Smoking behaviors, such as age at smoking initiation, smoking cessation, and number of cigarettes smoked per day (CPD), are partially genetically determined and have substantial heritability.1–4 Numerous loci and candidate genes have been suggested to contain genetic markers affecting smoking behaviors using genome-wide linkage scans 5 and genome wide association study approaches.67 Recent Genome Wide Association Studies (GWAS) have identified loci associated with smoking cessation (Dopamine Beta-Hydroxylase on chromosome 9q34) and CPD (e.g. nicotinic acetylcholine receptor locus on chromosome 15q25 and Cytochrome P2A6 (CYP2A6) locus on chromosome 19q13) in multiple populations,8–11 although GWAS of smoking behaviors specifically within COPD subjects have not been reported. Interestingly, the same single nucleotide polymorphisms (SNPs) in the 15q25 locus were previously associated with development of COPD,12 but the role of this locus in smoking behaviors in COPD patients and whether the sole effect of this locus on COPD susceptibility relates to smoking behavior remain unclear.
