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Traffic-Related Air Pollution, Participate Matter, and Autism

机译:与交通有关的空气污染,参与事项和自闭症

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Context: Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments. Objective: To examine the relationship between traffic-related air pollution, air quality, and autism. Design: This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development. Setting: Case-control study from California. Participants: A total of 279 children with autism and a total of 245 control children with typical development. Main Outcome Measures: Crude and multivariable adjusted odds ratios (AORs) for autism. Results: Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 mum in diameter (PM_(2.5) and PM_(10)) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]rexposure to PM_(2.5): AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM_(10): AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM_(2.5): AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM_(10): AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates. Conclusions: Exposure to traffic-related air pollution, nitrogen dioxide, PM_(2.5), and PM_(10) during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.
机译:背景:自闭症是一种异质性疾病,其遗传和环境因素可能是其起源的原因。对有害污染物的检查表明,自闭症病因中存在空气中毒的重要性,但很少有研究使用特定居住场所的暴露分配来检查其与当地空气污染水平的关系。目的:探讨与交通有关的空气污染,空气质量和自闭症之间的关系。设计:这项基于人群的病例对照研究包括从自闭症儿童和典型发育对照儿童获得的数据,这些儿童参加了加利福尼亚州遗传学和环境研究的儿童自闭症风险研究。出生证明中的母亲地址和居住史调查表中报告的地址用于估计怀孕每个月和生命的第一年的暴露水平。使用线源空气质量扩散模型,将交通相关的空气污染分配给每个位置。区域性空气污染物措施基于环境保护局的空气质量系统数据。逻辑回归模型比较了自闭症儿童和典型发育对照儿童的估计和测得的污染物水平。地点:来自加利福尼亚的病例对照研究。参与者:共有279名自闭症儿童和245名典型发育的对照儿童。主要结果指标:自闭症的粗略和多变量校正比值比(AOR)。结果:自闭症儿童更有可能住在妊娠期间(AOR,1.98 [95%CI,1.20-3.31])和出生后第一年(交通事故相关空气污染暴露四分之一的地方)。与对照组相比,AOR为3.10 [95%CI为1.76-5.57]。区域性二氧化氮和直径小于2.5和10毫米的颗粒物(PM_(2.5)和PM_(10))的暴露措施也与妊娠期自闭症相关(二氧化氮暴露:AOR,1.81 [95%CI,1.37 -3.09]暴露于PM_(2.5):AOR,2.08 [95%CI,1.93-2.25];暴露于PM_(10):AOR,2.17 [95%CI,1.49-3.16],并且在生命的第一年(暴露于二氧化氮:AOR,2.06 [95%CI,1.37-3.09];暴露于PM_(2.5):AOR,2.12 [95%CI,1.45-3.10];暴露于PM_(10):AOR,2.14 [95 %CI,1.46-3.12])。所有区域污染物估算值均按比例缩放为所有怀孕估算值分布的标准偏差的两倍。结论:在怀孕期间和生命的第一年,与交通有关的空气污染,二氧化氮,PM_(2.5)和PM_(10)的暴露与自闭症有关。进一步的流行病学和毒理学检查可能的生物学途径将有助于确定这些关联是否是因果关系。

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