Abstract only Background: A new form of lung injury was described in electronic cigarette users beginning July 2019 with patients presenting with respiratory distress. The condition is known as E-cigarette (eC) or vaping product use associated lung injury or EVALI and was thought to be related to Vit E oils used to dilute cannabis. Whether a single acute exposure of eC smoke can induce lung injury has not been reported. The purpose of this study was to determine if such an acute exposure with eC smoke heated with different heating elements and power levels induced inflammatory changes in the lungs and heart. Methods: Rats were exposed to pure air or received a single, 4-hour exposure to eC vapor (50% propylene glycol, 50% vegetable glycerin; tobacco flavoring, n=16 in each group). The devices used either a stainless steel (SS) or nichrome (NC) heating element randomized to a low or high atomization power (45 versus 70 Watts). Rats were euthanized within 48 hours of exposure and hematoxylin and eosin stained lung and cardiac histology sections were assessed. Inflammatory cells were counted from 12 random areas per section at 10 х magnification. Results: The lung alveoli appeared normal in the air group (Figure, panel A); the eC groups using the SS or NC heating element with high or low power showed accumulation of inflammatory cells (mainly macrophages) in bronchial lumen (B), near the pleura (C), and within the alveolar spaces (D). The numbers of inflammatory cells per field in the lung parenchyma were significantly greater in the rats exposed to eC using SS or NC heating element compared to the air control group (P < 0.05, One way ANOVA, Tukey multiple comparison test; panel E). Cardiac tissue appeared normal with no evidence of inflammation. Conclusion: One 4-hour exposure to eC vapor, in the absence of vitamin E oil or nicotine, significantly increased the number of inflammatory cells in the lung. Effects were seen after exposures to vapor generated using SS and NC heating elements at either high or low power.