Relationship between different particle size fractions and all-cause and cause-specific emergency ambulance dispatches.
ABSTRACT: BACKGROUND:Evidence on the relationship between different particle size fractions and emergency ambulance dispatches (EAD) remains limited and sparse. METHODS:We collected daily data of EAD, ambient air pollution and meteorological data from 2014 to 2018 in Guangzhou, China. We used a generalized additive model with covariate adjustments to estimate the associations between different particle size fractions and EAD related to all-cause, cardiovascular diseases, and respiratory diseases. Several subgroup and sensitivity analyses were also performed. RESULTS:Significant associations were observed between PM2.5, PM2.5-10, PM10 and EADs. A 10??g/m3 increase of PM2.5, PM2.5-10, and PM10 was associated with an increase of 0.98% (95% CI: 0.67, 1.28%), 2.06% (95% CI: 1.44, 2.68%), and 0.75% (95%CI: 0.53, 0.96%) in all-cause EAD, with an increase of 0.69% (95% CI: 0.00, 1.39%), 2.04% (95% CI: 0.64, 3.45%), and 0.60% (95%CI: 0.11,1.10%) in cardiovascular-related EAD, and an increase of 1.14% (95% CI: 0.25, 2.04%), 2.52% (95% CI: 0.72, 4.35%), and 0.89% (95%CI: 0.25,1.52%) in respiratory-related EAD at lag03, respectively. The results were robust in subgroup and sensitivity analyses. CONCLUSIONS:This study revealed that PM2.5, PM2.5-10 and PM10 were significantly related with risks of all-cause and cause-specific EAD. More evidence of high quality may be needed to further support our results in this ecological study.
Project description:Short-term health effects of ambient PM2.5 have been established with numerous studies, but evidence in Asian countries is limited. This study aimed to investigate the short-term effects of PM2.5 on acute health outcomes, particularly all-cause, cardiovascular, respiratory, cerebrovascular and neuropsychological outcomes. We utilized daily emergency ambulance dispatches (EAD) data from eight Japanese cities (2007-2011). Statistical analyses included two stages: (1) City-level generalized linear model with Poisson distribution; (2) Random-effects meta-analysis in pooling city-specific effect estimates. Lag patterns were explored using (1) unconstrained-distributed lags (lag 0 to lag 7) and (2) average lags (lag: 0-1, 0-3, 0-5, 0-7). In all-cause EAD, significant increases were observed in both shorter lag (lag 0: 1.24% (95% CI: 0.92, 1.56)) and average lag 0-1 (0.64% (95% CI: 0.23, 1.06)). Increases of 1.88% and 1.48% in respiratory and neuropsychological EAD outcomes, respectively, were observed at lag 0 per 10 µg/m³ increase in PM2.5. While respiratory outcomes demonstrated significant average effects, no significant effect was observed for cardiovascular outcomes. Meanwhile, an inverse association was observed in cerebrovascular outcomes. In this study, we observed that effects of PM2.5 on all-cause, respiratory and neuropsychological EAD were acute, with average effects not exceeding 3 days prior to EAD onset.
Project description:Short-term exposures to outdoor air pollutants have been associated with lower lung function, but the results are inconsistence. The effects of different pollutant levels on lung function changes are still unclear. We quantified the effects of outdoor air pollution exposure (NO2, PM10, O3, and PM2.5) on lung function among 1,694 female non-smokers from the Wuhan-Zhuhai Cohort in China by using linear mixed model. We further investigated the associations in the two cities with different air quality levels separately to quantify the effects of different pollutant level exposure on lung function. We found the moving averages of NO2, PM10, and PM2.5 concentrations were significantly associated with reduced FVC. In city at high pollutant level, the moving average of NO2, PM10, O3, and PM2.5 exposures were significantly associated with both FVC and FEV1 reductions. In the low-level air pollution city, PM10 (Lag03-Lag05) and O3 concentrations (Lag01-Lag03) were significantly associated with reduced FVC, while PM10 (Lag03-Lag05), O3 (Lag0-Lag03), and PM2.5 (Lag04-Lag06) exposure were significantly associated with reduced FEV1. Our results suggest that outdoor air pollution is associated with short-term adverse effects on lung function among female non-smokers. The adverse effects may persist for longer durations within 7 days at higher air pollutant levels.
Project description:BACKGROUND AND OBJECTIVES:Fine particulate matter (PM2.5, particulate matter with an aerodynamic diameter less than or equal to 2.5 ?m) has multiple adverse effects on human health, especially on the respiratory and circulatory system. The purpose of this study was to evaluate the short-term effect of PM2.5 on the mortality risk of non-accidental and circulatory diseases, and to explore the potential effect modification by sex, education and death location. METHODS:We collected daily mortality counts of Changchun (China) residents, daily meteorology and air pollution data, from January 1, 2014, to January 1, 2017. We focused on the elderly (?65 years old) population who died from non-accidental causes and circulatory diseases, and stratified them by sex, education, and death location. A generalized additive Poisson regression model (GAM) was used to analyse the impact of air pollutants on mortality. We fit single pollutant models to examine PM2.5 effects with different lag structures of single-day (distributed lag:lag0-lag3) and multi-day (moving average lag: lag01-lag03). To test the sensitivity of the model, a multi-pollutant model was established when the PM2.5 effect was strongest. RESULTS:In the single pollutant models, an increment of PM2.5 by 10 ?g/m3 at lag0-3 was associated with a 0.385% (95% CI: 0.069% to 0.702%) increase in daily non-accidental mortality and a 0.442% (95% CI: 0.038% to 0.848%) increase in daily circulatory disease mortality. NO2 (lag1) and O3 (lag0, lag1, lag2, lag01,lag02, lag03) were associated with daily non-accidental death and NO2 (lag1, lag3, lag03) and O3 (lag0, lag1, lag01,lag02, lag03) were associated with daily circulatory disease mortality. In the co-pollutant models, the risk estimates for PM2.5 changed slightly. The excess mortality risk of non-accidental and circulatory diseases was higher for women, people with low education, and died outside hospital. CONCLUSIONS:We found that short-term exposure to PM2.5 increased the mortality risk of non-accidental and circulatory diseases among the elderly in Changchun. Women, people with low education and died outside hospital are more susceptible to PM2.5. NO2 and O3 were also associated with an increase in mortality from non-accidental and circulatory diseases and the O3 is a high effect.
Project description:BACKGROUND: Outbreaks of Saharan-Sahel dust over Euro-Mediterranean areas frequently induce exceedances of the Europen Union's 24-hr standard of 50 ?g/m3 for particulate matter (PM) with aerodynamic diameter ? than 10 ?m (PM10). OBJECTIVES: We evaluated the effect of Saharan dust on the association between different PM fractions and daily mortality in Rome, Italy. METHODS: In a study of 80,423 adult residents who died in Rome between 2001 and 2004, we performed a time-series analysis to explore the effects of PM2.5, PM2.5-10, and PM10 on natural, cardiac, cerebrovascular, and respiratory mortality. We defined Saharan dust days by combining light detection and ranging (LIDAR) observations and analyses from operational models. We tested a Saharan dust-PM interaction term to evaluate the hypothesis that the effects of PM, especially coarse PM (PM2.5-10), on mortality would be enhanced on dust days. RESULTS: Interquartile range increases in PM2.5-10 (10.8 ?g/m3) and PM10 (19.8 ?g/m3) were associated with increased mortality due to natural, cardiac, cerebrovascular, and respiratory causes, with estimated effects ranging from 2.64% to 12.65% [95% confidence interval (CI), 1.18-25.42%] for the association between PM2.5-10 and respiratory mortality (0- to 5-day lag). Associations of PM2.5-10 with cardiac mortality were stronger on Saharan dust days (9.73%; 95% CI, 4.25-15.49%) than on dust-free days (0.86%; 95% CI, -2.47% to 4.31%; p = 0.005). Saharan dust days also modified associations between PM10 and cardiac mortality (9.55% increase; 95% CI, 3.81-15.61%; vs. dust-free days: 2.09%; 95% CI, -0.76% to 5.02%; p = 0.02). CONCLUSIONS: We found evidence of effects of PM2.5-10 and PM10 on natural and cause-specific mortality, with stronger estimated effects on cardiac mortality during Saharan dust outbreaks. Toxicological and biological effects of particles from desert sources need to be further investigated and taken into account in air quality standards.
Project description:BACKGROUND: Few studies have investigated the independent health effects of different size fractions of particulate matter (PM) in multiple locations, especially in Europe. OBJECTIVES: We estimated the short-term effects of PM with aerodynamic diameter ? 10 ?m (PM10), ? 2.5 ?m (PM2.5), and between 2.5 and 10 ?m (PM2.5-10) on all-cause, cardiovascular, and respiratory mortality in 10 European Mediterranean metropolitan areas within the MED-PARTICLES project. METHODS: We analyzed data from each city using Poisson regression models, and combined city-specific estimates to derive overall effect estimates. We evaluated the sensitivity of our estimates to co-pollutant exposures and city-specific model choice, and investigated effect modification by age, sex, and season. We applied distributed lag and threshold models to investigate temporal patterns of associations. RESULTS: A 10-?g/m3 increase in PM2.5 was associated with a 0.55% (95% CI: 0.27, 0.84%) increase in all-cause mortality (0-1 day cumulative lag), and a 1.91% increase (95% CI: 0.71, 3.12%) in respiratory mortality (0-5 day lag). In general, associations were stronger for cardiovascular and respiratory mortality than all-cause mortality, during warm versus cold months, and among those ? 75 versus < 75 years of age. Associations with PM2.5-10 were positive but not statistically significant in most analyses, whereas associations with PM10 seemed to be driven by PM2.5. CONCLUSIONS: We found evidence of adverse effects of PM2.5 on mortality outcomes in the European Mediterranean region. Associations with PM2.5-10 were positive but smaller in magnitude. Associations were stronger for respiratory mortality when cumulative exposures were lagged over 0-5 days, and were modified by season and age.
Project description:OBJECTIVE:To estimate the attributable and targeted avoidable deaths (ADs; TADs) of outdoor air pollution by ambient particulate matter (PM10), PM2.5 and O3 according to specific WHO methodology. DESIGN:Health impact assessment. SETTING:City of Valladolid, Spain (around 300?000 residents). DATA SOURCES:Demographics; mortality; pollutant concentrations collected 1999-2008. MAIN OUTCOME MEASURES:Attributable fractions; ADs and TADs per year for 1999-2008. RESULTS:Higher TADs estimates (shown here) were obtained when assuming as 'target' concentrations WHO Air Quality Guidelines instead of Directive 2008/50/EC. ADs are considered relative to pollutant background levels. All-cause mortality associated to PM10 (all ages): 52 ADs (95% CI 39 to 64); 31 TADs (95% CI 24 to 39).All-cause mortality associated to PM10 (<5?years): 0 ADs (95% CI 0 to 1); 0 TADs (95% CI 0 to 1). All-cause mortality associated to PM2.5 (>30?years): 326 ADs (95% CI 217 to 422); 231 TADs (95% CI 153 to 301). Cardiopulmonary and lung cancer mortality associated to PM2.5 (>30?years): Cardiopulmonary: 186 ADs (95% CI 74 to 280); 94 TADs (95% CI 36 to 148). Lung cancer : 51 ADs (95% CI 21 to 73); 27 TADs (95% CI 10 to 41).All-cause, respiratory and cardiovascular mortality associated to O3 (all ages): All-cause: 52ADs (95% CI 25 to 77) ; 31 TADs (95% CI 15 to 45). Respiratory: 5ADs (95% CI -2 to 13) ; 3 TADs (95% CI -1 to 8). Cardiovascular: 30 ADs (95% CI 8 to 51) ; 17 TADs (95% CI 5 to 30). Negative estimates which should be read as zero were obtained when pollutant concentrations were below counterfactuals or assumed risk coefficients were below one. CONCLUSIONS:Our estimates suggest a not negligible negative impact on mortality of outdoor air pollution. The implementation of WHO methodology provides critical information to distinguish an improvement range in air pollution control.
Project description:A body of literature has suggested an elevated risk of lung cancer associated with particulate matter and traffic-related pollutants.We examined the relation of lung cancer incidence with long-term residential exposures to ambient particulate matter and residential distance to roadway, as a proxy for traffic-related exposures.For participants in the Nurses' Health Study, a nationwide prospective cohort of women, we estimated 72-month average exposures to PM2.5, PM2.5-10, and PM10 and residential distance to road. Follow-up for incident cases of lung cancer occurred from 1994 through 2010. Cox proportional hazards models were adjusted for potential confounders. Effect modification by smoking status was examined.During 1,510,027 person-years, 2,155 incident cases of lung cancer were observed among 103,650 participants. In fully adjusted models, a 10-?g/m3 increase in 72-month average PM10 [hazard ratio (HR) = 1.04; 95% CI: 0.95, 1.14], PM2.5 (HR = 1.06; 95% CI: 0.91, 1.25), or PM2.5-10 (HR = 1.05; 95% CI: 0.92, 1.20) was positively associated with lung cancer. When the cohort was restricted to never-smokers and to former smokers who had quit at least 10 years before, the associations appeared to increase and were strongest for PM2.5 (PM10: HR = 1.15; 95% CI: 1.00, 1.32; PM2.5: HR = 1.37; 95% CI: 1.06, 1.77; PM2.5-10: HR = 1.11; 95% CI: 0.90, 1.37). RESULTS were most elevated when restricted to the most prevalent subtype, adenocarcinomas. Risks with roadway proximity were less consistent.Our findings support those from other studies indicating increased risk of incident lung cancer associated with ambient PM exposures, especially among never- and long-term former smokers.
Project description:BACKGROUND:Although particulate matter (PM) has not been consistently associated with breast cancer risk, two studies have reported harmful associations for breast cancer survival. We examined PM exposures and breast cancer survival in two U.S.-based prospective cohort studies. METHODS:The Nurses' Health Study (NHS) and NHSII are cohorts with detailed data on medical history, lifestyle factors, and causes of death. Women with Stage I-III breast cancer (n = 8,936) were followed through June 2014. Residential PM was estimated using spatio-temporal models. We performed Cox regression to estimate hazard ratios (HR) of breast cancer-specific mortality and all-cause mortality for 10 ?g/m3 increases in post-diagnosis PM. RESULTS:There were 1,211 breast cancer-specific deaths. Overall, PM was not associated with breast cancer-specific mortality [PM2.5: HR, 1.09; 95% confidence interval (CI), 0.87-1.36; PM2.5-10: HR, 1.03; 95% CI, 0.85-1.24; PM10: HR, 1.05; 95% CI, 0.89-1.24], but was associated with modest increases in all-cause mortality (PM2.5: HR, 1.12; 95% CI, 0.96-1.30; PM2.5-10: HR, 1.12; 95% CI, 1.00-1.24; PM10: HR, 1.09; 95% CI, 1.01-1.18). However, among participants with Stage I disease, PM2.5 was associated with higher breast cancer-specific mortality (HR, 1.64; 95% CI, 1.11-2.43). CONCLUSIONS:PM was not associated with breast cancer-specific death overall; however, higher PM was associated with all-cause mortality. Higher PM2.5 was associated with higher breast cancer-specific mortality among patients with Stage I breast cancer even after adjustment. IMPACT:Studies on ambient PM and breast cancer survival demonstrate that PM2.5 may have broader health effects than previously recognized and warrants further research on breast tumor progression.
Project description:Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35-65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject's 1-year average exposure to traffic-related air pollutants with particulate matter diameters ? 10 ?m (PM10) and ? 2.5 ?m (PM2.5) and the absorbance levels of PM2.5 (PM2.5abs), nitrogen dioxide (NO2), and nitrogen oxides (NOx) in the urban environment.One-year average air pollution exposures were 44.21 ± 4.19 ?g/m3 for PM10, 27.34 ± 5.12 ?g/m3 for PM2.5, and (1.97 ± 0.36) × 10-5/m for PM2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10-5/m increase in PM2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-?g/m3 increase in PM10; 2.81% (95% CI: 0.32, 5.31) per 20-?g/m3 increase in NO2; and 0.74% (95% CI: 0.08, 1.41) per 10-?g/m3 increase in NOx. The associations were not evident for right CIMT, and PM2.5 mass concentration was not associated with the outcomes.Long-term exposures to traffic-related air pollution of PM2.5abs, PM10, NO2, and NOx were positively associated with subclinical atherosclerosis in middle-aged adults.
Project description:BACKGROUND AND PURPOSE:Currently there are more and more studies on the association between short-term effects of exposure to particulate matter (PM) and the morbidity of stroke attack, but few have focused on stroke subtypes. The objective of this study is to assess the relationship between PM and stroke subtypes attack, which is uncertain now. METHODS:Meta-analyses, meta-regression and subgroup analyses were conducted to investigate the association between short-term effects of exposure to PM and the morbidity of different stroke subtypes from a number of epidemiologic studies (from 1997 to 2012). RESULTS:Nineteen articles were identified. Odds ratio (OR) of stroke attack associated with particular matter ("thoracic particles" [PM10]<10 µm in aerodynamic diameter, "fine particles" [PM2.5]<2.5 µm in aerodynamic diameter) increment of 10 µg/m3 was as effect size. PM10 exposure was related to an increase in risk of stroke attack (OR per 10 µg/m3 = 1.004, 95%CI: 1.001 ? 1.008) and PM2.5 exposure was not significantly associated with stroke attack (OR per 10 µg/m3 = 0.999, 95%CI: 0.994 ? 1.003). But when focused on stroke subtypes, PM2.5 (OR per 10 µg/m3 = 1.025; 95%CI, 1.001?1.049) and PM10 (OR per 10 µg/m3 = 1.013; 95%CI, 1.001 ? 1.025) exposure were statistically significantly associated with an increased risk of ischemic stroke attack, while PM2.5 (all the studies showed no significant association) and PM10 (OR per 10 µg/m3 = 1.007; 95%CI, 0.992 ? 1.022) exposure were not associated with an increased risk of hemorrhagic stroke attack. Meta-regression found study design and area were two effective covariates. CONCLUSION:PM2.5 and PM10 had different effects on different stroke subtypes. In the future, it's worthwhile to study the effects of PM to ischemic stroke and hemorrhagic stroke, respectively.