Electronic cigarette aerosols contain numerous chemicals that can affect the central nervous system through mechanisms involving oxidative stress, inflammatory processes, and blood–brain barrier dysfunction. When the liquid is heated, aldehydes, heavy metals, free radicals, and pyrolysis products of propylene glycol and glycerine are formed. These compounds lead to damage to endothelial structures, degradation of tight junction proteins, and increased blood–brain barrier permeability, which promotes the penetration of pro-inflammatory cytokines and the activation of microglia and astroglia. Preclinical studies have shown increased production of inflammatory mediators, disturbances in mitochondrial homeostasis, and changes in the functioning of transporters responsible for neuronal metabolism. Nicotine present in aerosols modulates the activity of nicotinic acetylcholine receptors, affecting dopaminergic, glutamatergic, and GABAergic transmission. These changes lead to neuroadaptation within the mesolimbic reward system and promote the reinforcement of addictive behaviours. Some aromatic compounds, including menthol and farnesol, may further exacerbate oxidative stress and enhance the effects of nicotine. Evidence from animal studies indicates that chronic exposure to electronic cigarette aerosols may lead to cognitive impairment, behavioural changes, and increased susceptibility to neurodegenerative processes, especially during developmental periods. Despite the growing number of mechanistic studies, clinical data remain limited. This paper summarises the current state of knowledge on the neurotoxic potential of electronic cigarette aerosols, with particular emphasis on molecular and cellular mechanisms, and highlights the need for further research into their long-term effects on the nervous system.

oxidative stress, nicotine, blood–brain barrier, electronic cigarettes, neuroinflammation