Mapping air pollution and idiopathic pulmonary fibrosis

See related article Although a relatively rare disease in the general community, idiopathic pulmonary fibrosis (IPF) is most common cause of chronic interstitial lung overall and its incidence increases markedly over age 60 years. With establishment IPF registries many countries, we are finally getting handle on epidemiology. It becoming clear that this not truly ‘idiopathic’ interactions between genetic susceptibility environmental exposures (especially smoking) responsible for cases. In general, fine particulate matter less than 2.5 μm diameter (PM2.5) major threat to cardiopulmonary health Asia Pacific region elsewhere around world.1 PM2.5 may also be marker other traffic-related air pollutants (TRAP) including nitrogen dioxide (NO2). These known have deleterious effects asthma obstructive (COPD),2 so it surprising investigators been studying context IPF. Thus, TRAP positively lower function, hospital admissions mortality (for example3, 4), with NO2 being particularly implicated. recent publication Respirology, Shull et al. report mapping helps identify geographic regions at higher risk prevalence.5 The authors recruited 503 patients from Catalonian registry, but only 75% could included analysis because missing data. was estimated by highly spatially temporally resolved model emissions, meteorology, chemical transport mineral dust models. Further validation provided ground-level measurements quality monitoring network. A map generated plotting patients' residential postcodes highest concentrations study were located areas traffic congestion, industrial areas, airport ports, prevalence Barcelona. Other factors such as family history, smoking inorganic exposure presented, even without these lived above World Health Organization (WHO) guidelines. Unfortunately, possible estimate prior diagnosis gaseous oxidant ozone (O3) examined. An earlier, similar geographic, Lombardy6 municipal level local cases IPF, found weak association levels particulates or O3. study5 did age-adjust data disease, although occurs predominantly more elderly. Nor take into account illustrated sharp seasonal peaks PM2.5, which might well influenced marked winds off Mediterranean Sea times. However, they point out heavily sea salt. agree retrospective semi-ecological studies hypothesis generating prospective cohort now required, taking all potentially confounding account. relevant occupational can described detail ‘inorganic dust’.5 We recently conducted case–control Australia examine factors,7 utilizing job matrices assess exposures. an increased associated second-hand smoke, respirable asbestos, specific organic, metal dusts. There some striking similarities pathogenesis COPD both epithelial activation/dysregulation their respective compartments, production transforming growth factor-beta (TGF-β) drivers sub-epithelial fibrosis, epithelial–mesenchymal transition (EMT) seemingly having roles diseases.8, 9 Both diseases strongly cigarette smoking, playing important aetiological role, likely through mechanisms. Furthermore, same telomere-related genes involved pre-disposition two conditions, different opposite allelic influences phenotypic outcomes each.10 gene underactivity leads short telomeres, while overactive alleles airway remodelling cancer. This latter complexity worsened protection TGF-β/EMT pathways. still much learn. So, what messages away progress area health? Clinicians should advise develop personal strategies minimize pollution,11 emphasizing there really no safe reduced low possible. Even so, within 200 m roads, is, those carrying significant amounts heavy diesel traffic.2 distance emphasized future research indeed clinical advice. Over next few decades, electrification road vehicles, accompanied hopefully end-game dramatically beneficial epidemiology TRAP-affected respiratory diseases. E.H.W. investigator NHMRC-awarded CRE Pulmonary Fibrosis. M.J.A. holds investigator-initiated grants Pfizer Boehringer-Ingelheim unrelated research. He has consultancy received assistance conference attendance Sanofi. speaker's fee GSK.