Toxicity Profiles
Condensed Toxicity Summary for 1,1-DICHLOROETHANE
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.
FEBRUARY 1994
Prepared by: Dennis M. Opresko, Ph.D., Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *
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.
1,1-Dichloroethane is used primarily as an intermediate in manufacturing vinyl chloride and 1,1,1-trichloroethane; it is also used as a cleaning agent and degreaser and as a solvent for plastics, oils, and fats (ATSDR, 1990).
The available evidence indicates that 1,1-dichloroethane can be readily absorbed following inhalation and oral exposures (ATSDR, 1990). The anesthetic effects of 1,1-dichloroethane are evidence that the chemical reaches the central nervous system (CNS). Acetic acid is a major metabolite, and 2,2-dichloroethanol, chloroacetic acid, and dichloroacetic acid are minor metabolites (McCall et al., 1983). In animal studies, orally administered 1,1-dichloroethane was excreted primarily in expired air as the unmetabolized chemical (Mitoma et al., 1985).
No information is available on the oral toxicity of 1,1-dichloroethane to humans. In animals, a drinking water concentration of up to 2500 mg/L for 52 weeks caused no adverse effects in male mice (Klaunig et al., 1986), and maximum gavage doses of 764 mg/kg/day (male Osborne-Mendel rats), 950 mg/kg (female Osborne-Mendel rats), 2885 mg/kg (male B6C3F1 mice), and 3331 mg/kg (female B6C3F1 mice), 5 days/week for 78 weeks (3 weeks on, 1 week off) resulted in no histopathological changes (NCI, 1978). A subchronic oral RfD of 1 mg/kg/day and a chronic oral RfD of 0.1 mg/kg/day (based on an inhalation study in rats and route-to-route extrapolation) are listed in HEAST (EPA, 1993a); however, an oral RfD is currently not found in IRIS. A U.S. Environmental Protection Agency (EPA) reassessment of the oral RfD is pending (EPA, 1993b).
At high vapor concentrations (26,000 ppm), 1,1-dichloroethane induces anesthesia and can cause cardiac arrhythmia in humans, but no fatalities have occurred (ATSDR, 1990). Adverse effects following subchronic or chronic exposures to humans have not been reported. In animal studies, 1,1-dichloroethane did not cause developmental or reproductive effects but did delay rib ossification in rats (Schwetz et al., 1974). Kidney damage was observed in cats exposed to 2025 mg/m3 (6 hours/day, 5 days/week) for 13 weeks followed by 4050 mg/m3 for an additional 13 weeks; however, similar effects were not seen in rats, rabbits, or guinea pigs. A subchronic RfC of 5 mg/m3 and a chronic RfC of 0.5 mg/m3 are listed in HEAST (EPA, 1993a). These RfCs are based on the adverse renal effects in cats following subchronic inhalation exposure. An RfC for 1,1-dichloroethane is not currently on IRIS although an EPA reassessment of the compound is pending (EPA, 1993b).
1,1-Dichloroethane is placed in Group C, possible human carcinogen (EPA, 1993b), based on no human data and limited evidence of carcinogenicity in two animal species (rats and mice), as shown by an increased incidence of mammary gland adenocarcinomas and hemangiosarcomas in female rats and an increased incidence of hepatocellular carcinomas and benign uterine polyps in mice (EPA, 1993b). Slope factors and unit risks have not been calculated.
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Last Updated 8/29/97