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      Long-term exposure to PM 10 and NO 2 in relation to lung function and imaging phenotypes in a COPD cohort

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          Abstract

          Background

          Ambient air pollution can contribute to the development and exacerbation of COPD. However, the influence of air pollution on objective COPD phenotypes, especially from imaging, is not well studied. We investigated the influence of long-term exposure to air pollution on lung function and quantitative imaging measurements in a Korean cohort of participants with and without COPD diagnosis.

          Methods

          Study participants ( N = 457 including 296 COPD cases) were obtained from the COPD in Dusty Areas (CODA) cohort. Annual average concentrations of particulate matter less than or equal to 10 μm in diameter (PM 10) and nitrogen dioxide (NO 2) were estimated at the participants’ residential addresses using a spatial air pollution prediction model. All the participants underwent volumetric computerized tomography (CT) and spirometry measurements and completed survey questionnaires. We examined the associations of PM 10 and NO 2 with FVC, FEV 1, emphysema index, and wall area percent, using linear regression models adjusting for age, gender, education, smoking, height, weight, and COPD medication.

          Results

          The age of study participants averaged 71.7 years. An interquartile range difference in annual PM 10 exposure of 4.4 μg/m 3 was associated with 0.13 L lower FVC (95% confidence interval (CI), − 0.22- -0.05, p = 0.003). Emphysema index (mean = 6.36) was higher by 1.13 (95% CI, 0.25–2.02, p = 0.012) and wall area percent (mean = 68.8) was higher by 1.04 (95% CI, 0.27–1.80, p = 0.008). Associations with imaging phenotypes  were not observed with NO 2.

          Conclusions

          Long-term exposure to PM 10 correlated with both lung function and COPD-relevant imaging phenotypes in a Korean cohort.

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          Most cited references37

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          An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease.

          Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.
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            Fine Particulate Air Pollution and Daily Mortality. A Nationwide Analysis in 272 Chinese Cities.

            Evidence concerning the acute health effects of air pollution caused by fine particulate matter (PM2.5) in developing countries is quite limited.
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              A joint ERS/ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework

              The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution.
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                Author and article information

                Contributors
                kamelon@hanmail.net
                seokhohong1972@gmail.com
                youngji@kangwon.ac.kr
                arsgnm17@gmail.com
                jhkimd29@gmail.com
                mikyeong.lee@nih.gov
                london2@niehs.nih.gov
                pulmo2@kangwon.ac.kr
                sykim@ncc.re.kr
                Journal
                Respir Res
                Respir. Res
                Respiratory Research
                BioMed Central (London )
                1465-9921
                1465-993X
                23 September 2020
                23 September 2020
                2020
                : 21
                : 247
                Affiliations
                [1 ]GRID grid.412011.7, ISNI 0000 0004 1803 0072, Biomedical Research Institutue, , Kangwon National University Hospital, ; Chuncheon, South Korea
                [2 ]GRID grid.412010.6, ISNI 0000 0001 0707 9039, Department of Internal Medicine and Environemntal Health Center, , Kangwon National University, ; Chuncheon, South Korea
                [3 ]GRID grid.412010.6, ISNI 0000 0001 0707 9039, Department of Environmental Science, , Kangwon National University, ; Chuncheon, South Korea
                [4 ]GRID grid.412010.6, ISNI 0000 0001 0707 9039, Department of Radiology, School of Medicine, , Kangwon National University, ; Chuncheon, South Korea
                [5 ]GRID grid.415619.e, ISNI 0000 0004 1773 6903, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, , National Medical Center, ; Seoul, South Korea
                [6 ]National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC USA
                [7 ]GRID grid.410914.9, ISNI 0000 0004 0628 9810, Department of Cancer Control and Population Health, , Graduate School of Cancer Science and Policy, National Cancer Center, ; Goyang-si, Gyeonggi-do South Korea
                Author information
                http://orcid.org/0000-0003-2927-370X
                Article
                1514
                10.1186/s12931-020-01514-w
                7513297
                32967681
                a2d83dba-89c0-4e7f-b012-8c08aa06b910
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 24 November 2019
                : 17 September 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100003725, National Research Foundation of Korea;
                Award ID: 2017R1A2B4003790, 2018R1A2B6004608
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000066, National Institute of Environmental Health Sciences;
                Award ID: ZO1 ES043012
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2020

                Respiratory medicine
                air pollution,copd,ct,lung function,traffic
                Respiratory medicine
                air pollution, copd, ct, lung function, traffic

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