Abstract

Background: Nicotine is responsible for smoking dependence and is mainly metabolised by CYP2A6. Several types of genetic polymorphism of CYP2A6 have been reported, but their relation to smoking habit and...

Highlights

  • IntroductionSeveral types of genetic polymorphism of CYP2A6 have been reported, but their relation to smoking habit and chronic obstructive pulmonary disease (COPD) phenotypes has not been fully clarified

  • Nicotine is responsible for smoking dependence and is mainly metabolised by CYP2A6

  • Contribution of CYP2A6del genotype to smoking habit Analysis of the results of lifelong cigarette consumption (CC) and CYP2A6del genotype frequency showed that the presence of this deletion allele prevented subjects from becoming heavy smokers (CC >60 pack years, table 2)

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Summary

Introduction

Several types of genetic polymorphism of CYP2A6 have been reported, but their relation to smoking habit and chronic obstructive pulmonary disease (COPD) phenotypes has not been fully clarified. Results: The percentage of subjects with a CYP2A6del allele (genotype D) was lower in heavy smokers (20.5%, n=88, CC >60 pack years) than in light smokers (37.4%, n=115, CC 10–59 pack years, χ2=6.8, p=0.01) or non-smokers (36.1%, n=122, χ2=6.0, p=0.01); lower in ex-smokers (20.7%, n=111) than in current smokers (41.3%, n=92, χ2=10.1, p8.0) than in those with a low LAA score (37.0%, n=127, LAA

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