Polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and new flame retardants (NFRs) are known thyroid hormone (TH) disruptors, but their disrupting mechanisms in humans are not completely understood. In this study, we aimed to explore the disrupting mechanisms of the aforementioned chemicals via examining TH-regulated proteins and gene expression in human serum. Adult participants from an e-waste dismantling (exposed group) and a control region (control group) in South China provided blood samples for the research. Some compounds of PCBs, PBDEs, and NFRs showed strong binding affinity to the thyroid-stimulating hormone (TSH), thyroglobulin, thyroxine-binding globulin (TBG), gene expression of TH receptor α (TRα) and β, and iodothyronine deiodinase I (ID1). The highly exposed individuals had lower levels of TBG, TSH, and expression of TRα, but higher expression of ID1 than those of the control group. The disruption of TH-regulated proteins and gene expression suggested the exertion of different and, at times, even contradictory effects on TH disruption. However, no statistically significant difference was found in the TH levels between the exposed and the control group, implying that the TH disruption induced by these chemicals depends on the combined influence of multiple mechanisms. Gene expression appears to be an effective approach for investigations of TH disruption and the potential health effects.

多氯联苯（PCB），多溴联苯醚（PBDE）和新型阻燃剂（NFR）是已知的甲状腺激素（TH）干扰物，但它们对人的破坏机理尚不完全清楚。在这项研究中，我们旨在通过检查TH调节蛋白和人类血清中的基因表达来探索上述化学物质的破坏机制。来自华南地区电子废物拆解（暴露组）和对照组（对照组）的成年参与者为研究提供了血液样本。PCB，PBDEs和NFR的某些化合物对甲状腺刺激激素（TSH），甲状腺球蛋白，甲状腺素结合球蛋白（TBG），TH受体α（TRα）和β的基因表达以及碘甲状腺素脱碘酶I（ ID1）。高暴露人群的TBG，TSH，和TRα的表达，但ID1的表达高于对照组。TH调节蛋白和基因表达的破坏表明对TH破坏的作用不同，有时甚至是矛盾的。但是，暴露组和对照组之间的TH水平没有统计学上的显着差异，这表明这些化学物质引起的TH破坏取决于多种机制的综合影响。基因表达似乎是研究TH破坏及其潜在健康影响的有效方法。在暴露组和对照组之间，TH水平没有发现统计学上的显着差异，这表明这些化学物质引起的TH破坏取决于多种机制的综合影响。基因表达似乎是研究TH破坏及其潜在健康影响的有效方法。在暴露组和对照组之间，TH水平没有统计学上的显着差异，这表明这些化学物质引起的TH破坏取决于多种机制的综合影响。基因表达似乎是研究TH破坏及其潜在健康影响的有效方法。