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      Differential toxicities of fine particulate matters from various sources

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          Abstract

          Fine particulate matters less than 2.5 µm (PM 2.5) in the ambient atmosphere are strongly associated with adverse health effects. However, it is unlikely that all fine particles are equally toxic in view of their different sizes and chemical components. Toxicity of fine particles produced from various combustion sources (diesel engine, gasoline engine, biomass burning (rice straw and pine stem burning), and coal combustion) and non-combustion sources (road dust including sea spray aerosols, ammonium sulfate, ammonium nitrate, and secondary organic aerosols (SOA)), which are known major sources of PM 2.5, was determined. Multiple biological and chemical endpoints were integrated for various source-specific aerosols to derive toxicity scores for particles originating from different sources. The highest toxicity score was obtained for diesel engine exhaust particles, followed by gasoline engine exhaust particles, biomass burning particles, coal combustion particles, and road dust, suggesting that traffic plays the most critical role in enhancing the toxic effects of fine particles. The toxicity ranking of fine particles produced from various sources can be used to better understand the adverse health effects caused by different fine particle types in the ambient atmosphere, and to provide practical management of fine particles beyond what can be achieved only using PM mass which is the current regulation standard.

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          The contribution of outdoor air pollution sources to premature mortality on a global scale.

          Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.
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            A simple technique for quantitation of low levels of DNA damage in individual cells

            Human lymphocytes were either exposed to X-irradiation (25 to 200 rads) or treated with H2O2 (9.1 to 291 microM) at 4 degrees C and the extent of DNA migration was measured using a single-cell microgel electrophoresis technique under alkaline conditions. Both agents induced a significant increase in DNA migration, beginning at the lowest dose evaluated. Migration patterns were relatively homogeneous among cells exposed to X-rays but heterogeneous among cells treated with H2O2. An analysis of repair kinetics following exposure to 200 rads X-rays was conducted with lymphocytes obtained from three individuals. The bulk of the DNA repair occurred within the first 15 min, while all of the repair was essentially complete by 120 min after exposure. However, some cells demonstrated no repair during this incubation period while other cells demonstrated DNA migration patterns indicative of more damage than that induced by the initial irradiation with X-rays. This technique appears to be sensitive and useful for detecting damage and repair in single cells.
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              An association between air pollution and mortality in six U.S. cities.

              Recent studies have reported associations between particulate air pollution and daily mortality rates. Population-based, cross-sectional studies of metropolitan areas in the United States have also found associations between particulate air pollution and annual mortality rates, but these studies have been criticized, in part because they did not directly control for cigarette smoking and other health risks. In this prospective cohort study, we estimated the effects of air pollution on mortality, while controlling for individual risk factors. Survival analysis, including Cox proportional-hazards regression modeling, was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities. Mortality rates were most strongly associated with cigarette smoking. After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 (95 percent confidence interval, 1.08 to 1.47). Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together. Mortality was most strongly associated with air pollution with fine particulates, including sulfates. Although the effects of other, unmeasured risk factors cannot be excluded with certainty, these results suggest that fine-particulate air pollution, or a more complex pollution mixture associated with fine particulate matter, contributes to excess mortality in certain U.S. cities.
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                Author and article information

                Contributors
                kpark@gist.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                19 November 2018
                19 November 2018
                2018
                : 8
                : 17007
                Affiliations
                [1 ]ISNI 0000 0001 1033 9831, GRID grid.61221.36, School of Earth Sciences and Environmental Engineering, , Gwangju Institute of Science and Technology (GIST), ; Gwangju, Republic of Korea
                [2 ]ISNI 0000 0004 0647 2631, GRID grid.443830.8, Department of Environmental Engineering, , Anyang University, ; Anyang, Republic of Korea
                [3 ]ISNI 0000 0004 1936 8091, GRID grid.15276.37, Department of Environmental and Global Health, , University of Florida, ; Gainesville, FL USA
                [4 ]ISNI 0000 0000 9611 0917, GRID grid.254229.a, Department of Industrial Plant Science & Technology, , Chungbuk National University, ; Cheongju, Republic of Korea
                [5 ]ISNI 0000 0004 0632 5092, GRID grid.497803.1, R&D Headquarter, KT&G, ; Daejeon, Republic of Korea
                [6 ]ISNI 0000 0001 2181 989X, GRID grid.264381.a, School of Pharmacy, , Sungkyunkwan University, ; Suwon, Republic of Korea
                [7 ]ISNI 0000 0004 0647 2973, GRID grid.256155.0, Department of Preventive Medicine, , Gachon University Graduate School of Medicine, ; Incheon, Republic of Korea
                [8 ]ISNI 0000 0000 9628 9654, GRID grid.411815.8, Department of Environmental Engineering, , Mokpo National University, ; Muan, Republic of Korea
                [9 ]ISNI 0000 0001 2171 7754, GRID grid.255649.9, Department of Environmental Science and Engineering, , Ewha Womans University, ; Seoul, Republic of Korea
                Author information
                http://orcid.org/0000-0001-8378-1954
                http://orcid.org/0000-0003-3228-8179
                Article
                35398
                10.1038/s41598-018-35398-0
                6242998
                30451941
                4da72853-a39d-4eac-b4e8-f9ba502be479
                © The Author(s) 2018

                Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 25 June 2018
                : 5 November 2018
                Funding
                Funded by: National Leading Research Laboratory program (NRF-2016R1A2A1A05005532) and the PM2.5 research consortium (NRF-2014M3C8A5028593 and NRF-2017M3D8A1092220), both funded by the Ministry of Science and ICT (MSIT) and the National Research Foundation (NRF) of Korea
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