Electric-cigarette/vaping-associated lung injury (EVALI) is a respiratory illness that causes respiratory failure in thousands of individuals due to an inhibitory physical interaction between vaping oil toxins and the pulmonary surfactant. Amongst possible vaping oil toxins, studies have proposed vitamin E acetate as a likely instigator of EVALI. Pulmonary surfactant is a phospholipid and protein complex lining pulmonary alveoli to achieve and maintain low surface tensions for proper respiration. The main mechanical properties that allow for this are interface stability and adsorption, which are dependent on surfactant dynamics and structure. To investigate this relationship, neutron spin echo (NSE), small angle neutron scattering (SANS) and Langmuir-Blodgett trough (LB) measurements were used on two pulmonary surfactant mimic systems. With NSE and LB highlighting membrane dynamics/mechanics and SANS highlighting structure-dependent properties, it was found that with the addition of increasing concentration, vitamin E acetate intercalates with surfactant lipids and nonlinearly increases membrane fluidity and area of compressibility to a plateau. With increased fluidity, lipid adsorption in inspiration is promoted and monolayer collapse in expiration is promoted. This suggests that monolayer collapse leads to pulmonary surfactant and subsequently respiratory failure, indicating a correlation between vitamin E acetate-associated collapse and observed EVALI pathology.

Mechanical mechanism for E-cigarette/vaping associated lung injury (EVALI)

ACS Spring 2022

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.