证据显示炎症在神经发育关键期（如孕期）影响着环境内分泌干扰物（EEDs）与孤独症谱系障碍（ASD）的关系，但在人类神经发育进程中这种关系的路径和影响机制还不清楚。本研究使用正在建立的天津市母婴队列，应用流行病学、儿少卫生学、免疫学、环境卫生学、分子生物学、生物统计等研究方法，以多溴联苯醚（PBDEs）及其代谢物为EEDs代表探讨其在孕期的暴露与婴幼儿期ASD患病的关系；探讨孕期PBDEs暴露造成促炎/抗炎细胞因子失衡与其孤独症患儿免疫发育异常的关系；探讨母亲遗传特征与其对PBDEs造成炎症应答之间关系。以证实研究假设，在炎症相关遗传背景下，PBDEs暴露引起母体炎性细胞因子变化、造成儿童外周循环促炎/抗炎细胞因子失衡、导致儿童神经发育异常出现ASD的作用路径。结果为孕期EEDs暴露造成ASD提供因果关系人群线索；助于理解炎症反应在EEDs不良健康效应中的作用，对ASD的病因和预防有重要意义

Increasing evidencesuggests that inflammation during critical period of neurodevelopment (e.g., during pregnancy) affects the relationship between environmental endocrine disruptors (EEDs) and autism spectrum disorders (ASD), but the pathway and mechanism of this relationship in the course of human neurodevelopment is not fully understood, and has become a research focus. This study is based on the establishing Tianjin Maternal and Child Health Cohort, using methods from Epidemiology, Maternal, Child and Adolescent Health, Immunology, Environment Health, Molecular biology and Biostatistics. We aim to explore the association between exposure to polybrominated diphenyl ethers (PBDEs) and its metabolites during pregnancy and ASD in infancy, to explore the relationship between imbalance of proinflammatory/anti-inflammatory cytokine caused by PBDEs exposure during pregnancy and immune developmental abnormalities in children with ASD, and the influence of genetic characteristics on inflammation caused by PBDEs exposure. To confirm our research hypothesis, PBDEs exposure induces maternal inflammatory cytokine changesin inflammation-related genetic background, causing children peripheral circulation of pro-inflammatory/anti-inflammatory cytokine imbalance, and bringing about neurobehavioral developmental abnormity in children, thus developing ASD. Our findings could provide population clues for causality of EEDs exposure during pregnancy causing ASD, help to understand the role of inflammatory response in the adverse health effects of EEDs, and has great significance for the etiology and early prevention of ASD.