Department of Preventive Medicine, Keck School of Medicine, Zilkha Neurogenetic Institute, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA 90089, USA.
JAMA Psychiatry. 2013 Jan;70(1):71-7. doi: 10.1001/jamapsychiatry.2013.266.
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.
To examine the relationship between traffic-related air pollution, air quality, and autism.
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.
Case-control study from California.
A total of 279 children with autism and a total of 245 control children with typical development.
Crude and multivariable adjusted odds ratios (AORs) for autism.
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 μm in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: 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 PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: 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.
Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 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.
自闭症是一种具有遗传和环境因素的异质障碍,这些因素可能导致其发生。对危险污染物的研究表明,空气毒物在自闭症的病因学中很重要,但很少有研究使用特定于居住地的暴露评估来研究其与当地空气污染水平的关系。
研究交通相关空气污染、空气质量与自闭症之间的关系。
本基于人群的病例对照研究包括来自加利福尼亚州参加儿童自闭症风险的遗传学和环境研究的自闭症儿童和具有典型发育的对照儿童的数据。母亲的出生证明上的地址和居住史调查问卷中报告的地址用于估计每个妊娠 trimester 和生命第一年的暴露情况。使用线源空气质量扩散模型为每个地点分配交通相关的空气污染。区域空气污染物测量值基于美国环境保护署的空气质量系统数据。使用逻辑回归模型比较自闭症儿童和具有典型发育的对照儿童的估计和测量污染物水平。
加利福尼亚州的病例对照研究。
共有 279 名自闭症儿童和共有 245 名具有典型发育的对照儿童。
自闭症的粗比值比(OR)和多变量调整比值比(AOR)。
与对照儿童相比,自闭症儿童在怀孕期间(OR,1.98 [95%CI,1.20-3.31])和生命的第一年(OR,3.10 [95%CI,1.76-5.57])更有可能居住在交通相关空气污染暴露最高四分位数的住所。怀孕期间的二氧化氮和小于 2.5 和 10 μm 直径的颗粒物(PM2.5 和 PM10)的区域暴露测量值也与自闭症相关(二氧化氮暴露:OR,1.81 [95%CI,1.37-3.09];PM2.5 暴露:OR,2.08 [95%CI,1.93-2.25];PM10 暴露:OR,2.17 [95%CI,1.49-3.16])和生命的第一年(二氧化氮暴露:OR,2.06 [95%CI,1.37-3.09];PM2.5 暴露:OR,2.12 [95%CI,1.45-3.10];PM10 暴露:OR,2.14 [95%CI,1.46-3.12])。所有区域污染物估计值均按妊娠所有估计值分布的标准差放大两倍。
怀孕期间和生命的第一年接触交通相关的空气污染、二氧化氮、PM2.5 和 PM10 与自闭症有关。对可能的生物学途径的进一步流行病学和毒理学研究将有助于确定这些关联是否具有因果关系。