A kinetic model has been constructed of the myeloperoxidase-hydrogen peroxide-chloride ion system of mammalian neutrophils. The model includes the reactions that form chlorinated species and those compounds formed through the reactions of phenolic compounds. Model calculations show that N-chlorotaurine is the primary long-lived product of this system, but that tyrosine peroxide is a major secondary product produced by the generation of tyrosyl radicals. While N-chlorotaurine is formed in much larger concentration than tyrosine peroxide, its lower toxicity may mean that tyrosine peroxide may be the more important mediator of toxic stress in the host associated with inflammatory processes. Care must be taken in the interpretation of dityrosine levels as indicating neutrophil derived oxidant damage. Tyrosine peroxide competes with the formation of dityrosine. Therefore, a high level of oxidative stress may be present even in the absence of significant levels of dityrosine.