Ambient air pollution and stroke.
Ontology highlight
ABSTRACT:
SUBMITTER: Ljungman PL
PROVIDER: S-EPMC4276028 | biostudies-literature | 2014 Dec
REPOSITORIES: biostudies-literature
Publications
Similar Datasets
Project description:Despite recent advances in treatment and prevention, stroke remains a leading cause of morbidity and mortality. There is a critical need to identify novel modifiable risk factors for disease, including environmental agents. A body of evidence has accumulated suggesting that elevated levels of ambient air pollutants may not only trigger cerebrovascular events in susceptible people (short-term exposures) but also increase the risk of future events (long-term average exposures). This review assesses the updated evidence for both short and long-term exposure to ambient air pollution as a risk factor for stroke incidence and outcomes. It discusses the potential pathophysiologic mechanisms and makes recommendations to mitigate exposure on a personal and community level. The evidence indicates that reduction in air pollutant concentrations represent a significant population-level opportunity to reduce risk of cerebrovascular disease.
| S-EPMC10421613 | biostudies-literature
Project description:BackgroundThe link between daily changes in level of ambient fine particulate matter (PM) air pollution (PM <2.5 μm in diameter [PM(2.5)]) and cardiovascular morbidity and mortality is well established. Whether PM(2.5) levels below current US National Ambient Air Quality Standards also increase the risk of ischemic stroke remains uncertain.MethodsWe reviewed the medical records of 1705 Boston area patients hospitalized with neurologist-confirmed ischemic stroke and abstracted data on the time of symptom onset and clinical characteristics. The PM(2.5) concentrations were measured at a central monitoring station. We used the time-stratified case-crossover study design to assess the association between the risk of ischemic stroke onset and PM(2.5) levels in the hours and days preceding each event. We examined whether the association with PM(2.5) levels differed by presumed ischemic stroke pathophysiologic mechanism and patient characteristics.ResultsThe estimated odds ratio (OR) of ischemic stroke onset was 1.34 (95% CI, 1.13-1.58) (P < .001) following a 24-hour period classified as moderate (PM(2.5) 15-40 μg/m(3)) by the US Environmental Protection Agency's (EPA) Air Quality Index compared with a 24-hour period classified as good (≤15 μg/m(3)). Considering PM(2.5) levels as a continuous variable, we found the estimated odds ratio of ischemic stroke onset to be 1.11 (95% CI, 1.03-1.20) (P = .006) per interquartile range increase in PM(2.5) levels (6.4 μg/m(3)). The increase in risk was greatest within 12 to 14 hours of exposure to PM(2.5) and was most strongly associated with markers of traffic-related pollution.ConclusionThese results suggest that exposure to PM(2.5) levels considered generally safe by the US EPA increase the risk of ischemic stroke onset within hours of exposure.
| S-EPMC3639313 | biostudies-literature
Project description:ObjectivesTo investigate the association between short-term changes in ambient pollution (particulate matter <2.5 μm in aerodynamic diameter (PM2.5) and ozone (O3)) and the risk of ischemic stroke among individuals living in a bi-ethnic community and whether this association is modified by ethnicity.MethodsWe identified incident ischemic stroke cases from the population-based Brain Attack Surveillance in Corpus Christi (BASIC) project between 2000 and 2012. Associations between PM2.5 (mean 24-h) and O3 (maximal 8-h) levels, measured on the same-day and lags of 1-3 days, and odds of ischemic stroke were assessed using a time-stratified case-crossover design and modeled using conditional logistic regression. We explored race/ethnicity (Mexican American versus non-Hispanic white) as a modifier by including interaction terms in the models.ResultsThere were 2948 ischemic strokes with median age 71 years (IQR: 59-80). We observed no overall associations between the air pollutants and odds of ischemic stroke at any lag. When stratified by ethnicity, higher O3 was consistently associated with greater odds of ischemic stroke for non-Hispanic whites, but not for Mexican Americans. Higher PM2.5 was generally associated with lower odds of ischemic stroke for non-Hispanic whites but modestly greater odds for Mexican Americans.ConclusionEthnic differences in the associations between ischemic stroke and short-term exposures to O3 and PM2.5 were suggested indicating that further study in diverse populations may be warranted.
| S-EPMC4641766 | biostudies-literature
Project description:Acute ischemic strokes (AIS) are closely linked with air pollution, and there is some evidence that traditional cardiovascular risk factors may alter the relationship between air pollution and strokes. We investigated the effect of atrial fibrillation (AF) on the association of AIS with air pollutants. This was a nationwide, population-based, case-only study that included all AIS treated in public healthcare institutions in Singapore from 2009 to 2018. Using multivariable logistic regression, adjusted for time-varying meteorological effects, we examined how AF modified the association between AIS and air pollutant exposure. A total of 51,673 episodes of AIS were included, with 10,722 (20.7%) having AF. The odds of AIS in patients with AF is higher than those without AF for every 1 µg/m3 increase in O3 concentration (adjusted OR [aOR]: 1.005, 95% CI 1.003-1.007) and every 1 mg/m3 increase in CO concentration (aOR: 1.193, 95% CI 1.050-1.356). However, the odds of AIS in patients with AF is lower than those without AF for every 1 µg/m3 increase in SO2 concentration (aOR: 0.993, 95% CI 0.990-0.997). Higher odds of AIS among AF patients as O3- and CO concentrations increase are also observed in patients aged ≥65 years and non-smokers. The results suggest that AF plays an important role in exacerbating the risk of AIS as the levels of O3 and CO increase.
| S-EPMC9503161 | biostudies-literature
Project description:Stroke is a leading cause of death, and air pollution is associated with stroke hospitalization. However, the susceptibility factors are unclear. Retrospective studies from 2014 to 2018 in Kaohsiung, Taiwan, were analyzed. Adult patients (>17 years) admitted to a medical center with stroke diagnosis were enrolled and patient characteristics and comorbidities were recorded. Air pollutant measurements, including those of particulate matter (PM) with aerodynamic diameters < 10 μm (PM10) and < 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3), were collected from air quality monitoring stations. During the study period, interquartile range (IQR) increments in PM2.5 on lag3 and lag4 were 12.3% (95% CI, 1.1-24.7%) and 11.5% (95% CI, 0.3-23.9%) concerning the risk of stroke hospitalization, respectively. Subgroup analysis revealed that the risk of stroke hospitalization after exposure to PM2.5 was greater for those with advanced age (≥80 years, interaction p = 0.045) and hypertension (interaction p = 0.034), after adjusting for temperature and humidity. A dose-dependent effect of PM2.5 on stroke hospitalization was evident. This is one of few studies focusing on the health effects of PM2.5 for patients with risk factors of stroke. We found that patients with risk factors, such as advanced age and hypertension, are more susceptible to PM2.5 impacts on stroke hospitalization.
| S-EPMC9324267 | biostudies-literature
Project description:BackgroundAmbient air pollution is associated with systemic increases in oxidative stress, to which sperm are particularly sensitive. Although decrements in semen quality represent a key mechanism for impaired fecundability, prior research has not established a clear association between air pollution and semen quality. To address this, we evaluated the association between ambient air pollution and semen quality among men with moderate air pollution exposure.MethodsOf 501 couples in the LIFE study, 467 male partners provided one or more semen samples. Average residential exposure to criteria air pollutants and fine particle constituents in the 72 days before ejaculation was estimated using modified Community Multiscale Air Quality models. Generalized estimating equation models estimated the association between air pollutants and semen quality parameters (volume, count, percent hypo-osmotic swollen, motility, sperm head, morphology and sperm chromatin parameters). Models adjusted for age, body mass index, smoking and season.ResultsMost associations between air pollutants and semen parameters were small. However, associations were observed for an interquartile increase in fine particulates ≤2.5 µm and decreased sperm head size, including -0.22 (95% CI -0.34, -0.11) µm2 for area, -0.06 (95% CI -0.09, -0.03) µm for length and -0.09 (95% CI -0.19, -0.06) µm for perimeter. Fine particulates were also associated with 1.03 (95% CI 0.40, 1.66) greater percent sperm head with acrosome.ConclusionsAir pollution exposure was not associated with semen quality, except for sperm head parameters. Moderate levels of ambient air pollution may not be a major contributor to semen quality.
| S-EPMC5878741 | biostudies-literature
Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.
| S-EPMC5089873 | biostudies-other
Project description:Purpose of reviewDuring the past century, exposure to particulate matter (PM) air pollution < 2.5 μm in diameter (PM2.5) has emerged as an all-pervading element of modern-day society. This increased exposure has come at the cost of heightened risk for cardiovascular (CV) morbidity and mortality. Not only can short-term PM2.5 exposure trigger acute CV events in susceptible individuals, but longer-term exposure over years augments CV risk to a greater extent in comparison with short-term exposure. The purpose of this review is to examine the available evidence for how ambient air pollution exposure may precipitate events at various time frames.Recent findingsRecent epidemiological studies have demonstrated an association between ambient PM2.5 exposure and the presence and progression of atherosclerosis in humans. Multiple animal exposure experiments over two decades have provided strong corroborative evidence that chronic exposure in fact does enhance the progression and perhaps vulnerability characteristics of atherosclerotic lesions. Evidence from epidemiological studies including surrogates of atherosclerosis, human translational studies, and mechanistic investigations utilizing animal studies have improved our understanding of how ambient air pollution may potentiate atherosclerosis and precipitate cardiovascular events. Even so, future research is needed to fully understand the contribution of different constituents in ambient air pollution-mediated atherosclerosis as well as how other systems may modulate the impact of exposure including adaptive immunity and the gut microbiome. Nevertheless, due to the billions of people continually exposed to PM2.5, the long-term pro-atherosclerotic effects of this ubiquitous air pollutant are likely to be of enormous and growing global public health importance.
| S-EPMC8379601 | biostudies-literature
Project description:BackgroundStroke and dementia are the leading causes of neurological disease burden. Detrimental effects of air pollution on both conditions are increasingly recognised, while the impacts on the dynamic transitions have not yet been explored, and whether critical time intervals exist is unknown.MethodsThis prospective study was conducted based on the UK Biobank. Annual average air pollution concentrations at baseline year 2010 estimated by land-use regression models were used as a proxy for long-term air pollution exposure. Associations between multiple air pollutants (PM2.5, PM2.5-10, and NO2) indicated by air pollution score and the dynamic transitions of stroke and dementia were estimated, and the impacts during critical time intervals were explored. The date cutoff of this study was February 29, 2020.FindingsDuring a median follow-up of 10.9 years in 413,372 participants, 6484, 3813, and 376 participants developed incident stroke, dementia, and comorbidity of stroke and dementia. For the overall transition from stroke to comorbid dementia, the hazard ratio (HR) for each interquartile range (IQR) increase in air pollution score was 1.38 (95% CI, 1.15, 1.65), and the risks were limited to two time intervals (within 1 year and over 5 years after stroke). As for the transition from dementia to comorbid stroke, increased risk was only observed during 2-3 years after dementia.InterpretationOur findings suggested that air pollution played an important role in the dynamic transition of stroke and dementia even at concentrations below the current criteria. The findings provided new evidence for alleviating the disease burden of neurological disorders related to air pollution during critical time intervals.FundingThe State Scholarship Fund of China Scholarship Council.
| S-EPMC10758736 | biostudies-literature
Project description:ObjectiveTo investigate the association between ambient air pollution and stroke morbidity in different subgroups and seasons.MethodsWe performed a time-series analysis based on generalised linear models to study the short-term exposure-response relationships between air pollution and stroke hospitalisations, and conducted subgroup analyses to identify possible sensitive populations.ResultsFor every 10 µg/m3 increase in the concentration of air pollutants, across lag 0-3 days, the relative risk of stroke hospitalisation was 1.029 (95% CI 1.013 to 1.045) for PM2.5, 1.054 (95% CI 1.031 to 1.077) for NO2 and 1.012 (95% CI 1.002 to 1.022) for O3. Subgroup analyses showed that statistically significant associations were found in both men and women, middle-aged and older populations, and both cerebral infarction and intracerebral haemorrhage. The seasonal analyses showed that statistically significant associations were found only in the winter.ConclusionsOur study indicates that short-term exposure to PM2.5, NO2 and O3 may induce stroke morbidity, and the government should take actions to mitigate air pollution and protect sensitive populations.
| S-EPMC7103818 | biostudies-literature