Institut National de Sante Publique du Quebec (INSPQ), Montreal, Quebec, Canada.
Department of Civil Engineering, University of Toronto, Toronto, Ontario, Canada.
Environ Res. 2020 Jun;185:109180. doi: 10.1016/j.envres.2020.109180. Epub 2020 Jan 25.
Despite evidence that ambient air pollution may play a role in the development of asthma, little is known about the potential contribution of industrial emissions.
We used a population-based birth cohort to investigate the association between asthma onset in childhood and residential exposure to industrial emissions, estimated from atmospheric dispersion modeling.
The study population comprised all children born in the province of Quebec, Canada, 2002-2011. Asthma onset were ascertained from health administrative databases with validated algorithms. We used atmospheric dispersion modeling to develop time-varying annual mean concentration of ambient PM, NO and SO at participants' residence from industries. For each pollutant, we assessed the association between industrial emissions exposure and childhood asthma onset using Cox proportional hazard model, adjusted for sex, material and social deprivation and calendar year. Sensitivity analysis included adjusting for long-term regional and traffic-related ambient PM and NO, and assessing potential confounding by unmeasured secondhand smoke.
The cohort included 722,667 children and 66,559 incident cases of asthma. For all pollutants, we found a non-linear association between childhood asthma onset and residential ambient air pollutant concentration from industries, with stronger effects at lower concentrations. A change from 25th to the 75th percentile in the mean annual ambient concentration of PM (0.13 μg/m), NO (1.0 μg/m) and SO (1.6 μg/m) from industrial emissions was associated with a 19% (95% CI: 17-20%), 21% (95% CI: 19-23%) and 23% (95% CI: 21-24%) increase in the risk of asthma onset in children, respectively. For PM and NO, associations were persisting after adjustments for long-term regional PM and traffic-related NO ambient concentration.
Residential exposure to industrial emissions estimated from dispersion modeling was associated with asthma onset in childhood. Importantly, associations were stronger at lower concentrations and independent from those of other sources, thus adding up to the burden of regional and traffic-related air pollution.
尽管有证据表明，环境空气污染可能在哮喘的发展中起作用，但对于工业排放物的潜在贡献知之甚少。
我们使用基于人群的出生队列研究，调查了大气扩散模型估计的儿童时期住宅暴露于工业排放物与哮喘发病之间的关联。
研究人群包括 2002 年至 2011 年期间在加拿大魁北克省出生的所有儿童。通过经过验证的算法从健康管理数据库中确定哮喘发病情况。我们使用大气扩散模型，根据工业的情况，为参与者的住所制定了随时间变化的每年环境 PM、NO 和 SO 的平均浓度。对于每种污染物，我们使用 Cox 比例风险模型评估了工业排放物暴露与儿童哮喘发病之间的关联，调整了性别、物质和社会剥夺以及日历年份。敏感性分析包括调整长期区域和交通相关的环境 PM 和 NO，并评估未测量的二手烟的潜在混杂因素。
该队列包括 722667 名儿童和 66559 例哮喘新发病例。对于所有污染物，我们发现儿童哮喘发病与工业排放的住宅环境空气污染物浓度之间存在非线性关联，在较低浓度下影响更大。每年环境 PM（0.13μg/m）、NO（1.0μg/m）和 SO（1.6μg/m）从工业排放的平均浓度从第 25 百分位到第 75 百分位的变化与儿童哮喘发病风险分别增加 19%（95%CI：17-20%）、21%（95%CI：19-23%）和 23%（95%CI：21-24%）相关。对于 PM 和 NO，在调整长期区域 PM 和交通相关 NO 环境浓度后，相关性仍然存在。
从扩散模型估计的住宅暴露于工业排放物与儿童哮喘发病有关。重要的是，在较低浓度下的关联更强，并且独立于其他来源的关联，因此增加了区域和交通相关空气污染的负担。
