Investigating Gene-Environment Interaction in Autism: Air Pollution x

研究自闭症基因与环境的相互作用：空气污染 x

• 批准号: 7844917
• 负责人: ROB S MCCONNELL
• 金额: $ 29.71万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-28 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7844917
• 关键词: Address; Affect; Air Pollutants; Air Pollution; American Psychiatric Association; Aromatic Polycyclic Hydrocarbons; Autistic Disorder; Behavior; Biological; Biological Markers; Brain; Candidate Disease Gene; Child; Childhood; Communication; Data; Development; Developmental Disabilities; Diagnostic; Disease; Environment; Environmental Exposure; Environmental Risk Factor; Etiology; Exposure to; Genes; Genetic; Genetic Risk; Genetic Variation; Genotype; Haplotypes; Home environment; Incidence; Inflammation; Inflammatory; Institutes; Location; Metabolism; Meteorology; Mind; Modeling; Monitor; Motor Vehicles; Oxidants; Oxidative Stress; Oxidative Stress Pathway; Particulate Matter; Pathway interactions; Perinatal; Play; Predisposition; Prevalence; Principal Investigator; Process; Processed Genes; Reporting; Research; Risk; Role; Single Nucleotide Polymorphism; Social Interaction; Societies; Source; Time; Work; autism spectrum disorder; base; case control; developmental disease; exhaust; gene environment interaction; genetic risk factor; improved; insight; pollutant; postnatal; prenatal; public health relevance; surveillance network; trafficking

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).

描述（由申请人提供）：过去 10 年来，自闭症谱系障碍 (ASD) 的患病率不断增加，社会负担不断增加。虽然遗传风险因素与自闭症谱系障碍广泛相关，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。目前对自闭症谱系障碍儿童氧化应激和炎症生物标志物的研究表明，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（一种引发炎症和氧化应激的常见暴露）与自闭症的关系。利用遗传和环境儿童自闭症风险研究 (CHARGE) 中收集的数据，我们将根据每个儿童家中产前、围产期和产后时间点每月的暴露情况，评估交通相关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 个单核苷酸多态性 (SNP) 进行基因分型，并检查 SNP 与空气污染的相互作用。这项工作可以为自闭症谱系障碍的病因学提供重要的见解，并为常见环境暴露带来的风险提供证据。 公共健康相关性：在这项研究中，我们试图检查交通造成的空气污染（一种常见的环境暴露）是否会增加患自闭症谱系障碍（ASD）的风险。我们还将检查体内处理污染物的基因，以确定这些基因在患有自闭症和非自闭症的儿童中是否有所不同，并看看这些基因是否与空气污染相互作用，从而增加自闭症风险。我们相信，这项工作可以为了解 ASD 的原因提供重要的见解，并提供因环境中常见暴露增加（与交通相关的空气污染）而导致的风险的证据。