. Author manuscript; available in PMC: 2021 Mar 1.

Published in final edited form as: Environ Sci Process Impacts. 2020 Feb 5;22(3):472–486. doi: 10.1039/c9em00537d

Table 1.

Mechanisms of TCE toxicity observed in placental models

Observed mechanism of TCE (or TCE metabolite) toxicity	Model utilized	Potential impact on placenta	Relevant Pregnancy outcome	References
Changes in energy metabolism pathways and macronutrient utilization by cells	HTR-8 cell line	Impaired trophoblast function during tissue remodeling; macronutrients diverted away from fetus to maintain placental sufficiency.	Preeclampsia; intrauterine growth restriction	¹¹⁵
Mitochondrial dysfunction; impaired mitochondrial adaptability	HTR-8 cell line	Insufficient metabolic energy capacity during tissue remodeling; impaired mitochondrial adaptability	Preeclampsia; intrauterine growth restriction	^{106, 107}
Apoptosis; lipid peroxidation	HTR-8 cell line	Insufficient extravillous trophoblast invasion, inadequate remodeling of spiral arteries	Preterm birth; preeclampsia	¹⁰⁵
Immunological responses; cytotoxicity	HTR-8 cell line	Increase in pro-inflammatory cytokines (e.g. IL-6), overall shift toward pro-inflammatory state in gestational compartment	Preterm birth; preeclampsia	¹⁰⁷
Oxidative stress	HTR-8 cell line; pregnant Wistar rats	Increased ROS in placental cells leading to activation of inflammatory pathways	Preterm birth, preeclampsia	^{103, 107}
Reduced fetal weight	Pregnant Wistar rats	Changes in macronutrient delivery to fetus	Intrauterine growth restriction; small-for-gestational-age; low birth weight	¹⁰³