Short-Term E-Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Cardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e-cigarettes are "safer/less harmful" than conventional cigarettes, their usage-among a variety of ages-has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e-cigarettes on the cardiovascular system, which is also the subject of significant debate.

We employed a passive e-Vape^TM vapor inhalation system and developed an in vivo whole-body e-cigarette mouse exposure protocol that mimics real-life human exposure scenarios/conditions and investigated the effects of e-cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e-cigarette-exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air-exposed platelets. E-cigarette-exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e-cigarette-exposed mice exhibited a shortened thrombosis occlusion and bleeding times.

Taken together, our data demonstrate for the first time that e-cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e-cigarette exposure should not be underestimated and warrant further investigation.