Extract
Asthma–COPD overlap (ACO) has recently been recognised as a separate phenotype of obstructive airway diseases and is included in several guidelines of asthma and COPD [1–5]. ACO patients have previously been shown to have lower diffusing capacity of the lung, higher blood neutrophil counts and higher interleukin-6 levels compared with asthma patients [6]. In COPD, fixed airway obstruction is considered to develop in response to chronic exposure to noxious inhaled particles [7]. In western countries, the most common cause of COPD is tobacco smoking, but occupational exposure to dusts and fumes has also been shown to increase the risk for developing COPD [7, 8]. However, the role of occupational exposures in the development of ACO is not known.
Abstract
Occupational exposure to vapours, gases, dusts or fumes (VGDF) increases the prevalence of asthma–COPD overlap (ACO) in adult-onset asthma. VGDF exposure is independently associated with ACO and an additive effect with smoking is proposed. http://bit.ly/2LiMiXW
Acknowledgements
We are grateful to Aino Sepponen (Seinäjoki Central Hospital, Seinäjoki, Finland) for her input with data management.
Footnotes
This study is registered at www.ClinicalTrials.gov with identifier number NCT02733016.
Author contributions: M. Tommola, P. Ilmarinen, L.E. Tuomisto, L. Lehtimäki and H. Kankaanranta designed the study and wrote the report. M. Tommola, P. Ilmarinen and H. Kankaanranta performed the statistical analyses. All authors contributed to interpretation of the data. All authors made critical revisions of the manuscript and approved the final version of the manuscript.
Conflict of interest: M. Tommola reports personal fees for lectures from AstraZeneca, Filha ry, GlaxoSmithKline, Pfizer and Chiesi, personal fees for lectures and consultation from Boehringer Ingelheim, and grants from the Orion Research Foundation, outside the submitted work.
Conflict of interest: P. Ilmarinen reports grants from AstraZeneca, and payment for lectures from Mundipharma, Orion and AstraZeneca, outside the submitted work.
Conflict of interest: L.E. Tuomisto reports compensation of costs for attending an international congress from Chiesi, Orion Pharma and Teva, for attending an international congress and costs for lectures from Boehringer Ingelheim, and for lectures from AstraZeneca, outside the submitted work.
Conflict of interest: L. Lehtimäki reports personal fees from AstraZeneca, Boehringer Ingelheim, Chiesi, GSK, Mundipharma, Novartis, Orion Pharma, Teva and ALK, outside the submitted work.
Conflict of interest: H. Kankaanranta reports grants from AstraZeneca, during the conduct of the study; as well as personal fees and non-financial support from AstraZeneca and Boehringer Ingelheim, personal fees from Chiesi Pharma AB, GlaxoSmithKline, Leiras-Takeda, MSD, Novartis, Mundipharma, Roche, Sanofi Genzyme and Orion Pharma, and non-financial support from Intermune, all outside the submitted work.
Support statement: Supported by Tampere Tuberculosis Foundation (Tampere, Finland), the Finnish Anti-Tuberculosis Association Foundation (Helsinki, Finland), the Research Foundation of the Pulmonary Diseases (Helsinki, Finland), Orion Research Foundation (Espoo, Finland), the Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital (Tampere, Finland) and the Medical Research Fund of Seinäjoki Central Hospital (Seinäjoki, Finland). None of the sponsors had any involvement in the planning, execution, drafting or write-up of this study. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received August 2, 2019.
- Accepted August 25, 2019.
- Copyright ©ERS 2019
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