There is limited information on the reproductive effects of trichloroethylene in humans. Experimental animal studies have shown that trichloroethylene does not adversely affect fertility, or embryo implantation and survival, and does not cause teratogenic effects. Trichloroethylene has, however, caused delayed development and decreased birth weight. In most studies, no neonatal mortality was observed unless maternal toxicity occurred (REPROTEXT document, 2001).
One study found that paternal occupational exposure to trichloroethylene was not associated with an increase in spontaneous abortion or congenital malformations (Taskinen et al., 1989). However studies have linked maternal occupational trichloroethylene exposure with an increase in spontaneous abortions (Hemminki et al., 1980; Windham et al., 1991). Epidemiological observations showed an increased number of congenital cardiac defects in children whose mothers resided in an area with drinking water contaminated by trichloroethylene and dichloroethylene as compared to mothers who did not live in a contaminated area (Goldberg et al., 1990).
Cardiac abnormalities have been described in chick embryos when eggs were injected with trichloroethylene. Experiments with rats showed that exposure to trichloroethylene or dichloroethylene in the period before pregnancy caused no increase in congenital cardiac defects. However, rats exposed to these agents both before and during pregnancy had a significantly greater number of fetuses with congenital cardiac malformations (Dawson et al., 1993; 1990). In another study, trichloroethylene did not cause significant maternal, embryonal or fetal toxicity and was not teratogenic in rats or mice (Schwetz et al., 1975).
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