da Silveira Fleck Alan, Vachon Julien, Buteau Stéphane, Laouan-Sidi Elhadji Anassour, Hatzopoulou Marianne, Weichenthal Scott, Smargiassi Audrey
Department of Environmental and Occupational Health, School of Public Health, University of Montreal, Montreal, Canada.
Center for Public Health Research (CReSP), University of Montreal and CIUSSS du Centre-Sud-de-l'Île-de-Montréal, Montreal, Canada.
Environ Epidemiol. 2022 Dec 14;7(1):e236. doi: 10.1097/EE9.0000000000000236. eCollection 2023 Feb.
Asthma is the most prevalent chronic respiratory disease in children. The role of ultrafine particles (UFPs) in the development of the disease remains unclear. We used a population-based birth cohort to evaluate the association between prenatal and childhood exposure to low levels of ambient UFPs and childhood-onset asthma.
The cohort included all children born and residing in Montreal, Canada, between 2000 and 2015. Children were followed for asthma onset from birth until <13 years of age. Spatially resolved annual mean concentrations of ambient UFPs were estimated from a land use regression model. We assigned prenatal exposure according to the residential postal code at birth. We also considered current exposure during childhood accounting for time-varying residence location. We estimated hazard ratios (HRs) using Cox proportional hazards models adjusted for age, sex, neighborhood material and social deprivation, calendar year, and coexposure to ambient nitrogen dioxide (NO) and fine particles (PM).
The cohort included 352,966 children, with 30,825 children developing asthma during follow-up. Mean prenatal and childhood UFP exposure were 24,706 particles/cm (interquartile range [IQR] = 3,785 particles/cm) and 24,525 particles/cm (IQR = 3,427 particles/cm), respectively. Both prenatal and childhood UFP exposure were not associated with childhood asthma onset in single pollutant models (HR per IQR increase of 0.99 [95% CI = 0.98, 1.00]). Estimates of association remained similar when adjusting for coexposure to ambient NO and PM.
In this population-based birth cohort, childhood asthma onset was not associated with prenatal or childhood exposure to low concentrations of UFPs.
哮喘是儿童中最常见的慢性呼吸道疾病。超细颗粒物(UFPs)在该疾病发展中的作用仍不清楚。我们使用了一个基于人群的出生队列来评估产前和儿童期暴露于低水平环境超细颗粒物与儿童期哮喘发病之间的关联。
该队列包括2000年至2015年在加拿大蒙特利尔出生并居住的所有儿童。对儿童从出生到未满13岁进行哮喘发病情况随访。利用土地利用回归模型估计环境超细颗粒物的空间分辨年平均浓度。我们根据出生时的居住邮政编码确定产前暴露情况。我们还考虑了儿童期的当前暴露情况,并考虑了随时间变化的居住地点。我们使用Cox比例风险模型估计风险比(HRs),该模型对年龄、性别、邻里物质和社会剥夺、日历年份以及与环境二氧化氮(NO)和细颗粒物(PM)的共同暴露进行了调整。
该队列包括352,966名儿童,其中30,825名儿童在随访期间患哮喘。产前和儿童期超细颗粒物暴露的平均值分别为24,706颗粒/立方厘米(四分位间距[IQR]=3,785颗粒/立方厘米)和24,525颗粒/立方厘米(IQR=3,427颗粒/立方厘米)。在单一污染物模型中,产前和儿童期超细颗粒物暴露均与儿童期哮喘发病无关(每IQR增加的HR为0.99[95%CI=0.98,1.00])。在调整了与环境NO和PM的共同暴露后,关联估计值仍然相似。
在这个基于人群的出生队列中,儿童期哮喘发病与产前或儿童期暴露于低浓度超细颗粒物无关。