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Thyroid hormones are essential regulators of metabolism, growth, and neurodevelopment, and disruptions in thyroid function can have profound health consequences, particularly during critical periods such as pregnancy and early childhood. Increasing evidence suggests that exposure to environmental pollutants, including persistent organic pollutants (POPs), bisphenols, heavy metals, pesticides, air pollutants, and per- and polyfluoroalkyl substances (PFAS), can adversely affect thyroid hormone balance. This review provides a comprehensive summary of epidemiological, experimental, and mechanistic studies linking environmental exposures to thyroid dysfunction. Epidemiological data consistently indicate associations between exposure to airborne pollutants (e.g., PM₂.₅, NO₂), endocrine-disrupting chemicals (e.g., BPA, phthalates), and heavy metals (e.g., lead, cadmium, mercury) with altered levels of thyroid-stimulating hormone (TSH), free and total thyroxine (T4), and triiodothyronine (T3). Exposure during prenatal and early-life stages is particularly concerning, as it may impair fetal thyroid development and have lasting effects on neurocognitive outcomes. Experimental and in vitro studies further demonstrate that these pollutants can disrupt thyroid hormone synthesis, metabolism, receptor binding, and gene expression. Mechanisms involved include oxidative stress, receptor antagonism, inhibition of iodide uptake, and epigenetic modifications. The evidence underscores the thyroid gland’s vulnerability to environmental insults and highlights the importance of enhanced monitoring, regulatory measures, and public health strategies to reduce exposure. Considering the pervasive presence of these pollutants, their impact on thyroid function represents a significant global health challenge. This review emphasizes the need for targeted interventions to limit exposure, particularly among sensitive populations, to safeguard thyroid health and prevent related diseases. • Environmental pollutants disrupt thyroid hormones via multiple biological pathways. • POPs, bisphenols, heavy metals, and PFAS affect thyroid homeostasis. • Prenatal exposures alter fetal thyroid function and impact neurodevelopment. • Key mechanisms include oxidative stress, receptor binding, and gene disruption. • Review supports stronger regulations to protect thyroid health and public safety.
Li et al. (Thu,) studied this question.