A new study by scientists at the University of California, Riverside, has revealed that heating e-cigarette liquids may produce toxic chemicals capable of damaging human lung cells, even at relatively low levels of exposure.
A new study by scientists at the University of California, Riverside, has revealed that heating e-cigarette liquids may produce toxic chemicals capable of damaging human lung cells, even at relatively low levels of exposure.
The research, published in Frontiers in Toxicology, found that two compounds—methylglyoxal and acetaldehyde—can form when propylene glycol, a main ingredient in most e-cigarette fluids, is heated during vaping. Both substances are known toxins, but their specific effects on lung tissue during vaping have remained unclear until now.
Using lab-grown human airway tissue, the researchers examined how these chemicals affect cellular health. The study found that both substances interfered with critical cell functions, though methylglyoxal caused more severe damage at lower concentrations. It disrupted mitochondrial activity—the process by which cells generate energy—and weakened the actin cytoskeleton, which helps cells maintain structure and strength.
“These changes are indicators of stress and injury that could contribute to long-term respiratory health problems if such exposure occurs repeatedly,” said Prof. Prue Talbot, lead author of the study and professor of the graduate division at UC Riverside.
While acetaldehyde is already recognised as a component of cigarette smoke linked to lung disease, Prof. Talbot noted that methylglyoxal may pose a greater risk. “Our results suggest that methylglyoxal could be even more toxic to airway cells despite appearing in smaller quantities,” she added.
Man Wong, a graduate student and first author of the paper, titled “Acetaldehyde and methylglyoxal: comparative analysis of toxic electronic cigarette degradation products in 3D and 2D exposure systems using human bronchial epithelial models,” said one of the more concerning findings was that lower-powered e-cigarette devices—often considered safer—might actually generate higher levels of methylglyoxal.
“Because nearly all e-cigarettes use propylene glycol, understanding how these byproducts form and how they affect lung cells is critical to assessing the long-term risks of vaping,” Wong said.
The study also observed that even brief exposure to these chemicals can alter cellular pathways involved in energy production, DNA repair, and structural integrity.
“Our findings provide insight into how vaping-related chemicals may contribute to lung injury,” Wong added. “We hope this research will inform future safety assessments of e-cigarette products.”
The work was carried out by Prof. Talbot, Wong, Teresa Martinez, and Nathan Hendricks, and was supported by grants from the National Institutes of Health, the US Food and Drug Administration Center for Tobacco Products, and the UCR Academic Senate.