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 Tim Borges, Ph.D., Chemical Hazard Evaluation Group, 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-Dichloroethene exists in two isomeric forms, cis-1,2-dichloroethene and trans-1,2-dichloroethene, that are colorless, volatile liquids with a slightly acrid odor. Although not used extensively in industry, 1,2-dichloroethene is used in the production of other chlorinated solvents and as a solvent for dyes, perfumes, and lacquers (Sax and Lewis 1989, Budavari et al. 1989). Humans are exposed to 1,2-dichloroethene primarily by inhalation, but exposure can also occur by oral and dermal routes.
Limited information exists on the absorption, distribution, and excretion of 1,2-dichloroethene in either humans or animals. In vitro studies have shown that the mixed function oxidases will metabolize 1,2-dichloroethene; the final metabolic products are dependent on the initial isomer of 1,2-dichloroethene (Costa and Ivanetich 1984, Henschler 1977, Liebman and Ortiz 1977).
Information on the toxicity of 1,2-dichloroethene in humans and animals is limited. Workers exposed to 1,2-dichloroethene have been reported to suffer from drowsiness, dizziness, nausea, fatigue, and eye irritation (ATSDR 1990). Acute and subchronic oral and inhalation animal studies of trans-1,2-dichloroethene and acute inhalation animal studies of cis-1,2-dichloroethene suggest that the liver is the primary target organ. The toxicity is expressed in increased activities of liver associated enzymes, fatty degeneration, and necrosis (McCauley et al. n.d., Barnes et al. 1985, Freundt et al. 1977). Secondary target organs include the central nervous system and lung.
Based on an unpublished study describing decreased hemoglobin and hematocrits in rats treated by gavage for 90 days, EPA (1994a,b) assigned a subchronic and chronic oral reference dose (RfD) for cis-1,2-dichloroethene of 1.00E-01 mg/kg/day and 1.00E-02 mg/kg/day, respectively. The RfDs were derived from a no-observed-adverse-effect-level/lowest-observed-adverse-effect-level (NOAEL/LOAEL) of 32 mg/kg/day. An inhalation reference concentration (RfC) for cis-1,2-dichloroethene has not been derived.
Subchronic and chronic RfDs of 2.00E-01 mg/kg/day and 2.00E-02 mg/kg/day, respectively, for trans-1,2-dichloroethene have been calculated (EPA 1994a, b). The RfDs were derived from a LOAEL of 175 mg/kg/day that was based on increased serum alkaline phosphatase activity in mice that received trans-1,2-dichloroethene in their drinking water (EPA 1994a,b). An RfC for trans-1,2-dichloroethene has not been derived.
No information was available concerning the chronic, developmental, or reproductive toxicity of
cis-1,2-dichloroethene or trans-1,2-dichloroethene. No cancer bioassays or epidemiological studies were
available to assess the carcinogenicity of 1,2-dichloroethene. EPA (1994b) has placed both
cis-1,2-dichloro-ethene and trans-1,2-dichloroethene in weight-of-evidence group D, not classifiable as to
human carcinogenicity, based on the lack of human or animal carcinogenicity data and on essentially
negative mutagenicity data. Oral and inhalation slope factors have not been calculated for these isomers.
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