Diesel exhausted particles (DEP), a kind of fine particles with aerodynamic diameters less than $2.5{mu}m$ (PM2.5), is of great concern to human health because they remain in atmosphere for long periods, invade an indoor air environment, and can be breathed most deeply into lung and reached the alveoli because of their small size ($0.1{sim}0.4;{mu}m$ in diameter). Epidemiological and experimental studies suggested that DEP may play an active role in the increased respiratory mortality and morbidity. In addition to their physical characteristics, the chemical components including polyaromatic hydrocarbon (PAH) are regarded as a carcinogen causing pulmonary tumors. PLD plays an important role in cell proliferation with various physiological phenomena and affects other enzymes by activating signal transduction pathway. We investigated the cytotoxic mechanism of DEP on RAW 264.7 cells focusing on the role in activation of PLD. Our results suggested DEP induced PLD activity through a specific signaling pathway involving phospholipase $A_2$, PLC, PKC and $Ca^{2+}$ mobilization.