5.3.1 Genetics
Greater understanding of the human genome has led to enquiry into whether genetics can affect an individual’s chances of taking up smoking. Data from family, adoption and, in particular, twin studies have suggested that genetic make-up could contribute to the likelihood of both experimentation and progression to established patterns of smoking.1-5 In 2010, the US Surgeon General reported that ‘genes appear to predispose persons to smoking initiation and persistence and possibly are related to the extent of difficulty a person has in smoking cessation’.6(page 156) Twin studies have variously reported that heritability for smoking (that is to say, the proportion in the variance in smoking that is attributable to genetic factors) ranges from about 50-80%, which is in keeping with heritability estimates for alcoholism, asthma and hypertension.3
While inherited factors influencing initiation and dependence are likely to overlap to some degree, there is evidence that independent genetic influences may mediate each stage of tobacco use.2,7-9 For example, one review of the data has estimated that, in twins, about 60% of the liability to initiate smoking can be attributed to genetic influences.1 However, environmental influences10 also play an important role in nicotine dependence and frequency of smoking,6,11 and genetic predisposition to tobacco use may be modified by individual and environmental factors such as family structure, religion and marital status.2
Interactions between genetic and environmental influence, and the causes of the relationships between social risk factors and substance use, may change significantly over the course of development. For example, evidence from twin research found that as twins developed from childhood to adulthood, the influence of shared environmental factors on church attendance (a consistent predictor of nicotine and alcohol consumption) declined dramatically, while the role of genetic factors increased.5 Frequent church attendance in adolescence appeared to reflect shared familial and social–environmental influences that were protective against substance use, while in adulthood the inverse relationship between church attendance and substance use became stronger, stemming largely from genetically influenced temperamental factors.5
Genetic influences may mediate the association between social factors (such as adolescents’ peer characteristics, including peer smoking) and smoking behaviour (including nicotine dependence) in other ways;10,12 for example, adolescents with specific genetic risk for nicotine dependence may be less affected by social context such as peer smoking than those with lower risk genotypes.12 The evidence regarding potential gender differences in the relative importance of genetic and shared environmental influences for adolescent smoking behaviour and nicotine dependence is mixed,6,13 while the extent of interaction between environmental and genetic risk factors in increasing susceptibility to nicotine addiction is unknown.14
Genetic variations, even at the level of a single gene, have been shown to affect performance in key behavioural circuits and subsequently impact on addiction risk.13 Behavioural circuits are being developed constantly due to interaction between genes and experience, resulting in the formation of attitudes, temperaments and, often, fixed behavioural patterns. During this maturation there are numerous opportunities to introduce risk or resilience into the system, as so many complex and overlapping developmental processes are taking place; this will influence subsequent individual tendencies such as those towards risk taking, for example.13
A large 2023 multi-ancestry genetic study15 drawing on electronic health records from almost 900,000 individuals has provided strong evidence that genetic factors play an important role in vulnerability to tobacco use disorder (TUD), with implications for the early uptake of smoking among young people. The study identified 72 independent genetic risk loci and prioritised more than 300 candidate genes, most of which are highly expressed in the brain and involved in neural pathways linked to reward, impulse control, learning and addiction. Key genes included those related to nicotinic acetylcholine receptors (such as CHRNA5, CHRNA4 and CHRNB2), as well as genes involved in dopaminergic and glutamatergic signalling, which influence sensitivity to nicotine and reinforcement processes. Importantly, genetic liability for TUD was strongly correlated with externalising behaviours, attention-deficit/hyperactivity disorder and other behavioural traits observable in childhood, even in tobacco-naïve young people, suggesting that genetic influences on smoking uptake may operate well before first use. These findings indicate that biological and genetic factors contribute to early susceptibility to tobacco use, interacting with social and environmental influences to increase the likelihood of experimentation and progression to regular smoking among some young people.15
Smoking is understood to be a highly complex behaviour, and where a genetic basis is postulated, it is with the recognition that many genes are likely to be involved, each individually contributing only a small degree of influence. Candidate genes for investigation in tobacco initiation, dependence and persistence have included several known to affect neurotransmitter pathways, nicotine-specific pathways and nicotine metabolism.2 The inheritance of genetic material may include polymorphisms of such genes, affecting individuals’ physiological responses to nicotine, such as the rate of nicotine metabolism, receptor sensitivity to nicotine and to certain neurotransmitters, and the levels of neurotransmitters available at neural synapses. These individual differences in response to nicotine are likely to affect the trajectory toward the development of nicotine dependence.6 Other genes connected with traits such as depression and anxiety are also being studied.2 There is also emerging evidence that genetic factors may influence an individual’s choice of friends, and that some individuals’ genetic make-up may make them more susceptible to the influence of peer groups.16
5.3.2 Effect of maternal smoking in utero on uptake of smoking in offspring
Several studies from Australia17,18 and internationally19-23 have reported an association between smoking during pregnancy and subsequent increased likelihood of uptake of smoking in offspring, even after controlling for a range of confounding factors. It may be that effects are different depending on the sex of the baby, with some research suggesting that female offspring exposed to tobacco smoke prenatally are more susceptible to taking up smoking as adolescents than male offspring similarly exposed.23
The relationship between maternal smoking and subsequent smoking uptake by offspring might be partially explained by their shared genetic background.6 Mothers who continue to smoke after pregnancy may also affect children’s attitude to smoking through role modelling.6 Findings of at least one study suggest that the effects of maternal smoking may not persist beyond early adolescence, after which social factors (such as mother’s current smoking behaviour and peer smoking) appear to become more important.24
However, a connection between maternal smoking and in utero effects on the brain is physiologically plausible. While the exact mechanisms and long-term consequences of these effects have not been fully elucidated25 it is known that nicotine (a toxic chemical) present in tobacco smoke reaches the unborn child through the placenta, binding with and activating neurotransmitters in the central and peripheral nervous system and negatively affecting neurodevelopment. Chronic exposure to nicotine during prenatal development has been shown in some animal studies to affect reward-related neural circuitry, in turn modifying the psychoactive effects of drugs in later life.26 A behavioural study among Canadian adolescents found that participants who had been prenatally exposed to maternal tobacco smoke were significantly more likely to use an addictive substance later in life, even after controlling for other variables such as age and peer drug use.26 Investigators suggested that prenatal exposure to maternal smoking could interfere with cortical development (important in decision-making) via modification of the gene that produced ‘brain-derived neurotrophic factor’ (BDNF); this in turn could influence adolescent susceptibility to addiction through abnormal processing of reward-associated cues, facilitating impulsive behaviours and subsequently higher substance abuse rates.13,26
For information on pregnancy and smoking see Section 3.7 and for more information on maternal smoking in utero and child health see Section 3.8.
5.3.3 Exposure to secondhand smoke
While exposure to secondhand smoke (SHS) has long been known to cause serious diseases,6 it has also been associated with increased risk for initiation,27 maintenance of cigarette smoking27-30 and intention to smoke in the future.27 Indoor and enclosed environments are of particular concern. SHS exposure in the home or car is associated with smoking initiation at a young age.27 It is possible that exposure to SHS can stimulate neural pathways which increase the brains sensitivity to nicotine prior to active smoking.27
People who do not smoke who are exposed to high levels of SHS may absorb amounts of nicotine similar to that of people who do smoke.30 For example, research examining the effects of SHS exposure on nicotinic acetylcholine receptors in the brain found that both smoking and non-smoking participants who were exposed to SHS for one hour as car passengers experienced significant receptor occupancy and increased plasma nicotine concentrations.28
An exploratory US study investigated whether sensitivity to SHS exposure (assessed with reaction measures commonly used to gauge subjective reactivity to the first experience with smoking cigarettes) among young people aged 8–13 years who have never smoked predicted susceptibility to smoking (measured through likelihood of future smoking).29 Those who reported more negative experiences with SHS exposure (such as coughing or feeling sick) tended to be less susceptible to smoking than those who experienced fewer unpleasant reactions. Some evidence was found for decreasing sensitivity to SHS with age.29 Children are especially susceptible to the effects of nicotine exposure through SHS, in part due to the differing effects of nicotine pharmacokinetics between children and adults.30
Exposure to smoke in social situations (quantified as the number of people who smoke in the social environment and number of situations where SHS exposure occurs), has been found to predict precursors to smoking initiation (including perceived nicotine dependence and smoking susceptibility) among adolescents who have never smoked.30 A large 2011 US survey involving students aged 12–17 years found exposure to secondhand smoke (as measured by frequency of exposure during the previous week and smoking in the home) was as influential in prompting uptake of smoking as peer pressure and exposure to tobacco advertising.31
In addition to a shared genetic predisposition to smoke and role modelling of smoking behaviour,30 cumulative exposure to secondhand smoke may increase risk for smoking uptake through additional exposure to nicotine during a time of critical brain development.29
See Section 4.17 for information on the health effects of secondhand smoke for infants and children.
5.3.4 Childhood illness and smoking uptake
Quality of life (QOL) and smoking have been shown to be related in studies among healthy and illness populations.32 The assumption that smoking causes a reduction in QOL was supported in some longitudinal studies, while other longitudinal research found that changes in smoking status did not predict QOL changes.32
The occurrence of asthma during childhood may be associated with reduced smoking uptake among male adolescents, but not females.33 A longitudinal study investigating whether the outcomes of asthma predicted smoking onset among adolescents with asthma found that poorer self-reported medication adherence and the maladaptive coping strategy of hiding asthma predicted smoking onset among both girls and boys, while poorer QOL predicted smoking in boys only.32 There is some evidence of an indirect relationship between asthma and smoking behaviour from a prospective population-based study conducted among Dutch adolescents. Participants with current asthma were more likely to report depressive feelings (as opposed to depression or depressive symptoms) than those without asthma: specifically, those with current, severe symptoms of asthma were more likely to report depressive feelings than respondents with mild and moderate symptoms. However, smoking behaviour was similar for adolescents with and without asthma. Depressive feelings and smoking were related both cross-sectionally and longitudinally.34
A systematic review investigating tobacco use among adolescents with physical disabilities found that those with physical disabilities were significantly more likely to use tobacco, compared to adolescents without physical disabilities.35 Similar to adolescents with severe asthma being more likely to report depressive feelings, adolescents with physical disabilities may also experience greater stressors and discrimination, which is associated with negative health behaviours such as tobacco use.35
There is a strong relationship between adolescent smoking and a range of psychiatric conditions; these are discussed further in Section 5.5.2 and Section 9A.3.
5.3.5 The influence of gender and sexuality
Tobacco use is generally higher among sexual and gender minority young people than their cisgender and heterosexual peers, with disparities beginning in adolescence and continuing into young adulthood.36 However, there are differences within sub-populations of gender and sexually diverse young people, as well as by specific tobacco products.37-40
Prevalence
The 2022–2023 Australian Secondary Students’ Alcohol and Drug (ASSAD) survey found that there were similar proportions of 12-to-17-year-old males (2%) and females (2%) who currently smoke.41 In the 2023–2024 Canadian Student Alcohol and Drugs Survey, however, gender is reported using a third category ‘gender diverse’ in addition to ‘boy’ and ‘girl’. Among students aged 12-to-18-years-old who reported smoking in the past 30 days, prevalence was similar for boys (5%), and girls (4%), however, higher for students identifying as gender diverse (12%).42
In the 2020–2021 iteration of ‘Writing Themselves In’, the largest health and wellbeing survey of LGBTQA+ young people aged 14-to-21-years in Australia, 12% of LGBTQA+ participants currently smoked, including 8% of participants aged 14-to-17-years, and 17% aged 18-to-21-years.37 Among participants aged 14-to-17, 13% of transgender females and 11% of transgender males currently smoked, and of those who identified as non-binary, 8% currently smoked. Among participants aged 18-to-21, 22% of transgender males currently smoked, followed by 18% of non-binary participants, and 14% of transgender females.37
According to the 2024 Report of the Surgeon General on Disparities in Tobacco Use and Exposure to Secondhand Tobacco Smoke the prevalence of tobacco use was higher overall among young people who identified as gay, lesbian, and bisexual than it was among young people who identified as heterosexual, however, the prevalence of tobacco use varied by different population groups, such as gay, lesbian, or bisexual populations, and by specific tobacco products.38 For instance, research in 2023 found that Californian adolescents who identified as asexual did not have a higher prevalence of tobacco use, or susceptibility to tobacco use, than their heterosexual and cisgendered peers.39 Researchers have called for future research to disaggregate subgroups of sexual and gender minority young people when conducting research as tobacco use is not universal among this population.40
Reasons for higher use/uptake
Qualitative research has identified three main motivations for tobacco uptake among the LGBTI community—image building, socialisation and stress. Smoking was used as a tool for building an image of one’s self or to attain a certain persona. In the LGBTI community smoking aids socialisation with some fearing loss of friends if they were to quit. Lastly, smoking was reported by the LGBTI community as a coping mechanism for stresses cause by the intersectionality of race, ethnicity and sexuality.43 As well as this, the LGBTI population has also been specifically targeted in tobacco advertising.44 A 2025 study45 examining factors associated with current use of e-cigarettes, cigarettes, and vaporised marijuana/cannabis among middle- and high-school students in the US, with a focus on sexual minority adolescents, found that among sexual minority students racial/ethnic minority identity and recent psychological distress were the top factors associated with an increased risk of smoking. Exposure to cigarette use at home or in vehicles and the belief that occasional cigarette use posed little to no harm were also strong predictors of tobacco use for sexual minority adolescents.45
A 2022 systematic review,46 informed by the minority stress model, examined factors associated with tobacco and nicotine use among transgender and gender-diverse people. Synthesising 35 studies, the review identified that environmental and general stressors including housing instability, low income, living with people who use substances were the most studied, and consistently associated with increased likelihood of tobacco and nicotine use, among transgender and gender-diverse adults, as well as external minority stressors such as discrimination and rejection. Protective factors such as family support, school connectedness, and positive relationships with teachers were associated with lower likelihood of use among transgender and gender-diverse young people. Other research has further emphasised that while discrimination may be a risk factor for tobacco use, fostering sexual and gender minority identity connectedness may be protective against tobacco use.36
Researchers emphasise that the evidence concerning tobacco use among gender minority young people remains limited by small samples, inconsistent measures of gender identity, and a lack of longitudinal and experimental studies, and argue that further high-quality research is needed to better understand causal pathways and inform effective prevention strategies.46
For more on smoking and the LGBTI community see InDepth 9A, Section, 9A.6.
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References
1. Sullivan P and Kendler K. The genetic epidemiology of smoking. Nicotine and Tobacco Research, 1999; 1(suppl.1):i51–7. Available from: https://academic.oup.com/ntr/article-abstract/1/Suppl_2/S51/1097866
2. Lerman C and Berrettini W. Elucidating the role of genetic factors in smoking behaviour and nicotine dependence. American Journal of Medical Genetics (Neuropsychiatric Genetics) 2003; 118B:48–54. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12627466
3. Batra V, Patkar A, Berrettini W, Weinstein S, and Leone F. The genetic determinants of smoking. Chest, 2003; 123(5):1730–39. Available from: https://www.sciencedirect.com/science/article/pii/S0012369215337284
4. Hall W, Madden P, and Lynskey M. The genetics of tobacco use: methods, findings and policy implications. Tobacco Control, 2002; 11:119–24. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/11/2/119.pdf
5. Kendler K and Myers J. A developmental twin study of church attendance and alcohol and nicotine consumption: a model for analyzing the changing impact of genes and environment. The American Journal of Psychiatry, 2009; 166(10):1150–5. Available from: http://ajp.psychiatryonline.org/cgi/content/full/166/10/1150
6. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/2010/index.htm.
7. Kendler K, Neale M, Sullivan P, Corey L, Gardner C, et al. A population-based twin study in women of smoking initiation and nicotine dependence. Psychological Medicine, 1999; 29:299–308. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10218922
8. Maes H, Sullivan P, Bulik C, Neale M, Prescott C, et al. A twin study of genetic and environmental influences on tobacco initiation, regular tobacco use and nicotine dependence. Psychological Medicine, 2004; 34:1251–61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15697051
9. Vink J, Willemsen G, and Boomsma D. Heritability of smoking initiation and nicotine dependence. Behavioral Genetics, 2005; 35:397–406. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15971021
10. Harakeh Z, Neiderhiser J, Spotts E, Engels R, Scholte R, et al. Genetic factors contribute to the association between peers and young adults smoking: univariate and multivariate behavioral genetic analyses. Addictive Behaviors, 2008; 33(9):1113–22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18584970
11. Agrawal A, Balasubramanian S, Smith E, Madden P, Bucholz K, et al. Peer substance involvement modifies genetic influences on regular substance involvement in young women. Addiction, 2010; 105(10):1844–53. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1360-0443.2010.02993.x/full
12. Johnson E, Chen L, Breslau N, Hatsukami D, Robbins T, et al. Peer smoking and the nicotinic receptor genes: an examination of genetic and environmental risks for nicotine dependence. Addiction, 2010; 105(11):2014–22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20840187
13. Baler R and Volkow N. Addiction as a systems failure: focus on adolescence and smoking. Journal of the American Academy of Child and Adolescent Psychiatry, 2011; 50(4):329–39. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21421173
14. Swan GE. Implications of genetic epidemiology for the prevention of tobacco use. Nicotine and Tobacco Research, 1999; 1(suppl.1):S49–56. Available from: http://ntr.oxfordjournals.org/content/1/Suppl_1/S49.abstract
15. Toikumo S, Jennings MV, Pham B, Lee H, Mallard TT, et al. Multi-ancestry meta-analysis of tobacco use disorders based on electronic health record data prioritizes novel candidate risk genes and reveals associations with numerous health outcomes. medRxiv, 2023. Available from: https://www.ncbi.nlm.nih.gov/pubmed/37034728
16. Harden K, Hill J, Turkheimer E, and Emery R. Gene-environment correlation and interaction in peer effects on adolescent alcohol and tobacco use. Behavioral Genetics, 2008; 38:339–47. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18368474
17. Al Mamun A, Lawlor D, Alati R, O'Callaghan M, Williams G, et al. Does maternal smoking during pregnancy have a direct effect on future offspring obesity? Evidence from a prospective birth cohort study. American Journal of Epidemiology 2006; 164(4):317−25. Available from: http://aje.oxfordjournals.org/cgi/content/full/164/4/317
18. O'Callaghan F, O'Callaghan M, Najman J, Williams G, Bor W, et al. Prediction of adolescent smoking from family and social risk factors at 5 years, and maternal smoking in pregnancy and at 5 and 14 years. Addiction 2006; 101(2):282–90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16445557
19. Buka S, Shenassa E, and Niaura R. Elevated risk of tobacco dependence among offspring of mothers who smoked during pregnancy: a 30-year prospective study. The American Journal of Psychiatry, 2003; 160:1978–84. Available from: http://ajp.psychiatryonline.org/cgi/content/full/160/11/1978
20. Oncken C, McKee S, Krishnan-Sarin S, O'Malley S, and Mazure C. Gender effects of reported in utero tobacco exposure on smoking initiation, progression and nicotine dependence in adult offspring. Nicotine and Tobacco Research, 2004; 6(5):829–33. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15700918
21. Lieb R, Schreier A, Pfister H, and Wittchen H. Maternal smoking and smoking in adolescents: a prospective community study of adolescents and their mothers. European Addiction Research, 2003; 9(3):120–30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12837990
22. Porath A and Fried P. Effects of prenatal cigarette and marijuana exposure on drug use among offspring. Neurotoxicological Teratology, 2005; 27(2):267–77. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15734278
23. Roberts K, Munafo M, Rodriguez D, Drury M, Murphy M, et al. Longitudinal analysis of the effect of prenatal nicotine exposure on subsequent smoking behaviour of offspring. Nicotine and Tobacco Research, 2005; 7(5):801–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16191751
24. Cornelius M, Leech S, Goldschmidt L, and Day N. Is prenatal tobacco exposure a risk factor for early adolescent smoking? A follow-up study. Neurotoxicological Teratology, 2005; 27:667–76. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16014324
25. Shea A and Steiner M. Cigarette smoking during pregnancy. Nicotine and Tobacco Research, 2008; 10(2):267–78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18236291
26. Lotfipour S, Ferguson E, Leonard G, Perron M, Pike B, et al. Orbitofrontal cortex and drug use during adolescence: role of prenatal exposure to maternal smoking and BDNF genotype. Archives of General Psychiatry, 2009; 66(11):1244. Available from: http://archpsyc.ama-assn.org/cgi/reprint/66/11/1244
27. Okoli CT and Kodet J. A systematic review of secondhand tobacco smoke exposure and smoking behaviors: Smoking status, susceptibility, initiation, dependence, and cessation. Addictive Behaviors, 2015; 47:22–32. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25863004
28. Brody A, Mandelkern M, London E, Khan A, Kozman D, et al. Effect of secondhand smoke on occupancy of nicotinic acetylcholine receptors in brain. Archives of General Psychiatry, 2011; 68(9):953–60. Available from: https://jamanetwork.com/journals/jamapsychiatry/article-abstract/1107271
29. Lessov-Schlaggar C, Wahlgren D, Liles S, Jones J, Ji M, et al. Sensitivity to secondhand smoke exposure predicts smoking susceptibility in 8-13-year-old never smokers. Journal of Adolescent Health, 2011; 48(3):234–40. Available from: http://www.jahonline.org/article/S1054-139X%2810%2900308-3/fulltext
30. Racicot S, McGrath J, and O'Loughlin J. An investigation of social and pharmacological exposure to secondhand tobacco smoke as possible predictors of perceived nicotine dependence, smoking susceptibility, and smoking expectancies among never-smoking youth. Nicotine and Tobacco Research, 2011; 13(10):926–33. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21622492
31. Voorhees C, Ye C, Carter-Pokras O, MacPherson L, Kanamori M, et al. Peers, tobacco advertising, and secondhand smoke exposure influences smoking initiation in diverse adolescents. American Journal of Health Promotion, 2011; 25(3):e1–11. Available from: https://journals.sagepub.com/doi/abs/10.4278/ajhp.090604-QUAN-180
32. Van De Ven M, Engels R, and Sawyer S. Asthma-specific predictors of smoking onset in adolescents with asthma: a longitudinal study. Journal of Pediatric Psychology, 2009; 34(2):118. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18567925
33. Verlato G, Bortolami O, Accordini S, Olivieri M, Cappa V, et al. Asthma in childhood reduces smoking initiation in subsequent teens among males. Journal of Adolescent Health, 2011; 48(3):253–8. Available from: http://www.jahonline.org/article/S1054-139X%2810%2900341-1/fulltext
34. Otten R, Van de Ven M, Engels R, and Van den Eijnden R. Depressive mood and smoking onset: a comparison of adolescents with and without asthma. Psychology & Health, 2009; 24(3):287–300. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20204994
35. Nagarajan VD and Okoli CT. A systematic review of tobacco use among adolescents with physical disabilities. Public Health, 2016. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26877065
36. Budenz A, Gaber J, Crankshaw E, Malterud A, Peterson EB, et al. Discrimination, identity connectedness and tobacco use in a sample of sexual and gender minority young adults. Tobacco Control, 2022. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36601779
37. Hill AO, Lyons A, Jones J, McGowan I, Carman M, et al. Writing Themselves In 4: The health and wellbeing of LGBTQA+ young people in Australia. National report, monograph series number 124, Melbourne: Australian Research Centre in Sex, Health and Society, La Trobe University, 2021. Available from: https://www.latrobe.edu.au/__data/assets/pdf_file/0010/1198945/Writing-Themselves-In-4-National-report.pdf.
38. U.S. Department of Health and Human Services. Eliminating Tobacco-Related Disease and Death: Addressing Disparities—A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2024. Available from: https://www.hhs.gov/sites/default/files/2024-sgr-tobacco-related-health-disparities-full-report.pdf.
39. Harlow AF, Liu F, Young LE, Coreas SI, Rahman T, et al. Sexual and Gender Identity Disparities in Nicotine and Tobacco Use Susceptibility and Prevalence: Disaggregating Emerging Identities Among Adolescents from California, USA. Nicotine and Tobacco Research, 2023. Available from: https://www.ncbi.nlm.nih.gov/pubmed/37493636
40. Figueroa W, Jankowski E, Curran H, Ennis AC, Poteat T, et al. Minority stressors and tobacco use among a US sample of sexual and gender minority young adults. Drug and Alcohol Dependence, 2024; 261:111356. Available from: https://www.ncbi.nlm.nih.gov/pubmed/38889573
41. Scully M, Bain E, Koh I, Wakefield M, and Durkin S. ASSAD 2022–2023: Australian secondary school students’ use of tobacco and e-cigarettes. Centre for Behavioural Research in Cancer: Cancer Council Victoria, 2023. Available from: https://www.health.gov.au/sites/default/files/2024-04/australian-secondary-school-students-use-of-tobacco-and-e-cigarettes-2022-2023.pdf.
42. Health Canada. Alcohol and Drug Use among Students in Canada, 2023–24. Government of Canada: Ottawa 2025. Available from: https://www.canada.ca/en/health-canada/services/canadian-student-tobacco-alcohol-drugs-survey/2023-2024-key-findings.html
43. Jannat-Khah DP, Dill LJ, Reynolds SA, and Joseph MA. Stress, Socializing, and Other Motivations for Smoking Among the Lesbian, Gay, Bisexual, Transgender, and Queer Community in New York City. American Journal of Health Promotion, 2017:890117117694449. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28318307
44. Tang H, Greenwood G, Cowling D, Lloyd J, Roeseler A, et al. Cigarette smoking among lesbians, gays, and bisexuals: how serious a problem? (United States). Cancer Causes and Control, 2004; 15:797–803. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15456993
45. Lin MY, Lockhart D, and Denlinger-Apte R. Exploring Factors Shaping Tobacco and Marijuana Use Among Sexual Minority Adolescents. Nicotine and Tobacco Research, 2025. Available from: https://www.ncbi.nlm.nih.gov/pubmed/40326389
46. Wolford-Clevenger C, Hill SV, and Cropsey K. Correlates of Tobacco and Nicotine Use Among Transgender and Gender Diverse People: A Systematic Review Guided by the Minority Stress Model. Nicotine and Tobacco Research, 2022; 24(4):444-52. Available from: https://pubmed.ncbi.nlm.nih.gov/34375426/