Prenatal Air Pollution Exposure and Placental Vasculature Development among Participants of the UPSIDE Cohort Study.

BACKGROUND:Air pollution exposure during pregnancy has been associated with reduced fetal growth and birth weight, but mechanisms mediating this association are not well understood. OBJECTIVES:We examined whether pregnancy air pollution exposures were associated with altered placental vascularization. METHODS:We studied pregnant women (N = 163) from the UPSIDE cohort study, part of the Environmental Influences on Child Health Outcomes (ECHO) Study. Using placenta photographs taken at birth (gestational weeks 37-42), we derived seventeen chorionic plate surface vessel outcomes in 7 groups: arterial area, arterial branches, arterial arc length, arterial endpoint distance to perimeter, arterial branch angle, arterial tortuosity, and artery-vein distances. Distributed lag nonlinear models were used to determine if/when gestational week mean PM2.5 and NO2 concentrations were associated with the seventeen chorionic plate surface vessel outcomes. RESULTS:Placental measures were more strongly associated with weekly NO2 than PM2.5. Higher early-pregnancy NO2 concentrations were associated with lower measures of the arterial area and arterial endpoint distance to perimeter groups, and greater measures of the arterial tortuosity group (e.g., each 9-ppb increase in NO2 concentration in gestational weeks 0-12 was associated with lower arterial surface area; cumulative β = -1.46 cm2; 95 % CI = -2.73, -0.19). Higher NO2 in late-pregnancy was associated with increased measures of the arterial area, arc length, tortuosity, and artery-vein distances groups, and decreased measures of the arterial branch group (e.g., 9-ppb increases in NO2 concentration in gestational weeks 18-37 were associated with lower numbers of arterial generations; cumulative β = -1.30 generations; 95 % CI = -2.22, -0.38). CONCLUSION:Residential traffic pollution exposure in early-pregnancy was associated with altered chorionic surface arterial vasculature, potentially leading to worse perfusion, while late-pregnancy positive associations may represent a compensatory response.