Endothelial Cell Inflammatory Reactions Are Altered in the Presence of E-Cigarette Extracts of Variable Nicotine.

Abstract

Exposure to tobacco smoke has been associated with heightened endothelial cell activities associated with cardiovascular diseases (CVD). Conversely, the exposure to nicotine both activates and inhibits particular endothelial cell functions. However, which constituent(s) of tobacco smoke is responsible for these changes is unknown, since toxic gases and fine particulate matter cannot be isolated. Electronic cigarette vapor allows us to isolate these constituents, providing us the ability to evaluate individual constituents. Here, we used e-cigarettes to (1) identify which constituents of tobacco products are most responsible for altered CVD functions and (2) elucidate the underlying risk of e-cigarette exposure. To accomplish this goal, endothelial cells were exposed to extracts produced from tobacco cigarettes or e-cigarettes. Endothelial cell inflammatory processes, viability, density and metabolic activity were observed. In general, a significant increase in complement deposition, the expression of the receptors for C1q, coupled with a decrease in cell proliferation and metabolic activity was observed. These results were independent of nicotine and the exposure to e-vapor was just as harmful as tobacco smoke extracts. Thus, the exposure to fine particulate matter and not toxic combustion gases or nicotine may be the most critical for regulating CVD progression.