Beyond the lungs: Autonomic nervous system disruption and respiratory injury associated with electronic cigarette use

Electronic cigarette (e-cigarette) use has risen rapidly over the past decade, particularly among adolescents and young adults, driven by perceptions of reduced harm compared with combustible cigarettes. Despite the absence of tobacco combustion, e-cigarette aerosols contain ultrafine particles, toxic chemicals, and heavy metals capable of inducing airway inflammation, oxidative stress, and epithelial injury. Increasing evidence links vaping to respiratory symptoms, asthma, and obstructive airway disease, even among never-smokers. Emerging data further indicate that e-cigarette use disrupts autonomic nervous system function, with nicotine exposure promoting sympathetic activation, suppressing parasympathetic tone, and reducing heart rate variability, thereby reflecting autonomic imbalance and potential cardiovascular risk. Although e-cigarettes are widely promoted as smoking-cessation tools, evidence remains inconsistent, with high rates of dual use and persistent nicotine dependence. Overall, e-cigarettes are not physiologically benign and are associated with both respiratory injury and autonomic dysregulation, while their role in smoking cessation remains uncertain. Further mechanistic and longitudinal studies are required to better define their long-term cardiopulmonary effects.