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.