Citation

DiPasquale M, Gbadamosi O, Nguyen MHL, Castillo SR, Rickeard BW, Kelley EG, Nagao M, Marquardt D. Chem. Res. Toxicol. 2020; ePub(ePub): ePub.

Copyright

(Copyright © 2020, American Chemical Society)

DOI

10.1021/acs.chemrestox.0c00212

PMID

32842741

Abstract

The outbreak of electronic-cigarette/vaping associated lung injury (EVALI) has made thousands ill. This lung injury has been attributed to a physical interaction between toxicants from the vaping solution and the pulmonary surfactant (PS). In particular, studies have implicated vitamin E acetate as a potential instigator of EVALI. Pulmonary surfactant is vital to proper respiration through the mechanical properties of adsorption and interface stability to achieve and maintain low surface tension at the air-liquid interface. Using neutron spin echo spectroscopy, we investigate the impact of vitamin E acetate on the mechanical properties of two lipid-only pulmonary surfactant mimics: pure 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) and a more comprehensive lipid mixture. It was found that increasing vitamin E acetate concentration non-linearly increased membrane fluidity and area compressibility to a plateau. Softer membranes would promote adsorption to the air-liquid interface during inspiration as well as collapse from the interface during expiration. These findings indicate the potential for the failure of the pulmonary surfactant upon expiration, attributed to monolayer collapse. This collapse could contribute to the observed EVALI signs and symptoms, including shortness of breath and pneumonitis.

Language: en