Abstract
Smoking of tobacco products continues to be widespread, despite recent progress in decreasing use. Both in the United States and worldwide, cigarette smoking is a major cause of morbidity and mortality. Growing evidence indicates that acute respiratory distress syndrome (ARDS) is among the consequences of cigarette smoking. Based on the topic from the 2017 Grover Conference, we review evidence that cigarette smoking increases lung vascular permeability using both acute and longer exposures of mice to cigarette smoke (CS). We also review studies indicating that CS extract disrupts cultured lung endothelial cell barrier function through effects on focal adhesion contacts, adherens junctions, actin cytoskeleton, and microtubules. Among the potentially injurious components of CS, the reactive aldehyde, acrolein, similarly increases lung vascular permeability and disrupts barrier function. We speculate that inhibition of aldehyde-induced lung vascular permeability may prevent CS-induced lung injury.