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Risk of Incident Diabetes in Relation to Long-term Exposure to Fine Particulate Matter in Ontario, Canada

Background: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM(2.5) and diabetes is sparse, particularly for incident d...

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Detalles Bibliográficos
Autores principales: Chen, Hong, Burnett, Richard T., Kwong, Jeffrey C., Villeneuve, Paul J., Goldberg, Mark S., Brook, Robert D., van Donkelaar, Aaron, Jerrett, Michael, Martin, Randall V., Brook, Jeffrey R., Copes, Ray
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute of Environmental Health Sciences 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701997/
https://www.ncbi.nlm.nih.gov/pubmed/23632126
http://dx.doi.org/10.1289/ehp.1205958
Descripción
Sumario:Background: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM(2.5) and diabetes is sparse, particularly for incident diabetes. Objectives: We conducted a population-based cohort study to determine whether long-term exposure to ambient PM(2.5) is associated with incident diabetes. Methods: We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM(2.5) at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics. Results: There were 6,310 incident cases of diabetes over 484,644 total person-years of follow-up. The adjusted hazard ratio for a 10-µg/m(3) increase in PM(2.5) was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates. Conclusions: This study suggests that long-term exposure to PM(2.5) may contribute to the development of diabetes.