Evaluating the effects of pod-based electronic cigarettes on human endothelial cell function

Pod-based electronic (e-) cigarettes more efficiently deliver nicotine
using a protonated formulation. The cardiovascular effects associated with
these devices are poorly understood. We evaluated whether pod-based
e-liquids and their individual components impair endothelial cell
function.  We isolated endothelial cells from people who are pod
users (n=10), tobacco never users (n=7), and combustible cigarette users
(n=6). After a structured use, pod users had lower acetylcholine-mediated
endothelial nitric oxide synthase (eNOS) activation compared with never
users and was similar to levels from combustible cigarette users (overall
P=0.008, P=0.01 pod vs never; P=0.96 pod vs combustible cigarette). The
effects of pod-based e-cigarettes and their constituents on vascular cell
function were further studied in commercially available human aortic
endothelial cells (HAECs) incubated with flavored JUUL e-liquids or
propylene glycol (PG):vegetable glycerol (VG) at 30:70 ratio with or
without 60 mg/mL nicotine salt for 90 min. A progressive increase in cell
death with JUUL e-liquid exposure was observed across 0.0001-1% dilutions;
PG:VG vehicle with and without nicotine salt-induced cell death.
A23187-stimulated nitric oxide production was decreased with all JUUL
e-liquid flavors, PG:VG and nicotine salt exposures. Aerosols generated by
JUUL e-liquid heating similarly decreased stimulated nitric oxide
production. Only mint-flavored e-liquids increased inflammation and
menthol-flavored e-liquids enhanced oxidative stress in HAECs. In
conclusion, pod e-liquids and their individual components appear to impair
endothelial cell function. These findings indicate the potential harm of
pod-based devices on endothelial cell function and thus may be relevant to
cardiovascular injury in pod-type e-cigarette users.