Exposure to environmental endocrine disrupting chemicals and effects on thyroid function
Preston, Emma Virginia
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BACKGROUND: Proper thyroid function is critical for normal fetal growth and neurodevelopment, as well as regulation of multiple systems in adults. There is growing evidence indicating that exposure to environmental chemicals may disrupt human thyroid function. Organophosphate flame retardants (PFRs) and per- and polyfluoroalkyl substances (PFASs) are two classes of potential thyroid disrupting chemicals commonly used in consumer products. OBJECTIVES: We characterized exposures to triphenyl phosphate (TPHP), a common PFR, and PFASs in two different U.S. populations. We assessed associations between TPHP and thyroid hormones in adults, as well as individual and joint associations of prenatal PFASs with maternal and neonatal thyroid hormones. METHODS: Analyses were conducted in two Boston, Massachusetts cohort studies: the Flame Retardant Exposure Study (FlaRE) and Project Viva, a longitudinal pre-birth cohort. In FlaRE, we used linear mixed effects models to assess covariate-adjusted associations between urinary DPHP concentrations and serum thyroid hormone levels in repeated samples from male and female adults (n=51). In Project Viva, we used both linear regression and weighted quantile sum regression to assess covariate-adjusted individual and joint associations of prenatal plasma PFAS concentrations measured in early pregnancy with maternal (n=726) and neonatal (n=465) thyroid hormone levels. RESULTS: In FlaRE, higher urinary DPHP was associated with higher total thyroxine (T4) levels in female but not male participants. We saw no associations between DPHP and free T4, total triiodothyronine, or thyroid stimulating hormone (TSH). In Project Viva, we found that higher prenatal exposure to PFASs was associated with lower maternal Free T4 Index (FT4I) and lower neonatal T4 in male infants, but was not associated with maternal T4 or TSH. Combined exposure to multiple PFASs was associated with lower maternal FT4I and neonatal T4 levels, but the relative contributions varied by individual PFAS. CONCLUSIONS: Exposures to both DPHP and PFASs were associated with altered thyroid hormone levels in these populations. Observed associations of DPHP and PFASs with thyroid hormone levels varied by sex, suggesting potential differences in susceptibility or mechanism of action. Associations between PFASs and thyroid hormones also differed across chemicals, suggesting potential differences in toxicological mechanism or potency.
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