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Trichloroethylene in drinking water throughout gestation did not produce congenital heart defects in Sprague Dawley rats
Author(s) -
DeSesso John M.,
Coder Prägati S.,
York Raymond G.,
Budinsky Robert A.,
Pottenger Lynn H.,
Sen Shiladitya,
Lucarell Joelle M.,
Bevan Christopher,
Bus James S.
Publication year - 2019
Publication title -
birth defects research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.845
H-Index - 17
ISSN - 2472-1727
DOI - 10.1002/bdr2.1531
Subject(s) - gestation , trichloroethylene , fetus , developmental toxicity , teratology , toxicity , pregnancy , physiology , medicine , metabolite , inhalation , inhalation exposure , trichloroacetic acid , toxicology , chemistry , anesthesia , biology , environmental chemistry , biochemistry , genetics
Background Trichloroethylene (TCE) was negative for developmental toxicity after inhalation and oral gavage exposure of pregnant rats but fetal cardiac defects were reported following drinking water exposure throughout gestation. Because of the deficiencies in this latter study, we performed another drinking water study to evaluate whether TCE causes heart defects. Methods Groups of 25 mated Sprague Dawley rats consumed water containing 0, 0.25, 1.5, 500, or 1,000 ppm TCE from gestational day 1–21. TCE concentrations were measured at daily formulation, when placed into water bottles each day and when water bottles were removed from cages. Four additional mated rats per group were used for plasma measurements. At termination, fetal hearts were carefully dissected fresh and examined. Results All TCE concentrations were >90% of target when initially placed in water bottles and when bottles were placed on cages. All dams survived with no clinical signs. Rats in the two higher dose groups consumed less water/day than other groups but showed no changes in maternal or fetal weights. The only fetal cardiac observation was small (<1 mm) membranous ventricular septal defect occurring in all treated and water control groups; incidences were within the range of published findings for naive animals. TCE was not detected in maternal blood, but systemic exposure was confirmed by detecting its primary oxidative metabolite, trichloroacetic acid, although only at levels above the quantitation limit in the two higher dose groups. Conclusions Ingesting TCE in drinking water ≤1,000 ppm throughout gestation does not cause cardiac defects in rat offspring.