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Background and Aim  Sparse evidence suggests a possible link between exposure to airborne nanoparticles (NPs) and cardiovascular (CV) risk, perhaps through mechanisms involving oxidative stress and inflammation. We assessed the effects of TiO 2  and Co 3 O 4  NPs in human circulating angiogenic cells (CACs), which take part in vascular endothelium repair/replacement.    Methods  CACs were isolated from healthy donors’ buffy coats after culturing lymphomonocytes on fibronectin-coated dishes in endothelial medium for 7 days. CACs were pre-incubated with increasing concentration of TiO 2  and Co 3 O 4  (from 1 to 100 μg/ml) to test the effects of NP – characterized by Transmission Electron Microscopy – on CAC viability, apoptosis (caspase 3/7 activation), function (fibronectin adhesion assay), oxidative stress and inflammatory cytokine gene expression.    Results  Neither oxidative stress nor cell death were associated with exposure to TiO 2  NP (except at the highest concentration tested), which, however, induced a higher pro-inflammatory effect compared to Co 3 O 4  NPs (p<0.01). Exposure to Co 3 O 4  NPs significantly reduced cell viability (p<0.01) and increased caspase activity (p<0.01), lipid peroxidation end-products (p<0.05) and pro-inflammatory cytokine gene expression (p<0.05 or lower). Notably, CAC functional activity was impaired after exposure to both TiO 2  (p<0.05 or lower) and Co 3 O 4  (p<0.01) NPs.    Conclusions  In vitro exposure to TiO 2  and Co 3 O 4  NPs exerts detrimental effects on CAC viability and function, possibly mediated by accelerated apoptosis, increased oxidant stress (Co 3 O 4  NPs only) and enhancement of inflammatory pathways (both TiO 2  and Co 3 O 4  NPs). Such adverse effects may be relevant for a potential role of exposure to TiO 2  and Co 3 O 4  NPs in enhancing CV risk in humans.

Effects of TiO2 and Co3O4 Nanoparticles on Circulating Angiogenic Cells