{
  "abstract": "Evidence supporting an idiopathic aetiology for many interstitial pneumonias is increasingly being challenged. It is now apparent that increasingly well-understood gene-environment interactions result in the various forms of pulmonary fibrosis to which we still apply the idiopathic moniker. Environmental factors play a significant role in the pathogenesis of pulmonary fibrosis, even for genetically predisposed individuals, perhaps acting as a ‘second-hit’ phenomenon.1 The proportional reduction in idiopathic pulmonary fibrosis (IPF) that would result from exposure elimination to vapour, gas, dust and fumes (VGDF) is estimated to be 26%.2 It has been shown that air pollution is associated with clinical worsening, radiological progression and declining lung function in IPF.3 4 Our understanding of how environmental exposures contribute to disease pathophysiology is evolving, with emerging evidence suggesting that pollutants may induce epigenetic changes that impact collagen production and fibroblast function in patients with fibrotic interstitial lung disease (ILD).5 While a cure for pulmonary fibrosis remains the short-term objective, the long-term vision is prevention, for which addressing environmental factors will be critical.",
  "authors": [
    {
      "affiliations": [
        "Department of Thoracic Medicine, The Prince Charles Hospital, Chermside, Queensland, Australia"
      ],
      "name": "Ramey Bajwa"
    },
    {
      "affiliations": [
        "Department of Thoracic Medicine, The Prince Charles Hospital, Chermside, Queensland, Australia",
        "Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia"
      ],
      "name": "John Mackintosh"
    }
  ],
  "title": "Clearing the haze around familial interstitial lung abnormalities",
  "uid": "c014b32c-382b-522e-a699-86aa2637d863"
}