Investigating Gene-Environment Interaction in Autism: Air Pollution x

描述（由申请人提供）：自闭症谱系障碍（ASD）的患病率在过去10年中一直在增加，给社会带来了越来越大的负担。虽然遗传风险因素与ASD广泛相关，但目前的增加不太可能仅由遗传因素引起，环境因素可能会增加已知的遗传风险。目前研究ASD儿童氧化应激和炎症的生物标志物表明，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，会引起炎症和氧化应激。使用作为遗传学和环境研究（CHARGE）儿童自闭症风险的一部分收集的数据，我们将评估交通相关空气污染物在自闭症风险中的作用，基于每个孩子在产前，围产期和产后时间点的家中每月暴露。我们计划对17个候选基因中的384个单核苷酸多态性（SNP）进行基因分型，并研究SNP与空气污染的相互作用。这项工作可能会提供重要的洞察自闭症的病因和证据的风险，由于共同的环境暴露。 公共卫生相关性：在这项研究中，我们试图检查由于交通造成的空气污染，一种常见的环境暴露，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，以确定它们在患有和没有自闭症的儿童中是否不同，并观察这些基因是否与空气污染相互作用以增加自闭症风险。我们相信，这项工作可能会提供重要的见解，什么原因导致ASD和风险的证据，由于一个共同的暴露增加的环境（交通相关的空气污染）。

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).