Ambient air pollution and the risk of stillbirth.
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ABSTRACT:
SUBMITTER: Faiz AS
PROVIDER: S-EPMC3491970 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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: 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: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:Background and aimsThe coronavirus disease 2019 (COVID-19) pandemic is severely threatening and challenging public health worldwide. Epidemiological studies focused on the influence of outdoor air pollution (AP) on COVID-19 risk have produced inconsistent conclusions. We aimed to quantitatively explore this association using a meta-analysis.MethodsWe searched for studies related to outdoor AP and COVID-19 risk in the Embase, PubMed, and Web of Science databases. No language restriction was utilized. The search date entries were up to August 13, 2021. Pooled estimates and 95% confidence intervals (CIs) were obtained with random-/fixed-effects models. PROSPERO registration number: CRD42021244656.ResultsA total of 35 articles were eligible for the meta-analysis. For long-term exposure to AP, COVID-19 incidence was positively associated with 1 μg/m3 increase in nitrogen dioxide (NO2; effect size = 1.042, 95% CI 1.017-1.068), particulate matter with diameter <2.5 μm (PM2.5; effect size = 1.056, 95% CI 1.039-1.072), and sulfur dioxide (SO2; effect size = 1.071, 95% CI 1.002-1.145). The COVID-19 mortality was positively associated with 1 μg/m3 increase in nitrogen dioxide (NO2; effect size = 1.034, 95% CI 1.006-1.063), PM2.5 (effect size = 1.047, 95% CI 1.025-1.1071). For short-term exposure to air pollutants, COVID-19 incidence was positively associated with 1 unit increase in air quality index (effect size = 1.001, 95% CI 1.001-1.002), 1 μg/m3 increase NO2 (effect size = 1.014, 95% CI 1.011-1.016), particulate matter with diameter <10 μm (PM10; effect size = 1.005, 95% CI 1.003-1.008), PM2.5 (effect size = 1.003, 95% CI 1.002-1.004), and SO2 (effect size = 1.015, 95% CI 1.007-1.023).ConclusionsOutdoor air pollutants are detrimental factors to COVID-19 outcomes. Measurements beneficial to reducing pollutant levels might also reduce the burden of the pandemic.
| S-EPMC8440008 | 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:Exposure to ambient air pollution and noise is ubiquitous globally. A strong body of evidence links air pollution, and recently noise, to cardiovascular conditions that eventually may also affect cognition in the elderly. Data that support a broader influence of these exposures on cognitive function during aging is just starting to emerge. This review summarizes current findings and discusses methodological challenges and opportunities for research. Although current evidence is still limited, especially for chronic noise exposure, high exposure has been associated with faster cognitive decline either mediated through cerebrovascular events or resulting in Alzheimer's disease. Ambient environmental exposures are chronic and affect large populations. While they may yield relatively modest-sized risks, they nevertheless result in large numbers of cases. Reducing environmental pollution is clearly feasible, though lowering levels requires collective action and long-term policies such as standard setting, often at the national level as well as at the local level.
| S-EPMC6544148 | 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: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