Familial aggregation of allergen-specific sensitization and asthma

Authors

  • Margaret Kurzius-Spencer,

    1. Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA
    2. Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
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  • Stefano Guerra,

    1. Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
    2. Center for Research in Environmental Epidemiology, IMIM-Hospital del Mar, CIBERESP, Barcelona, Spain
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  • Duane L. Sherrill,

    1. Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA
    2. Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
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  • Marilyn Halonen,

    1. Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
    2. Department of Pharmacology, University of Arizona, Tucson, AZ, USA
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  • Robert C. Elston,

    1. Department of Epidemiology and Biostatistics, Case Western Reserve University School of Medicine, Cleveland, OH, USA
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  • Fernando D. Martinez

    1. Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
    2. BIO5 Institute, University of Arizona, Tucson, AZ, USA
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Margaret Kurzius-Spencer, Mel and Enid Zuckerman College of Public Health, University of Arizona, PO Box 245215, Tucson, AZ 85724, USA.
Tel.: 520 626 9869
Fax: 520 626 5051
E-mail: mkurzius@email.arizona.edu

Abstract

To cite this article: Kurzius-Spencer M, Guerra S, Sherrill DL, Halonen M, Elston RC, Martinez FD. Familial aggregation of allergen-specific sensitization and asthma. Pediatric Allergy Immunology 2012: 23: 21–27.

Abstract

Background:  Familial aggregation of specific response to allergens and asthma adjusted for age and sensitization to multiple allergens was assessed in two large population cohorts.

Methods:  Allergen skin prick tests (SPTs) were administered to 1151 families in the Tucson Children’s Respiratory Study (CRS) and 435 families in the Tucson Epidemiological Study of Airway Obstructive Disease (TESAOD). Sensitization was defined by wheal size ≥3 mm; physician-diagnosed asthma at age ≥8 yr was based on questionnaires. Using s.a.g.e. 6.1 software assoc and fcor, familial correlations of crude and adjusted phenotypes were evaluated.

Results:  Crude estimates of parent–offspring (P–O) and sibling correlations were statistically significant for most allergens, ranging from 0.03 to 0.29. After adjusting for age of assessment and ‘other atopy’ (SPT-positive response to additional allergens), correlations were reduced by 14–71%. Sibling correlations for specific response to allergens were consistently higher than P–O correlations, but this difference was significant only for dust mite and weed mix in the TESAOD population. Familial correlation for atopic status (any positive SPTs vs. none) tended to be higher than for specific allergens. Asthma, with and without adjustment, showed greater familial correlation than either specific or general SPT response and significantly higher sibling correlation in TESAOD than in CRS, probably due to the older age of the siblings and the longer period of ascertainment.

Conclusions:  Significant familial aggregation of specific response to allergen after adjustment for other atopy appears to reflect a genetic propensity toward atopy, dependent on shared familial exposures. Results also suggest that inheritance of asthma is independent of atopic sensitization.

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