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

期刊

ENVIRONMENTAL RESEARCH
卷 208, 期 -, 页码 -

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2021.112590

关键词

Effect modification; Air pollution; Autism; Susceptibility; Interaction

资金

  1. National Institutes of Environmental Health Sciences [R01 ES029963, R56ES028121, P30ES007048]
  2. USC Dana and David Dornsife College of Letters, Arts and Sciences/Graduate School Fellowship

向作者/读者索取更多资源

This systematic review examined the modifying roles of social, child, genetic and maternal characteristics in associations between prenatal and early postnatal air pollution exposure and autism spectrum disorder (ASD).
Background: 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. Objective: 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. Methods: A systematic literature search in PubMed and Embase was conducted. Studies that examined modifiers of the association between air pollution and ASD were included. Results: 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 mu m (PM2.5) and 10 mu m (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. Conclusions: 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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