Human neuroblastoma cell SH-SY5Y was applied as a cell line model in order to explore its inflammatory responses to ozone oxidized black carbon (OBC) and also to investigate the potential roles of the nuclear factor-κB (NF-κB) and phosphatidylin-ositol- 3-kinase/protein kinase B (PI3K/Akt) pathways. The results showed that mitochondrial membrane potential (MMP) decreased and the degree of DNA damage increased signifi-cantly in a time- and concentration-dependent manner in SH-SY5Y cells after treatment with OBC. Interleukin-4 (IL-4) leakage and the expression of tumor necrosis factor-α (TNF-α)mRNA were found to increase concentration-dependently, suggesting that OBC could lead to inflammatory responses in SH-SY5Y cells. Meanwhile, significantly elevated in-tracellular reactive oxygen species (ROS) levels and the mRNA expression of superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) demonstrated that OBC caused oxidative stress in SH-SY5Y cells. OBC activated the NF-κB and PI3K/Akt pathways, indicated by significant changes seen in certain proteins. In summary, the NF-κB and PI3K/Akt pathways probably played important roles in OBC promoted oxidative stress and the in-flammatory responses seen in SH-SY5Y cells.