Maternal Plasma per- and Polyfluoroalkyl Substance Concentrations in Early Pregnancy and Maternal and Neonatal Thyroid Function in a Prospective Birth Cohort: Project Viva (USA)

BACKGROUND: Prenatal exposure to some per- and polyfluoroalkyl substances (PFASs) may disrupt maternal and neonatal thyroid function, which is critical for normal growth and neurodevelopment. OBJECTIVES: We examined associations of PFAS exposure during early pregnancy with maternal and neonatal thyroid hormone levels. METHODS: We studied 732 mothers and 480 neonates in Project Viva, a longitudinal prebirth cohort in Boston, Massachusetts. We quantified six PFASs, including perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PROS), and maternal thyroid hormones [thyroxine (T-4), Free T-4 Index (FT4I), thyroid stimulating hormone (TSH)] in plasma samples collected at a median 9.6 wk gestation and neonatal T-4 levels from postpartum heel sticks. We estimated associations of PEAS concentrations with thyroid hormone levels using covariate-adjusted linear regression models and explored effect measure modification by maternal thyroid peroxidase antibody (TPOAb) status and infant sex. RESULTS: PFAS concentrations were not associated with maternal T-4, but PFOA, perfluorohexane sulfonate (PFHxS), and 2-(N-methyl-perfluorooctane sulfonamido) acetate (MeFOSAA) were inversely associated with maternal FT4I [e.g., -1.87% (95% confidence interval (CI): -3.40, -0.31) per interquartile (IQR) increase in PFOA]. PFAS concentrations [PFOA, PFOS, and perfluorononanoate (PENA)] were inversely associated with TSH levels in TPOAb-positive women only. Prenatal PFOS, PFOA, and PFHxS concentrations were inversely associated with T-4 levels in male [e.g., PFHxS, quartile 4 vs.1: -2.51 mu g/dL (95% CI: -3.99, -1.04)1, but not female neonates [0.40 mu g/dL (95% Cl: -0.98, 1.79)1. CONCLUSIONS: In this study, prenatal exposure to some PFASs during early pregnancy was inversely associated with maternal FT4I and neonatal T-4 in male infants. These results support the hypothesis that prenatal exposure to PFASs influences thyroid function in both mothers and infants.