Micro and nanoplastic inhalation during gestation disrupts placentation in the Sprague-Dawley rat.

Micro and nanoplastics (MNPs) are a ubiquitous environmental contaminant that humans are exposed through multiple routes. Multiple studies have demonstrated that MNPs deposit in human placental tissues and can translocate across the placental barrier. Maternal blood enters the placenta through uterine spiral arteries. During development of the placenta, trophoblasts enter the arteriolar lumen and invade the endothelial layer. This remodeling reduces vascular contractility and maintains maternal blood flow into the placenta. Simultaneously, the placenta increases surface area through angiogenic branching, facilitating the indirect contact of maternal and fetal blood spaces and promoting maternal-fetal exchange. To date, no groups have investigated how maternal MNP exposure affects these key steps of placentation. Therefore, in this study, pregnant Sprague Dawley rats were exposed to air containing polyamide-12 MNP throughout gestation. Placental morphology, invasion of spiral arteries, and angiogenic signaling were evaluated in male and female placentas at GD16 and GD20. Maternal MNP inhalation significantly reduced the relative distance of trophoblast invasion into the placental region that houses maternal spiral arteries. Additionally, MNP exposure increased staining of smooth muscle actin around maternal spiral arteries, indicating poor remodeling and likely reducing uteroplacental blood flow. Likewise, inhalation of MNPs altered the size and number of maternal and fetal blood spaces, favoring less surface area for maternal-fetal exchange. Lastly, significant changes in the expression and spatial distribution of angiogenic and antiangiogenic mRNAs that regulate vascular branching and surface area were observed. Future studies are needed to characterize the mechanisms by which polyamide-12 MNP influences placental hemodynamics.