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.
Prepared by Dennis M. Opresko, Ph.D., Chemical Hazard Evaluation and Communication Program, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.
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.
1,2-Dichloroethane is used primarily in the manufacture of vinyl chloride, as well as in the synthesis of tetrachloroethylene, trichloroethylene, 1,1,1-trichloroethane, vinylidene chloride, aziridines, and ethylenediamines (U.S. Air Force 1989, ATSDR 1992). It is added to gasoline as a lead-scavenging agent, and, in the past, has been used as a metal degreasing agent; a solvent; and a fumigant for grain, upholstery, and carpets. It has also been used in paints, coatings, adhesives, varnishes, finish removers, soaps, and scouring agents (U.S. Air Force 1989, ATSDR 1992).
1,2-Dichloroethane is expected to be highly mobile in most soils, and consequently, contamination of groundwater is possible. Adsorption to soil particles is low, particularly for soils with a low organic carbon content. Volatilization from soils and surface waters may be an important transport process. Microbial biodegradation is not expected to be significant.
1,2-Dichloroethane is absorbed through the lungs, gastrointestinal system, and skin (ATSDR 1992). It is distributed throughout the body but may be concentrated in adipose tissue. The compound can also accumulate in breast milk (Urusova 1953) and may cross the placenta (Withey and Karpinski 1985, Vozovaya 1977). Metabolism of 1,2-dichloroethane most likely involves conjugation with glutathione (ATSDR 1992). Urinary metabolites are likely to include thiodiglycolic acid, chloroacetic acid, and N-acetyl-S-carboxymethyl-L-cysteine (NTP 1991). Excretion occurs primarily through elimination of soluble urinary metabolites (Reitz et al. 1982, Spreafico et al. 1980).
Bronchitis, hemorrhagic gastritis and colitis, hepatocellular damage, renal tubular necrosis, central nervous system depression, and histopathological changes in the brain have been reported in cases of acute oral poisoning of humans (ATSDR 1992, NIOSH 1976). Animal data indicate that short-term exposures may produce immune system deficiencies (Munson et al. 1982), and subchronic or chronic oral exposures may affect the liver or kidney (NTP 1991, Alumot et al. 1976). Subchronic or chronic oral reference doses for 1,2-dichloroethane have not been adopted by the United States Environmental Protection Agency (EPA) (EPA 1993a); however, a provisional reference dose (RfD) of 0.03 mg/kg/day has been calculated by the Superfund Health Risk Technical Support Center (EPA, 1994) from a no-observed-adverse-effects level (NOAEL) of 26 mg/kg/day for rats tested in a subchronic gavage study (NTP 1991). Use of this value in risk assessment reports for specific sites must be approved by the Support Center.
Acute inhalation exposures to 1,2-dichloroethane (75-125 ppm) can result in irritation of the eyes, nose and throat, dizziness, nausea, vomiting, increasing stupor, cyanosis, rapid pulse, delirium, anesthesia, partial paralysis, loss of tactile sense, degenerative changes in the myocardium, abnormal EEG, liver and kidney damage, pulmonary edema, and hemorrhages throughout the body (NIOSH 1976, CEC 1986, ATSDR 1992, Nouchi et al. 1984). Short-term exposures to animals have resulted in central nervous system depression (inactivity or stupor, tremors, uncertain gait, narcosis); pulmonary congestion; renal tubular degeneration; fatty degeneration of the liver and, less commonly, necrosis and hemorrhage of the adrenal cortex; chronic splenitis; fatty infiltration of the myocardium; and immuno-deficiency (Spencer et al. 1951, Heppel et al. 1946, Storer et al. 1984, Sherwood et al. 1987). Chronic occupational exposure to 1,2-dichloroethane may result in central nervous systems effects including irritability, sleeplessness, and decreased heart rate; loss of appetite; nausea; vomiting; epigastric pain, as well as irritation of the mucous membranes; and liver and kidney impairment (NIOSH 1976). Subchronic or chronic inhalation exposures to animals resulted in pathological lesions in the kidney, liver, heart, lungs, and testes (Heppel et al. 1946, Spencer et al. 1951, Cheever et al. 1990). A subchronic or chronic inhalation reference concentration for 1,2-dichloroethane has not been adopted and verified by EPA (EPA 1993a); however, a provisional RfC of 0.005 mg/m3 has been calculated by the Superfund Health Risk Technical Support Center (EPA 1994) from a LOAEL (gastrointestinal disturbances and liver and gallbladder disease) of 10 mg/m3 for occupationally exposed workers (Kozik 1957). Use of this value in risk assessment reports for specific sites must be approved by the Support Center.
1,2-Dichloroethane is classified by EPA in Group B2 as a probable human carcinogen by both the oral and inhalation exposure routes, based on evidence for the induction of several types of tumors in rats and mice. Male rats treated by gavage with 1,2-dichloroethane exhibited increased incidences of fibromas of the subcutaneous tissue; hemangiosarcomas of the spleen, liver, pancreas, and adrenal gland; and squamous-cell carcinomas of the forestomach. Female rats treated by gavage developed mammary adenocarcinomas. Increased incidences of hepatocellular carcinomas and pulmonary adenomas were observed in male mice treated by gavage, and increased incidences of mammary adenocarcinomas, pulmonary adenocarcinomas, and endometrial polyps and sarcomas were observed in female mice (NCI 1978). Mice treated by topical application of 1,2-dichloroethane exhibited an increased incidence of lung papillomas (Van Duuren et al., 1979). The oral slope factor for 1,2-dichloroethane is 9.1E-2 (ug/kg/day)-1, and the drinking water unit risk is 2.6E-6 (ug/L)-1. The inhalation slope factor is 9.1E-2 (ug/kg/day)-1, and the inhalation unit risk is 2.6E-5 (ug/m3)-1 (EPA 1993a, 1993b). Retrieve Toxicity Profiles Formal Version
Last Updated 10/31/97