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Smoke exposure interacts with ADAM33 polymorphisms in the development of lung function and hyperresponsiveness

  1. N. E. Reijmerink1,2,
  2. M. Kerkhof3,
  3. G. H. Koppelman4,
  4. J. Gerritsen4,
  5. J. C. De Jongste5,
  6. H. A. Smit6,
  7. B. Brunekreef7,8,
  8. D. S. Postma1

Article first published online: 19 FEB 2009

DOI: 10.1111/j.1398-9995.2009.01939.x

Issue

Allergy

Allergy

Volume 64, Issue 6, pages 898–904, June 2009

Additional Information

How to Cite

Reijmerink, N. E., Kerkhof, M., Koppelman, G. H., Gerritsen, J., De Jongste, J. C., Smit, H. A., Brunekreef, B. and Postma, D. S. (2009), Smoke exposure interacts with ADAM33 polymorphisms in the development of lung function and hyperresponsiveness. Allergy, 64: 898–904. doi: 10.1111/j.1398-9995.2009.01939.x

Author Information

  1. 1

    Department of Pulmonology

  2. 2

    Beatrix Children's Hospital

  3. 3

    Department of Epidemiology

  4. 4

    Department of Paediatric Pulmonology and Paediatric Allergology, Beatrix Children’s Hospital, University Medical Centre Groningen, University of Groningen, Groningen

  5. 5

    Department of Paediatrics, Erasmus University Medical Centre, Sophia Children’s Hospital, Rotterdam

  6. 6

    National Institute of Public Health and the Environment, Bilthoven

  7. 7

    Institute for Risk Assessment Sciences, University of Utrecht, Utrecht

  8. 8

    Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, the Netherlands

*Prof. D. S. Postma Department of Pulmonology University Medical Center Groningen University of Groningen PO Box 196 9700 AD Groningen the Netherlands

Publication History

  1. Issue published online: 11 MAY 2009
  2. Article first published online: 19 FEB 2009
  3. Accepted for publication 22 September 2008

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Keywords:

  • ADAM33;
  • asthma;
  • bronchial hyperresponsiveness;
  • in utero cigarette smoke exposure;
  • lung function

Introduction: ADAM33 is the first identified asthma gene by positional cloning, especially asthma combined with bronchial hyperresponsiveness (BHR). Moreover, ADAM33 is associated with early-life lung function and decline of forced expiratory volume in 1 s (FEV1) in the general population. In utero and postnatal cigarette smoke exposure (CSE) are associated with reduced lung function, and development of BHR and asthma. We hypothesized that this may occur via interaction with ADAM33.

Aim:  To replicate the role of ADAM33 in childhood lung function and development of BHR and asthma. Furthermore, we investigated gene–environment interaction of ADAM33 with in utero and postnatal CSE in the Dutch PIAMA cohort.

Methods:  Six ADAM33 single-nucleotide polymorphisms (SNPs) were genotyped. Rint was measured at age 4 and 8 years, FEV1 and BHR at age 8 years; asthma was based on questionnaire data at age 8.

Results:  In the total cohort, the rs511898 A, rs528557 C, and rs2280090 A alleles increased the risk to develop asthma (+BHR). There existed interaction between in utero but not postnatal CSE and the rs528557 and rs3918396 SNPs with respect to development of BHR, the rs3918396 SNP with Rint at age 8 and the rs528557 SNP with FEV1% predicted.

Conclusions:  We confirm associations between ADAM33 and the development of asthma (+BHR). This is the first study suggesting that interaction of in utero CSE with ADAM33 results in reduced lung function and the development of BHR, which needs further confirmation.

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