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Evidence of susceptibility to autism risks associated with early life ambient air pollution: A systematic review

环境卫生 空气污染 自闭症 医学 社会经济地位 怀孕 人口 精神科 生物 生态学 遗传学
作者
Xinran Yu,Md. Mostafijur Rahman,Zhongying Wang,Sarah A. Carter,Joel Schwartz,Zhanghua Chen,Sandrah P. Eckel,Daniel A. Hackman,Jiu‐Chiuan Chen,Anny H. Xiang,Rob McConnell
出处
期刊:Environmental Research [Elsevier]
卷期号:208: 112590-112590 被引量:17
标识
DOI:10.1016/j.envres.2021.112590
摘要

Many studies have found associations between early life air pollution exposure and subsequent onset of autism spectrum disorder (ASD). However, characteristics that affect susceptibility remain unclear.This systematic review examined epidemiologic studies on the modifying roles of social, child, genetic and maternal characteristics in associations between prenatal and early postnatal air pollution exposure and ASD.A systematic literature search in PubMed and Embase was conducted. Studies that examined modifiers of the association between air pollution and ASD were included.A total of 19 publications examined modifiers of the associations between early life air pollution exposures and ASD. In general, estimates of effects on risk of ASD in boys were larger than in girls (based on 11 studies). Results from studies of effects of family education (2 studies) and neighborhood deprivation (2 studies) on air pollution-ASD associations were inconsistent. Limited data (1 study) suggest pregnant women with insufficient folic acid intake might be more susceptible to ambient particulate matter less than 2.5 μm (PM2.5) and 10 μm (PM10) in aerodynamic diameter, and to nitrogen dioxide (NO2). Children of mothers with gestational diabetes had increased risk of ozone-associated ASD (1 study). Two genetic studies reported that copy number variations may amplify the effect of ozone, and MET rs1858830 CC genotype may augment effects of PM and near-roadway pollutants on ASD.Child's sex, maternal nutrition or diabetes, socioeconomic factors, and child risk genotypes were reported to modify the effect of early-life air pollutants on ASD risk in the epidemiologic literature. However, the sparsity of studies on comparable modifying hypotheses precludes conclusive findings. Further research is needed to identify susceptible populations and potential targets for preventive intervention.
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