A person who regularly uses e-cigarettes will inhale a mixture of chemicals into their lungs. This mixture contains very low concentrations of numerous chemicals that are known to cause cancer. Heavy use means inhaling these chemicals hundreds of times a day, every day, for many years. It is currently unknown whether this extent of exposure is sufficient to cause cancer. However, there are signs of cellular damage and exposure to cancer-causing chemicals in people who use e-cigarettes that have led to concern that e-cigarette use may cause cancer. Furthermore, people who quit smoking but continue e-cigarette use have a higher risk of lung cancer compared to people who quit smoking without e-cigarette use afterwards.1,2
Cancer is a condition that often arises 20 years or more after the initiation of tobacco use. Since e-cigarettes are a relatively new product, becoming popular after 2010 (see Section 18.3), the vast majority of people who use them have not been exposed for this length of time. A comprehensive Australian review has found no prospective studies of sufficient quality on which to assess the risk of cancer for people who use e-cigarettes.3,4
The current lack of extensive epidemiological evidence that e-cigarette use causes cancer cannot be taken to mean that e-cigarette use cannot cause cancer. Assessing such risk will take a longer timeframe than is possible given the recency of the introduction of e-cigarettes to the market.
Studies of the long-term risk of cancer from e-cigarette use are hampered by a number of issues:
- the relatively short period of time that e-cigarettes have been used
- many of the people who using e-cigarettes having a history of smoking (which is known to causes cancer)
- rapid changes in the types of e-cigarette devices, their modes of use and e-liquid composition, meaning that previous studies may not reflect the risks of contemporary and future e-cigarette use.
Numerous lines of evidence support the biological plausibility that long-term exposure to e-cigarette aerosols could increase the risk of cancer. There are chemicals present at concentrations in e-cigarette aerosols that are low but nevertheless capable of causing cancer (see Section 18.5.4).5-7 Some experiments using laboratory-grown cells show that e-cigarette chemicals can induce damage of the type that is known to lead to cancer (see Section 18.6.4.2). Biological samples from people who use e-cigarette contain evidence of various toxic compounds at levels higher than in non-users (see Sections 18.6.4.2 and 18.6.4.4). People who regularly use e-cigarettes have signs of cellular damage of the same type that is associated with the formation of cancer (see Section 18.6.4.4). On the basis of such evidence, a 2025 qualitative risk assessment from Australia concluded that nicotine-based e-cigarettes are likely to be carcinogenic (cancer causing) to humans who use them and to cause lung cancer and oral cancer8,9 (see Section 18.6.4.5 below).
18.6.4.1 Chemicals in e-cigarettes that can cause cancer
Numerous carcinogens (chemicals that are known causes of cancer in humans and/or animals) have been found in e-liquids and/or the aerosols from e-cigarettes. The carcinogens found in e-cigarette aerosols include benzo[a]pyrene, acrolein, arsenic, benzene, cadmium, formaldehyde, styrene and toluene (see Table 18.5.1)10,11 as well as other toxic metals and N-nitrosamines (some of which are derived from nicotine).8 Compared with tobacco smoke, e-cigarette emissions have much lower concentrations of most carcinogens12-14 (see Section 18.5.4.4 for a discussion of the health concerns of the chemicals found in e-cigarettes). A study that detected carcinogenic aldehydes and polycyclic aromatic hydrocarbons (PAHs) in e-cigarette aerosols found that these chemicals were present at much lower concentrations compared to heated tobacco products and conventional cigarettes. For example, the highest powered of the three e-cigarettes in this study produced 64.5 ng of formaldehyde per puff compared to 156.9 ng from the heated tobacco product and 255.5 ng from the cigarette. Benzo[a]pyrene, a carcinogenic PAH, was detected at only 1.1 pg per puff compared to 25.6 pg from the heated tobacco product and 457 pg from the cigarette (noting that pg refers to picogram, which is 1/1000th of a nanogram and one millionth of a microgram).
A number of studies and major reviews predict that the presence of toxic metals in e-cigarettes may be at a similar or even higher level than in conventional cigarettes, which may pose a risk for cancer.13,15-17
The US Surgeon General’s 2014 report stated that there is insufficient data to conclude that nicotine causes or contributes to cancer.18 The International Agency for Research on Cancer Advisory Group have not designated nicotine as a carcinogen and are not planning any evaluation of nicotine as a carcinogen as of 2024.19 Experiments testing the cancer-causing potential of nicotine are described in Section 3.3.1.1.
18.6.4.2 Laboratory studies on the risk of cancer from e-cigarette exposure
The early events that underlie cancer formation have been studied in laboratories for decades, and many forms of cellular damage that lead to cancer are well characterised.20,21 Results from some experiments exposing cells grown in laboratories to e-cigarette chemicals are consistent with promotion of the type of damage that triggers cancer formation. Furthermore, samples of cells from people who use e-cigarettes show these types of damage.
An extensive risk assessment has reviewed the evidence from laboratory studies to show that many chemicals from e-cigarettes show a variety of key characteristics of carcinogens, as summarised.8
There is considerable evidence that chemicals in e-cigarettes are genotoxic (lead to mutations in DNA that may trigger the start of cancer).6 A subset of these called mutagenic chemicals damage DNA by changing its sequence. Once they enter the body, they are often modified in biochemical reactions before binding to DNA at specific sites (called DNA adducts, see Section 3.3.2.2). E-cigarette aerosols can induce DNA strand breaks and oxidative DNA damage cells grown in the laboratory and the formation of DNA adducts in the lung, heart and bladder of mice.22 DNA adducts (regions of DNA bound to mutagenic chemicals, where mutations are likely to occur) have been found at elevated levels in tissue samples from people who use e-cigarettes compared to non-users.23,24 DNA damage has been demonstrated in cells exposed to 33 different e-liquids in one study.25 Studies of lung cells grown in the laboratory have shown that exposure to e-cigarette chemicals can lead genotoxicity.26,27 E-liquids or aerosol induced DNA damage in oral cells grown in the laboratory.28 Two major reviews have concluded that e-cigarettes show genotoxicity.29,30
Laboratory experiments also show that e-cigarette exposure can induce a state of oxidative stress, which causes a type of cellular damage that can lead to cancer.27,31 Human oral and lung cells grown in laboratories showed signs of increased oxidative stress when exposed to e-cigarette emissions, or in animals exposed to e-cigarettes.8,31
A 2025 Australian risk assessment also presented evidence for the presence of other key characteristics of carcinogens in cells exposed to e-cigarette chemicals, including induction of chronic inflammation, epigenetic alterations (in which DNA is modified but the sequence remains the same) and alterations to DNA repair mechanisms, among others.8,32,33 In one study, similar types of epigenetic alterations were found in the oral cells of people who use e-cigarettes and who smoke tobacco. These alterations are suspected to be involved in the formation of cancer.34
Applying e-cigarette chemicals to lung cancer cells has been shown to increase the rate of an event known as epithelial-to-mesenchymal transition,35 which is considered a first step in the transition to metastasis (the spreading of cancer). Application of e-cigarette chemicals to oral cancer cells could induce invasive activity of these cells, a mechanism that could contribute to spreading of cancer (metastasis).36 E-cigarette chemicals may also have epigenetic effects (altering DNA but without changing the sequence) in lab grown cells and animal experiments that are related to cancer formation.37,38
18.6.4.3 Animal studies on the risk of cancer from e-cigarette exposure
Some experimental studies in rodent models of disease indicate the potential of e-cigarette exposure to trigger lung tumour growth, consistent with a risk for cancer in humans.8
Mice exposed to e-cigarette aerosols for 12 weeks sustained DNA damage in lungs, heart, and bladder cells and diminished DNA repair (a situation that can promote the development of cancer) in the lungs.39 After 54 weeks of exposure, nine out of 40 mice developed lung cancer tumours (adenocarcinoma) and 23 developed a precancerous bladder condition (bladder urothelial hyperplasia).40 However, this experiment found tumours in much greater numbers that seen in similar experiments, such as those described below.
In one study, three months of exposure to e-cigarette emissions led to mice developing DNA mutation damage in their lungs, bladders and tongues.41 In another study, rats exposed to the chemicals from e-cigarettes over four weeks showed signs of toxicological damage. These effects included oxidative damage and genotoxic damage, which may increase the risk of cancer developing. However, tumour growth in these animals was not reported.42 An increase in lung tumours was also absent in mice exposed to e-cigarettes for eight weeks, but changes to the lung microbiome were seen in these animals that may favour tumour growth.43 Another study has demonstrated that e-cigarette exposure resulted in oxidative stress in the lungs and liver in mice.27 Genotoxic effects, however, were not seen in these mice, even after six months of exposure.27
Mice exposed to e-cigarette emissions were more likely to have colorectal adenomas, as seen by increases in polyps in their colons, compared to unexposed mice.44 Among the changes seen with e-cigarette exposure were increased inflammation, DNA damage, and increase of cancer cell markers.44
18.6.4.4 Human studies on the risk of cancer from e-cigarette exposure
18.6.4.4.1 Biomarkers of exposure and damage in people who use e-cigarettes
A biomarker is a substance in the body that can be measured to indicate exposure to specific chemicals. Biomarkers of exposure might be detected in people’s breath, saliva, urine, blood and other samples. Biomarkers may also indicate damage—or the potential for damage—to human systems (called biomarkers of potential damage), and may predict the risk of disease. Biomarkers of e-cigarette exposure and biomarkers of potential harm are described in more detail in Section 18.5.6.
Biomarkers of potential harm:
Biomarkers of potential harm have been found in tissue samples from people who use e-cigarettes. These include DNA adducts, markers of oxidative stress and inflammation discussed above in Section 18.6.4.2. DNA adducts are parts of DNA that are bound to chemicals that can cause mutations known to contribute to cancer formation. An example is acrolein-DNA adducts found at elevated levels in the mouths of people who use e-cigarettes, compared to non-users. These adducts consist of acrolein bound to DNA, which indicates a risk of DNA damage from this carcinogen.24
A systematic review has found substantial evidence for a significant association between e-cigarette use and biomarkers of potential harm that indicate a risk of cancer: oxidative stress, cellular apoptosis, DNA damage, genotoxicity, and tumour growth.45
Biomarkers of exposure:
Biological samples from people who use e-cigarette have been shown to contain biomarkers for various toxic chemicals and of damage at levels higher than for non-users. A potential limitation of these studies is that these chemicals may have entered the body from other sources of pollution.
Biomarkers of exposure to toxic chemicals, including carcinogens, were detected in samples from wave 1 (2013-2014), of the Population Assessment of Tobacco and Health (PATH) Study.46 This is a nationally representative, prospective study from the US. People who exclusively used e-cigarettes had higher levels of biomarkers for the carcinogens NNK (4-(methylnitros-amino)-1-(3-pyridyl)-1-butanone), lead, cadmium and acrylonitrile than never users. However e-cigarette-only users had lower levels of the carcinogens NNK, cadmium, acrylonitrile and acrolein than those who smoked tobacco.46 See Section 18.5.6 for more detail about carcinogen biomarkers in people who use e-cigarettes.
A longitudinal study of exposure to e-cigarettes found that acrolein biomarkers in urine were significantly higher in e-cigarette users than non-users/non-smokers after four to six months of exposure.47 Biomarkers of carcinogens that are associated with bladder cancer have been found in the urine of e-cigarette users.48
18.6.4.4.2 Rates of cancer among people who use e-cigarettes
Cancer in people who exclusively use e-cigarettes
The relatively short time frame in which e-cigarette use has been popular—and the long time period necessary for cancer to form after exposure to chemicals—means there has been insufficient time to obtain robust estimate the rates of cancer for people who use e-cigarettes. A major Australian review found no long-term prospective studies of the kind necessary for predicting the long-term risks of cancer, as of 2021.3,4 A systematic review from 2025 found some cross-sectional studies and one longitudinal study that addressed the risk of cancer from e-cigarette use. There was no consistent finding of an increased risk in these studies, likely due to the short time period covered.45
One short-term prospective study has measured self-reported health outcomes for 343 people who used e-cigarettes only, 693 who used tobacco and 319 dual users. There was no significant difference in the rates of cancer diagnosis after two years of follow-up in the study that will run for five years.49 However, the limited time-frame and sample size means this study may not be informative about long-term cancer risk.49
Some cross-sectional studies had found an association between e-cigarette use and lung cancer, but this study design should not be used to imply causation.50,51 Two case reports have documented cancer diagnoses for people who use e-cigarettes, such as lung or oral cancer.52,53 A systematic review has found an association between e-cigarette use and lung cancer, but most of the data came from cross-sectional studies.54 One longitudinal study using data from the All of Us Research Program found evidence that breast cancer patients who use e-cigarettes may experience a shorter time to metastasis (i.e. their cancers spread sooner).55
Cancer in people who switch from smoking to e-cigarettes
There is evidence that use of e-cigarettes after smoking cessation is associated with a higher risk of lung cancer compared to those who quit smoking and don’t take up e-cigarette use. That is, e-cigarette use after quitting smoking appears to diminish the benefits of smoking cessation for reducing lung cancer risk.1
A large longitudinal study from South Korea compared lung cancer outcomes (after 5 years’ follow-up) for people : who continued to smoke cigarettes; who quit in the short-term (4 to 6 yrs): and who quit in the longer-term (≥6 yrs). People who quit smoking but used e-cigarettes afterwards had a higher risk of lung cancer, and death from lung cancer, compared to those who quit both smoking without subsequent e-cigarette use. However, an improvement in all-cause mortality for people who used e-cigarettes after quitting smoking was seen. This indicates that there are likely some health benefits from smoking cessation followed by e-cigarette use, even if the rates of lung cancer and lung cancer mortality were not improved.1,2
Another study from South Korea tracked the health of people who smoke and were diagnosed with COPD (chronic obstructive pulmonary disease). Of over 23,000 people, 64% continued smoking, 30.3% quit, and 5.7% switched to e-cigarettes. Those who quit completely had a lower risk of lung cancer compared with those who continued smoking. Similar to the study above, switching from cigarettes to e-cigarettes failed to reduce the risk of lung cancer among people with COPD that is usually seen among people who quit smoking.2
A retrospective cohort study using data collected from 2018 to 2023 found that for people who smoke who have chronic hepatitis B, those who switched to e-cigarette use had a higher risk of liver cancer than those who quit smoking and did not use e-cigarettes, although the results did not reach statistical significance.56
Risk of cancer in dual users
A case-control study has identified dual use of e-cigarettes and conventional cigarettes as increasing the risk of early-onset lung cancer.57 In this study, people < 50 years old who smoked and used e-cigarettes had an almost 3-fold higher risk of lung cancer. This study was limited, however, as the results were not adjusted for smoking intensity or past smoking.57
18.6.4.5 Predicting the risk of cancer from e-cigarette use
An extensive qualitative risk assessment published in 2025 concluded that nicotine-based e-cigarettes are likely to be carcinogenic to humans who use them and to cause lung cancer and oral cancer.8 These conclusions were based on evidence 1) that aerosols produced by using e-cigarettes contain multiple known carcinogens, 2) that cellular and DNA damage seen in in human samples and laboratory grown cells exposed to e-cigarettes is consistent with the mechanisms of cancer development, and 3) that animal studies show similar damage, with some developing cancer.8 The conclusions of this report stated:
´Nicotine-based e-cigarettes are likely to be carcinogenic to humans who use them.
E-cigarettes are likely to cause lung cancer and oral cancer.’8
Some studies have used toxicological data to quantitatively predict the risk of cancer from e-cigarette use and to compare this to risks associated with other tobacco products.7 These studies commonly predict lesser risks of cancer from e-cigarettes than conventional cigarettes, but greater than ambient air. As e-cigarette device types are rapidly evolving, the accuracy of past studies to predict the risks from contemporary and future e-cigarette types is uncertain.
A study from 2023 assessed the cancer risk from numerous chemicals found in e-cigarette aerosols, finding the highest average risk came from chromium, followed by formaldehyde, nickel, acetaldehyde then arsenic. The risks from each of these five substances was above acceptable levels.58
A study from 2020 estimated the risk of cancer from metal contamination in e-cigarette aerosols.16 The authors estimated cancer risk by multiplying the cancer slope factor (an estimate of the risk of cancer) for specific metals by the estimated daily dose of exposure. Their results estimated that chromium and nickel were the leading contributors to cancer risk, with minor contributions from cadmium, lead, and arsenic. They concluded that some e-cigarettes may be significant sources of metal exposures, capable of increasing the risk of cancer.16
A similar study from 2017 compared estimated cancer risks of e-cigarettes to conventional cigarettes, heated tobacco products and nicotine inhalers (used for cessation), taking into account the exposure to 15 different carcinogens.13 The estimated mean lifetime risk of cancer from first and second generation (see Section 18.1.1) e-cigarette use was less than 1% of that estimated for conventional cigarettes, but 10-fold more than that for nicotine inhalation devices used for cessation. However, newer devices with variable power settings were much more varied, with some ranging more closely to the risk from conventional cigarettes. The higher risks were likely associated with the higher levels of carbonyl reaction products such as carcinogenic aldehydes that are generated at higher power levels.
Related reading
Relevant news and research
A comprehensive compilation of news items and research published on this topic
Read more on this topic
Test your knowledge
References
1. Kim YW, Park EJ, Kwak KI, Yoon TH, Kang HR, et al. Electronic cigarette use after smoking cessation and lung cancer risk. Nature Medicine, 2026; 32(7):2410-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/42260103
2. Kim T, Kim H, Shin SH, Choi S, Jeong E, et al. E-cigarette switching in COPD: reduced cardiovascular events without improvement in respiratory outcomes. Respiratory Research, 2026; 27(1). Available from: https://www.ncbi.nlm.nih.gov/pubmed/41680780
3. Banks E, Yazidjoglou A, Brown S, Nguyen M, Martin M, et al. Electronic cigarettes and health outcomes: systematic review of global evidence. Report for the Australian Department of Health, 2022, National Centre for Epidemiology and Population Health: Canberra. Available from: https://www.nhmrc.gov.au/sites/default/files/documents/attachments/ecigarettes/Electronic_cigarettes_and_health_outcomes_%20systematic_review_of_evidence.pdf.
4. Banks E, Yazidjoglou A, Brown S, Nguyen M, Martin M, et al. Electronic cigarettes and health outcomes: umbrella and systematic review of the global evidence. Medical Journal of Australia, 2023; 218(6):267-75. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36939271
5. National Academies of Sciences Engineering and Medicine. Public health consequences of e-cigarettes. The National Academies Press, Washington, DC 2018. Available from: http://nationalacademies.org/hmd/Reports/2018/public-health-consequences-of-e-cigarettes.aspx.
6. El Bouz M, Neto C, Mansuy T, Becher R, Valen H, et al. Health hazards of e-cigarettes and heated tobacco products: A comprehensive analysis of hazardous substances and regulatory gaps,. Nicotine & Tobacco Research, 2026; 28(5):710-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41351476
7. Shaw IC, Woollett AR, Dickie NM, Kennedy MJ, Liddle JT, et al. Is it safe to vape? Assessing the carcinogenic risk of "vape smoke". New Zealand Medical Journal, 2026; 139(1633):104-11. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41990383
8. Stewart B. E-cigarettes and cancer: A qualitative risk assessment. Clinical Oncology Society of Australia; Sydney.: COSA, 2025. Available from: https://www.cosa.org.au/COSA/COSA/Reports/E-Cigarettes-and-Cancer-Research-Report.aspx
9. Stewart BW, Marshall H, Bonevski B, Griffin HJ, Hopkins AM, et al. The carcinogenicity of e-cigarettes: a qualitative risk assessment. Carcinogenesis, 2025; 47(1). Available from: https://www.ncbi.nlm.nih.gov/pubmed/41910510
10. National Industrial Chemicals Notification and Assessment Scheme (NICNAS). Non-nicotine liquids for e-cigarette devices in Australia: chemistry and health concern. Australian Government Department of Health, 2019. Available from: https://www.industrialchemicals.gov.au/sites/default/files/2020-08/Non-nicotine%20liquids%20for%20e-cigarette%20devices%20in%20Australia%20chemistry%20and%20health%20concerns%20%5BPDF%201.21%20MB%5D.pdf.
11. National Health and Medical Research Council. Inhalation toxicity of non-nicotine e-cigarette constituents: risk assessments, scoping review and evidence map. 2022. Available from: https://www.nhmrc.gov.au/file/18287/download?token=Z5D5_sam.
12. Goniewicz ML, Knysak J, Gawron M, Kosmider L, Sobczak A, et al. Levels of selected carcinogens and toxicants in vapour from electronic cigarettes. Tobacco Control, 2014; 23(2):133-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/23467656
13. Stephens WE. Comparing the cancer potencies of emissions from vapourised nicotine products including e-cigarettes with those of tobacco smoke. Tobacco Control, 2017:10-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28778971
14. Dusautoir R, Zarcone G, Verriele M, Garcon G, Fronval I, et al. Comparison of the chemical composition of aerosols from heated tobacco products, electronic cigarettes and tobacco cigarettes and their toxic impacts on the human bronchial epithelial BEAS-2B cells. Journal of Hazardous Materials, 2021; 401:123417. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32763707
15. Gaur S and Agnihotri R. Health effects of trace metals in electronic cigarette aerosols-a systematic review. Biological Trace Element Research, 2019; 188(2):295-315. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29974385
16. Fowles J, Barreau T, and Wu N. Cancer and non-cancer risk concerns from metals in electronic cigarette liquids and aerosols. International Journal of Environmental Research and Public Health, 2020; 17(6). Available from: https://www.ncbi.nlm.nih.gov/pubmed/32213824
17. Williams M, Bozhilov K, Ghai S, and Talbot P. Elements including metals in the atomizer and aerosol of disposable electronic cigarettes and electronic hookahs. PLoS One, 2017; 12(4):e0175430. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28414730
18. U.S. Department of Health and Human Services. The health consequences of smoking: 50 years of progress. 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, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf.
19. Berrington de Gonzalez A, Masten SA, Bhatti P, Fortner RT, Peters S, et al. Advisory Group recommendations on priorities for the IARC Monographs. Lancet Oncology, 2024; 25(5):546-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/38621402
20. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. Atlanta, Georgia: Centers for Disease Control and Prevention, 2010. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53017/.
21. de Conti A, Madia F, Schubauer-Berigan MK, and Benbrahim-Tallaa L. Carcinogenicity of some metals evaluated by the IARC Monographs: A synopsis of the evaluations of arsenic, cadmium, cobalt, and antimony. Toxicology and Applied Pharmacology, 2025; 504:117506. Available from: https://www.ncbi.nlm.nih.gov/pubmed/40780533
22. Tang MS, Lee HW, Weng MW, Wang HT, Hu Y, et al. DNA damage, DNA repair and carcinogenicity: Tobacco smoke versus electronic cigarette aerosol. Mutation Research - Reviews in Mutation Research, 2022; 789:108409. Available from: https://www.ncbi.nlm.nih.gov/pubmed/35690412
23. Morgil GK and Cok I. Evaluation and comparison of DNA alkylation and oxidative damage in e-cigarette and heated tobacco users. Toxicology Mechanisms and Methods, 2025; 35(2):125-35. Available from: https://www.ncbi.nlm.nih.gov/pubmed/39138671
24. Cheng G, Guo J, Carmella SG, Lindgren B, Ikuemonisan J, et al. Increased acrolein-DNA adducts in buccal brushings of e-cigarette users. Carcinogenesis, 2022; 43(5):437-44. Available from: https://www.ncbi.nlm.nih.gov/pubmed/35239969
25. Al-Saleh I, Elkhatib R, Al-Rajoudi T, Al-Qudaihi G, Manogarannogaran P, et al. Cytotoxic and genotoxic effects of e-liquids and their potential associations with nicotine, menthol and phthalate esters. Chemosphere, 2020; 249:126153. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32058129
26. Khalil C, Chahine JB, Haykal T, Al Hageh C, Rizk S, et al. E-cigarette aerosol induced cytotoxicity, DNA damages and late apoptosis in dynamically exposed A549 cells. Chemosphere, 2021; 263:127874. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33297006
27. Platel A, Dusautoir R, Kervoaze G, Dourdin G, Gateau E, et al. Comparison of the in vivo genotoxicity of electronic and conventional cigarettes aerosols after subacute, subchronic and chronic exposures. Journal of Hazardous Materials 2022; 423(Pt B):127246. Available from: https://www.ncbi.nlm.nih.gov/pubmed/34844363
28. Guo J and Hecht SS. DNA damage in human oral cells induced by use of e-cigarettes. Drug Testing and Analysis, 2023; 15(10):1189-97. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36169810
29. Armendariz-Castillo I, Guerrero S, Vera-Guapi A, Cevallos-Vilatuna T, Garcia-Cardenas JM, et al. Genotoxic and carcinogenic potential of compounds associated with electronic cigarettes: A systematic review. Biomedicine Research International, 2019; 2019:1386710. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31950030
30. Keith R and Bhatnagar A. Cardiorespiratory and immunologic effects of electronic cigarettes. Current Addiction Reports 2021; 8(2):336-46. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33717828
31. Lerner CA, Sundar IK, Yao H, Gerloff J, Ossip DJ, et al. Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung. PLoS One, 2015; 10(2):e0116732. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25658421
32. Tellez CS, Grimes MJ, Juri DE, Do K, Willink R, et al. Flavored E-cigarette product aerosols induce transformation of human bronchial epithelial cells. Lung Cancer, 2023; 179:107180. Available from: https://www.ncbi.nlm.nih.gov/pubmed/36989612
33. Tellez CS, Juri DE, Phillips LM, Do K, Yingling CM, et al. Cytotoxicity and genotoxicity of e-cigarette generated aerosols containing diverse flavoring products and nicotine in oral epithelial cell lines. Toxicological Sciences, 2021; 179(2):220-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33226417
34. Herzog C, Jones A, Evans I, Raut JR, Zikan M, et al. Cigarette smoking and e-cigarette use induce shared DNA methylation changes linked to carcinogenesis. Cancer Research, 2024; 84(11):1898-914. Available from: https://www.ncbi.nlm.nih.gov/pubmed/38503267
35. Zahedi A, Phandthong R, Chaili A, Remark G, and Talbot P. Epithelial-to-mesenchymal transition of A549 lung cancer cells exposed to electronic cigarettes. Lung Cancer, 2018; 122:224-33. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30032837
36. Kinney R, Ponder L, Patel N, Chatterjee A, Vu K, et al. Comparative effects of cigarette smoke and e-cigarette vapor on oral squamous cell carcinoma: Unraveling distinct molecular pathways. Dental Research and Oral Health, 2025; 8(3):97-103. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41048327
37. Kopa-Stojak PN and Pawliczak R. Comparison of carcinogenic potential of alternative tobacco products. A systematic review. Toxicology Mechanisms and Methods, 2025; 35(9):1161-75. Available from: https://www.ncbi.nlm.nih.gov/pubmed/40741827
38. Awada C, Klein CB, Gordon T, Raja A, Pinkerton KE, et al. Exposure to electronic cigarette aerosols triggers alterations in genomic DNA methylation that impacts cancer pathways in mice. Inhalation Toxicology, 2026; 38(6):297-320. Available from: https://www.ncbi.nlm.nih.gov/pubmed/42021672
39. Lee HW, Park SH, Weng MW, Wang HT, Huang WC, et al. E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells. Proc Natl Acad Sci U S A, 2018; 115(7):E1560-E9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29378943
40. Tang MS, Wu XR, Lee HW, Xia Y, Deng FM, et al. Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice. Proc Natl Acad Sci U S A, 2019; 116(43):21727-31. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31591243
41. Chhaya D, Gress M, Raja A, Kosinska W, Gordon T, et al. Effects of e-cigarette (e-cig) aerosols on mutagenesis in selected organs in a C57 lacI (BigBlue(TM)) mouse model. International Journal of Environmental Research and Public Health, 2024; 21(12). Available from: https://www.ncbi.nlm.nih.gov/pubmed/39767534
42. Canistro D, Vivarelli F, Cirillo S, Babot Marquillas C, Buschini A, et al. E-cigarettes induce toxicological effects that can raise the cancer risk. Scientific Reports, 2017; 7(1):2028. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28515485
43. Velasco WV, Grimaldo MT, Karimi N, Clowers MJ, Krishna A, et al. Comparative effects of combustible cigarette versus electronic cigarette exposures on KRAS mutant lung cancer promotion. Neoplasia, 2025; 67:101185. Available from: https://www.ncbi.nlm.nih.gov/pubmed/40516145
44. Sayed IM, Chakraborty A, Inouye K, Dugan L, Tocci S, et al. E-cigarettes increase the risk of adenoma formation in murine colorectal cancer model. Archives of Toxicology, 2025; 99(3):1223-36. Available from: https://www.ncbi.nlm.nih.gov/pubmed/39786590
45. Kundu A, Sachdeva K, Feore A, Sanchez S, Sutton M, et al. Evidence update on the cancer risk of vaping e-cigarettes: A systematic review. Tobacco Induced Diseases, 2025; 23. Available from: https://www.ncbi.nlm.nih.gov/pubmed/39877383
46. Goniewicz ML, Smith DM, Edwards KC, Blount BC, Caldwell KL, et al. Comparison of nicotine and toxicant exposure in users of electronic cigarettes and combustible cigarettes. JAMA Network Open, 2018; 1(8):e185937. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30646298
47. Chen M, Carmella SG, Lindgren BR, Luo X, Ikuemonisan J, et al. Increased levels of the acrolein metabolite 3-hydroxypropyl mercapturic acid in the urine of e-cigarette users. Chemical Research in Toxicology, 2023; 36(4):583-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/35858275
48. Bjurlin MA, Matulewicz RS, Roberts TR, Dearing BA, Schatz D, et al. Carcinogen biomarkers in the urine of electronic cigarette users and implications for the development of bladder cancer: A systematic review. European Urology Oncology, 2021; 4(5):766-83. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32192941
49. Manzoli L, Flacco ME, Ferrante M, La Vecchia C, Siliquini R, et al. Cohort study of electronic cigarette use: effectiveness and safety at 24 months. Tobacco Control, 2017; 26(3):284-92. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27272748
50. Akinboro O, Nwabudike S, Elias R, Balasire O, Ola O, et al. Electronic cigarette use among survivors of smoking-related cancers in the United States. Cancer Epidemiology, Biomarkers & Prevention, 2019; 28(12):2087-94. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31501150
51. Gambaryan M, Kalinina A, Popovich M, Starovoytov M, and Drapkina O. Electronic cigarette use strongly associated with respiratory diseases: Results from Russian Tobacco Control Policy evaluation survey. European Respiratory Journal 2020:1875. Available from: https://publications.ersnet.org/content/erj/56/suppl64/1875.abstract
52. Nguyen H, Kitzmiller JP, Nguyen KT, Nguyen CD, and Bui TC. Oral carcinoma associated with chronic use of electronic cigarettes. Otolaryngology: Open Access, 20-17; 7:304. Available from: https://www.omicsonline.org/open-access/oral-carcinoma-associated-with-chronic-use-of-electronic-cigarettes-2161-119X-1000304.php?aid=88343
53. Klawinski D, Hanna I, Breslin NK, Katzenstein HM, and Indelicato DJ. Vaping the venom: Oral cavity cancer in a young adult with extensive electronic cigarette use. Pediatrics, 2021; 147(5). Available from: https://www.ncbi.nlm.nih.gov/pubmed/33926987
54. Mohapatra S, Tiwari A, Kandala A, Winayak R, Ghose A, et al. The risk of lung cancer from vaping or e-cigarette usage: a systematic review. ESMO Open, 2025; 10(12):105910. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41259896
55. Pillai DG, Chau CH, Price DK, and Figg WD. Vaping and cancer metastasis: novel preclinical insights and results from the All of Us Research Program. Oncologist, 2025; 30(7). Available from: https://www.ncbi.nlm.nih.gov/pubmed/40589063
56. Song BG, Lee M, Cho J, Gwak GY, Kang D, et al. E-cigarette switching, smoking cessation, and the risk of hepatocellular carcinoma in patients with chronic hepatitis B: A nationwide cohort study in South Korea. Preventive Medicine, 2026; 205:108530. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41654088
57. Bittoni MA, Carbone DP, and Harris RE. Vaping, smoking and risk of early onset lung cancer. Frontiers in Oncology, 2025; 15:1741978. Available from: https://www.ncbi.nlm.nih.gov/pubmed/41568369
58. Zhao S, Zhang X, Wang J, Lin J, Cao D, et al. Carcinogenic and non-carcinogenic health risk assessment of organic compounds and heavy metals in electronic cigarettes. Scientific Reports, 2023; 13(1):16046. Available from: https://www.ncbi.nlm.nih.gov/pubmed/37749131