Trichloroethylene-induced pneumotoxicity in fetal and neonatal mice.

Trichloroethylene (TCE) has previously been shown, in adult mouse lung, to alter the distribution of phospholipid associated with the pulmonary surfactant and to affect the activity of phospholipase A2, an enzyme involved in synthesis of the surfactant. However there are no data available on the effects of maternal exposure to TCE on fetal lung development. To determine if maternal TCE exposure may affect fetal pulmonary development, pregnant mice were treated with TCE (3000 mg/kg body wt.) administered intraperitoneally on day 17 of pregnancy. Fetuses were examined on the 18th and 19th gestational days and the 1st, 5th and 10th postnatal days. TCE caused increased mortality among 18- and 19-day-old fetuses and 1-day-old newborn mice. In addition mean body weight was reduced on the 1st postnatal day in animals exposed to TCE. Specific lung weights were also significantly reduced on both the 18th and 19th gestational days. More importantly, total lung phospholipid content was depressed immediately before birth; total DNA was not affected. These results suggest that prenatal maternal exposure to TCE may delay pulmonary maturation during the critical period when surfactant synthesis is initiated.