Stinna Skaaby1, Esben Meulengracht Flachs1, Peter Lange2,3,4,5, Vivi Schlünssen6,7, Jacob Louis Marott4,5, Charlotte Brauer1, Børge G Nordestgaard4,5,8, Steven Sadhra9, Om Kurmi10,11, Jens Peter Ellekilde Bonde1,2. 1. Department of Occupational and Environmental Medicine, Bispebjerg Frederiksberg Hospital, Copenhagen University Hospital, Copenhagen, Denmark. 2. Section of Epidemiology, Institute of Public Health, University of Copenhagen, Copenhagen, Denmark. 3. Department of Medicine, Herlev Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark. 4. Copenhagen City Heart Study, Bispebjerg Frederiksberg Hospital, Copenhagen University Hospital, Copenhagen, Denmark. 5. Copenhagen General Population Study, Herlev Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark. 6. Department of Public Health, Environmental, Work and Health, Danish Ramazzini Centre, University of Aarhus, Aarhus, Denmark. 7. National Research Center for the Working Environment, Copenhagen, Denmark. 8. Department of Clinical Biochemistry, Herlev Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark. 9. Institute of Occupational and Environmental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom. 10. Faculty of Health and Life Sciences, Coventry University, Coventry, United Kingdom. 11. Division of Respirology, Department of Medicine, McMaster University, Hamilton, Canada.
Abstract
PURPOSE: Recent studies suggest that occupational inhalant exposures trigger exacerbations of asthma and chronic obstructive pulmonary disease, but findings are conflicting. METHODS: We included 7,768 individuals with self-reported asthma (n = 3,215) and/or spirometric airflow limitation (forced expiratory volume in 1 second (FEV1)/ forced expiratory volume (FVC) <0.70) (n = 5,275) who participated in The Copenhagen City Heart Study or The Copenhagen General Population Study from 2001-2016. Occupational exposure was assigned by linking job codes with job exposure matrices, and exacerbations were defined by register data on oral corticosteroid treatment, emergency care unit assessment or hospital admission. Associations between occupational inhalant exposure each year of follow-up and exacerbation were assessed by Cox regression with time varying exposure and age as the underlying time scale. RESULTS: Participants were followed for a median of 4.6 years (interquartile range, IQR 5.4), during which 870 exacerbations occurred. Exacerbations were not associated with any of the selected exposures (high molecular weight sensitizers, low molecular weight sensitizers, irritants or low and high levels of mineral dust, biological dust, gases & fumes or the composite variable vapours, gases, dusts or fumes). Hazards ratios ranged from 0.8 (95% confidence interval: 0.7;1.0) to 1.2 (95% confidence interval: 0.9;1.7). CONCLUSION: Exacerbations of obstructive airway disease were not associated with occupational inhalant exposures assigned by a job exposure matrix. Further studies with alternative exposure assessment are warranted.
PURPOSE: Recent studies suggest that occupational inhalant exposures trigger exacerbations of asthma and chronic obstructive pulmonary disease, but findings are conflicting. METHODS: We included 7,768 individuals with self-reported asthma (n = 3,215) and/or spirometric airflow limitation (forced expiratory volume in 1 second (FEV1)/ forced expiratory volume (FVC) <0.70) (n = 5,275) who participated in The Copenhagen City Heart Study or The Copenhagen General Population Study from 2001-2016. Occupational exposure was assigned by linking job codes with job exposure matrices, and exacerbations were defined by register data on oral corticosteroid treatment, emergency care unit assessment or hospital admission. Associations between occupational inhalant exposure each year of follow-up and exacerbation were assessed by Cox regression with time varying exposure and age as the underlying time scale. RESULTS:Participants were followed for a median of 4.6 years (interquartile range, IQR 5.4), during which 870 exacerbations occurred. Exacerbations were not associated with any of the selected exposures (high molecular weight sensitizers, low molecular weight sensitizers, irritants or low and high levels of mineral dust, biological dust, gases & fumes or the composite variable vapours, gases, dusts or fumes). Hazards ratios ranged from 0.8 (95% confidence interval: 0.7;1.0) to 1.2 (95% confidence interval: 0.9;1.7). CONCLUSION: Exacerbations of obstructive airway disease were not associated with occupational inhalant exposures assigned by a job exposure matrix. Further studies with alternative exposure assessment are warranted.
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