Fine Particulate Air Pollution and Hospital Utilization for Upper Respiratory Tract Infections in Beijing, China.
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ABSTRACT:
SUBMITTER: Zhang D
PROVIDER: S-EPMC6406703 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature
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Fine Particulate Air Pollution and Hospital Utilization for Upper Respiratory Tract Infections in Beijing, China.
Zhang Daitao D Tian Yaohua Y Zhang Yi Y Cao Yaying Y Wang Quanyi Q Hu Yonghua Y
International journal of environmental research and public health 20190213 4
Few studies have examined the association between fine particulate matter (PM<sub>2.5</sub>) and upper respiratory tract infections (URTI) in urban cities. The principal aim of the present study was to evaluate the short-term impact of PM<sub>2.5</sub> 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 PM<sub>2.5</sub> concentra ...[more]
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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: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:BACKGROUND:Little is known about the effect of ambient fine particulate matter (PM2.5) on chronic obstructive pulmonary disease (COPD) in China. The objective of this study was to explore the short-term effects of PM2.5 on outpatient and inpatient visits for COPD in Beijing, China. METHODS:A total of 3,503,313 outpatient visits and 126,982 inpatient visits for COPD between January 1, 2010, and June 30, 2012, were identified from the Beijing Medical Claim Data for Employees. A generalized additive Poisson model was applied to estimate the percentage change with 95% confidence interval (CI) in hospital visits for COPD in relation to an interquartile range (IQR) (90.8 ?g/m3) increase in PM2.5 concentrations. RESULTS:Short-term exposure to PM2.5 was significantly associated with increased use of COPD-related health services. There were clear exposure-response associations of PM2.5 with COPD outpatient and inpatient visits. An IQR increase in the concurrent day PM2.5 concentrations was significantly associated with a 2.38% (95% CI, 2.22%-2.53%) and 6.03% (95% CI, 5.19%-6.87%) increase in daily outpatient visits and inpatient visits, respectively. Elderly people were more sensitive to the adverse effects. The estimated risk was higher during the warm season compared to the cool season. CONCLUSIONS:Short-term exposure to PM2.5 was associated with increased risk of hospital visits for COPD. Our findings contributed to the limited evidence concerning the effects of ambient PM2.5 on COPD morbidity in developing countries.
| S-EPMC6389038 | biostudies-literature
Project description:MicroRNAs (miRNAs) are post-transcriptional gene suppressors and potential mediators of environmental effects. In addition to human miRNAs, viral miRNAs expressed from latent viral sequences are detectable in human cells.In a highly exposed population in Beijing, China, we evaluated the associations of particulate air pollution exposure on blood miRNA profiles.The Beijing Truck Driver Air Pollution Study (BTDAS) included 60 truck drivers and 60 office workers. We investigated associations of short-term air pollution exposure, using measures of personal PM2.5 (particulate matter ? 2.5 ?m) and elemental carbon (EC), and ambient PM10 (? 10 ?m), with blood NanoString nCounter miRNA profiles at two exams separated by 1-2 weeks.No miRNA was significantly associated with personal PM2.5 at a false discovery rate (FDR) of 20%. Short-term ambient PM10 was associated with the expression of 12 miRNAs in office workers only (FDR < 20%). Short-term EC was associated with differential expression of 46 human and 7 viral miRNAs, the latter including 3 and 4 viral miRNAs in office workers and truck drivers, respectively. EC-associated miRNAs differed between office workers and truck drivers with significant effect modification by occupational group. Functional interaction network analysis suggested enriched cellular proliferation/differentiation pathways in truck drivers and proinflammation pathways in office workers.Short-term EC exposure was associated with the expression of human and viral miRNAs that may influence immune responses and other biological pathways. Associations between EC exposure and viral miRNA expression suggest that latent viral miRNAs are potential mediators of air pollution-associated health effects. PM2.5/PM10 exposures showed no consistent relationships with miRNA expression.
| S-EPMC4786978 | 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:ImportanceIncreased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown.ObjectiveTo investigate the association of PM2.5 exposure with KT outcomes.Design, setting, and participantsThis retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021.ExposuresExposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3).Main outcomes and measuresAcute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated.ResultsAmong 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs.Conclusions and relevanceThis cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.
| S-EPMC8498852 | biostudies-literature
Project description:BackgroundFew studies have used spatially resolved ambient particulate matter with an aerodynamic diameter of <10 μm (PM10) to examine the impact of PM10 on ischemic heart disease (IHD) mortality in China. The aim of our study is to evaluate the short-term effects of PM10 concentrations on IHD mortality by means of spatiotemporal analysis approach.MethodsWe collected daily data on air pollution, weather conditions and IHD mortality in Beijing, China during 2008 and 2009. Ordinary kriging (OK) was used to interpolate daily PM10 concentrations at the centroid of 287 township-level areas based on 27 monitoring sites covering the whole city. A generalized additive mixed model was used to estimate quantitatively the impact of spatially resolved PM10 on the IHD mortality. The co-effects of the seasons, gender and age were studied in a stratified analysis. Generalized additive model was used to evaluate the effects of averaged PM10 concentration as well.ResultsThe averaged spatially resolved PM10 concentration at 287 township-level areas was 120.3 ± 78.1 μg/m3. Ambient PM10 concentration was associated with IHD mortality in spatiotemporal analysis and the strongest effects were identified for the 2-day average. A 10 μg/m3 increase in PM10 was associated with an increase of 0.33% (95% confidence intervals: 0.13%, 0.52%) in daily IHD mortality. The effect estimates using spatially resolved PM10 were larger than that using averaged PM10. The seasonal stratification analysis showed that PM10 had the statistically stronger effects on IHD mortality in summer than that in the other seasons. Males and older people demonstrated the larger response to PM10 exposure.ConclusionsOur results suggest that short-term exposure to particulate air pollution is associated with increased IHD mortality. Spatial variation should be considered for assessing the impacts of particulate air pollution on mortality.
| S-EPMC4293109 | biostudies-literature
Project description:Chronic exposure to ambient particulate matter (PM) increases the risk of cardiovascular disease (CVD). One proposed mechanism linking PM exposure and CVD is the induction of low-grade systemic inflammation that underlies disease progression. However, the intermediaries that relay signals from the proximal sites of inflammation to the periphery remain unknown. We have previously shown that fine PM (PM2.5) alter red blood cell distribution width. Therefore, the overall goal of this study was to elucidate how PM exposure impacts the spleen and splenic macrophages which are primarily responsible for the turnover of aged and damaged red blood cells.
2024-12-02 | GSE262906 | GEO
Project description:RationaleThere are unexplained geographical and seasonal differences in the short-term effects of fine particulate matter (PM(2.5)) on human health. The hypothesis has been advanced to include the possibility that such differences might be due to variations in the PM(2.5) chemical composition, but evidence supporting this hypothesis is lacking.ObjectivesTo examine whether variation in the relative risks (RR) of hospitalization associated with ambient exposure to PM(2.5) total mass reflects differences in PM(2.5) chemical composition.MethodsWe linked two national datasets by county and by season: (1) long-term average concentrations of PM(2.5) chemical components for 2000-2005 and (2) RRs of cardiovascular and respiratory hospitalizations for persons 65 years or older associated with a 10-microg/m(3) increase in PM(2.5) total mass on the same day for 106 U.S. counties for 1999 through 2005.Measurements and main resultsWe found a positive and statistically significant association between county-specific estimates of the short-term effects of PM(2.5) on cardiovascular and respiratory hospitalizations and county-specific levels of vanadium, elemental carbon, or nickel PM(2.5) content.ConclusionsCommunities with higher PM(2.5) content of nickel, vanadium, and elemental carbon and/or their related sources were found to have higher risk of hospitalizations associated with short-term exposure to PM(2.5).
| S-EPMC2695497 | biostudies-literature
Project description:Air pollutants are associated with cardiovascular death; however, there is limited evidence of the effects of different pollutants on out-of-hospital cardiac arrests (OHCAs) in Beijing, China. We aimed to investigate the associations of OHCAs with the air pollutants PM2.5-10 (coarse particulate matter), PM2.5 (particles ≤2.5 μm in aerodynamic diameter), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (CO), and ozone (O₃) between 2013 and 2015 using a time-stratified case-crossover study design. We obtained health data from the nationwide emergency medical service database; 4720 OHCA cases of cardiac origin were identified. After adjusting for relative humidity and temperature, the highest odds ratios of OHCA for a 10 μg/m³ increase in PM2.5 were observed at Lag Day 1 (1.07; 95% confidence interval (CI): 1.04-1.10), with strong associations with advanced age (aged ≥70 years) (1.09; 95% CI: 1.05-1.13) and stroke history (1.11; 95% CI: 1.06-1.16). PM2.5-10 and NO₂ also showed significant associations with OHCAs, whereas SO₂, CO, and O₃ had no effects. After simultaneously adjusting for NO₂ and SO₂ in a multi-pollutant model, PM2.5 remained significant. The effects of PM2.5 in the single-pollutant models for cases with hypertension, respiratory disorders, diabetes mellitus, and heart disease were higher than those for cases without these complications; however, the differences were not statistically significant. The results support that elevated PM2.5 exposure contributes to triggering OHCA, especially in those who are advanced in age and have a history of stroke.
| S-EPMC5409624 | biostudies-literature