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Résumé (anglais)

Highlights * We studied childhood asthma onset and residential exposure to industrial emissions. * We used a population-based birth cohort in Quebec, Canada, 2002–2011. * Residential exposure to industrial emissions was estimated from dispersion modeling. * Ambient PM2.5, NO2 and SO2 from industries was associated with asthma onset. * Associations were independent from those of regional PM2.5 and traffic-related NO2. Abstract Background 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. Objective 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. Methods 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 PM2.5, NO2 and SO2 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 PM2.5 and NO2, and assessing potential confounding by unmeasured secondhand smoke. Results 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 PM2.5 (0.13 -g/m3), NO2 (1.0 -g/m3) and SO2 (1.6 -g/m3) 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 PM2.5 and NO2, associations were persisting after adjustments for long-term regional PM2.5 and traffic-related NO2 ambient concentration. Conclusion: 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.