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      International Journal of COPD (submit here)

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      Serum cytokine levels related to exposure to volatile organic compounds and PM 2.5 in dwellings and workplaces in French farmers – a mechanism to explain nonsmoking COPD

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          Abstract

          Although French farmers smoke less on average than individuals from the general population, they suffer more from COPD. Exposure to biological and chemical air pollutants in the farm may be the cause of these higher COPD rates. This study investigates the role of bio-contaminants, including the relationship of exposure to volatile organic compounds (VOCs) and fine particulate matter (of diameter of 2.5 µm [PM 2.5]) objectively measured in the farm settings (dwellings and workplaces) to serum cytokines involved in COPD, in a sample of 72 farmers from 50 farms in the Auvergne region, France. Mean concentrations of VOCs were highest inside the home, while levels of PM 2.5 were highest in workplaces (stables and granaries). After adjusting for confounders, high exposure to PM 2.5 was significantly associated with a decreased level of serum cytokines (among others, IL13: β: −0.94, CI: −1.5 to −0.2, P-value =0.004; IL8: β: −0.82, CI: −1.4 to −0.2, P-value =0.005) and high exposure to VOCs according to a VOC global score with a decreased IL13 level (β: −0.5, CI: −0.9 to −0.1, P-value =0.01). Moreover, respiratory symptoms and diseases, including COPD, were associated with a decreased level of serum cytokines significantly in the case of IL5. An alteration of immune response balance in terms of cytokine levels in relation to indoor chemical air pollution exposure may contribute to respiratory health impairment in farmers.

          Most cited references41

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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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            T helper type 17-related cytokine expression is increased in the bronchial mucosa of stable chronic obstructive pulmonary disease patients.

            There are increased numbers of activated T lymphocytes in the bronchial mucosa of stable chronic obstructive pulmonary disease (COPD) patients. T helper type 17 (Th17) cells release interleukin (IL)-17 as their effector cytokine under the control of IL-22 and IL-23. Furthermore, Th17 numbers are increased in some chronic inflammatory conditions. To investigate the expression of interleukin (IL)-17A, IL-17F, IL-21, IL-22 and IL-23 and of retinoic orphan receptor RORC2, a marker of Th17 cells, in bronchial biopsies from patients with stable COPD of different severity compared with age-matched control subjects. The expression of IL-17A, IL-17F, IL-21, IL-22, IL-23 and RORC2 was measured in the bronchial mucosa using immunohistochemistry and/or quantitative polymerase chain reaction. The number of IL-22(+) and IL-23(+) immunoreactive cells is increased in the bronchial epithelium of stable COPD compared with control groups. In addition, the number of IL-17A(+) and IL-22(+) immunoreactive cells is increased in the bronchial submucosa of stable COPD compared with control non-smokers. In all smokers, with and without disease, and in patients with COPD alone, the number of IL-22(+) cells correlated significantly with the number of both CD4(+) and CD8(+) cells in the bronchial mucosa. RORC2 mRNA expression in the bronchial mucosa was not significantly different between smokers with normal lung function and COPD. Further, we report that endothelial cells express high levels of IL-17A and IL-22. Increased expression of the Th17-related cytokines IL-17A, IL-22 and IL-23 in COPD patients may reflect their involvement, and that of specific IL-17-producing cells, in driving the chronic inflammation seen in COPD.
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              Long-term air pollution exposure and risk factors for cardiovascular diseases among the elderly in Taiwan.

              To investigate changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation associated with changes in long-term exposure to ambient air pollutants. We conducted secondary analyses of data on blood pressure and blood biochemistry markers from the Social Environment and Biomarkers of Aging Study in Taiwan and air pollution data from the Taiwan Environmental Protection Administration in 2000. Associations of 1-year averaged criteria air pollutants (particulate matter with aerodynamic diameters <10 μm (PM(10)) and <2.5 μm (PM(2.5)), ozone (O(3)), nitrogen dioxide (NO(2)), sulfur dioxide and carbon monoxide) with systolic blood pressure, diastolic blood pressure, total cholesterol, triglycerides, high-density lipoprotein cholesterol, fasting glucose, haemoglobin A1c (HbA1c), interleukin 6 (IL-6) and neutrophils were explored by applying generalised additive models. After controlling for potential confounders, we observed that increased 1-year averaged particulate air pollutants (PM(10) and PM(2.5)) and NO(2) were associated with elevated blood pressure, total cholesterol, fasting glucose, HbA1c, IL-6 and neutrophils. Associations of increased 1-year averaged O(3) with elevated blood pressure, total cholesterol, fasting glucose, HbA1c and neutrophils were also observed. In particular, our two-pollutant models showed that PM(2.5) was more significantly associated with end-point variables than two gaseous pollutants, O(3) and NO(2). Changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation are associated with long-term exposure to ambient air pollutants. This might provide a link between air pollution and atherosclerotic cardiovascular diseases.
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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
                2017
                05 May 2017
                : 12
                : 1363-1374
                Affiliations
                [1 ]Sorbonne Universités, UPMC Univ Paris 06, INSERM, Institut Pierre Louis d’Epidémiologie et de Santé Publique, UMRS 1136, Epidemiology of Allergic and Respiratory Diseases Department, Medical School Saint-Antoine, Paris
                [2 ]Mutualité Sociale Agricole, Clermont-Ferrand, Auvergne
                [3 ]Centre du Thorax de Nantes INSERM, UMR1087, Institut du thorax, Nantes
                [4 ]Respiratory Diseases Department, CHU Clermont-Ferrand, Clermont-Ferrand, Auvergne, France
                Author notes
                Correspondence: Nour Baïz, Sorbonne Universités, UPMC Univ Paris 06, INSERM, Institut Pierre Louis d’Epidémiologie et de Santé Publique, UMRS 1136, Epidemiology of Allergic and Respiratory Diseases Department, Medical School Saint-Antoine, F75012 Paris, France, Tel +33 1 44 73 86 58, Fax +33 1 44 73 84 54, Email baiz.nour@ 123456gmail.com
                [*]

                These authors contributed equally to this work

                Article
                copd-12-1363
                10.2147/COPD.S117866
                5426466
                28503065
                9c82d972-021f-4fcc-99aa-985703fe7021
                © 2017 Audi 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.

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                Original Research

                Respiratory medicine
                indoor rural air pollution,copd,french farmers,vocs,pm2.5,cytokines
                Respiratory medicine
                indoor rural air pollution, copd, french farmers, vocs, pm2.5, cytokines

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