Karin Grahn1, Per Gustavsson2, Tomas Andersson3, Anders Lindén4, Tomas Hemmingsson5, Jenny Selander6, Pernilla Wiebert7. 1. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden; Centre for Occupational and Environmental Medicine, Region Stockholm, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden. Electronic address: karin.grahn@ki.se. 2. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden; Centre for Occupational and Environmental Medicine, Region Stockholm, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden. Electronic address: per.gustavsson@ki.se. 3. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden; Centre for Occupational and Environmental Medicine, Region Stockholm, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden. Electronic address: tomas.andersson@ki.se. 4. Department of Respiratory Medicine and Allergology, NB6:03 Karolinska University Hospital, SE-171 76, Stockholm, Sweden; Institute of Environmental Medicine, Unit for Lung & Airway Research, Karolinska Institutet, PO Box 210, SE-171 77, Stockholm, Sweden. Electronic address: anders.linden@ki.se. 5. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden; Department of Public Health Sciences, Stockholm University, SE-106 91, Stockholm, Sweden. Electronic address: tomas.hemmingsson@ki.se. 6. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden. Electronic address: jenny.selander@ki.se. 7. Institute of Environmental Medicine, Unit for Occupational Medicine, Karolinska Institutet, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden; Centre for Occupational and Environmental Medicine, Region Stockholm, Solnavägen 4, Plan 10, SE-113 65, Stockholm, Sweden. Electronic address: pernilla.wiebert@ki.se.
Abstract
OBJECTIVES: Chronic Obstructive Pulmonary Disease (COPD) is a common respiratory disorder. Next to tobacco smoking, occupational exposure is the most important risk factor for COPD in high-income countries. To enable preventative measures, more knowledge is needed on which specific occupational exposures that are related to risk of developing COPD in men and women. METHODS: A population-based cohort was formed from subjects responding to the Stockholm Public Health Surveys in 2002, 2006, and 2010, followed up until 2014. The dataset was linked to a quantitative job exposure matrix via occupational titles from the 1990 nation-wide Population and housing census. We identified COPD among subjects having medication for COPD and/or reporting a physician's diagnosis of COPD. The gender-specific risks to develop COPD from occupational particle-exposure were estimated by proportional hazards regression model, adjusted for age and individual data on tobacco-smoking. RESULTS: Men exposed to respirable crystalline silica (RCS) (HR 1.46, CI 1.13-1.90), gypsum and insulation material (HR 1.56, CI 1.18-2.05), diesel exhaust (HR 1.18, CI 0.99-1.41) and high levels of particles from asphalt/bitumen (HR 1.71, CI 1.06-2.76) as well as welding fumes (HR 1.57, CI 1.12-2.21) had an increased smoking-adjusted risk for developing COPD. An increased risk was also observed among women highly exposed to various organic particles from soil, leather, plastic, soot, animal, textile, flour (HR 1.53, CI 1.15-2.04). Furthermore, a significant positive exposure-response trend was found among men exposed to RCS, iron dust, gypsum and insulation material, and diesel exhaust. A tendency towards an exposure-response relationship was also seen among both men and women exposed to welding fumes and various organic particles, and among men exposed to particles from asphalt/bitumen. The population attributable fraction for COPD from occupational exposure to particles was 10.6% among men and 6.1% among women. CONCLUSIONS: This study indicates an increased smoking-adjusted risk of developing of COPD due to occupational exposure to particles. A positive exposure-response relationship was found for RCS, gypsum and insulation, diesel exhaust, and welding fumes. Also, exposure to high levels of asphalt/bitumen and various organic particles was associated with a higher risk for COPD. Reduction of these exposures in the work environment are important to prevent future cases of COPD. More studies are needed to investigate exposure-response relationships further, but this study indicates that the European occupational exposure limit (OEL) for RCS needs to be re-evaluated.
OBJECTIVES:Chronic Obstructive Pulmonary Disease (COPD) is a common respiratory disorder. Next to tobacco smoking, occupational exposure is the most important risk factor for COPD in high-income countries. To enable preventative measures, more knowledge is needed on which specific occupational exposures that are related to risk of developing COPD in men and women. METHODS: A population-based cohort was formed from subjects responding to the Stockholm Public Health Surveys in 2002, 2006, and 2010, followed up until 2014. The dataset was linked to a quantitative job exposure matrix via occupational titles from the 1990 nation-wide Population and housing census. We identified COPD among subjects having medication for COPD and/or reporting a physician's diagnosis of COPD. The gender-specific risks to develop COPD from occupational particle-exposure were estimated by proportional hazards regression model, adjusted for age and individual data on tobacco-smoking. RESULTS:Men exposed to respirable crystalline silica (RCS) (HR 1.46, CI 1.13-1.90), gypsum and insulation material (HR 1.56, CI 1.18-2.05), diesel exhaust (HR 1.18, CI 0.99-1.41) and high levels of particles from asphalt/bitumen (HR 1.71, CI 1.06-2.76) as well as welding fumes (HR 1.57, CI 1.12-2.21) had an increased smoking-adjusted risk for developing COPD. An increased risk was also observed among women highly exposed to various organic particles from soil, leather, plastic, soot, animal, textile, flour (HR 1.53, CI 1.15-2.04). Furthermore, a significant positive exposure-response trend was found among men exposed to RCS, iron dust, gypsum and insulation material, and diesel exhaust. A tendency towards an exposure-response relationship was also seen among both men and women exposed to welding fumes and various organic particles, and among men exposed to particles from asphalt/bitumen. The population attributable fraction for COPD from occupational exposure to particles was 10.6% among men and 6.1% among women. CONCLUSIONS: This study indicates an increased smoking-adjusted risk of developing of COPD due to occupational exposure to particles. A positive exposure-response relationship was found for RCS, gypsum and insulation, diesel exhaust, and welding fumes. Also, exposure to high levels of asphalt/bitumen and various organic particles was associated with a higher risk for COPD. Reduction of these exposures in the work environment are important to prevent future cases of COPD. More studies are needed to investigate exposure-response relationships further, but this study indicates that the European occupational exposure limit (OEL) for RCS needs to be re-evaluated.
Authors: Bengt Sjögren; Maria Albin; Karin Broberg; Per Gustavsson; Håkan Tinnerberg; Gunnar Johanson Journal: Scand J Work Environ Health Date: 2021-11-25 Impact factor: 5.024
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