Airway epithelium represents a well-investigated target for environmental pollutants such as PM. Exposure of airway epithelium to airborne PM causes altered cytokine/chemokine gene expression and increased production of IL-1β, IL-6, IL-8 and TNF-α [5, 6] . Now, the lung endothelium is also gaining attention as a viable PM target tissue. Exposure of the endothelium to PM or its active components in the systemic circulation induces significant systemic endothelial inflammation and dysfunction, even at low levels of exposure [7, 8] . The water soluble fraction of PM (up to 35-50%) can easily diffuse through the epithelium/endothelial barrier to the systemic circulation. Bioavailable transition metals present in urban PM catalyze redox reactions in human lung endothelium, which cause oxidative stress, increase the production of inflammatory cytokines, and increase the activation of NF-κB signaling pathways, all of which trigger further endothelial damage [9] . Increased endothelial monolayer permeability is also observed in inflammatory pulmonary conditions such as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and sepsis; devastating lung disorders with mortality exceeding 30%, as well as in more subacute and chronic inflammatory disorders such as asthma [10, 11] .