injuries poisoning
Riot Control Chemical Agents
Pathophysiology of Riot Control Chemical Injuries
CN and CS alkylate enzymes such as lactic dehydrogenase; this mechanism may be responsible for transient tissue injury that resolves with rapid replacement of the inactivated enzymes. Release of cytokines such as bradykinin contributes to the pain caused by these compounds, as does generation of hydrochloric acid at high doses. CR appears to have a similar mechanism of action. DM is thought to exert its effects partly via the oxidation of its arsenic moiety from As(III) to As(V) and the subsequent release of chlorine. OC causes pain by binding to transient receptor potential vanilloid (TRPV1) receptors in neurons that are then stimulated to release neurokinin A,calcitonin-gene-related peptide, and substance P. These compounds induce neurogenic inflammation associated with pain, capillary leakage, edema, mucous production, and bronchoconstriction. 