Éric Lavigne1, Robert Talarico2, Aaron van Donkelaar3, Randall V Martin4, David M Stieb5, Eric Crighton6, Scott Weichenthal7, Marc Smith-Doiron8, Richard T Burnett9, Hong Chen10. 1. Air Health Science Division, Health Canada, Ottawa, Ontario, Canada; School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Ontario, Canada; Institute for Clinical Evaluative Sciences, Ottawa, Ontario, Canada. Electronic address: eric.lavigne@hc-sc.gc.ca. 2. Institute for Clinical Evaluative Sciences, Ottawa, Ontario, Canada. 3. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, Nova Scotia, Canada; Department of Energy, Environmental and Chemical Engineering, Washington University in St. Louis, St. Louis, MO, USA. 4. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, Nova Scotia, Canada; Department of Energy, Environmental and Chemical Engineering, Washington University in St. Louis, St. Louis, MO, USA; Harvard-Smithsonian Centre for Astrophysics, Cambridge, MA, USA. 5. School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Ontario, Canada; Population Studies Division, Health Canada, Ottawa, Ontario, Canada. 6. Institute for Clinical Evaluative Sciences, Ottawa, Ontario, Canada; Department of Geography, Environment and Geomatics, University of Ottawa, Ottawa, Ontario, Canada. 7. Air Health Science Division, Health Canada, Ottawa, Ontario, Canada; Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada. 8. Population Studies Division, Health Canada, Ottawa, Ontario, Canada. 9. School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Ontario, Canada. 10. Institute for Clinical Evaluative Sciences, Ottawa, Ontario, Canada; Population Studies Division, Health Canada, Ottawa, Ontario, Canada; Public Health Ontario, Toronto, Ontario, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada.
Abstract
BACKGROUND: Several studies have found positive associations between outdoor fine particulate air pollution (≤2.5 μm, PM2.5) and childhood asthma incidence. However, the impact of PM2.5 composition on children's respiratory health remains uncertain. OBJECTIVE: We examined whether joint exposure to PM2.5 mass concentrations and its major chemical components was associated with childhood asthma development. METHODS: We conducted a population-based cohort study by identifying 1,130,855 singleton live births occurring between 2006 and 2014 in the province of Ontario, Canada. Concentrations of PM2.5 and its seven major chemical components were assigned to participants based on their postal codes using chemical transport models and remote sensing. The joint impact of outdoor PM2.5 concentrations and its major components and childhood asthma incidence (up to age 6) were estimated using Cox proportional hazards models, allowing for potential nonlinearity. RESULTS: We identified 167,080 children who developed asthma before age 6. In adjusted models, outdoor PM2.5 mass concentrations during childhood were associated with increased incidence of childhood asthma (Hazard Ratio (HR) for each 1 μg/m3 increase = 1.026, 95% CI: 1.021-1.031). We found that the joint effects of PM2.5 and its components on childhood asthma incidence may be 24% higher than the conventional approach. Specific components/source markers such as black carbon, ammonium, and nitrate appeared to play an important role. CONCLUSIONS: Early life exposure to PM2.5 and its chemical components is associated with an increased risk of asthma development in children. The heterogeneous nature of PM2.5 should be considered in future health risk assessments. Crown
BACKGROUND: Several studies have found positive associations between outdoor fine particulate air pollution (≤2.5 μm, PM2.5) and childhood asthma incidence. However, the impact of PM2.5 composition on children's respiratory health remains uncertain. OBJECTIVE: We examined whether joint exposure to PM2.5 mass concentrations and its major chemical components was associated with childhood asthma development. METHODS: We conducted a population-based cohort study by identifying 1,130,855 singleton live births occurring between 2006 and 2014 in the province of Ontario, Canada. Concentrations of PM2.5 and its seven major chemical components were assigned to participants based on their postal codes using chemical transport models and remote sensing. The joint impact of outdoor PM2.5 concentrations and its major components and childhood asthma incidence (up to age 6) were estimated using Cox proportional hazards models, allowing for potential nonlinearity. RESULTS: We identified 167,080 children who developed asthma before age 6. In adjusted models, outdoor PM2.5 mass concentrations during childhood were associated with increased incidence of childhood asthma (Hazard Ratio (HR) for each 1 μg/m3 increase = 1.026, 95% CI: 1.021-1.031). We found that the joint effects of PM2.5 and its components on childhood asthma incidence may be 24% higher than the conventional approach. Specific components/source markers such as black carbon, ammonium, and nitrate appeared to play an important role. CONCLUSIONS: Early life exposure to PM2.5 and its chemical components is associated with an increased risk of asthma development in children. The heterogeneous nature of PM2.5 should be considered in future health risk assessments. Crown
Authors: Kaitlyn G Lawrence; Nicole M Niehoff; Alexander P Keil; W Braxton Jackson; Kate Christenbury; Patricia A Stewart; Mark R Stenzel; Tran B Huynh; Caroline P Groth; Gurumurthy Ramachandran; Sudipto Banerjee; Gregory C Pratt; Matthew D Curry; Lawrence S Engel; Dale P Sandler Journal: Environ Int Date: 2022-07-27 Impact factor: 13.352