Biological Report 85(1.10) Contaminant Hazard Reviews

April 1987 Report No. 10 

MERCURY HAZARDS TO FISH, WILDLIFE, AND INVERTEBRATES: 

A SYNOPTIC REVIEW 

by 

Ronald Eisler 

U. S. Fish and Wildlife Service 

Patuxent Wildlife Research Center 

Laurel, MD 20708 
SUMMARY 

Available literature on the ecological and toxicological aspects of mercury (Hg) in the environment, with 

special reference to fish and wildlife resources, is reviewed and summarized. Subdivisions include sources, 

chemical properties, background concentrations, acute and chronic toxicity, sublethal effects, and proposed

criteria to protect sensitive resources. 

Mercury has been used by man for at least 2,300 years, most recently as a fungicide in agriculture, in the 

manufacture of chlorine and sodium hydroxide, as a slime control agent in the pulp and paper industry, in the 

production of plastics and electrical apparatus, and in mining and smelting operations. Mercury burdens in 

some environmental compartments are estimated to have increased up to 5X precultural levels, primarily as a 

result of man's activities. The construction of artificial reservoirs, for example, which releases Hg from flooded 

soils, has contributed to the observed elevation of Hg concentrations in fish tissues from these localities. 

Elevated levels of Hg in living organisms in Hg-contaminated areas may persist for as long as 100 years after 

the source of pollution has been discontinued. One major consequence of increased mercury use, coupled with 

careless waste disposal practices, has been a sharp increase in the number of epidemics of fatal mercury 

poisonings in humans, wildlife, and aquatic organisms. 

Most authorities agree on six points: (1) mercury and its compounds have no known biological function, and 

the presence of the metal in the cells of living organisms is undesirable and potentially hazardous; (2) forms of 

mercury with relatively low toxicity can be transformed into forms of very high toxicity, such as methylmercury, 

through biological and other processes; (3) mercury can be bioconcentrated in organisms and biomagnified

through food chains; (4) mercury is a mutagen, teratogen, and carcinogen, and causes embryocidal, 

cytochemical, and histopathological effects; (5) some species of fish and wildlife contain high concentrations of 

Hg that are not attributable to human activities; (6) anthropogenic use of Hg should be curtailed, as the 

difference between tolerable natural background levels of Hg and harmful effects in the environment is 

exceptionally small. 

Concentrations of total Hg lethal to sensitive, representative, nonhuman species range from 0.1 to 2.0 ug/l 

(ppb) of medium for aquatic organisms; from 2,200 to 31,000 ug/kg body weight (acute oral) and 4,000 to 

40,000 ug/kg (dietary) for birds; and from 100 to 500 ug/kg body weight (daily dose) and 1,000 to 5,000 ug/kg 

diet for mammals. Organomercury compounds, especially methylmercury, are always more toxic than inorganic 

Hg compounds. Numerous biological and abiotic factors modify the toxicity of Hg compounds--sometimes by an 

order of magnitude or more--but the mechanisms of action are not clear. Significant adverse sublethal effects 

were observed among selected aquatic species at water concentrations of 0.03 to 0.1 ug Hg/l. For some birds, 

adverse effects--predominantly on reproduction--have been associated with total Hg concentrations (in ug/kg 

fresh weight) of 5,000 in feather, 900 in egg, and 50 to 100 in diet; and with daily intakes of 640 ug/kg body 

weight. Sensitive nonhuman mammals showed significant adverse effects of Hg when daily intakes were 250 

ug/kg body weight, when dietary levels were 1,100 ug/kg, or when tissue concentrations exceeded 1,100 ug/kg. 

The most recent mercury criteria proposed by the U.S. Environmental Protection Agency for protection of 

freshwater aquatic life are 0.012 ug/l medium (4-day average), not to exceed 2.4 ug/l on an hourly average; 

however, these criteria offer only limited protection to freshwater ecosystems. The saltwater criteria of 0.025 ug 

Hg/l medium (4-day average), not to exceed 2.1 ug/l hourly, are unsatisfactory for the protection of marine life. 

For the protection of sensitive species of mammals and birds that regularly consume fish and other aquatic 

organisms, total Hg concentrations in these prey items should probably not exceed 100 ug/kg fresh weight for 

birds, and 1,100 ug/kg for small mammals. The significance of elevated Hg levels in tissues of fish and wildlife 

is not fully understood; some species of marine pinnipeds, for example, normally contain high concentrations of 

Hg in various tissues without apparent adverse effects. Usually, however, concentrations in excess of 1,100 

ug/kg fresh weight of tissue (liver, kidney, blood, brain, hair) should be considered as presumptive evidence of 

an environmental mercury problem. 

2
Four courses of action now seem warranted. First, toxic mercurials in agriculture and industry should be 

replaced by less toxic substitutes. Second, controls should be applied at the point of origin to prevent the 

discharge of potentially harmful Hg wastes. Third, continued periodic monitoring of Hg in fish and wildlife is

needed for identification of potential problem areas., and for evaluation of ongoing mercury curtailment 

programs. And fourth, additional research is merited on mechanisms of mercury accumulation and detoxication 

in comparatively pristine ecosystems. 

DISCLAIMER 

Mention of trade names or commercial products does not constitute U.S. Government endorsement or 

recommendation for use. 

This report should be cited as follows: 

Eisler, R. 1987. Mercury hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish and 

Wildlife Service Biological Report 85(1.10). 

3
SUMMARY 

DISCLAIMER 

ACKNOWLEDGMENTS 

INTRODUCTION 

SOURCES OF ENVIRONMENTAL MERCURY 

CHEMICAL PROPERTIES 

MERCURY IN MINAMATA, JAPAN 

BACKGROUND CONCENTRATIONS 

 GENERAL 

 NONBIOLOGICAL 

 BIOLOGICAL

ACUTE AND CHRONIC TOXICITY 

 GENERAL 

 AQUATIC ORGANISMS 

 BIRDS 

 MAMMALS 

 OTHER GROUPS 

SUBLETHAL EFFECTS 

 GENERAL 

 AQUATIC ORGANISMS

 BIRDS 

 MAMMALS 

 OTHER GROUPS 

CURRENT RECOMMENDATIONS 

LITERATURE CITED 

TABLES 

Number 

1 Industrial and other uses of mercury in the United States in 1959 and in 1969. All values are in

metric tons (modified from Montague and Montague 1971) 

2 Amount of mercury in some global reservoirs (NAS 1978), and residence times (Clarkson et al. 

1984) 

3 Some properties of mercury and its compounds 

4 Mercury concentrations in selected biological and nonbiological materials collected from Minamata 

Bay, Japan, and environs. Concentrations are in mg Hg/kg (ppm) fresh weight (FW), or dry weight 

(DW) 

5 Mercury concentrations in water and sediments 

6 Mercury concentrations in field collections of selected species of flora and fauna. Values shown are 

in mg Hg/kg fresh weight (FW), or dry weight (DW) 

7 Toxicities of inorganic and organic mercury compounds to selected species of aquatic organisms 

8 Toxicity to birds of mercury administered by oral, dietary, or other routes 

9 Toxicity of organomercury compounds to selected mammalian species 

10 Sublethal effects of organomercury compounds administered to selected species of mammals

11 Proposed mercury criteria for protection of various resources and human health 

FIGURES 

Number 

1 Major transformations of mercury in the environment (modified from Beijer and Jernelov 1979) 

2 Mercury concentrations in livers of four species of pinniped mammals (from Eisler 1984) 

ACKNOWLEDGMENTS 

I thank J. Higgis and I. Moore for secretarial help; L.J. Garrett and J.E. Haber for literature retrieval; W.N. 

Beyer, T.A. Haines, M.C. Perry, J.G. Wiener, and M.R. Winfrey for reviewing the manuscript; and P.H. 

Eschmeyer and J.R. Zuboy for editorial services. 

4
INTRODUCTION 

The element mercury (Hg) and its compounds have no known normal metabolic function. Their presence in 

the cells of living organisms represents contamination from natural and anthropogenic sources; all such 

contamination must be regarded as undesirable and potentially hazardous (NAS 1978). 

The most important ore of mercury, cinnabar (mercuric sulfide), has been mined continuously since 415 BC 

(Clarkson and Marsh 1982). In the period before the industrial revolution, Hg was used extensively in gold 

extraction and in the manufacture of felt hats and mirrors; in the 1800's, it was used in the chloralkali industry, in 

the manufacture of electrical instruments, and as a medical antiseptic; and since 1900, it has been used in 

pharmaceuticals, in agricultural fungicides, in the pulp and paper industry as a slimicide, and in the production of 

plastics (Clarkson and Marsh 1982). Current world use of mercury is estimated at 10,000 to 15,000 metric tons 

annually (Boudou and Ribeyre 1983), of which the United States accounts for about 18% (Clarkson and Marsh 

1982). 

The first cases of fatal mercury poisoning were reported for two men in a European chemical laboratory in 

1865 (Das et al. 1982). The first documented human poisoning from an agricultural exposure to methylmercury 

occurred in 1940 (Das et al. 1982). As summarized by Elhassani (1983), exposure of humans to mercury 

compounds may result from dermal application (e.g., 1,600 infants in Argentina showed symptoms of Hg 

poisoning after a laundry treated their diapers with a Hg disinfectant), from diet (i.e., ingestion of Hgcontaminated fish, pork, seafoods, or grains), and from contact by respiratory routes (e.g., occupational 

exposure of mercury fungicide applicators in Nicaragua). Sporadic incidences of human poisonings have

occurred in the United States, the Soviet Union, and Canada; and major epidemics have been reported in 

Japan, Pakistan, Guatemala, Ghana, Yugoslavia, and Iraq (Clarkson and Marsh 1982; Das et al. 1982; 

Elhassani 1983; Greener and Kochen 1983). In 1972, for example, there were 6,530 hospital admissions within 

18 months (459 hospital deaths) among Iraqi farmers who ate bread made from seed wheat treated with a 

methylmercury fungicide. A water soluble red dye was washed off the wheat, with the assumption that the 

mercury would be equally soluble. Before the wheat was consumed by humans, it was fed (without apparent 

effect) to chickens and other :livestock for only a few days; it was not realized that a lengthy latency period was 

involved (Das et al. 1982; Elhassani 1983). There is no effective antidote to counteract the effects of 

methylmercury on the central nervous system (Elhassani 1983). 

Poisoning of game birds and other wildlife in Sweden, apparently by seeds treated with organomercurials, 

was noticed in 1960 (Das et al 1982). Massive kills of the grey heron (Ardea cinerea) in the Netherlands during 

1976, were attributed to a combination of low temperatures, undernourishment, and high body burdens of 

mercury (Van der Molen et al. 1982). Mercury contamination has resulted in the closure of pheasant and 

partridge hunting areas in Alberta, Canada (Mullins et al. 1977). In 1967, the Swedish medical board banned

the sale of fish that contained high concentrations of organomercury salts, originating from about 40 lakes and 

rivers (Das et al. 1982). In 1970, after the discovery of high levels of mercury in fish from Lake St. Clair, 

Canada, restrictions on fishing and the sale of fish were imposed in many areas of the United States and 

Canada (Das et al. 1982). Since 1970, a total of 26 of the 48 States in the conterminous United States have

reported mercury pollution in their waters as a direct result of human activities. These States have banned sport 

or commercial fishing in Hg-contaminated waters, or have issued health warnings about the consequences of 

eating Hg-contaminated fish or seafood from selected water courses, or have placed restrictions on fish

consumption from certain streams, lakes, or rivers polluted with mercury (NAS 1978). In general, the number of 

Hg-contaminated fish and wildlife habitats has progressively increased--almost all as a direct result of 

anthropogenic activities (Boudou and Ribeyre 1983). 

Most authorities on Hg ecotoxicology agree on six points. First, Hg and its compounds have no known 

biological function, and its presence in living organisms is undesirable and potentially hazardous. Second,

forms of mercury with relatively low toxicity can be transformed into forms with very high toxicity through 

biological and other processes. Third, methylmercury can be bioconcentrated in organisms and biomagnified

through food chains, returning mercury directly to man and other upper trophic level consumers in concentrated 

form. Fourth, mercury is a mutagen, teratogen, and carcinogen, and causes embryocidal, cytochemical, and 

histopathological effects. Fifth, high body burdens of mercury normally encountered in some species of fish and 

wildlife from remote locations emphasize the complexity of natural mercury cycles and human impacts on these 

cycles. And finally, the anthropogenic use of mercury should be curtailed, because the difference between 

5
tolerable natural background levels of mercury and harmful effects in the environment is exceptionally small. 

These, and other aspects of mercury and its compounds in the environment as a result of anthropogenic or 

natural processes, have been the subject of many reviews, including those by Montague and Montague (1971), 

D'Itri (1972), Friberg and Vostal (1972), Jernelov et al. (1972, 1975), Keckes and Miettinen (1972), Buhler

(1973), Holden (1973), D'Itri and D'Itri (1977), Eisler (1978, 1981), NAS (1978), Birge et al. (1979),.Magos and 

Webb (1979), Nriagu (1979), EPA (1980, 1985), Jenkins (1980), Clarkson and Marsh (1982), Das et al. (1982), 

Boudou and Ribeyre (1983), Elhassani (1983), Clarkson et al. (1984), Robinson and Touvinen (1984), and Wren 

(1986). 

This report was prepared in response to requests for information from environmental specialists of the U.S.

Fish and Wildlife Service. it is part of a continuing series of synoptic reviews on chemical contaminants and

natural resources. 

SOURCES OF ENVIRONMENTAL MERCURY 

As a direct result of human activities, mercury levels in river sediments have increased fourfold since precultural 

times, and twofold to fivefold in sediment cores from lakes and estuaries (Das et al. 1982). During the past 100 

years, it has been estimated that more than 500,000 metric tons of Hg entered the atmosphere, hydrosphere, 

and surface soils, with eventual deposition in subsurface soils and sediments (Das et al. 1982). Several 

activities that contribute significantly to the global input of Hg include the combustion of fossil fuels; mining and 

reprocessing of gold, copper, and lead; operation of chloralkali plants; and disposal of batteries and fluorescent 

lamps (NAS 1978; Das et al. 1982). The atmosphere plays an important role in the mobilization of Hg; 25% to 

30% of the total atmospheric Hg burden is of anthropogenic origin (NAS 1978). 

In the United States, mercury consumption rose from 1,305 metric tons in 1959 to 2,359 tons in 1969 (Table 1). 

The major use of mercury has been as a cathode in the electrolytic preparation of chlorine and caustic (Nriagu 

1979). In 1968 this use accounted for about 33% of the total U.S. demand for Hg (EPA 1980). Of recent U.S. 

mercury consumption, electrical apparatus have accounted for about 27%; industrial and control instruments, 

such as switches, thermometers, and barometers, and general laboratory appliances, 14%; antifouling and

mildew-proofing paints, 12%; Hg formulations to control fungal diseases of seeds, bulbs, and vegetables, 5%; 

and dental amalgams, pulp and paper manufacturers, pharmaceuticals, metallurgy and mining, and catalysts, 

9% (EPA 1980). Mercury, however, is no longer registered for use in antifouling paints, or for the control of 

fungal diseases of bulbs (EPA 1980). 

Mercury from natural sources enters the biosphere directly as a gas, in lava (from terrestrial and oceanic 

volcanic activity), in solution, or in particulate form; cinnabar (HgS), for example, is a common mineral in hot

spring deposits and a major natural source of mercury (Das et al. 1982). The global cycle of Hg involves

degassing of the element from the Earth's crust and evaporation from natural bodies of water, atmospheric 

transport (mainly in the form of Hg vapor), and deposition of Hg back onto land and water. Oceanic effluxes of 

Hg are tied to equatorial upwelling and phytoplankton activity and may significantly affect the global cycling of

this metal. If volatilization of Hg is proportional to primary production in the world's oceans, oceanic 

phytoplankton activity represents about 36% of the yearly Hg flow to the atmosphere, or about 2,400 tons per 

year (Kim and Fitzgerald 1986). Mercury finds its way into sediments, particularly oceanic sediments, where the 

retention time can be lengthy (Table 2), and where it may continue to contaminate aquatic organisms (Lindsay 

and Dimmick 1983). Estimates of the quantities of Hg entering the atmosphere from degassing of the surface of 

the planet vary widely, but a commonly quoted figure is 30,000 tons annually (Clarkson et al. 1984). In aquatic 

ecosystems, removal of the source of anthropogenic Hg results in a slow decrease in the Hg content of 

sediments and biota (NAS 1978). The rate of loss depends, in part, on the initial degree of contamination, the 

chemical form of Hg, physical and chemical conditions of the system, and the hydraulic turnover time (NAS

1978). 

6
Table 1. Industrial and other uses of mercury in the United States in 1959 and in 1969. All values are in metric 

tons (modified from Montague and Montague 1971). 

 1959 1969 

 –———————— ——————————

Use Tons Percent Tons Percent 

Chloralkali process 201 15.5 716 30.4 

Electrical apparatus 308 23.6 644 27.3 

Antifouling and mildew paints 121 9.3 336 14.2 

Control devices 213 16.3 241 10.2 

Dental preparations 63 4.8 105 4.5 

Catalysts 33 2.5 102 4.3 

Agriculture 110 8.4 93 3.9 

Laboratory 38 2.9 71 3.0 

Pharmaceuticals 59 4.5 25 1.1 

Pulp and paper mill 150 11.5 19 0.8 

Metal amalgamation 9 0.7 7 0.3 

Total 1,305 2,359 

Table 2. Amount of mercury in some global reservoirs (NAS 1978), and residence time (Clarkson et al. 1984). 

 Hg content Residence

Reservoir (metric tons) time 

Atmosphere 850 6 to 90 days 

Soils 21,000,000 1,000 years

Freshwater 200 -

Freshwater biota (living) 4 - 

Ocean water 4,150,000,000 2,000 years 

Oceanic biota (living) 3 - 

Ocean sediments 330,000,000,000 >1 million years 

CHEMICAL PROPERTIES

Mercury, a silver-white metal that is liquid at room temperature and is highly volatile, can exist in three 

oxidation states: elemental mercury (Hgo), mercurous ion (Hg2

2+), and mercuric ion (Hg2+). It can be part of 

both inorganic and organic compounds (EPA 1980; Clarkson et al. 1984; Table 3). All mercury compounds 

interfere with thiol metabolism, causing inhibition or inactivation of proteins containing thiol ligands and 

ultimately leading to mitotic disturbances (Das et al. 1982; Elhassani 1983). The mercuric species is the most 

toxic inorganic chemical form, but all three forms of inorganic Hg may have a common molecular mechanism of 

damage in which Hg2+ is the toxic species (Clarkson and Marsh 1982; Figure 1).

Chemical speciation is probably the most important variable influencing ecotoxicology of Hg, but Hg 

speciation is difficult, especially in natural environments (Boudou and Ribeyre 1983). Mercury compounds in an 

aqueous solution are chemically complex. Depending on pH, alkalinity, redox, and other variables, a wide 

7
variety of chemical species are liable to be formed, having different electrical charges and solubilities. For 

example, HgCl2 in solution can speciate into Hg(OH)2, Hg2+, HgCl+, Hg(OH)-, HgCl3

-, and HgCl42-; anionic 

forms predominate in saline environments (Boudou and Ribeyre 1983). In the aquatic environment, under

naturally occurring conditions of pH and temperature, Hg may also become methylated by biological or chemical 

processes, or both (Beijer and Jernelov 1979; EPA 1980; Ramamoorthy and Blumhagen 1984; Figure 1) -- 

although abiological methylation is limited (Callister and Winfrey 1986). Methylmercury is the most hazardous 

mercury species due to its high stability, its lipid solubility, and its possession of ionic properties that lead to a 

high ability to penetrate membranes in living organisms (Beijer and Jernelov 1979). 

All mercury discharged into rivers, bays, or estuaries as elemental (metallic) mercury, inorganic divalent 

mercury, phenylmercury, or alkoxyalkyl mercury can be converted into methylmercury compounds by natural 

processes (Jernelov 1969). The mercury methylation in ecosystems depends on mercury loadings, microbial 

activity, nutrient content, pH and redox condition, suspended sediment load, sedimentation rates, and other 

variables (NAS 1978; Compeau and Bartha 1984; Berman and Bartha 1986; Callister and Winfrey 1986; 

Jackson 1986). The finding that certain microorganisms are able to convert inorganic and organic forms of Hg 

into the highly toxic methylmercury or dimethylmercury has made it clear that any form of Hg is highly hazardous 

to the environment (EPA 1980, 1985). The synthesis of methylmercury by bacteria from inorganic Hg 

compounds present in the water or in the sediments is the major source of this molecule in aquatic 

environments (Boudou and Ribeyre 1983). This process can occur under both aerobic and anaerobic 

conditions (Beijer and Jernelov 1979; Clarkson et al. 1984), but seems to favor anaerobic conditions (Olson and 

Cooper 1976; Callister and Winfrey 1986). Transformation of inorganic mercury to an organic form by bacteria 

alters its biochemical reactivity and hence its fate (Windom and Kendall 1979; Figure 1). Methylmercury is 

decomposed by bacteria in two phases. First, hydrolytic enzymes cleave the C-Hg bond, releasing the methyl 

group. Second, a reductase enzyme converts the ionic Hg to the elemental form, which is then free to diffuse 

from the aquatic environment into the vapor phase. These demethylating microbes appear to be widespread in 

the environment; they have been isolated from water, sediments, and soils and from the gastrointestinal tract of 

mammals--including humans (Clarkson et. al. 1984). 

Table 3. Some properties of mercury and its compounds.a 

 Elemental Mercurous Mercuric Methylmercury

Property mercury chloride chloride chloride 

Empirical formula Hg Hg2Cl2 HgCl2 CH3HgCl

Molecular weight 200.59 472.09 271.52 251.09c 

Chlorine, % 0 15.02 26.12 14.12c 

Mercury, % 100 84.98 73.88 79.89c 

Melting point, o C –38.87 sublimes at 277 170c 

 400–500 

Density 13.534 7.15 5.4 4.063c 

Solubility, mg/L (ppm) 

 In water 0.056 2.0 74,070 ~1,016d 

 In benzene 2.387b insol. 5,000 ~6,535e 

aAll data from Merck Index (1976), except where indicated. 

bSpencer and Voigt (1968). cWeast and Astle (1982).

dEisler (unpubl.), 72 h equilibrium value. eEisler (unpubl.), 24 h equilibrium value. 

8
Methylmercury is produced by methylation of inorganic mercury present in both freshwater and saltwater 

sediments, and accumulates in aquatic food chains in which the top-level predators usually contain the highest 

concentrations (Clarkson and Marsh 1982). Organomercury compounds other than methylmercury decompose 

rapidly in the environment, and behave much like inorganic Hg compounds (Beijer and Jernelov 1979). In 

organisms near the top of the food chain, such as carnivorous fishes, almost all Hg accumulated is in the 

methylated form, primarily as a result of the consumption of prey containing methylmercury; methylation also 

occurs at the organism level by way of mucous, intestinal bacteria, and enzymatic processes, but these 

pathways are not as important as diet (Huckabee et al. 1979; Boudou and Ribeyre 1983). 

The biological cycle of Hg is delicately balanced, and small changes in input rates and the chemical form of 

Hg may result in increased methylation rates in sensitive systems (NAS 1978). For example, the acidification of 

natural bodies of freshwater is statistically associated with elevated concentrations of methylmercury in the 

edible tissues of predatory fishes (Clarkson et al. 1984). In chemically sensitive waterways, such as poorly 

buffered lakes, the combined effects of acid precipitation and increased emissions of Hg to the atmosphere (with 

subsequent deposition) pose a serious threat to the biota if optimal biomethylation conditions are met (NAS

1978). 

Mercury binds strongly with sulfhydryl groups, and has many potential target sites during embryogenesis; 

phenylmercury and methylmercury compounds are among the strongest known inhibitors of cell division (Birge 

et al. 1979). Organomercury compounds, especially methylmercury, cross placental barriers and can enter 

mammals by way of the respiratory tract, gastrointestinal tract, skin, or mucous membranes (Elhassani 1983). 

When compared with inorganic mercury compounds, organomercurials are more completely absorbed, are 

more soluble in organic solvents and lipids, pass more readily through biological membranes, and are slower to 

be excreted (Clarkson and Marsh 1982; Elhassani 1983; Greener and Kochen 1983). Biological membranes, 

including those at the blood-brain interface and placenta, tend to discriminate against ionic and inorganic Hg,

but allow relatively easy passage of methylmercury and dissolved Hg vapor (Greener and Kochen 1983). As 

judged by membrane model studies, it appears that electrically neutral mercurials are responsible for most of 

the diffusion transport of Hg, although this movement is modified significantly by pH and Hg speciation. It 

seems, however, that the liposolubility of methylmercury is not the entire reason for its toxicity and does not play 

a major role in its transport. This hypothesis needs to be examined further in studies with living membranes 

(Boudou et al. 1983). 

Mercury-antagonistic drugs include 2,3-dimercaptopropanol, polythiol resins, selenium salts, vitamin E, and 

sulfhydral agents (in J.O. Nriagu (ed.). The biogeochemistry of mercury in the environment. Elsevier/NorthHolland Biomedical Press, New York.Magos and Webb 1979; Elhassani 1983). Thiols (R-SH), which compete 

with Hg for protein binding sites, are the most important antagonists of inorganic mercury salts, and have been 

used extensively in attempts to counteract Hg poisoning in humans (Das et al. 1982). The protective action of 

selenium (Se) against adverse or lethal effects induced by inorganic or organic mercury salts has been reported 

for algae, aquatic invertebrates, fish, and mammals (Magos and Webb 1979; Heisinger 1979; Chang et al. 1981; 

Lawrence and Holoka 1981; Das et al. 1982; Gotsis 1982; Eisler 1985; Satoh et al. 1985). Selenite salts can 

release methylmercury from its linkage to proteins, and there is general agreement that a true antagonism exists 

between Se and Hg, although the exact mechanism is not fully established (Das et al. 1982). In marine

mammals and humans, for example, Se and Hg concentrations are closely related, almost linearly in a 1:1 molar 

ratio, but this relation blurs in teleosts (in which Se is abundant) and fails in birds (Eisler 1985). 

MERCURY IN MINAMATA, JAPAN 

One of the earliest and most extensively documented cases of mercury poisoning occurred in the 1950's at 

Minamata Bay, in southwestern Kyushu, Japan--especially among fishermen and their families (Fujiki 1963, 

1980; Irukayama 1967; Matida and Kumada 1969; Kojima and Fujita 1973; NAS 1978; Elhassani 1983; 

Nishimura and Kumagai 1983; Doi et al. 1984). The source of the mercury was in waste discharged from an 

acetaldehyde plant that used inorganic Hg as a catalyst; between 1932 and 1968, Minamata Bay received at 

least 260 tons of mercury, and perhaps as much as 600 tons. A severe neurological disorder was recognized in 

late 1953 and had reached epidemic proportions by 1956; 111 cases of poisoning were reported by the end of 

1960 and 41 deaths by August 1965. By 1982, there were 1,800 verified human victims of mercury poisoning in 

a total regional population of 200,000; however, the total number of victims remains unconfirmed. Symptoms 

evidenced by human victims included sensory impairment, constriction of visual fields, hearing loss, ataxia, and 

9
speech disturbances. Congenital cases were accompanied by disturbance of physical and mental development; 

about 6% of babies born in Minamata had cerebral palsy (vs. 0.5% elsewhere). 

"Minamata disease" resulted from the discharge of methylmercury from chemical factories into Minamata 

Bay. Once diluted and diffused in the water, it was concentrated to a high level in fish and filter-feeding shellfish 

by several routes, including bioconcentration and food chain biomagnification. When these fish and shellfish 

were consumed by humans, methylmercury gradually accumulated to exceed a threshold value, causing 

intoxication. Spontaneously poisoned cats, dogs, rats, waterfowl, and pigs behaved erratically and died; flying 

crows and grebes suddenly fell into the sea and drowned; and large numbers of dead fish were seen floating on 

the sea surface (Doi et al. 1984). In laboratory studies, cats and rats fed shellfish from the Bay developed the 

same signs as those seen in animals affected spontaneously. Abnormal Hg content--i.e., more than 30 mg/kg 

fresh weight--was measured in fish, shellfish, and muds from the Bay, and in organs of necropsied humans and 

cats that had succumbed to the disease. Mercury contamination of fish and sediments was still evident in 1981, 

although discharges from the acetaldehyde plant ceased in 1971 (Doi et al. 1984). 

There is a strong relation between the food of birds from Minamata and the Hg content in feathers; the 

content is highest in fish-eating seabirds and lowest in herbivorous waterfowl (Doi et al. 1984; Table 4). This 

same relation held in birds collected from China and Korea, although concentrations were significantly lower 

(Doi et al. 1984). There are close correlations between Hg contents of zooplankton and suspended particulate 

matter, and of sediments and fish muscle, suggesting a pathway from sediment to fish by way of suspended

matter and zooplankton. The conversion from inorganic Hg to methylmercury is believed to have occurred

primarily in zooplankton (Nishimura and Kumagai 1983). 

Table 4. Mercury concentrations in selected biological and nonbiological materials collected from Minamata

Bay, Japan and environs. Concentrations are in mg Hg/kg (ppm) fresh weight (FW), or dry weight (DW). 

Sample, year of 

collection, and Concentration 

other variables (mg/kg) Referencea 

Phytoplankton 

1974 Max. 0.32 DW Nishimura and 

 Kumagai 1983

Invertebrates 

 1961 

 Coelenterates 9.6 DW Matida and 

 Tunicates 35–56 DW Kumada 1969

 Molluscs 

 Pacific scallop,

 Chlamys ferrei nipponensis 

 Soft parts 48 DW 

 Pacific oyster,

 Crassostrea gigas 

 Soft parts 10 DW; 5.6 FW 

 Clam, Hormomya mutabilis 

 Foot 18–48 DW Fujiki 1963 

 Ganglion 181 DW 

10
 Other tissues 20–73 DW 

 Crustacean

 Crab, Neptunus pelagicus 

 Muscle 39 DW

 Filter-feeding molluscs 

 Soft parts

 1962 Max. 43 DW Fujiki 1980 

 1963 Max. 40 DW 

 1965 Max. 35 DW 

 1967 Max. 60 DW 

 1969 Max. 16 DW 

 1971 Max. 16 DW 

 1972 Max. 4 DW 

 Zooplankton

 1974 Max. 1.1 DW Nishimura and 

 Kumagai 1983

Fish 

 1961 

 Largescale blackfish, 

 Girella punctata 

 Viscera 18–27 DW Matida and 

 Muscle 12–20 DW Kumada 1969

 Scarbreast tuskfish, 

 Choerodon azurio

 Muscle 309.1 DW Fujiki 1963 

 Liver 85.0 DW 

 Heart 36.4 DW 

 Gill 13.3 DW 

 Digestive gland 1.3 DW 

 Black porgy, Sparus macrocephalus 

 Muscle 16.5 DW 

 Liver 32.2 DW 

 Heart 18.3 DW 

 Gill 9.1 DW 

 Digestive gland 4.0 DW 

 Muscle 

 1961 23.0 DW Fujiki 1980 

 1963 3.5 DW 

 1965 11.5 DW 

 1966–72 <0.6 DW 

1974 Max. 0.6 FW Nishimura and 

 Kumagai 1983

Birds 

11
 1955–80 

 Feather 

 Fish-eating seabirds 7.1 DW Doi 

Omnivorous waterfowl 5.5 DW et al. 1984 

 Predators 3.6 DW 

 Omnivorous terrestrial birds 1.5 DW 

 Herbivorous waterfowl 0.9 DW 

1965-66, found dead 

 Feather 4.6–13.4 FW Kojima and 

 Fujita 1973 

Mammals 

 Cat, Felis domesticus, 1961 

 Hair

 Naturally poisoned 40–52 DW Jenkins 1980

 Experimentally poisoned 22–70 DW 

Seawater 

 1961 

 Total 0.0016–0.0036 FW EPA 1980 

 1974 

 Filtered 0.0001 FW Nishimura and 

Suspended particulates 0.000075 FW Kumagai 1983

 Mud 

 1963 28–713 DW Fujiki 1980 

 1969 19–908 DW 

 1970 8–253 DW 

 1971 14–586 DW 

Sediments 

 1973 >15–600 DW Nishimura and 

 Kumagai 1983

aEach reference applies to the values in the same row and in the rows that follow for which no other reference is

indicated. 

In aquatic environments where point sources of industrial contamination have been identified, the 

elimination of Hg discharges has usually improved environmental quality. Such improvement has been reported 

for Minamata Bay (Table 4); for sediments in Saguenay Fjord, Quebec, when chloralkali wastes were limited; for 

fish residues in Canada's Lake St. Clair after two chloralkali plants were closed; and in various sections of 

Europe and North America when industrial discharges were eliminated (Barber et al. 1984). 

BACKGROUND CONCENTRATIONS 

GENERAL 

Mercury burdens in sediments and other nonbiological materials are estimated to have increased up to 5X 

prehuman levels, primarily as a result of man's activities (NAS 1978). The residence time of mercury is 

comparatively short (about 11 days) in the atmosphere, but is much longer (at least 1,000 years) in oceanic 

waters, soils, and sediments (Clarkson 1984). 

12
An elevated concentration of mercury (i.e., >1.0 mg/kg fresh weight), usually as methylmercury, in any 

biological sample is often associated with proximity to human use of mercury. The elimination of Hg pointsource discharges has usually been successful in improving environmental quality. However, elevated levels of 

mercury in biota may persist in contaminated areas long after the source of pollution has been discontinued 

(Rada et al. 1986). For example, Hg remains elevated today in resident biota of Lahontan Reservoir, Nevada, 

which received about 7,500 tons of mercury as a result of gold and silver mining operations during the period

1865 to 1895 (Cooper 1983). It is noteworthy that some groups of organisms with consistently elevated Hg 

residues may have acquired these concentrations as a result of natural processes, rather than from 

anthropogenic activities. These groups include older specimens of long-lived predatory fishes, marine

mammals (especially pinnipeds), and organisms living near natural Hg-ore-cinnabar deposits. 

NONBIOLOGICAL

Mercury burdens have increased 2X to 5X precultural levels in freshwater and estuarine sediments and 

freshwater lakes and rivers, but estimated increases in oceanic waters and terrestrial soils have been negligible 

(NAS 1978). Total mercury concentrations in uncontaminated natural waters (presumably unfiltered) now range 

from about 0.001 to 0.050 ug/l (Table 5). In sediments that were anthropogenically contaminated with Hg, 

concentrations were significantly elevated (usually >20.0 mg/kg) when compared with uncontaminated 

sediments (usually <1.0 mg/kg). The residence time of Hg in nonbiological materials is variable, and depends 

on a number of physicochemical conditions. Estimated half-time residence values for Hg are 11 days in the 

atmosphere, 1,000 years in terrestrial soils, 2,100 to 3,200 years in ocean waters, And >250 million years in

oceanic sediments (NAS 1978, as quoted in Boudou and Ribeyre 1983); the estimate was 1 month to 5 years 

for water from the contaminated Saguenay River in Quebec (Smith and Loring 1981). 

Table 5. Mercury concentrations in water and sediments. 

Material (units) Concentration Referencea 

Water (μg/L)

 Open ocean 0.0053 + 0.0022 Nishimura et al. 1983 

Open ocean <0.01 Fitzgerald 1979 

 Coastal seawater <0.02 

 Estuarine seawater <0.05 

Rivers and lakes 0.01 (Max. 0.05) 

 Rainwater 

 Open ocean 0.001 

 Coastal ocean 0.01 

 Continents Often >0.05 

 Sediment interstitial 

 water 0.1 

 Glacial waters 0.01 

 Ground waters 0.05 

Sediments (mg/kg) 

 Contaminated areas 

 Near chloralkali 

 plant 

 Quebec, Canada 12.0 Smith and Loring 1981 

 Norway 250 (90.0–350.0) Skei 1978 

 Thailand 8.4–58.0 Suckcharoen and 

 Lodenius 1980 

13
 Near gold mining 

 operations

 South Dakota 0.1–4.1 Martin and Hartman 1984

 Australia 120.0 Bycroft et al. 1982 

 Near Hg-fungicide

 plant 

 Denmark 22.0 Kiorboe et al. 1983 

 Near acetaldehyde 

 plant 

 Minamata Bay, Japan 28.0–713.0 Skei 1978 

Near pulp and paper 

 mill 

 Finland 746.0 Paasivirta et al. 1983 

 Uncontaminated areas 

North Central U.S. 0.02–0.06 Martin and Hartman 1984

 (Max. 0.11) 

 South Dakota 0.02–0.1 

 Thailand 0.03 Suckcharoen and 

 Finland 0.02 Lodenius 1980 

Various lakes Usually <10.0, Skei 1978 

 frequently <1.0 

aEach reference applies to the value in the same row and in the rows that follow for which no other reference is

indicated. 

Levels of mercury in sediments may be reflected by an increased mercury content in epibenthic fauna. For 

example, Hg concentrations in sediments near the Hyperion sewer outfall in Los Angeles, which ranged up to 

820 ug/kg and decreased with increasing distance from the outfall, were reflected in the Hg content of crabs, 

scallops, and whelks. Concentrations of Hg were highest in organisms collected nearest the discharge, and

lowest in those collected tens of kilometers away (Klein and Goldberg 1970). 

BIOLOGICAL 

Information on mercury residues in field collections of living organisms is especially abundant; accordingly, 

only a few selected data points are shown in Table 6. Additional, more extensive, information was given by 

Jenkins (1980), Eisler (1981), and Wren (1986). 

In general, mercury concentrations in biota were usually <1.0 mg/kg fresh weight tissue in organisms 

collected from locations not directly affected by man's use of the element. However, they exceed 1.0 mg/kg--

and are sometimes markedly higher--in animals and vegetation from the vicinity of chloralkali plants; agricultural 

users of mercury; smelteries; mining operations; pulp and paper mills; factories producing Hg-containing paints, 

fertilizers, and insecticides; sewer outfalls; sludge disposal areas; and other anthropogenic point sources of 

mercury. (Several notable exceptions to this generalization are discussed later.) 

Certain species of macrophytes strongly influence mercury cycling. For example, Spartina alterniflora--a 

dominant salt marsh plant in Georgia estuaries--accounted for almost half the total mercury budget in that 

ecosystem (Windom et al. 1976). Mangrove vegetation plays a similarly important role in mercury cycling in the 

Florida Everglades (Tripp and Harriss 1976). These findings suggest that more research is needed on the role 

of higher plants in the mercury cycle. 

14
Mercury was detectable in the tissues of almost all freshwater fishes examined, with the majority of the Hg 

(>80%) present as methylmercury (Huckabee et al. 1979). Methylmercury is absorbed more efficiently than 

inorganic Hg from water, and probably from food, and is retained longer regardless of the uptake pathway 

(Huckabee et al. 1979). Reservoir construction has often been inferred to be a cause of elevated mercury 

concentrations in fish. It is hypothesized that increases in mercury levels observed in fish were due to bacterial 

methylation of naturally occurring Hg in the flooded soils (Bodaly et al. 1984). Other factors that enhance 

accumulation of Hg in predatory teleosts from recently created reservoirs include low pH, high humus content, 

and low bioproduction (Lodenius 1983; Lodenius et al. 1983). In general, mercury levels are higher in fish from 

younger oligotrophic reservoirs, and lower in fish from older eutrophic reservoirs; in both situations, tissue Hg 

levels usually decline as the reservoirs age (Abernathy and Cumbie 1977). Concentrations >0.5 mg/kg (but <1.0 

mg/kg) fresh weight have been reported in trout from several wilderness lakes in northern Maine (Akielaszak 

and Haines 1981) and from the Adirondacks region of New York (Sloan and Schofield 1983); these values are 

considerably higher than might be expected for fish inhabiting remote lakes. These elevated concentrations 

were usually associated with lakes of low pH, low calcium, low dissolved organic carbon concentrations, and low 

water hardness and alkalinity. 

Table 6. Mercury concentrations in field collections of selected species of flora and fauna. Values shown are in 

mg Hg/kg fresh weight (FW), or dry weight (DW). 

Taxonomic group, organism, Concentrationa 

tissue, and other variables (ppm) Referenceb 

Fungi, Lichens, Mosses, Plants 

 Mandarin orange, Citrus tachibana 

 Japan 

 Sprayed with Hg 

 Fruit skin 0.03–0.24 FW Jenkins 1980

 Fruit pulp 0.01-0.4 FW

 Unsprayed

 Skin and pulp 0.01–0.05 FW 

 Fungi, Cortinarius spp.

 Near smelter 9.5–35.0 DW 

 Moss, Dicranum scoparium, whole 

 Tennessee 

Exposed to fly ash 1.1 DW 

 Remote areas 0.1 DW

 Great Smoky Mountains 0.07 DW 

 Hawaii 0.16 DW 

 Iceland 0.03 DW 

 Water hyacinth, Eichhornia crassipes 

 From sewage lagoon in 

 Bay St. Louis, Mississippi 

 Leaves 70.0 DW Chigbo et al. 1982 

 Lichen, Hypogymnia physodes, whole 

 Finland, 1982–83 

 Distance, in km, from 

 chloralkali plant 

15
 0–1 18.0 FW Lodenius and

 1–5 2.0 FW Tulisalo 1984

 5–20 0.4 FW 

 20–100 0.3 FW 

 >100 0.3 FW

 Labrador tea, Ledum sp. 

 Alaska, over cinnabar deposit 

 Stem 1.0–3.5 DW Jenkins 1980

 Alfalfa, Medicago sativa 

From soil containing 0.4 ppm Hg 

 Root 90.0 FW 

 Leaf 0.13–0.4 FW

 From soil with <0.4 ppm Hg 

 Leaf 0.16 FW 

 Tobacco, Nicotiana tabacum

 Leaf 

 Treated with Hg (Japan) 1.0–1.6 FW

 Untreated (USA) <0.2 FW 

 Rice, Oryza sativa, grain 

 Sprayed with Hg 0.1–0.7 FW

 Unsprayed 0.02–0.1 FW

 Marine flowering plant, 

 Posidonia oceanica 

 Near sewer outfall, 

 Marseilles, France 

 Rhizomes 2.5 DW Augier 

 Leaves 51.5 DW et al. 1978 

 Roots 0.6 DW 

 Cherry, Prunus avium

 Europe (Slovenia), bark 

 Uncontaminated areas 0.06 FW Jenkins 1980

 High Hg in soil 6.0 FW 

 Factory area 59.0 FW 

 Mosses, Sphagnum spp., whole 

 Finland, 1982–83 

 Distance (km) from

 chloralkali plant 

 0–1 3.8 (1.5–16.0) FW Lodenius and

 1–5 0.8 (0.2–2.6) FW Tulisalo 1984

 5–20 0.09 (0.04–0.2) FW 

 20–100 0.05 (0.0–0.8) FW 

 >100 0.02 FW

Aquatic Invertebrates 

16
 Freshwater

 Annelids, 2 families 

 From Hg-contaminated areas 0.3–0.6 FW Huckabee 

From uncontaminated areas 0.03–0.05 FW et al. 1979 

 Arthropods

 Sow bug, Asellus sp.

 Sweden, whole 

 20 km below paper mill 1.9 FW Jenkins 1980

 1–15 km above paper mill 0.06 FW 

 Crustaceans, 2 families 

 From Hg-contaminated areas 1.9–10.0 FW Huckabee 

From uncontaminated areas 0.06–0.56 FW et al. 1979 

 Insects, 8 families 

 From Hg-contaminated areas 0.5–5.0 FW

 From uncontaminated areas 0.05–0.21 FW 

 Stonefly, Isoperla sp. 

 Whole, Sweden 

 17 km below paper mill 2.4 FW Jenkins 1980

 15 km above paper mill 0.07 FW 

 Crayfish, Orconectes virilis 

 Ontario, whole 

 Central location 0.09–0.49 FW 

 From chloralkali

 plant location 1.4–7.4 FW

 Crayfish, Pacifiastacus sp. 

 Lahontan Reservoir, Nevada, 

 1981 

 Abdomen 5.7 FW Cooper 1983

 Molluscs 

 From Hg-contaminated areas 0.02–2.1 FW Huckabee 

From uncontaminated areas 0.05 FW et al. 1979 

 Marine 

Annelids, whole, 3 spp. 

 Georgia, USA, estuaries 

 Hg-contaminated estuary 

 Total Hg 0.7–4.5 DW Windom and

 Methyl Hg Max. 0.8 DW Kendall 1979

 Control estuary 

 Total Hg 0.1–0.6 DW 

 Methyl Hg Max. 0.13 DW

 Arthropods

 Crustaceans, whole, 2 spp.

 Georgia, USA, estuaries 

17
 Hg-contaminated estuary 

 Total Hg 0.4–1.8 DW 

 Methyl Hg Max. 1.0 DW 

 Control estuary

 Total Hg 0.1–0.4 DW 

 Methyl Hg Max 0.05 DW

 American lobster, 

 Homarus americanus 

 Muscle

 Chesapeake Bay 0.03–0.06 FW Jenkins 1980

 NW Atlantic 0.25–1.6 DW 

 Nova Scotia 0.15–1.5 FW

 Spiny lobster,

 Nephrops norvegicus 

 Tyrrhenian Sea, 1981 

 Muscle 2.9 FW Schreiber 1983 

 Shrimp

 Edible portions 

 Total Hg 0.77 FW Cappon 

 Methyl Hg 0.4 FW and Smith 1982 

 Echinoderms 

Sea stars, 3 spp., 1981 

 Venezuela, polluted area 

 Gonads 3.8–8.7 DW; Iglesias and 

 0.9–1.6 FW Panchaszadeh 

 1983 

 Molluscs 

 From vicinity chloralkali plant, 

 Israel, 1980–82, soft parts

 Gastropod,

 Arcularia gibbosula 18.2–38.7 DW Hornung et al. 

 Bivalve, 1984 

 Donax venustus Max. 6.4 DW 

 Bivalves, soft parts

 From Hg-polluted area, 

 Denmark

 Deposit feeders 1.4–4.4 FW Kiorboe 

 Suspension feeders 0.9–1.9 FW et al. 1983 

 Edible portions 

 Total Hg 0.04–0.22 FW Cappon and 

 Methyl Hg Max. 0.09 FW Smith 1982 

 Soft parts, 2 spp. 

 Georgia, USA, estuaries 

18
 Hg-contaminated estuary 0.5–1.2 DW Windom and

 Control estuary 0.1–0.2 DW Kendall 1979

 Mussel, Mytilus californianus 

 Soft parts

 Nationwide <0.4 DW Flegal 

 California 0.6–2.5 DW et al. 1981 

 Mussel, Mytilus edulis 

 Soft parts

 Belgium 1.0 DW

 Spain 1.5 DW 

 New Brunswick 0.1 FW 

 Netherlands 0.1–0.3 FW

 Great Britain 0.02–0.7 FW

 New Zealand 0.02–0.48 FW 

 Norway 0.2–0.65 DW 

 Softshell clam, Mya arenaria 

 Soft parts

 Chesapeake Bay, MD 0.01–0.05 FW 

 Nova Scotia 0.03–0.13 FW 

 New Brunswick

 3 km below pulp mill 0.9 FW 

 3 km below chloralkali 

 plant 3.6 FW 

Terrestrial Invertebrates 

 Aphid, Macrosiphium gei 

 Whole, Illinois 

 Fed on Hg-treated 

 tomato plants 0.3–11.5 FW

 Control 0.08–0.81 FW 

 Lacewing, Chrysopa carnea

 Whole, Illinois 

 Fed on Hg-treated 0.6–31.4 FW

 tomato plants

 Control 0.0–1.1 FW

Fish 

 Rock bass, Ambloplites rupestris

 Muscle

 Ontario 0.6–4.6 FW

 Michigan 0.4 FW 

 Western Ontario 1.1–10.9 FW

 Lake St. Clair 0.5–2.0 FW

 Blue hake, Antimora rostrata 

NW Atlantic, 2500 m depth

19
 Muscle

 1880 0.51 FW Barber

 1970 0.34 FW et al. 1984 

 Freshwater drum, Aplodinotus 

 grunniens 

 Whole 

 Age 0 0.05 FW Busch 1983 

 Age I 0.13 FW 

 Age II 0.18 FW 

 Blacktail, Diplodus sargus, muscle 

 Hg-polluted area 0.3–1.7 FW Hornung 

Unpolluted area 0.04–0.64 FW et al. 1984 

 Northern pike, Esox lucius, muscle

 Sweden 0.2–9.8 FW Jenkins 1980

 Quebec 0.3–0.8 FW

 Norway 0.1 FW 

 Saskatchewan 0.7–10.6 FW

 Canada (normal) 0.1 FW 

 Canada (polluted) 0.5–0.7 FW

 Lake St. Clair 2.0–3.0 FW

NW Ontario mining area 5.6 FW 

 Wisconsin 0.9–1.4 FW

 Manitoba, manmade reservoir 

 Preimpoundment (1971–73) 0.25–0.35 FW Bodaly 

 Postimpoundment (1979–82) 0.67–0.95 FW et al. 1985 

 Fish 

 Muscle

 Freshwater

 Total Hg 0.27–1.7 FW Cappon and 

 Methyl Hg Max. 1.4 FW Smith 1982 

 Marine

 Total Hg 0.11–5.7 FW

 Methyl Hg Max. 4.5 FW

Lahontan Reservoir, Nevada, 1981 

Muscle, 5 spp. Max. 2.3–3.9 FW Cooper 1983

Liver, 5 spp. Max. 2.4–8.3 FW 

Heart, 4 spp. Max. 1.1–2.1 FW 

Louisiana, Atchafalaya River, 1981 

Whole, 8 spp. 0.06–0.79 FW Winger and Andreasen 1985

 Nationwide, USA, whole 

1969–70 0.26 (0.05–1.7) FW Henderson and 

Pacific Coast and Alaska 0.25 (0.05–1.7) FW Shanks 1973

 Southwest 0.08 (<0.05–0.14) FW

20
 North Central 0.20 (<0.05–0.05) FW

 Northeast 0.23 (<0.05–0.08) FW

 Southeast 0.23 (<0.05–1.0) FW 

 1972 0.15 FW 

1976–77 0.11 FW Lowe et al. 

 1978–79 0.11 (0.01–1.1) FW 1985 

 1980–81 0.11 (0.01–0.77) FW

 Thailand 

 Muscle

 Near chloralkali plant 

 No waste water system,

 1975–76 0.32–3.6 FW Suckcharoen

 With waste water system, and Lodenius

 1978 0.1–1.4 FW 1980 

 Control location 0.01–0.3 FW

 Various species 

 Muscle

From unpolluted areas 0.04–0.15 FW NAS 1978 

 From moderately Hg-polluted 

 areas >1.0 FW

From highly polluted areas 10.0–24.0 FW 

 Blackfish, Gadopsis marmoratus

 Muscle

 From Hg-contaminated 

 sediments Max. 0.64 FW Bycroft 

From uncontaminated sediments Max. 0.06 FW et al. 1982 

 Channel catfish, Ictalurus punctatus 

 Muscle

 Lake Erie 0.3–1.8 FW Jenkins 1980

 Lake St. Clair 0.5–2.0 FW

 Ohio 0.1–0.4 FW

 Illinois 0.03–0.2 FW

 Oregon 0.02–1.5 FW

 Georgia 0.1–1.9 FW

 Texas 0.2–2.5 FW

 Pumkinseed, Lepomis gibbosus 

16 lakes, Ontario, Canada, 1981 

Muscle 0.09–0.54 FW Wren and MacCrimmon 1984 

 Black marlin, Makaira indica 

 Muscle

 Pacific Ocean 0.6–4.3 Cappon and 

 NE Australia 0.5–16.5 FW Smith 1982 

 Blue marlin, Makaira nigricans 

21
 Muscle

 Hawaii 0.4–14.0 FW

 Total Hg 0.4–0.9 FW

 Methyl Hg Max. 0.16 FW 

 Largemouth bass, 

 Micropterus salmoides 

 Muscle

 Texas 0.1 FW Jenkins 1980

 Utah 0.3–7.3 FW

 California 0.1–0.6 FW

 Oregon 0.2–1.8 FW

 Washington 0.1–0.3 FW

 Georgia 0.1–5.4 FW

 Michigan 0.2–0.9 FW

 Illinois 0.03–1.2 FW

 Arizona 0.3 FW

 Striped bass, Morone saxatilis 

 Lahontan Reservoir, Nevada, 

 1981 

 Single specimen, 16 years old 

 Muscle 9.5 FW Cooper 1983

 Heart 5.6 FW

 Liver 23.7 FW 

 Muscle

 Body weight 

 <3.2 kg <0.5 FW Alexander 

 3.2–5.7 kg 0.5 FW et al. 1973 

 >5.7 kg >0.5 FW 

 Yellow perch, Perca flavescens

 Whole 

 Age 0 0.07 FW Busch 1983 

 Age I 0.13 FW 

 Age II 0.22 FW 

 Round whitefish, 

 Prosopium cylindraceum

 Saginaw Bay, Michigan

 1977–78 

 Fillets 

 Methyl Hg Max. 0.05 FW Miller and 

 Total Hg Max. 0.1 FW Jude 1984 

 Trout, Salmo spp. 

 Missouri

 Liver and muscle 

22
 1946–50 3.0 FW Lloyd 

 1973 0.1–0.3 FW et al. 1977 

 Brook trout, Salvelinus fontinalis 

Adirondack lakes (15), New York

Whole <1.0 FW Sloan and Schofield 1983 

 Lake trout, Salvelinus namaycush 

 Muscle

 British Columbia 1.1–10.5 FW Jenkins 1980

 Ontario 0.3–1.3 FW

 Quebec 0.3–1.2 FW

 New York 0.3–0.6 FW

Sharks, Australia, 1980 

 Muscle, 7 spp. 

 Carcharhinus spp. Max. 4.3 FW Lyle 1984 

 Sphyrna spp. Max. 4.9 FW 

 Walleye, 

 Stizostedion vitreum vitreum

 Manitoba, manmade reservoir 

 Muscle

 Preimpoundment (1971–77) 0.2–0.3 FW Bodaly 

 Postimpoundment et al. 1984 

 (1978–92) 0.6–0.8 FW

Tunas, 1981, 5 spp. 

 Muscle 1.0–6.3 FW Schreiber 1983 

 Swordfish, Xiphias gladius

 Muscle

NW Atlantic 2.0 FW; 8.1 DW Jenkins 1980

 Peru 1.1–1.8 FW

 Pacific 0.5–1.7 FW

 W. Atlantic 0.05–4.9 FW

 Gibralter Strait 1.0–2.0 FW

Amphibians and Reptiles

 European toad, Bufo bufo 

 Yugoslavia 

 Control area 

 Liver 1.5 FW 

 Kidney 1.2 FW 

 Lung 0.2 FW 

 Muscle 0.2 FW

 Egg 0.06 FW 

 Polluted mercury mining area 

 Liver 21.8–25.5 FW Jenkins 1980; 

 Kidney 22.8–24.0 FW Terhivuo et al. 1985 

23
 Lung 1.7 FW 

 Muscle 2.3–2.9 FW

 Egg 2.3 FW 

 Loggerhead sea turtle, 

 Caretta caretta 

 Egg 0.01 FW Hall 1980 

 Crocodile, Crocodylus acutus 

 Egg 0.7 FW 

 Bullfrog, Rana catesbeiana 

 Lake St. Clair 

 Carcass 0.1 FW Jenkins 1980

 Liver 0.3 FW 

 Leopard frog, Rana pipiens 

 Lake St. Clair 

 Carcass 0.1–0.2 FW

 Liver 0.5–1.1 FW

 Florida 

 Liver 0.1 FW 

 Frog, Rana temporaria 

 Yugoslavia, 1975 

 From Hg-mining area

 Liver 21.0 FW Terhivuo

 Kidney 16.2 FW et al. 1984 

 Muscle 3.4 FW

 Egg 1.3 FW 

 From uncontaminated area

 All tissues <0.08 FW

Birds 

 Goshawk, Accipiter gentilis 

 Sweden 

 Feather 

 1860–1946 2.2 FW Jenkins 1980

 1947–65 29.0 FW 

 1967–69 3.1–5.1 FW

 Finnish sparrowhawk, 

 Accipiter nisus 

 Feather 

 Finland 

 1899–1960 4.1 (2.1–7.7) DW Solonen and

 1961–70 11.1 (2.3–42.0) DW Lodenius 1984 

 1971–82 7.4 (1.0–29.0) DW 

 Germany

 1972–73 4.9 (0.4–20.3) DW 

24
 Norway

 1976 2.0–20.0 DW 

 Wood duck, Aix sponsa

 Tennessee, 1972–73 

 Juveniles 

 Liver 0.4 (0.1–1.1) FW Lindsay and 

 Muscle 0.1 (0.05–0.4) FW Dimmick 1983

 Fat 0.1 (0.01–0.4)

 Adults

 Liver 0.2 (0.1–0.3) FW 

 Muscle 0.08 (0.06–0.11) FW

 Fat 0.06 (0.01–0.11) FW

 Blue-winged teal, Anas discors 

 Muscle

Lake St. Clair 0.1–2.3 FW Jenkins 1980

 Ontario 3.8–10.4 FW

 Wisconsin 0.0–0.5 FW

 Illinois 0.05 FW 

Great blue heron, Ardea herodius

 Liver

Lake St. Clair 97.0 (14.6–175.0) FW

 New Brunswick 4.5 FW 

 Lake Erie 0.7–4.3 FW

 Wisconsin 0.5 (0.2–1.1) FW 

 Birds

 Antarctic

 Liver

 1977–79 

 4 spp. 0.5–1.3 FW Norheim 

 3 spp. 2.7–2.9 FW et al. 1982 

 1980 

 5 spp. 0.5–2.1 FW Norheim and

 Kjos-Hanssen

 1984 

 Belgium, 1970–81 

 Liver, 30 spp. 

 Aquatic birds 0.11–35.0 FW Delbeke 

 Terrestrial birds ND-14.0 FW et al. 1984 

 Hawaiian, 1980 

Egg, 3 spp. 0.12–0.36 FW Ohlendorf and 

 Harrison 1986

 North America 

 Feather 

25
 From areas with

 mercury-treated seed dressing 

 Seed-eating songbirds 1.6 DW NAS 1978 

 Upland game birds 1.9 DW 

 From untreated areas 

 Seed-eating songbirds 0.03 DW 

 Upland game birds 0.35 DW 

 Northwestern Ontario, Canada 

 From a heavily mercury- 

 contaminated freshwater system 

 Liver

 Scavengers 57.0 (13.8–121) FW Fimreite 1979

 Fish eaters 39.5 (1.7–91) FW 

 Omnivores 26.6 (9.5–53) FW 

 Invertebrate feeders 12.4 (3.2–28) FW 

 Vegetarians 6.2 (1.9–28) FW 

 Diving ducks Max. 175.0 NAS 1978 

 Muscle

 Diving ducks Max. 23.0 FW 

 Mallard, Anas platyrhynchos Max. 6.1 FW 

 Eagle-owl, Bubo bubo 

 Sweden, 1963–76 

 Feather 

 Inland populations 3.2 DW Broo and 

 Coastal populations 6.5 DW Odsjo 1981 

 1829–1933 0.3–3.6 FW Jenkins 1980

 1964–65 12.8–41.0 FW 

 Peregrine, Falco peregrinus

 Feather 

 1834–1849 2.5 DW NAS 1978 

 1941–65 >40.0 DW 

 Swedish gyrfalcon, Falco rusticolus 

 Nestlings, feather 

Percent aquatic birds in diet

 None 0.035 FW Lindberg 1984

 4.8% biomass 0.66 FW 

 10.6% biomass 1.22 FW 

American bald eagle, 

 Haliaeetus leucocephalus

 Egg 

 Maine (highest concentrations 

 Nationwide) 

 1974 0.35–0.58 FW Wiemeyer

26
 1975 0.22–0.63 FW et al. 1984 

 1976 0.22–0.66 FW 

 1977 0.28–0.90 FW 

 1978 0.30 FW 

 1979 0.84–1.2 FW

Ringed herring gull, 

 Larus argentatus 

 Denmark, 1975–76 

 Liver 0.65 (0.08–2.34) FW Karlog and 

 Clausen 1983 

 Ontario

 Egg 1.5–15.8 FW Jenkins 1980

 Albumin 16.1–22.7 FW 

 Yolk 3.4–3.5 FW

 California seagull, 

 Larus californicus 

Lahontan Reservoir, Nevada, 1981 

 Muscle 0.4 FW Cooper 1983

 Liver 1.0 FW 

 Egg 0.1–0.2 FW

 Osprey, Pandion haliaetus

 Sweden 

 Feather 

 1840–1940 3.5–5.0 FW Jenkins 1980

 1940–66 >17.0 FW

 Brown pelican, 

 Pelecanus occidentalis

 Egg 

 South Carolina 0.3–0.5 FW

 Florida 0.4 FW 

 California 0.4 FW 

 Liver 0.75 DW Ohlendorf 

Kidney 0.68 DW et al. 1985 

 Feather 0.97 DW 

 Ring-necked pheasant, 

 Phasianus colchicus 

 Muscle

 Denmark 0.01 FW Jenkins 1980

 Idaho 0.0–15.0 FW

 Indiana 0.06 FW 

 Oregon <0.5 FW

 Wyoming 0.2–0.6 FW

 Colorado 0.04–0.6 FW

27
 Utah 0.15 (0.01–2.1) FW 

 California 1.6–4.7 FW

 Wisconsin 0.01–0.08 FW 

 Illinois 0.02–0.03 FW 

 Great crested grebe, 

 Podiceps cristata 

 Sweden 

 Feather 

 1865–1940 <10.0 FW

 1940–66 >14.0 FW

 Mourning dove, Zenaida macroura 

 Liver

 Eastern United States 0.07–0.67 FW 

Mammals

Australian fur seal, 

 Arctocephalus pusillus 

 Muscle 0.9 (0.1–1.9) FW Bacher 1985

 Liver 62.3 (1.0–170.0) FW 

 Kidney 0.6 (0.1–1.7) FW 

 Spleen 1.3 (0.0–3.8) FW 

 Brain 0.7 (0.0–2.5) FW 

 Hair 9.6 (1.1–19.8) DW 

 Woodmouse, Apodemus sylvaticus

 Great Britain

 In field with Hg-treated 

 wheat seed

 Liver Max. 7.1 FW Jenkins 1980

 Kidney Max. 11.7 FW 

 In chloralkali area 

 Liver Max. 0.5 FW 

 Kidney Max. 1.3 FW 

 Control area 

 Liver Max. 0.07 FW 

 Kidney Max. 0.3 FW 

 Roe deer, Capreolus capreolus 

 Males, Poland, 1977–78 

 From Hg-contaminated habitat 

 Muscle 0.047 FW Krynski 

 Liver 0.036 FW et al. 1982 

 Kidney 0.053 FW

 From uncontaminated area

 Muscle 0.013 FW

 Liver 0.015 FW

28
 Kidney 0.027 FW

 Beaver, Castor canadensis 

 Wisconsin, 1972–75 

 All tissues <0.09 FW Sheffy and 

 St. Amant 1982 

 Cat, Felis domesticus 

Ate fish from below chloralkali 

 plant, NW Ontario 

 Brain 6.9–16.4 FW Jenkins 1980

 Pancreas 4.3–4.9 FW

 Kidney 0.8–13.4 FW

 Liver 14.2–67.1 FW 

 Fur 121.0–392.0 FW 

 River otter, Lutra canadensis 

 Winnipeg River, 

 Manitoba, Canada, 1979–81

 Males

 Liver Max. 8.9 FW Kucera 1983

 Kidney Max. 6.5 FW 

 Brain Max. 3.1 FW 

 Females

 Liver Max. 3.9 FW 

 Kidney Max. 1.8 FW 

 Brain Max. 0.6 FW 

 Wisconsin, 1972–75 

 Brain 0.7 FW Sheffy and 

 Muscle 1.4 FW St. Amant 1982 

 Liver 3.3 (Max. 23.6) FW 

 Kidney 8.5 (Max. 20.9) FW 

 Fur

 Industrial area 9.5 (Max. 63.2) FW 

 Nonindustrial area 3.8 FW 

 Bobcat, Lynx rufus

 Hair

 Georgia USA

 Upper coastal plain 13.1 DW Jenkins 1980

 Lower coastal plain 0.9 DW 

 Mink, Mustela vision 

 Wisconsin, 1972–75 

 Brain 0.5 FW Sheffy and 

 Muscle 1.3 FW St. Amant 1982 

 Liver 2.1 (Max. 17.4) FW 

 Kidney 2.3 (Max. 12.5) FW 

29
 Fur

 Industrial area 10.5 (Max. 41.2) FW 

 Nonindustrial area 3.0 FW 

 Winnipeg River, 

 Manitoba, Canada, 1979–81

 Males

 Liver Max. 9.9 FW Kucera 1983

 Kidney Max. 6.4 FW 

 Brain Max. 2.4 FW 

 Females

 Liver Max. 10.7 FW 

 Kidney Max. 8.1 FW 

 Brain Max. 2.1 FW 

 Muskrat, Ondatra zibethicus

 Wisconsin, 1972–75 

 All tissues <0.06 FW Sheffy and 

 St. Amant 1982 

 Sheep, Ovis aries 

Grazing for 23 months on

 Hg-contaminated field 

 Diet (grass) 

 Winter 6.5 DW Edwards and

 Summer 1.9 DW Pumphery 1982 

 Lung Max. 4.0 FW 

 Kidney Max. 3.1 FW 

 Liver Max. 2.4 FW 

 Brain Max. 1.1 FW 

 Flesh <1.0 FW

 Harbor seal, 

 Phoca vitulina richardi 

 Liver

 California 269.0 (81.0–700.0) FW Jenkins 1980

 Oregon 0.3–68.0 FW

 Washington 1.3–60.0 FW

 Pribilof Islands 0.6–8.9 FW

 Raccoon, Procyon lotor 

 Wisconsin, 1972–75 

 Brain <0.02 FW Sheffy and 

 Muscle 0.08 FW St. Amant 1982 

 Kidney 1.4 FW 

 Liver 2.0 FW 

 Fur 3.8 FW 

 Gray squirrel, Sciurus carolinensis 

30
 Hair, Florida, 1974 

 Rural areas 0.43 FW Jenkins 1980

 Urban

 Age 0–1 1.0 (0.07–6.7) FW 

 Age >2 2.7 (0.30–9.2) FW 

 Striped dolphin, 

 Stenella coeruleoalba 

 Adults, Japan, 1977–80 

 Muscle

 Total Hg 15.2 FW Itano 

 Methyl Hg 5.3 FW et al. 1984a 

 Liver

 Total Hg 205.0 FW

 Methyl Hg 7.0 FW

 Kidney 

 Total Hg 14.7 FW 

 Methyl Hg 3.2 FW

 Whole body 

 Age 1 year 

 Total Hg 0.8 FW Itano 

 Methyl Hg 0.4 FW et al. 1984b 

 Age 3 years 

 Total Hg 1.8 FW

 Methyl Hg 1.0 FW

 Age 4 years 

 Total Hg 3.0 FW

 Methyl Hg 1.5 FW

 Age 14 years 

 Total Hg 4.5 FW

 Methyl Hg 2.6 FW

 Age 20 years 

 Total Hg 10.7 FW 

 Methyl Hg 3.5 FW

 Red fox, Vulpes vulpes

 Hair

 Georgia, USA 

 Upper coastal plain 2.3 DW Jenkins 1980

 Lower coastal plain 0.5 DW 

 Wisconsin, 1972–75 

 Fur 0.6 FW Sheffy and 

 Other tissues <0.14 FW St. Amant 1982 

California sea lion, 

 Zalophus californianus 

31
 Liver

 Mother 73.0–1,026.0 DW Jenkins 1980

 Pup 0.9–16.0 DW 

 Kidney 

 Mother 4.1–43.2 DW 

 Pup 0.6–6.7 DW 

aConcentrations are listed as mean, range, or maximum (Max.). 

bEach reference applies to the value in the same row and in the rows that follow for which no other reference is

indicated. 

Nationwide monitoring of whole fish during the period 1969 to 1981 demonstrated that the highest Hg 

concentrations (0.33 to 1.7 mg/kg FW) were in northern squawfish (Ptychocheilus oregonensis) from the 

Columbia River basin in the Pacific Northwest (Henderson and Shanks 1973; Lowe et al. 1985). Elevated Hg 

concentrations in this piscivorous species were attributed primarily to the presence of major cinnabar deposits 

and with Hg use associated with mineral mining in the Columbia River basin. Northern squawfish may have a 

natural tendency to accumulate high concentrations of mercury in their flesh--as is well known for older 

specimens of long-lived predatory fishes such as tunas, billfishes, bluefish (Pomatomus saltatrix), striped bass

(Morone saxatilis), northern pike (Esox lucius), and many species of sharks--but Hg uptake kinetics in squawfish 

requires further research (Lowe et al. 1985). 

Of 159 species of finfish and sharks from the coastal waters of Alaska, Hawaii, and the conterminous United 

States, mercury concentrations in muscle were usually less than 0.3 mg/kg fresh weight (Hall et al. 1978). Mean 

Hg concentrations in excess of 0.5 mg/kg fresh weight muscle were recorded in 31 species, including 10 

species of sharks and 4 species of billfishes; however, these 31 species accounted for less than 0.65% of the 

catch intended for human consumption (Hall et al. 1978). 

In birds, it is generally acknowledged that mercury concentrations are highest in species that eat fish and 

other birds. Residues were highest in kidney and liver, but total Hg contents were significantly modified by food 

preference and availability, and by migratory patterns (NAS 1978; Delbeke et al. 1984). Also, there is an inverse 

relationship between total Hg and percent methylmercury in tissues of various avian species (Norheim et al. 

1982; Karlog and Clausen 1983)--a pattern that seems to hold for all vertebrate organisms for which data are 

available. Diet and migration are the most important Hg modifiers in birds. For example, the higher levels of Hg 

in juvenile than in adult wood ducks (Aix sponsa) from Tennessee were related to dietary patterns: juveniles 

preferred insects, whereas adults preferred pondweed tubers; Hg residues were higher in the insects than in the 

pondweeds (Lindsay and Dimmick 1983). Concentrations of Hg in livers of Antarctic birds reflected Hg body 

burdens accumulated during migration, while the birds were overwintering near industrialized areas. 

Concentrations were highest in species that ate higher trophic levels of prey and were especially pronounced for 

skuas, Catharacta spp.; however, significant inherent interspecies differences were evident (Norheim et al. 

1982; Norheim and Kjos-Hanssen 1984). 

The significance of Hg residues in birds is not fully understood. For example, all eggs of the American bald 

eagle (Haliaeetus leucocephalus) collected Nationwide contained detectable levels of Hg, but the mean was 

0.15 mg Hg/kg (fresh weight basis) in eggs from unsuccessful nests vs. 0.11 in eggs from successful nests 

(Wiemeyer et al. 1984). Many other contaminants--especially organochlorine compounds--were in eagle eggs, 

and several were present at levels that potentially interfere with eagle reproduction (Wiemeyer et al. 1984). It is 

not now possible to implicate Hg as a major cause of unsuccessful eagle reproduction. 

Bird feathers have been used for some time as indicators of Hg loadings in terrestrial and marine 

environments. The keratin in bird feathers is not easily degradable, and Hg is probably associated firmly with the 

disulphide bonds of keratin. Consequently, it has been possible to compare Hg contents of feathers recently 

sampled with those from museum birds, thereby establishing a time series (Applequist et al. 1984). The most 

probable source of recent elevated Hg residues in feathers of the Finnish sparrowhawk (Accipiter nisus) was 

from consumption of avian granivores that had become contaminated as a result of eating seeds treated with

32
organomercury compounds; in 1981, 5.6 tons of methoxyethylmercury compounds were used in Finnish 

agriculture for protection of seeds against fungi (Solonen and Lodenius 1984). Captive Swedish eagle-owls 

(Bubo bubo), with low Hg content in feathers (<1.0 mg/kg DW), that were introduced into coastal areas quickly 

reflected the high (6.5 mg/kg) Hg levels in feathers of wild eagle-owls from that region. Captive birds released

into inland territories, where Hg levels were near background, did not accumulate Hg in feathers (Broo and

Odsjo 1981). Mercury levels in feathers of nestling Swedish gyrfalcons (Falco rusticolus) showed a better 

correlation with Hg levels in actual food items than with levels based on adult feathers. Mercury concentrations 

in feathers were higher in nestlings fed partly with aquatic bird species containing >0.07 mg Hg/kg in pectoral 

muscle than in nestlings fed willow grouse (Lagopus lagopus) and ptarmigan (Lagopus mutus), both of which 

contained <0.01 mg Hg/kg in pectoral muscle (Lindberg 1984). In some instances there was a substantial time 

lag, up to 10 years, between the introduction of a pesticide, such as alkylmercury, its subsequent banning, and 

measurable declines of Hg in feathers of several species of Swedish raptors; this was the case for various 

species of Falco, Haliaeetus, Bubo, Buteo, and Accipiter (Wallin 1984). Accordingly, a reduction in Hg content 

in feathers of free-living birds may be sufficient to establish an improved situation. 

Among mammals, marine pinnipeds usually contained the highest reported concentrations of Hg in tissues 

(Table 6). The relatively high concentrations appeared to be a result of natural processes rather than of 

anthropogenic activities, however, and probably did not represent a significant risk to pinniped health. In 

general, Hg concentrations increased significantly with increasing age of the organism, as shown (Figure 2) in 

the livers of harbor seal (Phoca groenlandica), grey seal (Halichoerus grypus), California sea lion (Zalophus 

californianus), and northern fur seal (Callorhinus ursinus). The mechanisms to account for this phenomenon in 

pinnipeds are similar to those reported by Itano et al. (1984 a,b, c) for the striped dolphin (Stenella 

coeruleoalba). They showed that tissue concentrations of mercury in striped dolphins increased with increasing 

age of the animal, reaching a plateau in 20 to 25 years; were highest in liver, although muscle accounted for 

about 90% of the total body Hg burden; were present in the methylated form in fetal and suckling stages, but the 

proportion of methylmercury decreased over time with no absolute increase after age 10 years; were excreted 

slowly by all developmental stages, and slowest in older dolphins (resulting in higher accumulations); and were 

correlated strongly with selenium concentrations in all age groups. It is probable that inorganic Hg and selenium 

were complexed in a 1:1 molar ratio, in a form biologically unavailable to marine mammals (and probably other 

mammals), thereby significantly decreasing the risk of mercury toxicosis to individuals with grossly elevated Hg 

body burdens (Eisler 1984, 1985). Large colonies of pinnipeds and, to a lesser extent, marine birds along the

western coast of the United States may make Hg available to mussels (Mytilus californianus) through fecal 

elimination of large amounts of Hg, resulting in abnormally high Hg levels in mussels from several west coast 

sites (Flegal et al. 1981). 

Among furbearers in the Wisconsin River drainage system, Hg burdens were higher in fish-eating than in

herbivorous species--i.e., river otter (Lutra canadensis) > mink (Mustela vison) > raccoon (Procyon lotor) > red 

fox (Vulpes fulva) > muskrat (Ondatra zibethicus) > beaver (Castor canadensis) (Sheffy and St. Amant 1982). In 

general, fur contained the highest Hg levels, followed by liver, kidney, muscle, and brain, in that order (Table 6; 

Sheffy and St. Amant 1982). Mercury levels in piscivorous furbearers collected from the Wisconsin River basin 

paralleled Hg levels in fish, crayfish, and bottom sediments from that system; levels in all compartments were 

highest about 30 km downstream from an area that supported 16 pulp and paper mills and a chloralkali plant 

(Sheffy and St. Amant 1982). Mink and river otter accumulated about 10X more Hg than did predatory fishes

from the same drainage areas--suggesting that these furbearers can serve as sensitive indicators of mercury, 

even at very low levels of Hg contamination (Kucera 1983). 

Domestic sheep (Ovis sp.) allowed to graze for 23 months on grass contaminated with Hg (up to 6.5 mg/kg 

dry weight) caused by atmospheric emissions of a nearby chloralkali site, retained about 0.1% of the total Hg 

taken in by ingestion and inhalation, although residues in flesh were negligible (Edwards and Pumphery 1982). 

It was concluded that contamination of grass as a result of atmospheric discharges of inorganic He from 

chloralkali sites causes no hazard, either directly to grazing animals or indirectly to humans who might ultimately 

consume their flesh. 

33
ACUTE AND CHRONIC TOXICITY 

GENERAL 

For all organisms tested, early developmental stages were the most sensitive, and organomercury 

compounds--especially methylmercury--were more toxic than inorganic forms. Numerous biological and abiotic 

factors modify the toxicity of Hg compounds, sometimes by an order of magnitude or more, but the mechanisms 

of action are not clear. 

Lethal concentrations of total Hg to sensitive, representative organisms varied from 0.1 to 2.0 ug/l of 

medium for aquatic fauna; from 2.2 to 31.0 mg/kg body weight (acute oral) and 4.0 to 40.0 mg/kg (dietary) for 

birds; and from 0.1 to 0.5 mg/kg body weight (daily dose) and 1.0 to 5.0 mg/kg (dietary) for mammals. 

AQUATIC ORGANISMS 

Toxic concentrations of mercury salts ranged from less than 0.1 ug/l to more than 200 ug/l for representative 

species of marine and freshwater organisms (Table 7). The lower concentrations of <2.0 ug/l recorded were

usually associated with early developmental stages, long exposures, and flowthrough tests (Table 7). Among 

metals tested, mercury was the most toxic to aquatic organisms, and organomercury compounds showed the 

greatest biocidal potential (Eisler 1981). In general, toxicity was higher at elevated temperatures (Armstrong

1979), at reduced salinities in marine organisms (McKenney and Costlow 1981), and in the presence of other 

metals such as zinc and lead (Parker 1979). 

Signs of acute mercury poisoning in fish included flaring of gill covers, increased frequency of respiratory 

movements, loss of equilibrium, and sluggishness (Armstrong 1979). Signs of chronic mercury poisoning 

included emaciation (due to appetite loss), brain lesions, cataracts, diminished response to change in light

intensity, inability to capture food, abnormal motor coordination, and various erratic behaviors (Armstrong 1979; 

Hawryshyn et al. 1982). Mercury residues in severely poisoned fish that died soon thereafter ranged (in mg/kg 

fresh weight) from 26 to 68 in liver, 16 to 20 in brain, and 5 to 7 in whole body (Armstrong 1979). 

Table 7. Toxicities of inorganic and organic mercury compounds to selected species of aquatic organisms. 

Chemical species, ecosystem, taxonomic Concentration 

group, species, and other variables Effecta (μg Hg/L medium) Reference 

Inorganic Mercury

 Freshwater

 Crustaceans 

 Crayfish, Orconectes limosus LC-50 (30 d) 2.0 EPA 1980 

 Cladoceran, Daphnia magna LC-50 (96 h) 5.0 EPA 1980 

 Cladoceran, Daphnia magna LC-50 (LT) 1.3–1.8 EPA 1980 

 Scud, Gammarus pseudolimnaeus LC-50 (96 h) 10.0 EPA 1980 

 Fish

 Rainbow trout, Salmo gairdneri 

 Juveniles LC-50 (96 h) 155.0–200.0 EPA 1980 

 Embryo-larva

 Static test LC-50 (28 d) 4.7 Birge et al. 1979 

Flowthrough test LC-50 (28 d) <0.1 Birge et al. 1979 

 Channel catfish, Ictalurus punctatus 

 Embryo-larva

34
 Static test LC-50 (10 d) 30.0 Birge et al. 1979 

Flowthrough test LC-50 (10 d) 0.3 Birge et al. 1979 

 Largemouth bass, Micropterus salmoides 

 Embryo-larva

Static test LC-50 (8 d) 140.0 Birge et al. 1979 

Flowthrough test LC-50 (8 d) 5.3 Birge et al. 1979 

 Brook trout, Salvelinus fontinalis LC-50 (LT) 0.3–0.9 EPA 1980 

 Fish, Notopterus notopterus LC-50 (96 h) 440.0 Verma and Tonk 1983 

 Amphibians 

 Narrow-mouthed toad, 

 Gastrophryne carolinensis

Embryo-larva LC-50 (96 h) 1.3 Birge et al. 1979 

 Treefrogs, Hyla spp. 

 Embryo-larva, 5 spp. LC-50 (96 h) 2.4–2.8 Birge et al. 1979 

 Leopard frog, Rana pipiens 

Embryo-larva LC-50 (96 h) 7.3 Birge et al. 1979 

 Cricket frog, Acris sp. 

Embryo-larva LC-50 (96 h) 10.4 Birge et al. 1979 

 Anurans, 4 spp. 

Embryo-larva LC-50 (96 h) 36.8–67.2 Birge et al. 1979 

 Marbled salamander, Ambystoma opacum

Embryo-larva LC-50 (96 h) 107.5 Birge et al. 1979 

 Marine 

 Protozoans 

 Ciliate, Uronema marinum LC-50 (24 h) 6.0 Parker 1979 

 Molluscs 

 Softshell clam, Mya arenaria LC-50 (168 h) 4.0 Eisler and 

 Hennekey 197 

 Hardshell clam, Mercenaria mercenaria

 Larva LC-50 (48 h) 4.8 EPA 1980 

 Larva LC-5 (9 d) 4.0 EPA 1980 

 American oyster, Crassostrea virginica 

 Embryo LC-5 (12 d) 3.3 EPA 1980 

 Larva LC-50 (48 h) 5.6 EPA 1980 

 Adults LC-50 (48 h) 5.5–10.2 EPA 1980 

 Blue mussel, Mytilus edulis LC-50 (96 h) 5.8 EPA 1985 

 Slipper limpet, Crepidula fornicata 

 Larva LC-50 (96 h) 60.0 Thain 1984 

 Adults LC-50 (96 h) 330.0 Thain 1984 

 Bay scallop, Argopecten irradians 

 Juveniles LC-50 (96 h) 89.0 Nelson 

 et al. 1976 

 Crustaceans 

35
 Fiddler crab, Uca pugilator 

 Zoea LC-50 (8 d) 1.8 EPA 1980 

 Mysid shrimp, Mysidopsis bahia 

Juveniles LC-50 (96 h) 3.5 Gentile et al. 1983 

Egg to egg LC-50 (LT) 1.8 Gentile et al. 1983 

 Dungeness crab, Cancer magister 

 Larva LC-50 (96 h) 6.6 Glickstein 1978 

 Copepod, Acartia tonsa, adult LC-50 (96 h) 10.0–15.0 EPA 1980 

 Prawn, Penaeus indicus 

 Postlarva LC-50 (48 h) 16.1 McClurg 1984 

 Postlarva LC-50 (96 h) 15.3 McClurg 1984 

 Annelids 

 Polychaete, Capitella capitata 

 Larva LC-50 (96 h) 14.0 EPA 1980 

 Fish

 Haddock, Melanogrammus aeglifinus

 Larvae LC-50 (96 h) 98.0 EPA 1980 

Organic Mercury

 Freshwater

 Planarians

 Flatworm, Dugesia dorotocephala 

Adult LC-0 (10 d) 200.0 Best et al. 1981 

 Adult LC-100 (5 d) 500.0 Best et al. 1981 

 Crustaceans 

 Cladoceran, Daphnia magna LC-50 (LT) 0.9–3.2 EPA 1980 

 Fish

 Rainbow trout 

 Larva LC-50 (96 h) 24.0 EPA 1980 

 Juvenile LC-50 (96 h) 5.0–42.0 EPA 1980 

 Brook trout 

 Yearling LC-50 (96 h) 65.0 EPA 1980 

 Marine 

 Crustaceans 

 Amphipod, Gammarus duebeni LC-50 (96 h) 150.0 EPA 1980 

aAbbreviations: LT = lifetime exposure; h = hours; d = days. 

BIRDS 

Signs of mercury poisoning in birds included muscular incoordination, falling, slowness, fluffed feathers, 

calmness, withdrawal, hyporeactivity, hypoactivity, and eyelid drooping. In acute oral exposures, signs appeared

as soon as 20 minutes postadministration in mallards and 2.5 hours in pheasants. Deaths occurred between 4 

and 48 hours in mallards and 2 and 6 days in pheasants; remission took up to 7 days (Hudson et al. 1984). In 

studies with coturnix (Coturnix coturnix coturnix), (Hill 1981) found that methylmercury was always more toxic 

than inorganic mercury, and that young birds were usually more sensitive than older birds. Furthermore, some 

birds poisoned by inorganic mercury recovered after treatment was withdrawn, but chicks that were fed 

36
methylmercury and later developed toxic signs usually died, even if treated feed was removed. Coturnix 

subjected to inorganic mercury, regardless of route of administration, showed a violent neurological dysfunction 

that ended in death 2 to 6 hours posttreatment. The withdrawal syndrome in coturnix poisoned by Hg 2+ was

usually preceded by intermittent, nearly undetectable tremors, coupled with aggressiveness towards cohorts; 

time from onset to remission was usually 3 to 5 days, but sometimes extended to 7 days. Coturnix poisoned by 

methylmercury appeared normal until 2 to 5 days posttreatment; then, ataxia and low body carriage with 

outstretched neck were often associated with walking. In advanced stages, coturnix lost locomotor coordination 

and did not recover; in mild to moderate clinical signs, recovery usually took at least 1 week (Hill 1981). 

Mercury toxicity to birds varies with the form of the element, dose, route of administration, species, sex, age, 

and physiological condition (.Fimreite 1979). For example, in northern bobwhite chicks fed diets containing 

methylmercury chloride, mortality was significantly lower when the solvent was acetone than when it was 

another carrier such as propylene glycol or corn oil (Spann et al. 1986). In addition, organomercury compounds 

interact with elevated temperatures and pesticides, such as DDE and parathion, to produce additive or morethan-additive toxicity, and with selenium to produce less-than-additive toxicity (Fimreite 1979). Acute oral 

toxicities of various mercury formulations ranged between 2.2 and about 31.0 mg/kg body weight for most avian 

species tested (Table 8). Similar data for other routes of administration were 4.0 to 40.0 mg/kg for diet and 8.0 

to 15.0 mg/kg body weight for intramuscular injection (Table 8). 

Residues of mercury in experimentally poisoned passerine birds usually exceeded 20 mg/kg fresh weight, 

and were similar to concentrations reported in wild birds that died of mercury poisoning (Finley et al. 1979). 

Mercury levels in tissues of poisoned wild birds were highest (45 to 126 mg/kg fresh weight) in red-winged 

blackbirds (Agelaius phoeniceus), intermediate in starlings (Sturnus vulgaris) and cowbirds (Molothrus ater), and 

lowest (21 to 54) in grackles (Quiscalus quiscula); in general, Hg residues were highest in the brain, followed by 

the liver, kidney, muscle, and carcass. Some avian species are more sensitive than passerines (Solonen and 

Lodenius 1984): liver residues (in mg Hg/kg dry weight) in birds experimentally killed by methylmercury ranged 

from 17 in red-tailed hawks (Buto jamaicensis) to 70 in jackdaws (Corvus monedula); and values were 

intermediate in ring-necked pheasants, kestrels (Falco tinnunculus), and magpies (Pica pica). Experimentally

poisoned grey herons (Ardea cinerea) seemed to be unusually resistant to Hg; lethal doses produced residues 

of 415 to 752 mg Hg/kg dry weight of liver (Van der Molen et al. 1982). However, levels of this magnitude were 

frequently encountered in livers from grey herons collected during a massive die-off in the Netherlands during a 

cold spell in 1976; the interaction effects of cold stress, mercury loading, and poor physical condition of the 

herons are unknown ((Ardea cinerea) in the Netherlands. Ardea 70:173-184Van der Molen et al. 1982). 

Table 8. Toxicity to birds of mercury administered by oral, dietary, or other routes. 

Route of administration 

(units), organism, and Exposure 

mercury formulation Concentration interval Effect Referencea 

Acute oral (mg Hg/kg 

body weight) 

 Chukar, Alectoris chukar

 Ethyl 26.9 Within 14 d LD-50 Hudson

 posttreatment et al. 1984 

 Mallard, Anas platyrhynchos

 Methyl 2.2–23.5 " LD-50 

 Ethyl 75.7 " LD-50 

 Phenyl 524.7 " LD-50 

 Northern bobwhite, 

 Colinus virginianus 

37
 Methyl 23.8 " LD-50 

 Coturnix, 

 Coturnix coturnix coturnix 

 Methyl 11.0–27.0 " LD-50 Hill 1981 

 Inorganic 26.0–54.0 " LD-50 

 Japanese quail,

 Coturnix japonica 

 Methyl 14.4–33.7 " LD-50 Hill and 

 Soares 1984;

 Hudson

 et al. 1984 

 Ethyl 21.4 " LD-50 Hudson

 et al. 1984 

 Inorganic 31.1 " LD-50 Hill and 

 Soares 1984

 Rock dove, Columba livia 

 Ethyl 22.8 " LD-50 Hudson

 et al. 1984 

 Fulvous whistling duck, 

 Dendrocygna bicolor 

 Methyl 37.8 " LD-50 

 Domestic chicken,

 Gallus domesticus 

 Phenyl 60.0 " LD-50 Mullins 

 et al. 1977 

 House sparrow,

 Passer domesticus 

 Methyl 12.6–37.8 Within 14 d LD-50 Hudson

 posttreatment et al. 1984 

 Gray partridge, Perdix perdix 

 Ethyl 17.6 " LD-50 

 Ring-necked pheasant, 

 Phasianus colchicus 

 Ethyl 11.5 " LD-50 

 Methyl 11.5–26.8 " LD-50 

 Phenyl 65.0–101.0 " LD-50 Mullins 

 et al. 1977; 

 Hudson

 et al. 1984 

 Prairie chicken, 

 Tympanuchus cupido

 Ethyl 11.5 " LD-50 Hudson

 et al. 1984 

38
Dietary (mg Hg/kg diet) 

 Coturnix

 Inorganic 32.0 Hatch-9 weeks LD-0 Hill 1981 

Inorganic 2,956–5,086 5 d + 7 d pt LD-50 

 Methyl 4.0 Hatch-9 weeks LD-0 

 Methyl 8.0 5 d Some Hill and 

 deaths Soares 1984

Methyl 31.0–47.0 5 d + 7 d pt LD-50 Hill 1981 

 Ring-necked pheasant 

 Ethyl 4.2 70 d LD-0b Spann 

Ethyl 12.5 70 d LD-50 et al. 1972 

 Ethyl 37.4 28 d LD-50 

 Ethyl 112.0 15 d LD-50 

 Japanese quail 

 Inorganic 

 In dry salt 500 28 d LD-86 El-Begearmi 

 In ethanol, et al. 1980 

 methanol, or water 500 28 d LD-55 

 In casein premix 500 28 d LD-33 

Birds, 4 spp. 

Methyl 40.0 6 to 11 d LD-33 Finley 

 et al. 1979 

Intramuscular injection 

(mg Hg/kg body weight) 

 Coturnix

 Methyl 8.0–33.0 Single dose LD-50 Hill 1981 

 Inorganic 15.0–50.0 Single dose LD-50 

 Rock dove

 Inorganic 10.0 Daily, 17 d Some Leander 

 deaths et al. 1977 

Yolk sac injection 

(ug Hg/egg) 

 Chicken 

 Methyl 15.0 Single dose Some Greener and

 deaths Kochen 1983

 Methyl 40.0-50.0 Single dose LD-50 

Applied to Egg Surface 

ug Hg/egg 

 Mallard 

 Methyl 3.0 Single dose LD-0 Hoffman and

 Methyl 9.0 Single dose Some Moore 1979 

 deaths

39
In drinking water (mg Hg/L) 

 Chicken 

 Inorganic 500.0 3 d Some Grissom and

 deaths Thaxton 1985

aReference cited applies to data in the same row and in the rows that immediately follow for which no reference 

is indicated. 

bReduction in egg production, 55% to 80%; embryonic survival sharply reduced.

Table 9. Toxicity of organomercury compounds to selected mammalian species. 

Dose, route of

 administration, and 

Organism other variables Effects Reference 

Dog, 0.1 to 0.25 mg/kg body High incidence Khera 1979 

Canis familiaris weight during entire of stillbirths 

pregnancy; oral route 

Cat, 0.25 mg/kg body Mean survival Eaton 

Felis domesticus weight daily for 90 time 78 days. et al. 1980 

days (total 80–90 Convulsions 

mg Hg); dietary starting at day 

route 68; all with 

signs by day 90. 

 Liver residues

 of survivors 

were 40.2 and 

 18.1 mg/kg 

 fresh weight for 

 total mercury and 

 inorganic mercury, 

 respectively 

Pig, Sus spp. 0.5 mg/kg body weight High incidence Khera 1979 

 during pregnancy; oral of stillbirths 

 route 

Rhesus monkey, 0.5 mg/kg body weight Maternally Khera 1979 

Macaca mulatta during days 20–30 of toxic, and 

 pregnancy abortient 

Mink, 1.0 mg/kg in diet Fatal to 100% Sheffy and 

Mustela vison in about 2 months St. Amant 1982 

 2 months 

River otter, >2.0 mg/kg in diet Fatal Kucera 1983

40
Lutra canadensis

Mink 5.0 mg/kg in diet All dead in 30 Sheffy and 

to 37 days. St. Amant 1982 

 Elevated residues 

 in kidney 

 (37.7 mg/kg 

 fresh weight) 

and liver (55.6) 

prior to death

Humans Various Lethal residues Khera 1979 

in tissues, in 

 mg/kg fresh 

 weight, were

>6.0 in brain,

>10.0 in liver,

 and >17.0 in 

 whole body 

Mule deer, 17.88 mg/kg LD-50 Hudson

Odocoileus hemionus body weight; single et al. 1984 

hemionus oral dose 

Harp seal, 25.0 mg/kg body Dead in 20 to Ronald 

Pagophilus weight daily; oral 26 days. et al. 1977 

groenlandicus route Blood Hg levels 

 just before 

 death were 

26.8 to 30.3 mg/L 

MAMMALS 

Methylmercury affects the central nervous system in man--especially the sensory, visual, and auditory areas 

concerned with coordination; the most severe effects lead to widespread brain damage, resulting in mental 

derangement, coma, and death (Clarkson and Marsh 1982). In mule deer (Odocoileus hemionus hemionus), 

after acute oral Hg poisoning was induced experimentally, additional signs included belching, bloody diarrhea, 

piloerection (hair more erect than usual), and loss of appetite (Hudson et al. 1984). The kidney is the probable 

critical organ in adult mammals due to the rapid degradation of phenylmercurials and methoxyethylmercurials to 

inorganic Hg compounds and subsequent translocation to the kidney (Suzuki 1979), whereas in the fetus the 

brain is the principal target (Khera 1979). Most human poisonings were associated with organomercury 

compounds used in agriculture as fungicides to protect cereal seed grain (Elhassani 1983); judging from 

anecdotal evidence, many wildlife species may have been similarly afflicted. Organomercury compounds, 

especially methylmercury, were the most toxic mercury species tested. Among sensitive species of mammals, 

death occurred at daily organomercury concentrations of 0.1 to 0.5 mg/kg body weight, or 1.0 to 5.0 mg/kg in 

the diet (Table 9). Larger animals such as mule deer and harp seals appear to be more resistant to Hg than 

smaller mammals such as mink, cats, dogs, pigs, monkeys, and river otters; the reasons for this difference are 

unknown, but may be related to differences in metabolism and detoxication rates. Tissue residues in fatally 

poisoned mammals (in mg Hg/kg fresh weight) were 6.0 in brain, 10.0 to 55.6 in liver, 17.0 in whole body, about 

30.0 in blood, and 37.7 in kidney (Table 9). 

41
OTHER GROUPS 

Methylmercury compounds at concentrations of 25.0 mg Hg/kg in soil were fatal to all tiger worms (Eisenia 

foetida) in 12 weeks; at 5.0 mg/kg, however, only 21% died in a similar period (Beyer et al. 1985). Inorganic 

mercury compounds were also toxic to earthworms (Octochaetus pattoni); in 60 days, 50% died at soil Hg levels 

of 0.79 mg/kg, and all died at 5.0 mg/kg (Abbasi and Soni 1983). 

SUBLETHAL EFFECTS 

GENERAL 

Mercury is a known mutagen, teratogen, and carcinogen. At comparatively low concentrations in birds and

mammals, it adversely affects reproduction, growth and development, behavior, blood and serum chemistry, 

motor coordination, vision, hearing, histology, and metabolism. It has a high potential for bioaccumulation and 

biomagnification, and is slow to depurate. Organomercury compounds were more effective in producing 

adverse effects than were inorganic Hg compounds; however, effects were significantly enhanced or 

ameliorated by numerous biotic and nonbiological modifiers. For sensitive aquatic species, adverse effects 

were observed at water concentrations of 0.03 to 0.1 ug Hg/l. For sensitive species of birds, harmful levels were 

640 ug Hg/kg body weight daily, or 50 to 500 ug Hg/kg in the diet; for sensitive mammals, these levels were 250 

ug Hg/kg body weight daily, or 1,100 ug Hg/kg diet. 

AQUATIC ORGANISMS 

Mercury at comparatively low concentrations adversely affects the reproduction, growth, behavior, 

metabolism, blood chemistry, osmoregulation, and oxygen exchange of marine and freshwater organisms. In 

general, the accumulation of mercury by aquatic biota is rapid, and depuration is slow. It is emphasized that

organomercury compounds, especially methylmercury, were significantly more effective than inorganic mercury 

compounds in producing adverse effects and accumulations. 

Reproduction was inhibited among sensitive species of aquatic organisms at water concentrations of 0.03 to 

1.6 ug Hg/l. In the planarian (Best et al. 1981); in the slipper limpet (Crepidula fornicata), spawning was delayed 

and fecundity was decreased at 0.25 ug Hg2+/l (Thain 1984); in the zebrafish (Brachydanio rerio), hatching 

success was reduced at 0.1 ug Hg2+/l and egg deposition was reduced at 0.8 ug/l (Armstrong 1979); fathead 

minnows (Pimephales promelas) exposed to 0.12 ug methylmercury/l for 3 months failed to reproduce (Birge et 

al. 1979); the leopard frog (Rana pipiens) did not metamorphose during exposure to 1.0 ug methylmercury/l for 

4 months (EPA 1980); and in the mysid shrimp (Mysidopsis bahia), the abortion rate increased and population 

size decreased after lifetime (i.e., 28 days) exposure to 1.6 ug/l of mercury as mercuric chloride (Gentile et al. 

1983). For sensitive marine invertebrates such as hydroids, protozoans, and mysid shrimp, reproduction was 

inhibited at concentrations between 1.1 and 2.5 ug Hg2+/l; this range was 5 to 71 ug/l for more resistant species

of marine invertebrates (Gentile et al. 1983). 

Reduced growth of sensitive species of aquatic organisms has been recorded at water concentrations of 

0.04 to 1.0 ug Hg/l. The rainbow trout (Salmo gairdneri) was the most sensitive species tested; growth 

reduction was observed after 64 days in 0.04 ug Hg/l as methylmercury, or 0.11 ug Hg/l as phenylmercury (EPA 

1980). In adults of the marine mollusc Crepidula fornicata, growth was reduced after 16 weeks in 0.25 ug

Hg2+/1 (Thain 1984). Growth inhibition was recorded in freshwater algae after exposure of 24 hours to 10 days 

to 0.3 to 0.6 ug organomercury/l, in brook trout (Salvelinus fontinalis) alevins after exposure for 21 days to 0.79 

ug organomercury/l (EPA 1980), and in the marine alga Scripsiella faeroense exposed to 1.0 ug Hg2+/l for 24 

hours (Kayser 1976). 

Adverse effects of mercury to aquatic organisms, in addition to those listed on reproduction and growth, 

have been documented at water concentrations of 0.88 to 5.0 ug/l: enzyme disruption in brook trout (Salvelinus 

fontinalis) embryos immersed for 17 days in solutions containing 0.88 ug/l, as methylmercury (EPA 1980); an 

increased incidence of frustule abnormalities and burst thecae in two species of marine algae during exposure 

to 1.0 ug Hg2+/l for 24 hours (Kayser 1976; Saboski 1977); arrested development of sea urchin larvae at 3.0 ug 

Hg2+/l for 40 hours (EPA 1980); decreased rate of intestinal transport of glucose, fructose, glycine, and 

42
tryptophan in the murrel (Channa punctatus) at 3.0 ug Hg2+/l for 30 days (Sastry et al. 1982); altered blood 

chemistry in striped bass (Morone saxatilis) at 5.0 ug Hg2+/l in 60 days (Dawson 1982); and decreased

respiration in striped bass 30 days postexposure after immersion for 30 to 120 days in 5.0 ug Hg2+/l (Armstrong 

1979; EPA 1980). In marine molluscs exposed to water concentrations of 6 to 10 ug Hg2+/l for 96 hours, the 

feeding of adults ceased and the swimming rate of larval stages declined (Thain 1984). At 44 ug Hg2+/l for 30 

days, the freshwater fish Notopterus notopterus showed generalized metabolic derangement (Verma and Tonk 

1983). In freshwater planarians exposed to 80 to 100 ug/l as methylmercury, behavior was modified and 

regeneration retarded (Best et al. 1981). And at high sublethal concentrations of methylmercury, rainbow trout 

were listless and darkly pigmented; appetite was reduced, and digestion was poor (Rodgers and Beamish 

1982). 

At lower trophic levels, the efficiency of mercury transfer was low through natural aquatic food chains; 

however, in animals of higher trophic levels, such as predatory teleosts and fish-eating birds and mammals, the 

transfer was markedly amplified (Eisler 1978, 1981).

High uptake and accumulation of mercury from the medium by representative species of marine and 

freshwater teleosts and invertebrates have been documented (Kopfler 1974; Eisler 1978, 1981; Birge et al. 

1979; Huckabee et al. 1979; EPA 1980, EPA. 1985; Stokes et al. 1981; Rodgers and Beamish 1982; Hirota et 

al. 1983; Clarkson et al. 1984; McClurg 1984; Niimi and Lowe-Jinde 1984; Ramamoorthy and Blumhagen 1984; 

Ribeyre and Boudou 1984; Thain 1984). Accumulation patterns were enhanced or significantly modified by 

numerous biological and abiotic factors (NAS 1978; Eisler 1978, 1981, 1984, 1985; EPA 1980, 1985; Stokes et 

al. 1981;Rodgers and Beamish 1982; Clarkson et al. 1984; Ramamoorthy and Blumhagen 1984; Ribeyre and 

Boudou 1984). In general, the accumulation of mercury was markedly enhanced at elevated water 

temperatures, reduced water salinity or hardness, reduced water pH, increased age of the organism, and 

reduced organic matter content of the medium; in the presence of zinc, cadmium, or selenium in solution; after 

increased duration. of exposure; and in the presence of increased nominal concentrations of protein-bound 

mercury. Uptake patterns were significantly modified by sex, sexual condition, prior history of exposure to Hg 

salts, the presence of complexing and chelating agents in solution, dietary composition, feeding niche, tissue 

specificity, and metabolism; however, trends were not consistent between species and it is difficult to generalize. 

In one example, Ribeyre and Boudou (1984) immersed rainbow trout in solutions containing 0.1 ug Hg/l, as 

methylmercury: after 30 days, bioconcentration factors (BCF) ranged from 28,300 for brain to 238,000 for 

spleen; values were intermediate for muscle (30,000), whole fish (36,000), blood (102,000), liver (110,000), 

kidney (137,000), and gill (163,000). The values may have been higher if exposure had extended beyond 30

days; Rodgers and Beamish (1982) showed that whole body Hg residues in rainbow trout subjected to mercury 

insult continued to increase for the first 66 days before stabilizing. When mercury was presented as inorganic 

mercuric ion at 0.1 ug/l for 30 days, BCF values were usually lower than in trout exposed to methylmercury: 

2,300 for muscle; 6,800 for brain; 7,000 for whole trout; 14,300 for blood; 25,000 for liver; 53,000 for kidney; 

68,600 for gill; and 521,000 for spleen (Ribeyre and Boudou 1984). The high BCF values recorded for rainbow 

trout were probably due to efficient uptake from water, coupled with slow depuration (Rodgers and Beamish 

1982). Whole body levels up to 100 mg Hg/kg were reportedly not lethal to rainbow trout, although 20 to 30

mg/kg were associated with reduced appetite, loss of equilibrium, and hyperplasia of gill epithelium (Niimi and 

Lowe-Jinde 1984). However, brook trout showed toxic signs and death at whole body residues of only 5 to 7 

mg/kg (Armstrong 1979). In another example, the marine copepod Acartia clausi, subjected to 0.05 ug/l of 

mercury and higher, reached equilibrium with the medium in only 24 hours. In that study (Hirota et al. 1983), 

BCF values for whole Acartia after 24-hour exposures were 14,360 for inorganic mercuric ion (0.05 ug/l) and, for 

methylmercury, 179,200 (0.05 ug/l) and 181,000 (0.1 ug/l). 

Elimination of accumulated mercury, both organic and inorganic, from aquatic organisms is a complex 

multicompartmental process, but appears to be largely dependent on its rate of biological assimilation. This 

rate, in turn, varies widely (20% to 90%) between species, for reasons as yet unexplained (NAS 1978). For 

example, mercury associated with dietary components that are not assimilated is eliminated rapidly with feces. 

The rest is absorbed across the gut and incorporated into tissues. This assimilated fraction of mercury is 

depurated much more slowly, at a rate positively correlated with the organism's metabolism (NAS 1978; 

Rodgers and Beamish 1982). Time to eliminate 50% of biologically assimilated mercury and its compounds (Tb 

1/2) is variable. Among various species of freshwater teleosts, Tb 1/2 values (in days) were 20 for guppies 

43
Poecilia reticulatus, 23 for goldfish Carassius auratus, 100 for northern pike, and 1,000 each for mosquitofish 

Gambusia affinis, brook trout, and rainbow trout (Huckabee et al. 1979). similar range in. Tb 1/2 values was 

recorded for invertebrates and marine fishes: 297 days for the crayfish Astacus fluviatilis, 435 days for mussel, 

481 days for the clam Tapes decussatus 1,030 days for the eel Anguilla vulgaris, and 1,200 days for the 

flounder Pleuronectes flesus (NAS 1978). 

Mercury-tolerant strains of bacteria (Colwell et al. 1976), protozoa (Berk et al. 1978), crustaceans (Green et

al. 1976; Weis 1976), and fish (Weis 1984) have been reported. It has been suggested that the mercuryresistant strains of bacteria that have been cultured or discovered may have application in mobilization or 

fixation of mercury from contaminated aquatic environments to the extent that polluted areas may become 

innocuous (Colwell et al. 1976). The marine protozoan Uronemia nigricans, after feeding on Hg-laden bacteria, 

acquired mercury tolerance within a single generation (Berk et al. 1978). The white shrimp (Penaeus setiferus), 

preexposed for 57 days to 1 ug Hg/l, did not differ from controls during either exposure or subsequent Hg stress 

experiments (Green et al. 1976); this observation suggested that nonsensitization or adaptation mechanisms 

are involved. The fiddler crab (Uca pugilator) seemed unusually resistant and showed negligible uptake or 

effects during exposure to 100 ug Hg/l for 2 weeks (Weis 1976). Reasons to account for Hg adaptation of the 

estuarine cyprinodontiform teleost Fundulus heteroclitus to both methylmercury and inorganic mercury are 

under investigation (Weis 1984). 

BIRDS 

Sublethal effects of mercury on birds, administered by a variety of routes, included adverse effects on 

growth, development, reproduction, blood and tissue chemistry, metabolism, and behavior; histopathology and 

bioaccumulation were also noted. 

The dietary route of administration is the most extensively studied pathway of avian Hg intake. Domestic 

chickens fed diets containing as little as 50 ug/kg of mercury, as methylmercury, contained elevated total Hg 

(2.0 mg/kg fresh weight) residues in liver and kidney after 28 weeks; at 150 ug/kg, residues ranged from 1.3 to 

3.7 mg/kg in heart, muscle, brain, kidney, and liver, in that general order; at 450 ug/kg in diets, residues in edible 

chicken tissues (3.3 to 8.2 mg/kg) were considered hazardous to human consumers, although no overt signs of 

mercury toxicosis were observed in the chickens (March et al. 1983). High inorganic mercury levels (500 mg/l) 

in drinking water of chickens decreased growth rate and food and water consumption, and elevated hemoglobin, 

hematocrit, and erythrocyte content within 3 days (Grissom and Thaxton 1985). The dietary concentration of 0.5 

mg Hg/kg dry weight (equivalent to about 0.1 mg/kg fresh weight) in the form of methylmercury was fed to three 

generations of mallards (Heinz 1979). Females laid a greater percentage of their eggs outside nest boxes than 

did controls, and also laid fewer eggs and produced fewer ducklings. Ducklings from parents fed methylmercury 

were less responsive than controls to tape-recorded maternal calls, but were hyperresponsive to a fright 

stimulus in avoidance tests. The tissues and eggs of ducks and other species of birds collected in the wild have 

sometimes contained levels of mercury equal to, or far exceeding, those associated with reproductive and 

behavioral deficiencies in domestic mallards (e.g., 9 to 11 mg/kg in feathers; >2.0 mg/kg in other tissues); 

therefore, it is possible that reproduction and behavior of wild birds have been modified by methylmercury 

contamination (Heinz 1979). Tissue mercury residues of wild-strain mallards and game-farm mallards were not 

significantly different after the birds were fed diets containing 0.5 mg Hg/kg as methylmercury for extended 

periods--indicating that game-farm mallards are suitable substitutes for wild mallards in toxicological evaluations 

(Heinz 1980). Dietary concentrations of 1.1 mg total Hg/kg have been associated with kidney lesions in juvenile 

starlings (Sturnus vulgaris) and with elevated residues in the liver (6.5 mg/kg dry weight and kidney (36.3 

mg/kg), after exposure for 8 >weeks (Nicholson and Osborn 1984). In American black ducks (Anas rubripes) 

fed diets containing 3.0 mg Hg/kg as methylmercury for 28 weeks, reproduction was significantly inhibited; 

tissue residues were elevated in kidney (16.0 mg/kg fresh weight) and liver (23.0 mg/kg); and brain lesions 

characteristic of mercury poisoning were present (Finley and Stendell 1978). Japanese quail (Coturnix

japonica) fed diets containing 8 mg Hg/kg of inorganic mercury for 3 weeks had depressed gonad weights; 

those fed 3 mg/kg inorganic mercury or 1 mg/kg methylmercury for 9 weeks showed alterations in brain and 

plasma enzyme activities (Hill and Soares 1984). Grossly elevated tissue residues of 400 mg/kg in feathers and 

17 to 130 mg/kg in other tissues were measured in gray partridge (Perdix perdix) after dietary exposure of 20 to 

25 mg total Hg/kg for 4 weeks (McEwen et al. 1973). 

44
Mercury exposure by immersion and oral administration have caused reproductive and behavorial 

modifications. Brief immersion of mallard eggs in solutions of methylmercury resulted in a significant incidence 

of skeletal embryonic aberrations at dosages of 1.0 ug Hg/egg, and higher; no increases in embryonic 

malformations were noted at 0.3 ug Hg/egg (Hoffman and Moore 1979). Reduced reproductive ability was 

noted in grey pheasants ingesting 640 ug Hg (as organomercury)/kg body weight daily for 30 days (McEwen et 

al. 1973); similar results were observed in ring-necked pheasants (Spann et al. 1972; Mullins et al. 1977). 

Behavioral alterations were noted in pigeons (Columba livia) given 3,000 ug inorganic Hg/kg body daily for 17 

days (Leander et al. 1977) or 1,000 ug/kg body weight of methylmercury for 5 weeks (Evans et al. 1982). 

Observed behavioral changes in posture and motor coordination of pigeons were permanent after the brain 

accumulated >12,000 ug Hg/kg fresh weight, and were similar to the "spastic paralysis" observed in wild crows 

during the Minamata, Japan, outbreak of the 1950's, although both species survived for years with these signs 

(Evans et al. 1982). 

Mercury residues of 790 to 2,000 ug/kg in egg, and 5,000 to 40,000 ug/kg in feathers, are linked to impaired 

reproduction in various bird species (Spann et al. 1972; NAS 1978; Heinz 1979; Fimreite 1979; Solonen and 

Lodenius 1984). Residues in eggs of 1,300 to 2,000 ug Hg/kg fresh weight were associated with reduced 

hatching success in white-tailed sea-eagles (Haliaeetus albicilla), the common loon (Gavia immer), and in 

several seed-eating species (Fimreite 1979); this range was 900 to 3,100 ug/kg for ring-necked pheasant 

(Spann et al. 1972), and 790 to 860 ug/kg for mallards (Heinz 1979). Residues of 5,000 to 11,000 ug Hg/kg in 

feathers of various species of birds have been associated with reduced hatch of eggs and with sterility (NAS

1978). Sterility was observed in the Finnish sparrow hawk (Accipiter nisus) at mercury concentrations of 40,000 

ug/kg in feathers (Solonen and Lodenius 1984). Chicks of the common tern (Sterna hirundo) from a colony in 

Long Island, New York, with abnormal feather loss, had significantly elevated mercury levels in blood and liver 

(Gochfeld 1980); however, the linkage of feather loss to mercury contamination requires further examination.

Interaction effects of mercury with other contaminants, such as herbicides and pesticides, could intensify 

hazards to avian populations (Mullins et al. 1977). For example, a striking parallel exists between levels of Hg 

and of DDT and its metabolites in birds of prey, suggesting the existence of common ecotoxicological 

mechanisms (Delbeke et al. 1984; Wiemeyer et al. 1984); additional research is clearly needed. 

MAMMALS 

Mercury has no known physiological function (EPA 1985). In humans and other mammals, it causes 

teratogenic, mutagenic, and carcinogenic effects; the fetus is the most sensitive life stage (NAS 1978; Chang 

1979; Khera 1979; EPA 1980, 1985; Elhassani 1983; Greener and Kochen 1983; Clarkson et al. 1984). 

Methylmercury irreversibly destroys the neurons of the central nervous system. Frequently, a substantial latent 

period intervenes between the cessation of exposure to Hg and the onset of signs and symptoms; this interval is 

usually measured in weeks or months, but sometimes in years (Clarkson et al. 1984). At high sublethal doses in 

man, mercury causes cerebral palsy, gross motor and mental impairment, speech disturbances, blindness,

deafness, microcephaly, intestinal disturbances, tremors, and tissue pathology (Chang 1979; EPA 1980, 1985; 

Elhassani 1983; Clarkson et al. 1984). Pathological and other effects of Hg may vary from organ to organ, 

depending on factors such as the effective toxic dose in the organ, the compound involved and its metabolism 

within the organ, the duration of exposure, and the other contaminants to which the animal is concurrently 

exposed (Chang 1979). Many compounds--especially salts of selenium--protect humans and other animals 

against mercury toxicity, although their mode of action is not clear (NAS 1978; Chang 1979; EPA 1980, 1985; 

Eisler 1985). 

Adverse effects of organomercury compounds to selected species of mammals have been recorded at 

administered doses of 0.25 mg Hg/kg body weight daily, dietary levels of 1.1 mg/kg, and blood Hg levels of 1.2 

mg/l (Table 10). 

Mercury transfer and biomagnification through mammalian food chains is well documented (Galster 1976; 

NAS 1978; Eaton et al. 1980; Eisler 1981; Huckabee et al. 1981; Sheffy and St. Amant 1982; Kucera 1983;

Clarkson et al. 1984; Wren 1986), but considerable variation exists. Among terrestrial mammals, for example, 

herbivores such as mule deer, moose (Alces alces), caribou (Rangifer tarandus), and various species of rabbits 

usually contained less than 1.0 mg Hg/kg fresh weight in liver and kidney, but carnivores such as the marten 

(Martes martes), polecat (Mustela putorius), and red fox (Vulpes vulpes) frequently contained more than 30

mg/kg NAS 1978). The usually higher mercury concentrations in fish-eating furbearers than in herbivorous 

45
species seemed to reflect the amounts of fish and other aquatic organisms in the diet. In river otter and mink

from the Wisconsin River drainage system, Hg levels paralleled those recorded in fish, crayfish, and bottom

sediments at that location. Highest Hg levels in all samples were recorded about 30 km downstream from an 

area that supported 16 pulp and paper mills and a chloralkali plant; residues were highest in the fur, followed by 

the liver, kidney, muscle, and brain (Sheffy and St. Amant 1982). 

In marine mammals, more than 90 % of the mercury content is inorganic; however, enough methylmercury 

occurs in selected tissues to result in the accumulation of high tissue concentrations of methylmercury in 

humans and wildlife consuming such meat (Clarkson et al. 1984). The liver of the ringed seal (Phoca hispida) 

normally contains 27,000 to 187,000 ug Hg/kg fresh weight, and is a traditional and common food of the coastal 

Inuit people (Eaton et al. 1980). Although levels of Hg in hair (109,000 ug/kg) and blood (37 ug/l) of Inuits were 

grossly elevated, no symptoms of Hg poisoning were evident in the coastal Inuits. Similar high concentrations 

have been reported for Alaskan Eskimo mothers who, during pregnancy, ate seal oil twice a day, and seal- meat 

or fish from the Yukon-Kuskokwim Coast every day (Galster 1976). Despite the extremely high total Hg content 

of seal liver, only the small organomercury component was absorbed and appeared in the tissues. Cats fed a 

diet of seal liver (26,000 ug Hg/kg fresh weight) for 90 days showed no neurologic or histopathologic signs 

(Eaton et al. 1980). It seems that the toxic potential of seal liver in terms of accumulated tissue levels in cats 

(up to 862 ug total Hg/l blood, and 7,600 ug total Hg/kg hair) is better indicated by the organomercury fraction in 

seal liver than by the concentration of total Hg (Eaton et al. 1980). 

Table 10. Sublethal effects of organomercury compounds administered to selected species of mammals. 

Dose, and other 

Organism variables Effect Reference 

Rhesus monkey, 16 μg/kg body No measurable Khera 1979 

 Macaca mulatta weight daily on eff ect on 

days 20 to 30 of reproduction

 pregnancy 

Human, adult 50 μg/day Risk of Clarkson 

paresthesia, et al. 1984 

 0.3% (burningprickling sensation of 

 skin) 

Human, adult 200 μg/day Risk of Clarkson 

paresthesia, 8% et al. 1984 

Cat, Felis 250 μg/kg body Increased Khera 1979 

 domesticus weight daily on incidence of 

days 10 to 58 of anomalous 

gestation; oral route fetuses

Harp seal, 250 μg/kg body Residues of Ronald 

 Pagophilus weight daily for 47,200 to et al. 1977; 

 groenlandicus 90 days; dietary 82,500 μg/kg Ramprashad

route fresh weight and Ronald 1977 

in liver, kidney, and 

 muscle; histopathology 

46
of middle ear 

Rat, Rattus sp. 500 μg/kg body Reduced Khera 1979 

 weight daily; fertility 

 oral route 

Human, adult 1,000 μg/day Risk of Clarkson et 

 paresthesia, 50% al. 1984 

Mink, 1,100 μg/kg Residues of Kucera 1983

 Mustela vison in diet 7,100 to 

 9,300 μg/kg 

 in brain; 

signs of poisoning 

Rat 2,000 μg/kg Adverse Suzuki 1979 

in diet (as behavioral 

Pacific blue changes in 

 marlin); gestation offspring 

 through postnatal day 16 

Rat 13,300 to Impaired Wu et al. 

 50,000 μg/kg cutaneous 1985 

 body weight sensitivity 

 daily for 5 and hearing 

days; up to one 

 subcutaneous year post- 

 injection treatment 

Monkeys, Various Visual disturbances Suzuki 1979 

 Macaca spp. at blood Hg levels 

of 1,200 to 4,000 

μg/L or brain Hg 

levels of 6,000 

to 9,000 μg/kg; tremors at

blood Hg levels of 2,000 to

 10,000 μg/L; 

kidney pathology at 

 brain Hg levels

of 1,500 μg/kg 

Human, adult Various Symptoms of Suzuki 1979 

 poisoning 

evident at residues of 

1,200 μg Hg/L 

 blood, 2,000 

to 3,000 μg/kg whole body, 

or 3,400 μg/kg hair 

47
Mice, Mus spp. Various Residues of Suzuki 1979 

2,000 to 5,000 

μg/kg hair or 

>10,000 μg/kg brain 

 associated with motor 

 incoordination 

 and decreased 

swimming ability; no 

observable effect at 

 <2,000 μg/kg hair 

Human, infant Various Severe effects Elhassani 

at blood Hg 1983 

levels of 3,000 μg/L 

Retention of mercury by mammalian tissues is longer for organomercury compounds (especially 

methylmercury) than for inorganic mercury compounds (NAS 1978; Clarkson and Marsh 1982; Elhassani 1983; 

Clarkson et al. 1984). Excretion of all Hg species follows a complex, variable, multicompartmental pattern; the 

longer-lived chemical Hg species have a biological half-life that ranges from about 1.7 days in human lung to 

1.36 years in whole body of various pinnipeds. 

OTHER GROUPS 

Methylmercury compounds have induced abnormal sex chromosomes in the fruit fly (Drosophila

melanogaster) (NAS 1978; Khera 1979). Earthworms (Eisenia foetida) exposed to soil containing 

methylmercury concentrations of 5.0 mg Hg/kg--typical of soil Hg levels near chloralkali plants--showed a 

significant reduction in the number of segments regenerated after 12 weeks, and contained 85 mg Hg/kg on a 

whole body fresh weight basis. Regeneration was normal at soil Hg levels of 1.0 mg/kg, although body burdens 

up to 27 mg/kg were recorded. It was concluded that soil contaminated with methylmercury posed a greater 

hazard to the predators of earthworms than to the earthworms (Beyer et al. 1985). Studies with a different 

species of earthworm (Octochaetus pattoni) and mercuric chloride, demonstrated a progressive initial increase 

in reproduction as soil mercury levels increased from 0.0 to the 60-day lethal level of 5.0 mg/kg (Abbasi and 

Soni 1983). 

CURRENT RECOMMENDATIONS 

Proposed mercury criteria for the protection of sensitive aquatic organisms, birds, and mammals, as well as 

human health, are shown in Table 11. In almost every instance, these criteria are listed as concentrations of 

total Hg, with most, if not all, the Hg present as an organomercury species. 

In 1980, the U.S. Environmental Protection Agency's proposed mercury criteria for freshwater aquatic life 

protection were 0.00057 ug/l (24-hour average), not to exceed 0.0017 ug/l at any time; these criteria seemed to 

afford a high degree of protection to freshwater biota, as judged by survival, bioconcentration, and 

biomagnification. Literature documented in this paper showed that mercury concentrations in water of 0.1 to 2.0 

ug/l were fatal to sensitive aquatic species and that concentrations of 0.03 to 0.1 ug/l were associated with 

significant sublethal effects. The 1980 proposed freshwater criteria provided safety factors for acute toxicities of 

175X to 3,508X based on the 24-hour average, and 58X to 1,176X based on the maximum permissible 

concentration (Table 11). For protection against sublethal effects, these values were 53X to 175X based on the 

24-hour mean, and 18X to 59X based on the maximum permissible concentration (Table 11). However, the 

most current freshwater criteria of 0.012 ug/l, not to exceed 2.4 ug/l (Table 11; EPA 1985), dramatically reduces 

the level of protection afforded aquatic biota: safety factors for acute toxicities are now 8X to 167X based on the 

96-hour average, and only 0.04X to 0.8X based on the maximum permissible concentration. For protection

against sublethal effects, these values were 2X to 8X based on the 4-day average, and only 0.01X to 0.04X 

based on the maximum permissible concentration, or essentially no significant protection. 

48
The proposed saltwater criteria of EPA (1980) for mercury and marine life were unsatisfactory. Proposed 

saltwater values of 0.025 ug/l (24-hour average), not to exceed 3.7 ug/l at any time (Table 11), provided safety 

factors of 4X to 80X against acute toxicity (based on 24-hour average), but less than 0.5X based on the 

maximum permissible level. For protection against sublethal damage effects, the safety factors computed were 

1.2X to 4X (based on 24-hour average) and less than 0.03X (based on maximum allowable concentration). The 

most recent saltwater criteria of 0.025 ug/l, not to exceed 2.1 ug/l (Table 11; EPA 1985), does not appear to 

offer a substantive increase in protection to marine life, when compared to criteria proposed 5 years earlier 

(EPA 1980). It seems that some downward modification is needed in the proposed Hg saltwater criteria if 

marine and estuarine biota are to be provided even minimal protection. 

Table 11. Proposed mercury criteria for protection of various resources and human health. 

Resource and criterion Mercury 

(units in parentheses) concentration Reference 

Aquatic life 

Freshwater Total recoverable Hg EPA 1980 

(μg/L) <0.00057 (24 h 

 average), not to 

 exceed 0.0017 at any 

 time

 <0.012, 4-day average EPA 1985 

 (not to be exceeded 

 more than once every 

 3 years; <2.4, one-hour

 average (not to be 

 exceeded more than once 

 every 3 years)a 

Saltwater Total recoverable Hg EPA 1980 

(μg/L) <0.025 (24 h

 average), not to 

 exceed 3.7 at any time 

 <0.025, 4-day average EPA 1985 

 (not to be exceeded 

 more than once every 

 3 years); <2.1, one-hour

 average (not to be 

 exceeded more than once 

 every 3 years)a 

 Freshwater (μg/L) 

Inland surface <10.0 from point source Abbasi and 

 waters, India discharge Soni 1983 

Fish (μg/kg fresh weight) 

 Brook trout, 

 Salvelinus fontinalis

49
 Whole body <5,000 EPA 1980, 1985 

Wildlife 

 Birds

 Tissue residues 

 (μg/kg fresh weight) 

 Feather <5,000 NAS 1978 

 Egg

 Mallard,

 Anas platyrhynchos <900 Heinz 1979 

 Ring-necked pheasant, 

 Phasianus colchicus <900 Spann et al. 1972 

 Various species 1,300–2,000 Fimreite 1979

Diet (μg/kg fresh weight) 50 to <100 Heinz 1979; 

 March et al. 1983 

Daily dose (μg/kg body 

weight) <640 Spann et al. 1972; 

 McEwen et al. 1973; 

 Mullins et al. 1977 

Mammals

Tissue residues (μg/kg 

 fresh weight) 

 Kidney <1,100 EPA 1980 

 Blood <1,200 Suzuki 1979 

 Brain <1,500 Suzuki 1979 

 Hair <2,000 Suzuki 1979 

Diet (μg/kg fresh weight) <1,100 Kucera 1979

 Daily dosage (μg/kg 

 body weight) <250 Ramprashad and 

 Ronald 1977;

 Ronald et al. 1977; 

 Khera 1979 

Human Health

 Tissue residues 

(μg/kg fresh weight) 

 Blood <200 Galster 1976 

Hair <6,000 Lodenius et al. 1983 

 Water (μg/L)

 Potable <2.0 NAS 1978 

 Protection from toxic

properties of Hg through 

 consumption of 

 contaminated aquatic 

 organisms <0.146 EPA 1980 

50
 Protection from toxic

properties of Hg from 

 ingestion of water 

 plus consumption of 

 resident aquatic 

 organisms <0.144 EPA 1980 

Fish and seafood 

 Acceptable intake (μg)

Daily, 60 kg adult 25 Khera 1979 

Weekly, 70 kg adult 200 Khera 1979 

Weekly, adult 500 Lodenius et al. 1983 

 Pregnant women 

(μg/kg fresh weight) <250 Khera 1979 

 Various locations 

 (μg/kg fresh weight) 

 Japan <400 NAS 1978 

 Canada, West Germany, 

 U.S.A. <500 NAS 1978 

 Australia <500 (mean), not 

 to exceed 1,500 

 in any sample Lyle 1984 

 Finland <1,000 Lodenius et al. 1983 

 Scandinavia <1,000 Suckcharoen and 

 Lodenius 1983 

 Sweden <1,000 NAS 1978 

 U.S.A. <1,000 EPA 1980, 1985; 

 Barber et al. 1984; 

 Miller and Jude 1984 

Foods of animal origin

(μg/kg fresh weight) 

Livestock tissues <500 Best et al. 1981 

Wildlife tissues <50 Krynski et al. 1982 

 Breast muscle

 Domestic poultry <500 NAS 1978 

 Ducks (wildlife) <1,000 Lindsay and 

 Dimmick 1983

 All foods 

Adult weekly intake (μg) 

 As total Hg <150 NAS 1978 

 As methylmercury <100 NAS 1978 

 Various locations 

 (μg/kg fresh weight) 

 Australia 10 to 100 NAS 1978 

51
 Benelux countries <30 NAS 1978 

 Brazil <50 NAS 1978 

 Canada <500 Bodaly et al. 1984 

 U.S.A. <1,000 Bodaly et al. 1984 

aAll mercury that passes through a 0.45-mm membrane filter after the sample is acidified to pH 1.5 to 2.0 with 

nitric acid. 

The significance of elevated Hg residues in tissues of aquatic organisms is not fully understood. 

Concentrations >1,000 ug Hg/kg fresh weight can occur in various tissues of selected species of fish and 

aquatic mammals eaten by humans. But it would be incorrect to assume that aquatic food chains--especially 

marine food chains--incorporate Hg exclusively from anthropogenic activities (Barber et al. 1984). Some 

organisms, however, do contain Hg tissue residues associated with known adverse effects to the organism and 

its predators. Thus, whole body residues of 5,000 to 7,000 ug Hg/kg fresh weight in brook trout eventually 

proved fatal to that species (EPA 1980). To protect sensitive species of mammals and birds that regularly 

consume fish and other aquatic organisms, total mercury concentrations in these food items should probably not 

exceed 100 ug/kg for avian protection, or 1,100 ug/kg for small mammals (Table 11). By comparison, proposed 

Hg levels in fish and seafood, in ug/kg fresh weight, for human health protection should not exceed 250 for 

expectant mothers, and 400 to 1,000 for adults worldwide (Table 11). 

Since long-lived, slow-growing, high-trophic-positon aquatic organisms usually contain the highest tissue 

mercury residues, some fisheries managers have proposed a legal maximum limit based on fish length or body 

weight, or alternatively, constraining the mean Hg concentration of the entire catch to a nominated level. In the 

Australian shark fishery, for example, implementation of a maximum length restriction (to a nominated level of 

500 ug Hg/kg), would result in retention of less than half of the present catch of seven species (Lyle 1984). 

Among sensitive avian species, adverse effects--predominantly on reproduction--have been reported at 

mercury concentrations (in ug/kg fresh weight) of 5,000 in feather, 900 in egg, 50 to 100 in diet, and daily 

administered doses of 640 on a body weight basis (Table 11). Although low Hg concentrations--e.g., 50 ug/kg 

in the diets of domestic chickens--sometimes produced no adverse effects on chickens, the tissue residues of 

Hg were sufficiently elevated to pose a hazard to human consumers (March et al. 1983). In contrast, in eggs of 

the American bald eagle (with 150 ug Hg/kg and low hatch), other contaminants present--especially 

organochlorine compounds--probably had a greater effect on hatchability than did Hg (Wiemeyer et al. 1984). 

Mammals, such as the domestic cat and the harp seal, showed birth defects, histopathology, and elevated

tissue residues at doses of 250 ug Hg/kg body weight daily (Table 11). The mink, at dietary levels of 1,100 ug 

Hg/kg, had signs of mercury poisoning; Hg residues in mink brain at this dietary level ranged from 7,100 to

9,300 ug/kg (Kucera 1983). Tissue residues in kidney, blood, brain, and hair in excess of 1,100 ug Hg/kg in

other nonhuman mammals are usually considered presumptive evidence of significant Hg contamination (Table 

11). 

At this point, it seems that four courses of action are warranted. First, toxic mercurials in agriculture and 

industry should be replaced by less toxic substitutes. Second, controls should be applied at the point of origin to 

prevent the discharge of potentially harmful Hg wastes. Third, continued periodic monitoring of fishery and 

wildlife resources is important, especially in areas with potential for reservoir development, in light of the 

hypothesis that increased flooding increases the availability of Hg to biota. And finally, additional research is

needed on mercury accumulation and detoxication in comparatively pristine ecosystems. 

52
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Figure 1. Major transformations of mercury in the environment (modified from Beijer and Jernelov 1979). 

62
Figure 2. Mercury concentrations in livers of four species of pinniped mammals (from Eisler 1984). 

63