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Mechanistic toxicity profiling of nicotine-rich e-liquids: mitochondrial and oxidative stress responses in ALI-exposed bronchial cells
Summary
Researchers examined the toxicity of four commercial nicotine-rich e-liquids on human bronchial epithelial cells using an air-liquid interface exposure system that mimics real-world inhalation conditions. They found that the e-liquid aerosols induced mitochondrial dysfunction and oxidative stress in the cells. The study suggests that while e-cigarettes may contain fewer combustion byproducts than traditional cigarettes, their aerosols can still cause measurable cellular damage in respiratory tissue.
Combustion byproducts contained in cigarette smoke are considered the main responsible for the occurring of serious chronic diseases. Aerosols from electronic cigarettes contain substantially fewer of these dangerous byproducts, potentially reducing health risks. This study examined the potential of four different commercial nicotine-rich e-liquids to induce cytotoxicity and mitochondrial dysfunction and oxidative stress in human bronchial epithelial cells (H292), using air-liquid interface (ALI) exposure. In addition to a qualitative control of the e-liquids, by dosing contaminants, we assessed cell viability, apoptosis, mitochondrial membrane potential, and reactive oxygen species (ROS) generation, by comparing e-cig aerosols to 1R6F reference cigarette smoke. All tested e-liquids showed very low levels of trace metals and microplastics, with contaminant concentrations below WHO drinking water limits. Furthermore, e-liquid aerosol induced significantly reduced cytotoxicity compared to 1R6F regular cigarette smoke, and mitochondrial integrity was preserved. Furthermore, no ROS generation was observed when using flavored e-cigarette aerosol. These results provide evidence of the lower potential toxicity of e-cigarettes compared to tobacco cigarettes in an in vitro model simulating real-world smoke exposure.