59 Placental vulnerability at the molecular level: The EGFR axis under chemical stress

Abstract Increasing evidence suggests that exposure to endocrine-disrupting chemicals (EDCs) during pregnancy can adversely affect maternal and fetal health. The placenta, a transient yet essential endocrine organ, is a sensitive target of such exposures. Among EDCs, bisphenol S (BPS)—a common replacement for bisphenol A—is frequently detected in pregnant individuals. Through in vivo models, primary human trophoblasts, and 3D microfluidic platforms, our work has shown that BPS disrupts placental function by antagonizing the epidermal growth factor receptor (EGFR), impairing trophoblast fusion and invasion. Building on these findings, we have recently investigated a mixture of EGFR-targeting environmental chemicals and demonstrated that this mixture alters trophoblast cell function and disrupts mitochondrial bioenergetics. These studies identify EGFR as a molecular target of environmental chemicals and illustrate how receptor-level disruptions may contribute to placental dysfunction. This talk will highlight mechanistic and functional findings on EGFR-targeting chemicals and their implications for pregnancy outcomes.