Prenatal Exposure to Per- and Polyfluoroalkyl Substances and Maternal Thyroid Function during Pregnancy in a Cohort with High Familial Likelihood of Autism Spectrum Disorder.

This study looked at how exposure to certain chemicals (PFAS) during pregnancy affects thyroid function in mothers and child development. Researchers followed 151 pregnant women and their children until age 3. They found that higher levels of some PFAS chemicals changed thyroid hormone levels in mothers. These changes were linked to increased likelihood of non-typical development in children, including autism.

The findings suggest these common environmental chemicals might affect brain development before birth.

This cohort study examined how prenatal exposure to per- and polyfluoroalkyl substances (PFAS) affects maternal thyroid function in 151 pregnant women from families with high autism likelihood. Researchers analyzed serum samples and tracked child development outcomes at age 3. Key findings showed that PFOS exposure was associated with increased total thyroxine (TT4) levels and decreased free thyroxine-to-total thyroxine ratio, while PFHxS showed opposite effects. Network analysis revealed PFAS had direct and indirect associations with non-typical development diagnosis, while total triiodothyronine was conditionally associated with non-typical development.

The study suggests prenatal PFAS exposure may disrupt maternal thyroid function, potentially affecting fetal brain development.

Findings suggest pregnant women should minimize PFAS exposure when possible, though specific prevention strategies require further research. Healthcare providers should be aware of potential thyroid disruption from environmental chemicals. More research needed to establish causal relationships and develop evidence-based prevention guidelines for PFAS exposure during pregnancy.

Single cohort study design limits generalizability. The study population had high familial autism likelihood, which may not represent general population. Observational design cannot establish causation between PFAS exposure and outcomes. Sample size and follow-up duration were not clearly specified.

Thyroid hormones supplied by the mother are essential for fetal brain development but could be disrupted by per- and polyfluoroalkyl substances (PFAS). We explored how prenatal PFAS exposures relate to maternal thyroid function in pregnant participants from the MARBLES cohort. We analyzed 212 serum samples from 151 pregnant women who later had a child with diagnosis of autism spectrum disorder (ASD), nontypical development (non-TD), or typical development (TD) by age 3. We quantified nine PFAS, total triiodothyronine (TT3), total thyroxine (TT4), free thyroxine (FT4), and thyroid-stimulating hormone.

We used a linear mixed effect model for individual and coexposure effects and Bayesian kernel machine regression (BKMR) for mixture effects. We conducted a mixed graphical model with a child neurodevelopmental classification as an exploratory analysis. Perfluorooctanesulfonate (PFOS) and perfluorohexanesulfonate (PFHxS) were associated with TT4 (per 1-unit increase in ln-transformed concentrations β [95% confidence interval, CI]: 1.005 [0.108, 1.903] for PFOS; -0.581 [-1.160, -0.002] for PFHxS) and FT4-to-TT4 ratio (-0.153 [-0.270, -0.036] for PFOS; 0.090 [0.013, 0.166] for PFHxS). In the network map, PFAS were directly and indirectly associated with non-TD diagnosis, while TT3 was conditionally associated with non-TD.

These findings indicate that prenatal PFAS exposure could interfere with maternal thyroid function, potentially impacting fetal neurodevelopment.