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BackgroundPrenatal exposure to some per- and polyfluoroalkyl substances (PFASs) may disrupt maternal and neonatal thyroid function, which is critical for normal growth and neurodevelopment.ObjectivesWe examined associations of PFAS exposure during early pregnancy with maternal and neonatal thyroid hormone levels.MethodsWe 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 (PFOS), and maternal thyroid hormones [thyroxine (T4), Free T4 Index (FT4I), thyroid stimulating hormone (TSH)] in plasma samples collected at a median 9.6 wk gestation and neonatal T4 levels from postpartum heel sticks. We estimated associations of PFAS 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.ResultsPFAS concentrations were not associated with maternal T4, 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 (PFNA)] were inversely associated with TSH levels in TPOAb-positive women only. Prenatal PFOS, PFOA, and PFHxS concentrations were inversely associated with T4 levels in male [e.g., PFHxS, quartile 4 vs.1: -2.51μg/dL (95% CI: -3.99, -1.04 )], but not female neonates [0.40μg/dL (95% CI: -0.98, 1.79)].ConclusionsIn this study, prenatal exposure to some PFASs during early pregnancy was inversely associated with maternal FT4I and neonatal T4 in male infants. These results support the hypothesis that prenatal exposure to PFASs influences thyroid function in both mothers and infants. https://doi.org/10.1289/EHP2534.

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are flame-retardant chemicals that are added to many consumer products. Multiple animal studies have shown PBDEs to be thyroid hormone (TH) disruptors. Epidemiologic evidence of PBDE exposure associated with TH disruption has been inconclusive. OBJECTIVES: We used repeated measures to estimate associations between serum PBDE concentrations and THs in a North American adult cohort. METHODS: From 2010 to 2011, we collected ≤ 3 serum samples at approximately 6-month intervals from 52 healthy adult office workers from Boston, Massachusetts, for analysis of PBDE congeners and THs. RESULTS: The geometric mean sum concentrations of the most prevalent PBDE congeners (BDE-28, BDE-47, BDE-99, BDE-100, and BDE-153) were 22 ng/g lipid in winter 2010, 23 ng/g lipid in summer 2010, and 19 ng/g lipid in winter 2011. BDE-47 was the predominant congener. Based on a multivariable mixed regression model, we estimated that on average, a 1-ng/g serum increase in BDE-47 was associated with a 2.6-µg/dL decrease in total thyroxine ([T.sub.4]) (95% CI: -4.7, -0.35). Total [T.sub.4] was inversely associated with each PBDE congener. Serum concentrations of PBDEs were not strongly associated with total triiodothyronine ([T.sub.3]), free [T.sub.4], or thyroid-stimulating hormone (TSH). CONCLUSION: These results are consistent with those from animal studies showing that exposure to PBDEs is associated with a decrease in serum [T.sub.4]. Because the other TH concentrations did not appear to be associated with BDE exposures, our findings do not indicate effects on the pituitary-thyroid axis. Taken together, our findings suggest that PBDE exposure might decrease the binding of [T.sub.4] to serum [T.sub.4] binding proteins. http://dx.doi.org/10.1289/ehp.1509755, Introduction Polybrominated diphenyl ethers (PBDEs) have been used since the 1970s as additive flame retardants. The technical formulation pentabromodiphenyl ether (pentaBDE), composed of PBDE congeners containing three to six bromines, [...]