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      Long-term air pollution exposure and cardio- respiratory mortality: a review

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          Abstract

          Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO 2) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric.

          There is a significant number of new studies on long-term air pollution exposure, covering a wider geographic area, including Asia. These recent studies support associations found in previous cohort studies on PM 2.5. The pooled effect estimate expressed as excess risk per 10 μg/m 3 increase in PM 2.5 exposure was 6% (95% CI 4, 8%) for all-cause and 11% (95% CI 5, 16%) for cardiovascular mortality. Long-term exposure to PM 2.5 was more associated with mortality from cardiovascular disease (particularly ischemic heart disease) than from non-malignant respiratory diseases (pooled estimate 3% (95% CI −6, 13%)). Significant heterogeneity in PM 2.5 effect estimates was found across studies, likely related to differences in particle composition, infiltration of particles indoors, population characteristics and methodological differences in exposure assessment and confounder control. All-cause mortality was significantly associated with elemental carbon (pooled estimate per 1 μg/m 3 6% (95% CI 5, 7%)) and NO 2 (pooled estimate per 10 μg/m 3 5% (95% CI 3, 8%)), both markers of combustion sources. There was little evidence for an association between long term coarse particulate matter exposure and mortality, possibly due to the small number of studies and limitations in exposure assessment. Across studies, there was little evidence for a stronger association among women compared to men. In subjects with lower education and obese subjects a larger effect estimate for mortality related to fine PM was found, though the evidence for differences related to education has been weakened in more recent studies.

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          Most cited references63

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          Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

          Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
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            Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults.

            Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.
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              Association of fine particulate matter from different sources with daily mortality in six U.S. cities.

              Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
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                Author and article information

                Journal
                Environ Health
                Environ Health
                Environmental Health
                BioMed Central
                1476-069X
                2013
                28 May 2013
                : 12
                : 43
                Affiliations
                [1 ]Institute of Risk Assessment Sciences, University of Utrecht, Utrecht, The Netherlands
                [2 ]University of Washington, Seattle, WA, USA
                [3 ]Institute of Epidemiology II, Helmholtz Zentrum München –German Research Center for Environmental Health, Neuherberg, Germany
                [4 ]Air Pollution Epidemiology Section, Office of Environmental Health Hazard Assessment, State of California, Oakland, CA, USA
                [5 ]Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands
                Article
                1476-069X-12-43
                10.1186/1476-069X-12-43
                3679821
                23714370
                834b8ecf-7783-4369-8cf6-23566a29146c
                Copyright ©2013 Hoek et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 December 2012
                : 2 April 2013
                Categories
                Review

                Public health
                air pollution,mortality,motorized traffic,cardiovascular,respiratory,particles
                Public health
                air pollution, mortality, motorized traffic, cardiovascular, respiratory, particles

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