Accumulating evidences indicate that pulmonary exposure to carbon nanotubes is associated with increased risk of lung diseases, whereas the effect on the vascular system is less studied. We investigated vascular effects of two types of multi-walled carbon nanotubes (MWCNT) in apolipoprotein E(-/-) mice, wild type mice and cultured cells. The ApoE(-/-) mice had accelerated plaque progression in aorta after five intracheal instillations of MWCNT (25.6 µg/mouse weekly for five weeks). The exposure was associated with pulmonary inflammation, lipid peroxidation and increased expression of inflammatory, oxidative stress, DNA repair and vascular activation response genes. The level of oxidatively damaged DNA in lung tissue was unaltered, probably due to increased DNA repair capacities. Despite upregulation of inflammatory genes in the liver, effects on systemic cytokines and lipid peroxidation were minimal. The exposure to MWCNTs in cultured human endothelial cells increased the expression of vascular adhesion molecules (ICAM1 and VCAM1). In co-cultures there was increased adhesion of monocytes to endothelial cells after exposure to MWCNT. The exposure to both types of MWCNT was also associated with increased lipid accumulation in monocytic-derived foam cells, which was dependent on concomitant oxidative stress since the antioxidant N-acetylcysteine inhibited the lipid accumulation. Collectively our results indicate that exposure to MWCNT is associated with accelerated progression of atherosclerosis, which could be related to both increased adherence of monocytes onto the endothelium and oxidative stress-mediated transformation of monocytes to foam cells.