Maternal PM2.5 exposure causes fetal growth restriction and alters placental morphology: Role of uterine inflammation.

Maternal exposure to fine particulate matter (PM2.5) correlates with low birthweight. The mechanism, however, remains elusive. We thus investigated the effects of maternal PM2.5 exposure on maternal uterus and placenta. To this end, female C57BL/6 J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) for 20 weeks and then mated with normal males. Placentas and fetus of gestation day 18.5 were harvested and analyzed. Pregnancy outcomes were also assessed, and after weaning, the uteri of those subgroups of dams were collected and analyzed either at estrus or diestrus stage. Maternal CAP exposure significantly reduced the fetal and placental weights but not fetal-placental weight ratio. Histological analysis of placenta showed smaller junction zone and bigger decidua due to maternal CAP exposure, accompanied by uterine natural killer (uNK) cell infiltration in decidua but not remarkable changes in vasculature and mRNA expression of nutrient transporters. Moreover, CAP exposure reduced uterine mass and increased uterine macrophage infiltration at estrus, but not diestrus, stage. As such, we demonstrate that PM2.5 exposure provokes endometritis, which may be responsible for the development of placental abnormalities and fetal growth restriction due to maternal PM2.5 exposure, shedding light on the mechanism whereby maternal PM2.5 exposure causes adverse reproductive outcomes.