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Original research
Impact of smoking on the development of idiopathic pulmonary fibrosis: results from a nationwide population-based cohort study
  1. Won Bae1,2,
  2. Chang-Hoon Lee1,
  3. Jinwoo Lee1,3,
  4. Young Whan Kim4,
  5. Kyungdo Han5,
  6. Sun Mi Choi1,3
  1. 1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea
  2. 2 Department of Pulmonary, Allergy and Critical Care Medicine, Seongnam Citizens Medical Center, Seongnam, Republic of Korea
  3. 3 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea
  4. 4 Department of Respiratory-Allergy & Clinical Immunology, Konkuk University Medical Center, Seoul, Republic of Korea
  5. 5 Department of Statistics and Actuarial Science, Soongsil University, Seoul, Republic of Korea
  1. Correspondence to Dr Sun Mi Choi, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital, Jongno-gu, Seoul, Korea (the Republic of); sunmich81{at}gmail.com

Abstract

Background Smoking has been considered an important risk factor for idiopathic pulmonary fibrosis (IPF) incidence. However, there are no population-based large-scale studies demonstrating the effects of smoking on the development of IPF. We aimed to evaluate the effect of smoking on IPF development using a nationwide population-based cohort.

Methods Using the Korean National Health Information Database, we enrolled individuals who had participated in the health check-up service between 2009 and 2012. Participants having a prior diagnosis of IPF were excluded. The history of smoking status and quantity was collected by a questionnaire. We identified all cases of incident IPF through 2016 on the basis of ICD-10 codes for IPF and medical claims. Cox proportional hazards models were used to calculate the adjusted HR (aHR) of the development of IPF.

Results A total of 25 113 individuals (0.11%) with incident IPF were identified out of 23 242 836 participants registered in the database. The risk of IPF was significantly higher in current and former smokers than in never smokers, with an aHR of 1.66 (95% CI 1.61 to 1.72) and 1.42 (95% CI 1.37 to 1.48), respectively. Current smokers had a higher risk of IPF than former smokers (aHR 1.17, 95% CI 1.13 to 1.21). The risk of IPF development increased as the smoking intensity and duration increased.

Conclusion Smoking significantly increased the risk of IPF development. Current smokers had a higher risk of IPF than former smokers. A dose–response relationship was observed between smoking and the development of IPF.

  • idiopathic pulmonary fibrosis
  • clinical epidemiology
  • tobacco and the lung

Data availability statement

No data are available. The data that support the findings of this study are available from the National Health Insurance Service in Korea but restrictions apply to the availability of these, which were used under license for the current study, and so are not publicly available.

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Data availability statement

No data are available. The data that support the findings of this study are available from the National Health Insurance Service in Korea but restrictions apply to the availability of these, which were used under license for the current study, and so are not publicly available.

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Footnotes

  • WB and C-HL contributed equally.

  • Contributors WB contributed to writing, figures and data interpretation. C-HL contributed to the study design and data interpretation. JL contributed to the literature search and data interpretation. YWK contributed to the literature search. KH contributed to the data collection and data analysis. SMC contributed to the study design, data interpretation and writing.

  • 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.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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