Despite decades of progress in tobacco control, smoking cessation success rates remain stubbornly low. Even with optimal pharmacological and behavioral interventions, sustained abstinence is achieved by a minority of individuals attempting to quit. This commentary advances the thirdhand smoke exposure nicotine → relapse hypothesis, proposing that residual tobacco smoke pollution in indoor environments represents an overlooked, modifiable determinant of nicotine relapse risk. Thirdhand smoke (THS), the persistent chemical residue of tobacco smoke that accumulates on surfaces, dust, and personal belongings, contains substantial nicotine reservoirs and emits a characteristic stale tobacco odor long after active smoking has ceased. We argue that THS undermine cessation through three interacting pathways: [1] biological re-exposure to nicotine via inhalation, dermal absorption, and ingestion; [2] psychological conditioning through olfactory cues that provoke craving and withdrawal-related distress; and [3] social and structural factors that disproportionately burden populations already at elevated risk for nicotine relapse. Emerging empirical evidence suggests that higher household THS contamination predicts shorter abstinence duration following quit attempts. We contend that incorporating environmental remediation of THS into cessation strategies represents a novel approach to improving long-term cessation outcomes. Future research directions and translational implications are discussed.

• Thirdhand smoke

• Smoking cessation

• Relapse

• Nicotine exposure

• Cue reactivity

THS: Thirdhand Smoke

Most people who smoke want to quit, yet only a small fraction succeeds. Population-level data consistently show that fewer than 10% of individuals who attempt to quit smoking in a given year maintain long-term abstinence [1, 2]. This pattern persists despite the availability of evidence-based pharmacotherapies, behavioral counseling, and combined treatment approaches delivered within healthcare systems [3]. While these interventions outperform unaided quit attempts, their absolute effectiveness remains modest [4].

The relatively low rate of successful cessation signals the presence of unaddressed factors that contribute to nicotine relapse. To date, smoking cessation research has focused overwhelmingly on individual-level biological dependence, motivation, cognition, and social context. What has been largely neglected is the post-cessationenvironment itself; specifically, whether residual tobacco smoke pollution continues to exert biological and psychological pressure on individuals who are actively trying to quit. This commentary argues that the chemical residue from thirdhand tobacco smoke (THS) represents a novel and plausible modifiable environmental factor that may help explain why cessation frequently fails even among motivated individuals using best-practice treatments.

Chemical Persistence and Reactivity

THS refers to the complex mixture of tobacco smoke pollutants that persist on indoor surfaces, in settled dust, and within porous materials long after smoking has stopped [5,6]. Unlike secondhand smoke, which is transient and inhaled during and shortly after active smoking, THS pollution of home environments may lead to chronic, involuntary, and often unnoticed exposure to tobacco smoke residue. Re-emissions of volatile and semivolatile 

compounds from this residue cause the smell of stale tobacco smoke. The largest THS constituent by mass is nicotine, with surface loadings that can exceed 1,000 µg/ m2 in homes of current and former smokers [7] and 10,000 µg/m2 in heavily smoked hospitality venues [8]. Nicotine is not only highly abundant in THS, but it also undergoes chemical reactions as it interacts with ambient oxidants (e.g., ozone, HONO) to form cancer-causing chemicals nitrosamines (e.g., NNA, NNK) [9].

Exposure Pathways beyond Inhalation

THS exposure differs in important ways from secondhand smoke exposure. THS exposure is not limited to inhalation but also occurs through dermal uptake and ingestion [5,6,10]. A person may involuntarily ingest THS when their mouth comes into contact with contaminated hands, food, or objects. A person may dermally absorb THS when their skin contacts contaminated objects, such as when wearing contaminated clothing or sleeping in bed with contaminated bedsheets and blankets. A person may also inhale THS that off-gasses from THS reservoirs into the air. THS pollution and exposure have been demonstrated in many settings where people had previously smoked, including apartments of nonsmokers in multiunit housing, used cars for sale, non-smoking rooms at hotels, rental cars, movie theaters, and hospital settings [11,12]. THS can also be transported on people and on polluted objects (e.g., clothes and furniture). People can expose each other to THS and spread this pollutant across environments because THS can stick to clothes, skin, and hair [10,13].

Disparities in Exposure

The tobacco industry invests billions of its profits each year in marketing campaigns to recruit new smokers and maintain addiction among individuals who use tobacco products. This includes targeting vulnerable populations, providing free or discounted products, and sponsoring sports, cultural, and youth-oriented events [14,15]. Although tobacco product use is widely recognized as the leading cause of preventable disease [16], legislators often condone the tobacco industry’s manipulative tactics because of its influence on the political process [17]. The people most burdened by tobacco use are non-White, lesbian, gay, bisexual, and/or transgender adults, those with lower education and household incomes, those without insurance, those from rural communities, Veterans, and those living in mobile or multi-unit housing [14,15]. Existing research shows that similar disparities exist for THS. Individuals in communities with higher smoking rates, no indoor smoking bans, multiunit housing, and lower incomes face higher THS exposure [18,19]. A review of sociodemographic disparities found that lower socioeconomic status, younger age (2-4 years), being Black, and living in multiunit housing increase children’s risk of THS exposure, especially due to persistent contamination in multiunit dwellings [20].

We propose that THS exposure undermines smoking cessation by sustaining or reactivating the biological and psychological mechanisms of nicotine dependence following a quit attempt. This may occur through three interacting pathways: biological, psychological, and social.

Exposure to THS includes exposure to nicotine, which may continue to affect biological dependence long after cessation. Nicotine dependence is driven by repeated stimulation of nicotinic acetylcholine receptors, resulting in dopaminergic reward signaling and the development of tolerance and withdrawal [21,22]. During cessation, the abrupt absence of nicotine produces aversive withdrawal symptoms, including craving, irritability, anxiety, and dysphoria, which are key predictors of nicotine relapse [21,22]. Nicotine users who are attempting to quit often relapse due to the intense aversive effects (e.g., strong cravings). THS-polluted environments can contain sufficient nicotine to plausibly interfere with this withdrawal process [5,6,12]. Chronic low-level nicotine exposure from contaminated dust, air, and surfaces may

(a) stimulate nicotinic receptors, signaling continued nicotine availability; (b) weaken extinction of conditioned dependence responses; and (c) prolong or destabilize withdrawal, increasing craving intensity. Evidence from secondhand smoke research shows that even low-dose involuntary nicotine exposure increases receptor occupancy and craving [23]. Given that THS reservoirs can persist at high concentrations in homes and vehicles, it is biologically plausible that THS exposure delivers a priming dose of nicotine sufficient to increase nicotine relapse risk.

As a chemical residue that emits compounds with the distinct odor of stale tobacco smoke, THS has olfactory properties that may evoke nicotine cravings through Pavlovian conditioning. Nicotine dependence develops in part through Pavlovian conditioning, in which individuals learn to respond to specific stimuli [24,25]. Pavlovian conditioning means that a stimulus initially without a 

relevant response (e.g., the smell of tobacco smoke) can become paired with the effect (e.g., cravings) caused by the unconditioned stimulus (e.g., nicotine deficits). After repeated pairings, the initially neutral cue becomes a conditioned stimulus that produces effects on its own (e.g., tobacco smell → cravings). Stimuli can be interoceptive, cues occurring on the inside (e.g., thoughts, emotions, sensations), or exteroceptive, cues occurring in the external world (e.g., smells, people). A meta-analysis of cue reactivity in cigarette smokers examined how nicotine-related cues relate to self-reported cravings [26]. The results showed that these cues produce significantly greater cravings than neutral cues. A systematic review and meta-analysis of ecological momentary assessment studies found a higher risk of a lapse due to nicotine-related environmental cues (e.g., nicotine-related smoking paraphernalia, presence of smokers) [27].

The stale tobacco odor emitted by THS is detectable at extremely low concentrations [5,6]. Unlike secondhand smoke, which is episodic, THS odor is persistent and, consequently, a continuous conditioned cue. Several studies support the idea that this odor may affect smoking behavior and cessation outcomes through Pavlovian conditioning. McRobbie, Hajek [28] studied reactions of patients attending a cessation treatment to other people’s cigarette smoke, finding that 54% of patients in cessation treatment found cigarette smoke tempting. Cortese, Uhde [29] found that smoking-related odors elicit higher cravings and increased skin conductance compared to odorless controls. Aslan, Sala [30] reported that tobacco odors were among the central symptoms of self-reported cigarette cravings among 505 adult smokers [30]. THS exposure may also activate other experiences that may increase nicotine relapse risk. In a controlled experimental THS exposure study using an animal model, THS was linked to hyperactivity as well as heightened anxiety [31], an interoceptive factor that is known to increase vulnerability to nicotine relapse during smoking cessation treatments [32]. In combination, these findings suggest that THS exposure may therefore function as a constant exteroceptive cue that maintains craving even in the absence of active smoking.

Social mechanisms may create circumstances in which THS exposure is more likely to be linked to nicotine relapse. Unfortunately, those disproportionately exposed to THS (see section titled Exposure Disparities) also live in social circumstances that may strengthen the relationship between THS exposure and nicotine relapse. For example, a person without insurance and in poverty may be at higher risk of nicotine relapse because they lack the income to remediate THS (see section titled Rethinking Smoking Cessation Strategies) or move to a dwelling without THS pollution. The existence of disparities in THS exposure also suggests that THS may function as an environmental amplifier of existing tobacco-related health disparities [14,15], undermining cessation efforts among those who stand to benefit most from quitting.

Although this research is nascent, early findings support the proposed THS exposure → nicotine relapse hypothesis (N = 2 studies). A longitudinal study of smokers attempting to quit has shown that substantial nicotine and carcinogen reservoirs persist in homes for months after cessation (e.g., in settled house dust, on surfaces, in furnishings) [12]. Nonsmokers living in these homes continue to exhibit THS exposure as measured by urinary biomarkers. Importantly, Matt, Mahabee-Gittens [33] found that higher nicotine levels in household dust at the time of quitting predicted shorter abstinence duration. A tenfold increase in dust nicotine was associated with a 50% increase in the odds of nicotine relapse, even after controlling for smoking history and demographic factors. While these findings are preliminary, they are consistent with established evidence on cue-induced craving and involuntary nicotine exposure [23,28-30,34].

Future Research Directions

To evaluate the proposed THS exposure → nicotine relapse hypothesis, we propose a series of laboratory and field studies to investigate the underlying biological, psychological, and social mechanisms. These studies include:

1. Quantify nicotine uptake from THS exposure during smoking cessation.
2. Examine neuropsychological markers of receptor activation following THS exposure, especially in comparison with SHS exposure.
3. Examine mediation effects of THS exposure on nicotine relapse via psychological and behavioral factors, such as THS exposure → anxiety or cravings→ nicotine relapse.
4. Identify social and structural moderators of the association between THS exposure and nicotine relapse.
5. Test the causal effects of THS remediation on smoking cessation outcomes.
6. Evaluate cost-effective remediation strategies in real-world settings.

Using observational, quasi-experimental, and randomized trials, such research can generate robust evidence to inform intervention strategies that disrupt the link between THS exposure and nicotine relapse, thereby supporting nicotine cessation.

Rethinking Smoking Cessation Strategies

Current smoking cessation interventions focus almost exclusivelyontheindividualtryingtoquit.Toourknowledge, none systematically addresses the role of contaminated environments in which individuals continue to live while quitting. Therefore, environmental remediation presents a potentially novel target for intervention. Potential actions for environmental remediation range in effort and cost, including (a) repeated deep cleaning of surfaces and dust; (b) air filtration and targeted ventilation strategies;

(c) washing or replacing clothing and soft materials; (d) removal of heavily contaminated furnishings (e.g., carpets, upholstery); (e) full gut remodel of an entire home; and

(e) leaving THS-polluted environments and moving to smoke-free ones [35, 36]. These remediation strategies may need to be tailored to an individual’s circumstances, including personal relationships, housing, and other resources. In parallel, cognitive-behavioral techniques could help individuals by (a) identifying THS-related triggers; (b) reducing exposure during vulnerable periods; and (c) coping with odor-induced craving without lapsing. Psychoeducation about THS has already been shown to promote healthier smoking-related behaviors, including adoption of smokefree homes and quit attempts [37]. The above strategies could be integrated into existing cessation programs, potentially enhancing their effectiveness in particularly high-risk populations.

When smokers quit, their immediate environments (e.g., homes, cars, personal belongings) remain contaminated with tobacco smoke chemicals that may biologically, psychologically, and socially undermine quit attempts. By reframing nicotine relapse risk as partly mediated and moderated by environmental factors, tobacco control gains new opportunities to target modifiable environmental factors to improve cessation outcomes. Reducing exposure to THS pollutants can inform environmental interventions to strengthen smoking cessation outcomes and reduce tobacco-related health disparities.

Mr. Garcia Alcaraz was supported by the UC San Diego SEED Fellowship and SDSU Graduate Fellowship. Dr. Matt was supported by the Tobacco-Related Disease Research Program (19CA-0164, T32PT6244, T33PC6863).

Conflicts of Interest: The authors have no conflicts of interest to disclose.

1. VanFrank B, Malarcher A, Cornelius ME, Schecter A, Jamal A, Tynan M. Adult smoking cessation - United States, 2022. MMWR Morb Mortal Wkly Rep. 2024; 73: 633–641.
2. American Cancer Society. Why people start smoking and why it’s hard to stop; 2024.
3. United States Public Health Service Office of the Surgeon G, National Center for Chronic Disease P, Health Promotion Office on S, Health. Publications and Reports of the Surgeon General. Smoking Cessation: A Report of the Surgeon General. Washington (DC): US Department of Health and Human Services; 2020.
4. Rigotti NA, Kruse GR, Livingstone-Banks J, Hartmann-Boyce J. Treatment of tobacco smoking: A review. JAMA. 2022; 327: 566-577.
5. Matt GE, Quintana PJ, Destaillats H, Gundel LA, Sleiman M, Singer BC, et al. Thirdhand tobacco smoke: Emerging evidence and arguments for a multidisciplinary research agenda. Environ Health Perspect. 2011; 119: 1218-1226.
6. Jacob P, 3rd, Benowitz NL, Destaillats H, Gundel L, Hang B, Martins-Green M, et al. Thirdhand smoke: New evidence, challenges, and future directions. Chem Res Toxicol. 2017; 30: 270-294.
7. Matt GE, Quintana PJE, Hoh E, Zakarian JM, Dodder NG, Record RA, et al. Persistent tobacco smoke residue in multiunit housing: Legacy of permissive indoor smoking policies and challenges in the implementation of smoking bans. Prev Med Rep. 2020; 18: 101088.
8. Matt GE, Quintana PJE, Hoh E, Zakarian JM, Chowdhury Z, Hovell MF, et al. A casino goes smoke free: A longitudinal study of secondhand and thirdhand smoke pollution and exposure. Tob Control. 2018; 27: 643-649.
9. Sleiman M, Gundel LA, Pankow JF, Jacob P, 3rd, Singer BC, DestaillatsH. Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proc Natl Acad Sci U S A. 2010; 107: 6576-6581.
10. Matt GE, Greiner L, Record RA, Wipfli H, Long J, Dodder NG, et al. Policy-relevant differences between secondhand and thirdhand smoke: Strengthening protections from involuntary exposure to tobacco smoke pollutants. Tob Control. 2024; 33: 798-806.
11. Lewinson T, Dasgupta A, Murphey JM, Onsando WM, NagovichJ. Tobacco in hotels: A study of smoke exposure and resident risk. Tobacco Use Insights. 2024; 17: 1179173x241272368.
12. Matt GE, Quintana PJE, Zakarian JM, Hoh E, Hovell MF, Mahabee-Gittens M, et al. When smokers quit: Exposure to nicotine and carcinogens persists from thirdhand smoke pollution. Tob Control. 2016; 26: 548-556.
13. Sheu R, Stönner C, Ditto JC, Klüpfel T, Williams J, Gentner DR. Human transport of thirdhand tobacco smoke: A prominent source of hazardous air pollutants into indoor nonsmoking environments. Sci Adv. 2020; 6: eaay4109.
14. Tobacco Education and Research Oversight Committee. Standing together against commercial tobacco & nicotine 2025–2026
15. Centers for Disease Control and Prevention. Improving tobacco-related health disparities; 2022.
16. Centers for Disease Control and Prevention. Current cigarette smoking among adults in the United States; 2024
17. Matheny J, Tegen A, Berkman M, Gray N, Verhagen B, Sree V. Combatting tobacco industry lobbyists in public health. Tob Induc Dis. 2023; 21: 1-3.
18. Samet JM, Chanson D, Wipfli H. The challenges of limiting exposure to THS in vulnerable populations. Curr Environ Health Rep. 2015; 2: 215-225.
19. Matt GE, Merianos AL, Quintana PJE, Hoh E, Dodder NG, Mahabee-Gittens EM. Prevalence and income-related disparities in thirdhand smoke exposure to children. JAMA Netw Open. 2022; 5: e2147184.
20. Hamzai L, Quintana PJE, Matt GE, Novotny TE, Mahabee-Gittens EM, Merianos AL, et al. Sociodemographic disparities in thirdhand smoke exposure among children in the United States: A narrative review. JEEA. 2024; 3: 29.
21. Le Foll B, Piper ME, Fowler CD, Tonstad S, Bierut L, Lu L, et al. Tobacco and nicotine use. Nat Rev Dis Prim. 2022; 8: 19.
22. Benowitz NL. Nicotine addiction. N Engl J Med. 2010; 362: 2295-2303.
23. Brody AL, Mandelkern MA, London ED, Khan A, Kozman D, Costello MR, et al. Effect of secondhand smoke on occupancy of nicotinic acetylcholine receptors in brain. Arch Gen Psychiatry. 2011; 68: 953-960.
24. Barrett ST, McNealy KR, Knabel ML, Burrichter RM, Steck KA, Bevins RA. The inside story: Interoceptive Pavlovian conditioning with the nicotine stimulus. J Exp Psychol Anim Learn Cogn. 2025; 51: 61-72.
25. Rupprecht LE, Smith TT, Schassburger RL, Buffalari DM, Sved AF, Donny EC. Behavioral mechanisms underlying nicotine reinforcement. Curr Top Behav Neurosci. 2015; 24: 19-53.
26. Betts JM, Dowd AN, Forney M, Hetelekides E, Tiffany ST. A meta-analysis of cue reactivity in tobacco cigarette smokers. Nicotine Tob Res. 2020; 23: 249-258.
27. Perski O, Kwasnicka D, Kale D, Schneider V, Szinay D, ten Hoor G, et al. Within-person associations between psychological and contextual factors and lapse incidence in smokers attempting to quit: A systematic review and meta-analysis of ecological momentary assessment studies. Addiction. 2023; 118 : 1216-1231.
28. McRobbie H, Hajek P, Locker J. Does the reaction of abstaining smokers to the smell of other people’s cigarettes predict relapse? Addiction. 2008; 103: 1883-1887.
29. Cortese BM, Uhde TW, LaRowe SD, Stein SV, Freeman WC, McClernon FJ, et al. Olfactory cue reactivity in nicotine-dependent adult smokers. Psychol Addict Behav. 2015; 29: 91-96.
30. Aslan M, Sala M, Gueorguieva R, Garrison KA. A network analysis of cigarette craving. Nicotine Tob Res. 2023; 25: 1155-1163.
31. Martins-Green M, Adhami N, Frankos M, Valdez M, Goodwin B, Lyubovitsky J, et al. Cigarette smoke toxins deposited on surfaces: Implications for human health. PLoS One. 2014; 9: e86391.
32. Zvolensky MJ, Stewart SH, Vujanovic AA, Gavric D, Steeves D. Anxiety sensitivity and anxiety and depressive symptoms in the prediction of early smoking lapse and relapse during smoking cessation treatment. Nicotine Tob Res. 2009; 11: 323-331.
33. Matt GE, Mahabee-Gittens EM, Zakarian JM, Quintana PJE, Hoh E, Myers M. Nicotine in thirdhand smoke residue predicts relapse from smoking cessation: A pilot study. Addict Behav. 2019; 98: 106041.
34. Okoli CT, Kodet J. A systematic review of secondhand tobacco smoke exposure and smoking behaviors: Smoking status, susceptibility, initiation, dependence, and cessation. Addict Behav. 2015; 47: 22-32.
35. Matt GE, Quintana PJE, Hoh E, Zakarian JM, Dodder NG, Record RA, et al. Remediating thirdhand smoke pollution in multiunit housing: Temporary reductions and the challenges of persistent reservoirs. Nicotine Tob Res. 2021; 23: 364-372.
36. Thirdhand Smoke Resource Center. Can I remove thirdhand smoke from my home? ; 2025.
37. Vanzi V, Marti F, Cattaruzza MS. Thirdhand smoke knowledge, beliefs and behaviors among parents and families: A systematic review. Healthcare. 2023; 11.