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      In Patients with Mild-to-Moderate COPD, Tobacco Smoking, and Not COPD, Is Associated with a Higher Risk of Cardiovascular Comorbidity

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          Comorbidities including cardiovascular diseases are very common in chronic obstructive pulmonary disease (COPD) secondary to tobacco smoking and contribute to the overall severity of the disease. In non-smoking COPD, which accounts for about 25% of COPD cases worldwide, current knowledge on the frequency and determinants of comorbidities remains scarce. The aims of the current study were to assess the frequency of major comorbidities and to evaluate their determinants in a group of non-selected patients with mild-to-moderate COPD who were exposed to organic dust (dairy farmers), to tobacco smoking, or to both, and in controls without COPD who were exposed to organic dust (dairy farmers), or to tobacco smoking, or to both, or who were without exposure.

          Patients and Methods

          A total of 4665 subjects (2323 dairy farmers and 2342 non-farmers) including 355 patients with COPD and 4310 controls with normal spirometry were recruited through a large COPD screening program. Self-reported physician-diagnosed diseases with plausible links to COPD were recorded in this cross-sectional study.


          Whatever the exposure, cardiovascular comorbidities were not more frequent in patients with COPD than their counterparts without airflow limitation. A higher risk of major cardiovascular comorbidities was associated with tobacco smoking and a lower risk was associated with exposure to organic dusts.


          Tobacco smoking (but not COPD) is associated with higher frequency of cardiovascular comorbidities. By contrast, being a dairy farmer exposed to organic dusts is associated with a lower frequency of the same comorbidities. This reinforces the crucial need for controlling established cardiovascular risk factors even in patients with mild-to-moderate COPD.

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          Most cited references 20

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          Chronic obstructive pulmonary disease in non-smokers.

          Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Tobacco smoking is established as a major risk factor, but emerging evidence suggests that other risk factors are important, especially in developing countries. An estimated 25-45% of patients with COPD have never smoked; the burden of non-smoking COPD is therefore much higher than previously believed. About 3 billion people, half the worldwide population, are exposed to smoke from biomass fuel compared with 1.01 billion people who smoke tobacco, which suggests that exposure to biomass smoke might be the biggest risk factor for COPD globally. We review the evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status.
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            Screening for and early detection of chronic obstructive pulmonary disease.

            Chronic obstructive pulmonary disease (COPD) is a substantially underdiagnosed disorder, with the diagnosis typically missed or delayed until the condition is advanced. Spirometry is the most frequently used pulmonary function test and enables health professionals to make an objective measurement of airflow obstruction and assess the degree to which it is reversible. As a diagnostic test for COPD, spirometry is a reliable, simple, non-invasive, safe, and non-expensive procedure. Early diagnosis of COPD should provide support for smoking cessation initiatives and lead to reduction of the societal burden of the disease, but definitive confirmation of both proves elusive. Despite substantial effort and investment, implementation of quality spirometry is deficient because of several hurdles and limitations, described in this Review. All in all, spirometry is recognised as the essential test for diagnosis and monitoring of COPD.
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              Biological dust exposure in the workplace is a risk factor for chronic obstructive pulmonary disease.

              Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality. Although the main risk factor is smoking, 15-19% of COPD even in smokers has been attributed to occupational exposures. The aim of this study was to investigate the association between occupational exposure and risk of COPD. Participants were part of a cross sectional study of risk factors for COPD. A total of 1232 completed a detailed respiratory questionnaire, spirometric testing and measurement of gas transfer. Job histories were coded according to the International Standard Classification of Occupations. These codes were then used to establish occupational exposures using the ALOHA job exposure matrix. The prevalence of emphysema was 2.4%, chronic obstructive bronchitis 1.8%, and COPD 3.4%. Subjects ever exposed to biological dusts had an increased risk of chronic obstructive bronchitis (OR 3.19; 95% CI 1.27 to 7.97), emphysema (OR 3.18; 95% CI 1.41 to 7.13), and COPD (OR 2.70, 95% CI 1.39 to 5.23). These risks were higher in women than in men. For biological dust, the risk of emphysema and COPD was also significantly increased in both the duration of exposure categories, again in women but not in men. No significant increased risks for COPD were found for mineral dust (OR 1.13; 95% CI 0.57 to 2.27) or gases/fumes (OR 1.63; 95% CI 0.83 to 3.22). In this general population sample of adults, occupational exposures to biological dusts were associated with an increased risk of COPD which was higher in women. Preventive strategies should be aimed at reducing exposure to these agents in the workplace.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of Chronic Obstructive Pulmonary Disease
                01 July 2020
                : 15
                : 1545-1555
                [1 ]Service de Pneumologie, Oncologie Thoracique et Allergologie Respiratoire, CHU de Besançon , Besançon, France
                [2 ]Equipe d’Epidémiologie Environnementale, Institute for Advanced Biosciences, Centre de Recherche UGA, INSERM U1209, CNRS UMR 5309 , Grenoble, France
                [3 ]Service de Pneumologie, Groupe Hospitalier Cochin, Site Val de Grâce, AP-HP and Université Paris Descartes (EA2511), Sorbonne-Paris-Cité , Paris, France
                [4 ]Epidemiology of Allergic and Respiratory Diseases UMR-S 707 Inserm/UPMC, Université Paris 6 , Paris, France
                [5 ]Centre Hospitalier Intercommunal de Créteil, Service de Pathologie Professionnelle et de l’Environnement , Créteil, France
                [6 ]Université Paris-Est Créteil, Faculté de Médecine , Créteil, France
                [7 ]Service de Pneumologie, CHU de Rennes , Rennes, France
                [8 ]Univ Rennes, CHU Rennes, Inserm, EHESP, Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en Santé, Environnement et Travail) – UMR-S 1085 , Rennes, France
                [9 ]Fédération des Maisons de Santé Comtoises (FéMaSaC) , Beure, France
                [10 ]Mutualité Sociale Agricole (MSA) , Besançon, France
                [11 ]UMR CNRS Chrono Environnement, Université de Franche-Comté , Besançon, France
                [12 ]Service Hospitalier Universitaire Pneumologie Physiologie, Pôle Thorax et Vaisseaux, CHU Grenoble , Alpes, France
                [13 ]Université Grenoble Alpes, INSERM U 1042 , Grenoble, France
                Author notes
                Correspondence: Thibaud Soumagne Email
                © 2020 Soumagne et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (

                Page count
                Figures: 2, Tables: 4, References: 26, Pages: 11
                Funded by: BALISTIC
                The COPD screening program (BALISTIC) was supported by a grant from Novartis Pharma.
                Original Research


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