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Stroke is a leading cause of long-term disability and the third leading cause of death after heart disease and cancer, both in the United States and globally. A large number of epidemiologic studies have found associations between short-term and long-term increases in particulate air pollution (PM) and risk of cardiovascular morbidity and mortality. However, the potential effects of PM on cerebrovascular morbidity and mortality have only recently been studied in detail. Large studies from the US, Europe, and Australia/New Zealand provide inconsistent support for an association between short-term increases in ambient PM levels and risk of cerebrovascular disease morbidity or mortality. The evidence in support of an association is more consistent among studies that have specifically evaluated hospitalization for ischemic stroke, although again, considerable heterogeneity across studies is observed. In contrast, findings from both ecological and cohort studies consistently show that long-term exposure to ambient PM is associated with increased risk of cerebrovascular morbidity and mortality. Given the well documented associations between ambient PM exposure and cardiac disease, as well as the putative mechanisms of these effects, it is plausible that ambient PM increase the risk of ischemic and/or hemorrhagic stroke. Studies to date broadly support this hypothesis, but additional studies are clearly needed.
Stroke is a leading cause of long-term disability and the third leading cause of death after heart disease and cancer, both in the United States and globally. A large number of epidemiologic studies have found associations between short-term and long-term increases in particulate air pollution (PM) and risk of cardiovascular morbidity and mortality. However, the potential effects of PM on cerebrovascular morbidity and mortality have only recently been studied in detail. Large studies from the US, Europe, and Australia/New Zealand provide inconsistent support for an association between short-term increases in ambient PM levels and risk of cerebrovascular disease morbidity or mortality. The evidence in support of an association is more consistent among studies that have specifically evaluated hospitalization for ischemic stroke, although again, considerable heterogeneity across studies is observed. In contrast, findings from both ecological and cohort studies consistently show that long-term exposure to ambient PM is associated with increased risk of cerebrovascular morbidity and mortality. Given the well documented associations between ambient PM exposure and cardiac disease, as well as the putative mechanisms of these effects, it is plausible that ambient PM increase the risk of ischemic and/or hemorrhagic stroke. Studies to date broadly support this hypothesis, but additional studies are clearly needed.
BackgroundStroke is a leading cause of death and long‐term disability in the United States. There is a well‐documented association between ambient particulate matter air pollution (PM) and cardiovascular disease morbidity and mortality. Given the pathophysiologic mechanisms of these effects, short‐term elevations in PM may also increase the risk of ischemic and/or hemorrhagic stroke morbidity and mortality, but the evidence has not been systematically reviewed.Methods and ResultsWe provide a comprehensive review of all observational human studies (January 1966 to January 2014) on the association between short‐term changes in ambient PM levels and cerebrovascular events. We also performed meta‐analyses to evaluate the evidence for an association between each PM size fraction (PM2.5, PM10, PM2.5‐10) and each outcome (total cerebrovascular disease, ischemic stroke/transient ischemic attack, hemorrhagic stroke) separately for mortality and hospital admission. We used a random‐effects model to estimate the summary percent change in relative risk of the outcome per 10‐μg/m3 increase in PM.ConclusionsWe found that PM2.5 and PM10 are associated with a 1.4% (95% CI 0.9% to 1.9%) and 0.5% (95% CI 0.3% to 0.7%) higher total cerebrovascular disease mortality, respectively, with evidence of inconsistent, nonsignificant associations for hospital admission for total cerebrovascular disease or ischemic or hemorrhagic stroke. Current limited evidence does not suggest an association between PM2.5‐10 and cerebrovascular mortality or morbidity. We discuss the potential sources of variability in results across studies, highlight some observations, and identify gaps in literature and make recommendations for future studies.
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