Eur Respir J 2007, doi:10.1183/09031936.00123206
B2 adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking
1 School of Paediatrics and Child Health, University of Western Australia, Perth, Australia
* To whom correspondence should be addressed. E-mail: Bradz{at}ichr.uwa.edu.au.
The aim of the study is to assess the possible interactions between (B2AR) gene polymorphisms and passive smoking on forced expiratory volume in 1 second (FEV1), forced expiratory vital capacity (FVC) and exhaled nitric oxide (eNO) in children at age 11. A cross-sectional analysis of the longitudinal cohort was conducted for associations between (B2AR) gene polymorphisms and lung function and eNO with regard to passive smoking. In children exposed to tobacco smoke, those with Arg16 (at least one Arg allele) had lower adjusted means of FEV1 (2.19 vs 2.38L; p=0.006) and FVC (2.43 vs 2.64L; p=0.011) compared with Gly16 homozygotes. Those with Gln27 (at least one Gln allele) also had a lower adjusted mean of FEV1 relative to Glu27 homozygotes (2.24L vs 2.39L; p=0.048). In children with no exposure to smoking those with Arg16 or Gln27 had lower adjusted geometric means of exhaled nitric oxide (eNO) compared with Gly16 homozygotes (15.4 vs.30.9 ppb; p=0.01) and Glu27 homozygotes (18.0 vs. 49.7 ppb; p=0.001), respectively. In conclusion, passive smoking had a significant effect on associations between B2 adrenoceptor polymorphisms and asthma-related phenotypes, enhancing the relationship between Arg16 and lung function and removing the relationship between Arg16 or Gln27 and eNO. Keywords: Asthma, exhaled nitrogen oxide, genetics, lung function, passive smoking
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