Riot-control agents are compounds that were initially developed for crowd control but that have also been used in military conflicts (see also Overview of Chemical-Warfare Agents Overview of Chemical-Warfare Agents Chemical-warfare (CW) agents are chemical mass-casualty weapons (MCWs) developed by governments for wartime use and include Toxic agents (intended to cause serious injury or death) Incapacitating... read more ). Riot-control agents are also referred to as harassing agents, tear agents, or lacrimators and are often misleadingly called tear gas, but in fact they do not exist as gases or vapors. Instead, they are solids that can be dispersed as liquids (by dissolving the solid agent to form a solution and then spraying the solution) or as aerosols (small particles released explosively or as smoke). Like anticholinergic agents, they are intended to cause incapacitation rather than serious injury or death, although deaths due to pulmonary edema (acute lung injury) have occurred.
Military versions of these agents include chloroacetophenone (CN, also marketed as Mace®), chlorobenzylidenemalononitrile (CS), dibenzoxazepine (CR), and diphenylaminoarsine (adamsite, or DM, a so-called vomiting agent). Oleoresin capsicum (OC, pepper spray) is a more recently developed riot-control agent used primarily for law enforcement and personal protection. Chloropicrin (PS) is a compound used during World War I that is occasionally regarded as a riot-control agent, although it is more properly classified as a pulmonary agent Pulmonary Chemical-Warfare Agents Pulmonary agents include traditional chemical-warfare “choking” agents such as chlorine, phosgene, diphosgene, and chloropicrin and some vesicants such as sulfur mustard, Lewisite, and phosgene... read more .
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.
Symptoms and Signs
Although there are minor differences between compounds, most riot-control agents cause nearly immediate irritation and pain involving the eyes, mucous membranes, and skin, which may also become briefly erythematous. Respiratory effects resulting from inhalation are typically obviously audible (eg, coughing, sneezing, and wheezing) due to type 1 damage, although type 2 damage (delayed-onset shortness of breath due to incipient acute lung injury) can occur with high doses. Deaths are usually due to pulmonary edema resulting from high doses delivered in confined spaces. The largely obsolete agent DM may cause either immediate or delayed-onset irritation along with vomiting.
Effects of all of the riot-control agents typically resolve within a half an hour, although agent left on the skin may cause blisters. Reactive airways dysfunction syndrome (RADS) can occur long after exposure and persist indefinitely, although it is impossible to predict which patients will develop this complication.
Diagnosis is made by history, signs (lacrimation, blepharospasm, erythema, type 1 respiratory signs), and symptoms (transient irritation and pain with, at high doses, delayed-onset shortness of breath or chest tightness). Chest x-rays are usually clear and not needed unless patients develop dyspnea, which suggests pulmonary edema. Laboratory studies do not contribute to diagnosis.
Casualties typically need prompt removal from exposure but are then usually triaged as delayed or minimal, since except at high doses effects are self-limiting. Evidence of incipient pulmonary edema should prompt urgent evacuation to a pulmonary intensive care unit.
Termination of exposure
If eye pain does not resolve spontaneously, eye decontamination
Cold compresses and analgesics if necessary for pain
At the first sign of exposure or potential exposure, masks are applied when available. People are removed from the affected area when possible.
Decontamination is by physical or mechanical removal (brushing, washing, rinsing) of solid or liquid agents. Water may transiently exacerbate the pain caused by CS and OC but is still effective, although fat-containing oils or soaps may be more effective against OC. Eyes are decontaminated by copious flushing with sterile water or saline or (with OC) open-eye exposure to wind from a fan. Referral to an ophthalmologist is needed if slit-lamp examination shows impaction of solid particles of agent.
Most effects resulting from riot-control agents are transient and do not require treatment beyond decontamination, and most patients do not need observation beyond 4 hours. However, patients should be instructed to return if they develop effects such as vesication or delayed-onset shortness of breath.
The views expressed in this article are those of the author and do not reflect the official policy of the Department of Army, Department of Defense, or the US Government.