON TOXICITY

Diamond et al. (1992) reported that water hardness had a significant effect on the
toxicity of cobalt. Their studies showed that in the hardness range of 50 to 200 mg/L
as CaC03, acute cobalt toxicity to both fish and invertebrates may be inversely

17

related to hardness. Toxicity of cobalt to fathead minnows appeared to increase at the
highest hardness tested, however the authors state that toxicity may have been a
result of the extreme hardness rather than cobalt toxicity. Diamond et al. (1992)
suggested that it is possible that Ca^' and Mg^' compete with cobalt for potential target
sites of toxic actions. Cobalt has a higher density and higher ionization potential than
these ions and thus cobalt adsorption on cell membranes may not be a stable
phenomenon given an abundance of more reactive cations available. This paper only
reported NOECs for fathead minnow, instead of effect concentrations. As such, it is
difficult to assess the true effects of hardness due to the possibility that toxic effects
may not occur In proportion to the respective NOECs. Buikema et al. (1984) was the
only other study that Investigated hardness effects on cobalt toxicity. They reported
that hardness had little effect on cobalt toxicity to rotifers over 96 hours.

3.Q BIQACCUMULATION

Cobalt may bioaccumulate in freshwater plants and invertebrates but does not
accumulate in fish tissues. Although freshwater algae can have cobalt concentrations
of 400 to 2x10*^ times the ambient levels, it is uncertain to whether this is due to actual
biological uptake or to physical adsorption (Cole and Carson 1981). Bioconcentration
factors range from 100-14 000 for freshwater molluscs; up to 10^ for Insect larvae; and
from 1-11 000 for other Invertebrates (Cole and Carson 1981). Various species of fish
sampled had cobalt concentrations ranging from 0.23 pg/g (fresh weight) to 4.7 pg/g In
Lake Erie; 0.16 pg/g to 1.1 pg/g in Lake Ontario; and 0.04 pg/g to 0.33 pg/g in the St.
Lawrence (Tong et al. 1972). The cobalt concentrations in lake trout {Salvelinus
namaycush) which averaged 0.0599 pg/g (fresh weight), were found not to vary
significantly with fish up to 12 years (Tong et al. 1974), suggesting that it does not
biomagnify. ASTDR (1991) reports that benthic bottom feeding fish do not appear to
significantly bioaccumulate cobalt from contaminated sediment.

Baudin and Fritsch (1989) examined the related contribution of food and water in the
accumulation of cobalt in fish. Carp fed Co^-contaminated snails were found to
accumulate Co only slightly. The authors report a trophic transfer rate (transfer of
contaminant residues from lower to higher trophic levels) of about 10^. Furthermore,
the fish were found to depurate cobalt, resulting in a retention factor of only 3x10'^
after 63 days. Fish exposed to waterborne cobalt had uptakes significantly higher
than those exposed through food, while fish exposed through both water and food had
the highest uptake. The authors concluded that water is the primary route of cobalt
uptake in carp and that accumulation from both food and water was additive.

4.0 IMPACT ON TASTE AND ODOUR OF WATER AND FISH TAINTING

in water cobaltous bromide has a slight odour and cobaltous chloride has a slight
sharp odour: cobaltous nitrate and sulfate are odourless (Weiss 1986).
Concentrations at which these odours were detectable were not given Organoleptic
data were not available for tainting of fish flesh.

5.0 MUTAGENICITY

A review of summary documents was undertaken to examine the likelihood of cobalt
causing mutagenic effects (ASTDR 1991, Smith and Carson 1981, IRIS 1994). A
recent special issue of the journal, "The Science of the Total Environment" (Volume
150, 1994) contained a number of papers on the toxicity, mutagenicity and
environmental fate of cobalt.

ASTDR (1991) reported that no studies were found describing genotoxic effects on
humans or animals through inhalation, oral or dennal exposure to cobalt. It was
reported that cobalt (II) was found to be generally non-mutagenic in bacteria and
yeast, while cobalt (III) garnered positive mutagenic responses in Salmonella
typhimurium and Escherichia coli. Further information suggested that cobalt was

19

genotoxic in in vitro experiments, causing genetic conversions in S. cerevisae.
clastogenic effects on mammalian cells, transformations in hamster cells and sister
chromatid exchanges in human lymphocytes. Sharma and Talukder (1987) report that
cobalt exerts very strong mutagenic effects on plant activity. When compared to other
inorganics, cobalt was found to be less toxic than arsenic and selenium, yet more
toxic than lead, zinc or cadmium based on clastogenic tests with onion root tips
{Allium sp). Effects reported include chromosome breaks, diplochromatids, erosion,
fragmentation and bridges. Cobalt salts reduced the rate of cell division, inhibited
passage of interphase into prophase and produced clumping and stickiness of
chromosomes in Vicia sp.

Nordberg (1994) reported that there was sufficient evidence of carcinogenicity for
cobalt (II) oxide, limited evidence of carcinogenicity for cobalt (II) sulphide and cobalt
(II) chloride, and inadequate evidence of carcinogenicity for cobalt aluminum spinel,
cobalt (II. Ill) oxide, cobalt naphtenate and cobalt (III) acetate in animals.

ASTDR (1991) reported that cobalt has not been shown to cause cancer in humans
by any exposure route. However, lARC (International Agency for Research on
Cancer) recently classified cobalt and cobalt compounds as possible human
carcinogens (Group B). This classification was based on limited evidence in humans,
and data from studies that concluded that soluble cobalt (II) compounds are genotoxic
to various organisms (Binderup and Wassermann 1994).

There is evidence that suggests that cobalt is teratogenic in mammalian systems
(ASTDR 1991). There is some indication that cobalt may cause terata in aquatic
invertebrates. Jaroensastraraks and McLaughlin (1974 as cited in Herndon et al.)
reported that eggs of the freshwater snail, Helisoma, treated with 1 mg/L of cobalt had
deformities of the shell and gut. Another study (Morrill 1963, in Herndon et al. 1981)
reported that concentrations as low as 0.16 pg/L caused abnormalities in the shell and
feet of gastropods. This study, could not be critically reviewed for this document, and

20

was not used in objective derivation. Data by Sundemnan (1992) suggested that low
concentrations of cobalt (30 mg/L) may cause abnormalities in Xenopus, however this
paper could not be obtained.

In summary, available information suggests that cobalt may exert genotoxic effects,
with cobalt (111) likely exhibiting the most significant mutagenic effects. Recent
evidence suggests that cobalt may cause cancer, and may result in terata in some
organisms, including aquatic invertebrates.

6.0 DERIVATION OF THE PROVINCIAL WATER QUAUTY OBJECTIVE

6.1 TOXICOLOGICAL DATA

For a PWQO to be developed, certain information requirements must be met (OMOE
1992a). These are summarized in Table 3. All requirements for developing a PWQO
could be met with the existing data, except for a mutagenicity assessment. While
cobalt has been shown to be mutagenic in lab animals, no primary data was available
for aquatic organisms. Until sufficient mutagenicity information becomes available, a
PWQO based solely on aquatic toxicity will be developed. It should be noted that this
value may not protect against mutagenic effects.

While there is evidence suggesting that cobalt toxicity is affected by water hardness,
there is insufficient toxicity data to allow development of a hardness-based PWQO.
Thus, the most conservative approach will be taken and the PWQO will be set as a
single value.

The lowest effect concentration of cobalt was 0.009 mg/L; based on a 28d LOEC
(reproduction) for D. magna (Kimball undated MS). The initial safety factor of 10
(OMOE 1992a) was applied to this value to derive a preliminary PWQO of 0.0009
mg/L (0.9 pg/L) for the protection of aquatic life.

21

6.2 BIOACCUMULATION

Cobalt does not appear to bioaccumulate in fish. Thus, for the purposes of criterion
development, bioaccumulation of cobalt was not considered significant. Therefore
bioaccumulation will not affect the preliminary PWQO calculated from toxicity data.

6.3 MUTAGENICITY

There were few studies available which examined mutagenic effects on aquatic
organisms. However, these data were from secondary literature sources and could
not be properly reviewed. Data for mammalian systems indicates that cobalt may
exert genotoxic effects, with cobalt (III) likely exhibiting the most significant mutagenic
effects. Recent evidence suggests that cobalt may cause cancer, and may result in
terata in some organisms. Therefore, the PWQO based on aquatic toxicity may not
protect against these effects.

6.4 TASTE AND ODOUR

There was no information in the literature that indicates that cobalt would affect the
taste and odour of water. In fact there is evidence to the contrary, it is tasteless and
odourless.

6.5 OTHER EFFECTS

There is no evidence to suggest that the PWQO should be lowered to protect
piscivorous wildlife.

22

6.6 DERMAL EFFECTS

The scant data available regarding dermal absorption of cobalt suggest that there
should be no detrimental effects on humans exposed to environmental concentrations
of cobalt while engaging in water based recreational activities (e.g. swimming).

ASTDR (1991) reported that no studies were found regarding lethal or significant non-
lethal effects on humans after dermal exposure to cobalt, nor were any studies
investigating rates of dermal absorption in humans found. Christie et al. (1976 in
Herndon et al. 1981) found that cobalt poorly penetrated normal skin but may
penetrate damaged skin more quickly. Herndon et al. (1981) reported that intermittent
dermal exposure to a 0.5 to 2.5% Co(N03)2 solution over periods ranging from 1 week
to 35 years resulted in dermatitis and eczema. There have been reports of some
people with severe dermal hypersensitivity to cobalt. Concentrations as low as 0.27%
cobalt chloride in distilled water have elicited an effect.

6.7 OMOEE LABORATORY DETECTION LIMITS

Boomer (pers. comm.) reported that the routine OMOEE laboratory detection limit for
cobalt in surface water is currently about 0.5 pg/L using pre-concentrated samples and
ICP/MS technology. This value is lower than the proposed PWQO of 0.9 pg/L.
However, there are problems when using this technique with samples containing high
concentrations of iron, which may result in laboratory detection limits 2 to 3 orders of
magnitude higher. Hence, in some instances, the PWQO may be below the detection
limit.

6.8 CONCLUSION

In summary, the recommended PWQO for total cobalt is 0.0009 mg/L based on
aquatic toxicity

23

7.0 RESEARCH NEEDS

Primary chronic and acute toxicity tests with vertebrates, especially coldwater North
American species are required to provide a more comprehensive data base. Although
there is fairly good breadth in the variety of species tested, there is very little depth in
terms of several tests on important species. In general, experimental procedure in the
future should include:

1 . reporting the effect concentration in terms of mg metal ion/L instead of
leaving it ambiguous and incomparable with other data. This is
especially important for cobalt which has significant differences in
molecular weight for hydrated and anhydrous salts, making conversions
from mg/L salt to mg/L metal ion impossible if the specific form of salt
used is not indicated.

2. studies on the toxic species and effects of water quality variables such
as pH and hardness.

3. since there is evidence suggesting cobalt may have mutagenic
properties, further investigations of these properties on aquatic organisms
are needed.

4. since the data from Kimball (undated) was never published, similar
experiments should be performed to assess the validity of the data.

5. The paper by Solski and Piontek (1987) reporting toxicity to Dugesia at
very low concentrations of cobalt should be obtained and assessed.

6. The two papers examining the mutagenicity of cobalt (Morrill 1963.
Sunderman 1992) should be obtained and assessed.

24

8.0 OBJECTIVES OF OTHER AGENCIES

There is no national Canadian cobalt guideline for the protection of freshwater aquatic
life (CCREM 1987). There are however guidelines for livestock watering and irrigation
water of 1.0 mg/L and 0.05 nng/L, respectively, for total cobalt (CCREf^ 1987). The
U.S. EPA (1987) has a permissible ambient goal of 0.7 mg/L based on human health
effects (Sittig 1985). A limit of 1.0 mg/L for cobalt in drinking water has been set in
the U.S.S.R. (Sittig 1985). The New York State ambient water quality standard for
cobalt of 5 |jg/L in surface water is based on chronic reproductive toxicity to aquatic
life (NYSDEC 1986).

25

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<

Table 3 : Data Requirements for
Provincial Water Quality Objectives

1. Toxicity

All data must be primary or chronic: marine or brackish
species are not permitted.

FISH

At Least:

One coldwater species - Rainbow trout (Birge 1978)

One warmwater species - Fathead minnow (Diamond et al
1992)

One other warmwater or coldwater species - Toad (Birge
1978)

With at least :

X

One species resident in Ontario (may be one of above)
Rainbow trout (Birge 19 78)

X

One early lifestage endpoint - 9d-ELS for fathead minnows
(Diamond et al . 1992)

X

one other whole oi"ganisms chronic endpoint - 28d-LC50 for
rainbow trout (Birge 1978)

INVERTEBRATES

At Least :

one crustacean - Daphnia magna (Diamond et al . 1992)

One other order - Crayfish (Boutet & Chaisemartin 1973)

With at Least:

X

no more than one tropical species

X

one early lifestage endpoint - 7d-L0EC (reproduction of
Daphnia as # of young per female) (Diamond et al . 1992)

X

one other chronic endpoint - 30d-LC50 with crayfish
(Boutet & Chaisemartin 1973)

40

ALGAE /AQUATIC PLANT

one algae or aquatic plant resident in temperate North
America using scientific procedures and test conditions
compatible with recognized algal bioassays - Green algae
{Coleman et aJ . 1971)

Bioaccumulation

One of :

Fish consumption limit {e.g. Health and Welfare Guideline)

an acceptable daily intake limit

contaminant residue in aquatic biota value

md :

A bioconcentration factor a 1000 (In the absence of
consumption limits, bioaccumulation may be significant and
the Guideline setting process should be followed)

or:

X

A bioconcentration factor s 1000 (In the absence of

consumption information, bioaccumulation is not considered

to be significant) .

If BCF data is unavailable:

Log Kow 2 4.00, then bioaccumulation is assumed to be
significant and the Guideline setting process should be
followed .

or :

Log Kow s 4.00, then bioaccumulation is assumed not to be
significant .

41

Mutagenicity

A) For Initial Assessment

Chemical is considered to be non-mutagenic (i.e. data from

a minimum of two test systems, including tests for

mutagenic as well as chromosomal damage endpoints, clearly

demonstrating .

or:

Chemical is considered to be mutagenic in aquatic or
mammalian systems. - Possibly, data is inconclusive

B) For Setting PWQOs (A total of three studies are required
for mutagenicity.

VERTEBRATES

(All data must be primary and measured in whole aquatic
organisms, Marine and brackish tests are not permitted)

Data

from at least one of the following three categories:

fish

- mutagenicity related diseases

fish

- mutagenicity or chromosomal aberrations

o t he r

vertebrate mutagenicity of chromosomal aberration

INVERTEBRATES

Data from a maximum of two of the following three categories:

invertebrate - mutagenicity or chromosomal aberration

aq^jatic plant - mutagenicity or chromosomal aberration

microbial - mutagenicity

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