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INTRODUCTION Prevention intervention programs reduce substance use, including smoking, but not all individuals respond. We tested whether response to a substance use prevention/intervention program varies based upon a set of five markers (rs16969968, rs1948, rs578776, rs588765, and rs684513) within the cluster of nicotinic acetylcholine receptor subunit genes (CHRNA5/A3/B4). METHODS Participants (N = 424) were randomly assigned to either control condition, or a family-based intervention in grade 6 and a school-based drug preventive intervention in grade 7. Smoking in the past month was assessed in grades 9-12 using a four-point scale (0 = never smoked, 1 = smoked but not in last month, 2 = one or a few times, 3 = about once a week or more). RESULTS There was a main effect of both the intervention (b = -0.24, P < .05) and genotype at rs16969968 (b = 0.14, P < .05) on high school smoking. Using dummy coding to allow for nonlinear effects, individuals with the A/A genotype smoked more often than those with G/G (b = 0.33, P < .05). A genotype × intervention effect was found with reduced smoking among those with A/A and G/A genotypes to levels similar to those with the G/G genotype (G/G vs. A/A: b = -0.67, P < .05; A/G vs. A/A: b = -0.61, P < .05; G/G vs. A/G ns). Results were nonsignificant for the other four markers. CONCLUSIONS Preventive interventions can reduce the genetic risk for smoking from rs16969968.

Maternal cigarette smoking is a risk factor for adolescent smoking. One possible explanation for increased smoking by human adolescents after maternal nicotine exposure is that exposure increases nicotine preference. However, it is difficult to separate the biological and social causes of smoking behavior in humans. This experiment examined the relationship between maternal nicotine exposure and nicotine preference in periadolescent offspring using a mouse model of oral nicotine consumption. Pregnant females were provided saccharin-flavored water containing 50 microg/ml nicotine (n = 4) or no nicotine (n = 5) from the ninth day of gestation through weaning on postnatal day (PD) 21. Offspring from these females were tested for nicotine preference during periadolescence (PDs 35-42) by providing access to both saccharin-only and nicotine solutions (50 microg/ml) 24 hr a day in the home cage in a two-bottle choice test. Male mice exposed maternally to nicotine (n = 9) exhibited an increased nicotine preference in adolescence compared to non-nicotine exposed controls (n = 12). Maternal nicotine exposure did not alter nicotine preference by periadolescent female mice. Nicotine consumption was confirmed by serum cotinine measurement. These data are consistent with human epidemiological reports that maternal nicotine exposure is associated with increased risk of cigarette smoking. Differential outcomes for males and females suggest that different processes underlie sex differences in nicotine consumption following maternal nicotine exposure.