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Introduction Brain functioning, as indexed by event‐related potentials (ERPs) representing smoking cue reactivity, inhibitory control, and reward processing, has been found to be compromised in smokers. However, whether environmental tobacco smoke (ETS) exposure in never smokers results in similar brain changes is unknown. This question is particularly relevant during adolescence, given ongoing brain maturation and a high risk of smoking initiation. The present study tested the associations between ETS exposure and ERPs reflecting cue reactivity (P3, LPP), inhibitory control (N2, P3), and reward processing (anticipation P3 (P3), feedback‐related negativity (FRN)) among never‐smoking adolescents. Methods Eighty‐four never‐smoking adolescents (nonexposed = 32, exposed = 52) performed a smoking cue reactivity, a Go/NoGo, and a monetary incentive delay (MID) task while ERPs were measured. Results Exposed and nonexposed groups did not differ in ERPs reflecting smoking cue reactivity, inhibitory control, and reward processing. A negative correlation between ETS exposure and the anticipatory P3 suggests reduced anticipatory reward sensitivity for nondrug rewards with increased levels of ETS exposure. However, since this effect was not consistent across analyses, no strong conclusions can be formulated. In the current study, few participants reported high levels of ETS exposure; therefore, further study is necessary. Conclusions Nevertheless, from this study, it can be concluded that low‐to‐moderate exposure to ETS during adolescence does not result in functional brain changes related to smoking cue reactivity, inhibitory control, and reward processing., This study tested the associations between ETS exposure and ERPs reflecting cue reactivity (P3, LPP), inhibitory control (N2, P3), and reward processing (anticipation P3 (P3), feedback‐related negativity (FRN)) among never‐smoking adolescents.

Contains fulltext : 236040.pdf (Publisher’s version ) (Open Access) Reduced anticipatory reward-related activity, especially in the ventral striatum (VS), may underly adolescent vulnerability to develop nicotine dependence. It remains unclear whether nicotine uptake caused by environmental tobacco smoke (ETS) exposure, known to be associated with future smoking, might prompt similar changes in the brain's reward system, rendering adolescents vulnerable for development of nicotine dependence. To address this question, we tested whether current ETS exposure and monthly smoking are associated with VS hypoactivity for non-drug rewards in experimental smoking adolescents. One-hundred adolescents performed a monetary incentive delay task while brain activity was measured using fMRI. To test the hypothesized relationship, we used a variety of approaches: (1) a whole-brain voxel-wise approach, (2) an region-of-interest approach in the VS using frequentist and Bayesian statistics and (3) a small volume voxel-wise approach across the complete striatum. The results converged in revealing no significant relationships between monthly smoking, ETS exposure and reward-related brain activation across the brain or in the (ventral) striatum specifically. However, Bayesian statistics showed only anecdotal evidence for the null hypothesis in the VS, providing limited insight into the (non-)existence of the hypothesized relationship. Based on these results, we speculate that blunted VS reward-related activity might only occur after relatively high levels of exposure or might be associated with more long term effects of smoking. Future studies would benefit from even larger sample sizes to reliably distinguish between the null and alternative models, as well as more objective measures of (environmental) smoking via using devices such as silicone wristbands. 11 p.

Introduction: Despite its well-established negative effects, environmental tobacco smoke (ETS) exposure remains highly prevalent worldwide. ETS exposure is associated with a wide range of physical and mental health-related problems among youth, including an increased likelihood to develop nicotine dependence. Up till now, neurocognitive effects of ETS exposure are largely unknown, while such effects could explain the role of ETS exposure in the development of nicotine dependence. Therefore, this preregistered study investigated the role of current ETS exposure in brain functioning associated with smoking cue-reactivity and inhibitory control. Method: Concurrent with functional magnetic resonance imaging, nonsmoking adolescents aged 14–18 years (N = 51) performed a smoking cue-reactivity task, assessing brain functioning to smoking cues, and a Go/NoGo task measuring inhibitory control. ETS exposure was measured using a self-report questionnaire and biochemically verified. Results: No significant associations were observed between current ETS exposure and brain functioning associated with smoking cue-reactivity and inhibitory control. Conclusion: These findings suggest that low-to-moderate levels of current ETS exposure are not associated with increased salience of smoking cues or deficits in inhibitory control in nonsmoking adolescents. Longitudinal research is needed to further clarify the exact effect of lifetime ETS exposure on brain functioning, as well as research focusing on the effects of higher levels of ETS exposure.