We assessed human lung microvascular EC barrier function as measured by transendothelial electrical resistance (TER), a highly sensitive measurement of permeability. PM challenge (10-100 μg/ml) induced doseand time-dependent reduction in TER (Additional file 1: Figure S1 ) or increases in FITC-dextran leakage through EC monolayer (Additional file 1: Figure S2 ) [20] , indicating a loss of EC barrier integrity. At the same time, PM induced a time-dependent (1-6 hr) reduction of the levels of tight junction proteins ZO-1 and ZO-2, but did not affect levels of adhesion junction proteins VE-cadherin or β-catenin ( Figure 1A ). No obvious cytotoxicity in the ECs was found after PM challenge (100 μg/ml, 0-16 hr) with MTT assay [13] or LDH release assay (Additional file 1: Figure S3 ).