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      Aeroparticles, Composition, and Lung Diseases

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          Abstract

          Urban air pollution is a serious worldwide problem due to its impact on human health. In the past 60 years, growing evidence established a correlation between exposure to air pollutants and the developing of severe respiratory diseases. Recently particulate matter (PM) is drawing more public attention to various aspects including historical backgrounds, physicochemical characteristics, and its pathological role. Therefore, this review is focused on these aspects. The most famous air pollution disaster happened in London on December 1952; it has been calculated that more than 4,000 deaths occurred during this event. Air pollution is a complex mix of gases and particles. Gaseous pollutants disseminate deeply into the alveoli, allowing its diffusion through the blood–air barrier to several organs. Meanwhile, PM is a mix of solid or liquid particles suspended in the air. PM is deposited at different levels of the respiratory tract, depending on its size: coarse particles (PM 10) in upper airways and fine particles (PM 2.5) can be accumulated in the lung parenchyma, inducing several respiratory diseases. Additionally to size, the composition of PM has been associated with different toxicological outcomes on clinical and epidemiological, as well as in vivo and in vitro animal and human studies. PM can be constituted by organic, inorganic, and biological compounds. All these compounds are capable of modifying several biological activities, including alterations in cytokine production, coagulation factors balance, pulmonary function, respiratory symptoms, and cardiac function. It can also generate different modifications during its passage through the airways, like inflammatory cells recruitment, with the release of cytokines and reactive oxygen species (ROS). These inflammatory mediators can activate different pathways, such as MAP kinases, NF-κB, and Stat-1, or induce DNA adducts. All these alterations can mediate obstructive or restrictive respiratory diseases like asthma, COPD, pulmonary fibrosis, and even cancer. In 2013, outdoor air pollution was classified as Group 1 by IARC based on all research studies data about air pollution effects. Therefore, it is important to understand how PM composition can generate several pulmonary pathologies.

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          Immunology of asthma and chronic obstructive pulmonary disease.

          Asthma and chronic obstructive pulmonary disease (COPD) are both obstructive airway diseases that involve chronic inflammation of the respiratory tract, but the type of inflammation is markedly different between these diseases, with different patterns of inflammatory cells and mediators being involved. As described in this Review, these inflammatory profiles are largely determined by the involvement of different immune cells, which orchestrate the recruitment and activation of inflammatory cells that drive the distinct patterns of structural changes in these diseases. However, it is now becoming clear that the distinction between these diseases becomes blurred in patients with severe asthma, in asthmatic subjects who smoke and during acute exacerbations. This has important implications for the development of new therapies.
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            Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.

            Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.
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              The physical characteristics of sulfur aerosols

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                Author and article information

                Contributors
                URI : http://frontiersin.org/people/u/283828
                URI : http://frontiersin.org/people/u/91092
                URI : http://frontiersin.org/people/u/49193
                URI : http://frontiersin.org/people/u/235942
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                20 January 2016
                2016
                : 7
                : 3
                Affiliations
                [1] 1Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México , Mexico City, Mexico
                [2] 2Departamento de Investigación en Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias , Mexico City, Mexico
                [3] 3Department of Pediatrics, University of Alberta , Edmonton, AB, Canada
                [4] 4Laboratorio de Inmunologia Integrativa, Instituto Nacional de Enfermedades Respiratorias , Mexico City, Mexico
                Author notes

                Edited by: Masaaki Murakami, Hokkaido University, Japan

                Reviewed by: Daisuke Kamimura, Hokkaido University, Japan; Hiroki Kimura, Hokkaido University, Japan

                *Correspondence: Patricia Segura-Medina, psegura@ 123456unam.mx

                Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Article
                10.3389/fimmu.2016.00003
                4719080
                26834745
                e6fac49a-95f4-4229-b9a1-e95cc6972a00
                Copyright © 2016 Falcon-Rodriguez, Osornio-Vargas, Sada-Ovalle and Segura-Medina.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 11 September 2015
                : 05 January 2016
                Page count
                Figures: 3, Tables: 1, Equations: 0, References: 117, Pages: 9, Words: 8304
                Funding
                Funded by: Secretarí-a de Ciencia, Tecnologí-a e Innovación del Distrito Federal 10.13039/501100007045
                Award ID: SECITI 042/13, SECITI 014/2014 and SECITI 019/2015
                Funded by: Consejo Nacional de Ciencia y Tecnologí-a 10.13039/501100007350
                Award ID: Scholarship 233789
                Categories
                Immunology
                Review

                Immunology
                air pollution,particulate matter,copd,asthma,fibrosis,inflammation
                Immunology
                air pollution, particulate matter, copd, asthma, fibrosis, inflammation

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