Electronic cigarettes can cause detrimental effects to human health and should be reconsidered as a smoking cessation tool, based on results from a recent study.
Electronic cigarettes (e-cigarettes) can cause detrimental effects to human health and should be reconsidered as a smoking cessation tool, based on results from a recent study published in the American Journal of Physiology: Lung Cellular and Molecular Physiology.
E-cigarettes have become a popular substitution for conventional cigarettes, with some in the medical community believing that they can help reduce the adverse consequences caused by smoking regular cigarettes. Although e-cigarettes are considered a potential alternative smoking cessation tool, their effects on human health have not been fully accounted for, especially regarding long-term exposure. In the study by Glynos et al, mice exposed to both e-cigarette vapor and cigarette smoke were compared based on established respiratory and inflammatory responses to determine any differences in health-related consequences.
Mice in this study were exposed to either cigarette smoke, e-cigarette vapor, or air for 3 days or 4 weeks to analyze the short-term and long-term effects. E-cigarettes were further separated into 3 categories of vapo: propylene glycol/vegetable glycerol (PG:VG), PG:VG with nicotine, or PG:VG with nicotine and flavoring.
Total cell counts in bronchoalveolar lavage fluid (BALF) of mice exposed to either e-cigarette vapor or cigarette smoke both increased, mainly due to an increase in the number of macrophages at 3 days. Protein content in BALF, however, only increased for those exposed to PG:VG with nicotine and flavoring compared with the other groups at 3 days. At 4 weeks of exposure, BALF cell counts were only elevated for the groups exposed to cigarette smoke and PG:VG with nicotine and flavoring, while BALF protein counts were only elevated in the PG:VG with nicotine and PG:VG with nicotine and flavoring groups.
Protein carbonyls and malondialdehyde were 2 oxidative stress markers that were analyzed in the BALF. At 3 days, increased levels of malondialdehyde were observed in the PG:VG and PG:VG with nicotine and flavoring groups, while increased protein carbonyls were seen in all cigarette and e-cigarette groups. Four weeks of exposure showed increased levels of malondialdehyde and protein carbonyl for those exposed to cigarette smoke, PG:VG with nicotine, and PG:VG with nicotine and flavoring.
At 3 days, oxidative stress in the lung tissue was seen through increased levels of malondialdehyde in the cigarette smoke, PG:VG, and PG:VG with nicotine and flavoring groups, and increased lung protein carbonyls were observed in the cigarette smoking and PG:VG with nicotine and flavoring groups. Four weeks of exposure revealed similar changes, except without increased stress biomarkers in the PG:VG group. These findings indicate that flavoring in e-cigarettes elevates oxidation markers while nicotine mitigates it.
Proinflammatory cytokines interleukin (IL)-1β and IL-6 were increased only in the PG:VG with nicotine and flavoring group at 3 days. After 4 weeks, the 2 cytokines were only elevated in the cigarette smoke group. Increased airway resistance and tissue elasticity and decreased static compliance were only significantly changed for the PG:VG group at 3 days, but long-term effects at 4 weeks seemed to only exist in the cigarette smoke—exposed mice. Airway hyperresponsiveness at 3 days occurred only in the groups exposed to cigarette smoke and PG:VG with nicotine and flavoring.
From this study, investigators found that e-cigarettes can invoke lung injuries and induce toxicities, although they had fewer harms compared with tobacco smoke regarding lung integrity. In addition, it seems that flavoring in e-cigarettes has the potential to augment these respiratory changes. This study indicates that e-cigarettes may not be any safer than classic cigarettes and could potentially be a harmful alternative smoking cessation tool.
Glynos C, Bibli SL, Katsaounou P, et al. Comparison of the effects of e-cigarette vapor with cigarette smoke on lung function and inflammation in mice [published online October 22, 2018]. Am J Physiol Lung Cell Mol Physiol. doi: 10.1152/ajplung.00389.2017.