Heavy metals as endocrine disruptors

Abstract

Heavy metals are widely recognized as endocrine-disrupting agents primarily originating from anthropogenic sources and persisting in soil, air, and water. This review aims to present an updated and comprehensive synthesis of current evidence regarding the endocrine-disrupting effects of heavy metals, with particular emphasis on their roles in the pathogenesis of common endocrine and metabolic disorders. The toxicological impact of these elements depends on the level and duration of exposure, their chemical form, and the biological susceptibility of target tissues. Chronic exposure, even at low doses, has been implicated in the development of diabetes mellitus, obesity, autoimmune thyroiditis, thyroid cancer, pubertal disorders, and infertility through mechanisms involving oxidative stress, inflammation, receptor interference, and hormonal dysregulation. Epidemiological data and experimental studies consistently demonstrate that metals such as cadmium, lead, mercury, arsenic, and nickel can disrupt hormonal signaling and alter metabolic and reproductive homeostasis. Despite accumulating evidence, safe exposure thresholds remain undefined, and the long-term consequences of chronic low-dose exposure are still poorly understood. Understanding these mechanisms is crucial for developing preventive strategies and informing public health policies aimed at reducing the endocrine and metabolic disease burden associated with heavy metal exposure.