James J Yang1, Esteban G Burchard2, Shweta Choudhry3, Christine C Johnson1, Dennis R Ownby4, David Favro5, Justin Chen6, Matthew Akana6, Connie Ha6, Pui-Yan Kwok6, Richard Krajenta1, Suzanne L Havstad1, Christine L Joseph1, Max A Seibold2, Mark D Shriver7, L Keoki Williams8. 1. Department of Biostatistics and Research Epidemiology, Henry Ford Health System, Detroit, Mich. 2. Department of Medicine, University of California San Francisco, San Francisco, Calif; Department of Biopharmaceutical Sciences, University of California San Francisco, San Francisco, Calif. 3. Department of Medicine, University of California San Francisco, San Francisco, Calif. 4. Department of Pediatrics, Medical College of Georgia, Augusta, Ga. 5. Center for Health Services Research, Henry Ford Health System, Detroit, Mich. 6. Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif. 7. Department of Anthropology, Pennsylvania State University, University Park, Pa. 8. Department of Biostatistics and Research Epidemiology, Henry Ford Health System, Detroit, Mich; Center for Health Services Research, Henry Ford Health System, Detroit, Mich; Department of Medicine, Henry Ford Health System, Detroit, Mich. Electronic address: kwillia5@hfhs.org.
Abstract
BACKGROUND: Many allergic conditions occur more frequently in African American patients when compared with white patients; however, it is not known whether this represents genetic predisposition or disparate environmental exposures. OBJECTIVE: We sought to assess the relationship of self-reported race and genetic ancestry to allergic sensitization. METHODS: We included 601 women enrolled in a population-based cohort study whose self-reported race was African American or white. Genetic ancestry was estimated by using markers that differentiate West African and European ancestry. We assessed the relationship between allergic sensitization (defined as > or =1 allergen-specific IgE results) and both self-reported race and genetic ancestry. Regression models adjusted for sociodemographic variables, environmental exposures, and location of residence. RESULTS: The average proportion of West African ancestry in African American participants was 0.69, whereas the mean proportion of European ancestry in white participants was 0.79. Self-reported African American race was associated with allergic sensitization when compared with those who reported being white (adjusted odds ratio, 2.19; 95% CI, 1.22-3.93), even after adjusting for other variables. Genetic ancestry was not significantly associated with allergic sensitization after accounting for location of residence (adjusted odds ratio, 2.09 for urban vs suburban residence; 95% CI, 1.32-3.31). CONCLUSION: Self-reported race and location of residence appeared to be more important predictors of allergic sensitization when compared with genetic ancestry, suggesting that the disparity in allergic sensitization by race might be primarily a result of environmental factors rather than genetic differences.
BACKGROUND: Many allergic conditions occur more frequently in African American patients when compared with white patients; however, it is not known whether this represents genetic predisposition or disparate environmental exposures. OBJECTIVE: We sought to assess the relationship of self-reported race and genetic ancestry to allergic sensitization. METHODS: We included 601 women enrolled in a population-based cohort study whose self-reported race was African American or white. Genetic ancestry was estimated by using markers that differentiate West African and European ancestry. We assessed the relationship between allergic sensitization (defined as > or =1 allergen-specific IgE results) and both self-reported race and genetic ancestry. Regression models adjusted for sociodemographic variables, environmental exposures, and location of residence. RESULTS: The average proportion of West African ancestry in African American participants was 0.69, whereas the mean proportion of European ancestry in white participants was 0.79. Self-reported African American race was associated with allergic sensitization when compared with those who reported being white (adjusted odds ratio, 2.19; 95% CI, 1.22-3.93), even after adjusting for other variables. Genetic ancestry was not significantly associated with allergic sensitization after accounting for location of residence (adjusted odds ratio, 2.09 for urban vs suburban residence; 95% CI, 1.32-3.31). CONCLUSION: Self-reported race and location of residence appeared to be more important predictors of allergic sensitization when compared with genetic ancestry, suggesting that the disparity in allergic sensitization by race might be primarily a result of environmental factors rather than genetic differences.
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