Investigating Gene-Environment Interaction in Autism: Air Pollution x

描述(由申请人提供)：在过去的10年里，随着社会负担的增加，自闭症谱系障碍(ASDS)的患病率一直在增加。虽然遗传风险因素与自闭症广泛相关，但目前的增加不太可能仅由遗传因素造成，环境因素可能会增加已知的遗传风险。目前对患有自闭症儿童氧化应激和炎症的生物标记物的研究表明，这些途径可能在病因学中发挥作用。我们建议研究空气污染与自闭症的关系。空气污染是一种常见的暴露，会导致炎症和氧化应激。使用从遗传学和环境研究(CHARGE)收集的儿童自闭症风险的数据，我们将根据每个孩子在产前、围产期和出生后时间点的每月暴露情况，评估与交通相关的空气污染物在自闭症风险中的作用。我们计划对17个候选基因中的384个单核苷酸多态(SNPs)进行分型，并研究SNP与空气污染的相互作用。这项工作可能会为自闭症的病因提供重要的见解，并为常见环境暴露的风险提供证据。 公共卫生相关性：在这项研究中，我们试图检查交通造成的空气污染是否会增加ASD的风险。我们还将检查处理体内污染物的基因，以确定患有自闭症和不患有自闭症的儿童的基因是否不同，并看看这些基因是否与空气污染相互作用，增加自闭症的风险。我们相信，这项工作可能会为导致自闭症的原因提供重要的见解，并提供由于环境中常见暴露增加(与交通相关的空气污染)而产生风险的证据。

DESCRIPTION (provided by applicant): The prevalence of autism spectrum disorders (ASDs) has been increasing during the last 10 years with increasing burden on society. While genetic risk factors are widely implicated in ASDs, the current increase is not likely to result from genetic factors alone and it is possible that environmental factors may augment known genetic risks. Current research examining biomarkers of oxidative stress and inflammation in children with an ASD suggests that these pathways may play a role in etiology. We propose to examine the association of air pollution, a common exposure that induces inflammation and oxidative stress, with autism. Using data collected as part of the Childhood Autism Risks from Genetics and the Environment Study (CHARGE) we will assess the role of traffic related air pollutants in autism risk based on monthly exposure at each child's home during prenatal, perinatal and postnatal time points. We plan to genotype 384 single nucleotide polymorphisms (SNPs) in 17 candidate genes and to examine SNP-air pollution interactions. This work may provide important insight into the etiology of ASDs and evidence for risk due to a common environmental exposure. PUBLIC HEALTH RELEVANCE: In this study we seek to examine if air pollution due to traffic, a common environmental exposure, increases risk for ASD. We will also examine genes that process pollutants in the body to determine if they are different in children with and without autism, and to see if these genes interact with air pollution to increase autism risk. We believe that this work may provide important insight into what causes ASDs and evidence for risk due to a common exposure increasing in the environment (traffic related air pollution).