In order to assess the health risk of cigarette smoke, crotonaldehyde-induced cell death and its mechanism in BEAS-2B cells were investigated. Cell survival rate, intracellular ATP level, apoptosis rate, cytochrome c released from mitochondria to cytoplasm, and caspase-9 and caspase-3/7 activities were determined by MTT, chemiluminescence, flow cytometry, flow cytometry combined with immunochemistry, and chemiluminescence methods, respectively. The results showed that crotonaldehyde induced cell apoptosis, and turned into necrosis along with the increase of crotonaldehyde dosage. Crotonaldehyde caused that intracellular ATP level declined rapidly, mitochondria membrane potential decreased, cytochrome c released from mitochondria to cytoplasm, and caspase-9 and caspase-3/7 were activated. It was concluded that crotonaldehyde induced and caspase mediated cell apoptosis.