Introduction Idiopathic pulmonary fibrosis (IPF) is a lung disease of unknown cause characterised by progressive scarring, with limited effective treatment and a median survival of only 2–3 years. Our aim was to identify potential occupational and environmental exposures associated with IPF in Australia.
Methods Cases were recruited by the Australian IPF registry. Population-based controls were recruited by random digit dialling, frequency matched on age, sex and state. Participants completed a questionnaire on demographics, smoking, family history, environmental and occupational exposures. Occupational exposure assessment was undertaken with the Finnish Job Exposure Matrix and Australian asbestos JEM. Multivariable logistic regression was used to describe associations with IPF as ORs and 95% CIs, adjusted for age, sex, state and smoking.
Results We recruited 503 cases (mean±SD age 71±9 years, 69% male) and 902 controls (71±8 years, 69% male). Ever smoking tobacco was associated with increased risk of IPF: OR 2.20 (95% CI 1.74 to 2.79), but ever using marijuana with reduced risk after adjusting for tobacco: 0.51 (0.33 to 0.78). A family history of pulmonary fibrosis was associated with 12.6-fold (6.52 to 24.2) increased risk of IPF. Occupational exposures to secondhand smoke (OR 2.1; 1.2 to 3.7), respirable dust (OR 1.38; 1.04 to 1.82) and asbestos (OR 1.57; 1.15 to 2.15) were independently associated with increased risk of IPF. However occupational exposures to other specific organic, mineral or metal dusts were not associated with IPF.
Conclusion The burden of IPF could be reduced by intensified tobacco control, occupational dust control measures and elimination of asbestos at work.
- idiopathic pulmonary fibrosis
- asbestos induced lung disease
- occupational lung disease
- tobacco and the lung
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Contributors MJA conceived and designed the case-control study, interpreted the analysis and wrote the first draft of the paper. TM, SMA and RW analysed and interpreted the data. GPB, SCD, RFH, RW, TJC and EHW conceived and designed the case–control study and interpreted the analysis. IG, PH, SK, YM, PNR, TJC and EHW established the Australian IPF Registry and were involved in acquisition of case data. SR acquired and analysed control data. All authors have revised the paper for important intellectual content and approve this version for publication. MJA and TJC act as guarantors.
Funding This project was funded by the National Health and Medical Research Council of Australia (Project Grant #1106601). Shyamali Dharmage, Paul Reynolds and E. Haydn Walters are also supported by NHMRC. Tamera Corte, Ian Glaspole, Yuben Moodley and E. Haydn Walters hold a Centre of Research Excellence Grant in Pulmonary Fibrosis from NHMRC. Lung Foundation Australia established the Australian IPF Registry with the generous support of a philanthropic family and industry sponsors including Boehringer Ingelheim, Roche Products, Galapagos and Bristol-Myers Squibb Australia.
Competing interests MJA holds investigator-initiated grants for unrelated research from Pfizer and Boehringer-Ingelheim. He has undertaken an unrelated consultancy for and received assistance with conference attendance from Sanofi. He has also received a speaker's fee from GSK. IG reports personal fees and non-financial support from Boehringer Ingelheim, personal fees from Roche, Avalyn, Pulmotect and Menarini, grants and non-financial support from Lung Foundation of Australia, grants from NHMRC, outside the submitted work. SK has received personal fees for preparing medicolegal reports for the courts on cases of interstitial lung disease. YM reports non-financial support from Roche and Boehringer Ingelheim, outside the submitted work. PNR reports other from GlaxoSmithKline and Boehringer Ingelheim, outside the submitted work. TJC reports grants and personal fees from Roche, grants, personal fees, non-financial support and other from Boehringer Ingleheim, grants from Actelion, personal fees from Astra Zeneca, grants and personal fees from BMS, and grants from Bayer, outside the submitted work.
Patient consent for publication Not required.
Ethics approval The study was approved by the Human Research Ethics Committees of the Royal Prince Alfred Hospital (HREC/15/RPAH/602) and Monash University (CF16/171 - 2016000071).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement No data are available.
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