Pancreatic Cancer Risk in Relation to Lifetime Smoking Patterns, Tobacco Type, and Dose-Response Relationships.
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Molina-Montes Esther, Van Hoogstraten Lisa, Gomez-Rubio Paulina, Löhr Matthias, Sharp Linda, Molero Xavier, Márquez Mirari, Michalski Christoph W, Farré Antoni, Perea José, O'Rorke Michael, Greenhalf William, Ilzarbe Lucas, Tardon Adonina, Gress Thomas M, Barberà Victor M, Crnogorac-Jurcevic Tatjana, Muñoz-Bellvis Luis, Domínguez-Muñoz Enrique, Balsells Joaquim, Costello Eithne, Iglesias Mar, Kleeff Jorg, Kong Bo, Mora Josefina, O'Driscoll Damian, Poves Ignasi, Scarpa Aldo, Yu Jingru, Ye Weimin, Hidalgo Manuel, Carrato Alfredo, Lawlor Rita, Real Francisco X, Malats Nuria, PanGenEU Study Investigators
Аннотация
METHODS: Tobacco smoking habits and other relevant information were obtained from 2,009 cases and 1,532 controls recruited in the PanGenEU study using standardized tools. Multivariate logistic regression analysis was performed to evaluate pancreatic cancer risk by smoking characteristics and interactions with other pancreatic cancer risk factors. Fractional polynomials and restricted cubic splines were used to test for nonlinearity of the dose-response relationships and to analyze their shape.
RESULTS: Relative to never-smokers, current smokers [OR = 1.72; 95% confidence interval (95% CI), 1.39-2.12], those inhaling into the throat (OR = 1.48; 95% CI, 1.11-1.99) or chest (OR = 1.33; 95% CI, 1.12-1.58), and those using nonfiltered cigarettes (OR = 1.69; 95% CI, 1.10-2.61), were all at an increased pancreatic cancer risk. Pancreatic cancer risk was highest in current black tobacco smokers (OR = 2.09; 95% CI, 1.31-3.41), followed by blond tobacco smokers (OR = 1.43; 95% CI, 1.01-2.04). Childhood exposure to tobacco smoke relative to parental smoking was also associated with increased pancreatic cancer risk (OR = 1.24; 95% CI, 1.03-1.49). Dose-response relationships for smoking duration, intensity, cumulative dose, and smoking cessation were nonlinear and showed different shapes by tobacco type. Effect modification by family history of pancreatic cancer and diabetes was likely.
CONCLUSIONS: This study reveals differences in pancreatic cancer risk by tobacco type and other habit characteristics, as well as nonlinear risk associations.
IMPACT: This characterization of smoking-related pancreatic cancer risk profiles may help in defining pancreatic cancer high-risk populations.