■在关键的神经发育窗口中暴露于内分泌干扰化学物质(EDC)与自闭症特征的风险有关。这项对流行病学研究的系统评价研究了孕妇在怀孕期间暴露于EDC与后代自闭症谱系障碍(ASD)风险之间的关系。
■我们搜索了PubMed,WebofScience,Scopus,和GoogleScholar从成立到2022年11月17日,用于调查产前暴露于EDCs与ASD相关结果之间的关联。两名独立审核员筛选了符合资格的研究,提取的数据,并评估了偏差的风险。该评论在PROSPERO(CRD42023389386)中注册。
■我们纳入了27项评估产前邻苯二甲酸盐暴露的观察性研究(8项研究),多氯联苯(8项研究),有机磷农药(8项研究),酚类(7项研究),全氟烷基物质(6项研究),有机氯农药(5项研究),溴化阻燃剂(3项研究),二恶英(1项研究),和对羟基苯甲酸酯(1项研究)。被检查的儿童数量从77到1,556不等,自闭症特征评估的年龄从3到14岁不等,大多数研究使用社会反应量表评估自闭症特征。除一项研究外,所有研究都被认为具有较低的偏倚风险。总的来说,孕妇在怀孕期间暴露于特定的ECD与后代自闭症特征的发生之间没有关联.
■此处评估的流行病学研究结果不支持产前暴露于ECD与以后生活中自闭症特征的可能性之间的关联。这些发现不应被解释为EDC缺乏影响ASD风险的神经发育效应的明确证据。鉴于当前研究的局限性,如代表性暴露评估,小样本量,不足以评估性二态效应,或EDC混合物的影响。未来的研究应该仔细解决这些限制。
Exposure to endocrine-disrupting chemicals (EDCs) during critical neurodevelopmental windows has been associated with the risk of autistic traits. This systematic review of epidemiological studies examined the association between maternal exposure to EDCs during pregnancy and the risk of autism spectrum disorder (ASD) in the offspring.
We searched PubMed, Web of Science, Scopus, and Google Scholar from inception to November 17, 2022, for studies investigating the association between prenatal exposure to EDCs and outcomes related to ASD. Two independent reviewers screened studies for eligibility, extracted data, and assessed the risk of bias. The review was registered in PROSPERO (CRD42023389386).
We included 27 observational studies assessing prenatal exposure to phthalates (8 studies), polychlorinated biphenyls (8 studies), organophosphate pesticides (8 studies), phenols (7 studies), perfluoroalkyl substances (6 studies), organochlorine pesticides (5 studies), brominated flame retardants (3 studies), dioxins (1 study), and parabens (1 study). The number of examined children ranged from 77 to 1,556, the age at the assessment of autistic traits ranged from 3 to 14 years, and most studies assessed autistic traits using the Social Responsiveness Scale. All but one study was considered to have a low risk of bias. Overall, there was no association between maternal exposure to specific ECDs during pregnancy and the occurrence of autistic traits in offspring.
Findings from the epidemiological studies evaluated here do not support an association between prenatal exposure to ECDs and the likelihood of autistic traits in later in life. These findings should not be interpreted as definitive evidence of the absence of neurodevelopment effects of EDCs affecting ASD risk, given the limitations of current studies such as representative exposure assessment, small sample sizes, inadequacy to assess sexually dimorphic effects, or the effects of EDC mixtures. Future studies should carefully address these limitations.