prostate cancer and smoking
DESCRIPTION
PROSTATE CANCER AND SMOKING. Kym Hickey MBBS, MPH Repatriation Medical Authority, Australia. Prostate Cancer and Smoking. Master’s thesis on this topic Review article on prostate cancer and smoking (Hickey et al 2001, Epidemiologic Reviews 23(1): 115-125). Learning Objectives. - PowerPoint PPT PresentationTRANSCRIPT
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PROSTATE CANCER AND SMOKING
Kym Hickey MBBS, MPH
Repatriation Medical Authority, Australia
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Prostate Cancer and Smoking
• Master’s thesis on this topic
• Review article on prostate cancer and smoking (Hickey et al 2001, Epidemiologic Reviews 23(1): 115-125)
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Learning Objectives
• Be aware of data concerning prostate cancer and smoking
• Understand epidemiological criteria used to assess causality
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Performance Objectives
• How to assess new evidence on prostate cancer & smoking
• How to apply epidemiological criteria to other questions of causality
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Why Prostate Cancer & Smoking
• Role of smoking in prostate cancer unclear
• Important public health issue as both smoking and prostate cancer are prevalent in community
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Identification of Studies
• Medline search
• Review of bibliographies of identified studies
• Conference papers
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Assessment of Study Quality
• Study design / selection issues
• Measurement of prostate cancer & smoking
• Control of confounding
• Statistical issues
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Results
• 65 controlled studies reported results for pc & smoking
• Results for both current & past smoking varied from protective for pc to increasing the risk of pc
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Study No. cases RR, CI
1 1369 1.04, 0.85-1.27
2 69 0.56, 0.36-0.83
3 71 2.2, 1.2-4.4
4 180 0.49, 0.16-1.57
5 238 1.46, 1.07-1.94
6 198 1.0, 0.6-1.6
7 707 1.1, 0.9-1.3
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Study No. Cases RR, CI
8 174 0.87, 0.61-1.23
9 220 1.08, 0.90-1.30
10 2,368 1.11, 1.01-1.23
11 209 1.11, 0.90-1.36
12 109 0.82, 0.57-1.14
13 138 0.9, 0.40-1.73
14 406 1.00, 0.71-1.39
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Study No. Cases RR, CI
15 54 1.3, 0.61-2.79
16 166 0.76, 0.51-1.14
17 243 1.1, 1.0-1.3
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Study No. Cases RR, CI
1 103 1.58, 0.81-3.10
2 709 1.26, 1.06-1.50
3 1748 1.34, 1.16-1.56
4 134 1.75, 1.37-2.19
5 147 1.1, 0.7-1.5
6 4607 1.18, 1.09-1.28
7 569 0.99, 0.87-1.34
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Study No. Cases RR, CI
8 149 2.0, 1.1-3.7
9 32 1.83, 1.01-3.05
10 826 1.31, 1.13-1.52
11 319 1.02, 0.81-1.28
12 193 0.93, 0.72-1.18
13 30 1.38, 0.67-2.85
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Population-based Case-Control
• 10 out of 15 p-b case-control studies found no association between current or ever smoking & pc as did 4 out of 5 case-control studies that used hospital cases and population controls
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Hospital-based Case-Control
• 12 out of 16 hospital-based case-control studies found no association between current or ever smoking and prostate cancer
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Methodological Criticisms I
• ? Differential measurement of prostate cancer in mortality cohorts
• ? Differential screening of prostate cancer in mortality cohorts
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Methodological Criticisms II
• ? Confounding by dietary fat
• ? Differential treatment of prostate cancer by smoking status
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Causal Criteria - Consistency
• There was inconsistency between the results of the mortality cohorts (positive association between pc and current smoking) and incidence cohorts (no association)
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Causal Criteria – Strength of Association
• Association observed between current smoking and fatal prostate cancer was weak – about a 30% increase in risk
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Causal Criteria – Dose Response
• 2 cohorts found a D-R relation between current smoking and risk of incident pc
• 2 cohorts found a D-R relation between current or recent smoking and risk of fatal pc
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Prostate Cancer More Aggressive in Smokers ?
• Does the increased risk of advanced incident or fatal pc in recent or current smokers mean that pc follows a more aggressive course in smokers compared to nonsmokers ?
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Causal Criteria – Biological Plausibility
• Few studies on the effects of smoking on prostate cancer in animals
• Nitrosamines and pc in rats, tobacco smoke and pc tumor cell fraction in rats
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Causal Criteria – Biological Plausibility
• Various mechanisms proposed – cadmium, male hormones, genetic mutations, immune dysfunction – but none clearly established
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Male Hormones
• Probably most widely discussed of the proposed mechanisms
• Rests on two assumptions: smoking is anti-estrogenic and male sex hormones increase risk of prostate cancer but ??
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Male Hormones
• No diff. in mean serum level of T, free T, dihydroT, estrone, estradiol, androstenedione, DHEAS, between pc cases and controls in meta-analysis of 10 prospective studies (Eaton et al 1999 Br J Cancer 80: 930-4)
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Conclusion
• Positive association observed between smoking and fatal prostate cancer could be due to a methodological bias or prostate cancer may be more aggressive in smokers