Electronic cigarette (e-cigarette) use, or vaping, in the United States and worldwide is increasing. Their use is highly controversial from scientific, political, financial, psychological, and sociological ideologies. Given the controversial nature of e-cigarettes and vaping, how should medical care providers advise their patients? To effectively face this new challenge, health care professionals need to become more familiar with the existing literature concerning e-cigarettes and vaping, especially the scientific literature. Thus, the aim of this article is to present a review of the scientific evidence-based primary literature concerning electronic cigarettes and vaping. A search of the most current literature using the pubmed database dating back to 2008, and using electronic cigarette(s) or e-cigarette(s) as key words, yielded a total of 66 highly relevant articles. These articles primarily deal with (1) consumer-based surveys regarding personal views on vaping, (2) chemical analysis of e-cigarette cartridges, solutions, and mist, (3) nicotine content, delivery, and pharmacokinetics, and (4) clinical and physiological studies investigating the effects of acute vaping. When compared to the effects of smoking, the scant available literature suggests that vaping could be a “harm reduction” alternative to smoking and a possible means for smoking cessation, at least to the same degree as other Food and Drug Administration-approved nicotine replacement therapies. However, it is unclear if vaping e-cigarettes will reduce or increase nicotine addiction. It is obvious that more rigorous investigations of the acute and long-term health effects of vaping are required to establish the safety and efficacy of these devices; especially parallel experiments comparing the cardiopulmonary effects of vaping to smoking. Only then will the medical community be able to adequately meet the new challenge e-cigarettes and vaping present to clinical medicine and public health.

Introduction: ECIGs are currently under scrutiny concerning their safety, particularly in reference to the impact ECIG liquids (E-liquids) have on human health. One concern is that aerosolized E-liquids contain trace metals that could become trapped in respiratory tissues and induce pathology.Methods: To mimic this trapping, peristaltic pumps were used to generate and transport aerosol onto mixed cellulose ester (MCE) membranes where aluminum (Al), arsenic (As), cadmium (Cd), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), and zinc (Zn) were subsequently captured and quantified. The presence of trace metals on unexposed MCE membranes and on MCE membranes exposed to mainstream smoke served as control and comparison, respectively. The presence of these metals was also determined from the E-liquid before aerosolization and untouched by the ECIG device. All metals were quantified using ICP-MS. The ECIG core assembly was analyzed using scanning electron microscopy with elemental analysis capability.Results: The contents (μg) of Al, As, Cd, Cu, Fe, Mn, Ni, Pb, and Zn on control MCE membranes were 1.2 ± 0.2, 0.050 ± 0.002, 0.047 ± 0.003, 0.05 ± 0.01, 0.001 ± 0.001, 0.16 ± 0.04, 0.005 ± 0.003, 0.014 ± 0.006, and 0.09 ± 0.02, respectively. The contents of all trace metals on MCE membranes exposed to aerosol were similar to controls, except Ni which was significantly (p < 0.01) higher (0.024 ± 0.004 μg). In contrast, contents of Al, As, Fe, Mn, and Zn on MCE membranes exposed to smoke were significantly higher (p < 0.05) than controls. The contents of Al, As, Cu, Fe, and Mn on smoke-exposed MCE membranes were also significantly higher (p < 0.05) than their content on aerosol-exposed membranes. The contents per cigarette equivalent of metals in E-liquid before aerosolization were negligible compared to amounts of aerosolized E-liquid, except for Fe (0.002 μg before and 0.001 μg after). Elemental analysis of the core assembly reveals the presence of several of these trace metals, especially Al, Fe, Ni, and Zn.Conclusions: In general, from the single ECIG-device/E-liquid combination used, the amount of trace metals from ECIG-generated aerosol are lower than in traditional mainstream smoke, Only Ni in the ECIG-generated aerosol was higher than control. The most probable source of Ni in this aerosol is the core assembly.

Background: Vaping has become a global health concern. As research continues, more studies are beginning to question the relative safety of E-liquid flavoring additives. The oral cavity is the first site of exposure to E-liquid aerosol, making it critical for investigation. Because of the importance of commensal bacterial biofilms for oral health, we sought to explore the effects of E-liquids ± flavors on the formation and growth of single- and multi-species biofilms and to investigate the mechanism of inhibition. Methods: Quantitative and confocal biofilm analysis, death curves, and colony-forming units (CFU) were evaluated with flavorless and flavored (tobacco, menthol, cinnamon, strawberry, blueberry) E-liquids using four strains of oral commensal bacteria (Streptococcus gordonii, Streptococcus intermedius, Streptococcus mitis, and Streptococcus oralis). Results: All flavoring agents show a dose-dependent inhibition in the growth of single-species and multi-species biofilms. Furthermore, CFUs, death curves, and light microscopy show that flavoring agents have a bactericidal mode of inhibition on the growth of these oral streptococci. Conclusions: These results show that flavored, rather than unflavored, E-liquids are more detrimental to biofilm formation and growth of oral commensal bacteria. Consequently, E-liquid flavorings agents could pose risks to the oral microenvironment, and by extension, to systemic health.

Background: While ECIGs are under scrutiny concerning safety, particularly in reference to the physiological impact that aerosolized ECIG liquid (E-liquid) may have on respiratory tissues, others believe that ECIGs are a “Harm Reduction” alternative to conventional cigarettes. Previous studies investigating ciliated respiratory epithelium indicate that smoking shortens cilia length, reduces cilia beat frequency and disrupts respiratory epithelium, which most likely contributes to the inhibition of mucocilliary clearance. Monitoring mucous clearance of respiratory tissues exposed to ECIG-generated aerosol or conventional cigarette smoke, as indexed by mucous transport velocity (MTV), is one way to gauge the impact aerosol and smoke have on the respiratory tract. Therefore, we designed an experiment to test the effect of ECIG-generated aerosol and smoke on MTV using the frog palate paradigm.Methods: Peristaltic pumps transport ECIG-generated aerosol and conventional cigarette smoke into custom-made chambers containing excised bullfrog palates. MTVs were determined before exposure, immediately after exposure and approximately 1 day following exposure. MTVs were also determined (at the same time points) for palates exposed to air (control). Surface and cross sectional SEM images of palates from all three groups were obtained to support MTV data.Results: The results indicate that ECIG-generated aerosol has a modest inhibitory effect (p < 0.05) on MTV 1 day post-exposure (0.09 ± 0.01) compared to control MTV (0.16 ± 0.03 mm/s). In contrast, smoke completely inhibits MTV from 0.14 ± 0.03 mm/s immediately before exposure to 0.00 mm/sec immediately after exposure and the MTV is unable to recover 1 day later. SEM images of control palates and palates exposed to ECIG-generated aerosol both show cilia throughout their epithelial surface, while some areas of palates exposed to smoke are completely devoid of cilia. Additionally, the epithelial thickness of aerosol-exposed palates appears thicker than control palates while smoke-exposed palates appear to be thinner due to epithelial disruption.Conclusions: These results indicate that ECIG-generated aerosol has only a modest effect on mucocilary clearance of bullfrog palates and aerosol sedimentation accounts for epithelial thickening. In accordance with the primary literature, conventional cigarette smoke dramatically inhibits mucociliary clearance and is, in part, due to decreased number of cilia and disruption of the smoke-exposed epithelium.

Background: The use of electronic cigarettes (ECIG) has become very common. Consequently, critical analysis of the biological effects of ECIG aerosol deserves attention. Flavorless ECIG aerosol is known to comprise fewer harmful constituents than cigarette smoke. Therefore, we hypothesize that aerosol has less immediate effect on the viability of oral commensal streptococci than smoke. Methods: Survival and growth of four strains of commensal streptococci were measured after exposure to flavorless ECIG aerosol ± nicotine and smoke. Peristaltic pumps were used to transport aerosol or smoke into chambers containing recently seeded colony-forming units (CFUs) of the oral commensal streptococci on agar plates. Bacterial survival and growth, based on colony counts and sizes, were determined 24 h post-exposure. Additionally, aerosol or smoke were delivered into chambers containing pre-adhered streptococci to plastic coverslips and biofilm formation was determined 24 h post-exposure via scanning electron microscopy. Results: The results suggest that flavorless aerosol ± nicotine has a modest effect on bacterial growth both as colonies on agar and as biofilms. In contrast, smoke dramatically decreased bacterial survival and growth in all parameters measured. Conclusion: Unlike cigarette smoke, flavorless ECIG aerosol has only a small effect on the survival and growth of oral commensal streptococci.