Differences in allergic sensitization by self-reported race and genetic ancestry

Received 20 May 2008; received in revised form 29 July 2008; accepted 30 July 2008.

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 ≥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.

Key words: Self-reported race, race-ethnicity, continental population group, IgE, allergic sensitization

Abbreviations used: AIM, Ancestral informative marker, gSD, Geometric SD, OR, Odds ratio, VIF, Variance inflation factor

a Department of Biostatistics and Research Epidemiology, Henry Ford Health System, Detroit, Mich

d Center for Health Services Research, Henry Ford Health System, Detroit, Mich

h Department of Medicine, Henry Ford Health System, Detroit, Mich

b Department of Medicine, University of California San Francisco, San Francisco, Calif

c Department of Biopharmaceutical Sciences, University of California San Francisco, San Francisco, Calif

f Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif

e Department of Pediatrics, Medical College of Georgia, Augusta, Ga

g Department of Anthropology, Pennsylvania State University, University Park, Pa

Reprint requests: L. Keoki Williams, MD, MPH, Center for Health Services Research, Henry Ford Health System, 1 Ford Place, 3A CHSR, Detroit, MI 48202.

Supported by grants from the Fund for Henry Ford Hospital, the Sandler Program for Asthma Research, and the National Institute of Allergy and Infectious Diseases (AI61774, AI50681, and AI59415) and the National Heart, Lung, and Blood Institute (HL79055), National Institutes of Health.

Disclosure of potential conflict of interest: E. G. Burchard has received research support from the National Institutes of Health (NIH) and the Flight Attendants Medical Research Institute and has served as a member of the American Thoracic Society (ATS). S. Choudhry has received research support from the ATS and the TRDRP. C. C. Johnson has received research support from the NIH and Henry Ford Hospital. D. R. Ownby has received research support from the National Institute of Allergy and Infections Diseases (NIAID), the American Academy of Pediatrics, and the Merck Childhood Asthma Network. P.-Y. Kwok has received research support from the NIH and has consulted on DNA analysis technology patent litigation. C. L. Joseph has received research support from the NIH. M. D. Shriver has consulting arrangements with DNAPrint Genomics and has received research support from the National Human Genome Research Institute, the NIH, the National Institute of Child Health and Human Development, the March of Dimes, and the National heart, Lung, and Blood Institute (NHLBI). L. K. Williams has received research support from the NIAID, the NIH, the NHLBI, and the Strategic Program for Asthma Research. The rest of the authors have declared that they have no conflict of interest.

PII: S0091-6749(08)01457-7

doi:10.1016/j.jaci.2008.07.044

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