Pod-based menthol and tobacco flavored e-cigarettes cause mitochondrial dysfunction in lung epithelial cells

Area of Science:

• Cellular and Molecular Toxicology
• Environmental Health
• Respiratory Medicine

Background:

• The U.S. FDA banned most flavored e-cigarette pods, exempting menthol and tobacco flavors.
• Prior studies linked menthol and tobacco e-cigarettes to mitochondrial reactive oxygen species.

Purpose of the Study:

• To investigate the effects of JUUL Menthol and Virginia Tobacco e-cigarette aerosols on mitochondrial respiration and electron transport chain (ETC) protein levels in lung epithelial cells.
• To determine if menthol or tobacco flavored e-cigarette aerosols induce mitochondrial dysfunction.

Main Methods:

• Human lung epithelial cells (Beas-2b) were exposed to JUUL Menthol and Virginia Tobacco aerosols.
• Mitochondrial respiration was measured using Seahorse XF analysis.
• Electron transport chain complex levels were assessed via Western blotting using total OXPHOS antibodies.

Main Results:

• Menthol aerosol exposure caused immediate increases in proton leak and decreased coupling efficiency, along with reduced levels of ETC complexes I, II, and IV.
• Twenty-four hours post-menthol exposure, cells showed decreased basal respiration, maximal respiration, and spare respiratory capacity, plus reduced complex I.
• Tobacco aerosol exposure did not significantly alter mitochondrial respiration but increased levels of ETC complexes I, IV, and V immediately post-exposure.

Conclusions:

• Exposure to menthol-flavored e-cigarette pods induces significant mitochondrial dysfunction in lung epithelial cells.
• Menthol flavor appears to be a key driver of cellular mitochondrial damage, unlike tobacco flavor in this study.