Family History of Asthma and Atopy: In-depth Analyses of the Impact on Asthma and Wheeze in 7- to 8-Year-Old Children

Author:

Bjerg Anders12,Hedman Linnea1,Perzanowski Matthew S.13,Platts-Mills Thomas4,Lundbäck Bo15,Rönmark Eva15

Affiliation:

1. Obstructive Lung Disease in Northern Sweden (OLIN) Studies, Department of Medicine, Sunderby Central Hospital of Norrbotten, Luleå, Sweden

2. Department of Respiratory Medicine and Allergy, University of Umeå, Umeå, Sweden

3. Department of Environmental Health Sciences, Columbia University, New York, New York

4. Asthma and Allergic Diseases Center, University of Virginia, Charlottesville, Virginia

5. Lung and Allergy Research, National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

Abstract

OBJECTIVES. Development of asthma in children is influenced by interactions between genetic and environmental factors. It is unclear whether paternal or maternal histories of disease confer different risks. Previous population-based studies have not stratified analyses by child gender and sensitization status. Our aim was to study in detail the hereditary component of childhood asthma. METHODS. A population-based cohort of 3430 (97% of invited) 7- to 8-year-old school children participated in an expanded International Study of Asthma and Allergy in Childhood survey, and two thirds were skin-prick tested. Heredity was defined as a family history of (1) asthma and (2) atopy (allergic rhinitis or eczema). Multivariate analyses corrected for known risk factors for asthma. RESULTS. At ages 7 to 8, prevalence of asthma was 5.3% among the children and 9.0% among the parents. In children without parental asthma or parental atopy, the prevalence of asthma was 2.8%. Corrected for parental asthma, parental atopy was a weak but significant risk factor. There were minor differences in the impact of parental disease between sensitized and nonsensitized children and between boys and girls. CONCLUSIONS. As risk factors for childhood asthma, there were major differences between parental asthma and parental atopy. Sibling asthma was only a marker of parental disease. Interactions between parental disease and the child's allergic sensitization or gender were not statistically significant. Asthma in both parents conferred a multiplicative risk, whereas the effect of parental atopy was additive, however limited. Asthma and atopy, despite their causal relationship, are separate entities and could be inherited differently. This large, population-based, and well-characterized cohort study does not confirm parent-of-origin effects found in previous studies.

Publisher

American Academy of Pediatrics (AAP)

Subject

Pediatrics, Perinatology, and Child Health

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