1

United States

Environmental Protection

Agency

Office of Water

4305

EPA-823-F-99-019

September 1999

Fact Sheet

Polychlorinated Biphenyls (PCBs) Update: Impact on Fish

Advisories

PCBs are a group of synthetic organic chemicals that contain 209 possible individual chlorinated biphenyl

compounds. These chemically related compounds are called congeners and vary in their physical and chemical

properties and toxicity. There are no known natural sources of PCBs. Although banned in the United States from

further production in 1979, PCBs are distributed widely in the environment because of their persistence and

widespread use. PCB mixtures found in the environment are different from the commercially produced PCB mixtures

(known as Aroclors in the United States) because of differences in chemical properties, persistence, and

bioaccumulation among the different congeners. The most common analytical method used to detect PCBs in the

environment is based on Aroclor analysis; however, congener-specific methods have been developed and currently

are being tested. PCB exposure is associated with a wide array of adverse health effects in experimental animals.

Experimental animal studies have shown toxic effects to the liver, gastrointestinal system, blood, skin, endocrine

system, immune system, nervous system, and reproductive system. In addition, developmental effects and liver

cancer have been reported. Skin rashes and a severe form of acne have been documented in humans; however,

other effects of PCB exposure in humans are not well understood. EPA has classified PCBs as probable human

carcinogens (Group B2). As of 1998, 37 states have issued 679 fish advisories for PCBs. These advisories inform

the public that high concentrations of PCBs 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 PCBs in the Environment

There are no known natural sources of PCBs;

therefore, all sources of PCBs are related to

commercial manufacture, use, storage, and disposal.

Manufacture of PCBs was banned in the United

States in 1979. However, PCB-containing materials

still in service at the time of the ban were not

required to be removed from use, and, therefore,

some are still in use. For example, the life

expectancy of electrical transformers that contain

PCBs is 30 years or more.

Currently, the major source of PCBs is environmental

reservoirs from past releases. PCBs have been

detected in soil, surface water, air, sediment, plants,

and animal tissue in all regions of the earth. PCBs

are highly persistent in the environment with reported

half-lives in soil and sediment ranging from months

to years. Because PCBs have very low solubility in

water and low volatility, most PCBs are contained in

sediments that serve as environmental reservoirs

from which PCBs may continue to be released over a

long period of time. PCBs may be mobilized from

sediments if disturbed (e.g., flooding, dredging).

Volatilization from land and surface water is also an

important source for the global distribution of PCBs

and is discussed below.

Fate and Transport of PCBs

The global cycling of PCBs results from their

evaporation from soils and surface waters to the

atmosphere and their redeposition back to land and

surface water. Adsorption to sediments and

revolatilization are the primary loss mechanisms

from surface water. 

PCBs are highly lipophilic (fat soluble) and are

rapidly accumulated by aquatic organisms and

bioaccumulated through the aquatic food chain.

Concentrations of PCBs in aquatic organisms may

be 2,000 to more than a million times higher than the

concentrations found in the surrounding waters, with

species at the top of the food chain having the

highest concentrations. Bioaccumulation factors vary

among the congeners and generally increase with

chlorine content from the trichlorobiphenyls up

through the hexachlorobiphenyls and then generally

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 PCBs. 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, mercury,

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

they become available.
2

decrease with higher chlorine content (hepta- and

octa-chlorobiphenyls).

PCBs have been included in several major fish

contaminant monitoring programs. A summary of the

National Contaminant Biomonitoring Program

(NCBP) data conducted by the U.S. Fish and Wildlife

Service, from 1976 through 1984, indicated a

significant downward trend in the geometric mean

concentration in whole fish samples of total PCBs

(from 0.89 ppm in 1976 to 0.39 ppm in 1984);

however, PCB residues in fish tissue remain

widespread, being detected at 91% of the sites

monitored in 1984. Maximum total PCB tissue

residue concentrations (wet weight) during this same

period also declined, from 70.6 ppm in 1976 to 6.7

ppm in 1984. Coinciding declines in tissue residue

concentrations of three Aroclors (1248, 1254, and

1260) were also observed. An analysis of the 1984-

1985 data from the NCBP study showed there was

no significant difference in residues in bottom feeding

and predatory fish for Aroclor 1248 and 1254;

however, there were significantly higher

concentrations of Aroclor 1260 in predator species as

compared to bottom feeders. Mean tissue concentrations of Aroclor 1248, 1254, and 1260 were 0.06 ±

0.32 0.21 ± 0.39, and 0.14 ± 0.24 ppm, respectively,

for bottom feeders (e.g., carp, white suckers, and

channel catfish) and 0.08 ± 0.31, 0.35 ± 0.69, and

0.23 ± 0.38 ppm, respectively, for predator species

(e.g., rainbow, brown, brook, and lake trout,

largemouth bass, and walleye).

Total PCBs also were detected at 91% of 374 sites

surveyed in EPA’s National Study of Chemical

Residues in Fish (NSCRF). Maximum, arithmetic

mean, and median total PCB concentrations reported

were 124, 1.89, and 0.209 ppm (wet weight),

respectively. As is shown in Table 1, the tri-, tetra-,

penta-, hexa-, and heptachlorobiphenyls were

detected in fish tissue samples at >50% of the sites.

Mean tissue concentrations were highest for the

tetra- and pentachlorobiphenyls with concentrations

of 0.696 and 0.565 ppm, respectively. The median

fish tissue concentrations were highest for the hexafollowed by the pentachlorobiphenyls with concentrations of 0.077 and 0.072 ppm, respectively. 

Potential Sources of Exposure and

Occurrence in Human Tissues

Exposure to PCBs is predominantly through the diet,

and especially from fish and seafood products. Red

meat, poultry, eggs, and dairy products also may be

important dietary sources of PCBs.

Individuals in the general population who may be

exposed to higher than average levels of PCBs

include recreational and subsistence fishers who

routinely consume large amounts of locally caught

fish, subsistence hunters who routinely consume the

meat and organ tissues of marine mammals, and

persons who live near hazardous waste sites

contaminated with PCBs.

Table 1. Summary of PCBs Detected in Fish Tissuea as Part of the National Study of Chemical

Residues in Fishb (1986-1989)

Congener Group

% of sites

where

 detected

ppm

Maximum Mean Median

Monochlorobiphenyl 13.8 0.235 0.001 ND

Dichlorobiphenyl 30.7 5.072 0.021 ND

Trichlorobiphenyl 57.5 18.344 0.150 0.002

Tetrachlorobiphenyl 72.4 60.764 0.696 0.023

Pentachlorobiphenyl 86.7 29.578 0.565 0.072

Hexachlorobiphenyl 88.7 8.862 0.356 0.077

Heptachlorobiphenyl 69.1 1.850 0.097 0.017

Octachlorobiphenyl 34.8 0.593 0.017 ND

Nonachlorobiphenyl 9.7 0.413 0.003 ND

Decachlorobiphenyl 3.3 0.038 0.001 0.003

Total PCBs* 91.4 ----- 1.898 0.209

* Total PCBs refers to the sum of the concentrations of compounds with 1 to 10 chlorines.

a

 Concentrations are reported on a wet weight basis.

b

 Species included freshwater, estuarine, and marine finfish; and a small number of marine shellfish.

Source: U.S. EPA, 1992.
3

Analytical methods are available to measure PCBs in

blood, tissue, breast milk, and environmental media.

However, currently there are no standard methods

for analyzing for PCB congeners. There is a standard

method for Aroclor analysis, but PCBs in environmental samples and human tissues are not

adequately characterized as Aroclors. In the absence

of peer-reviewed analytical methods for congener

specific chemical analysis of fish tissue, EPA’s Office

of Water recommends the continued use of total

Aroclor chemical analysis of fish tissue when

conducting human health risk assessment for PCBs.

Recently, new risk assessment methods for the PCB

congeners have been published and peer-reviewed.

However, the analytical methods for congener

analysis have not been verified or peer reviewed.

When standard methods for congener analysis have

been verified and peer reviewed, the Office of Water

will reevaluate the use of these methods because of

their increased accuracy and precision over Aroclor

analysis.

Fish Advisories

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 sensitive

subpopulations (such as pregnant women/fetus,

nursing mothers, and children). These advisories

inform the public that high concentrations of

chemical contaminants, such as PCBs, 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 (e.g., freshwater lakes or rivers). 

As of December 1998, PCBs were the chemical

contaminants responsible, at least in part, for the

issuance of 679 fish consumption advisories by 37

states, including the District of Columbia and the

U.S. Territory of American Samoa (see Figure 1).

Almost 27% of all advisories issued in the United

States are

Figure 1. 1998 Fish Advisories for PCBs.
4

a result of PCB contamination in fish and shellfish.

The number of advisories for PCBs is second only to

that for mercury advisories. Advisories for PCBs

have increased 112% from 319 advisories in 1993 to

679 advisories in 1998. The number of states that

have issued PCB advisories increased only slightly

from 31 to 35 states from 1993 to 1994 and then

declined to 34 states for 1995 and 1996. In 1997 and

1998, the number of states issuing advisories rose to

36 and 37, respectively. Advisories for PCBs

increased nearly 15% from 1997 (588 advisories) to

1998 (679 advisories).

Three states (Indiana, New York, and the District of

Columbia) have issued statewide advisories for

PCBs in their freshwater lakes and/or rivers. Another

6 states—Connecticut, Massachusetts, New Jersey,

New Hampshire, New York, and Rhode Island—have

statewide PCB advisories in effect for their coastal

marine waters. To date, 79% of the 679 PCB

advisories in effect have been issued by the following

10 states; Indiana (125), Michigan (104) Minnesota

(83), Wisconsin (54), New York (47), Ohio (37),

Georgia (25), Pennsylvania (22), Nebraska (22), and

Massachusetts (20).

General recommendations regarding food

preparation, such as trimming the fat and skinning

the fish prior to cooking, also may be included in the

general advisory information. Lipophilic chemicals,

such as PCBs, accumulate mainly in fatty tissues

(belly flap, lateral line, subcutaneous and dorsal fat,

dark muscle, gills, eye, brain, and internal organs).

Therefore, removal of internal organs and skin and

trimming the fat before cooking will decrease

exposure. In addition, various cooking procedures

can also reduce the amount of PCBs consumed (see

Appendix section "Dose Modification Due to Food

Preparation and Cooking" of EPA’s Guidance for

Assessing Chemical Contaminant Data for Use in

Fish Advisories, Volume 2).

Fish Consumption Limits—Table 2 shows the

recommended monthly fish consumption limits for

PCBs for fish consumers based on EPA’s default

values for risk assessment parameters. 

Consumption limits have been calculated as the

number of allowable fish meals per month, based on

the ranges of PCBs in the consumed fish tissue. The

following assumptions were used to calculate the

consumption limits:

# Consumer adult body weight of 72 kg

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

# Time-averaging period of 1 month (30.44 days)

# EPA’s reference dose for PCBs 

(2 × 10-5 mg/kg-d) from EPA’s Integrated Risk 

Information System (U.S. EPA, 1999)

# EPA’s cancer slope factor for PCBs 

(2 per mg/kg-d) from EPA’s Integrated Risk 

Information System (U.S. EPA, 1999c)

# Maximum acceptable cancer risk level (10-5 over

a 70-year lifetime) 

For example, when PCB levels in fish tissue are 0.05

ppm, then three 8-oz. meals per month (based on the

noncancer health endpoint—EPA’s reference dose)

or a half of an 8-oz. meal per month (based on the

cancer health endpoint—EPA’s cancer slope factor)

can safely be consumed. EPA recommends using

the more conservative of the two limits, for PCBs,

this is the consumption limit based on the cancer

endpoint.

For sensitive populations, such as pregnant women,

nursing mothers, and young children, some states

have issued either "no consumption" advisories or

"restricted consumption" advisories for PCBs.

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.

Toxicity of PCBs

Pharmacokinetics—PCBs are absorbed through the

gastrointestinal tract and distributed throughout the

body. Studies of individual chlorobiphenyl congeners

indicate, in general, that PCBs are readily absorbed,

with an oral absorption efficiency of 75% to greater

than 90%. Because of their lipophilic nature, PCBs,

especially the more highly chlorinated congeners

(tetra- through hexachlorobiphenyl), tend to

accumulate in lipid-rich tissues. Greater relative

amounts of PCBs are usually found in the liver,

adipose tissue, skin, and breast milk. It has been

shown that absorption by nursing infants of tetraand higher chlorinated congeners from breast milk

ranges from 90% to 100% of the dose. Offspring can

also be 

Table 2. Monthly Fish Consumption Limits

for PCBs

Risk-Based

Consumption

Limit

Noncancer

Health

Endpoints

Cancer

Health

Endpoints

Fish

Meals/Month

Fish Tissue

Concentrations

(ppm, wet weight)

Fish Tissue

Concentrations

(ppm, wet weight)

16 >0.006 - 0.012 >0.0015 - 0.003

12 >0.012 - 0.016 >0.003 - 0.004

8 >0.016 - 0.024 >0.004 - 0.006

4 >0.024 - 0.048 >0.006 - 0.012

3 >0.048 - 0.064 >0.012 - 0.016

2 >0.064 - 0.097 >0.016 - 0.024

1 >0.097 - 0.19 >0.024 - 0.048

0.5 >0.19 - 0.39 >0.048 - 0.097

None (<0.5)a >0.39 >0.097

aNone = 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.
5

exposed to PCBs through placental transfer. PCBs

have also been measured in other body fluids

including plasma, follicular fluid, and sperm fluid.

The retention of PCBs in fatty tissues is linked to the

degree of chlorination and also to the position of the

chlorine atoms in the biphenyl ring. In general, higher

chlorinated PCBs persist for longer periods of time.

Pharmacokinetic modeling of PCB disposition

indicates that PCB movement in the body is a

dynamic process, with exchanges between various

tissues that depend on fluctuating exposure levels to

specific congeners. The result is elimination of

congeners that are more easily metabolized and

retention of those that resist metabolism. In

occupationally-exposed individuals, lower chlorinated

congeners had half-lives between 1 and 6 years and

higher chlorinated PCBs had half-lives ranging from

8 to 24 years.

PCBs induce mixed function oxidases, and different

congeners induce specific forms (isozymes) of the

cytochrome P-450 system. Although there has been

much research into the mechanisms of PCB toxicity,

there is no clear definition of the mechanisms for

most congeners. The congeners appear to act by a

variety of mechanisms. Some PCB congeners are

similar to dioxins and bind to a cytosolic protein, the

Ah receptor, which regulates the synthesis of a

variety of proteins. The toxicity of these congeners is

similar to dioxins. The toxicity of other PCB

congeners seems to be unrelated to the Ah receptor.

Ultimately, the toxicity of a PCB mixture may depend

on the toxicity of the individual congeners and their

interactions.

Acute Toxicity—Acute high-level exposures of

laboratory animals to PCBs have resulted in liver and

kidney damage, neurological effects, developmental

effects, endocrine effects, hematological effects, and

death. LD50 values for Aroclor mixtures range from

about 1,000 mg/kg to more than 4,000 mg/kg. No

human deaths have been associated with acute

exposure to PCBs. 

Chronic Toxicity—In animal studies, numerous

effects have been documented, including hepatic,

gastrointestinal, hematological, dermal, body weight

changes, endocrine, immunological, neurological,

and reproductive effects. Most of the studies have

involved oral exposure. Despite the variety of adverse

effects observed in animals exposed to PCBs, overt

adverse effects in humans have been difficult to

document. This has been attributed to the fact that,

in most cases, the dosages tested in animals were

considerably higher than those found in occupational

exposures and the difficulties with interpreting

epidemiological studies. These include multiple

confounding factors, uncertain exposure estimates,

and statistical limitations. Skin rashes and a

persistent and severe form of acne (chloracne) have

been reported following exposures to PCBs.

Occupational and accidental exposures have

indicated that PCBs may affect many organs

including the gastrointestinal, respiratory, immune,

central nervous, and cardiovascular systems. 

Developmental Toxicity—PCB mixtures have been

shown to cause adverse developmental effects in

experimental animals. Some human studies have

suggested that PCB exposure may cause adverse

effects in children and in developing fetuses while

other studies have not shown effects. Reported

effects include lower IQ scores, low birth weight, and

lower behavior assessment scores. However, study

limitations, including lack of control for confounding

variables, deficiencies in the general areas of

exposure assessment, selection of exposed and

control subjects, the comparability of exposed and

control samples, and different findings from different

studies provide inconclusive evidence that PCBs

cause developmental effects in humans.

A study was conducted of pregnancy outcomes in

women who had consumed PCB-contaminated fish

from Lake Michigan over an average of 16 years

(exposure both prior to and during pregnancy).

Consumption of contaminated fish and levels of total

PCBs in cord serum correlated with lower birth

weight, smaller head circumference, and shorter

gestational age. Fish consumption was correlated

with delayed neuromuscular maturity, and, at 7

months, the children had subnormal visual

recognition memory. Children from this cohort were

examined at ages 4 and 11. At age 4, cord serum

PCB levels were associated with impaired short-term

memory. Activity level was inversely related to 4-year

serum PCB level and also to maternal milk PCB

level. At age 11, prenatal exposure to PCBs was

associated with lower full-scale and verbal IQ scores

after controlling for potential confounding variables

such as socio-economic status. The results from this

series of studies were confounded by possible

maternal exposure to other chemicals and by the fact

that the exposed group, on average, drank more

alcohol and caffeine prior to and during pregnancy,

weighed more, and took more cold medications

during pregnancy than the nonexposed group. 

Other relevant studies generally found no significant

differences between control groups and exposed

groups regarding stillbirths, multiple births, preterm

births, congenital anomalies, and low birth weight.

Information on chronic developmental toxicity is

available from studies in Rhesus monkeys. Exposure

periods ranged from 12 to 72 months. Inflammation

of tarsal glands, nail lesions, and gum recession

were noted in offspring of monkeys exposed to

Aroclor 1254. Adverse neurobehavioral effects were

reported following exposure to Aroclor 1016 and

Aroclor 1248. Other observed effects include

reduction in birth weight and increased infant death

for Aroclor 1248.
6

Exposure via lactation is a significant concern for

neonates. Animal studies indicate that lactational

exposure may be more significant than prenatal

exposure. In monkeys, signs of PCB intoxication

were observed in lactationally-exposed offspring, but

not in offspring exposed only prenatally.

Mutagenicity—The majority of mutagenicity assays

of PCBs have been negative. However, an increase

in the percentage of chromosomal aberrations in

peripheral lymphocytes and an increase in the sister

chromatid exchange rate were reported in a study of

workers manufacturing PCBs for 10 to 25 years.

Although workers and controls were matched for

smoking and drinking, concurrent exposure to other

known human genotoxic chemicals occurred.

Another study found an increased incidence of

chromatid exchanges in lymphocytes from workers

exposed to PCBs in an electric power substation fire

compared to unexposed controls. It is possible that

toxic chlorinated dioxins and/or furans generated

during the fire may have been responsible for the

effects.

The weight of evidence from the in vitro and in vivo

genotoxicity studies suggests that PCBs are not likely

to be genotoxic to humans. However, exposure to

PCBs may enhance the genotoxic activity of other

chemicals.

Carcinogenicity—PCBs are classified by EPA as

Group B2—probable human carcinogens. This is

based on studies that have found liver tumors in rats

exposed to Aroclors 1260, 1254, 1242, and 1016.

Evaluation of the animal data indicates that PCBs

with 54% chlorine content induces a higher yield of

liver tumors in rats than other PCB mixtures.

Human epidemiological studies of PCBs have not

yielded conclusive results. There is some suggestive

evidence that xenoestrogens, including PCBs, may

play a role in breast cancer induction. Some studies

have indicated an excess risk of several cancers

including: liver, biliary tract, gall bladder,

gastrointestinal tract, pancreas, melanoma, and nonHodgkins’s lymphoma. As with all epidemiological

studies, it is very difficult to obtain clear unequivocal

results because of the long latency period required

for cancer induction and the multiple confounders

arising from concurrent exposures, lifestyle

differences, and other factors. The currently available

evidence is considered inadequate, but suggestive

that PCBs may cause cancer in humans.

Special Susceptibilities—There is evidence that

embryos, fetuses, and neonates are more

susceptible to PCBs due to their under-developed

enzymatic systems, which may lead to increased

accumulation in the body. Breast-fed infants may

have an increased risk because of bioconcentration

of PCBs in breast milk and high intake rates relative

to body weights. In addition, there is evidence that a

steroid present in human milk inhibits glucuronyl

transferase activity which could in turn, inhibit

glucuronidation and excretion of PCB metabolites.

Other individuals with potentially greater risk include

those with liver and blood diseases or those with

syndromes associated with impairment to the

metabolic systems that help eliminate PCBs from the

body.

Interactive Effects—PCBs induce microsomal

enzymes; therefore, the effects of exposure to PCBs

or other compounds depend on the role of oxidative

metabolism. For example, preexposure to PCBs may

enhance the liver toxicity of some chemicals

(trichloroethylene, mirex, kepone, carbon

tetrachloride, tetrachloroethylene) but decrease the

liver toxicity of 1,1-dichloroethylene. Other interactive

effects include increased metabolism and excretion

of pentobarbital, increased genotoxicity of numerous

carcinogens, increased duodenal ulcerogenic activity

of acrylonitrile, and increased kidney toxicity of

trichloroethylene. 

Critical Data Gaps—The following studies could

help to fill in some of the key data gaps for PCBs:

congener-specific PCB levels in human tissues,

epidemiological studies of population living near PCB

contaminated sites and occupational settings where

exposure to PCBs still occurs; reproductive studies in

humans and animals including fertility studies in

males of a sensitive species; developmental and

neurodevelopmental studies; immunotoxicity studies

in humans and animals; neurotoxicity studies in

humans with high PCB body burdens and in animals;

chronic studies to determine the most sensitive

PCB Exposure and Development Effects—

The data from some studies in humans suggest

that exposure to PCBs may cause developmental effects. However, limitations of these

studies diminish the validity of the results.

Animal studies indicate that PCBs can cause

developmental effects following prenatal or

postnatal exposure.

Summary of EPA Health Benchmarks

# Chronic Toxicity-Reference Dose: 

2x10-5 mg/kg-d (Aroclor 1254) (U.S. EPA, 

1999c)

# Carcinogenicity: 1 (central estimate) to 2

(upper bound) per mg/kg-d (U.S. EPA,

1999c)

# Developmental Toxicity: 7x10-5 mg/kg-d

(Aroclor 1016) (U.S. EPA, 1999c)
7

animal target organ and species; and comparative

toxicity of Aroclors and bioaccumulated PCBs.

Sources of Information

ATSDR (Agency for Toxic Substances and Disease

Registry). 1998. Toxicological Profile for

Polychlorinated Biphenyls (Update). U.S. Department

of Health and Human Services, Public Health

Service, Atlanta, GA.

Cogliano, J.V. 1998. Assessing cancer risk from

environmental PCBs. Environmental Health

Perspectives, 106(6):317:323.

Delaware Department of Natural Resources and

Environmental Control. 1999. Chemical

Contaminants in Finfish from the Chesapeake and

Delaware Canal and Implications for Human Risk.

Delaware Department of Water Resources, March

31.

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.

Schmitt, C. J., J. L. Zabicek, and P. H. Peterman.

1990. National Contaminant Biomonitoring Program:

Residues of organochlorine chemicals in U.S.

freshwater fish, 1976-1984. Archives of

Environmental Contamination and Toxicology.

19:748-781.

U.S. Environmental Protection Agency. 1992.

National Study of Chemical Residues in Fish,

Volume I. Office of Science and Technology,

Washington, DC. EPA 823-R-92-008a.

U.S. Environmental Protection Agency. 1999a. Fact

Sheet: Update: National Listing of Fish and Wildlife

Advisories. Office of Water. EPA-823-F-99-005.

U.S. Environmental Protection Agency. 1999b.

Guidance for Assessing Chemical Contaminant Data

for Use in Fish Advisories. Volume 2, Third edition.

Risk Assessment and Fish Consumption Limits.

Office of Water. EPA 823-B-99-008. Washington,

DC.

U.S. Environmental Protection Agency. IRIS

(Integrated Risk Information System) for Aroclor

1254. 1999c. National Center for Environmental

Assessment, Office of Research and Development.

Cincinnati, OH.

U.S. Environmental Protection Agency, IRIS

(Integrated Risk Information System) for Aroclor

1016. 1999. National Center for Environmental

Assessment, Office of Research and Development.

Cincinnati, OH.

Zabik, M.E., A. M. Booren, M. J. Zabik, R. Welch,

and H. Humphrey. 1996. Pesticide residues, PCBs

and PAHs in baked, charbroiled, salt boiled, and

smoked Great Lakes’ lake trout. Food Chemistry

55(3): 231-239.

EPA Regulations and Advisories 

# Maximum Contaminant Level in drinking

water = 0.0005 mg/L

# Water Quality Criteria:

– Continuous chronic criteria (freshwater) = 0.014 μg/L

– Continuous chronic criteria

(saltwater) = 0.03 μg/L 

– Human health = 0.00017 μg/L

# Listed as a hazardous air pollutant under

Section 112 of the Clean Air Act

# Reportable quantity = 1 lb

# Listed as a hazardous substance

For more information about the National Fish

and Wildlife Contamination program, contact:

Mr. Jeffrey Bigler

U.S. Environmental Protection Agency

Office of Science and Technology

401 M St. S.W. (4305)

Washington, DC 20460

Bigler.Jeff@epa.gov

202 260-1305

202 260-9830 (fax)

The 1998 update of the database National

Listing of Fish and Wildlife Advisories is available

for downloading from the following Internet site:

http://www.epa.gov/OST