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Air Pollution and Subtypes, Severity and Vulnerability to Ischemic Stroke-A Population Based Case-Crossover Study.
PloS One 2016
BACKGROUND AND PURPOSE: Few studies have examined the association between air pollutants and ischemic stroke subtypes. We examined acute effects of outdoor air pollutants (PM10, NO2, O3, CO, SO2) on subtypes and severity of incident ischemic stroke and investigated if pre-existing risk factors increased susceptibility.
METHODS: We used a time stratified case-crossover study and stroke cases from the South London Stroke Register set up to capture all incident cases of first ever stroke occurring amongst residents in a geographically defined area. The Oxford clinical and TOAST etiological classifications were used to classify subtypes. A pragmatic clinical classification system was used to assess severity. Air pollution concentrations from the nearest background air pollution monitoring stations to patients' residential postcode centroids were used. Lags from 0 to 6 days were investigated.
RESULTS: There were 2590 incident cases of ischemic stroke (1995-2006). While there were associations at various lag times with several pollutants, overall, there was no consistent pattern between exposure and risk of ischemic stroke subtypes or severity. The possible exception was the association between NO2 exposure and small vessel disease stroke-adjusted odds ratio of 1.51 (1.12-2.02) associated with an inter-quartile range increase in the lag 0-6 day average for NO2. There were no clear associations in relation to pre-existing risk factors.
CONCLUSIONS: Overall, we found little consistent evidence of association between air pollutants and ischemic stroke subtypes and severity. There was however a suggestion that increasing NO2 exposure might be associated with higher risk of stroke caused by cerebrovascular small vessel disease.
METHODS: We used a time stratified case-crossover study and stroke cases from the South London Stroke Register set up to capture all incident cases of first ever stroke occurring amongst residents in a geographically defined area. The Oxford clinical and TOAST etiological classifications were used to classify subtypes. A pragmatic clinical classification system was used to assess severity. Air pollution concentrations from the nearest background air pollution monitoring stations to patients' residential postcode centroids were used. Lags from 0 to 6 days were investigated.
RESULTS: There were 2590 incident cases of ischemic stroke (1995-2006). While there were associations at various lag times with several pollutants, overall, there was no consistent pattern between exposure and risk of ischemic stroke subtypes or severity. The possible exception was the association between NO2 exposure and small vessel disease stroke-adjusted odds ratio of 1.51 (1.12-2.02) associated with an inter-quartile range increase in the lag 0-6 day average for NO2. There were no clear associations in relation to pre-existing risk factors.
CONCLUSIONS: Overall, we found little consistent evidence of association between air pollutants and ischemic stroke subtypes and severity. There was however a suggestion that increasing NO2 exposure might be associated with higher risk of stroke caused by cerebrovascular small vessel disease.
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