Associations of Gestational Exposure to Air Pollution and Polycyclic Aromatic Hydrocarbons with Placental Inflammation
Emily Craig, Yan Lin, Yihui Ge, Xiangtian Wang, Susan K. Murphy, Donald Harrington, Richard K. Miller, Sally W. Thurston, Philip K. Hopke, Emily S. Barrett, Thomas G. O’Connor, David Q. Rich, Junfeng Zhang
Abstract
High Resolution Image Download MS PowerPoint Slide Restricted fetal growth (RFG) is a leading contributor to perinatal mortality and has been associated with gestational exposure to air pollution, such as fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and polycyclic aromatic hydrocarbons (PAHs). This study examines the association between trimester-specific and weekly means of air pollution throughout gestation and placental inflammatory markers at delivery. In a prospective cohort study of 263 pregnant women in Rochester, NY, we measured interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in placental tissue and estimated gestational exposure to PM 2.5 and NO 2 using a high-resolution spatial-temporal model. Exposure to PAHs was estimated using urinary 1-hydroxypyrene (1-OHP) concentrations collected once per trimester. Using distributed lag models with a penalized spline function, each interquartile range (2.6 μg/m 3 ) increase in PM 2.5 concentration during gestational weeks 6–11 was associated with decreased placental IL-6 levels (−22.2%, 95% CI: −39.0%, −0.64%). Using multiple linear regression models, each interquartile range increase of 1-OHP was associated with an increase in TNF-α in the first trimester (58.5%, 95% CI: 20.7%, 74.2%), third trimester (22.9%, 95% CI: 0.04%, 49.5%), and entire pregnancy (29.6%, 95%CI: 3.9%,60.6%). Our results suggest gestational exposure to air pollution may alter the inflammatory environment of the placenta at delivery.