The current study found four different subgroups of nicotine exposure over a 7-day collection period among a sample of non-daily smokers. The clusters ranged from relatively high mean levels of cotinine that were similar to those measured among daily smokers [36], to consistently low mean cotinine levels similar to non-smokers exposed only to environmental smoke [37]. As expected, cotinine levels increased with more smoking days in the week and more cigarettes smoked per day. There was considerable variation in cotinine between days for some clusters, which confirms that high variability in smoking behavior for non-daily smokers can lead to similar variability in nicotine exposure. Cotinine did, however, remain fairly stable within the day, especially for the smokers who maintained low cotinine levels across days.
Nicotine exposure varied with some demographic and smoking characteristics. The high cotinine non-daily smokers had the lowest income of all groups and was comprised of menthol smokers only. This is consistent with research among daily smokers showing that rates of smoking, nicotine exposure, and levels of dependence are all higher among low income smokers compared to higher income smokers [2, 14, 18]. Higher cotinine levels among low versus high income smokers may be related to more perceived stress, easier access to cigarettes, and a lack of enforcement of smoking regulations where individuals live and work [18, 38, 39]. Among daily smokers, menthol smoking is often a correlate of lower SES as it was in the current sample [14]. The U.S. Food and Drug Administration (FDA) concluded that the use of menthol cigarettes is more common among low income smokers and related to higher rates of dependence [40]. Although there are some reports that menthol is associated with higher nicotine intake, an FDA review did not confirm this finding [40]. Higher cotinine levels among the current sample are likely due to more cigarettes smoked per day, rather than menthol preference.
We found a dose-response relationship between daily cotinine levels and nicotine dependence. The sub-group with the highest levels of cotinine also had the highest average dependence scores and were more likely to report smoking their first cigarette < 60 minutes after waking, which is a strong predictor of nicotine dependence [41]. Surprisingly, there was not a significant difference in the number of converted vs. native non-daily smokers between the clusters, which has been hypothesized to contribute to increasing dependence among light and non-daily smokers [6]. However, the results highlight that nicotine exposure is likely not the only factor determining dependence among non-daily smokers. Even the group with cotinine levels that were consistently above 200 ng/ml reported low levels of dependence and only 50% of this cluster reported that they smoke now because it’s hard to quit. Further, the group with cotinine levels near 0 ng/ml still endorsed aspects of dependence with over 20% of this group reporting that they continue to smoke now because it is hard for them to quit.
Prior research has shown that non-daily smokers have stronger stimulus control over their smoking than daily smokers [15]. Stimulus control occurs when a smokers’ mood, activity, and environmental context become important predictors of smoking behavior, rather than nicotine withdrawal alone [15]. This could explain why our subgroups with low levels of nicotine exposure still reported perceived symptoms of nicotine dependence. Our EMA results from the current study and a prior analysis of the sample found that smoking occurred most frequently during positive moods and activities of leisure [16]. Further, we found that the group with the lowest cotinine had more social smoking than the high cotinine cluster. Alternatively, participants with the highest levels of cotinine were more likely to report negative emotions during their smoking experiences and smoking during interactions such as phone calls and arguments. This is in part contrary to a laboratory study showing positive affect to be linked to higher nicotine boost among daily smokers [13]. This could have several explanations. Given the relatively higher levels of dependence among this group, these smokers may experience withdrawal symptoms that induce negative emotions, like irritability and anxiety, which precede and then accompany their next smoking experience. Another potential explanation is that the high cotinine group smokes to alleviate perceived stress. Experimentally induced stress has been shown to trigger negative affect and craving among heavy and light smokers and is commonly reported as a barrier to cessation [42, 43]. Future research exploring real-time smoking motives among non-daily smokers may help to elucidate why negative emotions are associated with higher cotinine levels for this group and how we might intervene on these emotions to reduce smoking behavior (see [44] for review).
The current study had several limitations. The sample, comprised primarily of non-Hispanic White smokers, was not nationally representative. For this reason our results may not generalize to Black and Hispanic smokers who are known to have higher rates of non-daily smoking than the general population [45]. In addition, our EMA relied on participants’ initiative to record each smoking session and some participants may have under-reported the number of cigarettes smoked; however, the sample’s self-reported CPD was consistent with prior studies of adults and adolescents [9]. Unexpectedly, the level of cotinine for cluster 1 was significantly higher than the other clusters while the average CPD was similar across cluster. This cluster was not comprised of slower nicotine metabolizers. Further research is needed to better understand the reasons for this discrepancy in cotinine values. Although it is possible that this group was underreporting their cigarettes per day, it would be unlikely for participants to also underreport their levels of dependence on items that are not face valid (e.g., time to first cigarette), suggesting that these were true non-daily smokers. Other factors could explain the high cotinine levels among this group, such as compensatory smoking.
In conclusion, the current study highlights that nicotine exposure among non-daily smokers is as variable as their self-reported patterns of smoking behavior. With a wide range in nicotine exposure and consistently low nicotine dependence and cessation rates, non-daily smokers may not fit with the long-held theory that nicotine is the primary factor that sustains smoking addiction [46]. Instead, these findings point to the need for more detailed assessments of smoking behavior to guide the development of effective cessation interventions for this group of smokers. Future research could inform our limited understanding of the biobehavioral mechanisms that contribute to individual differences in nicotine exposure among non-daily smokers and inform the development of personalized interventions that help non-daily smokers manage internal and external cues for smoking.