Acute effects of the JUUL e‐cigarette on blood pressure and peripheral sympathetic activity in young non‐smokers

Document Type

Article

Publication Date

4-18-2020

Department

Department of Biomedical Engineering; Department of Kinesiology and Integrative Physiology

Abstract

E‐cigarettes are aggressively marketed as an alternative to smoking for those who want to decrease the serious health risks of tobacco. However, e‐cigarette usage among adolescents and non‐smokers has increased dramatically, negating the previous decade‐decline in tobacco product usage among youth. JUUL™ has dominated the e‐cigarette market with their novel nicotine delivery system and sleek design. It is well known that tobacco cigarette smoking increases heart rate and arterial pressure while inhibiting muscle sympathetic nerve activity (MSNA) when acute increases in arterial pressure are not controlled. The purpose of our study was to investigate how acute usage of the JUUL e‐cigarette affects arterial pressure and sympathetic outflow. Ours was a randomized, crossover design that had participants inhale on a JUUL e‐cigarette containing nicotine (59 mg/ml) and a similar placebo e‐cigarette (0 mg/ml), separated by 1 month. Fifteen young, healthy non‐smokers (9 male, 6 female, 20±0.4 yr) participated. With subjects in a semi‐recumbent position, we recorded the electrocardiogram, beat‐by‐beat arterial pressure (finger plethysmography), and MSNA. Subjects rested quietly for 10 minutes while breathing in time to a computer display prompting them to breathe at a frequency of 15 breaths/min. Subjects then continued to breathe in time to the computer display, but inhaled once every thirty seconds on a randomized e‐cigarette that contained either nicotine or no nicotine for 10‐min followed by a 10‐min recovery. The last 5‐min of baseline (BASE) variables were averaged and compared to the last 5‐min of active vaping (VAPE) and the last 5‐min of recovery (REC). Variables were assessed with repeated measures ANOVA with significant condition‐by‐time interactions assessed with a Tukey post‐hoc test. Data were expressed as Δ means ± SE from BASE. Heart rate increased in the nicotine condition during VAPE and returned to BASE values in REC (5.0±1.3 nicotine vs. 0.1±0.8 b/min placebo, during VAPE; P<.01). Mean arterial pressure increased in the nicotine condition during VAPE and remained elevated during REC. (6.5±1.6 nicotine vs 2.6±1 mmHg placebo, during VAPE and 4.6.0±1.7 nicotine vs 1.4±1.4 mmHg placebo, during REC; all p<.05). MSNA burst frequency decreased from BASE to VAPE and did not restore during REC (−7.1±1.6 nicotine vs 2.6±2 bursts/min placebo, during VAPE and −5.8±1.7 nicotine vs .5±1.4 bursts/min placebo, during REC; all p<.05). MSNA burst incidence decreased from BASE to VAPE and did not restore during REC (−4.5.1±1.1 nicotine vs.1.8±1.4 bursts/100hb placebo at VAPE and −4.7±.9 nicotine vs .1±1.3 bursts/100hb placebo, during REC; all p<.05). Our results suggest that acute usage of the JUUL e‐cigarette delivers a stimulus that increases arterial pressure and heart rate while decreasing MSNA, likely through sympathetic baroreflex inhibition. Our findings draw similar conclusions to previous studies that investigated cigarette smoking and autonomic function in humans. We conclude that non‐smokers who use the JUUL e‐cigarette may put themselves at greater risk for acute and/or chronic hypertension.

Publication Title

The FASEB Journal

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