The sulphur mustard, 2-chloroethylethyl sulphide (CEES), is a sulfur mustard vesicant, which alkylates with a broad range of biological molecules. Since CESS can be used as weapon of mass destruction, it is of importance to improve our understanding of CEES-induced pathologies, especially of the lung. Primary macrophages (Mφ) are key residents of the lung and are responsible for tissue housekeeping; however, uncontrolled activation of these immune cells can be injurious to the lung. Since previous studies investigated the effects of CEES on monocyte/macrophage cell-lines, our efforts were focused on determining the effects of CEES on Mφ. Mφ exposed to CEES released no primary inflammatory cytokines (e.g. IL-1, TNFα, IL-8) or chemokines (e.g. MIP-1α, MIP-1β). However, Mφ production of nitric oxide, a known immune mediator, did increase three- to four-fold above untreated-Mφ. Additional studies were performed that investigated the biological pathways of CEES-induced apoptosis (program cell death). Our preliminary findings suggest that CEES triggers poly (ADP-ribose) polymerase (PARP) activation, mitochondrial damage, and caspase protein cleavage, which are key components in apoptosis. To prevent these upstream apoptotic events, we cultured CEES-treated Mφ with N-acetylcyteine (NAC), PARP inhibitors, or caspase inhibitors one-hour after exposure to CEES. Our preliminary finding suggests that NAC more efficiently protects Mφ from CEES-induced apoptosis than PARP or caspase inhibitors. Collectively, our findings suggest that CEES effects vary among tissues and regulation of the cellular redox state may serve as a possible therapeutic option for acute exposure to CEES.