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1.
BACKGROUND AND OBJECTIVE: RESPIRE, a randomized trial of an improved cookstove, was conducted in Guatemala to assess health effects of long-term reductions in wood smoke exposure. Given the evidence that ambient particles increase blood pressure, we hypothesized that the intervention would lower blood pressure. METHODS: TWO STUDY DESIGNS WERE USED: a) between-group comparisons based on randomized stove assignment, and b) before-and-after comparisons within subjects before and after they received improved stoves. From 2003 to 2005, we measured personal fine particle (particulate matter with aerodynamic diameter < 2.5 microm; PM(2.5)) exposures and systolic (SBP) and diastolic blood pressure (DBP) among women > 38 years of age from the chimney woodstove intervention group (49 subjects) and traditional open wood fire control group (71 subjects). Measures were repeated up to three occasions. RESULTS: Daily average PM(2.5) exposures were 264 and 102 microg/m(3) in the control and intervention groups, respectively. After adjusting for age, body mass index, an asset index, smoking, secondhand tobacco smoke, apparent temperature, season, day of week, time of day, and a random subject intercept, the improved stove intervention was associated with 3.7 mm Hg lower SBP [95% confidence interval (CI), -8.1 to 0.6] and 3.0 mm Hg lower DBP (95% CI, -5.7 to -0.4) compared with controls. In the second study design, among 55 control subjects measured both before and after receiving chimney stoves, similar associations were observed. CONCLUSION: The between-group comparisons provide evidence, particularly for DBP, that the chimney stove reduces blood pressure, and the before-and-after comparisons are consistent with this evidence.  相似文献   

2.
Elevated indoor air pollution exposures associated with the burning of biomass fuels in developing countries are well established. Improved cookstoves have the potential to substantially reduce these exposures. However, few studies have quantitatively evaluated exposure reductions associated with the introduction of improved stoves, likely due to the cost and time-intensive nature of such evaluations. Several studies have demonstrated the value of estimating indoor air pollution exposures by evaluating personal cooking practices and household parameters in addition to stove type. We assessed carbon monoxide (n=54) and fine particulate matter (PM2.5) (n=58) levels among non-smoking Honduran women cooking with traditional or improved wood-burning cookstoves in two communities, one semi-urban and one rural. Exposure concentrations were assessed via 8-h indoor monitoring, as well as 8-h personal PM2.5 monitoring. Housing characteristics were determined to indicate ventilation that may affect carbon monoxide and PM2.5. Stove quality was assessed using a four-level subjective scale representing the potential for indoor emissions, ranging from poorly functioning traditional stoves to well-functioning improved stoves. Univariately, the stove scale as compared to stove type (traditional versus improved) accounted for a higher percent of the variation in pollutant concentrations; for example, the stove scale predicted 79% of the variation and the stove type predicted 54% of the variation in indoor carbon monoxide concentrations. In multivariable models, the stove scale, age of the stove, and ventilation factors predicted more than 50% of the variation in personal and indoor PM2.5 and 85% of the variation in indoor carbon monoxide. Results indicate that using type of stove alone as a proxy for exposure may lead to exposure misclassification and potentially biased exposure and health effects relationships. Utilizing stove quality and housing characteristics that influence ventilation may provide a viable alternative to the more time- and cost-intensive pollutant assessments for larger-scale studies. Designing kitchens with proper ventilation structures could lead to improved indoor environments, especially important in areas where biomass will continue to be the preferred and necessary cooking fuel for some time.  相似文献   

3.
Background: A growing body of evidence indicates a relationship between household indoor air pollution from cooking fires and adverse neonatal outcomes, such as low birth weight (LBW), in resource-poor countries.Objective: We examined the effect of reduced wood smoke exposure in pregnancy on LBW of Guatemalan infants in RESPIRE (Randomized Exposure Study of Pollution Indoors and Respiratory Effects).Methods: Pregnant women (n = 266) either received a chimney stove (intervention) or continued to cook over an open fire (control). Between October 2002 and December 2004 we weighed 174 eligible infants (69 to mothers who used a chimney stove and 105 to mothers who used an open fire during pregnancy) within 48 hr of birth. Multivariate linear regression and adjusted odds ratios (ORs) were used to estimate differences in birth weight and LBW (< 2,500 g) associated with chimney-stove versus open-fire use during pregnancy.Results: Pregnant women using chimney stoves had a 39% reduction in mean exposure to carbon monoxide compared with those using open fires. LBW prevalence was high at 22.4%. On average, infants born to mothers who used a stove weighed 89 g more [95% confidence interval (CI), –27 to 204 g] than infants whose mothers used open fires after adjusting for maternal height, diastolic blood pressure, gravidity, and season of birth. The adjusted OR for LBW was 0.74 (95% CI, 0.33–1.66) among infants of stove users compared with open-fire users. Average birth weight was 296 g higher (95% CI, 109–482 g) in infants born during the cold season (after harvest) than in other infants; this unanticipated finding may reflect the role of maternal nutrition on birth weight in an impoverished region.Conclusions: A chimney stove reduced wood smoke exposures and was associated with reduced LBW occurrence. Although not statistically significant, the estimated effect was consistent with previous studies.  相似文献   

4.
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   

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: The long-term health effects of coarse particular matter (PM10–2.5) are challenging to assess because of a limited understanding of the spatial variation in PM10–2.5 mass and its chemical components.Objectives: We conducted a spatially intensive field study and developed spatial prediction models for PM10–2.5 mass and four selected species (copper, zinc, phosphorus, and silicon) in three American cities.Methods: PM10–2.5 snapshot campaigns were conducted in Chicago, Illinois; St. Paul, Minnesota; and Winston-Salem, North Carolina, in 2009 for the Multi-Ethnic Study of Atherosclerosis and Coarse Airborne Particulate Matter (MESA Coarse). In each city, samples were collected simultaneously outside the homes of approximately 40 participants over 2 weeks in the winter and/or summer. City-specific and combined prediction models were developed using land use regression (LUR) and universal kriging (UK). Model performance was evaluated by cross-validation (CV).Results: PM10–2.5 mass and species varied within and between cities in a manner that was predictable by geographic covariates. City-specific LUR models generally performed well for total mass (CV R2, 0.41–0.68), copper (CV R2, 0.51–0.86), phosphorus (CV R2, 0.50–0.76), silicon (CV R2, 0.48–0.93), and zinc (CV R2, 0.36–0.73). Models pooled across all cities inconsistently captured within-city variability. Little difference was observed between the performance of LUR and UK models in predicting concentrations.Conclusions: Characterization of fine-scale spatial variability of these often heterogeneous pollutants using geographic covariates should reduce exposure misclassification and increase the power of epidemiological studies investigating the long-term health impacts of PM10–2.5.Citation: Zhang K, Larson TV, Gassett A, Szpiro AA, Daviglus M, Burke GL, Kaufman JD, Adar SD. 2014. Characterizing spatial patterns of airborne coarse particulate (PM10–2.5) mass and chemical components in three cities: the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 122:823–830; http://dx.doi.org/10.1289/ehp.1307287  相似文献   

7.
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   

8.

Background

Epidemiologic studies show that exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] increases the total daily cardiovascular mortality. Impaired cardiac autonomic function, which manifests as reduced heart rate variability (HRV), may be one of the underlying causes. However, the cellular mechanism(s) by which PM2.5 exposure induces decreased HRV is not known.

Objectives

We tested the hypothesis that exposure to PM2.5 impairs HRV by decreasing the excitability of the cardiac vagal neurons in the nucleus ambiguus. We also detemined the effect of iron on PM-exposure–induced decrease in HRV.

Methods

We measured 24-hr HRV in time domains from electrocardiogram telemetry recordings obtained in conscious, freely moving mice after 3 days of exposure to PM2.5 in the form of soot only or iron-soot. In parallel studies, we determined the intrinsic properties of identified cardiac vagal neurons, retrogradely labeled with a fluorescent dye applied to the sinoatrial node.

Results

Soot-only exposure decreased short-term HRV (root mean square of successive difference). With the addition of iron, all HRV parameters were significantly reduced. In nonexposed mice, vagal blockade significantly reduced all HRV parameters, suggesting that HRV is, in part, under vagal regulation in mice. Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05). The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

Conclusions

The data suggest that PM-induced neuroplasticity of cardiac vagal neurons may be one mechanism contributing to the cardiovascular consequences associated with PM2.5 exposure seen in humans.  相似文献   

9.
Background: High ambient levels of ozone (O3) and fine particulate matter (PM2.5) are associated with cardiovascular morbidity and mortality, especially in people with preexisting cardiopulmonary diseases. Enhanced susceptibility to the toxicity of air pollutants may include individuals with metabolic syndrome (MetS).Objective: We tested the hypothesis that cardiovascular responses to O3 and PM2.5 will be enhanced in rats with diet-induced MetS.Methods: Male Sprague-Dawley rats were fed a high-fructose diet (HFrD) to induce MetS and then exposed to O3, concentrated ambient PM2.5, or the combination of O3 plus PM2.5 for 9 days. Data related to heart rate (HR), HR variability (HRV), and blood pressure (BP) were collected.Results: Consistent with MetS, HFrD rats were hypertensive and insulin resistant, and had elevated fasting levels of blood glucose and triglycerides. Decreases in HR and BP, which were found in all exposure groups, were greater and more persistent in HFrD rats compared with those fed a normal diet (ND). Coexposure to O3 plus PM2.5 induced acute drops in HR and BP in all rats, but only ND rats adapted after 2 days. HFrD rats had little exposure-related changes in HRV, whereas ND rats had increased HRV during O3 exposure, modest decreases with PM2.5, and dramatic decreases during O3 plus PM2.5 coexposures.Conclusions: Cardiovascular depression in O3- and PM2.5-exposed rats was enhanced and prolonged in rats with HFrD-induced MetS. These results in rodents suggest that people with MetS may be prone to similar exaggerated BP and HR responses to inhaled air pollutants.Citation: Wagner JG, Allen K, Yang HY, Nan B, Morishita M, Mukherjee B, Dvonch JT, Spino C, Fink GD, Rajagopalan S, Sun Q, Brook RD, Harkema JR. 2014. Cardiovascular depression in rats exposed to inhaled particulate matter and ozone: effects of diet-induced metabolic syndrome. Environ Health Perspect 122:27–33; http://dx.doi.org/10.1289/ehp.1307085  相似文献   

10.
Background: Almost half of the world’s population uses coal and biomass fuels for domestic energy. Limited evidence suggests that exposure to air pollutants from indoor biomass combustion may be associated with elevated blood pressure (BP).Objective: Our aim was to assess the relationship between air pollution exposure from indoor biomass combustion and BP in women in rural China.Methods: We measured 24-hr personal integrated gravimetric exposure to fine particles < 2.5 µm in aerodynamic diameter (PM2.5) and systolic BP (SBP) and diastolic BP (DBP) in the winter and summer among 280 women ≥ 25 years of age living in rural households using biomass fuels in Yunnan, China. We investigated the association between PM2.5 exposure and SBP and DBP using mixed-effects models with random intercepts to account for correlation among repeated measures.Results: Personal average 24-hr exposure to PM2.5 ranged from 22 to 634 µg/m3 in winter and from 9 to 492 µg/m3 in summer. A 1-log-µg/m3 increase in PM2.5 exposure was associated with 2.2 mm Hg higher SBP [95% confidence interval (CI), 0.8 to 3.7; p = 0.003] and 0.5 mm Hg higher DBP (95% CI, –0.4 to 1.3; p = 0.31) among all women; estimated effects varied by age group. Among women > 50 years of age, a 1-log-µg/m3 increase in PM2.5 exposure was associated with 4.1 mm Hg higher SBP (95% CI, 1.5 to 6.6; p = 0.002) and 1.8 mm Hg higher DBP (95% CI, 0.4 to 3.2; p = 0.01). PM2.5 exposure was positively associated with SBP among younger women, but the association was not statistically significant.Conclusion: PM2.5 exposure from biomass combustion may be a risk factor for elevated BP and hence for cardiovascular events. Our findings should be corroborated in longitudinal studies.  相似文献   

11.
An improved efficient stove is the mainstay intervention to reduce household air pollution (HAP) associated with biomass fuel use. It potentially addresses the adverse health outcomes by reducing smoke exposure, fuel consumption, and cooking time. This study evaluated two stove intervention programs and compared them for health effects (respiratory and eye symptoms, lung function, blood pressure and burns) among women who were the main cook of the household. A total of 83 and 134 improved and 209 and 179 traditional stoves in Sindh and Punjab provinces of Pakistan, respectively, were evaluated after 3 months of installation, during June to September, 2014. Twenty-four-hour particulate matter (<2.5 μm) (PM2.5) and carbon monoxide (CO) levels were measured in the kitchens in a subsample (n = 40). Multivariate logistic regression and general linear model were used to determine the health impact of improved stoves among women. PM2.5 and CO levels were significantly less in improved stove kitchens. Among women in Sindh program, significantly less cough (aRR 0.27, CI 0.20, 0.38), phlegm (aRR 0.27, CI 0.18, 0.40), shortness of breath (aRR 0.16, CI 0.11, 0.22), chest tightness (aRR 0.23, CI 0.17, 0.31), attack of asthma (aRR 0.33, CI 0.22, 0.49) (p < 0.001), sandy eyes (aRR 0.63, CI 0.47, 0.97), and itching in eyes (aRR 0.62, CI 0.41, 0.95 (p < 0.050) were present. While in Punjab program, risk reduction for phlegm (aRR 0.60, CI 0.45, 0.81) and protection from burns (aRR 0.56, CI 0.34, 0.91) were observed among women. Mean peak expiratory flow was higher among women using improved stoves in Sindh program (31.58, CI 17.90, 45.25 L/min) only. Overall, the positive health impact was greater among those women using closed kitchens. Interventions with improved stoves can have favorable health impact among women. However, variations in health gains were noted among the two programs, as well as greater impact among women using closed kitchen.  相似文献   

12.
Background: Epidemiologic studies have reported associations between fine particles (aerodynamic diameter ≤ 2.5 µm; PM2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time.Objective: We addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures.Methods: We replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration–response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education.Results: Since 2001, average PM2.5 levels, for all six cities, were < 18 µg/m3. Each increase in PM2.5 (10 µg/m3) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration–response relationship was linear down to PM2.5 concentrations of 8 µg/m3. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results.Conclusions: These results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits.  相似文献   

13.
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   

14.
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   

15.
The association between traffic-related air pollution and adverse cardiovascular effects has been well documented; however, little is known about whether different commuting modes can modify the effects of air pollution on the cardiovascular system in human subjects in urban areas with heavy traffic. We recruited 120 young, healthy subjects in Taipei, Taiwan. Each participant was classified with different commuting modes according to his/her own commuting style. Three repeated measurements of heart rate variability (HRV) indices {standard deviation of NN intervals (SDNN) and the square root of the mean of the sum of the squares of differences between adjacent NN intervals (r-MSSD)}, particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), temperature, humidity and noise level were conducted for each subject during 1-h morning commutes (0900–1000 h) in four different commuting modes, including an electrically powered subway, a gas-powered bus, a gasoline-powered car, and walking. Linear mixed-effects models were used to investigate the association of PM2.5 with HRV indices. The results showed that decreases in the HRV indices were associated with increased levels of PM2.5. The personal exposure levels to PM2.5 were the highest in the walking mode. The effects of PM2.5 on cardiovascular endpoints were the lowest in the subway mode compared to the effects in the walking mode. The participants in the car and bus modes had reduced effects on their cardiovascular endpoints compared to the participants in the walking mode. We concluded that traffic-related PM2.5 is associated with autonomic alteration. Commuting modes can modify the effects of PM2.5 on HRV indices among young, healthy subjects.  相似文献   

16.

Background

Air pollutants have not been associated with ambulatory electrocardiographic evidence of ST-segment depression ≥ 1 mm (probable cardiac ischemia). We previously found that markers of primary (combustion-related) organic aerosols and gases were positively associated with circulating biomarkers of inflammation and ambulatory blood pressure in the present cohort panel study of elderly subjects with coronary artery disease.

Objectives

We specifically aimed to evaluate whether exposure markers of primary organic aerosols and ultrafine particles were more strongly associated with ST-segment depression of ≥ 1 mm than were secondary organic aerosols or PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) mass.

Methods

We evaluated relations of air pollutants to ambulatory electrocardiographic evidence of cardiac ischemia over 10 days in 38 subjects without ST depression on baseline electrocardiographs. Exposures were measured outdoors in retirement communities in the Los Angeles basin, including daily size-fractionated particle mass and hourly markers of primary and secondary organic aerosols and gases. Generalized estimating equations were used to estimate odds of hourly ST-segment depression (≥ 1 mm) from hourly air pollution exposures and to estimate relative rates of daily counts of ST-segment depression from daily average exposures, controlling for potential confounders.

Results

We found significant positive associations of hourly ST-segment depression with markers of combustion-related aerosols and gases averaged 1-hr through 3–4 days, but not secondary (photochemically aged) organic aerosols or ozone. The odds ratio per interquartile increase in 2-day average primary organic carbon (5.2 μg/m3) was 15.4 (95% confidence interval, 3.5–68.2). Daily counts of ST-segment depression were consistently associated with primary combustion markers and 2-day average quasi-ultrafine particles < 0.25 μm.

Conclusions

Results suggest that exposure to quasi-ultrafine particles and combustion-related pollutants (predominantly from traffic) increase the risk of myocardial ischemia, coherent with our previous findings for systemic inflammation and blood pressure.  相似文献   

17.

Background

Past time-series studies of the health effects of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] have used chemically nonspecific PM2.5 mass. However, PM2.5 is known to vary in chemical composition with source, and health impacts may vary accordingly.

Objective

We tested the association between source-specific daily PM2.5 mass and hospital admissions in a time-series investigation that considered both single-lag and distributed-lag models.

Methods

Daily PM2.5 speciation measurements collected in midtown Manhattan were analyzed via positive matrix factorization source apportionment. Daily and distributed-lag generalized linear models of Medicare respiratory and cardiovascular hospital admissions during 2001–2002 considered PM2.5 mass and PM2.5 from five sources: transported sulfate, residual oil, traffic, steel metal works, and soil.

Results

Source-related PM2.5 (specifically steel and traffic) was significantly associated with hospital admissions but not with total PM2.5 mass. Steel metal works–related PM2.5 was associated with respiratory admissions for multiple-lag days, especially during the cleanup efforts at the World Trade Center. Traffic-related PM2.5 was consistently associated with same-day cardiovascular admissions across disease-specific subcategories. PM2.5 constituents associated with each source (e.g., elemental carbon with traffic) were likewise associated with admissions in a consistent manner. Mean effects of distributed-lag models were significantly greater than were maximum single-day effect models for both steel- and traffic-related PM2.5.

Conclusions

Past analyses that have considered only PM2.5 mass or only maximum single-day lag effects have likely underestimated PM2.5 health effects by not considering source-specific and distributed-lag effects. Differing lag structures and disease specificity observed for steel-related versus traffic-related PM2.5 raise the possibility of distinct mechanistic pathways of health effects for particles of differing chemical composition.  相似文献   

18.
Background: Epidemiologic studies of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in residential infiltration efficiencies (Finf) will affect epidemiologic study results.Objective: We aimed to develop models to predict Finf for > 6,000 homes in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study of PM2.5 exposure, subclinical cardiovascular disease, and clinical outcomes.Methods: We collected 526 two-week, paired indoor–outdoor PM2.5 filter samples from a subset of study homes. PM2.5 elemental composition was measured by X-ray fluorescence, and Finf was estimated as the indoor/outdoor sulfur ratio. We regressed Finf on meteorologic variables and questionnaire-based predictors in season-specific models. Models were evaluated using the R2 and root mean square error (RMSE) from a 10-fold cross-validation.Results: The mean ± SD Finf across all communities and seasons was 0.62 ± 0.21, and community-specific means ranged from 0.47 ± 0.15 in Winston-Salem, North Carolina, to 0.82 ± 0.14 in New York, New York. Finf was generally greater during the warm (> 18°C) season. Central air conditioning (AC) use, frequency of AC use, and window opening frequency were the most important predictors during the warm season; outdoor temperature and forced-air heat were the best cold-season predictors. The models predicted 60% of the variance in 2-week Finf, with an RMSE of 0.13.Conclusions: We developed intuitive models that can predict Finf using easily obtained variables. Using these models, MESA Air will be the first large epidemiologic study to incorporate variation in residential Finf into an exposure assessment.  相似文献   

19.
Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI).Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI.Results: An interquartile range (IQR) increase in area PM2.5 (0.59 μg/m3) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM2.5 (area + local, 1.05 μg/m3) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11).Conclusions: Residential exposure to PM2.5 may best be represented by a combination of area and local PM2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.  相似文献   

20.
Background: Numerous studies have linked fine particles [≤ 2.5 µm in aerodynamic diameter (PM2.5)] and health. Most studies focused on the total mass of the particles, although the chemical composition of the particles varies substantially. Which chemical components of fine particles that are the most harmful is not well understood, and research on the chemical composition of PM2.5 and the components that are the most harmful is particularly limited in Asia.Objectives: We characterized PM2.5 chemical composition and estimated the effects of cause-specific mortality of PM2.5 mass and constituents in Seoul, Korea. We compared the chemical composition of particles to those of the eastern and western United States.Methods: We examined temporal variability of PM2.5 mass and its composition using hourly data. We applied an overdispersed Poisson generalized linear model, adjusting for time, day of week, temperature, and relative humidity to investigate the association between risk of mortality and PM2.5 mass and its constituents in Seoul, Korea, for August 2008 through October 2009.Results: PM2.5 and chemical components exhibited temporal patterns by time of day and season. The chemical characteristics of Seoul’s PM2.5 were more similar to PM2.5 found in the western United States than in the eastern United States. Seoul’s PM2.5 had lower sulfate (SO4) contributions and higher nitrate (NO3) contributions than that of the eastern United States, although overall PM2.5 levels in Seoul were higher than in the United States. An interquartile range (IQR) increase in magnesium (Mg) (0.05 μg/m3) was associated with a 1.4% increase (95% confidence interval: 0.2%, 2.6%) in total mortality on the following day. Several components that were among the largest contributors to PM2.5 total mass—NO3, SO4, and ammonium (NH4)—were moderately associated with same-day cardiovascular mortality at the p < 0.10 level. Other components with smaller mass contributions [Mg and chlorine (Cl)] exhibited moderate associations with respiratory mortality on the following day (p < 0.10).Conclusions: Our findings link PM2.5 constituents with mortality and have implications for policy making on sources of PM2.5 and on the relevance of PM2.5 health studies from other areas to this region.  相似文献   

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