1

United States

Environmental Protection

Agency

Office of Water

4305

EPA-823-F-01-011

June 2001

Fact Sheet

Mercury Update: Impact on Fish Advisories

Mercury is distributed throughout the environment from both natural sources and human activities. Methylmercury

is the main form of organic mercury found in the environment and is the form that accumulates in both fish and

human tissues. Several instances of methylmercury poisoning through consumption of contaminated food have

occurred; these resulted in central nervous system effects such as impairment of vision, motor in-coordination,

loss of feeling, and, at high doses, seizures, very severe neurological impairment, and death. Methylmercury has

also been shown to be a developmental toxicant, causing subtle to severe neurological effects. EPA considers

there is sufficient evidence for methylmercury to be considered a developmental toxicant, and to be of concern for

potential human germ cell mutagenicity. As of December 2000, 41 states have issued 2,242 fish advisories for

mercury. These advisories inform the public that concentrations of mercury have been found in local fish at levels

of public health concern. State advisories recommend either limiting or avoiding consumption of certain fish from

specific waterbodies or, in some cases, from specific waterbody types (e.g., all freshwater lakes or rivers).

Sources of Mercury in the Environment 

Mercury is found in the environment in the metallic

form and in different inorganic and organic forms.

Most of the mercury in the atmosphere is elemental

mercury vapor and inorganic mercury; most of the

mercury in water, soil, plants, and animals is

inorganic and organic mercury (primarily methylmercury). 

Mercury occurs naturally and is distributed

throughout the environment by both natural

processes and human activities. Solid waste

incineration and fossil fuel combustion facilities

contribute approximately 87% of the emissions of

mercury in the United States. Other sources of

mercury releases to the air include mining and

smelting, industrial processes involving the use of

mercury such as chlor-alkali production facilities

and production of cement. 

Mercury is released to surface waters from naturally

occurring mercury in rocks and soils and from

industrial activities, including pulp and paper mills,

leather tanning, electroplating, and chemical

manufacturing. Wastewater treatment facilities may

also release mercury to water. An indirect source of

mercury to surface waters is mercury in the air; it is

deposited from rain and other processes directly to

water surfaces and to soils. Mercury also may be

mobilized from sediments if disturbed (e.g.,

flooding, dredging).

Sources of mercury in soil include direct application

of fertilizers and fungicides and disposal of solid

waste, including batteries and thermometers, to

landfills. The disposal of municipal incinerator ash

in landfills and the application of sewage sludge to

crop land result in increased levels of mercury in

soil. Mercury in air may also be deposited in soil and

sediments.

Fate and Transport of Mercury

The global cycling of mercury is a complex process. 

Mercury evaporates from soils and surface waters to

the atmosphere, is redeposited on land and surface

water, and then is absorbed by soil or sediments.

After redeposition on land and water, mercury is

commonly volatilized back to the atmosphere as a

gas or as adherents to particulates.

Mercury exists in a number of inorganic and organic

forms in water. Methylmercury, the most common

organic form of mercury, quickly enters the aquatic

food chain. In most adult fish, 90% to 100% of the

The purpose of this fact sheet is to summarize current information on sources, fate and transport, occurrence

in human tissues, range of concentrations in fish tissue, fish advisories, fish consumption limits, toxicity, and

regulations for mercury. The fact sheets also illustrate how this information may be used for developing fish

consumption advisories. An electronic version of this fact sheet and fact sheets for dioxins/furans, PCBs,

and toxaphene are available at http://www.epa.gov/OST/fish. Future revisions will be posted on the web as

they become available.
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mercury is methylmercury. Methylmercury is found

primarily in the fish muscle (fillets) bound to

proteins. Skinning and trimming the fish does not

significantly reduce the mercury concentration in the

fillet, nor is it removed by cooking processes. 

Because moisture is lost during cooking, the

concentration of mercury after cooking is actually

higher than it is in the fresh uncooked fish.

Once released into the environment, inorganic

mercury is converted to organic mercury

(methylmercury) which is the primary form that

accumulates in fish and shellfish. Methylmercury

biomagnifies up the food chain as it is passed from

a lower food chain level to a subsequently higher

food chain level through consumption of prey

organisms or predators. Fish at the top of the

aquatic food chain, such as pike, bass, shark and

swordfish, bioaccumulate methylmercury

approximately 1 to 10 million times greater than

dissolved methylmercury concentrations found in

surrounding waters.

In 1984 and 1985, the U.S. Fish and Wildlife Service

collected 315 composite samples of whole fish from

109 stations nationwide as part of the National

Contaminant Biomonitoring Program (NCBP). The

maximum, geometric mean, and 85th percentile

concentrations for mercury were 0.37, 0.10, and 0.17

ppm (wet weight), respectively. An analysis of

mercury levels in tissues of bottom-feeding and

predatory fish using the data from the NCBP study

showed that the mean mercury tissue concentration

of 0.12 ± 0.08 ppm in predatory fish species (e.g.,

trout, walleye, largemouth bass) was significantly

higher than the mean tissue concentration of 0.08 ±

0.06 ppm in bottom feeders (e.g., carp, white sucker,

and channel catfish).

Mercury, the only metal analyzed as part of EPA’s

1987 National Study of Chemical Residues in Fish

(NSCRF), was detected at 92% of 374 sites

surveyed. Maximum, arithmetic mean, and median

concentrations in fish tissue were 1.77, 0.26, and

0.17 ppm (wet weight), respectively. Mean mercury

concentrations in bottom feeders (whole body

samples) were generally lower than concentrations

for predator fish (fillet samples) (see Table 1). Most

of the higher tissue concentrations of mercury were

detected in freshwater fish samples collected in the

Northeast.

In 1998, the northeast states and eastern Canadian

provinces issued their own mercury study, including

a comprehensive analysis of mercury

concentrations in a variety of freshwater sportfish

collected from the late 1980s to 1996. Top level

predatory fish such as walleye, chain pickerel, and

large and smallmouth bass were typically found to

exhibit the highest concentrations, with mean tissue

residues greater than 0.5 ppm and maximum

residues exceeding 2 ppm. One largemouth bass

sample was found to contain 8.94 ppm of mercury,

while a smallmouth bass sampled contained 5

ppm. Table 2 summarizes the range and the mean

concentrations found in eight species of sportfish

sampled.

Table 3 provides national ranges and mean

concentrations for several species of freshwater fish

collected by states from the late 1980s to early 2001. 

43 states have provided EPA with 90,000 records of

chemical contaminant fish tissue data. These data

are available in the online National Listing of Fish

and Wildlife Advisories (U.S. EPA 2001b) at

www.epa.gov/ost/fish. 

Table 1. Mean Mercury Concentrations in

Freshwater Fisha

Species

Mean

concentration (ppm)b

Bottom Feeders

Carp 0.11

White sucker 0.11

Channel catfish 0.09

Predator Fish

Largemouth bass 0.46

Smallmouth bass 0.34

Walleye 0.52

Brown trout 0.14

a EPA National Study of Chemical Residues in Fish 1987;

b Concentrations are reported on wet weight basis

Source: Bahnick et al., 1994.

Table 2. Mercury Concentrations for Selected Fish

Species in the Northeast

Species

Mean

concentrationa

(ppm)

Minimummaximum

rangea

(ppm)
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Largemouth

bass

0.51 0-8.94

Smallmouth

bass

0.53 0.08-5.0

Yellow perch 0.40 0-3.15

Eastern chain

pickerel

0.63 0-2.81

Lake trout 0.32 0-2.70

Walleye 0.77 0.10-2.04

Brown

bullhead

0.20 0-1.10

Brook trout 0.26 0-0.98

a

 Concentrations are reported on a wet weight basis.

Source: NESCAUM, 1998.

Table 3. Mercury Concentrations for Selected Fish

Species in the U.S.

Species

Mean

concentrati

ona (ppm) Range

Largemouth

bass

0.52 0.0005 - 8.94

Smallmouth

bass

0.32 0.005 - 3.34

Yellow perch 0.25 0.005 - 2.14

Eastern

chain

pickerel

0.61 0.014 - 2.81

Lake trout 0.27 0.005 - 2

Walleye 0.43 0.005 - 16

Northern

Pike

0.36 0.005 - 4.4

a

 Concentrations are reported on a wet weight basis.

Source: NLFWA, 2000.

Because of the higher cost of methylmercury

analysis, EPA recommends that total mercury rather

than methylmercury concentrations be determined in

state fish contaminant monitoring programs. EPA

also recommends that the assumption be made that

all mercury is present as methylmercury in order to

be most protective of human health.

Potential Sources of Exposure and

Occurrence in Human Tissues

Potential sources of human exposure to mercury

include food contaminated with mercury, inhalation of

mercury vapors in ambient air, and exposure to

mercury through dental and medical treatments.

Dietary intake is by far the dominant source of

exposure to mercury for the general population. Fish

and other seafood products are the main source of

methylmercury in the diet; studies have shown that

methylmercury concentrations in fish and shellfish 

are approximately 1,000 to 10,000 times greater

than in other foods, including cereals, potatoes,

vegetables, fruits, meats, poultry, eggs, and milk. 

Individuals who may be exposed to higher than

average levels of methylmercury include recreational

and subsistence fishers who routinely consume

large amounts of locally caught fish and

subsistence hunters who routinely consume the

meat and organ tissues of marine mammals.

Analytical methods are available to measure

mercury in blood, urine, tissue, hair, and breast milk. 

Fish Advisories
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The states have primary responsibility for protecting

their residents from the health risks of consuming

contaminated noncommercially caught fish. They do

this by issuing consumption advisories for the

general population, including recreational and

subsistence fishers, as well as for sensitive

subpopulations (such as pregnant women/fetus,

nursing mothers and their infants, and children).

These advisories inform the public that high

concentrations of chemical contaminants, such as

mercury, have been found in local fish. The

advisories recommend either limiting or avoiding

consumption of certain fish from specific waterbodies

or, in some cases, from specific waterbody types

(such as lakes or rivers). 

As of December 2000, mercury was the chemical

contaminant responsible, at least in part, for the

issuance of 2,242 fish consumption advisories by 41

states. Almost 79% of all advisories issued in the

United States are at least partly due to mercury

contamination in fish and shellfish. Advisories for

mercury have increased steadily, by 149% from 899

advisories in 1993 to 2,242 advisories in 2000. The

number of states that have issued mercury

advisories also has risen steadily from 27 states in

1993 to 41 states in 2000. Advisories for mercury

increased nearly 8% from 1999 (2,073 advisories) to

2000 (2,242 advisories). 

Thirteen states have issued statewide advisories for

mercury in their freshwater lakes and/or rivers: 

Connecticut, Kentucky, Indiana, Maine,

Massachusetts, Michigan, Minnesota, New

Hampshire, New Jersey, North Carolina, Ohio,

Vermont and Wisconsin. Another nine states

(Alabama, Florida, Georgia, Louisiana, Maine,

Mississippi, North Carolina, and Texas) have

statewide mercury advisories in effect for their coastal

marine waters. Figure 1 shows the total number of

fish advisories for mercury in each state in 2000 (U.S.

EPA, 2001a).

Fish Consumption Limits—EPA indicated in the

Mercury Study Report to Congress (U.S. EPA, 1997)

that the typical U.S. consumer was not in danger of

consuming harmful levels of methylmercury from fish

and was not advised to limit fish consumption on the

basis of mercury content. This advice is appropriate

for typical consumers who eat less than 10 grams of

fish and shellfish per day with mercury

concentrations averaging between 0.1 and 0.15 ppm. 

At these rates of fish intake, methylmercury

exposures are considerably less than the reference

dose (RfD) of 1 x 10-4 mg/kg-d. However, eating more

fish than is typical or eating fish that are more

contaminated, can increase the risk to a developing

fetus.

Two groups of women of childbearing age are of

concern: (1) those who eat more than 10 grams of

fish a day and (2) those who eat fish with higher

methylmercury levels. Ten grams of fish is a little

over one-quarter cup of tuna per week or about one

fish sandwich per week. Based on diet surveys,

10% of women of childbearing age eat five times or

more fish than does the average consumer. If the

fish have average mercury concentrations of 0.1 to

0.15 ppm, the women’s mercury exposures range

from near or slightly over the RfD to about twice the

RfD.

The second group of women of concern are those

who eat fish with higher mercury concentrations

(e.g., 0.5 ppm and higher). Examples of fish with

above average mercury levels are king mackerel,

various bass species, pike, swordfish, and shark.

Even women eating average amounts of fish (i.e., <10

g/d) have mercury exposures near the RfD, if the

mercury concentration is 0.5 ppm. If women eat

these fish species and their average fish intake is

between 40 and 70 grams/day (or about a quarter

cup per day), their mercury exposures would range

from three to six times the RfD. Consumers who eat

fish with 1 ppm mercury (e.g., swordfish and shark)

at the level of 40 to 70 g/d have intakes that range

from 6 to nearly 12 times the RfD.

Some women of childbearing age in certain ethnic

groups (Asians, Pacific Islanders, and Native

Americans) eat much more fish than the general

population. Because of the higher amounts of fish in

their diets, women in these ethnic groups need to

be aware of the level of mercury in the fish they eat.

The RfD is not a “bright line” between safety and

toxicity; however, there is progressively greater

concern about the likelihood of adverse effects

above this level. Consequently, people are advised

to consume fish in moderate amounts and be

aware of the amount of mercury in the fish they eat. 

For some populations, such as pregnant women,

nursing mothers, and young children, some states

have issued either "no consumption" advisories or

"restricted consumption" advisories for methylmercury. Additional information on calculating

specific limits for these sensitive populations is

available in EPA’s Guidance for Assessing

Chemical Contaminant Data for Use in Fish

Advisories, Volume 2, Section 3 (U.S. EPA 2000).

Table 4 shows the recommended monthly fish

consumption limits for methylmercury in fish for fish

consumers based on EPA’s default values for risk

assessment parameters. States may select other

scientifically defensible values for developing fish
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advisories. Consumption limits have been calculated

as the number of allowable fish meals per month

based on the ranges of methylmercury in the

consumed fish tissue. The following assumptions

were used to calculate the consumption limits:

# Consumer adult body weight of 70 kg

# Average fish meal size of 8 oz (0.227 kg)

# Time-averaging period of 1 mo (30.44 d)

# EPA’s reference dose for methylmercury (1x10-4

mg/kg-d) from EPA’s Water Quality Criterion for

the Protection of Human Health : Methylmercury 

(U.S. EPA, 2001c).

For example, when methylmercury levels in fish

tissue are 0.4 ppm, then two 8-oz. (uncooked weight)

meals per month can safely be consumed.

Table 4. Monthly Fish Consumption 

Limits for Methylmercury

Risk-based 

consumption limit

Noncancer 

health endpoints

Fish meals/month Fish tissue concentrations

(ppm, wet weight)

16 > 0.03–0.06

12 > 0.06–0.08

8 > 0.08–0.12

4 > 0.12–0.24

3 > 0.24–0.32

2 > 0.32–0.48

1 > 0.48–0.97

0.5 > 0.97–1.9

None (<0.5)a > 1.9

a

 None = No consumption recommended.

NOTE: In cases where >16 meals per month are

consumed, refer to EPA’s Guidance for Assessing

Chemical Contaminant Data for Use in Fish Advisories,

Volume 2, Section 3 for methods to determine safe

consumption limits.

Toxicity of Mercury

Pharmacokinetics—Methylmercury is rapidly and

nearly completely absorbed from the gastrointestinal

tract; 90% to 100% absorption is estimated. Methylmercury is somewhat lipophilic, allowing it to pass

through lipid membranes of cells and facilitating its

distribution to all tissues, and it binds readily to

proteins. Methylmercury binds to amino acids in fish

muscle tissue.

The highest methylmercury levels in humans are

generally found in the kidneys. Methylmercury in the

body is considered to be relatively stable and is only

slowly transformed to form other forms of mercury.

Methylmercury readily crosses the placental and

blood/brain barriers. Estimates for its half-life in the

human body range from 44 to more than 80 days. 

Excretion of methylmercury is via the feces, urine,

and breast milk. Methylmercury is also distributed to

human hair and to the fur and feathers of wildlife;

measurement of mercury in hair and these other

tissues has served as a useful biomonitor of

contamination levels.

Acute Toxicity—Acute high-level exposures to

methylmercury may result in impaired central

nervous system function, kidney damage and

failure, gastro- intestinal damage, cardiovascular

collapse, shock, and death. The estimated lethal

dose is 10 to 60 mg/kg.

Chronic Toxicity—Both elemental mercury and

methylmercury produce a variety of health effects at

relatively high exposures. While recent studies

indicate that lower dose exposure can have effects

on the cardiovascular and immune systems, 

neurotoxicity is the effect of greatest concern. This is

true whether exposure occurs to the developing

embryo or fetus during pregnancy or to adults and

children. Human exposure to methylmercury has

generally been through consumption of

contaminated food. Two major episodes of methylmercury poisoning through fish consumption have

occurred. The first occurred in the early 1950s

among people, fish consuming domestic animals

such as cats, and wildlife living near Minamata City

on the shores of Minamata Bay, Kyushu, Japan. The

source of the methylmercury contamination was

effluent from a chemical factory that used mercury

as a catalyst and discharged wastes into the bay

where it accumulated in fish and shellfish that were

a dietary staple of this population. Average fish

consumption was reported to be in excess of 300

g/d, 20 times greater than is typical for recreational

fishers in the United States. By comparison, about

3% to 5% of U.S. consumers routinely eat 100

grams of fish per day. Among women of

childbearing age, 3% routinely eat 100 grams of fish

per day. 

In 1965, another methylmercury poisoning incident

occurred in the area of Niigata, Japan. The signs

and symptoms of the disease in Niigata were

similar to those of methylmercury poisoning in

Minamata.

Methylmercury poisoning also occurred in Iraq

following consumption of seed grain that had been

treated with a fungicide containing methylmercury.

The first outbreak occurred prior to 1960; the second

occurred in the early 1970s. In this case, imported
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mercury-treated seed grains that arrived after the

planting season were ground into flour and baked

into bread. Unlike the long-term exposures in Japan,

the epidemic of methylmercury poisoning in Iraq was

short in duration lasting approximately 6 months. The

signs and symptoms of disease in Iraq were

predominantly in the nervous system: difficulty with

peripheral vision or blindness, sensory disturbances,

incoordination, impairment of walking, and slurred

speech. Both children and adults were affected.

Some infants born to mothers who had consumed

methylmercury contaminated grain (particularly

during the second trimester of pregnancy) showed

nervous system damage even though the mother

was only slightly affected or asymptomatic.

Three recent epidemiology studies in the Seychelles

Islands, New Zealand, and the Faroe Islands were

designed to evaluate childhood development and

neurotoxicity in relation to fetal exposures to

methylmercury in fish-consuming populations. 

Prenatal methylmercury exposures in these three

populations were within the range of some U.S.

population exposures. No adverse effects were

reported from the Seychelles Islands study, but

children in the Faroe Islands exhibited subtle doserelated deficits at 7 years of age. These effects

include abnormalities in memory, attention, and

language. In the New Zealand prospective study,

children at 4 and 6 years of age exhibited deficiencies

in a number of neuropsychological tests.

In addition to the three large epidemiological

studies, studies on both adults and children were

conducted in the Amazon; Ecuador; French Guiana;

Madeira; Mancora, Peru; northern Quebec; and

Germany. Effects of methylmercury on the nervous

system were reported in all but the Peruvian

population. 

There has been considerable discussion within the

scientific community regarding the level of exposure

to methylmercury that is likely to be without an

appreciable risk of deleterious health effects during a

lifetime. In 1999, the Congress directed EPA to

contract with the National Research Council (NRC) of

the National Academy of Sciences to evaluate the

body of data on the health effects of methylmercury.

NRC published their report, Toxicological Effects of

Methylmercury, in 2000. EPA generally concurred

with the NRC findings and recommendations and

used them in determining the EPA RfD for

methylmercury. EPA chose to base the RfD on data

from the Faroes study. The Seychelles study has no

findings of effects associated with methylmercury

exposure, and thus is not the best choice for a public

health protective risk estimate. While the New

Zealand study does show mercury-related effects it

relatively small by comparison to the other two. 

Benchmark dose analysis was chosen as the most

appropriate method of quantifying the dose-effect

relationship. This lower 95% limit (BMDL) on a 5%

effect level obtained by applying a K power model (K

$ 1) to Faroese dose-response data based on

mercury in cord blood. It was found that several

endpoints are sensitive measures of methylmercury

effects in the Faroese children. The BMDLs and

corresponding estimates of ingested methylmercury

are within a very small range and cluster around a

level of 1 :g/kg bw/day. Rather than choosing a

single measure for the RfD critical endpoint, EPA

considers that this RfD is based on several scores

which are indications of neuropsychological

processes related to the ability of a child to learn

and process information. An uncertainty factor of 10

was applied. This included a factor of 3 for

pharmacokinetic variability and uncertainty; one area

of pharmacokinetic uncertainty was introduced with

the assumption of equivalent cord blood and

maternal blood mercury levels. An additional factor

of 3 addressed pharmacokinetic variability and

uncertainty. Other areas of concern include inability

to quantify possible long-term sequelae for

neurotoxic effects, questions as to the possibility of

observing adverse impacts (such as cardiovascular

effects) below the BMDL, and lack of a twogeneration reproductive effects assay.

Developmental Toxicity—Data are available on

developmental effects in rats, mice, guinea pigs,

hamsters, and monkeys. Also, convincing data from

a number of human studies (i.e., Minamata, Iraq,

New Zealand, and the Faroe Islands) indicate that

methylmercury causes subtle to severe neurologic

effects depending on dose and individual

susceptibility. EPA considers methylmercury to have

sufficient human and animal data to be classified as

a developmental toxicant.

Methylmercury accumulates in body tissue;

consequently, maternal exposure occurring prior to

pregnancy can contribute to the overall maternal

body burden and result in exposure to the

developing fetus. In addition, infants may be

exposed to methyl-mercury through breast milk.

Therefore, it is advisable to reduce methylmercury

exposure to women with childbearing potential to

reduce overall body burden.

Mutagenicity and Reproductive Effects - Methylmercury appears to be clastogenic but not to be a

point mutagen; that is, mercury causes

chromosome damage but not small heritable

changes in DNA.

EPA has classified methylmercury as being of high

concern for potential human germ cell mutagenicity.

The absence of positive results in a heritable

mutagenicity assay keeps methylmercury from
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being included under the highest level of concern.

The data on mutagenicity are not sufficient, however,

to permit estimation of the amount of methylmercury

that would cause a measurable mutagenic effect in

the human population. There is no two-generation

study of reproductive effects, but shorter term studies

in rodents, guinea pigs and monkeys have reported

observations consistent with reproductive deficits.

Carcinogenicity - Three human studies have been

identified that examined the relationship between

methylmercury exposure and cancer. There was no

persuasive evidence of increased carcinogenicity

attributable to methylmercury exposure in any of

these studies. Interpretation of these studies was

limited by poor study design and incomplete

descriptions of methodology and/or results.

Experimental animal data suggest that methylmercury may be tumorigenic in animals. Chronic

dietary exposures of mice to methylmercury resulted

in significant increases in the incidences of kidney

tumors in males but not in females. The tumors were

seen only at toxic doses of methylmercury. EPA has

found methylmercury to have inadequate data in

humans and limited evidence in animals.

All of the carcinogenic effects in animals were

observed in the presence of profound damage to the

kidneys. Tumors may be formed as a consequence

of repair in the damaged organs. Evidence points to a

mode of action for methylmercury carcinogenicity that

operates at high doses certain to produce other types

of toxicity in humans. Given the levels of exposure

most likely to occur in the U.S. population, even

among consumers of large amounts of fish, methylmercury is not likely to present a carcinogenic risk. 

EPA has not calculated quantitative carcinogenic risk

 values for methylmercury.

Special Susceptibilities—The developing fetus is

thought to be at particular risk of neurotoxic effects

from methylmercury exposure. Data on children

exposed only after birth are insufficient to determine

if this group has increased susceptibility to the

adverse central nervous system effects of

methylmercury. Children are considered to be at

increased risk of methylmercury exposure by virtue

of their greater food consumption as a percentage of

body weight (mg food/kg body weight) compared to

adult exposures. Additional studies indicate that

aging populations may be particularly susceptible to

effects of mercury exposure. 

Interactive Effects—Potassium dichromate and

atrazine may increase the toxicity of mercury,

although these effects have been noted only with

metallic and inorganic mercury. Ethanol increases

the toxicity of methylmercury in experimental

animals. Vitamins D and E, thiol compounds,

selenium, copper, and possibly zinc are

antagonistic to the toxic effects of mercury.

Critical Data Gaps—Additional data are needed on

the exposure levels at which humans experience

subtle, but persistent, adverse neurological effects.

Data on immunologic effects and cardiovascular

effects are not sufficient for evaluation of low-dose

methylmercury toxicity.

Figure 1: Mercury Advisories for 2000

Summary of EPA Health Benchmarks

# Chronic Toxicity–Reference Dose: 

1x10-4 mg/kg-d (U.S. EPA, 2001)

# Carcinogenicity:Not likely to be human

carcinogen under conditions of exposure
8
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EPA Regulations and Advisories

# Maximum Contaminant Level inorganic mercury in drinking water = 0.002 mg/L

# Toxic Criteria for those States Not Complying with CWA Section 303(c)(2)(B) - criterion

concentration for priority toxic pollutants:

– Freshwater: maximum = 1.4 :g/L, continuous = 0.77 :g/L

S Saltwater: maximum = 1.80 :g/L, continuous = 0.94 :g/L

– Human health consumption of organisms = 0.3 mg/kg methylmercury fish tissue (wet

weight).

# Water Quality Guidance for the Great Lakes System—protection of aquatic life in ambient

water:

– acute water quality criteria for mercury total recoverable: maximum = 1.694 :g/L

– chronic water quality criteria for mercury total recoverable: continuous = 0.908 :g/L

– water quality criteria for protection of human health, drinking water and nondrinking

water: maximum = 1.8 x 10-3 :g/L

– water quality criteria for protection of human health (mercury including methylmercury) =

1.3 x 10-3 :g/L.

# Listed as a hazardous air pollutant under Section 112 of the Clean Air Act

# Emissions from mercury ore processing facilities and mercury chlor-alkali plants = 2,300 g

maximum/24 h 

# Emissions from sludge incineration plants, sludge drying plants, or a combination of these

that process wastewater treatment plant sludge = 3,200 g maximum/24 h

# Ban of phenylmercuric acetate as a fungicide in interior and exterior latex paints

# Reportable quantities: Mercury, mercuric cyanide = 1 lb; mercuric nitrate, mercuric sulfate,

mercuric thiocyanate, mercurous nitrate, mercury fulminate = 10 lb; phenylmercury acetate

= 100 lb.

# Listed as a hazardous substance: Mercuric cyanide, mercuric nitrate, mercuric sulfate,

mercuric thiocyanate, mercurous nitrate

# Reporting threshold for Toxic Release Inventory (proposed) = 10 lb
10

Sources of Information

Bahnick, D., C. Sauer, B. Butterworth, and D.W.

Kuehl. 1994. A national study of mercury

contamination in fish IV: Analytical methods and

results. Chemosphere 29(3):537-547.

Kidwell, J.M., L.J. Phillips, and G.F. Birchard. 1995.

Comparative analyses of contaminant levels in

bottom feeding and predatory fish using the National

Contaminant Biomonitoring Program Data. Bulletin

of Environmental Contamination and Toxicology.

54:919-923.

National Institute of Environmental Health Sciences.

1999. Scientific Issues Relevant to Assessment of

Health Effects from Exposure to Methylmercury. U. S.

Department of Health and Human Services, Public

Health Service, Research Triangle Park, NC.

http://www.niehs.nih.gov.

NESCAUM (Northeast States for Coordinated Air

Use Management). 1998. Northeast States and

Eastern Canadian Provinces Mercury Study. A

Framework for Action. Boston, Massachusetts. 

Porcella, D.B. 1994. Mercury in the Environment:

Biogeochemistry. In: Watras, C. J., Huckabee, J. W.,

eds., Lewis Publishers. Mercury Pollution

Integration and Synthesis, Boca Raton, Florida. 3-

19.

Schmitt, C. J., and W. G. Brumbaugh. 1990. National

Contaminant Biomonitoring Program:

Concentrations of arsenic, cadmium, copper, lead,

mercury, selenium, and zinc in U.S. freshwater fish,

1978-1984. Archives of Environmental

Contamination and Toxicololgy. 19:731-747.

U.S. EPA (Environmental Protection Agency). 1997.

Mercury Study Report to Congress. Office of Air

Quality Planning and Standards and Office of

Research and Development, Washington, DC.

http://www.epa.gov/ttn/uatw/112nmerc/mercury.html

 U.S. EPA (Environmental Protection Agency). 2000.

Guidance for Assessing Chemical Contaminant

Data for Use in Fish Advisories. Volume 2, 3rd

edition. Risk Assessment and Fish Consumption

Limits. EPA 823-B-00-008. Office of Water,

Washington, DC.

http://www.epa.gov/ost/fish/guidance.html

U.S. EPA (Environmental Protection Agency). 2001a.

Fact Sheet: Update: National Listing of Fish and

Wildlife Advisories. EPA-823-F-01-010. Office of

Water, Washington, DC.

http://www.epa.gov/ost/fish/listing.html

U.S. EPA (Environmental Protection Agency). 2001b.

National Listing of Fish and Wildlife Advisories

(NLFWA). Office of Water, Washington, DC.

http://www.epa.gov/ost/fish/listing.html

U.S. EPA (Environmental Protection Agency). 2001c. 

Water Quality Criterion for the Protection of Human

Health : Methylmercury. EPA-823-R-01-001. Office

of Water, Washington DC. 

http://www.epa.gov/waterscience/criteria/methylmerc

ury/criteria.html

For more information about the National

Fish and Wildlife Contamination Program,

contact:

Jeffrey Bigler

U.S. Environmental Protection Agency

Office of Science and Technology

1200Pennsylvania Ave NW (4305)

Washington, DC 20460

Bigler.Jeff@epa.gov

202 260-1305

202 260-9830 (fax)

Additional information regarding

contaminants in fish and health risks is

available from the following Internet site:

http://www.epa.gov/ost/fish