HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wilson, N. M. Articles by Bush, A. Search for Related Content PubMed PubMed Citation Articles by Wilson, N. M. Articles by Bush, A.

β₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking

Dept of Respiratory Paediatrics, Royal Brompton Hospital, London, UK.

To the Editors:

The article of Zhang et al. 1 was of particular interest to us for two reasons. First, this article reported reduced lung function at age 11 yrs in children with arginine 16, compared with those homozygous for glycine 16, among those exposed to tobacco smoke but not in unexposed children. The present authors’ report 2 of a similar association of reduced lung function with the presence of the arginine 16 allele was not mentioned in their discussion. Unlike Zhang et al. 1, we also found lung function to be reduced in children with any glutamine 27 alleles. However, in our study of a smaller birth cohort, the association of β₂-adrenoceptor polymorphisms and lung function (maximal expiratory flow at functional residual capacity) was found at 1 month of age, probably before there could be any influence of the post-natal environment. In this small study, no influence of maternal smoking was detected. This association was not found at 10 yrs, but only 26% had a smoking parent. Were any associations between β₂-adrenoceptor polymorphisms and lung function found at birth in the Australian cohort? If not, could population differences or even a more polluted intrauterine environment in the UK cohort explain why this association was only found in later childhood in Australia?

The second point of interest was the unexpected finding of an effect of β₂-adrenoceptor polymorphisms on exhaled nitric oxide in children without smoke exposure. This information was also available from the present authors’ study 2, and so we revisited our data, looking specifically at exhaled nitric oxide levels at age 10 yrs and β₂-adrenoceptor genotype. As has been reported before, atopy (any positive skin-prick test result) had a significant effect on exhaled nitric oxide but, surprisingly, β₂-adrenoceptor polymorphisms also showed similar significant effects (table 1). In the general linear model, there was no interaction between genotype and atopy, and no detectable effect of parental smoking. The present results confirm those of Zhang et al. 1, and suggest a sizeable effect since numbers in our study were small. The relevance of this is unclear, but the same occurrence in separate cohorts in different hemispheres suggests that they are real.

None declared.

REFERENCES

1. Zhang G, Hayden CM, Khoo S-K, et al. β₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking. Eur Respir J 2007;30:48–55.[Abstract/Free Full Text]
2. Wilson NM, Lamprill JR, Mak JCW, Clarke JR, Bush A, Silverman M. Symptoms, lung function, and β₂-adrenoceptor polymorphisms in a birth cohort followed for 10 years. Pediatr Pulmonol 2004; 38: 75–81

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wilson, N. M. Articles by Bush, A. Search for Related Content PubMed PubMed Citation Articles by Wilson, N. M. Articles by Bush, A.