Linda E Kelemen1,2, Sarah Abbott3, Bo Qin4, Lauren Cole Peres3, Patricia G Moorman5, Kristin Wallace6,7, Elisa V Bandera4, Jill S Barnholtz-Sloan8, Melissa Bondy9, Kathleen Cartmell10, Michele L Cote11, Ellen Funkhouser12, Lisa E Paddock13, Edward S Peters14, Ann G Schwartz11, Paul Terry15, Anthony J Alberg6,7, Joellen M Schildkraut3. 1. Department of Public Health Sciences, Medical University of South Carolina, Bioengineering Building, MSC955, 68 President Street, Charleston, SC, 29425, USA. kelemen@musc.edu. 2. Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA. kelemen@musc.edu. 3. Department of Public Health Sciences, University of Virginia, Charlottesville, VA, USA. 4. Department of Population Science, Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. 5. Department of Community and Family Medicine, Duke Cancer Institute, Durham, NC, USA. 6. Department of Public Health Sciences, Medical University of South Carolina, Bioengineering Building, MSC955, 68 President Street, Charleston, SC, 29425, USA. 7. Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA. 8. Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA. 9. Department of Medicine, Section of Epidemiology and Population Sciences, Baylor College of Medicine, Houston, TX, USA. 10. College of Nursing, Medical University of South Carolina, Charleston, SC, USA. 11. Department of Oncology and the Karmanos Cancer Institute, Population Studies and Disparities Research Program, Wayne State University School of Medicine, Detroit, MI, USA. 12. Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. 13. Cancer Surveillance Research, Rutgers Cancer Institute of New Jersey and Rutgers School of Public Health, New Jersey State Cancer Registry, New Brunswick, NJ, USA. 14. Epidemiology Program, Louisiana State University Health Sciences Center School of Public Health, New Orleans, LA, USA. 15. Departments of Public Health and Surgery, University of Tennessee-Knoxville, Knoxville, TN, USA.
Abstract
BACKGROUND: Smoking is a risk factor for mucinous ovarian cancer (OvCa) in Caucasians. Whether a similar association exists in African Americans (AA) is unknown. METHODS: We conducted a population-based case-control study of incident OvCa in AA women across 11 geographic locations in the US. A structured telephone interview asked about smoking, demographic, health, and lifestyle factors. Odds ratios and 95% confidence intervals (OR, 95% CI) were estimated from 613 cases and 752 controls using unconditional logistic regression in multivariable adjusted models. RESULTS: Associations were greater in magnitude for serous OvCa than for all OvCa combined. Compared to never smokers, increased risk for serous OvCa was observed for lifetime ever smokers (1.46, 1.11-1.92), former smokers who quit within 0-2 years of diagnosis (5.48, 3.04-9.86), and for total pack-years smoked among lifetime ever smokers (0-5 pack-years: 1.79, 1.23-2.59; >5-20 pack-years: 1.52, 1.05-2.18; >20 pack-years: 0.98, 0.61-1.56); however, we observed no dose-response relationship with increasing duration or consumption and no significant associations among current smokers. Smoking was not significantly associated with mucinous OvCa. Associations for all OvCa combined were consistently elevated among former smokers. The proportion of ever smokers who quit within 0-2 years was greater among cases (23%) than controls (7%). CONCLUSIONS: Cigarette smoking may be associated with serous OvCa among AA, which differs from associations reported among Caucasians. Exposure misclassification or reverse causality may partially explain the absence of increased risk among current smokers and lack of dose-response associations. Better characterization of smoking patterns is needed in this understudied population.
BACKGROUND: Smoking is a risk factor for mucinous ovarian cancer (OvCa) in Caucasians. Whether a similar association exists in African Americans (AA) is unknown. METHODS: We conducted a population-based case-control study of incident OvCa in AA women across 11 geographic locations in the US. A structured telephone interview asked about smoking, demographic, health, and lifestyle factors. Odds ratios and 95% confidence intervals (OR, 95% CI) were estimated from 613 cases and 752 controls using unconditional logistic regression in multivariable adjusted models. RESULTS: Associations were greater in magnitude for serous OvCa than for all OvCa combined. Compared to never smokers, increased risk for serous OvCa was observed for lifetime ever smokers (1.46, 1.11-1.92), former smokers who quit within 0-2 years of diagnosis (5.48, 3.04-9.86), and for total pack-years smoked among lifetime ever smokers (0-5 pack-years: 1.79, 1.23-2.59; >5-20 pack-years: 1.52, 1.05-2.18; >20 pack-years: 0.98, 0.61-1.56); however, we observed no dose-response relationship with increasing duration or consumption and no significant associations among current smokers. Smoking was not significantly associated with mucinous OvCa. Associations for all OvCa combined were consistently elevated among former smokers. The proportion of ever smokers who quit within 0-2 years was greater among cases (23%) than controls (7%). CONCLUSIONS: Cigarette smoking may be associated with serous OvCa among AA, which differs from associations reported among Caucasians. Exposure misclassification or reverse causality may partially explain the absence of increased risk among current smokers and lack of dose-response associations. Better characterization of smoking patterns is needed in this understudied population.
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