Exposure to heavy metals and metalloids in PM2.5 and thyroid hormones in pregnant women: a longitudinal study in China.

Previous epidemiological studies have established associations between fine particulate matter (PM2.5) exposure and maternal thyroid hormone suppression. However, as PM2.5 is a complex chemical mixture, the specific contribution of metallic constituents to PM2.5-induced thyroid disruption remains poorly characterized. This study aimed to evaluate the relationship between maternal thyroid function and exposure to metallic and metalloid components of PM2.5 during pregnancy. In a longitudinal study of 847 pregnant women recruited from three maternal and child healthcare hospitals, we collected fasting blood samples at 10, 17, and 32 weeks of gestation for thyroid hormone assessment. Concurrently, ambient PM2.5 monitoring stations near participating hospitals quantified 11 metallic/metalloid elements. Linear mixed-effects regression models assessed individual element associations with thyroid parameters, while weighted quantile sum (WQS) regression evaluated combined effects of metal mixtures. Significant inverse associations were observed between lead (Pb) exposure and serum thyroid stimulating hormone (TSH) levels. Multiple elements - including aluminum (Al), arsenic (As), cadmium (Cd), lead (Pb), antimony (Sb), selenium (Se) and thallium (Tl) - demonstrated negative correlations with free thyroxine (FT4) and free triiodothyronine (FT3) concentrations. WQS analysis revealed that each inter-decile rise in mixed metal exposure was associated with a 0.52% decrease in TSH (95% CI: -3.84%, 2.91%), a 1.52% reduction in FT₄ (95% CI: -1.95%, -1.09%), and a 1.18% decline in FT₃ (95% CI: -1.60%, -0.77%). Tl, Al, and As emerged as primary contributors to these effects, collectively accounting for 86%- 97% of the weighted mixture impact. These findings demonstrate that metallic components of PM2.5, particularly Tl, Al and As are significantly associated with suppressed maternal thyroid function during pregnancy. This highlights the importance of metal-specific toxicity in PM2.5-related endocrine disruption.