Idan Menashe1, William F Anderson, Ismail Jatoi, Philip S Rosenberg. 1. Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD 20852-7244, USA. menashei@mail.nih.gov
Abstract
BACKGROUND: In the United States, a black-to-white disparity in age-standardized breast cancer mortality rates emerged in the 1980s and has widened since then. METHODS: To further explore this racial disparity, black-to-white rate ratios (RRs(BW)) for mortality, incidence, hazard of breast cancer death, and incidence-based mortality (IBM) were investigated using data from the National Cancer Institute's Surveillance, Epidemiology, and End Results program on 244 786 women who were diagnosed with breast cancer from January 1990 through December 2003 and followed through December 2004. A counterfactual approach was used to examine the expected IBM RRs(BW), assuming equal distributions for estrogen receptor (ER) expression, and/or equal hazard rates of breast cancer death, among black and white women. RESULTS: From 1990 through 2004, mortality RR(BW) was greater than 1.0 and widened over time (age-standardized breast cancer mortality rates fell from 36 to 29 per 100 000 for blacks and from 30 to 22 per 100 000 for whites). In contrast, incidence RR(BW) was generally less than 1.0. Absolute hazard rates of breast cancer death declined substantially for ER-positive tumors and modestly for ER-negative tumors but were persistently higher for blacks than whites. Equalizing the distributions of ER expression in blacks and whites decreased the IBM RR(BW) slightly. Interestingly, the black-to-white disparity in IBM RR(BW) was essentially eliminated when hazard rates of breast cancer death were matched within each ER category. CONCLUSIONS: The black-to-white disparity in age-standardized breast cancer mortality was largely driven by the higher hazard rates of breast cancer death among black women, diagnosed with the disease, irrespective of ER expression, and especially in the first few years following diagnosis. Greater emphasis should be placed on identifying the etiology of these excess hazards and developing therapeutic strategies to address them.
BACKGROUND: In the United States, a black-to-white disparity in age-standardized breast cancer mortality rates emerged in the 1980s and has widened since then. METHODS: To further explore this racial disparity, black-to-white rate ratios (RRs(BW)) for mortality, incidence, hazard of breast cancer death, and incidence-based mortality (IBM) were investigated using data from the National Cancer Institute's Surveillance, Epidemiology, and End Results program on 244 786 women who were diagnosed with breast cancer from January 1990 through December 2003 and followed through December 2004. A counterfactual approach was used to examine the expected IBM RRs(BW), assuming equal distributions for estrogen receptor (ER) expression, and/or equal hazard rates of breast cancer death, among black and white women. RESULTS: From 1990 through 2004, mortality RR(BW) was greater than 1.0 and widened over time (age-standardized breast cancer mortality rates fell from 36 to 29 per 100 000 for blacks and from 30 to 22 per 100 000 for whites). In contrast, incidence RR(BW) was generally less than 1.0. Absolute hazard rates of breast cancer death declined substantially for ER-positive tumors and modestly for ER-negative tumors but were persistently higher for blacks than whites. Equalizing the distributions of ER expression in blacks and whites decreased the IBM RR(BW) slightly. Interestingly, the black-to-white disparity in IBM RR(BW) was essentially eliminated when hazard rates of breast cancer death were matched within each ER category. CONCLUSIONS: The black-to-white disparity in age-standardized breast cancer mortality was largely driven by the higher hazard rates of breast cancer death among black women, diagnosed with the disease, irrespective of ER expression, and especially in the first few years following diagnosis. Greater emphasis should be placed on identifying the etiology of these excess hazards and developing therapeutic strategies to address them.
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