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Interstitial lung disease encompasses a heterogeneous group of disorders characterised by excessive deposition of collagen within the extracellular matrix and thickening of the pulmonary insterstitium. Many interstitial lung diseases are linked with known environmental exposures including tobacco smoke (idiopathic pulmonary fibrosis), inhaled dust, mould or other irritants (hypersensitivity pneumonitis) and occupational exposures (ie, silicosis, asbestosis).1 However, the role of potentially relevant environmental exposures is difficult to establish due to the long latency period of these disorders (eg, 40–50 years for asbestosis). In a recent advance in the detection of early stage interstitial lung disease, interstitial lung abnormalities (ILA)—radiological abnormalities on chest CT—have been postulated as an indicator of subclinical interstitial lung disease,2 opening the door to further discoveries. Exposure to traffic-related air pollution has been postulated as being another potential risk factor. The proposed mechanism of action for this effect is pulmonary and systemic inflammation, oxidative stress and dysregulated fibrogenesis.3
In 2016, outdoor air pollution was responsible for >3 million premature deaths,4 and it is estimated that 91% of the world’s population lives in places where air pollution exceeds the limits stipulated by WHO guidelines.5 Exposure to air pollution has been linked to many conditions, including cardiovascular disease, obesity and neurological disorders, as well as an increase in the incidence of respiratory disorders and related mortality.4 The American Lung Association recently emphasised that high levels of air pollution could be priming an epidemic of chronic respiratory diseases, such as COPD.6 In the field of interstitial lung disease, however, air pollution has received very little attention to date.7–10
In Thorax, Rice et al 11 have shown, for the first time, that long-term exposure to elemental carbon (EC), a marker of traffic pollution, may increase the risk of the development and progression of ILA. …
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 None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer reviewed.
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