Low-dose sulfur mustard primes oxidative function and induces apoptosis in human polymorphonuclear leukocytes.

Although considerable work has focused on understanding the processes of direct tissue injury mediated by the chemical warfare vesicant, sulfur mustard (2,2'-bis-chloroethyl sulfide; SM), relatively little is known regarding the mechanisms of secondary injury caused potentially by the acute inflammatory response that follows SM exposure. Polymorphonuclear leukocytes (PMNs) play a central role in the initiation and propagation of inflammatory responses that, in some cases, result in autoimmune tissue damage. The potential for PMN-derived tissue damage following SM exposure may, in part, account for the protracted progression of the injury before it resolves.