Effects of endocrine disruptors on thyroid hormone synthesis and function and consequences of fetal exposure

Fetal development depends on complex maternal-fetal-placental interactions, with thyroid hormones playing a vital role in regulating growth and neurogenesis. Exposure to endocrine-disrupting chemicals (EDCs) during pregnancy has emerged as a significant risk factor for thyroid dysfunction and its associated developmental and cognitive disorders. EDCs, including bisphenol A (BPA), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), perfluoroalkyl substances, pesticides, and heavy metals, disrupt thyroid hormone synthesis, secretion, and metabolism. Mechanisms involve receptor binding, disruption of the hypothalamic-pituitary-thyroid axis, and inhibition of thyroid peroxidase activity. BPA exposure, for instance, reduces free and total T4 levels and interferes with deiodinase activity. Similarly, PCBs and PBDEs are associated with lower thyroxine concentrations and long-term behavioral abnormalities in offspring. Pesticides and heavy metals exacerbate thyroid dysfunction by interfering with hormone synthesis and receptor interactions. Genetic predisposition, iodine deficiency, and autoimmune conditions further increase susceptibility to EDC-related thyroid disorders. Considering the heightened vulnerability of early pregnancy and the widespread environmental presence of EDCs, reducing exposure and implementing regulatory measures are essential to mitigate their adverse effects on maternal and fetal thyroid health. Future research should prioritize elucidating the mechanisms of EDC-induced thyroid dysfunction and developing interventions to protect at-risk populations.