The thyroid hormone system is a main target of endocrine disruptor compounds (EDC) at all levels of its intricately fine-tuned feedback regulation, synthesis, distribution, metabolism and action of the ‘prohormone’ thyroxine and its active metabolites. Apart from classical antithyroid effects of EDC on the gland, the majority of known and suspected effects occurs at the pre-receptor control of T3 ligand availability to T3 receptors exerting ligand modulated thyroid hormone action. Tissue-, organ- and cell-specific expression and function of thyroid hormone transporters, deiodinases, metabolizing enzymes and T3-receptor forms, all integral components of the system, may mediate adverse EDC effects. Established evidence from nutritional, pharmacological and molecular genetic studies clearly support the functional, biological, and clinical relevance of these targets. Iodine-containing thyroid hormones and the organization of this system are highly conserved during evolution from primitive aquatic life forms, amphibia, birds throughout all vertebrates including humans. Mechanistic studies from various animal experimental models strongly support cause–effect relationships upon EDC exposure, hazards and adverse effects of EDC across various species. Retrospective case–control, cohort and population studies linking EDC exposure with epidemiological data on thyroid hormone-related (dys-)functions provide clear evidence that human development, especially of the fetal and neonatal brain, growth, differentiation and metabolic processes in adult and aging humans are at risk for adverse EDC effects. Considering that more than half of the world population still lives on inadequate iodine supply, the additional ubiquitous exposure to EDC and their mixtures is an additional threat for the essential thyroid hormone system, the health of the human population and their future progenies, animal life forms and our global environment.

甲状腺激素系统是内分泌干扰物化合物 (EDC) 的主要目标，在其复杂微调的反馈调节、合成、分布、代谢和“激素原”甲状腺素及其活性代谢物的作用的各个层面上。除了 EDC 对腺体的经典抗甲状腺作用外，大多数已知和可疑的作用发生在 T3 配体对 T3 受体发挥配体调节甲状腺激素作用的 T3 受体的前受体控制。甲状腺激素转运蛋白、脱碘酶、代谢酶和 T3 受体形式的组织、器官和细胞特异性表达和功能，所有系统的组成部分，都可能介导不良的 EDC 效应。来自营养、药理学和分子遗传学研究的既定证据明确支持功能、生物学、这些目标的临床相关性。在从原始水生生物、两栖动物、鸟类到包括人类在内的所有脊椎动物的进化过程中，含碘甲状腺激素和该系统的组织是高度保守的。来自各种动物实验模型的机制研究强烈支持 EDC 暴露、EDC 对不同物种的危害和不利影响的因果关系。将 EDC 暴露与甲状腺激素相关（功能障碍）功能的流行病学数据联系起来的回顾性病例对照、队列和人群研究提供了明确的证据，证明人类发育，尤其是胎儿和新生儿大脑的发育、成人和衰老过程中的生长、分化和代谢过程人类面临 EDC 不良反应的风险。