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1.
Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood.Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania.Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM2.5 nephelometer was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m3 increases in average PM2.5 over 30-min intervals and ectopy counts.Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM2.5 exposure was 13 ± 22 μg/m3, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m3 in average PM2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM2.5 was not significantly associated with PAC count.Conclusion: PM2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.  相似文献   

2.
Background: Epidemiologic evidence for a causative association between black carbon (BC) and health outcomes is limited.Objectives: We estimated associations and exposure–response relationships between acute respiratory inflammation in schoolchildren and concentrations of BC and particulate matter with an aerodynamic diameter of ≤ 2.5 μm (PM2.5) in ambient air before and during the air pollution intervention for the 2008 Beijing Olympics.Methods: We measured exhaled nitric oxide (eNO) as an acute respiratory inflammation biomarker and hourly mean air pollutant concentrations to estimate BC and PM2.5 exposure. We used 1,581 valid observations of 36 subjects over five visits in 2 years to estimate associations of eNO with BC and PM2.5 according to generalized estimating equations with polynomial distributed-lag models, controlling for body mass index, asthma, temperature, and relative humidity. We also assessed the relative importance of BC and PM2.5 with two-pollutant models.Results: Air pollution concentrations and eNO were clearly lower during the 2008 Olympics. BC and PM2.5 concentrations averaged over 0–24 hr were strongly associated with eNO, which increased by 16.6% [95% confidence interval (CI), 14.1–19.2%] and 18.7% (95% CI, 15.0–22.5%) per interquartile range (IQR) increase in BC (4.0 μg/m3) and PM2.5 (149 μg/m3), respectively. In the two-pollutant model, estimated effects of BC were robust, but associations between PM2.5 and eNO decreased with adjustment for BC. We found that eNO was associated with IQR increases in hourly BC concentrations up to 10 hr after exposure, consistent with effects primarily in the first hours after exposure.Conclusions: Recent exposure to BC was associated with acute respiratory inflammation in schoolchildren in Beijing. Lower air pollution levels during the 2008 Olympics also were associated with reduced eNO.  相似文献   

3.
Background: A growing body of evidence has associated maternal exposure to air pollution with adverse effects on fetal growth; however, the existing literature is inconsistent.Objectives: We aimed to quantify the association between maternal exposure to particulate air pollution and term birth weight and low birth weight (LBW) across 14 centers from 9 countries, and to explore the influence of site characteristics and exposure assessment methods on between-center heterogeneity in this association.Methods: Using a common analytical protocol, International Collaboration on Air Pollution and Pregnancy Outcomes (ICAPPO) centers generated effect estimates for term LBW and continuous birth weight associated with PM10 and PM2.5 (particulate matter ≤ 10 and 2.5 µm). We used meta-analysis to combine the estimates of effect across centers (~ 3 million births) and used meta-regression to evaluate the influence of center characteristics and exposure assessment methods on between-center heterogeneity in reported effect estimates.Results: In random-effects meta-analyses, term LBW was positively associated with a 10-μg/m3 increase in PM10 [odds ratio (OR) = 1.03; 95% CI: 1.01, 1.05] and PM2.5 (OR = 1.10; 95% CI: 1.03, 1.18) exposure during the entire pregnancy, adjusted for maternal socioeconomic status. A 10-μg/m3 increase in PM10 exposure was also negatively associated with term birth weight as a continuous outcome in the fully adjusted random-effects meta-analyses (–8.9 g; 95% CI: –13.2, –4.6 g). Meta-regressions revealed that centers with higher median PM2.5 levels and PM2.5:PM10 ratios, and centers that used a temporal exposure assessment (compared with spatiotemporal), tended to report stronger associations.Conclusion: Maternal exposure to particulate pollution was associated with LBW at term across study populations. We detected three site characteristics and aspects of exposure assessment methodology that appeared to contribute to the variation in associations reported by centers.  相似文献   

4.
Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)]. This is the first national-level cohort study to investigate these risks in Canada.Objective: We investigated the association between long-term exposure to ambient PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults.Methods: We assigned estimates of exposure to ambient PM2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m3 increase in concentrations of PM2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m3; interquartile range, 6.2 μg/m3) than those reported previously.  相似文献   

5.
Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure–response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure–response relationship for lung cancer are required for disease burden estimates and related public health policy assessments.Objectives: We compared exposure–response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5.Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS.Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2–3 for cigarette smoking.Conclusions: The exposure–response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important.  相似文献   

6.
Background: Inhaling fine particles (particulate matter with diameter ≤ 2.5 μm; PM2.5) can induce oxidative stress and inflammation, and may contribute to onset of preterm labor and other adverse perinatal outcomes.Objectives: We examined whether outdoor PM2.5 was associated with adverse birth outcomes among 22 countries in the World Health Organization Global Survey on Maternal and Perinatal Health from 2004 through 2008.Methods: Long-term average (2001–2006) estimates of outdoor PM2.5 were assigned to 50-km–radius circular buffers around each health clinic where births occurred. We used generalized estimating equations to determine associations between clinic-level PM2.5 levels and preterm birth and low birth weight at the individual level, adjusting for seasonality and potential confounders at individual, clinic, and country levels. Country-specific associations were also investigated.Results: Across all countries, adjusting for seasonality, PM2.5 was not associated with preterm birth, but was associated with low birth weight [odds ratio (OR) = 1.22; 95% CI: 1.07, 1.39 for fourth quartile of PM2.5 (> 20.2 μg/m3) compared with the first quartile (< 6.3 μg/m3)]. In China, the country with the largest PM2.5 range, preterm birth and low birth weight both were associated with the highest quartile of PM2.5 only, which suggests a possible threshold effect (OR = 2.54; CI: 1.42, 4.55 and OR = 1.99; CI: 1.06, 3.72 for preterm birth and low birth weight, respectively, for PM2.5 ≥ 36.5 μg/m3 compared with PM2.5 < 12.5 μg/m3).Conclusions: Outdoor PM2.5 concentrations were associated with low birth weight but not preterm birth. In rapidly developing countries, such as China, the highest levels of air pollution may be of concern for both outcomes.Citation: Fleischer NL, Merialdi M, van Donkelaar A, Vadillo-Ortega F, Martin RV, Betran AP, Souza JP, O´Neill MS. 2014. Outdoor air pollution, preterm birth, and low birth weight: analysis of the World Health Organization Global Survey on Maternal and Perinatal Health. Environ Health Perspect 122:425–430; http://dx.doi.org/10.1289/ehp.1306837  相似文献   

7.
BACKGROUND: Long-term exposure to particulate air pollution has been associated with an increased risk of dying from cardiopulmonary and ischemic heart disease, yet few studies have evaluated cardiovascular end points other than mortality. We investigated the relationship between long-term exposure to traffic and occurrence of acute myocardial infarction (AMI) in a case-control study. METHODS: A total of 5,049 confirmed cases of AMI were identified between 1995 and 2003 as part of the Worcester Heart Attack Study, a community-wide study examining changes over time in the incidence of AMI among greater Worcester, Massachusetts, residents. Population controls were selected from Massachusetts resident lists. We used cumulative traffic within 100 m of subjects' residence and distance from major roadway as proxies for exposure to traffic-related air pollution. We estimated the relationship between exposure to traffic and occurrence of AMI using logistic regression, and we adjusted for the following potential confounders: age, sex, section of the study area, point sources emissions of particulate matter with aerodynamic diameter < 2.5 microm, area socioeconomic characteristics, and percentage of open space. RESULTS: An increase in cumulative traffic near the home was associated with a 4% increase in the odds of AMI per interquartile range [95% confidence interval (CI), 2-7%], whereas living near a major roadway was associated with a 5% increase in the odds of AMI per kilometer (95% CI, 3-6%). CONCLUSIONS: These results provide support for an association between long-term exposure to traffic and the risk of AMI.  相似文献   

8.
Background: Although serious health effects associated with particulate matter (PM) with aerodynamic diameter ≤ 10 μm (PM10) and ≤ 2.5 μm (PM2.5; fine fraction) are documented in many studies, the effects of coarse PM (PM2.5–10) are still under debate.Objective: In this study, we estimated the effects of short-term exposure of PM2.5–10 on daily mortality in Stockholm, Sweden.Method: We collected data on daily mortality for the years 2000 through 2008. Concentrations of PM10, PM2.5, ozone, and carbon monoxide were measured simultaneously in central Stockholm. We used additive Poisson regression models to examine the association between daily mortality and PM2.5–10 on the day of death and the day before. Effect estimates were adjusted for other pollutants (two-pollutant models) during different seasons.Results: We estimated a 1.68% increase [95% confidence interval (CI): 0.20%, 3.15%] in daily mortality per 10-μg/m3 increase in PM2.5–10 (single-pollutant model). The association with PM2.5–10 was stronger for November through May, when road dust is most important (1.69% increase; 95% CI: 0.21%, 3.17%), compared with the rest of the year (1.31% increase; 95% CI: –2.08%, 4.70%), although the difference was not statistically significant. When adjusted for other pollutants, particularly PM2.5, the effect estimates per 10 μg/m3 for PM2.5–10 decreased slightly but were still higher than corresponding effect estimates for PM2.5.Conclusions: Our analysis shows an increase in daily mortality associated with elevated urban background levels of PM2.5–10. Regulation of PM2.5–10 should be considered, along with actions to specifically reduce PM2.5–10 emissions, especially road dust suspension, in cities.  相似文献   

9.
Background: Evidence on the short-term effects of fine and coarse particles on morbidity in Europe is scarce and inconsistent.Objectives: We aimed to estimate the association between daily concentrations of fine and coarse particles with hospitalizations for cardiovascular and respiratory conditions in eight Southern European cities, within the MED-PARTICLES project.Methods: City-specific Poisson models were fitted to estimate associations of daily concentrations of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5), ≤ 10 μm (PM10), and their difference (PM2.5–10) with daily counts of emergency hospitalizations for cardiovascular and respiratory diseases. We derived pooled estimates from random-effects meta-analysis and evaluated the robustness of results to co-pollutant exposure adjustment and model specification. Pooled concentration–response curves were estimated using a meta-smoothing approach.Results: We found significant associations between all PM fractions and cardiovascular admissions. Increases of 10 μg/m3 in PM2.5, 6.3 μg/m3 in PM2.5–10, and 14.4 μg/m3 in PM10 (lag 0–1 days) were associated with increases in cardiovascular admissions of 0.51% (95% CI: 0.12, 0.90%), 0.46% (95% CI: 0.10, 0.82%), and 0.53% (95% CI: 0.06, 1.00%), respectively. Stronger associations were estimated for respiratory hospitalizations, ranging from 1.15% (95% CI: 0.21, 2.11%) for PM10 to 1.36% (95% CI: 0.23, 2.49) for PM2.5 (lag 0–5 days).Conclusions: PM2.5 and PM2.5–10 were positively associated with cardiovascular and respiratory admissions in eight Mediterranean cities. Information on the short-term effects of different PM fractions on morbidity in Southern Europe will be useful to inform European policies on air quality standards.Citation: Stafoggia M, Samoli E, Alessandrini E, Cadum E, Ostro B, Berti G, Faustini A, Jacquemin B, Linares C, Pascal M, Randi G, Ranzi A, Stivanello E, Forastiere F, the MED-PARTICLES Study Group. 2013. Short-term associations between fine and coarse particulate matter and hospitalizations in Southern Europe: results from the MED-PARTICLES project. Environ Health Perspect 121:1026–1033; http://dx.doi.org/10.1289/ehp.1206151  相似文献   

10.
Background: A large body of evidence suggests that fine particulate matter (PM) air pollution is a cause of cardiovascular disease, but little is known in particular about the cardiovascular effects of indoor air pollution from household use of solid fuels in developing countries. RESPIRE (Randomized Exposure Study of Pollution Indoors and Respiratory Effects) was a randomized trial of a chimney woodstove that reduces wood smoke exposure.Objectives: We tested the hypotheses that the stove intervention, compared with open fire use, would reduce ST-segment depression and increase heart rate variability (HRV).Methods: We used two complementary study designs: a) between-groups comparisons based on randomized stove assignment, and b) before-and-after comparisons within control subjects who used open fires during the trial and received chimney stoves after the trial. Electrocardiogram sessions that lasted 20 hr were repeated up to three times among 49 intervention and 70 control women 38–84 years of age, and 55 control subjects were also assessed after receiving stoves. HRV and ST-segment values were assessed for each 30-min period. ST-segment depression was defined as an average value below –1.00 mm. Personal fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] exposures were measured for 24 hr before each electrocardiogram.Results: PM2.5 exposure means were 266 and 102 μg/m3 during the trial period in the control and intervention groups, respectively. During the trial, the stove intervention was associated with an odds ratio of 0.26 (95% confidence interval, 0.08–0.90) for ST-segment depression. We found similar associations with the before-and-after comparison. The intervention was not significantly associated with HRV.Conclusions: The stove intervention was associated with reduced occurrence of nonspecific ST-segment depression, suggesting that household wood smoke exposures affect ventricular repolarization and potentially cardiovascular health.  相似文献   

11.
Background: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources.Objective: We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease.Methods: We used data from the first (2000–2003) and second examination (2006–2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45–75 years of age). We estimated residential long-term exposure to local traffic- and industry-specific fine particulate matter (PM2.5) at participants’ residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations).Results: A 1-μg/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-μg/m3 increases in traffic- and industry-specific PM2.5, respectively. Results for PM10 were similar.Conclusions: Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with total PM.Citation: Hennig F, Fuks K, Moebus S, Weinmayr G, Memmesheimer M, Jakobs H, Bröcker-Preuss M, Führer-Sakel D, Möhlenkamp S, Erbel R, Jöckel KH, Hoffmann B, Heinz Nixdorf Recall Study Investigative Group. 2014. Association between source-specific particulate matter air pollution and hs-CRP: local traffic and industrial emissions. Environ Health Perspect 122:703–710; http://dx.doi.org/10.1289/ehp.1307081  相似文献   

12.
Background: Many epidemiological studies have linked daily counts of hospital admissions to particulate matter (PM) with an aerodynamic diameter ≤ 10 μm (PM10) and ≤ 2.5 μm (PM2.5), but relatively few have investigated the relationship of hospital admissions with coarse PM (PMc; 2.5–10 μm aerodynamic diameter).Objectives: We conducted this study to estimate the health effects of PMc on emergency hospital admissions for respiratory diseases in Hong Kong after controlling for PM2.5 and gaseous pollutants.Methods: We conducted a time-series analysis of associations between daily emergency hospital admissions for respiratory diseases in Hong Kong from January 2000 to December 2005 and daily PM2.5 and PMc concentrations. We estimated PMc concentrations by subtracting PM2.5 from PM10 measurements. We used generalized additive models to examine the relationship between PMc (single- and multiday lagged exposures) and hospital admissions adjusted for time trends, weather conditions, influenza outbreaks, PM2.5, and gaseous pollutants (nitrogen dioxide, sulfur dioxide, and ozone).Results: A 10.9-μg/m3 (interquartile range) increase in the 4-day moving average concentration of PMc was associated with a 1.94% (95% confidence interval: 1.24%, 2.64%) increase in emergency hospital admissions for respiratory diseases that was attenuated but still significant after controlling for PM2.5. Adjusting for gaseous pollutants and altering models assumptions had little influence on PMc effect estimates.Conclusion: PMc was associated with emergency hospital admissions for respiratory diseases in Hong Kong independent of PM2.5 and gaseous pollutants. Further research is needed to evaluate health effects of different components of PMc.  相似文献   

13.
Background: Outbreaks of Saharan-Sahel dust over Euro-Mediterranean areas frequently induce exceedances of the Europen Union''s 24-hr standard of 50 μg/m3 for particulate matter (PM) with aerodynamic diameter ≤ than 10 μm (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 μg/m3) and PM10 (19.8 μg/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.  相似文献   

14.
Background: During the summer of 2003 numerous fires burned in British Columbia, Canada.Objectives: We examined the associations between respiratory and cardiovascular physician visits and hospital admissions, and three measures of smoke exposure over a 92-day study period (1 July to 30 September 2003).Methods: A population-based cohort of 281,711 residents was identified from administrative data. Spatially specific daily exposure estimates were assigned to each subject based on total measurements of particulate matter (PM) ≤ 10 μm in aerodynamic diameter (PM10) from six regulatory tapered element oscillating microbalance (TEOM) air quality monitors, smoke-related PM10 from a CALPUFF dispersion model run for the study, and a SMOKE exposure metric for plumes visible in satellite images. Logistic regression with repeated measures was used to estimate associations with each outcome.Results: The mean (± SD) exposure based on TEOM-measured PM10 was 29 ± 31 μg/m3, with an interquartile range of 14–31 μg/m3. Correlations between the TEOM, smoke, and CALPUFF metrics were moderate (0.37–0.76). Odds ratios (ORs) for a 30-μg/m3 increase in TEOM-based PM10 were 1.05 [95% confidence interval (CI), 1.03–1.06] for all respiratory physician visits, 1.16 (95% CI, 1.09–1.23) for asthma-specific visits, and 1.15 (95% CI, 1.00–1.29) for respiratory hospital admissions. Associations with cardiovascular outcomes were largely null.Conclusions: Overall we found that increases in TEOM-measured PM10 were associated with increased odds of respiratory physician visits and hospital admissions, but not with cardiovascular health outcomes. Results indicating effects of fire smoke on respiratory outcomes are consistent with previous studies, as are the null results for cardiovascular outcomes. Some agreement between TEOM and the other metrics suggests that exposure assessment tools that are independent of air quality monitoring may be useful with further refinement.  相似文献   

15.
Background: Recent studies have shown an association of short-term exposure to fine particulate matter (PM) with transient increases in blood pressure (BP), but it is unclear whether long-term exposure has an effect on arterial BP and hypertension.Objectives: We investigated the cross-sectional association of residential long-term PM exposure with arterial BP and hypertension, taking short-term variations of PM and long-term road traffic noise exposure into account.Methods: We used baseline data (2000–2003) on 4,291 participants, 45–75 years of age, from the Heinz Nixdorf Recall Study, a population-based prospective cohort in Germany. Urban background exposure to PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10) was assessed with a dispersion and chemistry transport model. We used generalized additive models, adjusting for short-term PM, meteorology, traffic proximity, and individual risk factors.Results: An interquartile increase in PM2.5 (2.4 μg/m3) was associated with estimated increases in mean systolic and diastolic BP of 1.4 mmHg [95% confidence interval (CI): 0.5, 2.3] and 0.9 mmHg (95% CI: 0.4, 1.4), respectively. The observed relationship was independent of long-term exposure to road traffic noise and robust to the inclusion of many potential confounders. Residential proximity to high traffic and traffic noise exposure showed a tendency toward higher BP and an elevated prevalence of hypertension.Conclusions: We found an association of long-term exposure to PM with increased arterial BP in a population-based sample. This finding supports our hypothesis that long-term PM exposure may promote atherosclerosis, with air-pollution–induced increases in BP being one possible biological pathway.  相似文献   

16.
Background: Air pollution exposure increases cardiovascular morbidity and mortality and is a major global public health concern.Objectives: We investigated the benefits of reducing personal exposure to urban air pollution in patients with coronary heart disease.Methods: In an open randomized crossover trial, 98 patients with coronary heart disease walked on a predefined route in central Beijing, China, under different conditions: once while using a highly efficient face mask, and once while not using the mask. Symptoms, exercise, personal air pollution exposure, blood pressure, heart rate, and 12-lead electrocardiography were monitored throughout the 24-hr study period.Results: Ambient air pollutants were dominated by fine and ultrafine particulate matter (PM) that was present at high levels [74 μg/m3 for PM2.5 (PM with aerodynamic diamater <2.5 µm)]. Consistent with traffic-derived sources, this PM contained organic carbon and polycyclic aromatic hydrocarbons and was highly oxidizing, generating large amounts of free radicals. The face mask was well tolerated, and its use was associated with decreased self-reported symptoms and reduced maximal ST segment depression (–142 vs. –156 μV, p = 0.046) over the 24-hr period. When the face mask was used during the prescribed walk, mean arterial pressure was lower (93 ± 10 vs. 96 ± 10 mmHg, p = 0.025) and heart rate variability increased (high-frequency power: 54 vs. 40 msec2, p = 0.005; high-frequency normalized power: 23.5 vs. 20.5 msec, p = 0.001; root mean square successive differences: 16.7 vs. 14.8 msec, p = 0.007). However, mask use did not appear to influence heart rate or energy expenditure.Conclusions: Reducing personal exposure to air pollution using a highly efficient face mask appeared to reduce symptoms and improve a range of cardiovascular health measures in patients with coronary heart disease. Such interventions to reduce personal exposure to PM air pollution have the potential to reduce the incidence of cardiovascular events in this highly susceptible population.  相似文献   

17.

Background

Although studies have found that diabetes mellitus (DM) modifies the impact of exposures from air pollution on cardiovascular outcomes, information is limited regarding DM as an air pollution-associated outcome.

Objectives

Using two prospective cohorts, the Nurses’ Health Study (NHS) and the Health Professionals Follow-Up Study (HPFS), we investigated the relationship of incident type 2 DM with exposures to particulate matter (PM) <2.5 μm (PM2.5), PM <10 μm (PM10), and PM between 2.5 and 10 μm in aerodynamic diameter (PM10–2.5) in the previous 12 months and the distance to roadways.

Methods

Cases were reported and confirmed through biennial and supplemental questionnaires of diagnosis and treatment information. During follow-up from 1989 to 2002, questionnaires provided information on time-varying covariates and updated addresses. Addresses were geocoded and used to assign air pollution exposures from spatiotemporal statistical models.

Results

Among participants living in metropolitan areas of the northeastern and midwestern United States, there were 3,784 incident cases of DM in the NHS, and 688 cases in the HPFS. Pooled results from random effects meta-analysis of cohort-specific models adjusted for body mass index and other known risk factors produced hazard ratios (HRs) for incident DM with interquartile range (IQR) increases in average PM during the 12 months before diagnosis of 1.03 [95% confidence interval (CI), 0.96–1.10] for PM2.5, 1.04 (95% CI, 0.99–1.09) for PM10, and 1.04 (95% CI, 0.99–1.09) for PM10–2.5. Among women, the fully adjusted HR for living < 50 m versus ≥ 200 m from a roadway was 1.14 (95% CI, 1.03–1.27).

Conclusions

Overall, results did not provide strong evidence of an association between exposure to PM in the previous 12 months and incident DM; however, an association with distance to road (a proxy marker of exposure to traffic-related pollution) was shown among women.  相似文献   

18.

Background

Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events.

Objective

We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites.

Methods

We assigned pollution exposure during two decades preceding a clinical exam (2000–2002) using observed PM10 from monitors nearest participants’ residences and PM10 and PM2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young’s modulus (YM) from carotid artery ultrasound and large (C1) and small (C2) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m3 increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C1 and C2 models were further adjusted for heart rate, weight, and height.

Results

Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C1, or C2, and the few associations observed were not robust across metrics and adjustment schemes.

Conclusions

Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.  相似文献   

19.
Background: Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 μm (PM10)] and mortality in adults.Objectives: We investigated short-term effects of elevated PM10 levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger.Methods: In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM10 concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature.Results: During the study period (1998–2006), PM10 concentration averaged 31.9 ± 13.8 μg/m3. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0–8%; p = 0.045] for a 10-μg/m3 increase in daily mean PM10. However, this association was significant only for late neonates (2–4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1–22%; p = 0.028) per 10-μg/m3 increase in PM10. In this age class, infants were 1.74 (95% CI, 1.18–2.58; p = 0.006) times more likely to die on days with a mean PM10 above the EU limit value of 50 μg/m3 than on days below this cutoff.Conclusions: Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM10, which may be exceeded on 35 days/year, does not prevent PM10 from triggering mortality in late neonates.  相似文献   

20.
Background: Current air quality standards for particulate matter (PM) use the PM mass concentration [PM with aerodynamic diameters ≤ 10 μm (PM10) or ≤ 2.5 μm (PM2.5)] as a metric. It has been suggested that particles from combustion sources are more relevant to human health than are particles from other sources, but the impact of policies directed at reducing PM from combustion processes is usually relatively small when effects are estimated for a reduction in the total mass concentration.Objectives: We evaluated the value of black carbon particles (BCP) as an additional indicator in air quality management.Methods: We performed a systematic review and meta-analysis of health effects of BCP compared with PM mass based on data from time-series studies and cohort studies that measured both exposures. We compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM2.5 based on data from prior studies.Results: Estimated health effects of a 1-μg/m3 increase in exposure were greater for BCP than for PM10 or PM2.5, but estimated effects of an interquartile range increase were similar. Two-pollutant models in time-series studies suggested that the effect of BCP was more robust than the effect of PM mass. The estimated increase in life expectancy associated with a hypothetical traffic abatement measure was four to nine times higher when expressed in BCP compared with an equivalent change in PM2.5 mass.Conclusion: BCP is a valuable additional air quality indicator to evaluate the health risks of air quality dominated by primary combustion particles.  相似文献   

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