ArticleBirth defects research2019
Trichloroethylene in drinking water throughout gestation did not produce congenital heart defects in Sprague Dawley rats.
Article in Birth defects research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Direct potable reuse and birth defects prevalence in Texas: An augmented synthetic control method analysis of data from a population-based birth defects registry.Environmental epidemiology (Philadelphia, Pa.) · 2024Article
- Toxicity assessments of selected trichloroethylene and perchloroethylene metabolites in three in vitro human placental models.Reproductive toxicology (Elmsford, N.Y.) · 2022Article
- HNF4a transcription is a target of trichloroethylene toxicity in the embryonic mouse heart.Environmental science. Processes & impacts · 2020Article
- Trichloroethylene in drinking water throughout gestation did not produce congenital heart defects in Sprague Dawley rats.Birth defects research · 2019Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTrichloroethylene (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.
methodsGroups 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.
resultsAll 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.
conclusionsIngesting TCE in drinking water ≤1,000 ppm throughout gestation does not cause cardiac defects in rat offspring.
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