The effects of prenatal PM oxidative potential exposure on feto-placental vascular resistance and fetal weight: A repeated-measures study.

Background: Feto-placental hemodynamic deterioration is a critical contributing factor to fetal growth restriction. Whether PM oxidative potential (OP) affects feto-placental hemodynamics and what impact is on estimated fetal weight (EFW) have not been fully elucidated. We sought to evaluate the association of PM OP with EFW and to explore whether feto-placental vascular impedance hemodynamic change is a possible mediator in this association.

Methods: A repeated-measures study was conducted involving sixty pregnant women with at least 26 weeks of follow-up during pregnancy in Guangzhou, China, from September 2017 to October 2018. Daily filter-based PM samples were prospectively collected from ground monitors, and estimates of OP for PM and its metallic (OPv-metal) and non-metallic constituents (OPv-nonmental) were determined by dithiothreitol assay. Ultrasound data of fetal growth and umbilical arterial resistance, including estimated fetal weight (EFW), pulsatility index, resistance index, and systolic-to-diastolic ratio, were also obtained during gestation. Generalized estimating equations and polynomial distribution lag models were applied to analyze the associations of maternal exposure to PM OP with EFW and umbilical artery indices. Causal mediation analysis was used to evaluate the mediating role of umbilical arterial resistance.

Results: Prenatal exposure to ambient PM OP was significantly inversely associated with EFW. The magnitudes of effects of OPv-nonmetal on EFW were larger than those of OPv-metal. Significant mediation for the relationship between PM-related OP and EFW by increased impedance in the umbilical artery was observed, with the estimated percent mediated ranging from 31% to 61%. The estimated percent mediated for OPv-nonmetal was higher than those for OPv-metal.

Conclusions: Findings suggest that increased impedance in the umbilical artery may be one of the potential mediators of the relationship between PM oxidative potential exposure and low fetal weight.