Humberto Parada1, Marilie D Gammon2, Hope L Ettore3, Jia Chen4, Antonia M Calafat5, Alfred I Neugut6, Regina M Santella7, Mary S Wolff8, Susan L Teitelbaum9. 1. Division of Epidemiology and Biostatistics, School of Public Health, San Diego State University, San Diego, CA, USA; Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA. Electronic address: hparada@sdsu.edu. 2. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: gammon@unc.edu. 3. Division of Epidemiology and Biostatistics, School of Public Health, San Diego State University, San Diego, CA, USA. Electronic address: hetorre@sdsu.edu. 4. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: jia.chen@mssm.edu. 5. Centers for Disease Control and Prevention, Atlanta, GA, USA. Electronic address: aic7@cdc.gov. 6. Department of Medicine, Vagelos College of Physicians and Surgeons and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA. Electronic address: ain1@cumc.columbia.edu. 7. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA. Electronic address: rps1@cumc.columbia.edu. 8. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: mary.wolff@mssm.edu. 9. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: susan.teitelbaum@mssm.edu.
Abstract
BACKGROUND: Environmental phenols, compounds used widely in personal care and consumer products, are known endocrine disruptors. Few epidemiologic studies have examined the association of phenol biomarkers with breast cancer incidence and, to our knowledge, none have considered associations with mortality following breast cancer. We examined seven urinary phenol biomarkers in association with breast cancer incidence and subsequent mortality, and examined effect measure modification by body mass index (BMI). METHODS: Participants included 711 women with breast cancer and 598 women without breast cancer who were interviewed for the population-based Long Island Breast Cancer Study Project. Among women with breast cancer, phenol biomarkers were quantified in spot urine samples collected on average within three months of a first diagnosis of primary in situ or invasive breast cancer in 1996-1997. Women with breast cancer were monitored for vital status using the National Death Index. After a median follow-up of 17.6 years, we identified 271 deaths, including 98 deaths from breast cancer. We examined creatinine-corrected phenol concentrations and the sum of parabens (Σparabens) in association with breast cancer incidence using logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), and with mortality using Cox regression to estimate hazard ratios (HRs) and 95% CIs. We evaluated multiplicative effect measure modification using cross-product terms in nested models. RESULTS: The highest (vs lowest) quintiles of urinary methylparaben, propylparaben, and Σparabens were associated with risk of breast cancer with ORs ranging from 1.31 to 1.50. Methylparaben, propylparaben, and Σparabens were also associated with all-cause mortality HRs ranging from 0.68 to 0.77. Associations for breast cancer incidence were more pronounced among women with BMI < 25.0 kg/m2 than among women with BMI ≥ 25.0 kg/m2; however, associations for mortality were more pronounced among women with BMI ≥ 25 kg/m2 than among women with BMI < 25 kg/m2. CONCLUSIONS: Select parabens may have differential associations with risk of developing breast cancer and mortality following breast cancer.
BACKGROUND: Environmental phenols, compounds used widely in personal care and consumer products, are known endocrine disruptors. Few epidemiologic studies have examined the association of phenol biomarkers with breast cancer incidence and, to our knowledge, none have considered associations with mortality following breast cancer. We examined seven urinary phenol biomarkers in association with breast cancer incidence and subsequent mortality, and examined effect measure modification by body mass index (BMI). METHODS:Participants included 711 women with breast cancer and 598 women without breast cancer who were interviewed for the population-based Long Island Breast Cancer Study Project. Among women with breast cancer, phenol biomarkers were quantified in spot urine samples collected on average within three months of a first diagnosis of primary in situ or invasive breast cancer in 1996-1997. Women with breast cancer were monitored for vital status using the National Death Index. After a median follow-up of 17.6 years, we identified 271 deaths, including 98 deaths from breast cancer. We examined creatinine-corrected phenol concentrations and the sum of parabens (Σparabens) in association with breast cancer incidence using logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), and with mortality using Cox regression to estimate hazard ratios (HRs) and 95% CIs. We evaluated multiplicative effect measure modification using cross-product terms in nested models. RESULTS: The highest (vs lowest) quintiles of urinary methylparaben, propylparaben, and Σparabens were associated with risk of breast cancer with ORs ranging from 1.31 to 1.50. Methylparaben, propylparaben, and Σparabens were also associated with all-cause mortality HRs ranging from 0.68 to 0.77. Associations for breast cancer incidence were more pronounced among women with BMI < 25.0 kg/m2 than among women with BMI ≥ 25.0 kg/m2; however, associations for mortality were more pronounced among women with BMI ≥ 25 kg/m2 than among women with BMI < 25 kg/m2. CONCLUSIONS: Select parabens may have differential associations with risk of developing breast cancer and mortality following breast cancer.
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