Toxicity Profiles
Formal Toxicity Summary for HEPTACHLOR EPOXIDE
NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
- EXECUTIVE SUMMARY
- 1. INTRODUCTION
- 2. METABOLISM AND DISPOSITION
- 1. INTRODUCTION
- 2.1 ABSORPTION 2.2 DISTRIBUTION 2.3 METABOLISM 2.4 EXCRETION
- 3. NONCARCINOGENIC HEALTH EFFECTS
- 3.1 ORAL EXPOSURES 3.2 INHALATION EXPOSURES 3.3 OTHER ROUTES OF EXPOSURE 3.4 TARGET ORGANS/CRITICAL EFFECTS
- 4. CARCINOGENICITY
- 4.1 ORAL EXPOSURES 4.2 INHALATION EXPOSURES 4.3 OTHER ROUTES OF EXPOSURE 4.4 EPA WEIGHT-OF-EVIDENCE 4.5 CARCINOGENICITY SLOPE FACTORS
- 5. REFERENCES
The toxicity information included in this summary was researched and compiled by R. A. Faust, Ph.D., who is a member of the Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory.
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
EXECUTIVE SUMMARY
Heptachlor epoxide, an oxidation product of the cyclodiene insecticide heptachlor, is not produced commercially in the United States and is not known to occur naturally (ATSDR 1993, IARC 1979). In the environment, heptachlor is converted to the epoxide, a chemical that degrades more slowly and, as a result, is more persistent than heptachlor. Both compounds adsorb strongly to sediments and are bioconcentrated in terrestrial and aquatic organisms; biomagnification of both is significant. Heptachlor epoxide has been identified in at least 87 of the 1300 hazardous waste sites on the EPA's National Priorities List (NPL) (ATSDR 1993).
In the body, heptachlor epoxide is formed by epoxidation of heptachlor. It is distributed to various tissues, with highest levels occurring in adipose tissues, where it may persist for prolonged periods. Heptachlor epoxide has been found in human fat, milk, and also in blood and fat of stillborn infants, indicating transplacental transfer to the fetus (IARC 1979, EPA 1986).
No studies were available regarding the toxic effects in humans after exposure to heptachlor epoxide. In laboratory animals, the liver and central nervous system are the primary target organs for heptachlor epoxide toxicity. Acute oral LD50s for rats, mice, and rabbits range from 39 to 144 mg/kg (ATSDR 1993), indicating moderate acute oral toxicity. Hypoactivity, ruffled fur, and increased mortality occurred in mice given a single oral dose of 30 mg/kg of a 25:75 heptachlor:heptachlor epoxide mixture (Arnold et al. 1977), and muscle spasms in the head and neck region and convulsive seizures were observed in young calves fed 2.5 mg/kg/day of a heptachlor epoxide preparation for 3 days (Buck et al. 1959). Increased liver weights and hepatocytomegaly were reported in male and female CD-1 mice fed a diet containing 1 to 10 ppm of a 25:75 heptachlor:heptachlor epoxide mixture for 18 months (IRDC 1973). Increased liver weights were also seen in dogs administered diets containing 0.5 to 7.5 ppm heptachlor epoxide for 60 weeks (Dow Chemical Company 1958).
An oral reference dose (RfD) of 1.3E-5 mg/kg/day for subchronic (EPA 1995a) and chronic exposure (EPA 1995b) to heptachlor epoxide was calculated based on a lowest-observed-adverse-effect level (LOAEL) of 0.0125 mg/kg/day from a 60-week dietary study with dogs (Dow Chemical Company 1958). Increased relative liver weight was identified as the critical effect. An inhalation reference concentration (RfC) for heptachlor epoxide has not been derived.
No epidemiological studies or case reports addressing the carcinogenicity of heptachlor epoxide in humans were available. Studies with laboratory animals demonstrated that heptachlor epoxide causes liver cancer in mice and rats. Liver carcinomas developed in C3H mice fed 10 ppm heptachlor epoxide for 2 years (Davis 1965). Hepatic hyperplasia, hyperplastic nodules, and liver carcinomas developed in CD-1 mice fed 0.1 to 10 ppm of a 25:75 heptachlor:heptachlor epoxide mixture for 18 months (IRDC 1973) and in CFN rats fed 0.5 to 10 ppm heptachlor epoxide for 108 weeks (Epstein 1976).
Based on EPA guidelines, heptachlor epoxide was assigned to weight-of-evidence group B2, probable human carcinogen (EPA 1995b). For oral and inhalation exposure, the slope factor is 9.1 (mg/kg/day)-1 (EPA 1995b,a). The unit risk is 2.6E-4 (µ/L)-1 for oral exposure and 2.6E-3 (µ/m3)-1 for inhalation exposure (EPA 1995b).
1. INTRODUCTION
Heptachlor epoxide (CAS No. 1024-57-3), also known as 1,4,5,6,7,8,8-heptachloro-a,4,7,7a-tetrahydro-4,7-methanol-1H-indene, epoxyheptachlor, or HCE, is a white crystalline solid with a molecular weight of 389.4 and a chemical formula of C10H5Cl7O (IARC 1979). It has a melting point of 160-161.5C (IARC 1979) and a vapor pressure of 2.6 × 10-6 mm Hg at 20C (ATSDR 1993). It is slightly soluble in water (0.275 mg/L at 25C), but is soluble in most organic solvents. Heptachlor epoxide is an oxidation product of heptachlor and chlordane. It is not produced commercially in the United States (ATSDR 1993) and is not known to occur naturally (IARC 1979).
Heptachlor is converted to heptachlor epoxide and other degradation products in the environment. Heptachlor epoxide degrades more slowly and, as a result, is more persistent than heptachlor. Both compounds adsorb strongly to sediments and are bioconcentrated in terrestrial and aquatic organisms; biomagnification of both is significant. Heptachlor epoxide has been identified in at least 87 of the 1300 hazardous waste sites on the National Priorities List (NPL) (ATSDR 1993).
2. METABOLISM AND DISPOSITION
2.1. ABSORPTION
Absorption of heptachlor epoxide in humans by various routes of exposure can be inferred from reports of adipose tissue levels of heptachlor epoxide (EPA 1985). Heptachlor epoxide is absorbed after oral administration to rats; however, quantitative data were not provided (Gillett and Chan 1968). One study examined the respiratory intake in rabbits exposed to pesticides under environmental conditions (Arthur et al. 1975). Male and female rabbits were housed outdoors in an area of high pesticide use, and a second group was housed inside a building with low pesticide use. During a 3-month period, weekly air sampling revealed a concentration of 1.86 ng/m3 heptachlor epoxide in the outside (high-exposure) area. Respiratory intake of heptachlor epoxide was calculated to be 0.002 µg/day.
2.2. DISTRIBUTION
Heptachlor epoxide has been found in human fat and also in blood (0.001 mg/L) and fat (0.01 to 0.3 mg/kg) of stillborn infants, indicating transplacental transfer to the fetus. The sera of pregnant women in a rural agricultural area in the Mississippi Delta contained levels of residues of chlorinated hydrocarbon insecticides, including heptachlor epoxide, that were comparable to those in occupationally exposed men (IARC 1979).
Following absorption of heptachlor, the epoxide was identified in various tissues of rats and dogs, with adipose tissue serving as the major storage depot. Four hours following a single gavage dose of 120 mg heptachlor, the epoxide was detected in blood, liver, and adipose tissue of rats and persisted for 3 to 6 months. In rats administered dietary concentrations of 30 to 35 ppm heptachlor for 2 months, heptachlor epoxide levels in the adipose tissue of males and females averaged 43 µg/g and 384 µg/g tissue, respectively. Much lower levels were detected in liver, kidney, and muscle tissue. A similar distribution was seen for dogs that received a daily capsule containing 1 mg heptachlor for 12 to 18 months. Heptachlor epoxide was not detected in the brain of either rats or dogs (EPA 1986).
2.3. METABOLISM
Dehydrochlorination of heptachlor epoxide, followed by hydroxylation and double-bond rearrangement, leads to the formation of a metabolite (unidentified) that is the principal form in which heptachlor is excreted in the feces (Leber and Benya 1994). Incubation of pig and rabbit liver microsomes with heptachlor epoxide led to the formation of a metabolite, identified as heptachlor epoxide diol (EPA 1986).
2.4. EXCRETION
Heptachlor epoxide is excreted in milk of lactating women, thereby reducing the body burden of heptachlor epoxide in these women but increasing the exposure of breast-fed infants (EPA 1985). Heptachlor epoxide elimination via milk production was found to be highest within 3 to 7 days in cows that had grazed on pastures immediately following treatment with heptachlor (Gannon and Decker 1960).
Heptachlor and its epoxide are primarily excreted in the feces. Rats that consumed a diet containing 10 ppm heptachlor epoxide for 30 days (estimated total consumption 5 mg) excreted 950 µg of an unnamed metabolite and 66 µg unchanged heptachlor epoxide in the feces (Matsumara and Nelson 1971). Rats and rabbits given oral doses of 28 to 50 mg/kg of heptachlor excreted heptachlor epoxide over at least a 12-month period (EPA 1986).
3. NONCARCINOGENIC HEALTH EFFECTS
3.1. ORAL EXPOSURES
3.1.1. Acute Toxicity
3.1.1.1. Human
Information on the acute toxicity of heptachlor epoxide in humans following oral exposure was not available.
3.1.1.2. Animal
Acute oral LD50s for rats, mice, and rabbits range from 39 to 144 mg/kg (ATSDR 1993). Single oral doses of a 25:75 heptachlor:heptachlor epoxide mixture administered to mice resulted in moderate hypoactivity, ruffled fur, and 20% mortality at 30 mg/kg and severe hypoactivity and "partial" mortality at 100 mg/kg (Arnold et al. 1977).
Among calves given single doses of heptachlor epoxide preparation, three received 5, 10, or 15 mg/kg/day and two received 25 mg/kg/day. All died within 3 hours to 3 days. Young calves fed a heptachlor epoxide preparation (2.5 or 3.5 mg/kg/day for 3 days) had muscle spasms in the head and neck region, convulsive seizures, elevated body temperatures, and engorged brain blood vessels (Buck et al. 1959).
3.1.2. Subchronic Toxicity
Information on the subchronic toxicity of heptachlor epoxide in humans or animals following oral exposure was not available.
3.1.3. Chronic Toxicity
3.1.3.1. Human
Information on the chronic toxicity of heptachlor epoxide in humans following oral exposure was not available.
3.1.3.2. Animal
A 25:75 mixture of heptachlor:heptachlor epoxide was administered to groups of 100 male and 100 female CD-1 mice in the diet at 0, 1, 5, and 10 ppm for 18 months. At the 6-month interim sacrifice, decreased body weights were seen in high-dose females but not in other treated groups. Significantly increased liver weights and an increased incidence of hepatocytomegaly were seen in both sexes at 6 and 18 months. The increases were dose-related and more marked in males (liver weight) (IRDC 1973).
In studies reviewed by Hayes (1982), no adverse effects were observed in rats administered 5 ppm heptachlor epoxide (about 0.25 mg/kg/day) in the diet for 60 weeks. The same dietary level resulting in a dose of about 0.35 mg/kg/day for 50 weeks was found harmless to dogs in a 60-week study. Histological liver changes (unspecified) produced in rat liver by doses of 0.35 mg/kg/day for 50 weeks returned to normal 30 weeks after cessation of dosing.
Groups of beagle dogs (2 males and 3 females/group) were given diets containing 0, 0.5, 2.5, 5, or 7.5 ppm heptachlor epoxide for 60 weeks (Dow Chemical Company 1958). Significantly increased relative liver weights were seen for both males and females at all concentrations tested.
3.1.4. Developmental and Reproductive Toxicity
3.1.4.1. Human
Information on the developmental and reproductive toxicity of heptachlor epoxide in humans following oral exposure was not available.
3.1.4.2. Animal
In a dominant lethal assay, eight male CD-1 mice received single oral doses of 7.5 or 15 mg/kg of a 25:75 heptachlor:heptachlor epoxide mixture and were bred with three untreated females each week for 6 weeks. There were no adverse effects on the reproductive capacity of male mice (Arnold et al. 1977). Heptachlor epoxide alone was tested in another dominant lethal assay with mice at a dose of 8 mg/kg/day. The chemical did not produce early fetal deaths or preimplantation losses above the control limits (Epstein et al. 1972).
3.1.5. Reference Dose
3.1.5.1. Subchronic
ORAL RfD: 1.3E-5 mg/kg/day (EPA 1995a)
NOAEL: not established
LOAEL: 0.0125 mg/kg/day
UNCERTAINTY FACTOR: 1000
PRINCIPAL STUDY: Dow Chemical Company 1958
COMMENTS: The chronic oral RfD (see Sect. 3.1.5.2.) was adopted as the subchronic oral RfD.
3.1.5.2. Chronic
ORAL RfD: 1.3E-5 mg/kg/day (EPA 1995b)
NOAEL: not established
LOAEL: 0.0125 mg/kg/day
UNCERTAINTY FACTOR: 1000
CONFIDENCE:
Study: Low
Data Base: Medium
RfD: Low
VERIFICATION DATE: 9/16/86
PRINCIPAL STUDY: Dow Chemical Company 1958
COMMENTS: The chronic RfD is based on increased relative liver weights in male and female dogs fed a diet containing heptachlor epoxide for 60 weeks. An uncertainty factor of 10 each was applied for inter- and intraspecies variation and to account for the fact that a NOAEL was not attained.
3.2. INHALATION EXPOSURES
3.2.1. Acute Toxicity
Information on the acute toxicity of heptachlor epoxide in humans or animals following inhalation exposure was not available.
3.2.2. Subchronic Toxicity
Information on the subchronic toxicity of heptachlor epoxide in humans or animals following inhalation exposure was not available.
3.2.3. Chronic Toxicity
Information on the chronic toxicity of heptachlor epoxide in humans or animals following inhalation exposure was not available.
3.2.4. Developmental and Reproductive Toxicity
3.2.4.1. Human
Significantly higher levels of heptachlor epoxide were detected in the sera of a group of women identified through hospital records with premature delivery than in the sera of a control group with normal delivery. However, sera levels of 8 of the 10 organochlorine pesticides for which analytical data were obtained were also significantly higher in the premature delivery group (Wasserman et al. 1982).
3.2.4.2. Animal
Information on the developmental and reproductive toxicity of heptachlor epoxide in animals following inhalation exposure was not available.
3.2.5. Reference Concentration
An inhalation RfC for heptachlor epoxide has not been derived.
3.3. OTHER ROUTES OF EXPOSURE
3.3.1. Acute Toxicity
3.3.1.1. Human
Information on the acute toxicity of heptachlor epoxide in humans by other routes of exposure was not available.
3.3.1.2. Animal
The intraperitoneal LD50 for heptachlor epoxide is 18 mg/kg (EPA 1985). A single intraperitoneal dose of 200 mg/kg resulted in violent convulsions 5 hours after treatment, at which time the rats were killed for biochemical neurotoxicity evaluations of brain homogenates. Heptachlor epoxide was shown to inhibit ATPase (adenosine triphosphate enzyme) activity in brain synaptic vesicles (EPA 1985).
Single intraperitoneal doses of a 25:75 heptachlor:heptachlor epoxide preparation administered to mice resulted in moderate hypoactivity, ruffled fur, and 20% mortality at 30 mg/kg and severe hypoactivity and "partial" mortality at 100 mg/kg (Arnold et al. 1977).
3.3.2. Subchronic Toxicity
Information on the subchronic toxicity of heptachlor epoxide in humans or animals by other routes of exposure was not available.
3.3.3. Chronic Toxicity
Information on the chronic toxicity of heptachlor epoxide in humans or animals by other routes of exposure was not available.
3.3.4. Developmental and Reproductive Toxicity
Information on the developmental and reproductive toxicity of heptachlor epoxide in humans or animals by other routes of exposure was not available.
3.4. TARGET ORGANS/CRITICAL EFFECTS
3.4.1. Oral Exposures
3.4.1.1. Primary Target Organ(s)
Liver: Chronic exposure caused increased liver weights in rats and dogs and hepatocellular changes in rats.
3.4.1.2. Other Target Organ(s)
Nervous system: Although no central nervous system effects were reported in chronic studies, acute exposures resulted in hypoactivity, seizures, and muscle spasms in animals.
3.4.2. Inhalation Exposures
No primary or other target organs were identified.
3.4.3 Other Routes of Exposure
Nervous system: Intraperitoneal injections produced convulsions and hypoactivity in animals.
4. CARCINOGENICITY
4.1. ORAL EXPOSURES
4.1.1. Human
Information on the carcinogenicity of heptachlor epoxide in humans following oral exposure was not available.
4.1.2. Animal
Davis (1965) fed groups of 100 male and 100 female C3H mice a diet containing 0 or 10 ppm heptachlor epoxide for 2 years. Survival was low, with 9.5% of treated mice and 50% of controls alive after 2 years. A two-fold increase in benign liver lesions (hyperplasia and benign tumors) over controls was reported. A reevaluation of the study by Reuber (1977) revealed a significantly increased incidence of liver carcinomas in the treated groups (77/81 in females and 73/79 in males) compared with controls (2/53 in males and 22/73 in females).
IRDC (1973; also cited as Velsicol Chemical Co. 1973) tested a 25:75 mixture of heptachlor: heptachlor epoxide by administering groups of 100 male and 100 female CD-1 mice 0, 1, 5, or 10 ppm of the test material in the diet for 18 months. Both sexes in the 5 and 10 ppm dose groups had a significantly increased incidence of hepatic hyperplasia and hyperplastic nodules. A reevaluation of this study by Reuber (1977) and four independent pathologists found a greater incidence of hepatic carcinoma, with a corresponding decrease in the incidence of hyperplasia and hyperplastic nodules (EPA 1985).
Epstein (1976) reported a previously unpublished study in which groups of 25 male and 25 female CFN rats were administered heptachlor epoxide at dietary concentrations of 0.5 to 10 ppm for 108 weeks. An excess of hepatomas and a spectrum of unusual tumors were seen in the treated groups. Histological reevaluation revealed an excess of hepatic carcinomas in females given 5 and 10 ppm; males given 10 ppm also showed an excess of tumors when hepatic carcinomas and hyperplastic nodules were combined.
4.2. INHALATION EXPOSURES
Information on the carcinogenicity of heptachlor epoxide in humans or animals following inhalation exposure was not available.
4.3. OTHER ROUTES OF EXPOSURE
Information on the carcinogenicity of heptachlor epoxide in humans or animals by other routes of exposure was not available.
4.4. EPA WEIGHT-OF-EVIDENCE
Classification: Group B2, probable human carcinogen (EPA 1995b)
Basis: Sufficient evidence exists from rodent studies in which liver carcinomas were induced in two strains of mice (C3H and CD-1) of both sexes and in CFN female rats. Several structurally related compounds are liver carcinogens.
4.5. CARCINOGENICITY SLOPE FACTORS
4.5.1. Oral
SLOPE FACTOR: 9.1 (mg/kg/day)-1 (EPA 1995b)
UNIT RISK: 2.6E-4 (µg/L)-1 (EPA 1995b)
PRINCIPAL STUDIES: Davis 1965, Velsicol Chemical Corporation 1973
COMMENT: The estimated slope factor is the geometric mean of four slope factors derived from data sets using two strains of mice (C3H and CD-1).
4.5.2. Inhalation
SLOPE FACTOR: 9.1 (mg/kg/day)-1 (EPA 1995a)
UNIT RISK: 2.6E-3 (µg/m3)-1 (EPA 1995b)
PRINCIPAL STUDY: Davis 1965, Velsicol Chemical Corporation 1973
COMMENT: The risk estimates were calculated from oral data.
5. REFERENCES
Arnold, D. W., G. L. Kennedy, Jr., M. L. Keplinger, et al. 1977. Dominant lethal studies with technical chlordane, HCS-3260, and heptachlor:heptachlor epoxide. J. Toxicol. Environ. Health 2:547-555.
Arthur, R. D., J. D. Cain, and B. F. Barrantine. 1975. The effect of atmospheric levels of pesticides on pesticide residues in rabbit adipose tissue and blood sera. Bull. Environ. Contam. Toxicol. 14:760-764.
ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profile for Heptachlor/Heptachlor Epoxide. Prepared by Clement International Corporation, under Contract No. 205-88-0608. U.S. Public Health Service, TP-92/11.
Buck, W. B., R. D. Radeleff, J. B. Jackson, et al. 1959. Oral toxicity studies with heptachlor and heptachlor epoxide in young calves. J. Econ. Entomol. 52:1127-1129 (cited in ATSDR 1993).
Dow Chemical Company. 1958. MRID No. 00061912. Available form EPA. FOI, EPA, Washington, DC 20460 (cited in EPA 1995b).
Davis, K. 1965. Pathology Report on mice fed Aldrin, Dieldrin, Heptachlor and Heptachlor Epoxide for Two Years. Internal FDA memorandum to Dr. A. J. Lehman, July 19 (cited in EPA 1995b)
EPA (U.S. Environmental Protection Agency). 1985. Drinking Water Criteria Document for Heptachlor, Heptachlor Epoxide and Chlordane (Final Draft). ECAO-CIN-406; EPA-600/X-84-197-1; PB86-117991. Prepared by the Office of Environmental Criteria and Assessment Office, Cincinnati, OH, for the Office of Water Drinking Water.
EPA. 1986. Carcinogenicity Assessment of Chlordane and Heptachlor Epoxide. EPA/600-/6-87/004. Carcinogen Assessment Group, Office of Health and Environmental Assessment, Washington, D.C.
EPA. 1995a. Health Effects Assessment Summary Tables. Annual FY-95. Prepared for the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, for the Office of Emergency and Remedial Response, Washington, D.C.
EPA. 1995b. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Cincinnati, OH.
Epstein, S. S., E. Arnold, J. Andea, et al. 1972. Detection of chemical mutagens by the dominant lethal assay in the mouse. Toxicol. Appl. Pharmacol. 23:288-325.
Epstein, S. S. 1976. Carcinogenicity of heptachlor and chlordane. Sci. Total Environ. 6:103-154.
Gannon, N. and G. C. Decker. 1960. The excretion of dieldrin, DDT, and heptachlor epoxide in milk of dairy cows fed on pasture treated with dieldrin, DDT, and heptachlor. J. Econ. Entomol. 53:411-415 (cited in ASTDR 1993).
Gillett, J. W. and T. M. Chan. 1968. Cyclodiene insecticides as inducers, substrates, and inhibitors of microsomal epoxidation. J. Agr. Food Chem. 16:590-593 (cited in ATSDR 1993).
Hayes, W. J. 1982. Chlorinated hydrocarbon insecticides. In: Pesticides Studied in Man. Williams & Wilkins, Baltimore, pp. 233-234.
IARC (International Agency for Research on Cancer). 1979. Heptachlor and heptachlor epoxide. In: IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemical to Humans. Some Halogenated Hydrocarbons, Vol. 20. World Health Organization, Lyon, France, pp. 129-154.
IRDC (International Research and Development Corporation). 1973. Unpublished Report to Velsicol Chemical Corporation, Eighteen Month Oral Carcinogenicity Study in Mice, September 26 (cited in Epstein 1976).
Leber, A. P. and T. J. Benya. 1994. Chlorinated hydrocarbon pesticides. In: Patty's Industrial Hygiene and Toxicology, 4th ed., Volume II, Part E. G. D. Clayton and F. E. Clayton, eds. New York, John Wiley & Sons, pp. 1540-1545.
Matsumara, F. and J. O. Nelson. 1971. Identification of the major metabolic product of heptachlor epoxide in rat feces. Bull. Environ. Contam. Toxicol. 5:489 (cited in EPA 1985).
Reuber, M.D. 1977. Histopathology of carcinomas of the liver in mice ingesting heptachlor or heptachlor epoxide. Expl. Cell Biol. 45:147-157 (cited in EPA 1985).
Velsicol Chemical Corporation. 1973. MRID No. 00062678. Available from EPA. FOI, EPA, Washington, D.C (cited in EPA 1995b).
Wasserman, M., M. Ron, B. Bercovici, et al. 1982. Premature delivery and organochlorine compounds: Polychlorinated biphenyls and some organochlorine pesticides. Environ. Res. 28:106-112 (cited in ATSDR 1993).
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