E-cigarette use has been linked to mitochondrial dysfunction through exposure to reactive oxygen species (ROS), toxic aldehydes, metals, and flavoring agents. These constituents can damage mitochondrial DNA, impair oxidative phosphorylation, and disrupt calcium homeostasis, resulting in oxidative stress, inflammation, and programmed cell death. Mitochondrial impairment contributes to many systemic disorders, including respiratory, cardiovascular, and metabolic conditions. Preclinical findings suggest altered mitochondrial morphology, reduced adenosine triphosphate (ATP) production, and increased ROS, all of which can contribute to mitochondrial dysfunction following e-cigarette exposure. Certain flavorings and metals intensify these effects. While early human data suggest systemic mitochondrial stress, most research remains in vitro or animal-based. This review identifies mitochondrial dysfunction as a key mechanism in e-cigarette toxicity and calls for longitudinal research to elucidate its long-term health consequences.

1. IntroductionElectronic cigarettes have rapidly reshaped global nicotine use, particularly among adolescents and young adults, due to their perceived safety, technical customizability, and extens...

Electronic cigarettes are widely used by individuals in their reproductive years, yet polymer materials in pods, wicks, seals, and casings remain underexamined as possible contributors to inhaled particulate exposure. This narrative review evaluates whether e-cigarette device components could plausibly generate microplastics or nanoplastics during use and whether such particles, if present, could have reproductive relevance. Evidence from device-material studies, polymer degradation chemistry, aerosol physics, inhalation toxicology, and reproductive microplastic models was synthesized. Current devices place polycarbonate, polydimethylsiloxane, nylon, and other polymers near heating and aerosolization zones, where thermal cycling, solvent contact, and mechanical stress could theoretically promote oxidation, chain scission, embrittlement, or fragmentation. However, no study has chemically identified or quantified device-derived microplastics or nanoplastics in e-cigarette aerosols using polymer-resolving methods. Thus, links between e-cigarette use, inhaled polymer particles, and reproductive harm remain hypothetical. Evidence from non-e-cigarette models shows that micro- and nanoplastics can induce oxidative stress, inflammation, endocrine disruption, barrier interaction, and cellular injury, but these findings cannot be extrapolated without confirming particle formation, polymer identity, dose, and biodistribution. Future research should prioritize polymer-resolved aerosol testing under realistic puffing regimens, including unused and aged devices, e-liquids, condensates, and emitted aerosols. Key endpoints should include polymer identity, particles per puff, particles per mL of e-liquid consumed, particle size distribution, polymer mass, pulmonary deposition, systemic translocation, and reproductive or placental effects. Device-derived microplastics should be treated as a plausible particle-safety concern requiring direct experimental evaluation.