Evaluation of maternal exposure to PM2.5 and its components on maternal and neonatal thyroid function and birth weight: a cohort study.

BACKGROUND: Particulate matter (PM) air pollution is an environmental risk to public health. The prevalence of thyroid disease during pregnancy has increased rapidly in recent decades, but the available data on the relationships among air pollution, thyroid function and birth outcomes in pregnant women, particularly in China, are scarce. We aimed to evaluate the association between maternal exposure to PM2.5 and its components and maternal and neonatal thyroid function and to investigate whether thyroid function acts as a mediator between air pollution and birth weight.

METHODS: In this prospective birth cohort study, the levels of maternal exposure to PM2.5 and its components during the first trimester were assessed in 433 pregnant women in Nanjing, China, enrolled during 2014-2015. We evaluated the levels of maternal exposure to PM2.5 and its six main constituents-organic matter (OM), black carbon (BC), sulfate (SO42-), nitrate (NO3-), ammonium (NH4+) and soil dust-using the V4.CH.02 product of the Dalhousie University Atmospheric Composition Analysis Group. The maternal serum-free thyroxine (FT4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) levels during the second trimester were measured through electrochemiluminescent microparticle immunoassays. The neonatal TSH levels were detected using an AutoDELFIA Neonatal TSH kit within 72 hours after birth, and the birth weight Z-score of each newborn was estimated.

RESULTS: Higher exposure to maternal PM2.5 and some components (BC and NH4+) decreased the maternal FT4 level (p<0.05), and the birth weight Z-score was decreased (p<0.05) by higher exposure to maternal PM2.5 and some components (OM, BC, NO3- and NH4+). A mediation analysis clarified that the maternal FT4 levels explained 15.9%, 18.4%, and 20.9% of the associations of maternal PM2.5, BC and NH4+ exposure with the birth weight Z-score, respectively (p<0.05). After additional sensitivity analyses including only non-preterm participants (n=418) and non-TPOAb-positive participants (n=415), the models remained stable.

CONCLUSIONS: Our results suggest an inverse association between maternal exposure to PM2.5 and its components and the maternal FT4 levels. Maternal FT4 might act as a mediator between exposure to PM2.5 and its components and birth weight.