Several studies show that ultrafine particles have a larger surface area than coarse particles, thus causing a greater inflammatory response. In this study, we investigated chemical and biological oxidative effects of nanoparticles in vitro. Carbon black (CB) nanoparticles with mean aerodynamic diameters of 14, 56, and 95nm were examined. The innate oxidative capacity of the CB nanoparticles was measured by consumption of dithiothreitol (DTT) in cell-free system. The expression of heme oxygenase-1 (HO-1) in rat alveolar type II epithelial cell line (SV40T2) and alveolar macrophages (AM) exposed to CB nanoparticles was measured by ELISA. DTT consumption of 14nm CB was higher than that of other CB nanoparticles having the same particle weight. However, DTT consumption was directly proportional to the particle surface area. HO-1 protein in SV40T2 cells was significantly increased by the 14nm and 56nm CB, however, 95nm CB did not affect. HO-1 protein in AM was significantly increased by the 14, 56, and 95nm CB. The increase in HO-1 expression was diminished by N-acetyl-l-cysteine (NAC) treatment of each CB nanoparticles before exposure although the difference between the effects of NAC-treated and untreated 14nm CB did not achieve significant. In conclusion, CB nanoparticles have innate oxidative capacity that may be dependent on the surface area. CB nanoparticles can induce oxidative stress in alveolar epithelial cells and AM that is more prominent with smaller particles. The oxidative stress may, at least partially, be mediated by surface function of particles.