 this review is a a series of the authors ' studies designed to test the hypothesis that administration of trichloroethylene ( tce ) , dichloroethylene ( dce ) , their metabolites , and related compounds are responsible for fetal cardiac teratogenesis when given to pregnant rats during organogenesis . 
 identification of teratogenic compounds will allow more accurate assessment of environmental contaminants and public health risks . 
 epidemiologic studies and previous teratogenic studies using chick embryos and fetal rats have reported an increased number of congenital cardiac defects when exposed to tce or dce during fetal development . 
 metabolites of tce and dce studied in the drinking - water exposure study include trichloroacetic acid tcaa ) , monochloroacetic acid , trichloroethanol , carboxymethylcysteine , trichloroacetaldehyde , dichloroacetaldehyde , and dichlorovinyl cysteine . 
 varying doses of each were given in drinking water to pregnant rats during the period of fetal heart development . 
 rats receiving 2730 ppm tcaa in drinking water were the only metabolite group demonstrating a significant increase in the number of cardiac defects in fetuses on a per - litter basis ( p = 0.0004 wilcoxon test and p = 0.0015 exact permutation test ) . 
 maternal and fetal variables showed no statistically significant differences between treated and untreated groups . when treated with tcaa the increased cardiac defects , as compared to controls , 
 do not preclude the involvement of other metabolites as cardiac teratogens , but indicates tcaa as a specific cardiac teratogen . 
 further studies of drinking - water exposure and potential mechanisms of action on the developing heart are proceeding.imagesfigure 1 
Images