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Thorax 2004;59:569-573 doi:10.1136/thx.2003.016667
  • Asthma

Glutathione S transferase deficiency and passive smoking increase childhood asthma

  1. M Kabesch1,
  2. C Hoefler1,
  3. D Carr1,
  4. W Leupold2,
  5. S K Weiland3,
  6. E von Mutius1
  1. 1University Children’s Hospital Munich, Germany
  2. 2University Children’s Hospital Dresden, Germany
  3. 3Institute of Epidemiology, University of Ulm, Germany
  1. Correspondence to:
    Dr M Kabesch
    Children’s University Hospital, Ludwig Maximilians University Munich, Lindwurmstrasse 4, D-80337 München, Germany; Michael.Kabeschmed.uni-muenchen.de
  • Received 7 October 2003
  • Accepted 28 March 2004

Abstract

Background: It has been suggested that the genetically determined deficiency of glutathione S transferase (GST) enzymes involved in the detoxification of environmental tobacco smoke (ETS) components may contribute to the development of asthma.

Methods: A large population of German schoolchildren (n = 3054) was genotyped for deficiencies of the GST isoforms M1 and T1. The association between GSTM1 and GSTT1 genotypes and asthma as well as atopy was investigated with respect to current and in utero ETS exposure.

Results: In children lacking the GSTM1 allele who were exposed to current ETS the risk for current asthma (OR 5.5, 95% CI 1.6 to 18.6) and asthma symptoms such as wheeze ever (OR 2.8, 95% CI 1.3 to 6.0), current wheezing (OR 4.7, 95% CI 1.8 to 12.6) and shortness of breath (OR 8.9, 95% CI 2.1 to 38.4) was higher than in GSTM1 positive individuals without ETS exposure. Hints of an interaction between ETS exposure and GSTM1 deficiency were identified. In utero smoke exposure in GSTT1 deficient children was associated with significant decrements in lung function compared with GSTT1 positive children not exposed to ETS.

Conclusions: GSTM1 and GSTT1 deficiency may increase the adverse health effects of in utero and current smoke exposure.

Footnotes

  • This study was funded by the German Ministry of Education and Research as part of the German national genome research network, grant GS 01 0122. MK was also funded by the carrier development grant R186 from the University of Munich.

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