A systematic evaluation of the potential effects of trichloroethylene exposure on cardiac development

Reprod Toxicol. 2016 Oct:65:321-358. doi: 10.1016/j.reprotox.2016.08.014. Epub 2016 Aug 27.

Abstract

The 2011 EPA trichloroethylene (TCE) IRIS assessment, used developmental cardiac defects from a controversial drinking water study in rats (Johnson et al. [51]), along with several other studies/endpoints to derive reference values. An updated literature search of TCE-related developmental cardiac defects was conducted. Study quality, strengths, and limitations were assessed. A putative adverse outcome pathway (AOP) construct was developed to explore key events for the most commonly observed cardiac dysmorphologies, particularly those involved with epithelial-mesenchymal transition (EMT) of endothelial origin (EndMT); several candidate pathways were identified. A hypothesis-driven weight-of-evidence analysis of epidemiological, toxicological, in vitro, in ovo, and mechanistic/AOP data concluded that TCE has the potential to cause cardiac defects in humans when exposure occurs at sufficient doses during a sensitive window of fetal development. The study by Johnson et al. [51] was reaffirmed as suitable for hazard characterization and reference value derivation, though acknowledging study limitations and uncertainties.

Keywords: AOP; Cardiac; Malformations; TCE; Trichloroethylene.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dose-Response Relationship, Drug
  • Environmental Exposure / adverse effects*
  • Environmental Pollutants / toxicity*
  • Epithelial-Mesenchymal Transition
  • Female
  • Heart / drug effects*
  • Heart / embryology
  • Humans
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Solvents / toxicity*
  • Trichloroethylene / toxicity*

Substances

  • Environmental Pollutants
  • Solvents
  • Trichloroethylene