Key Laboratory of the Public Health Safety, Ministry of Education, Department of Environmental Health, School of Public Health, Fudan University, Shanghai 200032, China.
Key Laboratory of Health Technology Assessment, National Health Commission of the People's Republic of China, Fudan University, Shanghai 200032, China.
Environ Sci Technol. 2024 Oct 15;58(41):18177-18189. doi: 10.1021/acs.est.4c06287. Epub 2024 Oct 3.
Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are emerging environmental endocrine disruptors that may adversely affect the human endocrine system, particularly the thyroid gland, the largest endocrine gland in the human body. An epidemiologic survey was conducted involving 318 community residents in Shanghai, China, to assess PFAS exposure levels. The relationship between PFAS exposure and five thyroid function indicators was analyzed using Bayesian Kernel Regression (BKMR) and Weighted Quantile Sum Regression (WQS). Ten effector genes related to PFAS and thyroid diseases were identified through the Comparative Toxicogenomics Database (CTD) for bioinformatics analysis and pathways involved were explored through mediation analysis. In vivo validation of these effector genes was conducted using PCR, complemented by in vitro cellular experiments involving transcriptome sequencing and the construction of animal models to simulate mixed PFAS exposure in the general population. Mixed PFAS exposure was found to impact thyroid health primarily through pathways related to lipid metabolism in toxicogenomic studies and resulted in the upregulation of key genes associated with lipid metabolism in animal models. Our results demonstrate that PFAS exposure could affect the expression of lipid metabolism pathways through the modulation of transcription factors, contributing to the development of thyroid disease.
全氟烷基和多氟烷基物质(PFAS)是新兴的环境内分泌干扰物,可能会对人体内分泌系统,特别是人体最大的内分泌腺——甲状腺产生不良影响。本研究在中国上海进行了一项涉及 318 名社区居民的流行病学调查,以评估 PFAS 暴露水平。采用贝叶斯核回归(BKMR)和加权分位数和回归(WQS)分析了 PFAS 暴露与 5 项甲状腺功能指标之间的关系。通过比较毒理学基因组数据库(CTD)对与 PFAS 和甲状腺疾病相关的 10 个效应基因进行了生物信息学分析,并通过中介分析探讨了相关途径。通过 PCR 对这些效应基因进行了体内验证,并通过体外细胞实验(包括转录组测序和构建动物模型以模拟一般人群中混合 PFAS 暴露)进行了补充。毒理学研究表明,混合 PFAS 暴露主要通过与脂质代谢相关的途径影响甲状腺健康,导致与脂质代谢相关的关键基因在动物模型中上调。我们的研究结果表明,PFAS 暴露可能通过调节转录因子影响脂质代谢途径的表达,从而导致甲状腺疾病的发生。