The discrepancy between our findings and those among adults cannot be explained by the fact that adults smoke more cigarettes per day and have been smoking for longer; since neither the duration of adolescents’ smoking nor how many cigarettes they smoked influenced the direction of our findings. Further, existing research demonstrates that the half-life of cotinine is similar across age groups (38, 39), suggesting that early adolescents are unlikely to have different rates of nicotine metabolism compared with adults. As indicated by a growing body of literature in both human and rodent models (40–44), it is possible that there is something unique about this period of brain development that influences an adolescent’s response to nicotine exposure.
