1

United States

Environmental Protection

Agency

Office of Water

4305

EPA-823-F-99-018 

September 1999

Fact Sheet

Toxaphene Update: Impact on Fish Advisories

Toxaphene is the tradename for an organochlorine pesticide that is comprised of a mixture of at least

670 chlorinated camphenes. Toxaphene was first introduced in 1947 and was probably the most heavily used

pesticide in the United States during the 1970s after DDT was banned. In the United States, toxaphene was banned

for most uses in 1982 and all uses were banned in 1990. However, due to its relatively long half-life, toxaphene

persists in the environment. The soil half-life is approximately 1 to 14 years. Toxaphene can enter waterbodies from

soil runoff and can also volatilize and be transported to waterbodies via the atmosphere. Toxaphene absorbed by

organisms accumulates in fatty tissues and has been shown to affect the central nervous system and the liver. EPA

has classified toxaphene as a probable human carcinogen (Group B2). As of 1998, four states have issued a total of

six fish advisories for toxaphene. These advisories inform the public that high concentrations of toxaphene 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 Toxaphene in the

Environment

In the United States, all uses of toxaphene were

banned in 1990. As a result, no entries for toxaphene

are reported in EPA’s Toxic Chemical Release

Inventory (TRI). In the past, toxaphene entered the

environment as an insecticide. Toxaphene entered

surface waters through runoff from rain, by direct

application to lakes as a pesticide, by wastewater

release from manufacturing facilities, and through

activities related to disposal of waste pesticides.

Toxaphene adsorbs to soil particles, and may enter

waterbodies in this form. Virtually all of the

toxaphene in waterbodies is in the particulate and

sediment fractions. Toxaphene was also applied

directly to soil as an insecticide for agricultural crops. 

Fate and Transport of Toxaphene

Once toxaphene enters the environment, it breaks

down very slowly. Therefore, even though the use of

toxaphene has been banned in the United States for

more than 10 years, exposures may still occur. After

releases to surface water or soils or application to

crops, the more volatile components of toxaphene

readily partition to the atmosphere where they

persist. The atmosphere is the most important

environmental medium for the transport of toxaphene

and it can also be transported to surface water and

soil by wet and dry deposition. As a result, toxaphene

can be carried far from its original release site. In

soil, toxaphene binds to soil particles; therefore,

leaching to ground water is not of great concern. In

surface water, the toxaphene that does not volatilize

is eventually deposited in sediments.

Toxaphene can bioconcentrate in the tissues of

aquatic organisms and may also be biomagnified in

the aquatic food chain. In 1984 and 1985, the U.S.

Fish and Wildlife Service collected 321 composite

samples of whole fish from 112 stations nationwide

as part of the National Contaminant Biomonitoring

Program (NCBP). Toxaphene was detected in

freshwater fish at 69% of 112 stations sampled in the

NCBP study. Maximum and geometric mean tissue

concentrations of toxaphene in 1984 were 8.2 and

0.14 ppm (wet weight), respectively. An analysis of

all 1984-1985 data from the NCBP study on

toxaphene in bottom-feeding and predatory fish

species showed there was no significant difference in

residues in these two trophic groups of fish. Mean

tissue concentrations of toxaphene were 0.19 + 0.63

and 0.17 + 0.35 ppm, respectively, for bottom

feeders and predator species. Results of a more

recent study show the range of total toxaphene

concentrations (wet weight) measured in various fish

species in the Great Lakes from 1992-1994 (see

Table 1).

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 toxaphene. 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 PCBs, 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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Potential Sources of Exposure and

Occurrence in Human Tissues

Because the use of toxaphene was banned in the

United States, potential sources of exposure are

limited. Low-level exposures may occur in the

general population through ingestion of contaminated

food. Because toxaphene may accumulate in fish

and shellfish, persons who consume large quantities

of these foods may be at greater risk of higher level

exposure than the general population. Additionally,

persons who eat large quantities of wild game from

areas where toxaphene was heavily used as a

pesticide may also be at higher risk. An additional

source of potential exposure is contact with

toxaphene-contaminated media near toxaphene

waste disposal sites. Before toxaphene was banned,

major sources of exposure resulted during its

manufacture and use as an insecticide. These

exposures were primarily dermal or by inhalation. 

Analytical methods can be used to measure

toxaphene in blood, urine, breast milk, and body

tissues. Similar to PCBs, toxaphene analysis can be

conducted for specific congeners using high

resolution spectrometry or gas chromatography with

electron-capture negative ionization. However, there

currently are no standard methods for these

analyses. At this time, EPA’s Office of Water

recommends analysis of total toxaphene until further

development of congener-specific analyses.

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 toxaphene, 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 1998, toxaphene was the chemical

contaminant responsible, at least in part, for the

issuance of a total of six fish consumption advisories

by four states: Arizona (3), Georgia (1), Oklahoma

(1), and Texas (1) (see Figure 1). This contaminant

accounts for less than 0.2 % of all advisories issued

in the United States. The number of advisories for

toxaphene has remained relatively unchanged from

1993 through 1998. Currently, no states have issued

statewide or regionwide advisories for toxaphene in

their freshwater lakes and/or rivers or in their coastal

marine waters. 

Fish Consumption Limits—Table 2 shows the

recommended monthly fish consumption limits for

toxaphene for fish consumers based on EPA’s

default 

Table 1. Mean Concentrations of

Toxaphene Reported in Great 

Lakes Fisha (1992-1994)

Lake Species

Mean

Concentrationb

(ppm)

Standard

Error of

Mean

(ppm)

Superio

r

Lake

trout

4.9 1.4

Michig

an

Lake

trout

1.5 0.3

Huron Lake

trout

2.4 0.5

Ontario Lake

trout

0.54 0.2

Erie Walleye 0.13 0.02

Superio

r

Smelt 0.16 0.04

Michig

an

Smelt 0.059 0.006

Ontario Smelt 0.067 0.02

a Species included only freshwater finfish.

b Concentrations are reported on a wet weight basis.

Source: Glassmeyer et al., 1997.

Table 2. Monthly Fish Consumption

Limits for Toxaphene

Risk-Based

Consumption

Limit

Noncancer

Health

Endpoints

Cancer

Health

Endpoints

Fish

Meals/Month

Fish Tissue

Concentration

s (ppm, wet

weight)

Fish Tissue

Concentrations

(ppm, wet weight)

16 >0.075 - 0.15 >0.0027 - 0.0055

12 >0.15 - 0.2 >0.0055 - 0.0073

8 >0.2 - 0.3 >0.0073 - 0.011

4 >0.3 - 0.6 >0.011 - 0.022

3 >0.6 - 0.8 >0.022 - 0.029

2 >0.8 - 1.2 >0.029 - 0.044

1 >1.2 - 2.4 >0.044 - 0.088

0.5 >2.4 - 4.8 >0.088 - 0.18

None (<0.5)a >4.8 >0.18

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.
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Figure 1. Fish Advisories for Toxaphene.

values for risk assessment parameters. 

Consumption limits have been calculated as the

number of allowable fish meals per month, based on

the ranges of toxaphene 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 d)

# EPA’s reference dose for toxaphene

(2.5 x 10-4 mg/kg-d) from EPA’s Reference Dose

Tracking Report (U.S. EPA, 1997)

# EPA’s cancer slope factor for toxaphene 

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

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

# Maximum acceptable cancer risk level (10-5 over

a 70-year lifetime).

For example, when toxaphene levels in fish tissue are

1 ppm, then sixteen 8-oz. meals per month (based

on the noncancer health endpoint-EPA’s reference

dose) or a half 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

toxaphene, this is the consumption limit based on the

cancer health 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 toxaphene. Additional information on

calculating specific limits for these sensitive

populations is available in EPAs Guidance for

Assessing Chemical Contaminant Data for Use in

Fish Advisories, Volume 2, Section 3.

Toxicity of Toxaphene

Pharmacokinetics—Most of the components of

toxaphene are rapidly degraded in mammals via

dechlorination, dehydrodechlorination, and oxidation,

primarily through the action of the mixed function

oxidase system and other hepatic microsomal

enzymes. Conjugation may occur but is not a major

route of metabolism. Each component of toxaphene

has its own rate of biotransformation, making the

characterization of toxaphene pharmacokinetics

complex. Some components of toxaphene are highly

lipophilic and poorly metabolized; these components

may accumulate in body fat. 

Acute Toxicity—Acute high-level exposures to

toxaphene and toxaphene-contaminated food have
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resulted in death in adults and children with an

estimated minimum lethal dose of 2 to 7 g, which is

equivalent to 29 to 100 mg/kg for an adult male. LD50

values in rats were 80 mg/kg for females and 90

mg/kg for males. Transient liver and kidney effects

and periods of memory loss have been observed in

humans after single large oral exposures. In animals,

the most sensitive organ is the liver. Toxicity to the

central nervous system, kidneys, and adrenal glands

has also been observed.

Chronic Toxicity—Chronic exposure to toxaphene

may result in damage to the following organ

systems: liver, kidney, adrenal, immunological, and

neurological. Chronic exposure to toxaphene may

cause hormonal alterations. A study on chronic

exposure found increased levels of hepatic

metabolism of the hormones estradiol and estrone

and a decrease in their uterotropic action. Some

adverse effects of toxaphene that do not occur with a

single exposure may result from repeated exposure

totaling a lower cumulative dose. Exposures at 0.06

mg/kg-d over 5 weeks caused adrenal hormone

reductions, whereas a single dose of 16 mg/kg did

not cause effects.

Developmental Toxicity—Women exposed to

toxaphene after entering a field that had recently

been sprayed with the chemical exhibited a higher

incidence of chromosomal aberrations in cultured

lymphocytes than did unexposed women. Dermal

and inhalation uptake were the probable routes of

exposure; however, the exposure was not quantified.

Animal study results suggest that toxaphene does

not interfere with fertility in experimental animals at

the doses tested (up to 25 mg/kg-d).

Adverse developmental effects, including

immunosuppressive and behavioral, were noted in

experimental animals at levels below those required

to induce maternal toxicity. Immunosuppression

(reduction in macrophage levels, cell-mediated

immunity, and humoral immunity) was observed in

test animals exposed during gestation and nursing,

as were alterations in kidney and liver enzymes and

delayed bone development. Other adverse effects

noted in offspring of maternally exposed animals

included histological changes in the liver, thyroid,

and kidney.

Toxaphene is known to be rapidly conveyed into

breast milk after maternal exposure to the chemical.

The half-life of toxaphene in milk has been estimated

at 9 days. 

As noted above, toxaphene accumulates in body

tissue; consequently, exposure occurring prior to

pregnancy can contribute to the overall maternal

body burden and result in exposure to the developing

individual. Therefore, it is necessary to reduce

exposure to children and women with childbearing

potential to reduce overall body burden. Depending

on the timing and extent of an individual’s prior

exposure to toxophene, the outcome of that

pregnancy may be affected even if exposure is

reduced during pregnancy.

Mutagenicity—Changes in human genetic material

have been noted in workers exposed to toxaphene.

There are also numerous positive mutagenicity

assays of toxaphene: the Ames test, sister chromatid

exchange, chromosomal aberrations in toxapheneexposed humans, and forward mutation assays. The

implications of this for human germ cells are not

known. One assay designed to assess the dominant

lethal effects on implantations in mice yielded

negative results. Some data suggest that the polar

fraction of toxaphene may be more mutagenic than

the nonpolar fraction.

Carcinogenicity—Toxaphene is classified as a

probable human carcinogen (Group B2) by EPA

based on oral studies in animals. No conclusive

human epidemiological studies are available for

toxaphene. Oral administration of toxaphene resulted

in an increased incidence of hepatocellular

carcinomas and neoplastic nodules in mice and

thyroid tumors in rats.

Toxaphene has recently been observed to have

estrogenic effects on human breast cancer estrogensensitive cells. Xenoestrogens have been

hypothesized to have a role in human breast cancer.

In addition to potential carcinogenic effects,

toxaphene may also cause disruption of the

endocrine system due to its estrogenic activity.

Special Susceptibilities—A protein-deficient diet

may increase the toxicity of toxaphene approximately

threefold based on an LD50 study in rats. Individuals

with latent or clinical neurological diseases, such as

Children may be at greater risk for toxic

effects caused by toxaphene because their

immune systems are not fully developed until 10

to 12 years of age. Immunosuppressive effects

have been demonstrated in animals after

chronic exposure to toxaphene. These studies

have also suggested that immature animals

cannot detoxify a toxaphene mixture as

efficiently as they can the single components of

the mixture. 

Summary of EPA Health Benchmarks

# Chronic Toxicity—Reference Dose:

2.5 × 10-4 mg/kg-d (U.S. EPA, 1997)

# Carcinogenicity: 1.1 per mg/kg-d (U.S.

EPA, 1999b)
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epilepsy or behavioral disorders, may be at higher

risk for toxaphene toxicity. In addition, children may

be especially susceptible to toxaphene-induced

neurotoxicity based on early reports of acute

ingestion toxicity.

Other individuals who may be at higher risk are those

with diseases of the renal, nervous, cardiac, adrenal,

and respiratory systems. Individuals using certain

medications are also at potential risk due to the

induction of hepatic microsomal enzymes by

toxaphene (discussed further in the following

section).

Interactive Effects —Metabolism of some drugs and

alcohol may be affected by toxaphene’s induction of

hepatic microsomal enzymes. This was observed in

a man using warfarin as an anticoagulant while he

used toxaphene as an insecticide. The effectiveness

of the drug was reduced because toxaphene’s

induction of microsomal enzymes increased the

drug’s metabolism.

Based on acute studies in animals and anecdotal

reports of acute exposure in humans, exposure to

chemicals that increase microsomal mixed-function

oxidase systems (e.g., lindane) are likely to reduce

the acute toxicity of other chemicals detoxified by the

same system (e.g., toxaphene) because the system

is functioning at a higher than normal level.

Toxaphene, in turn, may reduce the acute toxicity of

chemicals that require this system for detoxification.

Critical Data Gaps —The following data gaps have

been identified for toxaphene.

# mammalian germ cell genotoxicity, 

# studies that investigate sensitive developmental

toxicity endpoints including behavioral effects,

# epidemiological and animal studies of

immunotoxicity, 

# long-term neurotoxicity studies in animals using

sensitive functional and neuropathological tests

and behavioral effects on prenatally exposed

animals, 

# epidemiological studies evaluating multiple

organ systems, and pharmacokinetic studies.

EPA Regulations and Advisories

# Maximum Contaminant Level in drinking water = 0.003 mg/L

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

# Reportable Quantity = 1 lb

# Toxaphene Effluent Standard = 0-15 μg/L discharge/day

# Effluent Guidelines and Standards: Electroplating—Definition of Total Toxic Organic = > 0.01 mg/L

# Effluent Guidelines and Standards: Metal Finishing—Definition of Total Toxic Organic = >0.01 mg/L

# Chemicals and chemical categories to which this part applies (Toxic Release Inventory) = 25,000 lb

manufactured or processed, 10,000 lb otherwise used

# Extremely Hazardous Substances and Their Threshold Planning Quantities (Camphechlor) = 

500/10,000 lb

# Municipal Solid Waste Landfills: Design Criteria—MCL for Upper Aquifer = 0.005 mg/L

# Municipal Solid Waste Landfills: Appendix II = 2 μg/L (Practical Quantitation Limit)
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Sources of Information

ATSDR (Agency for Toxic Substances and Disease

Registry). 1996. Toxicological Profile for Toxaphene

(Update). U.S. Department of Health and Human

Services, Public Health Service, Atlanta, GA.

Davis, D.L., H.L. Bradlow, M. Wolff, T. Woodruff,

D.G. Hoel, and H. Anton-Culver. 1993. Medical

hypothesis: Xenoestrogens as preventable causes of

breast cancer. Environmental Health Perspectives

101(5): 372-377. 

Glassmeyer S.T., D.S. Devault, T.R. Meyers, and

R.A. Hites. 1997. Toxaphene in Great Lakes fish: a

temporal, spatial, and trophic study. Environmental

Science and Technology 31(1):84-88.

HSDB (Hazardous Substance Data Bank). 1998.

National Library of Medicine, National Toxicology

Program, Bethesda, MD.

Kidwell, J.M., L.J. Phillips, and G.F. Burchard. 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.

MIXTOX. 1992. Database on toxicological

interactions available on disk for personal computers.

Version 1.5. Environmental Criteria and Assessment

Office, U.S. Environmental Protection Agency,

Cincinnati, OH.

Soto, A.M., K.L.Chung, and C. Sonnenschein.1994.

The pesticides endosulfan, toxaphene, and dieldrin

have estrogenic effects on human estrogen-sensitive

cells. Environmental Health Perspectives 102(4):380-

383.

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

Reference Dose Tracking Report. Office of Pesticide

Programs, Health Effects Division. Washington, DC.

U.S. EPA (Environmental Protection Agency). 1999a.

Guidance for Assessing Chemical Contaminant Data

for Use in Fish Advisories. Volume 2, 3rd edition. Risk

Assessment and Fish Consumption Limits. EPA

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

U.S. EPA (Environmental Protection Agency). 1999b.

IRIS (Integrated Risk Information System) for

Toxaphene. National Center for Environmental

Assessment, Office of Research and Development.

U.S. EPA (Environmental Protection Agency). 1999c.

Fact Sheet: Update: National Listing of Fish and

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

Water, Washington, D.C.

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 1997 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