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COPD at work: exposures are different than in the past, but still matter
  1. Dick Heederik1,
  2. David M Mannino2,3
  1. 1 Institute for Risk Assessment Sciences, Division of Environmental Epidemiology, University of Utrecht, Utrecht, The Netherlands
  2. 2 Department of Medicine, University of Kentucky College of Medicine, Lexington, Kentucky, USA
  3. 3 Medical Affairs, GlaxoSmithKline, Philadelphia, Pennsylvania, USA
  1. Correspondence to Dr Dick Heederik, Institute for Risk Assessment Sciences, Division of Environmental Epidemiology, University of Utrecht, Utrecht NL-3508 TD, The Netherlands; d.heederik{at}

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This present common knowledge about the role of occupational exposures in the development of COPD has not been without controversy and is generally accepted only for less than two decades.1 This is because the dominant cause of COPD in high-income countries is cigarette smoking. Despite the biological plausibility of other inhaled agents being causally implicated, only the role of tobacco smoke was accepted as a cause of COPD in the mid-1980s.2 3 At that time, chronic non-malignant lung disease characterised by airflow limitation became more common in occupational population studies as the incidence of TB and pneumoconiosis were decreasing in major heavy industries (mining, foundries). But it was not commonly accepted that occupational dust and fumes exposures could be a cause of this group of diseases, the reasons being that obstructive respiratory disease are multifactorial diseases, strongly associated to non-occupational factors. As a result, a heated discussion existed at that time in the literature on the role of occupational exposures in relation to what we now refer to as COPD. In the case of coal workers, perhaps the best studied occupational group at that time, some argued that airflow limitations were of minor degree and not sufficient to impair lung function and disable the worker unless he was a smoker as well.4–6 Others disagreed and argued that clinically relevant decreased in lung function could result from a lifetime exposure to coalmine dust.2 3 Some suggested that the lung function declines …

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  • Contributors Both authors have contributed to the writing and editing of this editorial.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests DMM is an employee and shareholder of GlaxoSmithKline. DH has no competing interest to declare.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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