Abstract
Exposure to air pollution during pregnancy that disrupts thyroid function can lead to adverse health outcomes in mother and child. We evaluated the overall effect and critical exposure window of residential ambient air pollution exposures on thyroid function in the MADRES pregnancy cohort. We also investigated whether these associations varied by iodine deficiency status and neighborhood deprivation. Early pregnancy (6-20 weeks) serum thyroid stimulating hormone (TSH) and free thyroxine (FT4) were measured for 217 mothers. Daily residential ambient air pollution exposures (PM(2.5), PM(10), NO(2) and O(3) 8hr max) were estimated using inverse-distance squared spatial interpolation from regulatory monitors. We used linear regression to assess effects of single ambient air pollutants on thyroid function, including exploration of effect modification by iodine deficiency and neighborhood deprivation (Area Deprivation Index and Gini Index of income inequality, dichotomized at the median). Distributed lag models (DLM) were used to assess critical windows of exposure for ambient air pollutants from 12 weeks preconception to first trimester. We found that one SD increase in PM(2.5) (2.4 μg/m(3)) and PM(10) (5.8 μg/m(3)) were associated with 18.9 % (95 % CI: 2.7, 37.8 %) and 16.8 % (95 % CI: 0.7, 35.6 %) higher TSH levels, respectively, with significant windows of susceptibility in the first trimester (GW 5-8 or 6-8). These associations were also modified by neighborhood deprivation, and iodine status. Our findings indicate that relatively low levels of PM exposures in early pregnancy are associated with increased TSH levels particularly among women with replete iodine levels and women living in neighborhoods with greater deprivation.