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ß₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking

School of Paediatrics and Child Health, University of Western Australia, Perth, Australia.

CORRESPONDENCE: G. Zhang, School of Paediatrics and Child Health, GPO Box D184, Perth WA 6840, Australia. Fax: 61 893882097. E-mail: Bradz{at}ichr.uwa.edu.au

Keywords: Asthma, exhaled nitric oxide, genetics, lung function, passive smoking

Received: September 20, 2006
Accepted March 23, 2007

The aim of the present study was to assess the effects of possible interactions between ß₂-adrenoceptor gene polymorphisms and passive smoking on forced expiratory volume in one second (FEV₁), forced vital capacity (FVC) and exhaled nitric oxide (eNO) in children aged 11 yrs.

A cross-sectional analysis of the longitudinal cohort was conducted for associations between ß₂-adrenoceptor gene polymorphisms and lung function and eNO with regard to passive smoking.

Among children exposed to tobacco smoke, those with Arg16 (at least one Arg allele) exhibited lower adjusted mean FEV₁ (2.19 versus 2.38 L) and FVC (2.43 versus 2.64 L) than Gly16 homozygotes. Those with Gln27 (at least one Gln allele) also exhibited a lower adjusted mean FEV₁ relative to Glu27 homozygotes (2.24 versus 2.39 L). Among children with no exposure to smoking, those with Arg16 or Gln27 showed lower adjusted geometric mean eNO levels compared with Gly16 homozygotes (15.4 versus 30.9 ppb) and Glu27 homozygotes (18.0 versus 49.7 ppb).

In conclusion, passive smoking had a significant effect on associations between ß₂-adrenoceptor gene polymorphisms and asthma-related phenotypes, enhancing the relationship between Arg16 and lung function and removing the relationship between Arg16 or Gln27 and exhaled nitric oxide levels.

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