The use of electronic cigarettes (e-cigarettes) or ‘vaping’ has been marketed as a safer alternative to tobacco cigarette smoking and as a potential smoking cessation tool. However, recent findings published in the European Respiratory Journal revealed that e-cigarette vapour may increase the risk for bacterial pneumonia.1 In their publication, Miyashita and colleagues demonstrated that e-cigarette smoking increased the expression of platelet-activating factor receptor (PAFR) in nasal epithelial cells of vaping adults. Vaping also increased pneumococcal adhesion to airway cells in vitro.
In the study, adults who vaped at least once a week as well as healthy adults who have never smoked were recruited. Among e-cigarette users, nasal cells were obtained immediately before and one hour after a five-minute vaping period. A statistically significant increase in PAFR expression was seen in the nasal epithelial cells obtained. These findings are important because PAFR plays a crucial role in the pathogenesis of bacterial pneumonia. Host-expressed PAFR is utilized by Streptococcus pneumoniae for epithelial cell adhesion and uses the receptor as a Trojan horse to enter airway cells when the receptor is internalised.2
In vitro experiments were also conducted to further investigate the effect of vaping on lower respiratory cells. Pneumococcal adhesion to human alveolar epithelial A549 cells was analysed using an in vitro adhesion assay.3 The investigators found that both nicotine-containing and nicotine-free e-cigarette vapour increased pneumococcal adhesion to airway cells in a dose-dependent and time-dependent manner. Furthermore, pneumococcal penetration into cells was also increased by both nicotine-free and by 5% nicotine-containing e-cigarette vapour. In mouse models, nicotine-containing e-cigarette vapour increased mouse nasal PAFR expression and nasopharyngeal pneumococcal colonization. Overall, these findings suggest that e-cigarette use may increase the susceptibility to pneumococcal infection.
Previous epidemiologic studies have suggested that inhalation of toxins increases the risk for airway bacterial infection. A study by Nuorti and colleagues showed that cigarette smoking was associated with a fourfold increase (95% confidence interval [CI]: 2.0–7.0) in the risk for invasive pneumococcal disease.4 Passive exposure to tobacco smoke, on the other hand, has been associated with a 1.5-fold increase (95% CI: 1.2–1.9) in the risk for pneumonia in children.5
The vapour from e-cigarettes is generated by the vaporisation of propylene glycol, nicotine, and flavourings in the e-cigarette liquid. Although e-cigarettes have been shown to contain fewer toxic compounds than tobacco smoke,6 Goel and colleagues reported that e-cigarette vapour contains up to 10×1013 free radicals per puff.7 This oxidative stress induced by e-cigarette smoke is believed to be an initial stimulus for PAFR-dependent adhesion. In mouse models, e-cigarette vapour has been shown to deplete lung antioxidants and consequently delayed the clearance of pneumococci from the lung.8 In vitro studies have shown that e-cigarette vapour is a potent inducer of oxidative stress response genes in bronchial epithelial cells.9 Oxidative stress from e-cigarette vapour is not only limited to the airways. Systemic increase in oxidative stress markers have also been shown among adults after vaping.10
The findings of Miyashita and colleagues lend valuable information on the effects of e-cigarette vaping on PAFR-dependent airway pneumococcal adherence. Further epidemiologic studies are needed to determine the impact of regular vaping on the risk of pneumococcal airway infection on a population level.
E-cigarette vapour may increase risk for pneumococcal infection Lisa Miyashita, Reetika Suri, Emma Dearing, Ian Mudway, Rosamund E Dove, Daniel R. Neill, Richard Van Zyl-Smit, Aras Kadioglu, Jonathan Grigg
European Respiratory Journal 2018 51: 1701592; DOI: 10.1183/13993003.01592-2017