Abstract
BackgroundDiabetes and neurological disorders are a growing burden among the elderly, and may also make them more susceptible to particulate air matter with aerodynamic diameter less than 2.5 μg (PM2.5). The same biological responses thought to effect cardiovascular disease through air pollution-mediated systemic oxidative stress, inflammation and cerebrovascular dysfunction could also be relevant for diabetes and neurodegenerative diseases.MethodsWe conducted multi-site case-crossover analyses of all-cause deaths and of hospitalizations for diabetes or neurological disorders among Medicare enrollees (>65 years) during the period 1999 to 2010 in 121 US communities. We examined whether 1) short-term exposure to PM2.5 increases the risk of hospitalization for diabetes or neurological disorders, and 2) the association between short-term exposure to PM2.5 and all-cause mortality is modified by having a previous hospitalization of diabetes or neurological disorders.ResultsWe found that short term exposure to PM2.5 is significantly associated with an increase in hospitalization risks for diabetes (1.14% increase, 95% CI: 0.56, 1.73 for a 10 μg/m3 increase in the 2 days average), and for Parkinson’s disease (3.23%, 1.08, 5.43); we also found an increase in all-cause mortality risks (0.64%, 95% CI: 0.42, 0.85), but we didn’t find that hospitalization for diabetes and neurodegenerative diseases modifies the association between short term exposure to PM2.5 and all-cause mortality.ConclusionWe found that short-term exposure to fine particles increased the risk of hospitalizations for Parkinson’s disease and diabetes, and of all-cause mortality. While the association between short term exposure to PM2.5 and mortality was higher among Medicare enrollees that had a previous admission for diabetes and neurological disorders than among Medicare enrollees that did not had a prior admission for these diseases, the effect modification was not statistically significant. We believe that these results provide useful insights regarding the mechanisms by which particles may affect the brain. A better understanding of the mechanisms will enable the development of new strategies to protect individuals at risk and to reduce detrimental effects of air pollution on the nervous system.
Highlights
Diabetes and neurological disorders are a growing burden among the elderly, and may make them more susceptible to particulate air matter with aerodynamic diameter less than 2.5 μg (PM2.5)
Among the subjects who died during the study period in all the communities, 13.7%, 3.8%, and 3.3% of subjects had a previous hospitalization noting as a cause or a comorbid condition diabetes, Alzheimer’s disease, and dementia respectively
This may limit generalization of these results. Another limitation though is due to Medicare reporting only the date of death and not the cause of death. In this multi-city study we found that short-term exposure to fine particles increased the risk of hospitalizations for Parkinson’s disease and diabetes and of all-cause mortality in Medicare enrollees
Summary
Diabetes and neurological disorders are a growing burden among the elderly, and may make them more susceptible to particulate air matter with aerodynamic diameter less than 2.5 μg (PM2.5). The same biological responses thought to effect cardiovascular disease through air pollution-mediated systemic oxidative stress, inflammation and cerebrovascular dysfunction could be relevant for diabetes and neurodegenerative diseases. There is clear evidence that long- and short-term exposures to particulate air pollution are associated with both acute and chronic mortality risk; multi-site studies have shown that ambient particulate pollution is associated with increased risk of deaths or hospitalizations for broadly defined cardiovascular disease [1,2,3,4,5,6,7,8,9]. Several studies have reported associations between short-term particulate matter (PM2.5) exposure and cerebrovascular disease and stroke [10,11,12,13,14,15]. The endothelial dysfunction induced by oxidative stress can release vascular endothelial growth factor and prostanoids, which promote vascular leakage, protein extravasation, and cytokine production [32]
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