Abstract
Bisphenol A (BPA) and its analogues are widely used industrial chemicals in the production of polycarbonate plastics, epoxy resins, and related polymeric materials. Their extensive production and application have led to pervasive environmental contamination, enabling human exposure via ingestion, inhalation, and dermal absorption. As endocrine disruptors, BPA and its analogues (such as bisphenol S and bisphenol F) can influence thyroid homeostasis through interference with hormone synthesis, metabolism, and receptor signaling pathways. Recent studies suggest that exposure to bisphenols may contribute to thyroid dysfunction, autoimmune thyroid disease, and possibly thyroid carcinogenesis. Although some BPA alternatives appear to exert thyroid disrupting effects comparable to BPA, limited epidemiological evidence precludes a clear assessment of their relative safety. Given the ongoing rise in global bisphenol exposure, clarifying molecular mechanisms, defining susceptible subpopulations, and improving regulatory oversight are critical steps toward reducing thyroid-related health risks.