Apoptotic and proinflammatory effect of combustion-generated organic nanoparticles in endothelial cells

- Flame-generated organic carbon nanoparticles (OC NPs) simulate combustion exhausts.
- OC NPs can be produced by controlling flame operating conditions.
- We investigate the toxicological effect of OC NPs on endothelial cells (EC).
- OC NPs induce growth inhibition and massive apoptosis as revealed by FACS analysis.
- OC NPs also induce a time-dependent increase of proinflammatory lysophospholipid.

Air pollution exposure in industrialized cities is associated with an increased risk of morbidity and mortality attributed to cardiovascular diseases. Combustion exhausts emitted from motor vehicles and industries represent a major source of nanoparticles in the atmosphere. Flame-generated organic carbon nanoparticles (OC NPs) provide interesting model nanoparticles that simulate fresh combustion emissions near roadways or combustion sources. These model nanoparticles can be produced by controlling flame operating conditions and used to test possible toxicological mechanisms responsible for the observed health effects. OC NPs were used to investigate their possible effect on endothelial cells (EC) growth and production of proinflammatory lipid mediators. Results indicated a dose and time-dependent reduction in cell viability following incubation of EC with OC NPs for 24 and 48 h. Fluorescence-activated cell sorting revealed that EC treated with OC NPs showed a cell proliferation index significantly lower than that of control cells and an increased apoptotic cell death. The annexin assay confirmed the increased apoptotic cell death. Moreover, OC NPs also induced a time-dependent increase of proinflammatory lysophospholipid production. These results, establishing that OC NPs induce EC proinflammatory lysophosholipid production and apoptotic cell death, provide the first evidence of the detrimental effect of OC NPs on EC.