Introduction and objective:
Bisphenol A (BPA) is among the most extensively studied endocrine-disrupting chemicals. Because its chemical structure resembles that of endogenous hormones, BPA and its analogues are capable of interacting with intracellular pathways, including those governed by thyroid hormones. The this aim of the review is to outline the molecular mechanisms through which bisphenols exert their effects, and to evaluate how these interactions may influence thyroid function.

Brief description of the state of knowledge:
BPA and its structural analogues are widely present in the environment, which has stimulated ongoing interest in their potential effects on thyroid physiology. Epidemiological studies suggest that higher concentrations of urinary or serum BPA may be linked to changes in T4, T3 and TSH levels, although findings remain inconsistent across populations. Experimental evidence from cellular and animal models provides additional support, showing that BPA can impair thyroid hormone synthesis, alter glandular architecture, and influence the expression of genes essential for hormone production. BPA has also been shown to interfere with thyroid hormone receptor activity, thereby modifying downstream signalling. Comparable effects have been observed for several BPA substitutes, including BPS and BPF.

Summary:
Available evidence indicates that BPA and its analogues can interfere with thyroid hormone signalling through multiple molecular mechanisms. Experimental studies demon-strate effects on receptor activity, non-genomic signalling and local hormone metabolism, while animal models support thyroid related effects in vivo. Human data remain heteroge-neous and suggest modest associations, underscoring the need for well designed longitudinal studies to clarify clinical relevance.