E‐Liquid Base Solution Used in Electronic Cigarettes Impairs Cerebovascular Reactivity

Abstract

Electronic cigarettes (E-cigs) have been marketed as a safer alternative to traditional cigarettes and as a smoking cessation aid. The main components comprising the E-cig liquid are vegetable glycerin (VG) and propylene glycol (PG), but few studies have examined the chronic effects of either VG or PG e-cig aerosol on cerebrovascular health. Wild type C57BL/6J mice (n=6/group) were placed in whole-body chambers (SCIREQ InExpose) and exposed to aerosol produced from e-cigs (Joyetech eGrip OLED using 5-sec puffs at 17.5 W) with either 100% VG or 100% PG liquid using 60 puffs/day, 5 days/week, for 4 weeks. Control group of mice were exposed to ambient air. One-day after the last exposure, the mice were sacrificed and the middle cerebral artery (MCA) responsiveness to acetylcholine (ACh; 10-9M to 10-4M), phenylephrine (PE; 10-9M to 10-4M), and sodium nitroprusside (SNP; 10-9M to 10-4M) were examined using a pressure myography. Maximal MCA dilation to ACh (10-4M) was impaired by ~50% in both VG and PG exposed groups (max response = 8.2±1.1 and 8.2±1.8 μm, respectively, p<0.05) compared to control mice (17.2±0.8 μm). Maximal endothelial-independent dilator response to SNP (10-4 M) showed 25-42% impairment with VG (14.8±2.7 μm) and PG (13.0±2.9 μm) compared to control mice (17.4±0.9 μm, p<0.05). Maximal vasoconstriction response to PE (10-4 M) was 15% lower (-12.8±1.9 μm) with VG and 40% lower (-9.0±2.6 μm, p<0.05) with PG compared to control mice (-15.0±2.4 μm). Mice exposed to e-cig aerosol produced solely from base compounds used in e-liquid (VG or PG) show significant cerebrovascular dysfunction (up to 50%), with a greater deficit observed in endothelial-dependent mechanisms. However, endothelial-independent mechanisms are also involved.