Gene-environment interactions contributing to other cigarette use behaviors, such as adolescent smoking, cigarettes smoked per day, nicotine dependence, and cessation have yielded significant findings as well. A couple of measures of the parental environment moderated genetic influences on adolescent smoking (8,35). Specifically, significant interactions were found between parental monitoring and rs16969968 of CHRNA5 (33) and maternal smoking during pregnancy and rs1051730 of CHRNA3 (35) for smoking at age 14. Meanwhile, social pressures to smoke, prevalence of smoking among popular students, marketing and vending restrictions on the sale of cigarettes, and school-level smoking moderated the heritability of daily smoking among adolescents (39,95,96). Only one molecular genetic study investigated and found a significant interaction between 5-HTTLPR and school tobacco use in influencing tobacco use frequency, such that the greater the number of short alleles, the stronger the individual’s response to the school health behavioral environment (39). In adulthood, the experience of traumatic events and neighborhood social cohesion interacted with aggregated genetic risk to influence the number of cigarettes smoked per day. The interaction between the experience of traumatic events and neighborhood social
