Ambient Air Pollution and Risk for Stroke Hospitalization: Impact on Susceptible Groups.
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ABSTRACT:
SUBMITTER: Chang CH
PROVIDER: S-EPMC9324267 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC4276028 | 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:Air pollution is associated with a diversity of health effects, and evidence for a causal relationship with specific diseases exists. Exposure to air pollution is ubiquitous and typically beyond the control of the individual; the resulting health burden for the population can be high. Disproportionate effects are seen in individuals who have increased susceptibility to air pollution owing to individual- or community-level characteristics. As studies grow increasingly sophisticated, the understanding of who comprises the susceptible population continuously expands. Characteristics of susceptibility include genetic predisposition; socioeconomic factors; life stage; the presence of preexisting diseases, such as asthma, chronic obstructive pulmonary disease, cystic fibrosis; and the unique population of lung transplant recipients. This review explores how select populations, namely individuals with preexisting pulmonary disease and those living in communities of low socioeconomic status, have an increased susceptibility to the health effects of ambient air pollution. Genetic susceptibility, though a fundamental determinant of risk, is beyond the scope of this review and is not discussed. Strategies designed to mitigate air pollution-related health effects are discussed using a framework that addresses pollution exposure at multiple levels-government, state, community, and the individual. Emission reduction strategies remain the basis for public health protection; however, ancillary harm reduction measures are explored that can be adopted by susceptible communities and individuals.
| S-EPMC5955035 | 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: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:Air pollution has been linked to hypertension in the general population, but data on gestational hypertension (GH) are limited. We investigated criteria air pollutants and air toxics during the period before conception and in early gestation in relation to GH risk in the Consortium on Safe Labor/Air Quality and Reproductive Health Study (United States, 2002-2008). Modified Community Multi-scale Air Quality models estimated air pollution exposures for 6,074 singleton pregnancies in which GH was present and 199,980 normotensive pregnancies. Generalized estimating equations estimated relative risks per interquartile-range increment for pollutants and high exposure (?75th percentile) for air toxics after adjustment for major risk factors. For an interquartile-range increment, GH risk was significantly increased by 18% for sulfur dioxide during the 3 months before conception and, during gestational weeks 1-20, 17% for nitrogen oxides, 10% for particulate matter with an aerodynamic diameter <2.5 ?m, 7% for particulate matter with an aerodynamic diameter <10 ?m, and 22% for sulfur dioxide. High exposures to several polycyclic aromatic hydrocarbons before conception and during the first trimester were significantly associated with 8%-20% higher risk of GH. Further, preconceptional exposures to several volatile organic compounds were significantly associated with 11%-19% higher risk. Our findings suggest that early exposures to criteria air pollutants, particularly from transport emissions, and high exposure to several air toxics before conception may increase GH risk.
| S-EPMC5860464 | biostudies-literature
Project description:The purpose of the present study was to examine the risk of stillbirth associated with ambient air pollution during pregnancy. Using live birth and fetal death data from New Jersey from 1998 to 2004, the authors assigned daily concentrations of air pollution to each birth or fetal death. Generalized estimating equation models were used to estimate the relative odds of stillbirth associated with interquartile range increases in mean air pollutant concentrations in the first, second, and third trimesters and throughout the entire pregnancy. The relative odds of stillbirth were significantly increased with each 10-ppb increase in mean nitrogen dioxide concentration in the first trimester (odds ratio (OR) = 1.16, 95% confidence interval (CI): 1.03, 1.31), each 3-ppb increase in mean sulfur dioxide concentration in the first (OR = 1.13, 95% CI: 1.01, 1.28) and third (OR = 1.26, 95% CI: 1.03, 1.37) trimesters, and each 0.4-ppm increase in mean carbon monoxide concentration in the second (OR = 1.14, 95% CI: 1.01, 1.28) and third (OR = 1.14, 95% CI: 1.06, 1.24) trimesters. Although ambient air pollution during pregnancy appeared to increase the relative odds of stillbirth, further studies are needed to confirm these findings and examine mechanistic explanations.
| S-EPMC3491970 | biostudies-literature
Project description:BackgroundEcologic analyses suggest that living in areas with higher levels of ambient fine particulate matter air pollution (PM2.5) is associated with higher risk of adverse COVID-19 outcomes. Studies accounting for individual-level health characteristics are lacking.MethodsWe leveraged the breadth and depth of the US Department of Veterans Affairs national healthcare databases and built a national cohort of 169,102 COVID-19 positive United States Veterans, enrolled between March 2, 2020 and January 31, 2021, and followed them through February 15, 2021. Annual average 2018 PM2.5 exposure, at an approximately 1 km2 resolution, was linked with residential street address at the year prior to COVID-19 positive test. COVID-19 hospitalization was defined as first hospital admission between 7 days prior to, and 15 days after, the first COVID-19 positive date. Adjusted Poisson regression assessed the association of PM2.5 with risk of hospitalization.ResultsThere were 25,422 (15.0%) hospitalizations; 5,448 (11.9%), 5,056 (13.0%), 7,159 (16.1%), and 7,759 (19.4%) were in the lowest to highest PM2.5 quartile, respectively. In models adjusted for State, demographic and behavioral factors, contextual characteristics, and characteristics of the pandemic a one interquartile range increase in PM2.5 (1.9 µg/m3) was associated with a 10% (95% CI: 8%-12%) increase in risk of hospitalization. The association of PM2.5 and risk of hospitalization among COVID-19 individuals was present in each wave of the pandemic. Models of non-linear exposure-response suggested increased risk at PM2.5 concentrations below the national standard 12 µg/m3. Formal effect modification analyses suggested higher risk of hospitalization associated with PM2.5 in Black people compared to White people (p = 0.045), and in those living in socioeconomically disadvantaged neighborhoods (p < 0.001).ConclusionsExposure to higher levels of PM2.5 was associated with increased risk of hospitalization among COVID-19 infected individuals. The risk was evident at PM2.5 levels below the regulatory standards. The analysis identified those of Black race and those living in disadvantaged neighborhoods as population groups that may be more susceptible to the untoward effect of PM2.5 on risk of hospitalization in the setting of COVID-19.
| S-EPMC8040542 | biostudies-literature
Project description:BackgroundAlthough growing evidence links air pollution to stroke incidence, less is known about the effect of air pollution on atrial fibrillation (AF), an important risk factor for stroke.ObjectivesWe assessed the associations between air pollution and incidence of AF and stroke. We also sought to characterize the shape of pollutant-disease relationships.MethodsThe population-based cohort comprised 5,071,956 Ontario residents, age 35–85 y and without the diagnoses of both outcomes on 1 April 2001 and was followed up until 31 March 2015. AF and stroke cases were ascertained using health administrative databases with validated algorithms. Based on annual residential postal codes, we assigned 5-y running average concentrations of fine particulate matter ([Formula: see text]), nitrogen dioxide ([Formula: see text]), and ozone ([Formula: see text]) from satellite-derived data, a land-use regression model, and a fusion-based method, respectively, as well as redox-weighted averages of [Formula: see text] and [Formula: see text] ([Formula: see text]) for each year. Using Cox proportional hazards models, we estimated the hazard ratios (HRs) and 95% confidence intervals (95% CIs) of AF and stroke with each of these pollutants, adjusting for individual- and neighborhood-level variables. We used newly developed nonlinear risk models to characterize the shape of pollutant–disease relationships.ResultsBetween 2001 and 2015, we identified 313,157 incident cases of AF and 122,545 cases of stroke. Interquartile range increments of [Formula: see text], [Formula: see text], [Formula: see text], and [Formula: see text] were associated with increases in the incidence of AF [HRs (95% CIs): 1.03 (1.01, 1.04), 1.02 (1.01, 1.03), 1.01 (1.00, 1.02), and 1.01 (1.01, 1.02), respectively] and the incidence of stroke [HRs (95% CIs): 1.05 (1.03, 1.07), 1.04 (1.01, 1.06), 1.05 (1.03, 1.06), and 1.05 (1.04, 1.06), respectively]. Associations of similar magnitude were found in various sensitivity analyses. Furthermore, we found a near-linear association for stroke with [Formula: see text], whereas [Formula: see text], [Formula: see text]-, and [Formula: see text] relationships exhibited sublinear shapes.ConclusionsAir pollution was associated with stroke and AF onset, even at very low concentrations. https://doi.org/10.1289/EHP4883.
| S-EPMC6792368 | biostudies-literature
Project description:BackgroundPreterm birth is a major perinatal health problem, but factors leading to it are still not completely understood.ObjectivesOur goal was to identify the relation between acute increase in ambient air pollution in a few hours before onset of labor and the risk of preterm birth.MethodsWe collected registered birth outcome data and hourly ambient air pollution measurements during 2009‒2013 in Brisbane, Australia. Using a time-stratified case-crossover design and conditional logistic regression models with natural cubic splines, we assessed the shape of air pollution-preterm birth curve, after controlling for potential confounders. We also examined the effect modification of other factors.ResultsThe association between air pollution [nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO)] and preterm birth was nonlinear. Threshold concentrations for the mean of 0‒24 hr NO2, 24‒48 hr SO2, and 24‒48 hr CO before onset of labor were 7.6 parts per billion (ppb), 3.8 ppb, and 162.5 ppb, respectively. Increases in air pollution concentrations above thresholds were associated with increased risks of preterm birth. The odds ratios of preterm birth at the 95th percentile of NO2, SO2, and CO against the thresholds were 1.17 (95% CI: 1.08, 1.27), 1.01 (95% CI: 0.99, 1.04), and 1.18 (95% CI: 1.06, 1.32), respectively. The associations were modified by demographic factors, such as maternal smoking and socioeconomic status.ConclusionAcute increases in ambient air pollution concentrations above certain levels before onset of labor may stimulate preterm birth.CitationLi S, Guo Y, Williams G. 2016. Acute impact of hourly ambient air pollution on preterm birth. Environ Health Perspect 124:1623-1629; http://dx.doi.org/10.1289/EHP200.
| S-EPMC5047774 | biostudies-literature