Didecyldimethylammonium chloride (DDAC) is a commonly used biocide that can cause lung inflammation and fibrosis. However, the mechanism of this pulmonary toxicity is unclear. Thus, we examined the mechanism for the DDAC-induced pulmonary toxicity at the cellular level by using lung epithelial cells. DDAC induced cell damage, including injury of mitochondria and lysosomes with the release of lactate dehydrogenase (LDH), as well as caused cell morphological changes and necrotic reactions. In a clonogenic assay, treatment with a low concentration of DDAC ($5{mu}m$) for 10 days reduced both the number and size of the colonies, which are indexes of cell growth. In addition, DDAC increased intracellular reactive oxygen species (ROS) production while it decreased glutathione (GSH) activity. Therefore, our results suggest that exposure to even a low concentration of DDAC may inhibit cell growth and cause oxidative stress in lung epithelial cells.