title: Association of asthma with beta(2)-adrenergic receptor gene polymorphism and cigarette smoking.
abstract: Recent studies have suggested that two polymorphisms of the beta(2)-adrenergic receptor (beta(2)AR) gene at codons 16 (arginine to glycine) and 27 (glutamine to glutamate) affect an individual's airway responsiveness, or response to acute or chronic beta(2)-agonist therapy but are not risk factors for asthma. We hypothesize that there is an interaction effect on asthma between the beta(2)AR gene polymorphisms and cigarette smoking. A case-control study was conducted in 128 asthma cases and 136 control individuals identified from 10,014 studied subjects in rural Anqing, China. Allele-specific polymerase chain reaction (PCR) was used to genotype beta(2)AR gene polymorphisms. Multiple logistic regression was used to adjust for potential confounding factors. We found a marginally significant interaction between cigarette smoking and beta(2)AR-16 genotype after adjusting for important confounding factors (p = 0.06). Specifically, we found that compared with never-smoking Gly-16 homozygotes, those ever-smokers who are Arg-16 homozygotes had a significantly increased risk of asthma (odds ratio [OR] = 7.81; 95% confidence interval [CI]: 2.07 to 29.5). This association showed a clear dose-response relationship with the number of cigarettes smoked. However, there was no significant association of asthma with polymorphisms of the beta(2)AR at position 27 (OR = 1.38; 95% CI: 0.69 to 2.73). Our study suggests a gene-environment interaction between the Arg-16 genotype and ever cigarette smoking with respect to the susceptibility of an individual to asthma.
authors.affiliation: Program for Population Genetics, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Wang
authors.forename: C
authors.initials: C
authors.lastname: Chen
authors.forename: T
authors.initials: T
authors.lastname: Niu
authors.forename: D
authors.initials: D
authors.lastname: Wu
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.forename: B
authors.initials: B
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Fang
authors.forename: C N
authors.initials: CN
authors.lastname: Yandava
authors.forename: J M
authors.initials: JM
authors.lastname: Drazen
authors.forename: S T
authors.initials: ST
authors.lastname: Weiss
authors.forename: X
authors.initials: X
authors.lastname: Xu
mesh_terms: D000328:Adult; D001249:Asthma / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology*; D016022:Case-Control Studies; D002681:China / Q000453:epidemiology; D015986:Confounding Factors, Epidemiologic; D005260:Female; D005541:Forced Expiratory Volume; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006720:Homozygote; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D015995:Prevalence; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics*; D012307:Risk Factors; D017678:Sex Distribution; D012907:Smoking / Q000009:adverse effects*; D011795:Surveys and Questionnaires
chemical_list: D018343:Receptors, Adrenergic, beta-2