Increased mortality in COPD among construction workers exposed to inorganic dust

Our plain-English summary of Increased mortality in COPD among construction workers exposed to inorganic dust, by I.A. Bergdahl, K. Torén, K. Eriksson, et al (The European Respiratory Journal, 2004).

The study

• Authors: I.A. Bergdahl, K. Torén, K. Eriksson, U. Hedlund, T. Nilsson, R. Flodin, B. Järvholm
• Journal: The European Respiratory Journal
• Published: 2004;23(3):402-6
• Cited by: 119 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The aim of this study was to find out if occupational exposure to dust, fumes or gases, especially among never-smokers, increased the mortality from chronic obstructive pulmonary disease (COPD). A cohort of 317,629 Swedish male construction workers was followed from 1971 to 1999. Exposure to inorganic dust (asbestos, man-made mineral fibres, dust from cement, concrete and quartz), gases and irritants (epoxy resins, isocyanates and organic solvents), fumes (asphalt fumes, diesel exhaust and metal fumes), and wood dust was based on a job-exposure matrix. An internal control group with "unexposed" construction workers was used, and the analyses were adjusted for age and smoking. When all subjects were analysed, there was an increased mortality from COPD among those with any airborne exposure (relative risk 1.12 (95% confidence interval (CI) 1.03-1.22)). In a Poisson regression model, including smoking, age and the major exposure groups, exposure to inorganic dust was associated with an increased risk (hazard ratio (HR) 1.10 (95% CI 1.06-1.14)), especially among never-smokers (HR 2.30 (95% CI 1.07-4.96)). The fraction of COPD among the exposed attributable to any airborne exposure was estimated as 10.7% overall and 52.6% among never-smokers. In conclusion, occupational exposure among construction workers increases mortality due to chronic obstructive pulmonary disease, even among never-smokers.

In plain English

This Swedish study followed 317,629 male construction workers from 1971 to 1999 and looked at deaths from chronic obstructive pulmonary disease (COPD). Exposure was estimated from each man's job title at his first health examination, using a job-exposure matrix. Asbestos was not analysed on its own. It was grouped with man-made mineral fibres, cement, concrete and quartz as "inorganic dust". Workers in jobs rated unexposed served as the comparison group, and the analyses took smoking and age into account. There were 523 COPD deaths among exposed workers and 200 in the comparison group. Workers with any airborne exposure had a relative risk of COPD death of 1.12 (95% CI 1.03–1.22). In a model including smoking, age and all exposure groups, inorganic dust had a hazard ratio of 1.10 (1.06–1.14) in the whole cohort; a separate model limited to never-smokers gave 2.30 (1.07–4.96). The authors concluded that occupational dust exposure increases COPD mortality, even in never-smokers. They noted that exposure rested only on the first job title and that the 1970s-based matrix may have missed earlier asbestos exposure.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Prospective cohort study (register-based, with an internal comparison group of unexposed construction workers)
• Who was studied: 317,629 Swedish male construction workers who attended occupational health examinations, followed from 1971 to the end of 1999. Of these, 200,735 were in exposed jobs and 116,894 were in jobs rated nonexposed (the comparison group).
• Exposure: Exposure was assigned from the job title at the first health examination, using a job-exposure matrix based on a mid-1970s survey. There were four exposure groups. Inorganic dust covered asbestos, man-made mineral fibres, cement, concrete and quartz. Gases and irritants covered epoxy resins, isocyanates and organic solvents. Fumes covered diesel exhaust, metal fume and asphalt. The fourth group was wood dust. Asbestos was not analysed separately.
• Main results:
  • There were 523 COPD deaths among workers with any airborne exposure and 200 among the controls.
  • In the whole cohort, using the person-year method stratified for smoking and age, workers with any airborne exposure had a relative risk of COPD death of 1.12 (95% CI 1.03–1.22) compared with controls.
  • In the whole cohort, the relative risk was 1.16 (95% CI 1.05–1.28) for workers exposed to inorganic dust and 1.22 (95% CI 1.04–1.42) for workers exposed to fumes. For wood dust it was 0.77 (0.53–1.07).
  • Among never-smokers only, workers with any airborne exposure had a relative risk of COPD death of 2.11 (95% CI 1.43–3.00). For the inorganic dust group it was 2.38 (1.59–3.44), based on 28 deaths compared with 7 among never-smoking controls.
  • In a Poisson regression of the whole cohort that included all exposure groups, smoking and age, inorganic dust had a hazard ratio of 1.10 (95% CI 1.06–1.14). The risk declined for gases and irritants (1.02, 0.96–1.08) and for fumes (0.98, 0.93–1.03).
  • In a separate Poisson regression restricted to never-smokers, with exposure groups and age as predictors, the hazard ratio was 2.30 (1.07–4.96) for inorganic dust. It was 3.85 (2.50–5.94) for gases and irritants and 4.44 (2.80–7.04) for fumes.
  • Among the exposed, the fraction of COPD attributable to work was estimated at 10.7% overall and 52.6% among never-smokers.
• The authors' conclusion: The authors concluded that occupational exposure to dust increases mortality from COPD, even in never-smokers. They added that the dust exposure is construction-related and the results cannot be directly applied to the general population.
• Limitations the authors state:
  • Control workers had probably been exposed to dust at lower levels, which may underestimate the risks.
  • Cumulative exposure could not be estimated, because exposure was based only on the occupation reported at the first health examination.
  • The matrix reflected 1970s exposures, so earlier asbestos exposure may not have been captured. The authors suggested that past asbestos exposure among plumbers may explain the raised COPD risk in the metal fume group.
  • The exposure groups overlapped considerably.
  • Smoking was recorded only at the start of follow-up and was not updated over time.
  • Some deaths may have been misclassified between asthma and COPD, particularly before 1987.
  • The never-smoker estimate rests on a small number of deaths.

Topics

Medical terms in this study, explained in our Lexicon: COPD, Occupational Exposure, Relative Risk, confidence interval, Hazard Ratio.

Related studies

• Increased mortality from infectious pneumonia after occupational exposure to inorganic dust, metal fumes and chemicals — K. Torén, I. Qvarfordt, et al. (2011)
• Airways obstruction among older construction and trade workers at Department of Energy nuclear sites — J.M. Dement, L. Welch, et al. (2010)
• Mortality due to asbestos-related causes among railway carriage construction and repair workers — G. Battista, S. Belli, et al. (1999)
• Acute effects of multi-walled carbon nanotubes on primary bronchial epithelial cells from COPD patients — S. Beyeler, S. Chortarea, et al. (2018)
• Airway wall remodeling induced by occupational mineral dusts and air pollutant particles — A. Churg, J.L. Wright (2002)
• Exposure to chrysotile mining dust and digestive cancer mortality in a Chinese miner/miller cohort — S. Lin, X. Wang, et al. (2014)

Browse more research in The European Respiratory Journal, or return to medical research.