Faculty of Health Sciences, Simon Fraser University, Vancouver, British Columbia, Canada.
Centre of Hip Health and Mobility, Vancouver Coastal Health Research Institute, Vancouver, British Columbia, Canada.
JAMA Pediatr. 2019 Jan 1;173(1):86-92. doi: 10.1001/jamapediatrics.2018.3101.
The etiology of autism spectrum disorder (ASD) is poorly understood, but prior studies suggest associations with airborne pollutants.
To evaluate the association between prenatal exposures to airborne pollutants and ASD in a large population-based cohort.
DESIGN, SETTING, AND PARTICIPANTS: This population-based cohort encompassed nearly all births in Metro Vancouver, British Columbia, Canada, from 2004 through 2009, with follow-up through 2014. Children were diagnosed with ASD using a standardized assessment with the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule. Monthly mean exposures to particulate matter with a diameter less than 2.5 µm (PM2.5), nitric oxide (NO), and nitrogen dioxide (NO2) at the maternal residence during pregnancy were estimated with temporally adjusted, high-resolution land use regression models. The association between prenatal air pollution exposures and the odds of developing ASD was evaluated using logistic regression adjusted for child sex, birth month, birth year, maternal age, maternal birthplace, and neighborhood-level urbanicity and income band. Data analysis occurred from June 2016 to May 2018.
Mean monthly concentrations of ambient PM2.5, NO, and NO2 at the maternal residence during pregnancy, calculated retrospectively using temporally adjusted, high-resolution land use regression models.
Autism spectrum disorder diagnoses based on standardized assessment of the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule. The hypothesis being tested was formulated during data collection.
In a cohort of 132 256 births, 1307 children (1.0%) were diagnosed with ASD by the age of 5 years. The final sample size for the PM2.5-adjusted model was 129 439 children, and for NO and NO2, it was 129 436 children; of these, 1276 (1.0%) were diagnosed with ASD. Adjusted odds ratios for ASD per interquartile range (IQR) were not significant for exposure to PM2.5 during pregnancy (1.04 [95% CI, 0.98-1.10] per 1.5 μg/m3 increase [IQR] in PM2.5) or NO2 (1.06 [95% CI, 0.99-1.12] per 4.8 ppb [IQR] increase in NO2) but the odds ratio was significant for NO (1.07 [95% CI, 1.01-1.13] per 10.7 ppb [IQR] increase in NO). Odds ratios for male children were 1.04 (95% CI, 0.98-1.10) for PM2.5; 1.09 (95% CI, 1.02-1.15) for NO; and 1.07 (95% CI, 1.00-1.13) for NO2. For female children, they were for 1.03 (95% CI, 0.90-1.18) for PM2.5; 0.98 (95% CI, 0.83-1.13) for NO; and 1.00 (95% CI, 0.86-1.16) for NO2.
In a population-based birth cohort, we detected an association between exposure to NO and ASD but no significant association with PM2.5 and NO2.
自闭症谱系障碍（ASD）的病因尚不清楚，但先前的研究表明与空气污染物有关。
在一个大型基于人群的队列中评估产前暴露于空气污染物与 ASD 之间的关联。
设计、地点和参与者：本基于人群的队列包括 2004 年至 2009 年期间不列颠哥伦比亚省大温哥华地区几乎所有的出生，随访至 2014 年。使用经过标准化评估的自闭症诊断访谈修订版和自闭症诊断观察时间表对儿童进行 ASD 诊断。在妊娠期间，使用时间调整的高分辨率土地利用回归模型估算母体居住地的 PM2.5、一氧化氮（NO）和二氧化氮（NO2）的每月平均暴露量。使用逻辑回归调整儿童性别、出生月份、出生年份、母亲年龄、母亲出生地和邻里城市化和收入带，评估产前空气污染暴露与 ASD 发病几率之间的关联。数据分析于 2016 年 6 月至 2018 年 5 月进行。
使用时间调整的高分辨率土地利用回归模型， retrospectively 计算母体居住地在妊娠期间的 PM2.5、NO 和 NO2 的月平均浓度。
根据自闭症诊断访谈修订版和自闭症诊断观察时间表进行的标准化评估得出的 ASD 诊断。正在测试的假设是在数据收集过程中制定的。
在 132256 名出生的儿童中，有 1307 名（1.0%）在 5 岁时被诊断为 ASD。PM2.5 调整模型的最终样本量为 129439 名儿童，NO 和 NO2 的最终样本量为 129436 名儿童；其中 1276 名（1.0%）被诊断为 ASD。与 ASD 相关的调整后的 OR 值在妊娠期间 PM2.5 暴露（每增加 1.5 μg/m3 [IQR]，PM2.5 增加 1.04 [95%CI，0.98-1.10]）或 NO2（每增加 4.8 ppb [IQR]，NO2 增加 1.06 [95%CI，0.99-1.12]）方面没有统计学意义，但 NO 的 OR 值有统计学意义（每增加 10.7 ppb [IQR]，NO 增加 1.07 [95%CI，1.01-1.13]）。对于男性儿童，PM2.5 的 OR 值为 1.04（95%CI，0.98-1.10）；NO 的 OR 值为 1.09（95%CI，1.02-1.15）；NO2 的 OR 值为 1.07（95%CI，1.00-1.13）。对于女性儿童，PM2.5 的 OR 值为 1.03（95%CI，0.90-1.18）；NO 的 OR 值为 0.98（95%CI，0.83-1.13）；NO2 的 OR 值为 1.00（95%CI，0.86-1.16）。
在基于人群的出生队列中，我们发现暴露于 NO 与 ASD 之间存在关联，但与 PM2.5 和 NO2 之间没有显著关联。
