Impact of Oxidant Gases on the Relationship between Outdoor Fine Particulate Air Pollution and Nonaccidental, Cardiovascular, and Respiratory Mortality.
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ABSTRACT:
SUBMITTER: Weichenthal S
PROVIDER: S-EPMC5703979 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Short term changes in exposure to outdoor fine particulate matter (PM2.5) concentrations are associated with an increased risk of mortality. However, less is known about how oxidant gases may modify the acute health effects of PM2.5. Our objective was to investigate whether associations between acute exposure to PM2.5 and mortality were modified by the oxidant gases O3 and NO2 using their redox-weighted average (Ox). We conducted a multi-city case-crossover study in 24 cities across Canada between 1998-2011 including 1,179,491 nonaccidental mortality events. Interquartile increases in lag-0 and 3-day mean PM2.5 and Ox concentrations were each associated with small increases in nonaccidental and cardiovascular mortality. In stratified analyses, associations between PM2.5 and nonaccidental and cardiovascular mortality tended to be greatest in the highest tertile of Ox with a significant interaction observed between lag 0 PM2.5 and 3-day mean Ox (interaction p-value?=?0.04). There was no evidence of effect modification by Ox in the relationship between PM2.5 and respiratory mortality. Overall, the relationship between short-term changes in outdoor PM2.5 and nonaccidental mortality may be greater when oxidant gas concentrations are also elevated. In some regions, reductions in oxidant gas concentrations may also reduce the acute health impacts of PM2.5.
| S-EPMC6208424 | biostudies-literature
Project description:Fine particulate matter (PM2.5) air pollution and environmental temperatures influence cardiovascular morbidity and mortality. Recent evidence suggests that several air pollutants can promote dyslipidemia; however, the impact of ambient PM2.5 and temperature on high-density lipoprotein (HDL) function remains unclear. We hypothesized that daily exposures to higher levels of ambient PM2.5 and colder outdoor temperatures would impair HDL functionality. Lipoproteins, serum cholesterol efflux capacity (CEC), and HDL oxidation markers were measured twice in 50 healthy adults (age 32.1 ± 9.6 years) living in southeast Michigan and associated with ambient and personal-level exposures using mixed models. Although previous 7-day mean outdoor temperature (4.4 ± 9.8°C) and PM2.5 levels (9.1 ± 1.8 µg/m3) were low, higher ambient PM2.5 exposures (per 10 µg/m3) were associated with significant increases in the total cholesterol-to-HDL-C ratio (rolling average lag days 1 and 2) as well as reductions in CEC by -1.93% (lag day 5, p = 0.022) and -1.62% (lag day 6, p = 0.032). Colder outdoor temperatures (per 10°C) were also associated with decreases in CEC from -0.62 to -0.63% (rolling average lag days 5 and 7, p = 0.027 and 0.028). Previous 24-hour personal-level PM2.5 and temperature exposures did not impact outcomes, nor were any exposures associated with changes in HDL-oxidation metrics. In conclusion, we provide the first evidence that ambient PM2.5 (even at low levels) and outdoor temperatures may influence serum CEC, a critical antiatherosclerotic HDL function.
| S-EPMC6133768 | biostudies-literature
Project description:Few studies have examined the association between fine particulate matter (PM2.5) and upper respiratory tract infections (URTI) in urban cities. The principal aim of the present study was to evaluate the short-term impact of PM2.5 on the incidence of URTI in Beijing, China. Data on hospital visits due to URTI from 1 October 2010 to 30 September 2012 were obtained from the Beijing Medical Claim Data for Employees, a health insurance database. Daily PM2.5 concentration was acquired from the embassy of the United States of America (US) located in Beijing. A generalized additive Poisson model was used to analyze the effect of PM2.5 on hospital visits for URTI. We found that a 10 μg/m³ increase in PM2.5 concentration was associated with 0.84% (95% CI, 0.05⁻1.64%) increase in hospital admissions for URTI at lag 0⁻3 days, but there were no significant associations with emergency room or outpatient visits. Compared to females, males were more likely to be hospitalized for URTI when the PM2.5 level increased, but other findings did not differ by age group or gender. The study suggests that short-term variations in PM2.5 concentrations have small but detectable impacts on hospital utilization due to URTI in adults.
| S-EPMC6406703 | biostudies-literature
Project description:Using daily fine particulate matter (PM2.5) composition data from the 2000-2005 U.S. EPA Chemical Speciation Network (CSN) for over 200 sites, we applied multivariate methods to identify and quantify the major fine particulate matter (PM2.5) source components in the U.S. Novel aspects of this work were: (1) the application of factor analysis (FA) to multi-city daily data, drawing upon both spatial and temporal variations of chemical species; and, (2) the exclusion of secondary components (sulfates, nitrates and organic carbon) from the source identification FA to more clearly discern and apportion the PM2.5 mass to primary emission source categories. For the quantification of source-related mass, we considered two approaches based upon the FA results: 1) using single key tracers for sources identified by FA in a mass regression; and, 2) applying Absolute Principal Component Analysis (APCA). In each case, we followed a two-stage mass regression approach, in which secondary components were first apportioned among the identified sources, and then mass was apportioned to the sources and to other secondary mass not explained by the individual sources. The major U.S. PM2.5 source categories identified via FA (and their key elements) were: Metals Industry (Pb, Zn); Crustal/Soil Particles (Ca, Si); Motor Vehicle Traffic (EC, NO2); Steel Industry (Fe, Mn); Coal Combustion (As, Se); Oil Combustion (V, Ni); Salt Particles (Na, Cl) and Biomass Burning (K). Nationwide spatial plots of the source-related PM2.5 impacts were confirmatory of the factor interpretations: ubiquitous sources, such as Traffic and Soil, were found to be spread across the nation, more unique sources (such as Steel and Metals Processing) being highest in select industrialized cities, Biomass Burning was highest in the U.S. Northwest, while Residual Oil combustion was highest in cities in the Northeastern U.S. and in cities with major seaports. The sum of these source contributions and the secondary PM2.5 components agreed well with the U.S. PM2.5 observed during the study period (mean=14.3 ug/m3; R2= 0.91). Apportionment regression analyses using single-element tracers for each source category gave results consistent with the APCA estimates. Comparisons of nearby sites indicated that the PM2.5 mass and the secondary aerosols were most homogenous spatially, while traffic PM2.5 and its tracer, EC, were among the most spatially representative of the source-related components. Comparison of apportionment results to a previous analysis of the 1979-1982 IP Network revealed similar and correlated major U.S. source category factors, albeit at lower levels than in the earlier period, suggesting a consistency in the U.S. spatial patterns of these source-related exposures over time, as well. These results indicate that applying source apportionment methods to the nationwide CSN can be an informative avenue for identifying and quantifying source components for the subsequent estimation of source-specific health effects, potentially contributing to more efficient regulation of PM2.5.
| S-EPMC3951912 | biostudies-literature
Project description:Short-term changes in levels of fine ambient particulate matter (PM2.5) may increase the risk of acute ischemic stroke; however, results from prior studies have been inconsistent. We examined this hypothesis using data from a multicenter prospective stroke registry.We analyzed data from 9202 patients hospitalized with acute ischemic stroke, having a documented date and time of stroke onset, and residing within 50 km of a PM2.5 monitor in 8 cities in Ontario, Canada. We evaluated the risk of ischemic stroke onset associated with PM2.5 in each city using a time-stratified case-crossover design, matching on day of week and time of day. We then combined these city-specific estimates using random-effects meta-analysis techniques. We examined whether the effects of PM2.5 differed across strata defined by patient characteristics and ischemic stroke etiology.Overall, PM2.5 was associated with a -0.7% change in ischemic stroke risk per 10-?g/m increase in PM2.5 (95% confidence interval = -6.3% to 5.1%). These overall negative results were robust to a number of sensitivity analyses. Among patients with diabetes mellitus, PM2.5 was associated with an 11% increase in ischemic stroke risk (1% to 22%). The association between PM2.5 and ischemic stroke risk varied according to stroke etiology, with the strongest associations observed for strokes due to large-artery atherosclerosis and small-vessel occlusion.These results do not support the hypothesis that short-term increases in PM2.5 levels are associated with ischemic stroke risk overall. However, specific patient subgroups may be at increased risk of particulate-related ischemic strokes.
| S-EPMC3102528 | biostudies-literature
Project description:BackgroundOutdoor physical activity (PA) brings important health benefits, but exposure to polluted air increases health risks. This study aimed to quantify the tradeoff of PA under fine particulate matter (PM2.5) air pollution by estimating the optimal PA duration under various pollution levels.MethodsA risk-benefit analysis was performed to estimate the optimal outdoor moderate-intensity PA (MPA) duration under varying PM2.5 concentrations.ResultsAn inverse nonlinear relationship was identified between optimal MPA duration and background PM2.5 concentration levels. When background PM2.5 concentration increased to 186 µg/m3, the optimal outdoor MPA duration decreased to 2.5 h/week, the minimum level recommended by current PA guidelines. When background PM2.5 concentration further increased to 235 µg/m3, the optimal outdoor MPA duration decreased to 1 h/week. The relationship between optimal MPA duration and background PM2.5 concentration levels was stronger when exercising at a location closer to a source of air pollution. Compared to the general adult population, adults aged 60 years and older had substantially steeper curves-the optimal outdoor MPA duration decreased to 2.5 h/week when background PM2.5 concentration reached 45 µg/m3.ConclusionThe health benefit of outdoor MPA by far outweighs the health risk of PM2.5 pollution for the global average urban background concentration (22 μg/m3). This modeling study examined a single type of air pollutant and suffered from measurement errors and estimation uncertainties. Future research should examine other air pollutants and indoor PA, incorporate short- and mid-term health effects of MPA and air pollution into the risk-benefit analysis, and provide estimates specific for high-risk subgroups.
| S-EPMC7537654 | biostudies-literature
Project description:Heavy fine particulate matter (PM2.5) air pollution occurs frequently in China. However, epidemiological research on the association between short-term exposure to PM2.5 pollution and respiratory disease morbidity is still limited. This study aimed to explore the association between PM2.5 pollution and hospital emergency room visits (ERV) for total and cause-specific respiratory diseases in urban areas in Beijing.Daily counts of respiratory ERV from Jan 1 to Dec 31, 2013, were obtained from ten general hospitals located in urban areas in Beijing. Concurrently, data on PM2.5 were collected from the Beijing Environmental Protection Bureau, including 17 ambient air quality monitoring stations. A generalized-additive model was used to explore the respiratory effects of PM2.5, after controlling for confounding variables. Subgroup analyses were also conducted by age and gender.A total of 92,464 respiratory emergency visits were recorded during the study period. The mean daily PM2.5 concentration was 102.1±73.6 ?g/m3. Every 10 ?g/m3 increase in PM2.5 concentration at lag0 was associated with an increase in ERV, as follows: 0.23% for total respiratory disease (95% confidence interval [CI]: 0.11%-0.34%), 0.19% for upper respiratory tract infection (URTI) (95%CI: 0.04%-0.35%), 0.34% for lower respiratory tract infection (LRTI) (95%CI: 0.14%-0.53%) and 1.46% for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) (95%CI: 0.13%-2.79%). The strongest association was identified between AECOPD and PM2.5 concentration at lag0-3 (3.15%, 95%CI: 1.39%-4.91%). The estimated effects were robust after adjusting for SO2, O3, CO and NO2. Females and people 60 years of age and older demonstrated a higher risk of respiratory disease after PM2.5 exposure.PM2.5 was significantly associated with respiratory ERV, particularly for URTI, LRTI and AECOPD in Beijing. The susceptibility to PM2.5 pollution varied by gender and age.
| S-EPMC4824441 | biostudies-other
Project description:ObjectiveFew studies investigating associations between fine particulate air pollution and hemorrhagic stroke have considered subtypes. Additionally, less is known about the modification of such association by factors measured at the individual level. We aimed to investigate the risk of fatal intracerebral hemorrhage (ICH) incidence in case of PM2.5 (particles ??2.5??m in aerodynamic diameter) exposure.MethodsData on incidence of fatal ICH from 1 June 2012 to 31 May 2014 were extracted from the acute stroke mortality database in Shanghai Municipal Center for Disease Control and Prevention (SCDC). We used the time-stratified case-crossover approach to assess the association between daily concentrations of PM2.5 and fatal ICH incidence in Shanghai, China.ResultsA total of 5286 fatal ICH cases occurred during our study period. The averaged concentration of PM2.5 was 77.45??g/m3. The incidence of fatal ICH was significantly associated with PM2.5 concentration. Substantial differences were observed among subjects with diabetes compared with those without; following the increase of PM2.5 in lag2, the OR (95% CI) for subjects with diabetes was 1.26 (1.09-1.46) versus 1.05 (0.98-1.12) for those without. We did not find evidence of effect modification by hypertension and cigarette smoking.ConclusionsFatal ICH incidence was associated with PM2.5 exposure. Our results also suggested that diabetes may increase the risk for ICH incidence in relation to PM2.5.
| S-EPMC6545210 | biostudies-literature
Project description:BackgroundMaternal exposure to fine particulate air pollution (PM2.5) during pregnancy is associated with lower newborn birthweight, which is a risk factor for chronic disease. Existing studies typically report the average association related with PM2.5 increase, which does not offer information about potentially varying associations at different points of the birthweight distribution.MethodsWe retrieved all birth records in Massachusetts between 2001 and 2013 then restricted our analysis to full-term live singletons (n = 775,768). Using the birthdate, gestational age, and residential address reported at time of birth, we estimated the average maternal PM2.5 exposure during pregnancy of each birth. PM2.5 predictions came from a model that incorporates satellite, land use, and meteorologic data. We applied quantile regression to quantify the association between PM2.5 and birthweight at each decile of birthweight, adjusted for individual and neighborhood covariates. We considered effect modification by indicators of individual and neighborhood socioeconomic status (SES).ResultsPM2.5 was negatively associated with birthweight. An interquartile range increase in PM2.5 was associated with a 16 g [95% confidence interval (CI) = 13, 19] lower birthweight on average, 19 g (95% CI = 15, 23) lower birthweight at the lowest decile of birthweight, and 14 g (95% CI = 9, 19) lower birthweight at the highest decile. In general, the magnitudes of negative associations were larger at lower deciles. We did not find evidence of effect modification by individual or neighborhood SES.ConclusionsIn full-term live births, PM2.5 and birthweight were negatively associated with more severe associations at lower quantiles of birthweight.
| S-EPMC6686872 | biostudies-literature
Project description:Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GRO? [growth-regulated protein ?], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNF? [tumor necrosis factor ?], IP-10 [interferon ?-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1?/? [macrophage inflammatory protein 1?/?], IL-6 [interleukin 6], and IL-1? [interleukin 1?]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
| S-EPMC5215745 | biostudies-literature