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Influence of male sex and parental allergic disease on childhood wheezing: role of interactions

Authors

  • E. Melén,

    1. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden,
    2. Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden,
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  • J. Kere,

    1. Department of Biosciences at Novum and Clinical Research Centre, Karolinska Institutet, Stockholm, Sweden,
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  • G. Pershagen,

    1. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden,
    2. Department of Occupational and Environmental Health, Stockholm County Council, Stockholm, Sweden,
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  • M. Svartengren,

    1. Department of Occupational and Environmental Health, Stockholm County Council, Stockholm, Sweden,
    2. Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden
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  • M. Wickman

    1. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden,
    2. Department of Occupational and Environmental Health, Stockholm County Council, Stockholm, Sweden,
    3. Sachs's Children's Hospital, Institute of Södersjukhuset, Karolinska Institutet, Stockholm, Sweden
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Erik Melén, Department of Occupational and Environmental Health, Norrbacka, Karolinska Hospital, SE-171 76 Stockholm, Sweden.
E-mail: erik.melen@imm.ki.se

Summary

Background Boys have been reported to be more susceptible to childhood wheezing, whereas girls are more susceptible later in life. This difference might be related to both genetic and environmental factors.

Objective To investigate the influence of male sex and parental allergic disease on the development of childhood wheezing.

Methods Infants (n=4089) born in Stockholm were recruited in a prospective study, BAMSE. Data on parental allergic diseases were obtained from questionnaires answered at the children's birth and on symptoms of wheezing at 1, 2 and 4 years of age. Sensitization to inhalant allergens and lung function was investigated at the age of 4 years.

Results Children were classified as having recurrent, transient (n=266), early-onset persistent (n=319) and late-onset wheezing (n=195). Boys were over-represented in all groups of wheezing (odds ratio, OR=1.4–1.5) and both maternal and paternal allergic disease was of importance for the wheezing outcomes. A dominating influence from maternal allergic disease was only seen in children with persistent wheezing. An interaction exceeding additivity was found between male sex and parental allergic disease, particularly in children with persistent wheezing (OR=2.9 and 95% confidence interval, CI 95% 2.1–4.0 for boys with any parental history vs. OR=1.4, CI 95% 1.0–2.1 for girls). Interaction between male sex and parental allergic disease was also observed in children who wheezed at the age of 4 years and were sensitized to inhalant allergens.

Conclusion Our data suggest an interaction between male sex and parental allergic disease in childhood wheezing, which may represent a sex-specific genetic influence.

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