Abstract
Bisphenols (BPs), and especially bisphenol A (BPA), are known endocrine disruptors (EDCs), capable of interfering with estrogen and androgen activities, as well as being suspected of other health outcomes. Given the crucial role of thyroid hormones and the increasing incidence of thyroid carcinoma in the last few decades, this review analyzes the effects of BPS on the thyroid, considering original research in vitro, in vivo, and in humans published from January 2000 to October 2019. Both in vitro and in vivo studies reported the ability of BPs to disrupt thyroid function through multiple mechanisms. The antagonism with thyroid receptors (TRs), which affects TR-mediated transcriptional activity, the direct action of BPs on gene expression at the thyroid and the pituitary level, the competitive binding with thyroid transport proteins, and the induction of toxicity in several cell lines are likely the main mechanisms leading to thyroid dysfunction. In humans, results are more contradictory, though some evidence suggests the potential of BPs in increasing the risk of thyroid nodules. A standardized methodology in toxicological studies and prospective epidemiological studies with individual exposure assessments are warranted to evaluate the pathophysiology resulting in the damage and to establish the temporal relationship between markers of exposure and long-term effects.
Highlights
Thyroid hormones (THs) play a critical role in the regulation of physical development, somatic growth, metabolism, and energy provision and are essential for normal brain development in humans [1]
This review aims at evaluating the extensive body of experimental and human studies that in the last two decades have attempted to explore the effects of bisphenol A (BPA), its substitutes, and its halogenated derivatives on the thyroid at different levels
Despite the variety of approaches applied and the heterogeneous and sometimes even conflicting results from the examined studies, a series of interesting indications supports the hypothesis of a role of BPs in interfering with the normal thyroid function
Summary
Thyroid hormones (THs) play a critical role in the regulation of physical development, somatic growth, metabolism, and energy provision and are essential for normal brain development in humans [1]. Thyroid cancer (TC) incidence rates have been rising in many western countries, including the United States where the incidence increased 3.6% per year during 1974 to 2013 [3]. 2030, it is estimated to become the fourth leading cancer diagnosis in the United States [4]. Papillary thyroid cancer (PTC), in particular, is the most frequent histotype with a typically excellent prognosis, accounting for 70% to 90% of well-differentiated thyroid malignancies, and though over diagnosis of small tumors is thought to contribute significantly to the increase in incidence, PTC incidence has significantly increased for every stage and tumor size category [3]. The thyroid is characterized by a low proliferation index, it is susceptible to environmental chemicals that may contribute to the increasing incidence of TC [6]
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