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Ambient Air Pollution and Stroke

2014; Lippincott Williams & Wilkins; Volume: 45; Issue: 12 Linguagem: Inglês

10.1161/strokeaha.114.003130

1524-4628

Petter Ljungman, Murray A. Mittleman,

Air Quality Monitoring and Forecasting

HomeStrokeVol. 45, No. 12Ambient Air Pollution and Stroke Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUBAmbient Air Pollution and Stroke Petter L. Ljungman, MD, PhD and Murray A. Mittleman, MD, DrPH Petter L. LjungmanPetter L. Ljungman From the Department of Medicine Cardiovascular Epidemiology Research Unit, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (P.L.L., M.A.M.); and Unit of Environmental Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.L.L.). and Murray A. MittlemanMurray A. Mittleman From the Department of Medicine Cardiovascular Epidemiology Research Unit, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (P.L.L., M.A.M.); and Unit of Environmental Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.L.L.). Originally published9 Oct 2014https://doi.org/10.1161/STROKEAHA.114.003130Stroke. 2014;45:3734–3741Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2014: Previous Version 1 Stroke is a leading cause of death in the United States1 and worldwide (http://www.who.int) and may lead to considerable neurological sequelae including aphasia, paraplegia, and dementia. The estimated healthcare costs of stroke in the United States exceed $36 billion per year.1 A large body of evidence supports the association between ambient air pollution exposure and increased cardiovascular mortality and morbidity,2 but only recently have several studies specifically demonstrated an association with increased stroke risk.BackgroundMajor sources of air pollution include traffic, power plants and in developing countries, biomass combustion. Both particles and gases are emitted through combustion. Particulate matter with aerodynamic diameter 60 years old, never-smokers, and among subjects with exposure levels <25 μg/m3 (current annual mean air quality standard in Europe). Studies that compared long-term air pollution exposure and hospital admissions according to specific stroke type reported positive associations for NO2, CO, and traffic density and admissions for both ischemic and hemorrhagic stroke19 in Edmonton, Canada, whereas NO28,20 in Denmark or NOx15 in London, UK, demonstrated associations consistent with ischemic stroke but not hemorrhagic stroke. Two studies from Scania, Sweden17,18 only including hospital admissions for ischemic stroke observed associations between higher long-term exposure to NOx and higher risk of hospital admission for ischemic stroke in participants with diabetes mellitus but found no association in the overall population, in smokers, or in participants with hypertension or atrial fibrillation. A recent population-based cohort study in Denmark studying long-term NO2 and traffic noise exposure and stroke incidence reported positive associations for ischemic stroke in separate analyses for both noise and NO2 but in combined analyses NO2 was only associated with fatal ischemic strokes.20Table 2. Studies of Long-Term Air Pollution Exposure and Hospitalization for StrokeStudyLocationStudy DesignStroke OutcomeRelative Risk (95% Confidence Intervals)ExposureMaheswaran et al6Sheffield, UKEcologicalAny stroke1.13 (0.99–1.29) PM10Highest to lowest quintile of modeled pollutant1.11 (0.99–1.25) CO1.13 (1.04–1.27) NOxAndersen et al8DenmarkCohortAny stroke1.05 (0.99–1.11)Per interquartile range increase (43%) in mean modeled NO2 since 1971Ischemic1.05 (0.95–1.17Hemorrhagic0.93 (0.81–1.07)Lipsett et al10CaliforniaCohortAny stroke1.06 (1.00–1.13) PM10Per 10 μg/m3 annual mean pollutant at closest monitor1.14 (0.99–1.32) PM2.5Miller et al1136 US citiesCohortAny stroke1.28 (1.01–1.61) PM2.5Per 10 μg/m3 mean of closest monitor during 2000Maheswaran et al15London, UKEcologicalIschemic1.22 (0.77–1.93) PM10Per 10 μg/m3 of modeled pollutant exposure1.11 (0.93–1.32) NO2Hemorrhagic0.52 (0.20–1.37) PM100.86 (0.60–1.24) NO2Atkinson et al14EnglandCohortAny stroke0.98 (0.95–1.01) PM10Per 3.0 μg/m3 PM100.99 (0.95–1.03) NO2Per 10.7 μg/m3 NO21.02 (1.00–1.05) SO2Per 2.2 μg/m3 SO21.00 (0.97–1.04) O3Per 3.0 μg/m3 O3 modeled annual meanStafoggia et al1611 cohorts, EuropeCohortAny stroke1.19 (0.88–1.62)Per 5 μg/m3 annual meanOudin et al17Scania, SwedenCase–controlIschemic0.95 (0.86–1.06)Annual mean modeled NOx of 20–30 vs <10 μg/m3Oudin et al18Scania, SwedenCase–controlIschemicIn diabetics:Modeled annual NOx:2.0 (1.2–3.4) high NOxHigh NOx ≥25 μg/m31.3 (1.1–1.6) low NOxLow NOx 20°CPM10 on days with ≤20°CQian et al29Wuhan, ChinaTime seriesAny strokePM10…Qian et al30Wuhan, ChinaTime seriesAny strokeNO2SO2 and O3Qian et al31Wuhan, ChinaTime seriesAny strokePM10 all days and NO2, SO2 on normal temperature daysO3 all days and NO2, SO2 on high temperature daysQian et al32Wuhan, ChinaTime seriesAny strokeNO2 in spring. PM10, NO2, SO2 in winterPM10 and SO2 in spring. All pollutants summer or fallTurin et al33Takashima, JapanTime seriesAny stroke…Suspended PM, NO2, SO2, and O3IschemicNO2Suspended PM, SO2, and O3Hemorrhagic…Suspended PM, NO2, SO2, and O3Yorifuji et al34Tokyo, JapanTime seriesAny strokePM2.5 and NO2…Ischemic…PM2.5 and NO2HemorrhagicPM2.5 and NO2…Yorifuji and Kashima 3547 Japanese citiesTime seriesAny stroke…PM10IschemicPM10…Hemorrhagic…PM10Zanobetti and Schwartz 36112 US citiesTime seriesAny strokePM2.5 and PMcoarseMaynard et al37Massachusetts, USACase crossoverAny strokeBlack carbonSO4Qian et al38Shanghai, ChinaCase crossoverAny strokePM10, NO2, and SO2…IschemicPM10, NO2, and SO2…HemorrhagicNO2 and SO2PM10Ren et al39Massachusetts, USACase crossoverAny strokeO3…Zeka et al4020 US citiesCase crossoverAny strokePM10…Zeka et al4120 US citiesCase crossoverAny strokePM10 if pneumonia or ≥75-y oldPM10 if no pneumonia or ≤75-y oldPM0.1 indicates ultrafine particles with <0.1 μm aerodynamic diameter; PM10, particles with aerodynamic diameter ≤10 μm; PM2.5, fine particles with aerodynamic diameter ≤2.5 μm; PMcoarse, coarse particles with aerodynamic diameter between 2.5 and 10 μm in aerodynamic diameter; and TSP, total suspended particles.*Positive associations with confidence intervals not including the null.†Associations with confidence intervals including the null.Short-Term Air Pollution Exposure and Hospitalization for StrokeStudies of short-term air pollution exposure and hospitalization for any stroke have reported mixed results.43–63 However, in contrast to studies investigating short-term exposure to air pollution and stroke mortality that typically use death certificate data, some studies of associations with hospital admissions for stroke have had more data on stroke type. These studies have reported associations between PM10,45,46,64,65 PM2.5,66–68 black carbon,68 CO,51,58,64 NO2,43,58,64,68 and O362,69,70 and ischemic stroke (Table 4; for detailed estimates, see Table II in the online-only Data Supplement). A majority did not observe associations between air pollutants and hemorrhagic stroke45,58,62,65,69 with a few exceptions56,57,63,64,71 including one study that specifically investigated days in Taiwan polluted by Asian dust storms originating from the Gobi desert.63 Of the studies with specific data on subtype of ischemic stroke, PM10, PM2.5, and O3 were associated with strokes characterized as large-artery atherosclerotic strokes, small-vessel occlusions, lacunar strokes, or transient ischemic attacks rather than cardioembolic strokes.46,67–69 Stronger associations were reported for recurrent ischemic strokes or history of stroke,58,70 in individuals with diabetes mellitus or on diabetes mellitus medication67,70 and with ≥1 cardiovascular risk factors.69,70 A few studies reported stronger associations between O3 and ischemic stroke in men than in women.62,69,72 Air pollution on warm days was more strongly associated with both hemorrhagic and ischemic stroke in Taiwan.64 Associations between air pollution and ischemic stroke were stronger in the warm season in Edmonton, Canada58 and Dijon, France70 in contrast to Wuhan61 where associations were stronger in the cold season. Differences may reflect better exposure classification because of time spent outdoors in climates such as Edmonton, Canada but may also be because of seasonal interactions between pollutants.Table 4. Studies of Short-Term Exposure to Air Pollution and Hospital Admissions for StrokeStudyLocationStudy DesignStroke OutcomePositive Associations*Null Associations†Ballester et al43Valencia, SpainTime seriesAny strokeNO2CO, SO2, and O3Burnett et al44Toronto, CanadaTime seriesAny stroke…PM10, CO, NO2, and O3Chan et al45Taipei, TaiwanTime seriesAny strokePM10, PM2.5, and O3CO, NO2, and SO2Ischemic…PM10, PM2.5, CO, NO2, SO2, and O3Hemorrhagic…PM10, PM2.5, CO, NO2, SO2, and O3Corea et al46Mantua, ItalyCase crossoverAny strokePM10…IschemicPM10 in all ischemic, large vessel, small vessel, and lacunarPM10 in cardioembolic. CO, NO2, SO2, and O3Jalaludin et al47Sydney, AustraliaTime seriesAny stroke…PM10, PM2.5, CO, NO2, SO2, and O3Larrieu et al488 French citiesTime seriesAny stroke…PM10, NO2, and O3Le Tertre et al498 European citiesTime seriesAny stroke…PM10 and black smokeLinn et al50Los Angeles, USATime seriesAny strokeCO and NO2 in springPM10 and O3Moolgavkar51Los Angeles, USATime seriesAny strokePM10, CO, NO2, and SO2PM2.5Nascimento et al52Sao Jose Campos, BrazilTime seriesAny strokePM10 and SO2O3Poloniecki et al53London, UKTime seriesAny stroke…Black smoke, CO, NO2, SO2, and O3Pönkä and Virtanen54Helsinki, FinlandTime seriesAny strokeNO2…IschemicTotal suspended particles…Sunyer et al557 European citiesTime seriesAny stroke…SO2Turin et al56Takashima, JapanTime seriesAny stroke…PM10,NO2, SO2, and O3Ischemic…PM10,NO2, SO2, and O3HemorrhagicSO2PM10,NO2, and O3Villeneuve et al57Edmonton, CanadaCase crossoverAny stroke…PM10, PM2.5, CO, NO2, SO2, and O3IschemicPM2.5CO, NO2, SO2, and O3TIA…PM10, PM2.5, CO, NO2, SO2, and O3HemorrhagicSO2PM10, PM2.5, CO, NO2, and O3Villeneuve et al58Edmonton, CanadaCase crossoverAny strokeCO in warm seasonPM2.5, NO2, SO2, O3, and CO all yearIschemicCO, NO2,O3 in warm seasonPM2.5, SO2. CO, NO2, and O3 all yearHemorrhagic…PM2.5, CO, NO2, SO2, and O3Wong et al59Hong Kong, ChinaTime seriesAny stroke…PM10, NO2, SO2, and O3Wordley et al60Birmingham, UKTime seriesAny strokePM10…Xiang et al61Wuhan, ChinaCase crossoverAny strokePM10 and NO2 in cold seasonPM10, NO2, and SO2 all year and in subtypes. PM10 and NO2 in warm seasonXu et al62Allegheny, USACase crossoverAny strokeO3…IschemicO3…Hemorrhagic…O3Yang et al63Taipei, TaiwanTime seriesAny stroke…Asian dustIschemic…Asian dustHemorrhagicAsian dust and intracerebralAsian dust and subarachnoidalTsai et al64Kaohsiung, TaiwanCase crossoverIschemicPM10, NO2, SO2, O3 warm days, CO all daysPM10, NO2, SO2, and O3 cool daysHemorrhagicPM10, CO, NO2, and O3 warm daysSO2 warm days, all pollutants cool daysWellenius et al659 US citiesCase crossoverIschemicPM10, CO, NO2, and SO2Hemorrhagic…PM10, CO, NO2, and SO2Lisabeth et al66Corpus Christi, USATime seriesIschemicPM2.5O3O'Donnell et al678 Canadian citiesCase crossoverIschemicPM2.5 in diabetics and noncardioembolicPM2.5 in ischemic strokes overallWellenius et al68Boston, USACase crossoverIschemicPM2.5, black carbon, NO2, and PM2.5 large and small vessel strokeCO, SO4, O3, and PM2.5 cardioembolic strokeHenrotin et al69Dijon, FranceCase crossoverIschemicO3 in all ischemic, large vessel, and TIAPM10, CO, NO2, and SO2HemorrhagicPM10, CO, NO2, SO2, and O3Henrotin et al70Dijon, FranceCase crossoverIschemicO3 in recurrent strokeO3 in incident strokeYamazaki et al71JapanCase crossoverIschemic…PM7, NO2, and O3 in 24 h averagesHemorrhagicPM7 2 h before intracerebral hemorrhage…Bedada et al72UKCase crossoverMinor strokeNOCO, NO2, SO2, and O3PM0.1 indicates ultrafine particles with less than 0.1 μm aerodynamic diameter; PM10, particles with aerodynamic diameter ≤10 μm; PM2.5, fine particles with aerodynamic diameter ≤2.5 μm; PMcoarse, coarse particles with aerodynamic diameter between 2.5 and 10 μm in aerodynamic diameter; and TIA, transient ischemic attack.*Positive associations with confidence intervals not including the null.†Associations with confidence intervals including the null.SummaryThe current evidence suggests that exposure to higher levels of air pollutants related to combustion increases the risk of stroke. Studies of both long-term and short-term air pollution exposure suggest consistent evidence of increased risk of ischemic stroke and moderately consistent evidence supporting an association with hemorrhagic stroke. A few studies exploring susceptible subgroups have indicated stronger associations in individuals with several cardiovascular risk factors, diabetes mellitus, previous stroke, and of older age. A recently published meta-analysis focusing on short-term air pollution exposure and stroke incidence or mortality reported significant associations for PM2.5, PM10, SO2, CO, NO2, and O3 for stroke with stronger associations for ischemic stroke.73Because much of the existing literature is based on linkage of administrative data, an important limitation of many available studies is limited ability to classify and validate specific stroke outcomes. Ischemic stroke and hemorrhagic stroke and their subtypes have in the majority of studies been analyzed as a combined outcome despite the clear possibility that air pollution may affect underlying pathophysiological pathways differently. Only some have separately analyzed ischemic stroke and hemorrhagic stroke and a handful have considered subtypes of ischemic stroke or hemorrhagic stroke. Similarly, only a handful used thorough chart reviews and adjudicated the diagnosis and onset time of stroke. This highlights the need for high-quality validated diagnostic characterization of stroke outcome in studies of air pollution. In a study of short-term air pollution exposure and stroke specifically investigating the bias introduced through misclassification of time of event of stroke found that incorrect temporal classification caused up to 66% bias toward the null.42 This may be especially relevant in mortality studies where the date of death from death certificates is used while not accounting for the time between stroke onset and death. In studies of long-term exposure to air pollution, the ability to investigate associations with stroke is dependent on the validity and resolution of the spatial exposure assessment and the adequate control for confounders related to both air pollution at place of residence and the risk of stroke, in particular socioeconomic factors.There is growing evidence to suggest that both accumulated exposure to higher air pollution during a period of years and higher mean levels during a period of days increase the risk of stroke. In addition to improving temporal classification of exposure by validating stroke onset time, future research efforts should be directed to careful characterization of stroke subtype because air pollution may variably affect the different pathophysiological pathways. Air pollution exposure and increased risk of stroke may represent a considerable public health problem and regulations have improved air quality in many countries in Europe and the United States, resulting in greater life expectancy.74 Yet, associations with stroke have been reported at levels in compliance with current standards,16,68 highlighting the continued importance of effective regulation and monitoring in high-income countries as well as extending efforts to address regulation in low- and middle-income countries where levels of air pollution and prevalence of stroke are on the rise.Sources of FundingThis work was supported by the US Environmental Protection Agency (grants R832416, RD83479801), National Institute of Environmental Health Sciences (grant P01-ES009825), Swedish Council for Working Life and Social Research Marie Curie International Postdoctoral Fellowship Programme, the Swedish Heart-Lung Foundation, the Swedish Society of Cardiology, and the Swedish Society for Medical Research. 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