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Background: Few studies have examined the relationship between long-term exposure to ambient fine particulate matter (PM2.5) and nonaccidental mortality in rural populations.Objective: We examined the relationship between PM2.5 and nonaccidental and cardiovascular mortality in the U.S. Agricultural Health Study cohort.Methods: The cohort (n = 83,378) included farmers, their spouses, and commercial pesticide applicators residing primarily in Iowa and North Carolina. Deaths occurring between enrollment (1993–1997) and 30 December 2009 were identified by record linkage. Six-year average (2001–2006) remote-sensing derived estimates of PM2.5 were assigned to participants’ residences at enrollment, and Cox proportional hazards models were used to estimate hazard ratios (HR) in relation to a 10-μg/m3 increase in PM2.5 adjusted for individual-level covariates.Results: In total, 5,931 nonaccidental and 1,967 cardiovascular deaths occurred over a median follow-up time of 13.9 years. PM2.5 was not associated with nonaccidental mortality in the cohort as a whole (HR = 0.95; 95% CI: 0.76, 1.20), but consistent inverse relationships were observed among women. Positive associations were observed between ambient PM2.5 and cardiovascular mortality among men, and these associations were strongest among men who did not move from their enrollment address (HR = 1.63; 95% 0.94, 2.84). In particular, cardiovascular mortality risk in men was significantly increased when analyses were limited to nonmoving participants with the most precise exposure geocoding (HR = 1.87; 95% CI: 1.04, 3.36).Conclusions: Rural PM2.5 may be associated with cardiovascular mortality in men; however, similar associations were not observed among women. Further evaluation is required to explore these sex differences.Citation: Weichenthal S, Villeneuve PJ, Burnett RT, van Donkelaar A, Martin RV, Jones RR, DellaValle CT, Sandler DP, Ward MH, Hoppin JA. 2014. Long-term exposure to fine particulate matter: association with nonaccidental and cardiovascular mortality in the Agricultural Health Study Cohort. Environ Health Perspect 122:609–615; http://dx.doi.org/10.1289/ehp.1307277  相似文献   

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Background

Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.

Methods

We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] exposure based on a small-scale dispersion and chemistry transport model was assigned to each home address. We calculated distances between residences and major roads. Long-term exposure to air pollution (annual PM2.5 and distance to high traffic) and concentration of inflammatory markers [high-sensitivity C-reactive protein (hs-CRP) and fibrinogen] on the day of the baseline visit were analyzed with sex-stratified multiple linear regression, controlling for individual-level risk factors.

Results

In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m3 in PM2.5 (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.

Conclusions

Our study indicates that long-term residential exposure to high levels of PM2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.  相似文献   

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Background: Experimental evidence and studies of children and adolescents suggest that ambient fine particulate matter [particulate matter 2.5μm in aerodynamic diameter (PM2.5)] air pollution may be obesogenic, but the relationship between PM2.5 and the risk of body weight gain and obesity in adults is uncertain.Objectives: Our goal was to characterize the association between PM2.5 and the risks of weight gain and obesity.Methods: We followed 3,902,440 U.S. Veterans from 2010 to 2018 (median 8.1 y, interquartile range: 7.3–8.4) and assigned time-updated PM2.5 exposures by linking geocoded residential street addresses with satellite-based estimates of surface-level PM2.5 mass (at 1-km2 resolution). Associations with PM2.5 were estimated using Cox proportional hazards models for incident obesity [body mass index (BMI)30kg/m2] and a 10-lb increase in weight relative to baseline and linear mixed models for associations with intra-individual changes in BMI and weight.Results: A 10-μg/m3 higher average annual PM2.5 concentration was associated with risk of incident obesity [n=2,325,769; hazard ratio (HR)=1.08 (95% CI: 1.06, 1.11)] and the risk of a 10-lb (4.54kg) increase in weight [HR=1.07 (95% CI: 1.06, 1.08)] and with higher intra-individual changes in BMI [0.140kg/m2 per year (95% CI: 0.139, 0.142)] and weight [0.968 lb/y (95% CI: 0.955, 0.981)]. Nonlinear exposure–response models indicated associations at PM2.5 concentrations below the national standard of 12μg/m3. As expected, a negative exposure control (ambient air sodium) was not associated with obesity or weight gain. Associations were consistent in direction and magnitude across sensitivity analyses that included alternative outcomes and exposures assigned at different spatial resolutions.Discussion: PM2.5 air pollution was associated with the risk of obesity and weight gain in a large predominantly male cohort of U.S. Veterans. Discussions about health effects of PM2.5 should include its association with obesity, and deliberations about the epidemiology of obesity should consider its association with PM2.5. Investigation in other cohorts will deepen our understanding of the relationship between PM2.5 and weight gain and obesity. https://doi.org/10.1289/EHP7944  相似文献   

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Atmospheric particulate matter (PM) was measured concurrently from September, 2012, to June, 2013, at two sites, urban and industrial suburban, in Tabriz, Iran. The annual average concentration of total suspended particulates (TSP), PM10, PM2.5, and PM1 at the urban site were 142.2 ± 76.3, 85.3 ± 43.9, 39 ± 19.1, and 28.4 ± 14.9 µg/m3 (mean ± SD), respectively. A total of 11 inorganic water-soluble ions in the TSP and PM10 were identified by ion chromatography. In the urban site, concentrations of total water-soluble ions in TSP and PM10 were 20.3 ± 20.8 and 16.0 ± 14.1 µg/m3, respectively. In this sampling site, secondary inorganic aerosols (i.e., Σ $ {\text{SO}}_{4}^{2 - } $ , $ {\text{NO}}_{3}^{ - } $ , and $ {\text{NH}}_{4}^{ + } $ concentrations) were the main measured water-soluble ions, which collectively accounted for 13.9 % of TSP mass and 17.7 % of PM10 mass. Correlations between $ {\text{NH}}_{4}^{ + } $ with $ {\text{NO}}_{3}^{ - } $ and $ {\text{SO}}_{4}^{2 - } $ indicated that the main source of these ions in PM was the combustion processes. Results of elemental analysis in the industrial suburban site showed that natural sources were the dominant source of PM in this area.  相似文献   

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大气颗粒物污染与人群死亡率变化流行病学研究进展   总被引:3,自引:0,他引:3  
大气污染已成为影响人类健康的主要危害因素之一。 1997年世界卫生组织 (WHO)和美国哈佛大学曾经评估了各种主要环境危险因素的全球疾病负担 ,发现全球由于大气污染而造成的失能调整生命年 (DALY)损失占其全部损失的 0 5 % ,我国则占 0 4% [1] 。而在大气污染相关的各种健康效应终点中 ,死亡是其中最显著的健康效应 ,在美国环保局 (EPA)定量评价的与大气污染有关的健康效应终点中 ,由死亡引起的经济损失可占全部损失的 89% [2 ] 。因此 ,近年来大气颗粒物 (PM)污染与人群死亡变化的关系已成为国际环境流行病学研究的热点之一 …  相似文献   

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大气细颗粒物污染与居民每日死亡关系的Meta分析   总被引:10,自引:1,他引:10  
目的综合分析国内外大气细颗粒物(PM2.5)短期暴露与人群死亡关系的流行病学资料,以获取大气PM2.5-居民死亡的暴露-反应关系。方法在联机检索文献的基础上,对多篇文献的综合评价采用Meta分析的方法进行,定量确定PM2.5居民每日死亡的暴露-反应关系。结果建立了居民短期接触大气PM2.5污染的暴露-反应关系,即大气PM2.5浓度每升高100μg/m^3,居民死亡发生增加的百分比为12.07%(95%可信区间:8.31%-15.82%)。结论本研究建立的暴露-反应关系,可用于我国及各城市大气细颗粒物污染的健康危险度评价工作。  相似文献   

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颗粒物污染空气,影响青少年肺功能的发育、新生婴儿的体质量、神经元功能、增加人群死亡率,其机理主要是通过炎性反应因子的激活,产生炎症前期反应和变态反应。空气颗粒物污染对人体的危害正受到人们的重视。海云可清除空气中部分颗粒物,但目前防止空气颗粒物污染的措施主要是控制颗粒物进入大气,人们减少到有严重颗粒物污染的场所。  相似文献   

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大气颗粒物健康效应生物学机制研究进展   总被引:10,自引:1,他引:10  
大量流行病学研究发现,大气颗粒物的污染水平与心肺系统疾病的超额发病、死亡存在密切关联,但其毒理学机制尚未阐明。本文对近年来大气颗粒物毒理学研究进行综述,包括大气颗粒物对呼吸系统、心血管系统及神经系统的毒性作用,并对氧化应激损伤、细胞钙稳态失衡及激活关键转录因子等分子毒理学机制进行了初步的阐述。  相似文献   

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Background: Few European studies have investigated the effects of long-term exposure to both fine particulate matter (≤ 2.5 µm; PM2.5) and nitrogen dioxide (NO2) on mortality.Objectives: We studied the association of exposure to NO2, PM2.5, and traffic indicators on cause-specific mortality to evaluate the form of the concentration–response relationship.Methods: We analyzed a population-based cohort enrolled at the 2001 Italian census with 9 years of follow-up. We selected all 1,265,058 subjects ≥ 30 years of age who had been living in Rome for at least 5 years at baseline. Residential exposures included annual NO2 (from a land use regression model) and annual PM2.5 (from a Eulerian dispersion model), as well as distance to roads with > 10,000 vehicles/day and traffic intensity. We used Cox regression models to estimate associations with cause-specific mortality adjusted for individual (sex, age, place of birth, residential history, marital status, education, occupation) and area (socioeconomic status, clustering) characteristics.Results: Long-term exposures to both NO2 and PM2.5 were associated with an increase in nonaccidental mortality [hazard ratio (HR) = 1.03 (95% CI: 1.02, 1.03) per 10-µg/m3 NO2; HR = 1.04 (95% CI: 1.03, 1.05) per 10-µg/m3 PM2.5]. The strongest association was found for ischemic heart diseases (IHD) [HR = 1.10 (95% CI: 1.06, 1.13) per 10-µg/m3 PM2.5], followed by cardiovascular diseases and lung cancer. The only association showing some deviation from linearity was that between NO2 and IHD. In a bi-pollutant model, the estimated effect of NO2 on mortality was independent of PM2.5.Conclusions: This large study strongly supports an effect of long-term exposure to NO2 and PM2.5 on mortality, especially from cardiovascular causes. The results are relevant for the next European policy decisions regarding air quality.  相似文献   

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Background: Fine particulate matter (PM) air pollution is associated with numerous adverse health effects, including increased blood pressure (BP) and vascular dysfunction. Coarse PM substantially contributes to global air pollution, yet differs in characteristics from fine particles and is currently not regulated. However, the cardiovascular (CV) impacts of coarse PM exposure remain largely unknown.Objectives: Our goal was to elucidate whether coarse PM, like fine PM, is itself capable of eliciting adverse CV responses.Methods: We performed a randomized double-blind crossover study in which 32 healthy adults (25.9 ± 6.6 years of age) were exposed to concentrated ambient coarse particles (CAP; 76.2 ± 51.5 μg/m3) in a rural location and filtered air (FA) for 2 hr. We measured CV outcomes during, immediately after, and 2 hr postexposures.Results: Both systolic (mean difference = 0.32 mmHg; 95% CI: 0.05, 0.58; p = 0.021) and diastolic BP (0.27 mmHg; 95% CI: 0.003, 0.53; p = 0.05) linearly increased per 10 min of exposure during the inhalation of coarse CAP when compared with changes during FA exposure. Heart rate was on average higher (4.1 bpm; 95% CI: 3.06, 5.12; p < 0.0001) and the ratio of low-to-high frequency heart rate variability increased (0.24; 95% CI: 0.07, 0.41; p = 0.007) during coarse particle versus FA exposure. Other outcomes (brachial flow-mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wave velocity) were not differentially altered by the exposures.Conclusions: Inhalation of coarse PM from a rural location is associated with a rapid elevation in BP and heart rate during exposure, likely due to the triggering of autonomic imbalance. These findings add mechanistic evidence supporting the biological plausibility that coarse particles could contribute to the triggering of acute CV events.Citation: Brook RD, Bard RL, Morishita M, Dvonch JT, Wang L, Yang HY, Spino C, Mukherjee B, Kaplan MJ, Yalavarthi S, Oral EA, Ajluni N, Sun Q, Brook JR, Harkema J, Rajagopalan S. 2014. Hemodynamic, autonomic, and vascular effects of exposure to coarse particulate matter air pollution from a rural location. Environ Health Perspect 122:624–630; http://dx.doi.org/10.1289/ehp.1306595  相似文献   

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我国大气污染与儿童呼吸系统疾病和症状的关系   总被引:2,自引:0,他引:2  
目的 描述我国主要大气污染物水平与儿童呼吸系统疾病和症状报告率的关系.方法 收集国内外1980至2008年公开发表的关于我国大气污染物与儿童呼吸系统疾病和症状关系的文献,最终有12篇文献人选.采用单因素线性回归和Pearson相关分析的方法分析我国主要大气污染物(TSP,PM10,PM2.5,SO2和NOx)与儿童呼吸系统疾病和症状(咳嗽、持续咳嗽、咯痰、持续咯痰、哮喘、喘呜、支气管炎和肺炎)的关系.结果 研究地区大气中颗粒物(TSP,PM10,PM2.5)的浓度与儿童呼吸系统疾病和症状报告率之间有很强的正相关关系;其中TSP浓度与儿童咳嗽、持续咳嗽、咯痰、持续咯痰和支气管炎的报告率呈明显的正相关关系,TSP浓度每增加10 μg/m3,以上疾病和症状的报告率分别增加0.50%,0.12%,0.43%,0.09%,0.51%;PM10浓度每增加10μg/m3,儿童咳嗽、咯痰以及支气管炎的报告率分别增加2.64%,2.27%和2.17%;PM2.5浓度每增加10μg/m3,儿童咳嗽、咯痰和支气管炎的报告率分别增加4.56%,3.49%和3.74%.大气中SO2浓度与喘鸣的相关关系较明显,SO2浓度每增加10μg/m3,儿童喘鸣的报告率增加0.55%;在大气中SO2浓度低于0.15mg/m,的地区,SO2浓度与儿童咳嗽和咯痰报告率的相关关系较明显,SO2浓度每增加10μg/m3,以上症状的报告率分别增加1.65%,1.50%.在NOx浓度低于0.10 mg/m3的地区,NOx浓度与儿童持续咳嗽、持续咯痰和支气管炎的报告率之间有较强的相关关系,NOx浓度每增加10μg/m3,以上疾病和症状的报告率分别增加0.86%,0.51%,3.21%.此外,北方地区大气污染物与儿童呼吸系统疾病和症状的报告率之间相关关系更显著.结论 我国大气污染物浓度是儿童呼吸系统疾病和症状的危险因素,并且北方地区大气污染物对儿童呼吸系统疾病和症状的影响更大.  相似文献   

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Background

Physical activity reduces, whereas exposure to air pollution increases, the risk of premature mortality. Physical activity amplifies respiratory uptake and deposition of air pollutants in the lung, which may augment acute harmful effects of air pollution during exercise.

Objectives

We aimed to examine whether benefits of physical activity on mortality are moderated by long-term exposure to high air pollution levels in an urban setting.

Methods

A total of 52,061 subjects (50–65 years of age) from the Danish Diet, Cancer, and Health cohort, living in Aarhus and Copenhagen, reported data on physical activity in 1993–1997 and were followed until 2010. High exposure to air pollution was defined as the upper 25th percentile of modeled nitrogen dioxide (NO2) levels at residential addresses. We associated participation in sports, cycling, gardening, and walking with total and cause-specific mortality by Cox regression, and introduced NO2 as an interaction term.

Results

In total, 5,534 subjects died: 2,864 from cancer, 1,285 from cardiovascular disease, 354 from respiratory disease, and 122 from diabetes. Significant inverse associations of participation in sports, cycling, and gardening with total, cardiovascular, and diabetes mortality were not modified by NO2. Reductions in respiratory mortality associated with cycling and gardening were more pronounced among participants with moderate/low NO2 [hazard ratio (HR) = 0.55; 95% CI: 0.42, 0.72 and 0.55; 95% CI: 0.41, 0.73, respectively] than with high NO2 exposure (HR = 0.77; 95% CI: 0.54, 1.11 and HR = 0.81; 95% CI: 0.55, 1.18, p-interaction = 0.09 and 0.02, respectively).

Conclusions

In general, exposure to high levels of traffic-related air pollution did not modify associations, indicating beneficial effects of physical activity on mortality. These novel findings require replication in other study populations.

Citation

Andersen ZJ, de Nazelle A, Mendez MA, Garcia-Aymerich J, Hertel O, Tjønneland A, Overvad K, Raaschou-Nielsen O, Nieuwenhuijsen MJ. 2015. A study of the combined effects of physical activity and air pollution on mortality in elderly urban residents: the Danish Diet, Cancer, and Health cohort. Environ Health Perspect 123:557–563; http://dx.doi.org/10.1289/ehp.1408698  相似文献   

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