Abstract
An increased incidence of lung cancer is well known among patients with idiopathic pulmonary fibrosis. It is not known whether interstitial lung abnormalities, i.e. early fibrotic changes of the lung, are a risk factor for lung cancer in the general population.
The study's objective was to assess whether interstitial lung abnormalities were associated with diagnoses of, and mortality from, lung cancer and other cancers. Data from the AGES-Reykjavik study, a cohort of 5764 older Icelandic adults, were used. Outcome data were ascertained from electronic medical records. Gray's tests, Cox proportional hazards models and proportional subdistribution hazards models were used to analyse associations of interstitial lung abnormalities with lung cancer diagnoses and lung cancer mortality as well as diagnoses and mortality from all cancers.
There was a greater cumulative incidence of lung cancer diagnoses (p<0.001) and lung cancer mortality (p<0.001) in participants with interstitial lung abnormalities than in others. Interstitial lung abnormalities were associated with an increased hazard of lung cancer diagnosis (hazard ratio 2.77) and lung cancer mortality (hazard ratio 2.89) in adjusted Cox models. Associations of interstitial lung abnormalities with all cancers were found in models including lung cancers but not in models excluding lung cancers.
People with interstitial lung abnormalities are at increased risk of lung cancer and lung cancer mortality, but not of other cancers. This implies that an association between fibrotic and neoplastic diseases of the lung exists from the early stages of lung fibrosis and suggests that interstitial lung abnormalities could be considered as a risk factor in lung cancer screening efforts.
Abstract
Interstitial lung abnormalities are associated with an increased hazard of lung cancer diagnosis and lung cancer mortality in a general population cohort. Cancers other than lung cancer were not associated with interstitial lung abnormalities. https://bit.ly/3hWdc6m
Footnotes
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Author contributions: Study design: G.T. Axelsson, R.K. Putman, T. Araki, H. Hatabu, V. Gudnason, G.M. Hunninghake and G. Gudmundsson; acquisition or interpretation of the data: G.T. Axelsson, R.K. Putman, T. Aspelund, E.F. Gudmundsson, T. Hida, T. Araki, M. Nishino, H. Hatabu, V. Gudnason, G.M. Hunninghake and G. Gudmundsson; critical revision of the manuscript for important intellectual content: G.T. Axelsson, R.K. Putman, T. Aspelund, E.F. Gudmundsson, T. Hida, T. Araki, M. Nishino, H. Hatabu, V. Gudnason, G.M. Hunninghake and G. Gudmundsson; statistical analysis: G.T. Axelsson, T. Aspelund, G.M. Hunninghake and E.F. Gudmundsson; obtained funding: G. Gudmundsson, V. Gudnason and G.M. Hunninghake.
Conflict of interest: G.T. Axelsson has nothing to disclose.
Conflict of interest: R.K. Putman reports grants from NIH, during the conduct of the study.
Conflict of interest: T. Aspelund has nothing to disclose.
Conflict of interest: E.F. Gudmundsson has nothing to disclose.
Conflict of interest: T. Hida has nothing to disclose.
Conflict of interest: T. Araki has nothing to disclose.
Conflict of interest: M. Nishino reports personal fees for consultancy from Daiichi Sankyo and AstraZeneca; honoraria from Roche; and grants from Merck, AstraZeneca, Canon Medical Systems and NIH (R01CA203636, U01CA209414, R01HL111024), outside the submitted work.
Conflict of interest: H. Hatabu reports grants from Canon Medical System Inc. and Konica-Minolta Inc., personal fees for consultancy from Mitsubishi Chemical Inc. and personal fees for advisory board work from Canon Medical System Inc., outside the submitted work.
Conflict of interest: V. Gudnason has nothing to disclose.
Conflict of interest: G.M. Hunninghake reports personal fees from Genentech, Boehringer Ingelheim, The Gerson Lehrman Group and Mitsubishi Chemical, outside the submitted work.
Conflict of interest: G. Gudmundsson has nothing to disclose.
Support statement: Supported by National Institutes of Health (NIH) grants K08 HL140087 (R.K. Putman); R01 CA203636 (M. Nishino); and R01 HL111024, R01 HL130974 and R01 135142 (G.M. Hunninghake); National Institute on Aging (NIA) grant 27120120022C (V. Gudnason); the Icelandic Research Fund, project grant 141513-051 (G. Gudmundsson, V. Gudnason and G.M. Hunninghake); Oddur Olafsson Fund; and Landspitali Scientific Fund A-2015-030 and A-2016-023 (G. Gudmundsson). The Age, Gene/Environment Susceptibility-Reykjavik Study was supported by NIH contracts N01-AG-1-2100 and HHSN27120120022C, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association) and the Althingi (the Icelandic Parliament). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received November 5, 2019.
- Accepted June 16, 2020.
- Copyright ©ERS 2020