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Effects of vaping on the human respiratory system have been observed. Serious lung illnesses such as chronic obstructive pulmonary disease, asthma, and possibly lung cancer is associated with the use of e-cigarettes.
Effects of vaping on the human respiratory system have been observed.[1] Serious lung illnesses such as chronic obstructive pulmonary disease, asthma,[2] and possibly lung cancer[3] is associated with the use of e-cigarettes.[2]
Potential effects of e-cigarette exposure on various organ systems in the human body
Potential effects of e-cigarette exposure on various organ systems in the human body[4]
Video on the facts of vaping by the Centers for Disease Control and Prevention[5]

The impact of traditional cigarettes on human health has been well-defined in both animal and human studies.[4] In contrast, little is known about the adverse effects of e-cigarette exposure on human health.[4] There is a lack of many long-term studies that can identify future health risks associated with e-cigarette use.[6] There is no sufficient evidence on their long-term organ effects.[4] Their long-term exposure health effects remain largely unknown.[4] Data on the prolonged use of e-cigarettes use among people with pre-existing chronic diseases are missing.[4] Long-term exposure to e-cigarettes may cause adverse effects on various organ systems.[4]

The long-term effects on lung function is unknown.[7] There is concern that e-cigarette use could result in respiratory diseases among youth.[8] Repeated exposure to acrolein, which is produced by heating the propylene glycol and glycerin in e-liquids, causes chronic pulmonary inflammation, reduction of host defense, neutrophil inflammation, mucus hypersecretion, and protease-mediated lung tissue damage, which are linked to the development of chronic obstructive pulmonary disease.[9] Vaping cannabinoid plants may lead to lung injury similar to that of smoking tobacco.[10] Vaping poses unique risks, as contaminants and additives to the vape medium may cause significant lung damage apart from cannabinoids.[10]

There is limited available evidence on their long-term cardiovascular effects.[11] Their cardiovascular effects in individuals who do not have cardiovascular disease is uncertain.[12] E-cigarettes may lead to adverse effects on the cardiovascular system through various mechanisms, such as oxidative stress, inflammation, endothelial dysfunction, atherosclerosis, hemodynamic effects, and platelet activity.[13] Research on the consequences of vaping on blood pressure is limited.[14] Compared to non-users, e-cigarette use increases the chance of experiencing a heart attack by 33%.[15] The evidence suggests that vaping has the ability to induce tachycardia-induced cardiomyopathy.[16]

The long-term effects of e-cigarette use on the brain is unknown.[17] Vaping may increase the risk of suicidal thoughts and suicide.[18] A 2021 observational study found an association between e-cigarette use and stroke.[19] The risk of early death is anticipated to be similar to that of smokeless tobacco.[20] There is a significant risk of long-lasting lung injury from vaping that may contribute to or lead to death, in old people.[21] Nicotine exposure leads to epigenetic changes that affect lung function in future generations.[22] Vaping or the use of any nicotine-based product during pregnancy, or both during pregnancy and the breastfeeding postpartum period, causes the "concurrent exposure of three generations to nicotine."[23]

Limited research

The long-term consequences from e-cigarette use on death and disease are unclear.[24] The risks from long-term use of nicotine as well as other toxicants that are unique to e-cigarettes are uncertain.[25] The potential long-term effects of e-cigarette consumption have been scarcely investigated.[26] The latency period for diseases caused by tobacco use encompasses a duration of at least 25 years.[27] Therefore, as of 2019, it will conservatively take two decades until firm conclusions from long-term research on e-cigarette use are accessible.[27] Epidemiological data on cancer findings takes at least 20 to 40 years to become available.[28] As of 2023, evidence of the harms of e-cigarettes has been unfolding slowly and has been documented in many reviews and reports worldwide.[29] E-cigarettes have the potential for benefit and harm, the nature and scale of each being uncertain in the absence of ample evidence.[30]

The health effects related to e-cigarette use is mostly unknown.[31] Most of the available articles reported are limited in their design, methodology, and the used exposure time and had a lack of long-term follow-up.[32] There is insufficient data regarding the health benefits of vaping.[33] There is limited available research regarding their effects on vulnerable groups such as minors.[34] The effect on population health from e-cigarettes is unknown.[7] The chemical characteristics of the short-lived free radicals and long-lived free radicals produced from e-cigarettes is unclear.[35] The knowledge of possible acute and long-term health effects of aerosols inhaled from e-cigarettes is limited partially due to incomplete awareness of physical phenomena related to e-cigarette aerosol dynamics.[36] There is a significant absence of inhalational toxicity data regarding the majority of the ingredients in e-cigarettes.[37]

Respiratory effects

Overview

Figure shows mechanisms of e-liquid flavorings effects on the lung innate immunity and the respiratory microbiota in lung injury. The respiratory tract is lined by a pseudostratified columnar ciliated epithelium (nasal cavity through the bronchi) transitioning to cuboidal on the bronchioles and squamous on the alveoli (AEC). The apical junctional complexes (AJC), including tight and adherens junctions, maintain the airways epithelial integrity and contribute to prevent contact between the respiratory microbiota and the phagocytic cells therefore, providing an immunotolerant environment an immunotolerant environment. At the AJC, the tight junctions regulate paracellular permeability, and the adherens junctions provide cell-to-cell communication, while connecting to cellular cytoskeletal proteins. The airway mucus constitutes the water-based apical layer of the airway surface liquid and the periciliary layer is the second sol-based layer that bathes the epithelium. The respiratory microbiota (RM) resembles the oral microbiota (OM). Members of the RM relies on the airway mucus to access nutrients including mucins (MUC5AC and MUC5B) and avoid contact with the epithelium, professional antigen presenter cells (DCs) and phagocytic cells such as alveolar macrophages (AMs) and neutrophils (PMNs). The airway epithelium secretes β-defensins and other host defense peptides and proteins (HDPs). In addition to the airway's epithelium, the innate immune response within the respiratory tract involves phagocytic cells including dendritic cells, alveolar macrophages, neutrophils; eosinophils; innate lymphoid cells and natural killer cells. The airway surface liquid represents an ecological niche for the respiratory microbiota, provides a source of specialized nutrients, and plays a role in immunomodulation by regulating the interaction between the respiratory microbiota and the immune system. E-cigarette flavorings such as cinnamaldehyde, menthol, or vanillin can disrupt microbial clearance in the respiratory tract by disrupting the AEC integrity and decreasing the levels of mucus, decreasing mucus clearance and antimicrobial secretion, and eliciting and inflammatory response, eventually producing lung injury. E-cigarette flavorings also impair the phagocytic activity of AMs and PMNs.
Figure shows mechanisms of e-liquid flavorings effects on the lung innate immunity and the respiratory microbiota in lung injury.[38] The respiratory tract is lined by a pseudostratified columnar ciliated epithelium (nasal cavity through the bronchi) transitioning to cuboidal on the bronchioles and squamous on the alveoli (AEC).[38] The apical junctional complexes (AJC), including tight and adherens junctions, maintain the airways epithelial integrity and contribute to prevent contact between the respiratory microbiota and the phagocytic cells therefore, providing an immunotolerant environment an immunotolerant environment.[38] At the AJC, the tight junctions regulate paracellular permeability, and the adherens junctions provide cell-to-cell communication, while connecting to cellular cytoskeletal proteins.[38] The airway mucus constitutes the water-based apical layer of the airway surface liquid and the periciliary layer is the second sol-based layer that bathes the epithelium.[38] The respiratory microbiota (RM) resembles the oral microbiota (OM).[38] Members of the RM relies on the airway mucus to access nutrients including mucins (MUC5AC and MUC5B) and avoid contact with the epithelium, professional antigen presenter cells (DCs) and phagocytic cells such as alveolar macrophages (AMs) and neutrophils (PMNs).[38] The airway epithelium secretes β-defensins and other host defense peptides and proteins (HDPs).[38] In addition to the airway's epithelium, the innate immune response within the respiratory tract involves phagocytic cells including dendritic cells, alveolar macrophages, neutrophils; eosinophils; innate lymphoid cells and natural killer cells.[38] The airway surface liquid represents an ecological niche for the respiratory microbiota, provides a source of specialized nutrients, and plays a role in immunomodulation by regulating the interaction between the respiratory microbiota and the immune system.[38] E-cigarette flavorings such as cinnamaldehyde, menthol, or vanillin can disrupt microbial clearance in the respiratory tract by disrupting the AEC integrity and decreasing the levels of mucus, decreasing mucus clearance and antimicrobial secretion, and eliciting and inflammatory response, eventually producing lung injury.[38] E-cigarette flavorings also impair the phagocytic activity of AMs and PMNs.[38]

When vaping, hundreds to thousands of chemicals are inhaled into the lungs.[39] The risks to the lungs are not fully understood,[40] and concern exists regarding the negative effects on lung function.[41] The long-term effects on lung function is unknown.[7] There is limited evidence on the long-term health effects to the lungs.[42] The long-term effect from vaping a base containing nicotine on lung tissue is unknown.[43] A 2025 review states that the current evidence on whether e-cigarettes pose respiratory risks is unclear, due to confounding by cigarette smoking.[44] Researchers have documented the harmful pulmonary effects of conventional tobacco smoking for more than 140 years.[45] In contrast, as of 2022, e‑cigarettes have been in widespread use for less than two decades, offering a comparatively limited period in which to identify and characterize pulmonary conditions linked to their use.[45]

Limited evidence suggests that e-cigarettes produce less short-term effects on lung function than with traditional cigarettes.[7] Some studies suggest that vaping may be just as hazardous to respiratory health as cigarette smoking.[46] Overall, research indicates that vaping produces effects on lung function comparable to those caused by cigarette smoking.[46] Many ingredients used in e-liquids have not been examined in the lung.[40] E-cigarettes increase the risk of developing asthma and chronic obstructive pulmonary disease.[47] Vaping may induce acute lung disease[42] and increase the risk of developing lung disease.[48] Vaping might cause sub-acute bronchial toxicity.[49] Little is known about the short- and long-term effects of e-cigarettes on the respiratory microbiota and their impact on the innate immune response.[38]

Effects

E-cigarette use can have deleterious effects on lung lipid metabolism regardless of nicotine content.[50] Lipid-laden macrophages, discovered in bronchoalveolar lavage fluid from e-cigarette users, suggest users are at risk for lipid-mediated lung injury and interfered pathogen clearance via macrophages.[51] The lipid concentrations may be related to aerosolization of propylene glycol and glycerin solvents in e-liquid.[51] Exposure to inhaled nicotine-containing e-cigarette fluids triggered effects normally associated with the development of a chronic obstructive lung disease-like tissue damage in a nicotine-dependent manner.[52] Preclinical research indicate that vaping escalates the virulence of drug resistant microorganisms and diminishes the capacity of lung cells to eliminate bacteria.[53] E-cigarettes have been correlated with pleural effusions.[54] A 2015 study found that e-cigarette vapors can induce oxidative stress in lung endothelial cells.[55]

Constant lung inflammation as a result of the e-cigarette vapor could result in lung pathogenesis and induce serious diseases, including chronic obstructive pulmonary disease and fibrosis.[31] There is strong evidence that e-cigarette vapors can result in acute endothelial cell injury, but the long-term effects regarding this matter on being exposed over a prolonged period of time to e-cigarette vapor is uncertain.[56] The use of nicotine-laden e-cigarettes can induce oxidative stress and disrupt autophagy due to nicotine exposure, which may act as a mechanism that causes to the onset of chronic obstructive pulmonary disease.[57] A 2014 case report observed the correlation between sub-acute bronchiolitis and vaping.[42] After quitting vaping the symptoms improved.[42] Vaping causes bronchospasm.[58] Adolescents who vaped had a higher frequency of chronic bronchitis symptoms.[59]

The long-term effects regarding respiratory flow resistance are unknown.[60] The available evidence indicates that e-cigarettes may result in respiratory effects that are like as well as unlike that of traditional cigarettes.[37] E-cigarettes, particularly the ones containing nicotine, decrease lung function, but to a considerable lower extent than with traditional cigarettes.[61] E-cigarette use lowers oxygen saturation.[62] E-cigarettes could harm the respiratory system.[63] Vaping induces irritation of the upper and lower respiratory system.[64] The immediate effects of e-cigarettes after five minutes of use on pulmonary function resulted in considerable increases in resistance to lung airflow.[65]

Vaping induces fundamental changes to the airway epithelial proteome that are unique from what has been observed in smokers.[66] These alterations are accompanied by visible modifications in airway appearance, with vapers exhibiting a noticeable reddish coloration consistent with erythema and heightened tissue fragility.[66] Research has observed an acute increase in airway resistance after the use of a single e-cigarette.[63] Higher levels of exhaled nitric oxide were found among test subjects in a 2014 study who vaped with a base of nicotine which was associated with lung inflammation.[67] Short-term usage of e-cigarettes results in an increase in respiratory resistance in a manner similar to that of tobacco smoking.[60] There is concern that e-cigarette use could result in respiratory diseases among youth.[8] Evidence from animal studies indicate that children or adolescents exposed to second-hand vapor containing nicotine may impede their lung development.[68]

The figure shows the effects of flavors in e-liquids reported in different experimental models
The figure shows the effects of flavors in e-liquids reported in different experimental models[69]

Data suggest that e-cigarette users produce significantly more sputum than smokers and show increased markers of inflammation in their airways.[70] As airway inflammation and mucus hypersecretion are central features underlying asthma pathology, asthmatics might be at increased risk for e-cigarette-induced health effects.[70] Adolescents with asthma who vape could have greater odds of having a higher number of respiratory symptoms and aggravations in contrast to their peers who do not vape.[71] Adolescents and children with other respiratory ailments who vape may be at greater chance for aggravating of respiratory symptoms.[71]

Comparable to a traditional cigarette, e-cigarette particles are tiny enough to enter the alveoli, enabling nicotine absorption.[65] These particles are also tiny enough to go deep in the lungs and enter into the systemic circulation.[72] Research indicates that e-cigarette vapor containing particulate matter with a diameter of 2.5 μm, just from one puff, enters the systemic circulation via the cardiopulmonary system, leading to a large amount being deposited in the respiratory tract.[58] Local pulmonary toxicity may occur because metal nanoparticles can deposit in the lung's alveolar sacs.[72] E-cigarettes companies state that the particulates produced by an e-cigarette are too tiny to be deposited in the alveoli.[73] Tinier particles deposit more nicotine in the alveoli.[49]

National Institute on Drug Abuse TV interview with Virginia Commonwealth University Professor of Psychology, Thomas Eissenberg, following his discussion on e-cigarette research.[74]
Vaping is an epidemic spreading amongst teenagers.[75] It can expose the lungs to acrolein, which can cause irreversible damage.[75]

Different devices generate different particle sizes and cause different depositions in the respiratory tract, even from the same nicotine liquid.[76] The aerosol production of e-cigarettes during vaping decreases, which requires a more forceful suction to create a similar volume of aerosol.[77] A more forceful suction could affect the deposition of substances into the lungs.[77] Compared to cigarette smoke, e-cigarettes produce on average smaller size particles, and the health effects of these smaller size particles is unclear.[78] Reports in the literature have shown respiratory and cardiovascular effects by these smaller size particles, suggesting a possible health concern.[79] Vaping is potentially harmful, especially to the critically ill, such as people with oncologic, lung, or cardiac diseases.[64] A 2019 case study of hard-metal pneumoconiosis was published in the European Respiratory Journal.[18] Researchers tested the patient's e-cigarette, which was used with cannabis.[18] Cobalt was found in the vapor, including other toxic metals-nickel, aluminum, manganese, lead, and chromium.[18] Metal-induced toxicity in the lung can result in long-term, if not, permanent scarring of the lungs.[18]

As with cardiovascular disease, evidence consistently indicates that exposure to e-cigarette aerosol is associated with adverse effects on lungs and pulmonary function.[9] Repeated exposure to acrolein, which is produced by heating the propylene glycol and glycerin in e-liquids, causes chronic pulmonary inflammation, reduction of host defense, neutrophil inflammation, mucus hypersecretion, and protease-mediated lung tissue damage, which are linked to the development of chronic obstructive pulmonary disease.[9] E-cigarette aerosol also exposes users to highly oxidizing free radicals.[9] Animal studies have also shown that e-cigarettes increase pulmonary inflammation and oxidative stress while inhibiting the immune system.[9]

Consistent with these experimental results, people who used e-cigarettes experienced decreased expression of immune-related genes in their nasal cavities, with more genes suppressed than among cigarette smokers, indicating immune suppression in the nasal mucosa.[9] E-cigarette use upregulates expression of platelet-activating factor receptor (PAFR) in users' nasal epithelial cells; PAFR is an important molecule involved in the ability of S.pneumoniae, the leading cause of bacterial pneumonia, to attach to cells it infects (adherence).[9] In light of the immunosuppressive effects observed in nasal mucosa, there is concern that e-cigarette use will predispose users toward more severe respiratory infections, as has been demonstrated in mouse studies.[9]

Case reports and small case series have linked e-cigarette use to a variety of diffuse parenchymal lung diseases which include small airway-centered fibrosis, constrictive bronchiolitis, and respiratory bronchiolitis-associated interstitial lung disease.[80] Vaping is reportedly connected to a range of lung injuries which include hypersensitivity pneumonitis, diffuse alveolar hemorrhage, acute eosinophilic pneumonia, diffuse alveolar damage, organizing pneumonia, lipoid pneumonia, and giant cell interstitial pneumonia.[81] Vaping cannabinoid plants may lead to lung injury similar to that of smoking tobacco.[10] Vaping poses unique risks, as contaminants and additives to the vape medium may cause significant lung damage apart from cannabinoids.[10]

Respiratory effects in youth and young adults

Overview

As of 2021, little information is available regarding the effect of e-cigarette exposure on children's respiratory health.[82] Available data on the respiratory effects among young people are mainly self-reported and may be subjected to recall bias, as of 2021.[82]

Effects

An infographic explaining that vaping can be harmful to youth, presented by the US Food and Drug Administration.
An infographic explaining that vaping can be harmful to youth, presented by the US Food and Drug Administration.[83]

A 2016 survey conducted on 44,662 Chinese students (mean age 14.6 years), reported that e-cigarette use was significantly associated with respiratory symptoms, e.g., cough or phlegm for 3 consecutive months in the past 12 months.[82] Likewise, in a 2017 study on 2,086 adolescents aged 16–18 years who took part in the Southern California Children's Health Study, self-reported wheeze in the last 12 months was associated with current but not past use of e-cigarette.[82] In the same study, chronic bronchitis symptoms during the previous year were associated with both past and present use of e-cigarette.[82] The risk of bronchitis symptoms was directly proportional to the number of days of e-cigarette use in the past month, compared with non-e-cigarette users.[82] Vaping among 11th-grade and 12th-grade students in California was linked with twice the chance of respiratory complaints, and the chance went up with vaping more regularly.[84] In a 2020 cohort study of 7,049 adolescents, the association of e-cigarette use alone with wheezing in the past 12 months proved not to be significant.[82]

A 2017 cross-sectional study investigating the effects of active, passive, and e-cigarette vaping in Korean adolescents, including 4,890 with asthma in the last 12 months, reported significant associations between active and passive smoking and asthma.[82] In addition, the authors found that asthma was significantly more frequent in the e-cigarette group.[82] In a 2016 cross-sectional study on a large sample of 35,904 high school students (mean age 16.4 years) in South Korea, the authors found that e-cigarette users had an increased association with asthma diagnosis in comparison with non-e-cigarette users, suggesting that e-cigarette use may be a risk factor for asthma.[82] Of note, current e-cigarette users had the highest risk for severe asthma, defined as the number of days (greater than or equal to 4) absent from school in the past year due to asthma symptoms, compared to non-e-cigarette users.[82]

Similarly, in a 2017 survey on 6089 adolescents (mean age 15.8 years) in Hawaii, the authors reported that current use of e-cigarettes showed a significant association with current asthma and a marginal one with asthma at any time.[82] A 2020 study on 21,532 U.S. adolescents (age range: 14–18 years), in which use of an e-vapor product was associated with asthma, showed an additional harmful effect on asthma of the combined use of vapor products with marijuana and cigarette smoking: use of an e-vapor product was associated with asthma, and this association was even more evident when its use was coupled with marijuana, particularly when cigarette smoking was also involved.[82] When adjusting for frequent cigarette smoking and marijuana use, frequent use of an e-vapor product (greater than or equal to 10 days per month) was significantly associated with asthma.[82]

Asthma exacerbations were found to be associated with e-cigarette vaping.[82] Data from the 2012 Florida Youth Tobacco Survey, involving 36,085 high school students, reported that prevalence of ever having used e-cigarette and having used them in the past 30 days among those who reported asthma was 10.4 and 5.3%, and this was significantly higher than in those without asthma.[82] Among students with asthma, use of e-cigarette in the past 30 days was positively associated with an asthma attack in the past 12 months.[82]

E-cigarette use is associated with a doubling of the risk of symptoms of chronic bronchitis among US high school juniors and seniors with higher risk associated with higher use; these risks persisted among former users.[9] Similarly, current e-cigarette use was associated with an increased diagnosis of asthma among Korean high school students among current (e-cigarette users who were never cigarette smokers).[9] E-cigarette users were also more likely to have had days absent from school due to severe asthma symptoms.[9]

Cardiovascular effects

Overview

Figure shows a cartoon-style comic illustrating the aerosolization process of e-cigarette and its relation to cardiovascular diseases. This comic provides a visual narrative, starting from the use of an e-cigarette to the potential harmful effects on the cardiovascular system. In the upper left part of the cartoon, it can be seen that e-cigarette aerosol contains many substances such as nicotine, flavorings, aldehydes, and metals, which may be harmful to human. In the upper right part of the cartoon is the design of an e-cigarette device. On the right side of the cartoon is the adverse effects of e-cigarette aerosol on blood vessels and heart. Through mechanisms such as oxidative stress, inflammation, and endothelial dysfunction, e-cigarette aerosol can increase heart rate, blood pressure, and clog blood vessels.
Figure shows a cartoon-style comic illustrating the aerosolization process of an e-cigarette and its relation to cardiovascular diseases.[13] This comic provides a visual narrative, starting from the use of an e-cigarette to the potential harmful effects on the cardiovascular system.[13] In the upper left part of the cartoon, it can be seen that e-cigarette aerosol contains many substances such as nicotine, flavorings, aldehydes, and metals, which may be harmful to human.[13] In the upper right part of the cartoon is the design of an e-cigarette device.[13] On the right side of the cartoon is the adverse effects of e-cigarette aerosol on blood vessels and heart.[13] Through mechanisms such as oxidative stress, inflammation, and endothelial dysfunction, e-cigarette aerosol can increase heart rate, blood pressure, and clog blood vessels.[13]
Diagram shows potential adverse cardiovascular effects induced by various constituents of e-cigarette aerosol.
Diagram shows potential adverse cardiovascular effects induced by various constituents of e-cigarette aerosol.[13]
Figure shows summary of pulmonary and cardiovascular dysfunction and their cellular basis. (a) E-cigarette use has been linked to disease and dysfunction in the heart and lungs. (b) i. Platelets are activated towards a pro-thrombotic phenotype in the vessel; ii. E-cigarette aerosol exposure promotes endothelial cell death and compromised barrier function, which facilitates immune cell extravasation into the surrounding tissue. Endothelial cells release inflammatory cytokines that enhance neutrophil recruitment; iii. Monocytes differentiate into macrophages upon extravasation. Neutrophils and macrophages remodel extracellular matrix in the interstitium as an inflammatory response, promoting compromise of the epithelium and endothelium; iv. Epithelial permeability is compromised and e-cigarette aerosol exposure is associated with epithelial cell apoptosis and necrosis; v. e-cigarette aerosol exposed macrophages and neutrophils enter the lung tissue and promote inflammation. Macrophages take up e-cigarette-associated lipids. Not to scale.
Figure shows summary of pulmonary and cardiovascular dysfunction and their cellular basis.[85] (a) E-cigarette use has been linked to disease and dysfunction in the heart and lungs.[85] (b) i. Platelets are activated towards a pro-thrombotic phenotype in the vessel; ii. E-cigarette aerosol exposure promotes endothelial cell death and compromised barrier function, which facilitates immune cell extravasation into the surrounding tissue.[85] Endothelial cells release inflammatory cytokines that enhance neutrophil recruitment; iii. Monocytes differentiate into macrophages upon extravasation.[85] Neutrophils and macrophages remodel extracellular matrix in the interstitium as an inflammatory response, promoting compromise of the epithelium and endothelium; iv. Epithelial permeability is compromised and e-cigarette aerosol exposure is associated with epithelial cell apoptosis and necrosis; v. e-cigarette aerosol exposed macrophages and neutrophils enter the lung tissue and promote inflammation.[85] Macrophages take up e-cigarette-associated lipids.[85] Not to scale.[85]
Figure shows testing outcomes for acute heart rate. Eight acute studies found no significant increase in heart rate with e-cigarette use within subject or compared to tobacco cigarettes. Three acute tests found a significant increase in heart rate for nicotine e-cigarettes, but in one test, the increase was not significantly different than tobacco cigarettes, and in another, it was a significantly lower increase than tobacco cigarettes. One additional acute study finding an increase in heart rate was seriously compromised due to excessive e-cigarette exposure. One study reported that acute non-nicotine e-cigarette use significantly raised heart rate compared to sham vaping; it conducted excessive e-cigarette exposure. Another study on non-nicotine e-cigarettes found that tobacco cigarettes significantly raised heart rate in comparison.
Eight acute studies found no significant increase in heart rate with e-cigarette use within subject or compared to tobacco cigarettes.[86] Three acute tests found a significant increase in heart rate for nicotine e-cigarettes, but in one test, the increase was not significantly different than tobacco cigarettes, and in another, it was a significantly lower increase than tobacco cigarettes.[86] One additional acute study finding an increase in heart rate was seriously compromised due to excessive e-cigarette exposure.[86] One study reported that acute non-nicotine e-cigarette use significantly raised heart rate compared to sham vaping; it conducted excessive e-cigarette exposure.[86] Another study on non-nicotine e-cigarettes found that tobacco cigarettes significantly raised heart rate in comparison.[86]

There is limited available evidence on their long-term cardiovascular effects.[11] Their cardiovascular effects in individuals who do not have cardiovascular disease is uncertain.[12] Although limited, there is supportive evidence that vaping adversely impacts endothelial function and arterial hardening.[11] Most of the cardiovascular effects of vaping are consistent with those of nicotine.[35] Despite the widespread use of e-cigarettes and the known detrimental cardiac consequences of nicotine, the effects of e-cigarettes on the cardiovascular system are not well-known.[87] E-cigarettes may lead to adverse effects on the cardiovascular system through various mechanisms, such as oxidative stress, inflammation, endothelial dysfunction, atherosclerosis, hemodynamic effects, and platelet activity.[13]

Blood pressure effects

Research on the consequences of vaping on blood pressure is limited.[14] Short-term physiological effects include increases in blood pressure and heart rate.[42]

A 2014 study demonstrated that short-term e-cigarette using caused a fractional increase in diastolic blood pressure.[32] In a 2015 study, a lower nicotine content was reported in the blood of persons vaping e-cigarettes than in the case of people smoking traditional cigarettes, which contributed to a smaller increase in arterial pressure and heart rate in this group.[32] Research by Vlachopoulos et al. in 2016 was conducted among people without cardiovascular risk.[32]

Research was conducted by Antoniewicz et al. in 2019 to assess acute influence of inhaling e-cigarettes with nicotine and without it within the period of 0, two, and four hours after exposure.[32] A significant increase in heart rate was reported in the case of vaping e-cigarettes containing nicotine and an increase in arterial blood pressure in both analyzed cases.[32]

In the study of Arastoo et al. in 2020 among 100 electronic and traditional smokers, including chronic smokers, the baseline heart rate variability as well as hemodynamics (blood pressure and heart rate) were analyzed.[32] In this research, the authors hypothesized that the changes in these parameters are caused by nicotine, and not by the non-nicotine components of the e-cigarette aerosol.[32] Based on the conducted research, it was shown that people who were chronic smokers of both types of cigarettes had a similar level of heart rate variability.[32] When assessing the effect of vaping e-cigarettes, a sharp increase in blood pressure and heart rate was noticed only after the use of e-cigarettes with nicotine, which confirmed the hypothesis.[32]

Abnormalities in heart rate during vaping e-cigarettes in comparison with non-smokers were demonstrated by Moheimani et al. in 2017.[32] The authors indicate that it was not caused by the nicotine content in the e-liquid, because it was untraceable in the plasma of the examined persons.[32] At the same time, they emphasize that it is nicotine metabolites that can produce adverse effects leading to a greater risk of cardiovascular diseases among people who use this type of cigarette.[32]

Effects

A 2023 systematic review and meta-analysis finds that nicotine-containing e-cigarettes cause a substantial, potentially harmful effect on several short-term cardiovascular parameters.[88] Their short-term use may result in adverse effects in vascular endothelial function.[89] Vaping might bring about some adverse cardiovascular effects to users, especially those who already have cardiovascular disease.[35] However, the risk is believed to be lower than that of cigarette smoking based on research comparing e-cigarette aerosol in contrast to cigarette smoke chemicals.[35] Compared to non-users, e-cigarette use increases the chance of experiencing a heart attack by 33%.[15]

Preliminary evidence indicates there may be a correlation between the use of e-cigarettes and a heightened risk of heart failure.[90] Using e-cigarettes could exacerbate heart failure symptoms, diminish quality of life, and lead to more frequent hospital admissions.[90] Nonetheless, existing research faces substantial challenges, such as a lack of long-term prospective studies, difficulties in accurately measuring exposure, and risks of confounding factors.[90]

There is a substantial amount of evidence that e-cigarettes can be equally (if not even more) harmful to the cardiovascular system than traditional tobacco.[91] Like classic tobacco smoking, e-cigarettes can also increase sympathetic nervous system activity, oxidative stress and inflammation, endothelial dysfunction, and platelet activation, leading to cardiac arrhythmias, atherosclerosis and plaque instability, thrombosis and acute ischemia, etc.[91] The effects of e-cigarettes on RAAS activity and specifically on aldosterone levels are presently not known.[91]

Given the similarity between their cardiovascular effects and those of traditional tobacco smoking, it is quite plausible that e-cigarette–derived nicotine also activates the RAAS axis and elevates circulating aldosterone levels, exactly as the nicotine delivered by traditional tobacco products does.[91]

The effects of aldehydes, particulates, and flavorings used in vaping devices on cardiovascular health is not clear.[35] Low amounts of aldehydes can still be a health concern, particularly among individuals with cardiovascular disease.[58] E-cigarettes reduce cardiac muscle function and increase inflammation, but these changes were only substantial with traditional cigarettes.[61] No published research is available on vaping and thrombosis, platelet reactivity, atherosclerosis, or blood vessel function.[42] The small particles generated from e-cigarette use have the ability to get through airways and enter circulation, which pose a potential risk to cardiovascular systems.[58]

The minute nicotine particles in the e-cigarette vapor could increase the risk of cardiac arrhythmias and hypertension which may put some users, particularly those with atherosclerosis or other cardiovascular risk factors, at significant risk of acute coronary syndrome.[92] There are many compounds in the e-cigarette vapor that have an impact on the onset and advancement of atherosclerosis.[93] Some case reports documented the possible cardiovascular adverse effects from using e-cigarettes, the majority associated was with improper use.[92] Even though e-cigarettes are anticipated to produce fewer harmful substances than traditional cigarettes, limited evidence recognizes they comparatively have a lowered raised cardiovascular risk.[92]

Preliminary studies have shown that using a nicotine containing e-cigarette for just five minutes causes similar lung irritation, inflammation, and effect on blood vessels as smoking a traditional cigarette, which may increase the risk of a heart attack.[94] E-cigarette use leads to sympathomimetic effects because of nicotine intake.[16] The evidence suggests that vaping has the ability to induce tachycardia-induced cardiomyopathy.[16] E-cigarettes containing nicotine may have a lower cardiovascular effect than traditional cigarettes containing nicotine.[95]

A 2016 study found vaping increases aortic stiffness in people who did not have cardiovascular risk factors, an effect that was lower than with cigarette smoking.[35] A 30-minute vaping session seems to induce an unfavorable effect on aortic stiffness similar to traditional smoking.[96] Habitual vaping was associated with oxidative stress and a shift towards cardiac sympathetic activity, which are both associated with a risk of developing cardiovascular disease.[57] A 2012 case report found a correlation between paroxysmal atrial fibrillation and vaping.[42] Research indicates a relationship between exposure to particulate matter with a diameter of 2.5 μm and the chance of developing cardiovascular disease.[58]

E-cigarettes adversely impact the cardiovascular system.[9] Although the specific role of nicotine in cardiovascular disease remains debated, nicotine is not the only biologically active component in e-cigarette aerosol.[9] E-cigarettes work by creating an aerosol of ultrafine particles to carry nicotine deep into the lungs.[9] These particles are as small as—and sometimes smaller than—those in traditional cigarettes.[9] These ultrafine particles are themselves biologically active, trigger inflammatory processes, and are directly implicated in causing cardiovascular disease and acute cardiovascular events.[9] The dose-response effect for exposure to particles is nonlinear, with substantial increases in cardiovascular risk with even low levels of exposure to ultrafine particles.[9] For example, exposure to second-hand cigarette smoke has nearly as large an effect on many risk factors for cardiovascular disease and the risk of acute myocardial infarction as does being an active smoker.[9] Like traditional cigarette smokers, e-cigarette users experience increased oxidative stress and increases in the release of inflammatory mediators.[9] E-cigarette aerosol also induces platelet activation, aggregation, and adhesion.[9] All these changes are associated with an increased risk of cardiovascular disease.[9] These physiological changes are manifest in rapid deterioration of vascular function following use of e-cigarettes.[9]

E-cigarette and traditional cigarette smoking in healthy individuals with no known cardiovascular disease exhibit similar inhibition of the ability of arteries to dilate in response to the need for more blood flow.[9] This change reflects damage to the lining of the arteries (the vascular endothelium), which increases both the risk of long-term heart disease and an acute event such as a myocardial infarction (heart attack).[9] Using e-cigarettes is also accompanied by a shift in balance of the autonomic (reflex) nervous system toward sympathetic predominance, which is also associated with increased cardiac risk.[9]

The biological stresses that e-cigarette use impose on the cardiovascular system are manifest as an increase in risk of acute myocardial infarction.[9] A cross-sectional analysis of data in the US 2014 and 2016 National Health Interview Surveys showed that daily e-cigarette use was associated with increased odds of having suffered a myocardial infarction, controlling for traditional cigarette smoking, demographic characteristics (age, gender, body mass index, family income) and health characteristics (hypertension, diabetes, and hypercholesterolemia).[9] Significantly, the effect of using e-cigarettes on the odds of myocardial infarction approached what was found with traditional cigarette smoking.[9]

Daily vaping represents an independent risk factor for myocardial infarction, synergically amplified by exposure to nicotine, a parasympathomimetic alkaloid increasing heart rate and blood pressure.[96] Nicotine has systemic hemodynamic effects that are mediated by the activation of the sympathetic nervous system.[87] Thus, acute nicotine treatment can stimulate cardiac output by producing systemic vasoconstriction and increasing heart rate.[87] In the context of e-cigarettes, by contributing to an increased sympathetic heart activity, can be also responsible for increased oxidative stress, which will cause an increased cardiovascular risk.[32] Moreover, the increased oxidative stress and inflammatory conditions can induce the development of atherosclerosis.[32]

Neurological diseases

Exposure to nicotine and e-cigarettes is possibly implicated in causing neurological diseases such as Alzheimer's disease and multiple sclerosis.[97] Nicotine independently promotes the development of neurodegenerative disorders,[57] induces oxidative stress, and inhibits the process of autophagy.[57] Out of 28 e-liquids tested from seven companies in 2014, the four most commonly found flavor additives were vanillin, ethyl maltol, ethyl vanillin, and menthol.[57] They are carcinogenic or toxic, which may contribute to causing cardiopulmonary diseases such as chronic obstructive pulmonary disease and neurodegenerative disorders such as Alzheimer's disease.[57] E-cigarette use results in oxidize stress, which play a role in contributing to cardiopulmonary diseases and neurodegenerative disorders.[57]

Brain effects

The long-term effects of e-cigarette use on the brain is unknown.[17] With long-term nicotine use, cellular adaptations (as the brain reacts to recurring periods of uptake and withdrawal) within the brain may result in almost permanent alterations in neurons and neural circuits.[66] While a clear positive correlation between e-cigarette use and depression has been established, the causality and mitigating factors affecting this relationship are largely undetermined.[17] There is growing evidence that vaping may increase the risk of depression which increases the risk of suicidal thoughts and suicide.[18]

Chronic farnesol administration increases the firing rate of nicotinic acetylcholine receptor-expressing neurons in the ventral tegmental area.[17] Thus, the addition of the green apple flavorant, which is acquired by adding the chemical farnesol, induces neurobiological changes in the brain’s reward-related circuitry, which enhances nicotine’s rewarding properties to reinforce continued product use.[17]

E-cigarette-emitted metal particulates have been shown to readily cross the blood–brain barrier, as evidenced by metal accumulation in the mouse brain.[17] Moreover, following e-cigarette exposure, arsenic, chromium, copper, iron, manganese, nickel, lead, selenium, strontium, and zinc were found to accumulate across different regions of the mouse brain, with the greatest accumulation observed in the anterior frontal cortex and striatum.[17] Specifically, in the anterior frontal cortex, copper and strontium were enriched, whereas arsenic, chromium, copper, iron, lead, and selenium were enriched in the striatum.[17] Like other types of e-cigarette emissions, the type and relative proportion of metals that might accumulate in the brain are expected to vary among commercially available brands due to differences in the vape liquid constituents and electronic cigarette device characteristics.[17]

Cerebrovascular disease effects

Adequate research is not available to ascertain the risk of long-term harm resulting in cerebrovascular disease.[98]

Effects on COVID-19

Figure shows the effects of e-cigarette use on lung and immune function in response to COVID-19 virus and similarities of pathogenicity.
Figure shows the effects of e-cigarette use on lung and immune function in response to COVID-19 virus and similarities of pathogenicity.[99]
Figure shows factors responsible for higher susceptibility of smokers or vapers against COVID-19. In normal individuals, the muco-ciliary epithelium and the mucous layers act as the first line of defense against the foreign pathogen (in this case SARS-CoV2). On smoking, this layer is damaged and so is the flow of the peri-ciliary fluid (mucous; indicated by arrows) which makes them more prone to infections. Smokers are also shown to have higher surface expression of ACE2 receptors (binding sites for SARS-CoV2) which allows the entry of pathogens into the host cell and protects the virus against the host surveillance. In normal individuals, the viral infection could be checked by the, (a) cytokine release from the type II pneumocytes, goblet, nasal epithelial/ciliated and oral mucosal cells and (b) immune cell (macrophages, neutrophils and lymphocytes) infiltration at the site of infection, to contain further spread. Smoking weakens the immune system enabling easy entry into the host cell, rapid multiplication of the virus followed by hyperinflammatory response triggered by 'cytokine storm' in the host body eventually leading to damaged lung tissue.
Figure shows factors responsible for higher susceptibility of smokers or vapers against COVID-19.[100] In normal individuals, the muco-ciliary epithelium and the mucous layers act as the first line of defense against the foreign pathogen (in this case SARS-CoV2).[100] On smoking, this layer is damaged and so is the flow of the peri-ciliary fluid (mucous; indicated by arrows) which makes them more prone to infections.[100] Smokers are also shown to have higher surface expression of ACE2 receptors (binding sites for SARS-CoV2) which allows the entry of pathogens into the host cell and protects the virus against the host surveillance.[100] In normal individuals, the viral infection could be checked by the, (a) cytokine release from the type II pneumocytes, goblet, nasal epithelial/ciliated and oral mucosal cells and (b) immune cell (macrophages, neutrophils and lymphocytes) infiltration at the site of infection, to contain further spread.[100] Smoking weakens the immune system enabling easy entry into the host cell, rapid multiplication of the virus followed by hyperinflammatory response triggered by 'cytokine storm' in the host body eventually leading to damaged lung tissue.[100]

Because of their possible acute lung and cardiovascular toxicity, vaping may pose a greater risk of severe sickness for individuals with COVID-19.[101] The impact of vaping on being more susceptible to being diagnosed with COVID-19 is unknown.[102] A 2020 study found a clear link between vaping and various COVID-19 cases and fatalities.[103]

Vaping habits, such as the hand-to-mouth actions as well as touching the face, could increase the chance of COVID-19 infection and spread of the virus.[104] Through the transmission of asymptomatic carriers, sharing vaping devices could contribute to the spread of the virus.[104] It is possible the surface of a vaping device can be a vehicle for the transmission of the virus.[105] This is because the virus can survive on surfaces for a few hours to days.[105] Due to their design, e-cigarettes devices are brought to the mouth and face to inhale repeatedly, and many users have an increased urge to cough or expectorate which can increase the transmission of COVID-19.[106] In addition, the aerosols generated by these devices could contribute to SARS-CoV-2 transmission.[106]

E-cigarettes which contain high amount of nicotine might contribute to overexpression of ACE2 and contribute in the serious COVID 19 associated complications.[99] Moreover, ACE2 is linked to nicotinic acetylcholine receptors (nAChRs), particularly alpha7nAChR receptors, further supporting the notion that vaping (nicotine) might be playing a significant role in the pathophysiology of COVID-19.[99] Furthermore, TMPRSS2 protease important in the virus entry into the host cells are is suggested to be altered by ACE2 in vapers.[99]

E-cigarette use impair mucociliary clearance, increased mucosal permeability, promote peribronchial inflammation, and fibrosis.[99] It is well-established that the mucociliary epithelium and the mucous layers act as the primary line of defense against pathogens.[99] Further, vaping induces oxidative stress and inflammatory responses which may further contribute to COVID-19 related complication in vapers.[99]

A 2020 analysis showed that the occurrence of COVID-19 was associated with the use of e-cigarettes or the use of e-cigarettes and cigarettes together.[99] COVID-19 diagnosis was five times more likely among e-cigarettes users and seven times more likely among ever-dual-users.[99] Further, the testing was nine times more likely among past 30-day dual-users and 2.6 times more likely among past 30-day e-cigarette only users.[99] A 2021 review speculates that dual users of e-cigarettes and alcohol may be at higher risk to complications of COVID-19.[51] Higher odds of COVID-19 symptoms and higher odds of confirmed/suspected COVID-19 diagnosis were found in dual users than in exclusive smoking of conventional cigarettes.[107]

A 2020 study showed that while the use of nicotine or flavor-containing e-cigarettes led to significant cytokine dysregulation and potential inflammasome activation, none of these effects were detected in non-flavored and non-nicotine-containing e-cigarettes.[26] Therefore, taking together these observations, e-cigarette use may still be a potent risk factor for severe COVID-19 development depending on the flavor and nicotine content.[26] While smoking is linked with progression to more dire cases of COVID-19, a 2020 review recommends to give up vaping to minimize the chance of developing a severe case of COVID-19.[108]

Vaping websites inquired abouts the risks related to e-cigarette use and COVID-19, and unverified statements that vaping and nicotine can be used to guard against COVID-19 spread across social media.[109] The use of-cigarettes and the possible greater chance of transmission and susceptibility to COVID-19, as well as the possible greater chance of severity to this illness is a public health concern.[110] Medical organizations and public health professional across the globe have voiced their concern that e-cigarette use may increase the likelihood for COVID-19 susceptibility, severity, and negative consequences.[110]

Erectile dysfunction effects

Vaping may cause oxidative stress, such as the creation of reactive oxygen species and hydroxyl radicals.[111] This can lead to endothelial dysfunction, which in turn may lead to erectile dysfunction.[111] Nicotine causes dysfunction of nitric oxide synthesis.[112] This may result in an inability to get penile erections, resulting in erectile dysfunction.[112] Multiple studies have shown endothelial dysfunction from vaping, from nicotine itself as well as additives and flavors in e-cigarette emissions.[111] No study has conclusively demonstrated vaping causes erectile dysfunction, although nicotine use has been demonstrated to cause erectile dysfunction.[111]

Esophagitis effects

The figure shows a 2024 case report of odynophagia secondary to esophageal candidiasis, herpes simplex virus esophagitis, and reflux esophagitis, all of which were associated with daily heavy vaping.
The figure shows a 2024 case report of odynophagia secondary to esophageal candidiasis, herpes simplex virus esophagitis, and reflux esophagitis, all of which were associated with daily heavy vaping.[113]

E-cigarettes have been associated with esophageal symptoms and are now considered potential triggers of esophagitis exacerbations.[96]

Effects on eye health

A 23-year-old male presented to the emergency department with three weeks of intermittent left-sided eye pressure and vision loss in 2022. Upon further evaluation by a retina specialist, he was found to have multiple Roth spots and an impending central retinal vein occlusion in his left eye, accompanied by decreased visual acuity. After thorough exclusion of organic causes, his significant vaping history was considered the likely etiology of this hypercoagulable state and resultant central retinal vein occlusion.
A 23-year-old male presented to the emergency department with three weeks of intermittent left-sided eye pressure and vision loss in 2022.[114] Upon further evaluation by a retina specialist, he was found to have multiple Roth spots and an impending central retinal vein occlusion in his left eye, accompanied by decreased visual acuity.[114] After thorough exclusion of organic causes, his significant vaping history was considered the likely etiology of this hypercoagulable state and resultant central retinal vein occlusion.[114]

Limited research is available on the consequences of vaping on eye health, though chemicals such as nicotine and aldehydes are possibly harmful to the eyes.[115] Exposure to toxic chemicals from e-liquid or its vapor may result in dry eye and tear film break-up.[115]

A case report published in 2022 described a 23-year-old male with a significant history of e-cigarette use who was diagnosed with central retinal vein occlusion.[116] He presented with partial vision loss affecting his left eye.[116] Infectious and autoimmune causes were excluded.[116] Imaging showed prothrombotic changes in the right middle cerebral artery and elevated pressure in the right side of the heart.[116] Genetic testing for hereditary thrombophilia was negative.[116] After ruling out other etiologies, the central retinal vein occlusion was attributed to e-cigarette-induced thrombotic activity.[116] Anticoagulation therapy led to symptom resolution.[116]

Reproductive effects

Overview

E-cigarettes are used with increasing frequency by teenagers, who are potential future parents.[117] E-cigarettes, even when nicotine-free, include many harmful substances (including endocrine disruptors) that disturb the hormonal balance and negatively affect the morphology and function of the reproductive organs.[117]

Male

Diagram explaining the effects of e-cigarette-mediated reproductive disruption.
Effects of e-cigarette-mediated reproductive disruption[118]
The figure shows the effects of e-liquid with and without nicotine on the male reproductive system.
The effects of e-liquid with and without nicotine on the male reproductive system[117]

While studies on the effect of e-cigarettes on human male reproduction are limited, numerous studies have investigated their effect in animal models.[118]

The figure shows the influence of aerosol components of e-cigarette on male and female reproductive system.
The influence of aerosol components of e-cigarette on the male and female reproductive system[117]

Exposure to e-cigarettes was reported to disturb the hypothalamo-pituitary axis, resulting in altered gonadal function and semen quality.[118] Wawryk-Gawda and collaborators in 2019 showed that in male rats exposed to e-cigarette vapor had increased apoptosis in spermatogonia and spermatocyte, an alteration of the morphology and function of the seminiferous epithelium, as well as unica albuginea malformations.[118] Other studies linked e-cigarette utilization with steroidogenesis disruption and global disorganization of the testes, accompanied by significant desquamation of germ cells.[118]

Moreover, low testicular weight and a higher apoptotic cell number in the testis was observed in the context of e-cigarette exposure.[118] Intraperitoneal injection of e-cigarette liquid in male rats induced toxicity and testicular inflammation, which, in turn, affected sperm production and sperm quality with lower sperm density, reduction of epididymal sperm number, and lower sperm viability.[118] When inhaled for 4 weeks by male rats, the same flavoring induced apoptosis in testes.[118] The sperm of rats exposed to e-cigarette vapor showed increased teratozoospermia (looped tail, flagellar angulation, and complete absence of flagellum).[118] Studies showed that sperm chromatin integrity could also be affected by e-cigarette exposure.[118] In fact, higher DNA damage was observed in both testis and sperm of exposed rats.[118] These findings suggest potential mutagenic effects of e-cigarettes on sperm.[118]

Little to no studies have corroborated these findings in humans.[118] A preliminary study, presented at the British Fertility Society Conference in 2017, investigating the effect of e-cigarette flavoring on human sperm, showed a significant decrease in motility in specimen cultured with e-liquid flavoring.[118] This study and the results obtained in animal models all suggest that vaping could have pathogenic effects on male reproduction and caution should be used when vaping and trying to conceive.[118]

Female

Evidence of the impact of e-cigarettes on female reproduction suggests that the female reproductive system is not left unaffected by exposure to e-cigarettes.[118] Unlike sperm, there is no evidence linking the impact of e-cigarette utilization on intrinsic oocyte quality and oocyte genome integrity.[118] However, some data suggests that ovarian function is impaired in animal models exposed to e-cigarettes.[118] A decreased percentage of normal follicles was described in the ovaries of female rats exposed to e-cigarette fluid.[118] Hormone levels were also affected in these animals, where a reduction in estrogen secretion was observed.[118] Implantation and pregnancy outcomes were also affected in mice exposed to e-cigarette vapor.[118] Microarray analysis showed an alteration in uterine receptivity transcripts in e-cigarette exposed mice.[118] These females experienced a delay in embryo implantation, although the animals showed high progesterone levels, resulting in a decreased offspring number.[118]

Although reproductive trials have demonstrated that e-cigarettes can be responsible for embryo implantation and development impairments in mice, studies have not yet been performed specifically regarding e-cigarette-associated exposure in mammal granulosa cells.[119] In a 2017 study carried out in pregnant smokers, it was observed that the use of e-cigarettes as a way to quit tobacco smoking was consideerably more common than any other US FDA-approved smoking cessation tool.[119] For this reason, both fertility and embryo implantation trials in 2019 have been performed in mice following exposure of the animals to e-cigarette-produced aerosol for 4 months.[119] Exposed dams showed a significant delay in the onset of the first litter and a noticeable impaired embryo implantation despite the detection of high progesterone levels, a known pregnancy indicator.[119] As a consequence, existing studies could indicate that e-cigarettes are capable of impairing pregnancy initiation and fetal health, further suggesting that their use on behalf of reproductive-aged women or during pregnancy should be considered with extreme caution, a 2020 review states.[119]

Effects on gastrointestinal system

The most common gastrointestinal symptoms associated with vaping were epigastric pain, nausea and vomiting, followed by diarrhea and hemorrhage, which Gaur et al. attributed to the trace metals copper and chromium in the aerosol if exposed to high levels.[120] Further reports have documented relapsed ulcerative colitis in two unrelated cases of heavy cigarette smokers after having stopped cigarette smoking and starting e-cigarette use.[120] In these cases, either the continued use of e-cigarettes or switching back to cigarette smoking helped alleviate the symptoms.[120]

In another case report of a pregnancy health effect linked to e-cigarette use, a one-day-old infant suffered gastrointestinal bleeding with abdominal distension and respiratory distress.[120] The infant recovered at six months, after having undergone double barrel ileostomy and subsequent surgical procedures.[120] Vaping might induce recurring ulcerative colitis.[49]

Effects on immunology

Concern exists regarding the immunological effects of e-liquid, and analysis on animals demonstrate that nicotine as well as e-liquid vapor, appear to have adverse effects on the immune system.[49] The health consequences of smoking are widely documented, but the immunological effects of e-cigarette use is not well understood.[34] The finding of the limited available research on the immunological effects appear to be contradictory.[34] There is a small amount of research available that is related to gastrointestinal and neurological health risks.[34] There were reports of e-cigarettes causing an immune system reaction involving inflammation of the gastrointestinal system.[31]

Nasal scrape biopsies from non-smokers, smokers, and vapers showed extensive immunosuppression at the gene level with e-cigarette use.[1] Neutrophils from chronic vapers have been found to have a greater propensity for neutrophil extracellular trap formation than those from cigarette smokers or non-smokers.[1] Given that e-cigarettes may also impair neutrophil phagocytosis, the available data suggests that neutrophil function may be impaired in e-cigarette users.[1]

Insulin resistance effects

Studies have shown that nicotine causes decreased sensitivity of tissues to insulin, thus increasing the risk of developing type 2 diabetes.[32] Nicotine contributes to an increase in the level of hormones antagonistic to insulin, i.e, catecholamines and cortisol.[32] In turn, research studies conducted on animals have shown a direct influence of nicotine on activation of protein kinase dependent on AMP in adipose tissue.[32] It increased the speed of lipolysis and promoted insulin resistance.[32] Insulin resistance, which causes the development of diabetes, is connected with prothrombotic inflammatory conditions and provokes atherogenic changes in blood lipids.[32] It increases the risk of ischemic heart disease, diseases of peripheral arteries, and brain stroke.[32]

Research on the influence of nicotine on the organism has demonstrated its ability to induce hyperglycemia by activating glycogenesis and gluconeogenesis.[32] El Golli et al. in 2016 conducted experiment on rats administered intraperitoneally exposed to pure nicotine (0.5 mg/kg of body weight), e-liquid with or without nicotine for 28 days, and a significant increase in the level of blood glucose was reported.[32] Additionally, a reduced level of liver proteins and increased transaminase activity were detected in all the examined groups, yet it was the rats exposed to e-cigarettes which achieved worse results than the rats exposed to pure nicotine.[32] This can suggest that the mechanism of disorders of glucose metabolism induced by e-cigarettes is different than in the case of nicotine alone.[32] A 2019 study demonstrated that e-cigarettes users were at a greater risk of being diagnosed with prediabetes than those who had never used this kind of cigarettes.[32]

Kidney effects

A 2016 study regarding e-liquid exposure in adults rats showed e-cigarettes have an adverse impact on the kidneys.[121]

Liver effects

Animal studies have shown that vaping can induce hepatic steatosis through heterogeneous mechanisms, involving oxidative stress, hepatocytes apoptosis and impairment of cholesterol and lipid metabolism.[96] A 2020 case report documented e-cigarettes-induced hepatic injury even in humans, describing an increase of liver enzymes in a young vaper presenting to the emergency department for fever, abdominal pain, vomiting, and diarrhea.[96]

Effects on medication

Two cases highlighted that the use of the e-cigarette increased their clozapine levels and one publication presenting a patient with epilepsy for whom it increased their seizure frequency.[122] Two of the patients were 16 years old and 23 years old females and there was one 52-year-old male.[122] The increased clozapine levels reported cases, demonstrate the effect of nicotine on medication plasma levels and raise wider concerns regarding potential interactions with other medications as well.[122] Switching between different e-cigarette products and vice versa, or planning on quitting smoking, might alter the serum levels of a person's medication.[122]

Thromboembolism

There is scarce information on the health effects of using oral contraceptive in conjunction with e-cigarettes.[116] The available research indicates that e-cigarettes can lead to thrombosis.[116] As a result, people with other hypercoagulability triggers who also use e-cigarettes may face an increased risk of thromboembolism.[116] Additionally, oral contraceptive use in young adolescents can induce a hypercoagulable state and thrombosis.[116] This serves as an independent risk factor for thromboembolism, even in women without genetic predispositions or other common risk factors.[116] The estrogen component of oral contraceptives alters hemostasis by boosting the plasma levels and activities of coagulation factors while reducing coagulation inhibitors.[116]

Metabolism

Metabolic effects

There is a limited amount of research available on the metabolic effects of vaping.[123] It has not been fully studied in humans as to whether vaping has the same negative effects on metabolic processes as cigarette smoking.[123] Though, animal studies show similar effects of vaping, even without being exposed to nicotine, on weight and metabolic processes, comparing cigarette smoking.[123] This shows other things are responsible for the metabolic effects than just nicotine.[123] Animal studies indicate that vaping has similar negative effects on weight, body fat, glucose and lipid profiles and other cardiovascular potential dangers as traditional cigarettes, but they may be less prominent.[123] A lot of these cardiometabolic effects happen even without nicotine being present.[123]

Metabolic syndrome effects

As of 2020, there have been very few publications demonstrating the influence of e-cigarettes on the risk of occurrence of metabolic syndrome in people.[32] Research on a group of 18,300 volunteers was conducted by Lequy et al. 2018.[32] The obtained results allowed the researchers to claim that the occurrence of metabolic syndrome was connected with using e-cigarettes, whenever patients were not on a diet.[32] Another study in 2020 has been conducted on a group of 7505 Korean males over 19 years of age to compare the frequency of occurrence of cardiovascular risk factors among: males smoking conventional cigarettes, dual users (e-cigarettes and traditional cigarettes users) and never-smokers.[32] The multivariate logistic regression analysis showed that, in the adjusted model, the odds ratio (OR) for the prevalence of metabolic syndrome equaled 2.79 (p < 0.001) in comparison with never-smokers and 1.57 (p = 0.038) in relation to cigarette-only smokers.[32] In this model, dual users were characterized by an increased waist circumference and triglycerides level, as well as reduced high-density lipoproteins (HDL) in comparison with both the people who had never smoked and those who smoked only traditional cigarettes; therefore, it may be concluded that dual users are more vulnerable to cardiovascular risk factors.[32]

Blood lipids

High levels of triglycerides and low levels of HDL are risk factors for cardiovascular disease.[87] Nicotine promotes loss of body weight and the disturbance of lipoprotein metabolism through the secretion of catecholamines, such as norepinephrine.[87] Catecholamine secretion favors the elevation of low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) and is also associated with decreased HDL levels.[87] Higher levels of LDL and VLDL are also known risk factors for cardiovascular diseases.[87] A health survey in Korean men showed significantly elevated triglyceride levels in dual users of conventional cigarettes and e-cigarettes compared to non-smokers.[87]

In addition, there was no significant difference in triglyceride levels between dual users and conventional cigarette-only smokers.[87] However, another work has shown that e-cigarette users have higher triglycerides and lower HDL than never users.[87] HDL cholesterol was significantly lower in both dual users and conventional cigarette only smokers compared to those who never have smoked.[87] E-cigarette vapers had increased levels of LDL and VLDL compared to nonsmokers.[87] Habitual e-cigarette users had increased oxidized LDL levels compared with non-user control individuals.[87] Oxidized LDL can lead to atherosclerosis as it can contribute to the buildup of atherosclerotic plaques.[87]

A 2019 study shows that e-cigarettes influence the lipid profile.[32] A comparison between nonsmokers, people smoking traditional cigarettes, and those using e-cigarettes demonstrated that the LDL fraction concentration was significantly higher in the group vaping e-cigarettes than in the control group, as opposed to those smoking traditional cigarettes, in whose case a negligible increase was reported.[32] In both groups also a slight decrease in the HDL fraction cholesterol was reported in comparison with the nonsmoking group, yet this decrease was greater in the group of people vaping e-cigarettes.[32] In turn, in the case of VLDL, the group of e-cigarettes users demonstrated a smaller increase in its concentration in blood serum.[32]

Effects on microbial pathogens

Vaping may weaken the body's ability to get rid of microbial pathogens, resulting in greater vulnerability to viral, fungal, or bacterial infections.[124] However, the effects of such findings continue to be unclear.[124]

Effects on multisystem inflammatory syndrome

Studies have shown an association between multisystem inflammatory syndrome and vaping, and a 2021 review speculates that adolescents who vape might be especially vulnerable to serious respiratory symptoms if they develop a hyper-inflammatory state multisystem inflammatory syndrome.[99]

Effects on nasal tissues

Research has been conducted on nasal tissues, partly due to a great number of e-cigarette users exhale via the nose.[103] There is a noticeable decline in gene expression associated with the immune system in the nasal epithelium, which suggests the immune genes had been impaired, and as consequence e-cigarette users may be more prone to infections.[103]

Effects on neuropsychiatric disorders

There is scant evidence on the neuropathological effects induced by nicotine exposure on the developing brain.[125] Due to this lack of knowledge, there is a rising public health concern when taking into account the surge in teen nicotine use and the emergence of innovative nicotine delivery devices like e-cigarettes.[125] There is persuasive evidence implying that teen nicotine exposure raises the likelihood of anxiety-associated behavior in the near term.[126] There is an association between teen nicotine exposure and a higher susceptibility of developing mood and anxiety-associated disorders in adulthood.[125] Exposure to nicotine and e-cigarettes is possibly implicated in causing schizophrenia.[97] Given the lack of data, there is currently no recommendation regarding dose adjustment of antipsychotics in the context of e-cigarette use.[127]

Data from rodents support findings from human studies associating e-cigarette exposure with anxiety- and depression-associated behaviors.[17] Specifically, withdrawal from nicotine was shown to induce persistent changes in anxiety-, depression- and compulsive-like behaviors following seven weeks of e-cigarette exposure, and surprisingly, these behavioral changes persisted 90 days following the last e-cigarette exposure in male mice.[17] Behavioral changes have also been observed even in the absence of nicotine, as nicotine-free e-cigarette vapor exposure was shown to result in anxiogenic phenotypes in both male and female mice.[17]

Abdominal obesity effects

Research conducted on rats demonstrated that exposure to nicotine contributes to significant adipocytes hypertrophy with increased expression of transcription factors of proadipogenic genes.[32] Such factors include the peroxisome proliferator activated receptor γ (PPAR-γ).[32] The result of the aforementioned situation is an increase in body weight and accumulation of adipose tissue.[32] The creation of mature adipocytes is also influenced by oxidative stress.[32]

So far not much has been learnt about the influence of e-cigarettes on adipose tissue and adipocyte functions.[32] The first such research was conducted by Zagoriti et al. in 2020.[32] It compared the influence of traditional cigarettes, e-cigarettes, and heated tobacco products on the differentiation of preadipocytes into beige adipocytes.[32] The increased activity of this kind of adipocytes (so-called thermogenic ones) was suggested as a means of reducing obesity and metabolic disorders.[32]

It was demonstrated that the extract of traditional cigarettes, as opposed to the other two extracts, significantly disrupted the differentiation of preadipocytes into beige adipocytes, which can influence the metabolic function of adipose tissue.[32] In turn, the results of research on e-cigarettes conducted on mice demonstrated that pure nicotine did not fully answer for lower body weight.[32] Further studies involving exposure of mice to equivalent nicotine doses, through inhaling e-cigarette or traditional cigarette fumes, did not show any influence on the body weight reduction in those exposed to e-cigarettes.[32] It can suggest that it is other compounds in cigarettes that can participate in reducing body weight while smoking traditional cigarettes.[32] On the other hand, opposite results were obtained by El Goli et al. in 2001 and Werley et al. in 2016 in their research on rats.[32]

Effects on oral health

The figure shows the clinical aspects at (A) the initial examination, (B) the one-month follow-up, and (C) the six-month follow‑up. A 26‐year‐old male patient sought care complaining of a rough white plaque on the hard palate that had evolved for one month. He mentioned being a former smoker of industrialized cigarettes (about 30 cig/per day, over eight years). For four years, he used vape products exclusively and daily, with a nicotine concentration of 50 mg/mL, more than 15 times a day, for about two continuous minutes each time, consuming roughly four mL of fruity or sweetened essence. On average, this corresponds to 200 mg of nicotine consumption per day which corresponds up to five times the nicotine content of a pack of cigarettes. On clinical examination, chronic carious lesions were observed on teeth 26 and 36, presence of residual root of 27 and a well‐defined white plaque, with a rough surface, measuring approximately one cm in the posterior region of the palate. In the middle third of the palate, there were papules with a reddish central area, compatible with nicotinic stomatitis (figure A). Although the present investigation is limited by the description of only one case, the available evidence suggests that the use of vape may be associated with the development of hyperkeratotic lesions in the oral mucosa and may significantly alter salivary patterns, as vape liquids contain carcinogenic and cytotoxic components.
The figure shows the clinical aspects at (A) the initial examination, (B) the one-month follow-up, and (C) the six-month follow‑up.[128] A 26‐year‐old male patient sought care complaining of a rough white plaque on the hard palate that had evolved for one month.[128] He mentioned being a former smoker of industrialized cigarettes (about 30 cig/per day, over eight years).[128] For four years, he used vape products exclusively and daily, with a nicotine concentration of 50 mg/mL, more than 15 times a day, for about two continuous minutes each time, consuming roughly four mL of fruity or sweetened essence.[128] On average, this corresponds to 200 mg of nicotine consumption per day which corresponds up to five times the nicotine content of a pack of cigarettes.[128] On clinical examination, chronic carious lesions were observed on teeth 26 and 36, presence of residual root of 27 and a well‐defined white plaque, with a rough surface, measuring approximately oneone cm in the posterior region of the palate.[128] In the middle third of the palate, there were papules with a reddish central area, compatible with nicotinic stomatitis (figure A).[128] Although the present investigation is limited by the description of only one case, the available evidence suggests that the use of vape may be associated with the development of hyperkeratotic lesions in the oral mucosa and may significantly alter salivary patterns, as vape liquids contain carcinogenic and cytotoxic components.[128]

Research on potential oral health changes following e-cigarette exposure is limited and daily vaping is associated with poor oral health.[129] The tissues of the oral cavity are those first exposed to the inhaled e-aerosol and they interact directly with its toxicants and chemical components.[129] Nicotine can cause vasoconstriction and decreased blood flow, which results in a reduced oxygen and blood supply to the gums and a reduction in the ability of the gums to remain healthy.[130]

A 2020 pilot cross-sectional study was performed with volunteers to assess the effect of e-cigarette use on biomarkers of inflammation, oxidative stress, anti-inflammatory lipid mediators, tissue injury and repair and growth factors in saliva and gingival crevicular fluid. The obtained results were compared between four groups of participants as e-cigarette users, non-smokers, cigarette smokers and both e-cigarette and cigarette (dual) smokers.[129] There was significant increase between levels of myeloperoxidase and matrix metaloproteinase-9 in e-cigarette users vs. non-smokers, and between dual smokers and e-cigarette users in inflammatory mediators as receptor for advanced glycation end products, myeloperoxidase and recombinant human uteroglobin/CC10.[129]

The changes in antioxidant capacity of saliva in e-cigarette users and cigarette smokers comparing to non-smokers were observed in a study by in 2021.[129] The uric acid, hypoxanthine, xanthine, TAOS (total antioxidant status) and TEAC (Trolox equivalent antioxidant capacity) were determined in the samples of saliva patients.[129] The antioxidant capacity of saliva was affected in the e-cigarette users in a similar degree as in cigarette smokers when compared to the saliva of non-smokers.[129] The impaired antioxidant function of saliva can stimulate the formation of free radicals and reactive oxygen species (ROS), which play a role in the progression of periodontitis and destruction of tissue.[129]

The microorganisms, harboring over 700 species, that reside in the human oral cavity are described as the oral microbiome, oral microflora or oral microbiota.[129] The microorganisms play an important role in the maintenance of the proper environment in the oral cavity and encompasses oral niches, such as teeth surface, tongue, cheeks, subgingival and supragingival plaque, palates, tonsils and salivary.[129] A dysbiosis, an imbalance in the microbial ecosystem, can produce changes in their functional composition and can result in pathological conditions.[129] The flavoring compounds of e-liquids have various aromas and tastes, and some chemical components, such as saccharides and sucralose are added to provide a sweet taste, they may selectively disrupt the homeostasis of the oral microbiome and can be associated with a variety of oral diseases, such as periodontitis and caries.[129]

There is evidence that e-cigarette use is associated with a compositional and functional shift in the oral microbiome, with an increase in opportunistic pathogens and virulence traits.[129] Preliminary research indicates that the health risks of e-cigarettes to the oral microbiome may be comparable to or more than smoking.[131] The combination of glycerin and flavoring agent in e-liquid pods may be associated with a four-fold increase in microbial adhesion and a two-fold increase in biofilm formation.[130] Sticky aerosols produced by heated e-liquid encourage the caries-causing bacterium Streptococcus mutans to adhere to tooth enamel, leading to demineralization and caries.[130]

There is little evidence indicating that using e-cigarettes rather than continue to smoke will help with periodontal disease.[132] Vaping may be equally as dangerous or possibly more dangerous to oral health than tobacco smoking.[133] Vaping with or without nicotine or flavoring may help cause periodontal disease.[134] Nicotine as well as their flavoring may be damaging to periodontal ligament, stem cells, and gingival fibroblasts in cultures as a result of creation of aldehydes and/or carbonyls from e-cigarette vapor.[134] It is possible that e-cigarettes could harm the periodontium because of the effects of nicotine on gum tissues and the immune system.[135] A 2023 review found every study demonstrated an increased marginal bone loss, probing depth, and plaque index, as well as decreased bleeding on probing in e-cigarette users as opposed to non-smokers who had an implant-supported prosthesis with over a year in use.[136] Early research suggests that e-cigarettes have an adverse effect on the results of dental implants in males.[137] A 2016 study found 6.9-8.1% of e-cigarette users had a toothache compared with 3.9-16.7% in traditional cigarette users.[138]

The potential connection of e-cigarette use with dry mouth has not been fully investigated.[139] Dry mouth is one of the oral complaints related to e-cigarettes and the oral diagnoses related to their use include nicotine stomatitis, black hairy tongue, and angular cheilitis.[140] Dry mouth from using e-cigarette affects adults and youth.[139] E-cigarette users were more likely to have dry mouth than tobacco users.[139] Vaping can increase the risk of developing oral mucosal lesions, nicotine stomatitis, hyperplastic candidiasis, and black hairy tongue.[141] The oral mucosal lesions nicotine stomatitis, hyperplastic candidiasis, and black hairy tongue are more frequent in vapers than in previous smokers.[141] In 2015, after an individual was diagnosed with black hairy tongue they quit vaping and started smoking again, which cured her discolored tongue.[141] When she started vaping again, the discoloration came back.[141] Vaping may result in chronic bad breath.[142]

Otology effects

Although little is known about the effects of e-cigarettes in otology, preliminary in vitro studies have shown middle-ear epithelial cell cytotoxicity is associated with nicotine and propylene glycol.[143] A 2014 study on guinea pigs showed that nicotine causes injury at the cochlear outer hair cells, which were deformed in shape with vacuolated cytoplasm and heterochromatic nuclei.[143]

Effects on reversible cerebral vasoconstriction syndrome

A 2015 case report found that vaping might trigger the onset of reversible cerebral vasoconstriction syndrome.[49]

Effects on sleep health

A 2020 study reported that similar to conventional cigarettes, e-cigarettes were associated with worse sleep health in young adults.[4] A 2019 study showed a significant association between e-cigarettes use and higher odds of sleep-related problems in adolescents.[4] Research indicates that nicotine, a primary component in most e-cigarettes, disrupts sleep patterns due to its stimulating properties, leading to difficulty falling asleep and maintaining restful sleep.[144] Initiation or escalation of nicotine vaping has been linked to sleep disturbances.[145]

Adolescents and young adults are frequently impacted, with vaping linked to sleep deprivation, insomnia, and increased reliance on sleep medications.[144] A 2019 study demonstrates that e-cigarette use is associated with various sleep-related disturbances, including reduced sleep duration, increased sleep latency, poor sleep quality, and insomnia.[144] The findings show a notable association between e-cigarette use and reduced or insufficient sleep duration, comparable to the harmful effects associated with traditional cigarette smoking.[144]

Even irregular e-cigarette users experience negative impacts on sleep, including shortened sleep duration and altered sleep quality.[144] Sleep quality encompasses four key attributes: sleep efficiency, sleep latency, sleep duration, and wakefulness after sleep onset.[144] Multiple studies have consistently reported decreased sleep duration and overall poorer sleep quality among e-cigarette users sleep.[144] Furthermore, e-cigarette users are more likely to use medications to aid sleep, and conditions such as insomnia and parasomnias are more prevalent in this group compared to non-users.[144]

Effects on spine health

Due to the growing worldwide popularity of e-cigarette products advertised as a healthier alternative to tobacco, there is an increasing concern over health risks that are linked to vape use and how it affects bone health.[146] There is evidence that many of the major constituents of e-cigarettes, such as nicotine and carbonyl compounds can significantly impair osteoblast function, suggesting e-cigarette use may be detrimental to bone health.[147] The research on bone metabolism is limited.[148]

A 1995 study demonstrated systemic nicotine significantly increased pseudoarthrosis rate to 100% compared to 44% in control animals in a rabbit model of posterolateral spine fusion.[146] A 2000 study showed nicotine alone inhibits the expression of multiple cytokines with a variety of functions during spine fusion.[146] An e-cigarette solution containing nicotine can impact intervertebral disc health through the degeneration of both vasculature and nucleus pulposus and annulus fibrosus cells.[146]

Stroke effects

Exposure to nicotine and e-cigarettes is a prominent risk factor implicated in causing ischemic stroke.[97] A 2021 observational study found an association between e-cigarette use and stroke.[19] The role of e-cigarette use in the development of stroke is inconclusive, due to the strong effect of prior tobacco use as a risk factor for stroke.[149]

Effects on surgical outcomes

There is limited information on the physiologic effect of nicotine vaping on surgical outcomes.[150] Nicotine can induce vasoconstriction while in otologic surgery.[151] It is not known whether there is a benefit for vaping to aid with quitting smoking before surgery.[150] Vaping may have a considerable negative effect on wound healing[150] and may hamper tissue regeneration.[152]

Effects on thyroid function

The impact of nicotine-induced changes in thyroid function on cognitive processes remains limited.[153] Nicotine influences various parts of the endocrine system, including the thyroid gland, which plays a vital role in maintaining cognitive health.[153] Nicotine may influence thyroid function, and such alterations could contribute to its observed effects on cognition.[153] Furthermore, these disruptions could impair learning and memory processes, which potentially play a role in nicotine's addictive properties.[153]

Thyroid signaling plays a role in learning and memory through both hippocampus-dependent and hippocampus-independent mechanisms, which suggests its widespread influence in cognitive processes.[153] Consequently, nicotine-induced disruptions to thyroid function may impair cognition.[153] Thyroid hormone signaling are an integral part of both short- and long-term synaptic plasticity in healthy individuals, and nicotine-related alterations could interfere with these mechanisms.[153]

The evidence indicates that individuals who quit smoking have a heightened risk of autoimmune hypothyroidism, which suggests that withdrawal from prolonged nicotine use may also adversely affect thyroid function.[153] Additionally, nicotine withdrawal has been shown to substantially decrease serum T4 levels, while both prolonged exposure and withdrawal increase the T3-to-T4 ratio.[153] This indicates potential dysregulation of thyroid hormone activity.[153]

Rodent studies have shown that nicotine exposure during prenatal and perinatal periods interferes with thyroid function.[153] Evidence suggests that parental nicotine exposure may cause serious, persistent effects on thyroid hormone regulation in offspring.[153] Nicotine administration during gestation and lactation alters thyroid hormone levels in the developing young, which potentially leads to long-term impairments in cognition, learning, and memory.[153]

While nicotine can impair thyroid function, thyroid hormones may also play a direct role in modulating cholinergic signaling by regulating the gene that governs acetylcholine synthesis.[153] Nicotine from inhaled aerosol alters catecholamine levels.[148]

Effects on tuberculosis

Long-term e-cigarette use could increase the chance of developing tuberculosis.[154]

Effects on urologic health

Data on the impact of vaping on urologic health is not available.[155]

Vascular disease effects

A single use of an e-cigarette can cause an increase in 8-iso-prostaglandin, a marker for oxidative damage that is inversely correlated with nitric oxide levels, indicating endothelial dysfunction.[156] The lack of nitric oxide levels allows for the production of pro-inflammatory markers in blood vessels, attracting monocytes and other phagocytic cells and inducing endothelial and subendothelial damage.[156]

The detrimental effects of aerosols associated with e-cigarettes start at the endothelial level.[157] The oxidative stress reduces the bioavailability of nitric oxide which in turn plays a key role in endothelium dysfunction alongside peroxynitrite (produced by superoxide) which causes low-density lipoprotein oxidation and inflammatory cytokines.[157] A healthy endothelium is responsible for the production of vasodilators; however this function becomes impaired when the endothelium is injured (e.g., by cigarette smoke or toxic compounds found in e-cigarettes) leading to an imbalance between vasoconstrictors and vasodilators.[157] The damaged cells from the endothelium must be replaced in order to maintain vascular tone, an ability that is reduced in users of e-cigarettes.[157] Platelet activation, coagulation cascade stimulation, and impairment of anticoagulative fibrinolysis leads to vascular disease.[157]

Tooth discoloration

Little evidence is present for the exact mechanisms of how tobacco and nicotine products may discolor teeth.[158] Cigarette smoke considerably impacts the color stability of dental composites, the existing evidence indicates.[159] Although data is limited, e-cigarettes induce a decrease in color variation of dental composites compared to cigarette smoke.[159] There is some evidence to suggest that the e-liquid composition has some influence on staining.[158] Repolishing or whitening procedures can help with the changes in color to dental composites caused by vaping.[159]

Researchers used spectrophotometry to compare enamel specimens after exposure to e-liquid aerosol according to flavor and nicotine content and found discoloration of enamel in vitro.[130] The chemical substances used to flavor e-liquids, such as menthol, may be the reason behind the color alteration of enamel.[130] A 2020 study reported that exposure to e-cigarettes produced discoloration levels on prosthodontic materials that was similar to that associated with the smoking of tobacco products.[130] In their study, which included ceramics and resin materials with different surface properties, discoloration caused by both e-cigarettes and conventional tobacco cigarettes was below clinically perceptible levels for ceramic materials but was visually perceptible for composite resins.[130]

Although the effect of e-cigarettes on tooth color may be less pronounced than that of traditional cigarettes, long-term, high-dose exposure to e-cigarettes does cause tooth discoloration.[130] The rate of color change varies between natural tooth enamel and restoration materials composed of resin or ceramics.[130] The rate of color change may also be affected by the brand and flavor of the e-liquid.[130]

Effects on skin

Dermal exposure

The first case of contact dermatitis linked to vaping was reported in 2015.[141] Over the last three years leading up to 2019, there has been a rise in cases of contact dermatitis from e-cigarette nickel exposure.[141]

Contact dermatitis from nickel exposure has been reported, following e-cigarette use.[68] The nickel from the heating coil leaches out of the device, resulting in irritation to the hand from holding the device.[141] Cases of contact dermatitis have been treated with the avoidance of the e-cigarette.[122]

E-cigarette aerosol exposure

Little is known regarding the impacts of e-cigarette aerosol on the skin.[160] A 2014 study found HaCaT skin cells were injuried after directly being exposed to aerosolized Balsamic flavored e-liquid.[160] The aerosolized flavor free e-liquid did not exhibit any effects.[160]

Mortality

E-cigarette use induces an acute rise in cardiac sympathetic nerve activity.[161] This can trigger electrocardiogram abnormalities, and as a result, lead to a higher chance of sudden death in people with co-morbidities.[161] The risk of early death is anticipated to be similar to that of smokeless tobacco.[20] There is a significant risk of long-lasting lung injury from vaping that may contribute to or lead to death, in old people.[21]

Multigenerational effects

See also: Epigenetic effects of smoking, Environmental toxicants and fetal development, and Smoking and pregnancy

Nicotine exposure leads to epigenetic changes that affect lung function in future generations.[22] Vaping or the use of any nicotine-based product during pregnancy, or both during pregnancy and the breastfeeding postpartum period, causes the "concurrent exposure of three generations to nicotine."[23] Exposure to nicotine by fathers is strongly associated with brain and behavioral changes that span multiple generations, which, in part, is due to alterations in the epigenome.[23]

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    E-cigarette battery explosion injuries

References

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  32. ↑ 32.00 32.01 32.02 32.03 32.04 32.05 32.06 32.07 32.08 32.09 32.10 32.11 32.12 32.13 32.14 32.15 32.16 32.17 32.18 32.19 32.20 32.21 32.22 32.23 32.24 32.25 32.26 32.27 32.28 32.29 32.30 32.31 32.32 32.33 32.34 32.35 32.36 32.37 32.38 32.39 32.40 32.41 32.42 32.43 32.44 32.45 32.46 32.47 32.48 Górna, Ilona; Napierala, Marta; Florek, Ewa (2020). "Electronic Cigarette Use and Metabolic Syndrome Development: A Critical Review". Toxics. 8 (4): 105. doi:10.3390/toxics8040105. ISSN 2305-6304. PMC 7711672. PMID 33212878.{{cite journal}}: CS1 maint: unflagged free DOI (link) This article incorporates text by Ilona Górna, Marta Napierala, and Ewa Florek available under the CC BY 4.0 license.
  33. ↑ Gorlova, Olga Y; Xu, Ying; Guo, Yanfang; Liu, Kaiqian; Liu, Zheng; Wang, Xiaobo (2016). "E-Cigarette Awareness, Use, and Harm Perception among Adults: A Meta-Analysis of Observational Studies". PLOS ONE. 11 (11): e0165938. Bibcode:2016PLoSO..1165938X. doi:10.1371/journal.pone.0165938. ISSN 1932-6203. PMC 5115669. PMID 27861501.
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  39. ↑ Casey, AM; Muise, ED; Crotty Alexander, LE (October 2020). "Vaping and e-cigarette use. Mysterious lung manifestations and an epidemic". Current opinion in immunology. 66: 143–150. doi:10.1016/j.coi.2020.10.003. ISSN 0952-7915. PMC 7755270. PMID 33186869.
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  44. ↑ Caci, Grazia; Selya, Arielle; La Rosa, Giusy Rita Maria; Spicuzza, Lucia; Morjaria, Jaymin B.; Geraci, Giulio; Polosa, Riccardo (March 2025). "Respiratory effects of electronic cigarette use in individuals who never smoked: A systematic review". Clinical Medicine. 25 (2): 100295. doi:10.1016/j.clinme.2025.100295. PMC 11930579. PMID 39993529. This article incorporates text by Grazia Caci, Arielle Selya, Giusy Rita Maria La Rosa, Lucia Spicuzza, Jaymin B Morjaria 5, Giulio Geraci, and Riccardo Polosa available under the CC BY 4.0 license.
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  97. ↑ 97.0 97.1 97.2 Sharma, Sejal; Rahman Archie, Sabrina; Kanchanwala, Vrajesh; Mimun, Kyle; Rahman, Md Ashrafur; Zhang, Yong; Abbruscato, Thomas (26 April 2022). "Effects of Nicotine Exposure From Tobacco Products and Electronic Cigarettes on the Pathogenesis of Neurological Diseases: Impact on CNS Drug Delivery". Frontiers in Drug Delivery. 2. doi:10.3389/fddev.2022.886099.{{cite journal}}: CS1 maint: unflagged free DOI (link) This article incorporates text by Sejal Sharma, Sabrina Rahman, Archie Vrajesh Kanchanwala, Kyle Mimun, Ashrafur Rahman, Yong Zhang, and Thomas Abbruscato available under the CC BY 4.0 license.
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  101. ↑ Münzel, Thomas; Hahad, Omar; Kuntic, Marin; Keaney, John F; Deanfield, John E; Daiber, Andreas (2020). "Effects of tobacco cigarettes, e-cigarettes, and waterpipe smoking on endothelial function and clinical outcomes". European Heart Journal. 41 (41): 4057–4070. doi:10.1093/eurheartj/ehaa460. ISSN 0195-668X. PMC 7454514. PMID 32585699.
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  118. ↑ 118.00 118.01 118.02 118.03 118.04 118.05 118.06 118.07 118.08 118.09 118.10 118.11 118.12 118.13 118.14 118.15 118.16 118.17 118.18 118.19 118.20 118.21 118.22 Montjean, Debbie; Godin Pagé, Marie-Hélène; Bélanger, Marie-Claire; Benkhalifa, Moncef; Miron, Pierre (18 March 2023). "An Overview of E-Cigarette Impact on Reproductive Health". Life. 13 (3): 827. doi:10.3390/life13030827. PMC 10053939. PMID 36983982.{{cite journal}}: CS1 maint: unflagged free DOI (link) This article incorporates text by Debbie Montjean, Marie-Hélène Godin Pagé, Marie-Claire Bélanger, Moncef Benkhalifa, and Pierre Miron available under the CC BY 4.0 license.
  119. ↑ 119.0 119.1 119.2 119.3 119.4 Konstantinidou, Fani; Stuppia, Liborio; Gatta, Valentina (September 2020). "Looking Inside the World of Granulosa Cells: The Noxious Effects of Cigarette Smoke". Biomedicines. 8 (9): 309. doi:10.3390/biomedicines8090309. PMID 32867029.{{cite journal}}: CS1 maint: unflagged free DOI (link) This article incorporates text by Fani Konstantinidou, Liborio Stuppia, and Valentina Gatta available under the CC BY 4.0 license.
  120. ↑ 120.0 120.1 120.2 120.3 120.4 Seiler-Ramadas, Radhika; Sandner, Isabell; Haider, Sandra; Grabovac, Igor; Dorner, Thomas Ernst (October 2021). "Health effects of electronic cigarette (e‑cigarette) use on organ systems and its implications for public health". Wiener klinische Wochenschrift. doi:10.1007/s00508-020-01711-z. ISSN 0043-5325. PMC 8500897. PMID 32691214. This article incorporates text by Radhika Seiler-Ramadas, Isabell Sandner, Sandra Haider, Igor Grabovac, and Thomas Ernst Dorner available under the CC BY 4.0 license.
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  128. ↑ 128.0 128.1 128.2 128.3 128.4 128.5 128.6 128.7 Carvalho, Bruna Fernandes do Carmo; Faria, Natália de Carvalho; Foiani, Letícia; Nepomuceno, Gabrielle Luana Jimenez Teodoro; Cavalcanti, Desirée Rosa; Alves, Mônica Ghislaine Oliveira; Martinho, Herculano da Silva; Pérez‐Sayáns, Mário; Almeida, Janete Dias (August 2024). "Oral Mucosa and Saliva Alterations Related to Vape". Clinical and Experimental Dental Research. 10 (4). doi:10.1002/cre2.926. PMC 11226547. PMID 38970232. This article incorporates text by Bruna Fernandes do Carmo Carvalho, Natália de Carvalho Faria, Letícia Foiani, Gabrielle Luana Jimenez Teodoro Nepomuceno, Desirée Rosa Cavalcanti, Mônica Ghislaine Oliveira Alves, Herculano da Silva Martinho, Mário Pérez‐Sayáns, and Janete Dias Almeida available under the CC BY 4.0 license.
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