Consideration of the evidence for mechanisms of 1,1,2-trichloroethylene metabolism, including new identification of its dichloroacetic acid and trichloroacetic acid metabolites in mice.

Data derived from studies with vinylidene chloride (1,1-dichloroethylene)and 1,1,2-trichloroethylene suggest that similar mutagenic and tumorogenic properties in mice may be attributable to rearrangement of the 2 haloalkene-derived haloepoxides, respectively, into chloroacetyl chloride and dichloroacetyl chloride. On the other hand, the relative harmlessness of 1,1,2-trichloroethylene in rats and man is due to alternative rearrangement of 1,1,2-trichloroethylene oxide into chloral and the further products of its metabolism. The identification in mice of the new 1,1,2-trichloroethylene metabolite, dichloroacetic acid (in addition to trichloroacetic acid) strongly supports this supposition. The small proportion of dichloroacetic acid in relation to the large proportion of trichloroacetic acid in the urine of the treated mice is consistent with a spill-over model that is now tentatively proposed for 1,1,2-trichloroethylene metabolism in these animals.