Developing Genetic Education for Smoking Cessation

Background. Reducing cigarette smoking among adults is a major public health objective. Although the target prevalence for adult smoking is < 12% by 2010 (DHHS 2000), current estimates indicate that 20.8%, or 45.3 million adults, currently smoke (CDC, 2007). An estimated 44.2% of smokers tried to quit at least one day in the last 12 months (CDC, 2007), yet <10% of smokers who try to quit remain abstinent (Benowitz, 2008). Even with intensive treatment, only 11-20% of smokers are abstinent for 6 months (Sutherland, 2003). Smoking also results in an enormous economic burden, with health-care and lost productivity costs totaling approximately $167 billion per year (CDC, 2008). A limitation of current treatment guidelines is a lack of specificity for individual smokers. Completion of the sequencing of the human genome and the current focus on genomics (Collins, Green, Guttmacher, & Guyer, 2003) provides an unprecedented opportunity to study the biobehavioral factors influencing smoking. This research will contribute to individualized treatment by providing a better understanding of the effects of genetic, psychological, and environmental factors and their interaction on smoking initiation, maintenance, cessation, and relapse (Lerman, Schnoll & Munafo, 2007; Morgan et al., 2003; Swan et al., 2003). Both candidate gene studies to identify specific genes that affect smoking and pharmacogenomic studies that investigate the effects of selected genes on treatment response contribute to a growing body of knowledge about genetic influences on smoking. The anticipated outcome of these studies will be the ability to individualize type, dose, and duration of treatment based on smokers' genotypes (Lerman, Schnoll & Munafo). Ultimately, the long-term goal of this research is to decrease relapse and promote sustained abstinence.

The Genetic Education and Smoking Model provides a framework for investigating variables that potentially influence the ways smokers respond to information about: (a) genetic contributions to smoking and (b) the potential for genetically-informed cessation treatment. Based on social-cognitive theory and the Common Sense Model (CSM)(Cervone, 2004; Brownlee, Leventhal, & Leventhal, 2000), the Genetic Education and Smoking Model proposes that genetic education will influence smokers' mental representations and appraisals about genetics and smoking in addition to their smoking-related behaviors and affective responses.

As genetically-informed cessation treatment becomes a part of research and clinical care, smokers will need a degree of genetic literacy to make informed decisions (McInerney, 2002; Shields, Lerman, & Sullivan, 2004). There is a growing body of scientific knowledge to guide an educational program about genetic contributions to smoking and the potential for genetically-informed cessation treatment. Epidemiologic twin studies consistently support a genetic cause for smoking, with an estimated 56% of the variance for smoking initiation and 67% of progression to nicotine dependence due to additive genetic effects (Sullivan and Kendler, 1999). Findings from several genome-wide scans using linkage analysis have identified chromosomes 1, 2, 4, 5, 6, 9, 10, 11, 14, 17, 18, and 21 as containing possible susceptibility loci for smoking-related genes (Li,Cheng, Ma, & Swan, 2003; Li, Ma, & Beuten, 2004). Several candidate-genes for smoking heritability have been identified, including nicotinic acetylcholine receptors (nAChRs), dopamine receptor (DRD2 and DRD4) and transporter (SLC6A3) genes, the catechol-o-methyl-transferase (COMT) gene, the mu opioid receptor (OPRM1) gene, and the serotonin transporter (5-HTT) gene (Lerman, Schnoll, & Munafo, 2007; Schnoll, Johnson, & Lerman, 2007). Polymorphisms of CYP2A6, a cytochrome P450 enzyme, play a major role in the inactivation of nicotine to its metabolite, cotinine (Messina, Tyndale, & Sellers, 1997; Benowitz, 2008).

Specific Aims. The primary specific aim is to compare the effects of the experimental group to the attention control group on smoking-related mental representations, appraisals, behaviors, and affective responses over time. The primary aim will be achieved using a randomized, longitudinal, two-group repeated measures design to determine the direct effects of the intervention on smoking-related mental representations, appraisals, behaviors, and affective responses.

The secondary aim is to explore whether personality characteristics (trait negative affectivity and curiosity) and educational level moderate the effects of the genetic educational program on smoking-related mental representations, appraisals, behaviors, and affective responses.