Electronic cigarette vapour suppresses human neutrophil functions and alters phenotype, irrespective of nicotine content

Background: In the UK, around 2.7 million people use electronic (e-)cigarettes despite uncertainties in their long-term safety. Neutrophils play a central role in the pathophysiology of chronic obstructive pulmonary disease (COPD), a smoking-associated lung disease. Objective: To measure the impact of direct e-cigarette vapour exposure on the function and phenotype of human neutrophils. Methods: Peripheral blood neutrophils from non-smoker/vaper participants were exposed to 40 puffs (4s on/30s off) of e-cigarette vapour generated from e-cigarettes loaded with flavourless e-liquids with and without nicotine using second and third generation devices. Neutrophil functions were measured by microscopy and flow cytometry. Results: Neutrophil migration to CXCL8, phagocytosis of E. coli and S. aureus pHrodo bioparticles and generation of reactive oxygen species (ROS) were significantly reduced by e-cigarette vapour. Neutrophil extracellular trap (NET) formation was suppressed. Oxidative burst and glycolytic reserve were significantly impaired. Neutrophil phenotypic markers including CD62L were altered, suggesting an activated and immature phenotype. Conclusions: Neutrophils are functionally supressed after exposure to vapour from high power e-cigarette devices, even in the absence of nicotine. This is likely driven by the reported presence of reactive carbonyl species in the vapour of e-cigarettes, the production of which is directly tied to device power output. This work highlights the potentially damaging impact of vaping on respiratory health and increases the urgency of further research to uncover the long-term health implications of e-cigarettes.