Abstract
Vaping of flavored liquids has been touted as safe alternative to traditional cigarette smoking with decreased health risks. The popularity of vaping has dramatically increased over the last decade, particularly among teenagers who incorporate vaping into their daily life as a social activity. Despite widespread and increasing adoption of vaping among young adults, there is little information on long-term consequences of vaping and potential health risks. This study demonstrates vaping-induced pulmonary injury using commercial JUUL pens with flavored vape juice using an inhalation exposure murine model. Profound pathological changes to upper airway, lung tissue architecture, and cellular structure are evident within 9 wk of exposure. Marked histologic changes include increased parenchyma tissue density, cellular infiltrates proximal to airway passages, alveolar rarefaction, increased collagen deposition, and bronchial thickening with elastin fiber disruption. Transcriptional reprogramming includes significant changes to gene families coding for xenobiotic response, glycerolipid metabolic processes, and oxidative stress. Cardiac systemic output is moderately but significantly impaired with pulmonary side ventricular chamber enlargement. This vaping-induced pulmonary injury model demonstrates mechanistic underpinnings of vaping-related pathologic injury.
Highlights
Relative merit of vaping for “harm reduction” intervention that transitions smokers away from combustible cigarettes remains under attack because of widespread adoption of vaping as a social activity and lifestyle choice by “never smokers,” adolescents [1, 2, 3]
Such severe vaping-associated pulmonary injury (VAPI) cases arise in users of commercially available vaping products, unlike the electronic vaping-associated lung injury (EVALI) epidemic in 2019 traced back to black market “Dank Vapes” associated with ill-conceived mixing of Vitamin E acetate and THC into vape juice [48, 49]
Pathological processes culminating in severe VAPI are more obscure and slow to develop, in some cases occurring over months of frequent unrelenting vaping activity [10, 11, 12, 13, 14, 15, 16, 17]
Summary
Relative merit of vaping for “harm reduction” intervention that transitions smokers away from combustible cigarettes remains under attack because of widespread adoption of vaping as a social activity and lifestyle choice by “never smokers,” adolescents [1, 2, 3]. The electronic vaping-associated lung injury (EVALI) outbreak of 2019 serves as a sobering demonstration of potential dangers resulting from uninformed experimentation with vape juice composition [4, 5, 6]. Commercially sold vape juices and prefilled disposable devices typically do not provoke acute lung injury and respiratory distress as pointed out by vaping advocacy groups [7, 8, 9]. Vaping-associated pulmonary injury (VAPI) in a minority of users is a well-documented and growing concern in the clinical setting with multiple independent reports of severe respiratory illness including acute respiratory distress syndrome including potential pulmonary circulation impairment [10, 11, 12, 13, 14, 15, 16, 17]. Fundamental unresolved issues using commercial vaping products from reputable sources include [1] how do individualspecific biological factors influence susceptibility to VAPI; [2] what is the underlying pathogenesis of VAPI leading to respiratory distress; and [3] how does progression of VAPI precipitate pulmonary circuit failure? Immediacy of the problem in society, recency of modern electronic vaping, and the rapid evolution of vaping technology necessitate development of an innovative platform to study biological processes of VAPI
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