Aim: The association of smoking and development of ductal pancreatic cancer was studied experimentally and epidemiologically. Methods: Experimentally the tobacco derived carcinogen 4-(methylnitrosamino)-l-(3-pyridyl)-l-butanone (NKK) was measured in pancreatic juice of actively smoking and non-smoking or passively smoking patients undergoing surgery for disorders of the pancreatic gland by gas chromatography with mass spectrometric detection. Epidemiologically age at diagnosis of pancreatic cancer was compared among smoking and non-smoking patients. Results: NKK was detected in 14/17 (82%) samples of active smokers at levels from 1.37-604 ng/ml pancreatic juice whereas it ranged from not-detected (3 cases) to 96.8 ng/ml in non-smokers/passive smokers (p<0.05, Wilcoxon rank-sum test). Smoking patients (n=120) developed pancreatic cancer 6 years significantly earlier (p<0.05, t-test) than non-smokers (n=247, mean 58 vs 74 years, respectively) Conclusion: 1. The tobacco derived carcinogen NKK was detected for the first time in human pancreatic juice. 2. NKK levels in pancreatic juice were higher in actively smoking than in non-smoking or passively smoking patients. 3. Smokers acquire ductal pancreatic cancer earlier than non-smokers. 4. The carcinogen NKK, its metabolites but also other tobacco derived compounds may contribute to the development of pancreatic cancer in humans.
|Original language||English (US)|
|Number of pages||1|
|Journal||Langenbeck's Archives of Surgery|
|State||Published - Dec 1 2001|
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