Electronic cigarettes are battery powered devices that use a vape-liquid to produce a vapor that is inhaled. A consequence of the rise in e-cigarette usage was the 2019 emergence of a vaping-induced respiratory disease denoted as 'e-cigarette or vaping use-associated lung injury' (EVALI). One of the suspected causes of EVALI is Vitamin E Acetate (VEA), which was found to be a diluent in certain illicit vape-pens, whereas nicotine is commonly diluted in equal parts propylene glycol and vegetable glycerin (PG:VG). The prevalent use of e-cigarettes and the emergence of a novel illness has made understanding how e-cigarette vapors affect our respiratory tissues a public health concern. We have designed and produced a simple device that can operate e-cigarettes and deliver the vapor to a chamber containing a standard cell culture multi-well plate. Here we utilize our device to model the response of human airway mucociliary tissue after chronic exposure to vapors produced from either PG:VG or VEA. We note several differences between how PG:VG and VEA vapors interact with and alter airway tissue cultures and suggest potential mechanisms for how VEA-vapors can exacerbate EVALI symptoms. Our device combined with primary human airway tissue cultures make an economical and compact model system that allows for animal-free investigations into the acute and chronic consequences of e-cigarette vapors on primary respiratory cells.
Keywords: Air-liquid interface; Cytokines; E-cigarettes; Inflammation; Vaping.
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