The effect of volatile organic compounds on endothelial function and atherogenesis.

Abstract

Volatile organic compounds (VOCs) are a group of pervasive air pollutants that are released into the atmosphere from both anthropogenic and environmental sources. Recent epidemiological studies suggest that exposure to various VOCs is associated with an increased risk of cardiovascular disease. However, the relationship between VOCs and cardiovascular disease is not well-studied. Using animal models and three select VOCs, benzene, xylene, and trichloroethylene, we studied the effects of VOCs on endothelial injury and benzene-induced atherogenesis. We found that exposure to benzene and xylene increased circulating endothelial microparticles, depleted progenitor cells, and increased platelet activation. Following the exposure to the representative VOC, trichloroethylene (TCE), we saw a decrease in circulating endothelial microparticles, modest changes in platelet activation, and modest changes in progenitor cell populations. This suggests that petroleum products such as benzene and xylene may be playing a more deleterious role in endothelial injury and atherogenesis than chlorinated VOCs like TCE.