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Risk estimates of mortality attributed to low concentrations of ambient fine particulate matter in the Canadian community health survey cohort

BACKGROUND: Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM(2.5)) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM(2.5) are limi...

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Detalles Bibliográficos
Autores principales: Pinault, Lauren, Tjepkema, Michael, Crouse, Daniel L., Weichenthal, Scott, van Donkelaar, Aaron, Martin, Randall V., Brauer, Michael, Chen, Hong, Burnett, Richard T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750218/
https://www.ncbi.nlm.nih.gov/pubmed/26864652
http://dx.doi.org/10.1186/s12940-016-0111-6
Descripción
Sumario:BACKGROUND: Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM(2.5)) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM(2.5) are limited. Further, many existing studies lack individual-level information on potentially important behavioural confounding factors. METHODS: A prospective cohort study was conducted among a subset of participants in a cohort that linked respondents of the Canadian Community Health Survey to mortality (n = 299,500) with satellite-derived ambient PM2.5 estimates. Participants enrolled between 2000 and 2008 were followed to date of death or December 31, 2011. Cox proportional hazards models were used to estimate hazard ratios (HRs) for mortality attributed to PM(2.5) exposure, adjusted for individual-level and contextual covariates, including smoking behaviour and body mass index (BMI). RESULTS: Approximately 26,300 non-accidental deaths, of which 32.5 % were due to circulatory disease and 9.1 % were due to respiratory disease, occurred during the follow-up period. Ambient PM(2.5) exposures were relatively low (mean = 6.3 μg/m(3)), yet each 10 μg/m(3) increase in exposure was associated with increased risks of non-accidental (HR = 1.26; 95 % CI: 1.19-1.34), circulatory disease (HR = 1.19; 95 % CI: 1.07–1.31), and respiratory disease mortality (HR = 1.52; 95 % CI: 1.26–1.84) in fully adjusted models. Higher hazard ratios were observed for respiratory mortality among respondents who never smoked (HR = 1.97; 95 % CI: 1.24–3.13 vs. HR = 1.45; 95 % CI: 1.17–1.79 for ever smokers), and among obese (BMI ≥ 30) respondents (HR = 1.76; 95 % CI: 1.15-2.69 vs. HR = 1.41; 95 % CI: 1.04–1.91 for normal weight respondents), though differences between groups were not statistically significant. A threshold analysis for non-accidental mortality estimated a threshold concentration of 0 μg/m(3) (+95 % CI = 4.5 μg/m(3)). CONCLUSIONS: Increased risks of non-accidental, circulatory, and respiratory mortality were observed even at very low concentrations of ambient PM(2.5). HRs were generally greater than most literature values, and adjusting for behavioural covariates served to reduce HR estimates slightly. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12940-016-0111-6) contains supplementary material, which is available to authorized users.