Smoking Cessation and Pancreatic Cancer Risk in Individuals With Prediabetes and Diabetes: A Nationwide Cohort Study
Department of Healthcare Administration and Policy, School of Public Health, University of Nevada, Las Vegas, Las Vegas, Nevada
Search for other papers by Joo-Hyun Park in
Current site
Google Scholar
PubMed
Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
Department of Clinical Research Design and Evaluation, Samsung Advanced Institute for Health Science and Technology (SAIHST), Sungkyunkwan University, Seoul, Republic of Korea
Search for other papers by Jung Yong Hong in
Current site
Google Scholar
PubMed
Search for other papers by Jay J. Shen in
Current site
Google Scholar
PubMed
Search for other papers by Kyungdo Han in
Current site
Google Scholar
PubMed
Search for other papers by Young Suk Park in
Current site
Google Scholar
PubMed
Search for other papers by Joon Oh Park in
Current site
Google Scholar
PubMed
Background: Individuals with diabetes and prediabetes are at increased risk of pancreatic cancer. However, little is known about the effects of smoking or smoking cessation on pancreatic cancer risk in individuals with diabetes and prediabetes. We investigated the association between smoking status (particularly smoking cessation) and pancreatic cancer risk according to glycemic status. Patients and Methods: This nationwide cohort study included 9,520,629 adults without cancer who underwent the Korean National Health Screening in 2009 and were followed until 2018. Hazard ratios and 95% confidence intervals for pancreatic cancer were estimated after adjusting for potential confounders. Results: During the 78.4 million person-years of follow-up, 15,245 patients were newly diagnosed with pancreatic cancer. Among individuals with diabetes and prediabetes, current smoking synergistically increased pancreatic cancer risk (all P<.01). However, quitters with diabetes and prediabetes had a pancreatic cancer risk comparable to that of never-smokers (all P>.05). For pancreatic cancer in current smokers, quitters, and never-smokers, respectively, the hazard ratios were 1.48 (95% CI, 1.40–1.58), 1.11 (95% CI, 1.03–1.19), and 1.00 (reference) among individuals with normoglycemia; 1.83 (95% CI, 1.70–1.97), 1.28 (95% CI, 1.18–1.39), and 1.20 (95% CI, 1.14–1.26) among individuals with prediabetes; and 2.72 (95% CI, 2.52–2.94), 1.78 (95% CI, 1.63–1.95), and 1.63 (95% CI, 1.54–1.72) among individuals with diabetes. There were no differences in risk between quitters with a <20 pack-year smoking history and never-smokers in all glycemic status groups. Conclusions: Pancreatic cancer risk synergistically increased in current smokers with diabetes and prediabetes. However, smoking cessation reduced the synergistically increased risk of pancreatic cancer to the level of never-smokers, especially when smoking history was <20 pack-years. More individualized and intensive cancer prevention education should be underscored for individuals at an increased risk of pancreatic cancer beyond the one-size-fits-all approach.
Submitted March 24, 2023; final revision received June 16, 2023; accepted for publication July 19, 2023.
Author contributions: Study concept and design: J.H. Park, Hong, Shen, Han. Data acquisition: J.H. Park, Hong, Shen, Han. Data analysis and interpretation: All authors. Funding acquisition: J.H. Park. Manuscript preparation: J.H. Park, Hong, Shen, Han. Critical revision: All authors. J.H. Park had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Data availability statement: The data analyzed in this study are not available for public use. However, researchers can apply for the National Health Insurance data-sharing service based on Institutional Review Board approval. After review by the Korea National Health Insurance Sharing Service Institutional Data Access/Ethics Committee, researchers must pay a data access fee before accessing the data on the Health Insurance Data Service website (http://nhiss.nhis.or.kr), similar to the authors of this article.
Disclosures: Dr. Hong has disclosed serving as a consultant or advisor for AstraZeneca and Eisai. Dr. J.O. Park has disclosed serving as a consultant or advisor for Celgene, Merck Serono, Servier, AstraZeneca, and MediRama; and receiving grant/research support from Celgene, Medpacto, and Servier. The remaining authors have disclosed that they have not received any financial consideration from any person or organization to support the preparation, analysis, results, or discussion of this article.
Funding: Research reported in this publication was supported by the Basic Science Research Program through the National Research Foundation of Korea with funds from the Ministry of Education, Republic of Korea (2022R1I1A1A01054327, J.H. Park) and the Bio & Medical Technology Development Program of the National Research Foundation with funds from the Ministry of Scient and ICT, Republic of Korea (RS-2023-00222838, J.Y. Hong).
Supplementary Materials
- Supplemental Materials (PDF 451 KB)
© 2019-2024 National Comprehensive Cancer Network