vvEPA
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).
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.
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
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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, PCS residues in fish tissue remain
widespread, being detected at 91% of the sites
monitored in 1984. Maximum total PCS 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 concen-
trations 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 PCS 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 hexa-
followed by the pentachlorobiphenyls with concen-
trations of 0.077 and 0.072 ppm, respectively.
Table 1. Summary of PCBs Detected in Fish Tissue3 as Part of the National Study of Chemical
Residues in Fish' (1986-1989)
Congener Group
Monochlorobiphenyl
Dichlorobiphenyl
Trichlorobiphenyl
Tetrachlorobiphenyl
Pentachlorobiphenyl
Hexachlorobiphenyl
Heptachlorobiphenyl
Octachlorobiphenyl
Nonachlorobiphenyl
Decachlorobiphenyl
Total PCBs*
% of sites
where
detected
13.8
30.7
57.5
72.4
86.7
88.7
69.1
34.8
9.7
3.3
91.4
Maximum
0.235
5.072
18.344
60.764
29.578
8.862
1.850
0.593
0.413
0.038
ppm
Mean
0.001
0.021
0.150
0.696
0.565
0.356
0.097
0.017
0.003
0.001
1.898
Median
ND
ND
0.002
0.023
0.072
0.077
0.017
ND
ND
0.003
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.
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.
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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 PCS congeners. There is a standard
method for Aroclor analysis, but PCBs in environ-
mental samples and human tissues are not
adequately characterized as Aroclors. In the absence
of peer-reviewed analytical methods for congener
specific chemical analysis offish tissue, EPA's Office
of Water recommends the continued use of total
Aroclor chemical analysis offish tissue when
conducting human health risk assessment for PCBs.
Recently, new risk assessment methods for the PCS
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.
1998
D American Samoa = 1
D Guam
1—1 .,., .„ .„. _ .„
D Virgin Islands
D Puerto Rico
D States issuing advisory (37)
• Statewide Lake Advisories
A Statewide River Advisories
• Statewide Coastal Marine Advisories
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a result of PCS 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 PCS 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 PCS advisories in effect for their coastal
marine waters. To date, 79% of the 679 PCS
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 x 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 PCS 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.
Table 2. Monthly Fish Consumption Limits
for PCBs
Risk-Based
Consumption
Limit
Fish
Meals/Month
16
12
8
4
3
2
1
0.5
None (<0.5)a
Noncancer
Health
Endpoints
Fish Tissue
Concentrations
(ppm, wet weight)
>0.006-0.012
>0.012-0.016
>0.016-0.024
>0.024 - 0.048
>0.048 - 0.064
>0.064 - 0.097
>0.097-0.19
>0.19-0.39
>0.39
Cancer
Health
Endpoints
Fish Tissue
Concentrations
(ppm, wet weight)
=•0.0015-0.003
>0.003 - 0.004
>0.004 - 0.006
>0.006-0.012
>0.012-0.016
>0.016-0.024
>0.024 - 0.048
>0.048 - 0.097
>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.
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 tetra-
and higher chlorinated congeners from breast milk
ranges from 90% to 100% of the dose. Offspring can
also be
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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 PCS disposition
indicates that PCS 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 PCS toxicity,
there is no clear definition of the mechanisms for
most congeners. The congeners appear to act by a
variety of mechanisms. Some PCS 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 PCS
congeners seems to be unrelated to the Ah receptor.
Ultimately, the toxicity of a PCS 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—PCS mixtures have been
shown to cause adverse developmental effects in
experimental animals. Some human studies have
suggested that PCS 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
PCS levels were associated with impaired short-term
memory. Activity level was inversely related to 4-year
serum PCS level and also to maternal milk PCS
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.
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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 PCS intoxication
were observed in lactationally-exposed offspring, but
not in offspring exposed only prenatally.
PCB Exposure and Development Effects—
The data from some studies in humans suggest
that exposure to PCBs may cause develop-
mental 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.
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 non-
Hodgkins'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.
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)
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
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animal target organ and species; and comparative
toxicity of Aroclors and bioaccumulated PCBs.
EPA Regulations and Advisories
# Maximum Contaminant Level in drinking
water = 0.0005 mg/L
# Water Quality Criteria:
Continuous chronic criteria (fresh-
water) = 0.014 ug/L
Continuous chronic criteria
(saltwater) = 0.03 ug/L
Human health = 0.00017 ug/L
# Listed as a hazardous air pollutant under
Section 112 of the Clean Air Act
# Reportable quantity = 1 Ib
# Listed as a hazardous substance
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., LJ. 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.
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
202260-1305
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
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