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      In Vitro and In Vivo Experimental Studies of PM 2.5 on Disease Progression

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          Abstract

          Air pollution is a very critical issue worldwide, particularly in developing countries. Particulate matter (PM) is a type of air pollution that comprises a heterogeneous mixture of different particle sizes and chemical compositions. There are various sources of fine PM (PM 2.5), and the components may also have different effects on people. The pathogenesis of PM 2.5 in several diseases remains to be clarified. There is a long history of epidemiological research on PM 2.5 in several diseases. Numerous studies show that PM 2.5 can induce a variety of chronic diseases, such as respiratory system damage, cardiovascular dysfunction, and diabetes mellitus. However, the epidemiological evidence associated with potential mechanisms in the progression of diseases need to be proved precisely through in vitro and in vivo investigations. Suggested mechanisms of PM 2.5 that lead to adverse effects and chronic diseases include increasing oxidative stress, inflammatory responses, and genotoxicity. The aim of this review is to provide a brief overview of in vitro and in vivo experimental studies of PM 2.5 in the progression of various diseases from the last decade. The summarized research results could provide clear information about the mechanisms and progression of PM 2.5-induced disease.

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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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            The health effects of ambient PM2.5 and potential mechanisms

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              Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

              Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM10 and PM2.5) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                01 July 2018
                July 2018
                : 15
                : 7
                : 1380
                Affiliations
                [1 ]Department of Biological Science and Technology, National Chiao Tung University, 75 Boai Street, Hsinchu 300, Taiwan; ccjwo21@ 123456gmail.com (C.-C.C.); mict6009@ 123456gmail.com (C.-H.T.); ricechen@ 123456hotmail.com (C.-Y.C.); olulu789.bt05g@ 123456g2.nctu.edu.tw (H.-F.C.)
                [2 ]Division of Chest Medicine, Department of Internal Medicine, Hsinchu Mackay Memorial Hospital, 690 Section 2, Guangfu Road, Hsinchu 300, Taiwan; 4040@ 123456mmh.org.tw
                [3 ]Division of Pulmonary Medicine, Department of Internal Medicine, Tungs’ Taichung Metro Harbor Hospital, 699 Section 8, Taiwan Blvd., Taichung 435, Taiwan
                [4 ]Division of Nephrology, Department of Internal Medicine, Hsinchu Mackay Memorial Hospital, 690 Section 2, Guangfu Road, Hsinchu 300, Taiwan
                [5 ]Division of Endocrinology, Department of Internal Medicine, Hsinchu Mackay Memorial Hospital, 690 Section 2, Guangfu Road, Hsinchu 300, Taiwan
                Author notes
                [* ]Correspondence: lincs@ 123456mail.nctu.edu.tw ; Tel.: +886-3-513-1338
                Article
                ijerph-15-01380
                10.3390/ijerph15071380
                6068560
                29966381
                4f7337c4-f54e-46c6-8b0b-e5d43936562c
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 10 May 2018
                : 23 June 2018
                Categories
                Review

                Public health
                particulate matter (pm),pm2.5,animal model,in vitro study,disease progression
                Public health
                particulate matter (pm), pm2.5, animal model, in vitro study, disease progression

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