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      Harmful impact of air pollution on severe acute exacerbation of chronic obstructive pulmonary disease: particulate matter is hazardous

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          Abstract

          Introduction

          Particulate matter and air pollution in Korea are becoming worse. There is a lack of research regarding the impact of particulate matter on patients with COPD. Therefore, the purpose of this study was to investigate the effects of various air pollution factors, including particulate matter, on the incidence rate of severe acute exacerbations of COPD (AECOPD) events.

          Methods

          We analyzed the relationship between air pollutants and AECOPD events that required hospitalization at Guro Hospital in Korea from January 1, 2015 to May 31, 2017. We used general linear models with Poisson distribution and log-transformation to obtain adjusted relative risk (RR). We conducted further analysis through the Comprehensive Air-quality Index (CAI) that is used in Korea.

          Results

          Among various other air pollutants, particulate matter was identified as a major source of air pollution in Korea. When the CAI score was over 50, the incidence rate of severe AECOPD events was statistically significantly higher [RR 1.612, 95% CI, 1.065–2.440, P=0.024]. Additionally, the particulate matter levels 3 days before hospitalization were statistically significant [RR 1.003, 95% CI, 1.001–1.005, P=0.006].

          Conclusion

          Particulate matter and air pollution increase the incidence rate of severe AECOPD events. COPD patients should be cautioned against outdoor activities when particulate matter levels are high.

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          Most cited references 42

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          Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis

          Background Short-term exposure to outdoor fine particulate matter (particles with a median aerodynamic diameter <2.5 μm (PM2.5)) air pollution has been associated with adverse health effects. Existing literature reviews have been limited in size and scope. Methods We conducted a comprehensive, systematic review and meta-analysis of 110 peer-reviewed time series studies indexed in medical databases to May 2011 to assess the evidence for associations between PM2.5 and daily mortality and hospital admissions for a range of diseases and ages. We stratified our analyses by geographical region to determine the consistency of the evidence worldwide and investigated small study bias. Results Based upon 23 estimates for all-cause mortality, a 10 µg/m3 increment in PM2.5 was associated with a 1.04% (95% CI 0.52% to 1.56%) increase in the risk of death. Worldwide, there was substantial regional variation (0.25% to 2.08%). Associations for respiratory causes of death were larger than for cardiovascular causes, 1.51% (1.01% to 2.01%) vs 0.84% (0.41% to 1.28%). Positive associations with mortality for most other causes of death and for cardiovascular and respiratory hospital admissions were also observed. We found evidence for small study bias in single-city mortality studies and in multicity studies of cardiovascular disease. Conclusions The consistency of the evidence for adverse health effects of short-term exposure to PM2.5 across a range of important health outcomes and diseases supports policy measures to control PM2.5 concentrations. However, reasons for heterogeneity in effect estimates in different regions of the world require further investigation. Small study bias should also be considered in assessing and quantifying health risks from PM2.5.
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            Air pollution and markers of coagulation, inflammation, and endothelial function: associations and epigene-environment interactions in an elderly cohort.

            Previous studies suggest that air pollution is related to thrombosis, inflammation, and endothelial dysfunction. Mechanisms and sources of susceptibility are still unclear. One possibility is that these associations can be modified by DNA methylation states. We conducted a cohort study with repeated measurements of fibrinogen, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in 704 elderly men participating in the Veterans Administration Normative Aging Study (2000-2009). We investigated short- and intermediate-term air pollution effects on these blood markers, and epigene-environment interactions by DNA methylation of Alu, LINE-1, tissue factor (F3), Toll-like receptor 2 (TLR-2), and ICAM-1. We found effects of particle number, black carbon, nitrogen dioxide (NO(2)), and carbon monoxide (CO) on fibrinogen. Ozone was a predictor of C-reactive protein and ICAM-1. Particle number, black carbon, NO(2), CO, PM(2.5), and sulfates were associated with ICAM-1 and VCAM-1. An interquartile range increase in 24-hour exposure for NO(2) was associated with a 1.7% (95% confidence interval = 0.2%-3.3%) increase in fibrinogen for ozone; a 10.8% (2.2%-20.0%) increase in C-reactive protein for particle number; a 5.9% (3.6%-8.3%) increase in ICAM-1; and for PM(2.5), a 3.7% (1.7%-5.8%) increase in VCAM-1. The air pollution effect was stronger among subjects having higher Alu, lower LINE-1, tissue factor, or TLR-2 methylation status. We observed associations of traffic-related pollutants on fibrinogen, and both traffic and secondary particles on C-reactive protein, ICAM-1, and VCAM-1. There was effect modification by DNA methylation status, indicating that epigenetic states can convey susceptibility to air pollution.
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              Spatial and temporal variations of six criteria air pollutants in 31 provincial capital cities in China during 2013-2014.

              Long-term air pollution data with high temporal and spatial resolutions are needed to support the research of physical and chemical processes that affect the air quality, and the corresponding health risks. However, such datasets were not available in China until recently. For the first time, this study examines the spatial and temporal variations of PM2.5, PM10, CO, SO2, NO2, and 8 h O3 in 31 capital cities in China between March 2013 and February 2014 using hourly data released by the Ministry of Environmental Protection (MEP) of China. The annual mean concentrations of PM2.5 and PM10 exceeded the Chinese Ambient Air Quality Standards (CAAQS), Grade I standards (15 and 40 μg/m(3) for PM2.5 and PM10, respectively) for all cities, and only Haikou, Fuzhou and Lasa met the CAAQS Grade II standards (35 and 70 μg/m(3) for PM2.5 and PM10, respectively). Observed PM2.5, PM10, CO and SO2 concentrations were higher in cities located in the North region than those in the West and the South-East regions. The number of non-attainment days was highest in the winter, but high pollution days were also frequently observed in the South-East region during the fall and in the West region during the spring. PM2.5 was the largest contributor to the air pollution in China based on the number of non-attainment days, followed by PM10, and O3. Strong correlation was found between different pollutants except for O3. These results suggest great impacts of coal combustion and biomass burning in the winter, long range transport of windblown dust in the spring, and secondary aerosol formation throughout the year. Current air pollution in China is caused by multiple pollutants, with great variations among different regions and different seasons. Future studies should focus on improving the understanding of the associations between air quality and meteorological conditions, variations of emissions in different regions, and transport and transformation of pollutants in both intra- and inter-regional contexts.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2018
                28 March 2018
                : 13
                : 1053-1059
                Affiliations
                Division of Respiratory, Allergy and Critical Care Medicine, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Republic of Korea
                Author notes
                Correspondence: Jae Jeong Shim, Division of Respiratory and Critical Care Medicine, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, 148 Gurodong-ro, Guro-gu, Seoul 08308, Republic of Korea, Tel +82 2 2626 1029, Fax +82 2 2626 1166, Email jaejshim@ 123456kumc.or.kr
                Article
                copd-13-1053
                10.2147/COPD.S156617
                5881527
                © 2018 Choi et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Respiratory medicine

                air pollution, particulate matter, air quality index, acute exacerbation, copd

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