Nicotine in E-cigarette aerosol may lead to pulmonary inflammation

Background: Cigarette smoking stands as one of the leading causes of preventable death globally. Alternative tobacco products, such as e-cigarettes, have gained popularity due to the general perception of being less harmful. However, much is still unknown about the health implications of these novel products. In this study, we aimed to investigate if e-cigarettes could induce pulmonary inflammatory responses by measuring lung-related circulating extracellular vesicles (EVs) in the blood of healthy volunteers following brief e-cigarette vaping sessions, with and without nicotine. Methods: 22 healthy volunteers were included. Employing a randomized, double-blind, cross-over design all participants vaped 30 puffs of e-cigarette aerosol, with and without nicotine, over a 30-min period. Blood samples were collected at baseline, 30-and 105-min following exposure. Lung-related EVs were quantified using flow cytometry. Analyzed markers included angiotensin converting enzyme (ACE), aldehyde dehydrogenase 3B1 (ALDH3B1), palate, lung and epithelial clone (PLUNC), complement component 3 (C3), C-C motif chemokine ligand 3 (CCL3), also known as macrophage inflammatory protein 1 alpha (MIP-1 alpha), and uteroglobin, also known as club cell protein 16 (CC16). All these markers are associated with pulmonary inflammation. Results: E-cigarette use, with nicotine but not without, resulted in a significant increase in three out of the six lung-related inflammatory markers measured and clear increases though not statistically significant in the remaining three. Conclusion: The observed increase in levels of circulating lung-related inflammatory EV markers following vaping e-cigarette aerosol containing nicotine suggests that inhaled nicotine plays a central role in triggering pulmonary inflammation. Clinicaltrials.gov ID: NCT04175457.