Abstract
Objective: We examined the role of active cigarette smoking, smoking cessation, and environmental tobacco smoking (ETS) as determinants for pancreatic cancer in a large prospective cohort study.
Methods: The Netherlands Cohort Study consisted of 120,852 men and women who completed a baseline questionnaire in 1986. After 16.3 years of follow‐up, 520 pancreatic cancer cases were available for analysis.
Results: Compared to never cigarette smokers, both former and current cigarette smokers had an increased pancreatic cancer risk (multivariable‐adjusted hazard rate ratio (HR) = 1.34; 95% confidence interval (CI) = 1.02–1.75 and HR = 1.82; 95% CI = 1.40–2.38, respectively). We observed an increased pancreatic cancer risk of 38% (95% CI = 1.01–1.87) with smoking ≥20 cigarettes per day compared to never cigarette smoking. The trend test was significant (P = 0.03), but no clear dose‐response relation was present. For duration of smoking, we observed an increased pancreatic cancer risk per increment of 10 years (multivariable‐adjusted HR = 1.15; 95% CI = 1.08–1.22), with a clear dose response effect observing a 2‐fold increased cancer risk comparing ≥40 years of smoking to never cigarette smoking. Quitting smoking gradually reduced the risk of pancreatic cancer (HR = 1.83, 1.41, and 1.42 for currents smokers, ex‐smokers quitted 0.1–<10 yrs, and quitted 10–<20 yrs, respectively) and reached unity after ≥20 years of quitting smoking (multivariable‐adjusted HR = 1.17; 95% CI=0.80–1.70). Based on the current study, hypothetically 27% (95% CI = 15–37) of pancreatic cancer cases could be prevented if people would not smoke. We investigated which smoking aspect was most important in pancreatic cancer etiology by including smoking variables simultaneously in the model. Only duration remained significantly associated with pancreatic cancer risk (≥40 years of smoking vs. never cigarette smokers, multivariable‐adjusted HR = 1.87; 95% CI = 1.24–2.80); the risk estimates of other smoking variables attenuated and became non‐significant. When we investigated the interaction between ethanol intake and cigarette smoking, no significant interaction was found (P = 0.97). However, current smokers who consumed ≥30 g of ethanol daily experienced a significantly increased risk compared to abstainers who never smoked (multivariable‐adjusted HR = 2.40; 95% CI = 1.06–5.41). No association was observed for ETS and pancreatic cancer risk in women.
Conclusion: Overall, our findings confirmed that cigarette smoking is an important risk factor for pancreatic cancer, while quitting smoking reduced risk. Therefore from a public health perspective, quitting smoking would benefit the burden on pancreatic cancer incidence and mortality. No association was observed between ETS and pancreatic cancer.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B140.
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