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Occupational exposures and IPF: when the dust unsettles
  1. Cathryn T Lee1,
  2. Kerri A Johannson2
  1. 1 Department of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois, USA
  2. 2 Department of Medicine, University of Calgary, Calgary, Alberta, Canada
  1. Correspondence to Dr Kerri A Johannson, Department of Medicine, University of Calgary, Calgary, AB T3M1M4, Canada; kerri.johannson{at}ahs.ca

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The average person spends 90 000 hours at work over their lifetime, equating to nearly 6.5 million breaths taken in the workplace. Although work is an essential task for many, it may also carry risk. Inhaled exposures in the workplace contribute substantially to the burden of chronic respiratory conditions, including asthma, chronic obstructive pulmonary disease and bronchitis, with population attributable fractions (PAFs) of 15%–20%.1 Given the increasing global impact of chronic lung disease,2 prevention remains a key priority, through ongoing efforts to identify and mitigate risk factors.

Idiopathic pulmonary fibrosis (IPF) is a progressive chronic lung disease that accounts for 1% of adult deaths annually in the UK.3 It is increasingly diagnosed and associated with early morbidity, mortality and high healthcare utilisation.4 Conceptually, IPF is a disease of genes, environment and time, where a genetically susceptible individual with various inhalational insults manifests IPF with age. The genetic risks associated with IPF are increasingly understood, yet these inhalational insults remain poorly characterised. Smoking is the most robustly defined risk factor for IPF,5 though chronic air pollution and several work-related exposures have also been associated with disease.6 In the most comprehensive meta-analysis on this topic, multiple occupational exposures were associated with IPF with pooled PAFs of 3% for silica, 4% for wood dust, 8% for metal dust or fumes and 26% for vapours, gases, dust or fumes.1 The number of parent studies included …

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Footnotes

  • 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 CTL reports no disclosures. KAJ reports personal fees and other from Boehringer-Ingelheim, personal fees and other from Hoffman La Roche Ltd, personal fees and other from Theravance, personal fees and other from Blade Therapeutics, grants from Chest Foundation, grants from University of Calgary School of Medicine, grants from Pulmonary Fibrosis Society of Calgary, grants from UCB Biopharma SPRL, other from Three Lakes Foundation, outside the submitted work.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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