Long-term ambient hydrocarbons exposure and incidence of ischemic stroke.
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ABSTRACT:
SUBMITTER: Zhang HW
PROVIDER: S-EPMC6892494 | biostudies-literature | 2019
REPOSITORIES: biostudies-literature
Publications
Long-term ambient hydrocarbons exposure and incidence of ischemic stroke.
Zhang Han-Wei HW Kok Victor C VC Chuang Shu-Chun SC Tseng Chun-Hung CH Lin Chin-Teng CT Li Tsai-Chung TC Sung Fung-Chang FC Wen Chi Pang CP Hsiung Chao A CA Hsu Chung Y CY
PloS one 20191204 12
Exposure to air pollutants is known to have adverse effects on human health; however, little is known about the association between hydrocarbons in air and an ischemic stroke (IS) event. We investigated whether long-term exposure to airborne hydrocarbons, including volatile organic compounds, increased IS risk. This retrospective cohort study included 283,666 people aged 40 years or older in Taiwan. Cox proportional hazards regression analysis was used to fit single- and multiple-pollutant model ...[more]
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Project description:Particulate matter and volatile organic compounds, including total hydrocarbons (THCs), are major ambient air pollutants. Primary nonmethane hydrocarbons (NMHCs) originate from vehicle emissions. The association between air pollution and urinary bladder cancer (UBC) is debatable. We investigated whether long-term exposure to ambient hydrocarbons increases UBC risk among people aged ≥ 20 years in Taiwan. Linkage dataset research with longitudinal design was conducted among 589,135 initially cancer-free individuals during 2000-2013; 12 airborne pollutants were identified. Several Cox models considering potential confounders were employed. The study outcomes were invasive or in situ UBC incidence over time. The targeted pollutant concentration was divided into three tertiles: T1/T2/T3. The mean age of individuals at risk was 42.5 (SD 15.7), and 50.5% of the individuals were men. The mean daily average over 10 years of airborne THC concentration was 2.25 ppm (SD 0.13), and NMHC was 0.29 ppm (SD 0.09). Both pollutants show long-term monotonic downward trend over time using the Mann-Kendall test. There was a dose-dependent increase in UBC at follow-up. UBC incidence per 100,000 enrollees according to T1/T2/T3 exposure to THC was 60.9, 221.2, and 651.8, respectively; it was 170.0/349.5/426.7 per 100,000 enrollees, corresponding to T1/T2/T3 exposure to NMHC, respectively. Without controlling for confounding air pollutants, the adjusted hazard ratio (adj.HR) was 1.83 (95% CI 1.75-1.91) per 0.13-ppm increase in THC; after controlling for PM2.5, adj.HR was even higher at 2.09 (95% CI 1.99-2.19). The adj.HR was 1.37 (95% CI 1.32-1.43) per 0.09-ppm increase in ambient NMHC concentration. After controlling for SO2 and CH4, the adj.HR was 1.10 (95% CI 1.06-1.15). Sensitivity analyses showed that UBC development risk was not sex-specific or influenced by diabetes status. Long-term exposure to THC and NMHC may be a risk factor for UBC development. Acknowledging pollutant sources can inform risk management strategies.
| S-EPMC9718740 | biostudies-literature
Project description:This study aimed to investigate whether long-term exposure to airborne hydrocarbons, including volatile organic compounds, increases the risk of developing retinal vein occlusion (RVO) among the population of Taiwan. A retrospective cohort study involving 855,297 people was conducted. Cox proportional hazards regression analysis fitted the multiple pollutant models for two targeted pollutants, including total hydrocarbons (THC), nonmethane hydrocarbons (NMHC) were used, and the risk of RVO was estimated. The chi-squared test and one-way analysis of variance were used to test differences in demographics and comorbidity distribution among tertiles of the targeted pollutants. Before controlling for multiple pollutants, hazard ratios for the overall population were 19.88 (95% CI: 17.56-22.50) at 0.51-ppm increases in THC and 4.33 (95% CI: 3.97-4.73) at 0.27-ppm increases in NMHC. The highest adjusted hazard ratios for different multiple pollutant models of each targeted pollutant were statistically significant (all p values were ?0.05) for all patients at 29.67 (95% CI: 25.57-34.42) for THC and 16.24 (95% CI: 14.14-18.65) for NMHC. Our findings suggest that long-term exposure to THC and NMHC contribute to RVO development.
| S-EPMC6759191 | biostudies-literature
Project description:OBJECTIVE:To study the effect of long term exposure to ambient fine particulate matter of diameter ?2.5 ?m (PM2.5) on the incidence of total, ischemic, and hemorrhagic stroke among Chinese adults. DESIGN:Population based prospective cohort study. SETTING:Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) project carried out in 15 provinces across China. PARTICIPANTS:117?575 Chinese men and women without stroke at baseline in the China-PAR project. MAIN OUTCOME MEASURES:Incidence of total, ischemic, and hemorrhagic stroke. RESULTS:The long term average PM2.5 level from 2000 to 2015 at participants' residential addresses was 64.9 ?g/m3, ranging from 31.2 ?g/m3 to 97.0 ?g/m3. During 900?214 person years of follow-up, 3540 cases of incident stroke were identified, of which 63.0% (n=2230) were ischemic and 27.5% (n=973) were hemorrhagic. Compared with the first quarter of exposure to PM2.5 (<54.5 ?g/m3), participants in the highest quarter (>78.2 ?g/m3) had an increased risk of incident stroke (hazard ratio 1.53, 95% confidence interval 1.34 to 1.74), ischemic stroke (1.82, 1.55 to 2.14), and hemorrhagic stroke (1.50, 1.16 to 1.93). For each increase of 10 ?g/m3 in PM2.5 concentration, the increased risks of incident stroke, ischemic stroke, and hemorrhagic stroke were 13% (1.13, 1.09 to 1.17), 20% (1.20, 1.15 to 1.25), and 12% (1.12, 1.05 to 1.20), respectively. Almost linear exposure-response relations between long term exposure to PM2.5 and incident stroke, overall and by its subtypes, were observed. CONCLUSIONS:This study provides evidence from China that long term exposure to ambient PM2.5 at relatively high concentrations is positively associated with incident stroke and its major subtypes. These findings are meaningful for both environmental and health policy development related to air pollution and stroke prevention, not only in China, but also in other low and middle income countries.
| S-EPMC7190010 | biostudies-literature
Project description:Background and Purpose- China bears a heavy burden of stroke because of its large population of elderly people and the propensity for stroke. Previous studies have examined the association between air pollution and stroke mortality or hospital admission. However, the global evidence for adverse effects of air pollution on survival after stroke is scarce. Methods- We used the first national hospital-based prospective registry cohort of stroke in China, which included 12 291 ischemic stroke patients who visited hospitals during 2007 to 2008. All patients were followed for 1-year poststroke. Deaths during the follow-up period were recorded. Participants' 3-year prestroke exposures to ambient PM1, PM2.5, PM10 (particulate matter with aerodynamic diameters ≤1, ≤2.5, and ≤10 μm, respectively) and NO2 (nitrogen dioxide) were estimated by machine learning algorithms with satellite remote sensing, land use information, and meteorological data. Cox proportional hazards models were used to examine the association between air pollution and survival after ischemic stroke. Results- In total, 1649 deaths were identified during the 1-year follow-up period. After controlling for potential confounders, significant associations were observed between exposure to PM1 and PM2.5 and incident fatal ischemic stroke. The corresponding hazard ratios and 95% CIs associated with 10 µg/m3 increase in PM1 and PM2.5 were 1.05 (1.02-1.09) and 1.03 (1.00-1.06), respectively. No significant association was observed for PM10 or NO2 (hazard ratios and 95% CIs, 1.01 [1.00-1.03] and 1.03 [0.99-1.06], respectively). Higher hazard ratios (and 95% CIs) were observed for male, elderly and obese individuals. Conclusions- Prestroke exposure to PM1 and PM2.5 was associated with increased incident fatal ischemic stroke in the year following an ischemic stroke in China. Improved air quality may be beneficial for people to recover from stroke.
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Project description:ImportanceAccurate estimation of the association between transient ischemic attack (TIA) and risk of subsequent stroke can help to improve preventive efforts and limit the burden of stroke in the population.ObjectiveTo determine population-based incidence of TIA and the timing and long-term trends of stroke risk after TIA.Design, setting, and participantsRetrospective cohort study (Framingham Heart Study) of prospectively collected data of 14 059 participants with no history of TIA or stroke at baseline, followed up from 1948-December 31, 2017. A sample of TIA-free participants was matched to participants with first incident TIA on age and sex (ratio, 5:1).ExposuresCalendar time (TIA incidence calculation, time-trends analyses), TIA (matched longitudinal cohort).Main outcomes and measuresThe main outcomes were TIA incidence rates; proportion of stroke occurring after TIA in the short term (7, 30, and 90 days) vs the long term (>1-10 years); stroke after TIA vs stroke among matched control participants without TIA; and time trends of stroke risk at 90 days after TIA assessed in 3 epochs: 1954-1985, 1986-1999, and 2000-2017.ResultsAmong 14 059 participants during 66 years of follow-up (366 209 person-years), 435 experienced TIA (229 women; mean age, 73.47 [SD, 11.48] years and 206 men; mean age, 70.10 [SD, 10.64] years) and were matched to 2175 control participants without TIA. The estimated incidence rate of TIA was 1.19/1000 person-years. Over a median of 8.86 years of follow-up after TIA, 130 participants (29.5%) had a stroke; 28 strokes (21.5%) occurred within 7 days, 40 (30.8%) occurred within 30 days, 51 (39.2%) occurred within 90 days, and 63 (48.5%) occurred more than 1 year after the index TIA; median time to stroke was 1.64 (interquartile range, 0.07-6.6) years. The age- and sex-adjusted cumulative 10-year hazard of incident stroke for patients with TIA (130 strokes among 435 cases) was 0.46 (95% CI, 0.39-0.55) and for matched control participants without TIA (165 strokes among 2175) was 0.09 (95% CI, 0.08-0.11); fully adjusted hazard ratio [HR], 4.37 (95% CI, 3.30-5.71; P < .001). Compared with the 90-day stroke risk after TIA in 1948-1985 (16.7%; 26 strokes among 155 patients with TIA), the risk between 1986-1999 was 11.1% (18 strokes among 162 patients) and between 2000-2017 was 5.9% (7 strokes among 118 patients). Compared with the first epoch, the HR for 90-day risk of stroke in the second epoch was 0.60 (95% CI, 0.33-1.12) and in the third epoch was 0.32 (95% CI, 0.14-0.75) (P = .005 for trend).Conclusions and relevanceIn this population-based cohort study from 1948-2017, the estimated crude TIA incidence was 1.19/1000 person-years, the risk of stroke was significantly greater after TIA compared with matched control participants who did not have TIA, and the risk of stroke after TIA was significantly lower in the most recent epoch from 2000-2017 compared with an earlier period from 1948-1985.
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Project description:BackgroundNoise has been related to several cardiovascular diseases (CVDs) such as coronary heart disease and to their risk factors such as hypertension, but associations with stroke remain under-researched, even if CVD likely share similar pathophysiologic mechanisms.AimThe objective of the study was to examine the association between long-term residential exposure to total environmental noise and stroke incidence in Montreal, Canada.Materials and methodsWe created an open cohort of adults aged ≥45years, free of stroke before entering the cohort for the years 2000 to 2014 with health administrative data. Residential total environmental noise levels were estimated with land use regression (LUR) models. Incident stroke was based on hospital admissions. Cox hazard models with age as the time axis and time-varying exposures were used to estimate associations, which were adjusted for material deprivation, year, nitrogen dioxide, stratified for sex, and indirectly adjusted for smoking.ResultsThere were 9,072,492 person-years of follow-up with 47% men; 26,741 developed stroke (21,402 ischemic; 4947 hemorrhagic; 392 had both). LUR total noise level acoustic equivalent for 24 hours (LAeq24h) ranged 44 to 79 dBA. The adjusted hazard ratio (HR) for stroke (all types), for a 10-dBA increase in LAeq24h, was 1.06 [95% confidence interval (CI): 1.03-1.09]. The LAeq24h was associated with ischemic (HR per 10 dBA: 1.08; 95% CI: 1.04-1.12) but not hemorrhagic stroke (HR per 10 dBA: 0.97; 95% CI: 0.90-1.04).ConclusionThe results suggest that total environmental noise is associated with incident stroke, which is consistent with studies on transportation noise and other CVD.
| S-EPMC9703819 | biostudies-literature
Project description:Background Left atrial (LA) volumes and emptying fraction in the general population may address structural and functional aspects of atrial cardiomyopathy associated with long-term risk of ischemic stroke in the absence of atrial fibrillation or prior stroke. We investigated the association between LA volumes and function and ischemic stroke. Methods and Results In a community-based cohort, we measured LA minimal volume, LA maximal volume, and LA emptying fraction by transthoracic echocardiography. The primary end point was ischemic stroke. Participants with known atrial fibrillation or prior ischemic stroke were excluded, which resulted in 1866 participants. The mean age was 58±16 years, and 57% were women. During a median follow-up of 16.5 years (interquartile range: 11.4-16.8 years), 176 (9.4%) ischemic strokes occurred. In multivariable cause-specific regression models and competing risk models with death as a competing risk, LA emptying fraction was associated with ischemic stroke (hazard ratio [HR], 1.14 per 10% decrease [95% CI, 1.02-1.28]) and (subdistribution HR, 1.14 [95% CI, 1.01-1.29]). This association remained when adjusting for participants who developed atrial fibrillation during follow-up (HR, 1.12 per 10% decrease [95% CI, 1.00-1.26]). Indexed LA volumes were not associated with ischemic stroke in the same models. LA emptying fraction and indexed LA volumes were not associated with all-cause mortality. Conclusions Lower LA emptying fraction measured by transthoracic echocardiography was associated with future ischemic stroke independently of incident atrial fibrillation. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02993172.
| S-EPMC9683687 | biostudies-literature
Project description:BackgroundRoad traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution.MethodsTwenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (Lden [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM2.5 and PM10], nitrogen dioxide [NO2], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of Lden preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government's maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential Lden thresholds.ResultsOf 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of Lden and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98-1.14) per 10 dB, which attenuated to 1.01 (0.93-1.09) and 1.00 (0.91-1.09) in models further adjusted for PM2.5 or NO2, respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between Lden and stroke.ConclusionsLong-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air pollution.
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Project description:Little is known about the long-term health effects of ambient ultrafine particles (<0.1 ?m) (UFPs) including their association with respiratory disease incidence. In this study, we examined the relationship between long-term exposure to ambient UFPs and the incidence of lung cancer, adult-onset asthma, and chronic obstructive pulmonary disease (COPD).Our study cohort included approximately 1.1 million adults who resided in Toronto, Canada and who were followed for disease incidence between 1996 and 2012. UFP exposures were assigned to residential locations using a land use regression model. Random-effect Cox proportional hazard models were used to estimate hazard ratios (HRs) describing the association between ambient UFPs and respiratory disease incidence adjusting for ambient fine particulate air pollution (PM2.5), NO2, and other individual/neighbourhood-level covariates.In total, 74,543 incident cases of COPD, 87,141 cases of asthma, and 12,908 cases of lung cancer were observed during follow-up period. In single pollutant models, each interquartile increase in ambient UFPs was associated with incident COPD (HR = 1.06, 95% CI: 1.05, 1.09) but not asthma (HR = 1.00, 95% CI: 1.00, 1.01) or lung cancer (HR = 1.00, 95% CI: 0.97, 1.03). Additional adjustment for NO2 attenuated the association between UFPs and COPD and the HR was no longer elevated (HR = 1.01, 95% CI: 0.98, 1.03). PM2.5 and NO2 were each associated with increased incidence of all three outcomes but risk estimates for lung cancer were sensitive to indirect adjustment for smoking and body mass index.In general, we did not observe clear evidence of positive associations between long-term exposure to ambient UFPs and respiratory disease incidence independent of other air pollutants. Further replication is required as few studies have evaluated these relationships.
| S-EPMC5477122 | biostudies-literature
Project description:Evidence is still limited for the role of long-term PM2.5 exposure in cerebrovascular diseases among residents in high pollution regions. The study is aimed to investigate the long-term effects of PM2.5 exposure on stroke mortality, and further explore the effect modification of temperature variation on the PM2.5-mortality association in northern China. Based on a cohort data with an average follow-up of 9.8 years among 38,435 urban adults, high-resolution estimates of PM2.5 derived from a satellite-based model were assigned to each participant. A Cox regression model with time-varying exposures and strata of geographic regions was employed to assess the risks of stroke mortality associated with PM2.5, after adjusting for individual risk factors. The cross-product term of PM2.5 exposure and annual temperature range was further added into the regression model to test whether the long-term temperature variation would modify the association of PM2.5 with stroke mortality. Among the study participants, the annual mean level of PM2.5 concentration was 66.3 μg/m3 ranging from 39.0 μg/m3 to 100.6 μg/m3. For each 10 μg/m3 increment in PM2.5, the hazard ratio (HR) was 1.31 (95% CI: 1.04-1.65) for stroke mortality after multivariable adjustment. In addition, the HRs of PM2.5 decreased gradually as the increase of annual temperature range with the HRs of 1.95 (95% CI: 1.36-2.81), 1.53 (95% CI: 1.06-2.22), and 1.11 (95% CI: 0.75-1.63) in the low, middle, and high group of annual temperature range, respectively. The findings provided further evidence of long-term PM2.5 exposure on stroke mortality in high-exposure settings such as northern China, and also highlighted the view that assessing the adverse health effects of air pollution might not ignore the role of temperature variations in the context of climate change.
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