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      Mortality Risk and Fine Particulate Air Pollution in a Large, Representative Cohort of U.S. Adults

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          Abstract

          Background:

          Evidence indicates that air pollution contributes to cardiopulmonary mortality. There is ongoing debate regarding the size and shape of the pollution–mortality exposure–response relationship. There are also growing appeals for estimates of pollution–mortality relationships that use public data and are based on large, representative study cohorts.

          Objectives:

          Our goal was to evaluate fine particulate matter air pollution ( PM 2.5 ) and mortality using a large cohort that is representative of the U.S. population and is based on public data. Additional objectives included exploring model sensitivity, evaluating relative effects across selected subgroups, and assessing the shape of the PM 2.5 –mortality relationship.

          Methods:

          National Health Interview Surveys (1986–2014), with mortality linkage through 2015, were used to create a cohort of 1,599,329 U.S. adults and a subcohort with information on smoking and body mass index (BMI) of 635,539 adults. Data were linked with modeled ambient PM 2.5 at the census-tract level. Cox proportional hazards models were used to estimate PM 2.5 –mortality hazard ratios for all-cause and specific causes of death while controlling for individual risk factors and regional and urban versus rural differences. Sensitivity and subgroup analyses were conducted and the shape of the PM 2.5 –mortality relationship was explored.

          Results:

          Estimated mortality hazard ratios, per 10 μ g / m 3 long-term exposure to PM 2.5 , were 1.12 (95% CI: 1.08, 1.15) for all-cause mortality, 1.23 (95% CI: 1.17, 1.29) for cardiopulmonary mortality, and 1.12 (95% CI: 1.00, 1.26) for lung cancer mortality. In general, PM 2.5 –mortality associations were consistently positive for all-cause and cardiopulmonary mortality across key modeling choices and across subgroups of sex, age, race-ethnicity, income, education levels, and geographic regions.

          Discussion:

          This large, nationwide, representative cohort of U.S. adults provides robust evidence that long-term PM 2.5 exposure contributes to cardiopulmonary mortality risk. The ubiquitous and involuntary nature of exposures and the broadly observed effects across subpopulations underscore the public health importance of breathing clean air. https://doi.org/10.1289/EHP4438

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          Most cited references23

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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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            Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project

            Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. European Community's Seventh Framework Program (FP7/2007-2011). Copyright © 2014 Elsevier Ltd. All rights reserved.
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              Is Open Access

              Outdoor Particulate Matter Exposure and Lung Cancer: A Systematic Review and Meta-Analysis

              Background: Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on the evidence regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence. Objective: Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer. Methods: We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10-μg/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates. Results: The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers [1.44 (95% CI: 1.04, 1.22)], followed by never-smokers [1.18 (95% CI: 1.00, 1.39)], and then current smokers [1.06 (95% CI: 0.97, 1.15)]. In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively. Conclusion: The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources. Citation: Hamra GB, Guha N, Cohen A, Laden F, Raaschou-Nielsen O, Samet JM, Vineis P, Forastiere F, Saldiva P, Yorifuji T, Loomis D. 2014. Outdoor particulate matter exposure and lung cancer: a systematic review and meta-analysis. Environ Health Perspect 122:906–911; http://dx.doi.org/10.1289/ehp.1408092
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                Author and article information

                Journal
                Environ Health Perspect
                Environ. Health Perspect
                EHP
                Environmental Health Perspectives
                Environmental Health Perspectives
                0091-6765
                1552-9924
                24 July 2019
                July 2019
                : 127
                : 7
                : 077007
                Affiliations
                [1 ]Department of Economics, Brigham Young University , Provo, Utah, USA
                [2 ]MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London , London, UK
                [3 ]Department of Civil and Environmental Engineering, University of Washington , Seattle, Washington, USA
                [4 ]Department of Cancer Control and Population Health, Graduate School of Cancer Science and Policy, National Cancer Center , Goyang-si, Gyeonggi-do, Korea
                [5 ]Center for the Economics of Human Development, University of Chicago , Chicago, Illinois, USA
                [6 ]Cornerstone Research , San Francisco, California, USA
                [7 ]Department of Mechanical Engineering, Carnegie Mellon University , Pittsburgh, Pennsylvania, USA
                [8 ]Health Canada , Ottawa, Ontario, Canada
                Author notes
                Address correspondence to C. Arden Pope III, 142 FOB, Brigham Young University, Provo, UT 84602 USA. Telephone: (801) 422-2157. Email: cap3@ 123456byu.edu
                Article
                EHP4438
                10.1289/EHP4438
                6792459
                31339350
                3c088195-cdf8-43da-9fbd-b504556d43a4

                EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted.

                History
                : 06 September 2018
                : 09 May 2019
                : 22 May 2019
                : 27 September 2019
                Categories
                Research

                Public health
                Public health

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