Cannabidiol and Vitamin E Compromise the Interfacial Stability of Model Lung Surfactant Lipid Monolayers by Altering Their Thermodynamic and Rheological Properties.

Escobar E.; Ong E.; Atkins M.; Dhar P. · Langmuir : the ACS journal of surfaces and colloids · 2026

**Background & Methods** This laboratory study investigated how two common vaping additives—cannabidiol (CBD) and α-tocopherol (vitamin E)—affect lung surfactant film mechanics. Researchers used dipalmitoylphosphatidylcholine (DPPC) monolayers as a model system to simulate lung surfactant behavior, subjecting them to cyclic deformations mimicking breathing patterns. Both quasi-static surface properties (compression/expansion isotherms) and dynamic rheological properties (oscillatory barrier deformations) were evaluated using a Langmuir-Pockels trough and epifluorescence microscopy. **Key Findings** • Both cannabidiol and vitamin E altered the surface activity and rheological properties of DPPC monolayers in a concentration-dependent manner, compromising interfacial stability and film restructuring capacity during simulated breathing cycles. • Vitamin E demonstrated a substantially greater impact on lung surfactant film mechanics compared to cannabidiol across all concentrations tested, likely due to its bulkier molecular structure and greater lipophilicity. • When both additives were present simultaneously, vitamin E exhibited a dominant effect on film disruption, suggesting it may be the primary driver of surfactant dysfunction in real-world vaping scenarios involving multiple additives. **Dosage & Administration** Not reported. The study examined concentration-dependent effects of additives on model surfactant systems without specifying equivalent inhalation exposures or vaping product concentrations. **Safety & Adverse Effects** The study did not directly assess clinical adverse effects. However, findings suggest that chronic vaping exposure could disrupt lung surfactant film structure and mechanics, potentially contributing to reduced lung compliance and labored breathing characteristic of e-cigarette or vaping product use-associated lung injury (EVALI). **Evidence Quality** This is an *in vitro* mechanistic study with significant limitations regarding clinical applicability. While the Langmuir trough model provides controlled conditions to isolate molecular interactions, it does not fully replicate the complex biological environment of intact lungs, including immune responses, cellular interactions, and systemic absorption. The study uses simplified model systems rather than human tissue or animal models. Findings provide mechanistic insight into how vaping additives may disrupt surfactant function but cannot directly establish causation of human lung disease. Additional *in vivo* studies are needed to validate these mechanisms and determine clinical relevance to EVALI pathogenesis.

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