The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for CHLORDANE

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.

December 1994

Prepared by: Carol S. Forsyth, Ph.D., Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.


*Managed by Martin Marietta Energy Systems Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.

Technical grade chlordane is a mixture of structurally related compounds including trans-chlordane, cis-chlordane, -chlordene, heptachlor, and trans-nonachlor (ATSDR, 1994). Chlordane was used extensively as a pesticide in the United States from 1948 to 1988. Because the chemical is persistent in the environment, exposure can still occur from breathing the air of treated homes, consuming shellfish caught in contaminated waters, or eating food produced on contaminated farmlands (ATSDR, 1994). Chlordane is readily absorbed after oral, inhalation, or dermal exposure and is stored in adipose tissue. The chemical is excreted in the feces from the bile (Ewing et al., 1985), but metabolite residues have been detected in 46% of human milk samples from Arkansas/Mississippi, in 68% of samples from Mississippi, and in 100% of samples from Hawaii (ATSDR, 1994).

Death in humans from ingestion of chlordane was accompanied by vomiting, dry cough, agitation and restlessness, hemorrhagic gastritis, bronchopneumonia, muscle twitching, and convulsions (IARC, 1991). Nonlethal, accidental poisoning of children has resulted in convulsions, excitability, loss of coordination, dyspnea, and tachycardia; however, recovery was complete (IARC, 1991). When a municipal water supply was contaminated with chlordane in concentrations of up to 1.2 g/L, 13 persons had symptoms of gastrointestinal and neurological disorders (WHO, 1984). Signs of toxicity from chronic inhalation exposure in chlordane treated homes include sinusitis, bronchitis, dermatitis, neuritis, migraine (Menconi et al., 1988), gastrointestinal distress, fatigue, memory deficits, personality changes, decreased attention span, numbness or paresthesias, disorientation, loss of coordination, dry eyes, and seizures (Spyker et al., 1990). Blood dyscrasias, including production defects and thrombocytopenic purpura, have been described for both professional applicators and for home owners and their families following home termite treatment (Epstein and Ozonoff, 1987). An inhalation reference concentration (RfC) for chlordane is under review by EPA (EPA 1994a).

Liver enlargement occurred in mice exposed to 10 mg/m3 8 hours/day, 5 days/week for 90 days (IARC, 1991). Increased liver weights were found in female rats (5.8 mg/m3), increased liver and kidney weights occurred in male rats (28.2 mg/m3), serum chemistry changes indicative of liver damage and hypersensitivity occurred in females (28.2 mg/m3), and centrilobular hepatocyte enlargement occurred in males and females (28.2 mg/m3) exposed to chlordane by inhalation 8 hours/day, 5 days/week, for 28 days (ATSDR, 1994).

Long-term feeding studies with chlordane in laboratory animals resulted in significantly reduced weight gains in male (203.5 or 407.0 ppm; 80 weeks) and female (120.8 or 241.5 ppm; 80 weeks) rats, a dose-related trend in mortality of female rats and male mice (29.9 or 56.2 ppm; 80 weeks) (NCI, 1977), and liver hypertrophy of female rats (>=5 ppm; 130 weeks) (EPA, 1994a). In a 24-month feeding study with mice, hepatocellular swelling and necrosis occurred in males and increased liver weights occurred in males and females fed 5 ppm (ATSDR, 1994; EPA, 1994a). A chronic oral reference dose (RfD) of 6E-05 mg/kg/day for chlordane was calculated from a no-observed-adverse-effect level (NOAEL) of 0.055 mg/kg/day derived from a chronic feeding study with rats (EPA, 1994a). The subchronic oral RfD is also 6E-05 mg/kg/day (EPA, 1994b).

Altered endocrine (Cranmer et al., 1984) and immune (Shepard, 1983; Theus et al., 1991) functions have been observed in rat pups exposed to chlordane in utero.

Exposure of humans from chlordane treated homes has been associated with leukemia (Epstein and Ozonoff, 1987), skin neoplasms (Menconi et al., 1988), and neuroblastoma in children (IARC, 1991). An increased risk of non-Hodgkin's lymphoma has been found among farmers exposed to chlordane 20 or more days per year (Hoar Zahm et al., 1988). Hepatic carcinomas and hepatocellular adenomas have been described for several strains of male and female mice and male rats given chlordane in the diet (NCI, 1977; EPA, 1994a). EPA (1994a) has classified chlordane as group B2, probable human carcinogen. The carcinogenicity slope factor (q1*) for oral exposure is 1.3E+0 (mg/kg/day)-1 based on an increase of hepatocellular carcinomas in mice and hepatocellular adenomas in rats. A drinking water unit risk of 3.7E-5 (µg/L)-1 was calculated based on the q1* (EPA, 1994a). The q1* for inhalation exposure is 1.3E+0 (mg/kg/day)-1 (EPA, 1994b), and the inhalation unit risk value is 3.7E-4 (µg/m3)-1 (EPA, 1994a). The inhalation risk estimates were calculated from the oral data. Retrieve Toxicity Profiles Formal Version

Last Updated 8/29/97

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