The Journal of Allergy and Clinical Immunology
Volume 126, Issue 6 , Pages 1149-1156.e1, December 2010

Racial differences in biologic predictors of severe asthma: Data from the Severe Asthma Research Program

  • Christy Gamble, DrPHc, MPH

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa
    • Corresponding Author InformationReprint requests: Christy Gamble, MPH, 9 NW Montefiore Hospital, 3459 Fifth Ave, Pittsburgh, PA 15213.
  • ,
  • Evelyn Talbott, DrPH, MPH

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa
  • ,
  • Ada Youk, PhD

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa
  • ,
  • Fernando Holguin, MD, MPH

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa
  • ,
  • Bruce Pitt, PhD

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa
  • ,
  • Lori Silveira, MS

      Affiliations

    • National Jewish Health, Denver, Colo
  • ,
  • Eugene Bleecker, MD

      Affiliations

    • Wake Forest University, Winston-Salem, NC
  • ,
  • William Busse, MD

      Affiliations

    • University of Wisconsin, Madison, Wis
  • ,
  • William Calhoun, MD

      Affiliations

    • University of Texas-Galveston, Galveston, Tex
  • ,
  • Mario Castro, MD, MPH

      Affiliations

    • Washington University, St Louis, Mo
  • ,
  • Kian Fan Chung, MD, DSc

      Affiliations

    • Imperial College, London, United Kingdom
  • ,
  • Serpil Erzurum, MD

      Affiliations

    • Cleveland Clinics, Cleveland, Ohio
  • ,
  • Elliot Israel, MD

      Affiliations

    • Brigham and Women's Hospital, Boston, Mass
  • ,
  • Sally Wenzel, MD

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pa

Received 20 July 2010; received in revised form 24 August 2010; accepted 26 August 2010. published online 08 November 2010.

Background

Biologic factors are known to contribute to asthma severity. It is unknown whether these factors differentially contribute to asthma severity in black compared with white subjects.

Objective

We sought to assess the extent to which racial disparities between black and white subjects with severe asthma are attributable to physiologic, immunoinflammatory, and sociodemographic variables.

Methods

Black and white asthmatic adults enrolled in a cross-sectional study focused on severe asthma were evaluated. Severe asthma was identified by using the American Thoracic Society definition. After initial univariable analyses, unconditional logistic regression models were used to estimate the probability of having severe asthma for black and white subjects.

Results

Differences in severe asthma in black compared with white subjects were observed. In univariable analysis IgE level was not associated with severe asthma in black or white subjects, whereas in multivariable analysis IgE level was significantly associated with severe asthma for black subjects (P = .014) but not for white subjects. The odds of having severe asthma more than doubled for black subjects with 2 or more family members with asthma (P = .026), whereas the odds of severe asthma for white participants with a strong family history of asthma decreased by almost half (P = .05). Atopy was negatively associated with severe asthma in both races in univariable analysis but remained significant only in black subjects, whereas comorbidities were associated with severe asthma in white subjects.

Conclusion

Biologic factors were distinctly associated with severe asthma only in black subjects. Studies that incorporate comprehensive evaluation of biologic factors associated with asthma might lead to the development of therapies that target biologic abnormalities in black subjects.

Key words: Severe asthma, race, IgE, allergic sensitization, immunoinflammatory

Abbreviations used: BMI, Body mass index, FVC, Forced vital capacity, GERD, Gastroesophageal reflux disease, SARP, Severe Asthma Research Program, SES, Socioeconomic status

 

 Supported by Clinical and Translational Research Center funding: UL1 RR024153 (National Center for Research Resources). Grant support: HL69116, HL69130, HL69155, HL69167, HL69170, HL69174, HL69349, HL091762, M01 RR02635, M01 RR03186, M01 RR007122-14, 1UL1RR024153, 1UL1RR024989, 1UL1RR024992, 1UL1RR025011.

 Disclosure of potential conflict of interest: E. Bleecker has served as an advisor/consultant for Aerovance, AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline, Merck, Novartis, Pfizer, and Wyeth and has received research support from Aerovance, Amgen, AstraZeneca, Boehringer-Ingelheim, Centocor, Ception, Genentech, GlaxoSmithKline, Novartis, Pfizer, Wyeth, and the National Institutes of Health (NIH). W. Busse is on the advisory board for Altair, Amgen, Centocor, GlaxoSmithKline, Merck, Pfizer, Wyeth, and Johns & Johnson; is a consultant for AstraZeneca, Boehringer-Ingelheim, Novartis, TEVA, and GlaxoSmithKline; is a speaker for Merck; and has received research support from the NIH/National Institute of Allergy and Infectious Diseases (NIAID), the NIH/National Heart, Lung, and Blood Institute (NHLBI), Novartis, AstraZeneca, GlaxoSmithKline, MedImmune, and Ception. M. Castro is a consultant for Electrocore, NKTT, Schering-Plough, Asthmatx, and Cephalon; is on the advisory board for Genentech; is a speaker for AstraZeneca, Boehringer-Ingelheim, Pfizer, Merck, and GlaxoSmithKline; has received research support from Asthmatx, Amgen, Ception, Genentech, MedImmune, Merck, Novartis, the NIH, and GlaxoSmithKline; and has received royalties from Elsevier. K. F. Chung is a consultant for Gilead, is on the advisory board for Merck and GlaxoSmithKline, and has received research support from MRC UK, Asthma UK, and Wellcome Trust. S. Wenzel has served as a consultant for Merck and GlaxoSmithKline and as an advisory board member for Amira. The rest of the authors have declared that they have no conflict of interest.

PII: S0091-6749(10)01411-9

doi:10.1016/j.jaci.2010.08.049

The Journal of Allergy and Clinical Immunology
Volume 126, Issue 6 , Pages 1149-1156.e1, December 2010