OBJECTIVE: To evaluate the role of tobacco and alcohol consumption in the aetiology of prostate cancer. PATIENTS AND METHODS: In a case-control study conducted in the Netherlands, information on smoking and drinking habits was obtained from questionnaires completed by 345 patients exhibiting primary prostate cancer and by 1346 controls with benign prostate hyperplasia. The response rate was 79%. RESULTS: No association was observed between drinking habits and the risk of prostate cancer (324 cases versus 1237 controls; odds ratio 1.36; 95%CI 0.84-2.22). A significantly elevated odds ratio was found for individuals who had smoked at any time during their lives (329 cases versus 1212 controls; odds ratio 2.12; 95%CI 1.24-3.62). However, no relationship was observed between the number of cigarettes smoked, the duration of smoking, the age at which the subjects started smoking or with the calendar period in which they were born. Odds ratios calculated for individuals who smoked in consecutive 5-year periods between 1940 and 1989 did not show any trend. Furthermore, the risk of prostate cancer among ex-smokers did not differ significantly from the risk among current smokers, even when smoking was stopped more than 25 years previously. CONCLUSION: From these findings, which do not point to the causative agent, it would appear that neither smoking nor alcohol consumption seriously increases the risk of prostate cancer.
OBJECTIVE: To evaluate the role of tobacco and alcohol consumption in the aetiology of prostate cancer. PATIENTS AND METHODS: In a case-control study conducted in the Netherlands, information on smoking and drinking habits was obtained from questionnaires completed by 345 patients exhibiting primary prostate cancer and by 1346 controls with benign prostate hyperplasia. The response rate was 79%. RESULTS: No association was observed between drinking habits and the risk of prostate cancer (324 cases versus 1237 controls; odds ratio 1.36; 95%CI 0.84-2.22). A significantly elevated odds ratio was found for individuals who had smoked at any time during their lives (329 cases versus 1212 controls; odds ratio 2.12; 95%CI 1.24-3.62). However, no relationship was observed between the number of cigarettes smoked, the duration of smoking, the age at which the subjects started smoking or with the calendar period in which they were born. Odds ratios calculated for individuals who smoked in consecutive 5-year periods between 1940 and 1989 did not show any trend. Furthermore, the risk of prostate cancer among ex-smokers did not differ significantly from the risk among current smokers, even when smoking was stopped more than 25 years previously. CONCLUSION: From these findings, which do not point to the causative agent, it would appear that neither smoking nor alcohol consumption seriously increases the risk of prostate cancer.
Authors: T M Crisp; E D Clegg; R L Cooper; W P Wood; D G Anderson; K P Baetcke; J L Hoffmann; M S Morrow; D J Rodier; J E Schaeffer; L W Touart; M G Zeeman; Y M Patel Journal: Environ Health Perspect Date: 1998-02 Impact factor: 9.031