Prenatal Exposure to Per- and Polyfluoroalkyl Substances, Maternal Thyroid Dysfunction, and Child Autism Spectrum Disorder.
Prenatal Exposure to Per- and Polyfluoroalkyl Substances, Maternal Thyroid Dysfunction, and Child Autism Spectrum Disorder.
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DOI：
10.3803/enm.2022.1598
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发表时间：
2022-12
影响因子：
3.4
通讯作者：
Pearce, Elizabeth N.
中科院分区：
文献类型：
--
作者：
Shin, Hyeong-Moo;Oh, Jiwon;Schmidt, Rebecca J.;Pearce, Elizabeth N.
关键词：
自闭症谱系障碍（ASD）具有高昂的经济和社会成本，是一个日益严重的公共卫生问题，其患病率在过去二十年中稳步上升。尽管实际增加的发病率与改善的诊断仍然存在争议，但ASD患病率的增加表明非遗传因素可能是原因。越来越多的流行病学证据表明，怀孕期间母亲甲状腺功能异常与儿童ASD和其他神经发育障碍的风险增加有关。产前接触干扰内分泌的化学物质，如全氟烷基和多氟烷基物质（PFAS），已知会破坏甲状腺功能，并可能影响早期大脑发育；因此，假设甲状腺功能障碍介导了这种关系。从产前PFAS暴露通过甲状腺功能障碍到ASD病因的潜在途径的概念并不新鲜；然而，关于这一主题的现有文献很少。本综述的目的是评估和总结有关这一途径的潜在机制的报告。
Autism spectrum disorder (ASD), with its high economic and societal costs, is a growing public health concern whose prevalence has risen steadily over the last two decades. Although actual increased incidence versus improved diagnosis remains controversial, the increased prevalence of ASD suggests non-inherited factors as likely contributors. There is increasing epidemiologic evidence that abnormal maternal thyroid function during pregnancy is associated with increased risk of child ASD and other neurodevelopmental disorders. Prenatal exposure to endocrine-disrupting chemicals such as per- and polyfluoroalkyl substances (PFAS) is known to disrupt thyroid function and can affect early brain development; thus, thyroid dysfunction is hypothesized to mediate this relationship. The concept of a potential pathway from prenatal PFAS exposure through thyroid dysfunction to ASD etiology is not new; however, the extant literature on this topic is scant. The aim of this review is to evaluate and summarize reports with regard to potential mechanisms in this pathway.