CS, CN
Signs and Symptoms: burning and pain on exposed mucous membranes and skin, eye pain and tearing, burning in the nostrils, respiratory discomfort, and tingling of the exposed skin.
Detection: no detector.
Decontamination: Eyes: thoroughly flush with water, saline, or similar substance. Skin: flush with copious amounts of water, alkaline soap and water, or a mildly alkaline solution (sodium bicarbonate or sodium carbonate). Generally, decontamination is not needed if the wind is brisk. Hypochlorite exacerbates the skin lesion and should not be used.
Immediate management: Usually none is necessary; effects are self-limiting.
Riot-control agents, also called irritants, lacrimators, and "tear gas," produce transient discomfort and eye closure to render the recipient temporarily incapable of fighting or resisting. Law enforcement agencies use them for riot control, and military forces use them for training and in combat (see below). They have a high LCt50 and a low effective Ct50, and therefore have a high safety ratio. Their major activity is to cause pain, burning, or discomfort on exposed mucous membranes and skin; these effects occur within seconds of exposure but seldom persist more than a few minutes after exposure has ended.
Paris police used riot-control agents to dispel rioters before World War I, and these compounds were the first chemical agents deployed during that war. French soldiers used them with limited success in small skirmishes. About 30 riot-control agents were developed and used, but their use decreased following the advent of more potent compounds.
After World War I, military and law enforcement agencies used CN for various purposes until CS, a more potent and less toxic compound synthesized by Corson and Stoughton (hence the nomenclature) in 1928, replaced it in about 1959. Today CN is in commercially available devices for self-protection (MaceR), but CS is the agent otherwise used. The military forces of most countries use it in training as a confidence builder for the protective mask (the "gas chamber exercise"), and the United States used it extensively in Vietnam, primarily for tunnel denial. Worldwide, police forces of many countries, e.g., Ireland, France, Russia, and the United States, use it for crowd control or during riots.
The United States excludes these agents from international treaty provisions. They may be used in military situations by presidential order.
The agents in use today are CS and CN. CA is outmoded, CR is a British agent, and DM is neither used nor stockpiled.
PHYSICOCHEMICAL CHARACTERISTICS
Unlike most agents which are liquids under temperate conditions, riot-control agents are solids with low vapor pressures and are dispersed as fine particles or in solution. Dispersion devices include small, hand-held spray cans, large spray tanks, grenades, and larger weapons.
MECHANISM OF TOXICITY
The mechanism of biological activity is less well characterized for riot-control agents than for most other agents. Fortunately, a detailed knowledge of the mechanism of action is not necessary for appropriate medical management.
CS and CN are SN2 alkylating agents (mustard, in contrast, is an SN1 alkylator) and react readily at nucleophilic sites. Prime targets include sulfhydryl-containing enzymes such as lactic dehydrogenase. In particular, CS reacts rapidly with the disulfhydryl form of lipoic acid, a coenzyme in the pyruvate decarboxylase system. It has been suggested that tissue injury may be related to inactivation of certain of these enzyme systems.
Pain can occur without tissue injury and may be bradykinin mediated. CS causes bradykinin release in vivo and in vitro, and elimination of bradykininogen in vivo abolishes the systemic response to CS.
The initial response to aerosolized CS is an increase in blood pressure and irregular respiration, suggestive of the Sherrington pseudoaffective response. Bypassing the pain receptors of the nose and upper airway by endotracheal administration of CS leads to the same decrease in blood pressure and in respiration seen after intravenous injection. This suggests that the initial pressor effect and irregular respiration are responses to a noxious stimulus rather than pharmacological effects of CS.
The main effects of riot-control agents are pain, burning, and irritation of exposed mucous membranes and skin. These effects do not differ appreciably from one agent to another except in the case of DM, which will be discussed in a separate section.
Eyes: The eye is the organ most sensitive to riot-control agents. Contact with agent produces a sensation of conjunctival and corneal burning and leads to tearing, blepharospasm, and conjunctival injection. The severe blepharospasm causes the lids to close tightly and produces transient "blindness," an effect that could inhibit the recipient's ability to fight or resist. However, if the recipient opens his eyes, his vision is near normal even if a significant concentration of the agent persists.
Because these compounds are solids, it is possible for a particle or clump to become embedded in the cornea or conjunctiva to cause tissue damage. With the caveat noted below, there is no evidence that this complication has ever occurred; however, a recipient seeking medical care for eye pain after exposure should have his eyes thoroughly decontaminated and undergo thorough ophthalmic examination. It could be necessary to pick out the particles of agent from tissue.
Reviewers examined the evidence for permanent eye damage from riot-control agents. In each instance, the damage was from a weapon fired from close range (about 50% were self-inflicted). The reviewers concluded that the blast force driving the agent deep into tissue (with or without the wadding of the weapon) was the major cause of permanent injuries. This should not happen under normal use.
Nose and mouth: Contact with the delicate mucous membranes of the nose produces a burning sensation, rhinorrhea, and sneezing; a similar burning sensation accompanied by increased salivation occurs after contact with the mouth.
Airways: Inhalation causes burning and irritation of the airways with bronchorrhea, coughing, and a perception of a "tight chest" or an inability to breathe. However, pulmonary function studies done immediately after exposure have shown minimal alterations.
An inhaled irritating compound might be expected to exacerbate a chronic pulmonary disease such as asthma, emphysema, or bronchitis, but this appears not to happen after CS or CN, even though these agents have been used widely in mixed populations. The medical care provider should nevertheless anticipate airway problems in individuals with lung disease, particularly if they are exposed to higher than the average field use concentrations.
There is no evidence that CS causes permanent lung damage after one or several exposures to field concentrations. Following inhalation of lethal amounts, animals died from severe airway damage 12 to 24 hours post-exposure, but survivors from large exposures had minimal or no pulmonary abnormalities. After multiple (50 or more) daily exposures to smaller amounts, animals developed laryngitis and tracheitis.
Skin: Contact with the skin causes a tingling or burning sensation and may cause erythema, particularly if the skin is raw or freshly abraded (e.g., shortly after shaving). The erythema begins several minutes after exposure and generally subsides 45 to 60 minutes after termination of exposure.
Under conditions of high temperature, high humidity, and high concentration of agent, there may be more severe dermatitis starting with erythema hours after exposure and followed by vesication. Generally these are second-degree burns not unlike, but more severe than sunburn. Firemen who entered contaminated buildings after summer riots several decades ago developed these lesions. After stirring up the contaminating particles, they later developed erythema and blisters on their exposed skin. Hypersensitivity may develop. In one instance, an individual developed generalized vesication and high fever after an uneventful exposure to CS more than 20 years after his only and equally uneventful previous exposure.
Gastrointestinal tract: Gastrointestinal effects usually do not occur with most riot-control agents (DM is an exception), although there may be retching or vomiting if the agent concentration is high, exposure is prolonged, or the individual is sensitive.
Cardiovascular: A transient increase in heart rate and blood pressure has occurred in people immediately prior to an exposure to a riot-control agent or immediately after onset of exposure. The heart rate and blood pressure returned essentially to pre-test ranges while exposure continued and may have been caused by the anxiety or the initial pain rather than to a pharmacological effect of these agents. This "alarm reaction" may cause adverse effects in one with pre-existing cardiovascular disease.
Oral ingestion: Children occasionally eat CS, and several adults have swallowed CS pellets. Aside from bouts of diarrhea and abdominal cramps (which might have been from the cathartics and antacids used as therapy), their courses have been uneventful. In animals, the LD50 is about 200 mg/kg (which is about 14 grams/70-kg person), an amount unlikely to be ingested, even deliberately. A few animals fed lethal amounts (or greater) had gastric irritation or erosions, and several had signs of intestinal perforation. Recommended therapy after ingestion consists of cathartics, antacids, and surgical observation.
Lethality: CN, occasionally in combination with DM, has caused deaths in people who refused to exit a confined space. In each case the agent was used in excess. Death generally occurred hours after initial exposure, and post-mortem findings were those of severe airway damage similar to that seen in animals.
Metabolism: Animals given lethal amounts of CS by intravenous or intraperitoneal administration developed increased blood thiocyanate concentrations hours later, indicating that the malononitrile portion of CS had been metabolized to cyanide. Cyanide was not a factor in causing death (lung damage was). A significant increase in blood concentration of thiocyanate has not been noted after aerosol administration of CS. Several popular databases mention this cyanogenic potential of CS and suggest that treatment of a CS casualty might require therapy for cyanide poisoning (this recommendation is apparently based on the i.v. or i.p. administration data). After receiving lethal amounts of CS by inhalation, animals died 12 to 24 hours later from severe airway damage; cyanide was not implicated in their deaths.
The effects of usual field concentrations of DM are similar to those of the other riot-control agents, except that DM has little irritancy to the skin. However, at higher concentrations, DM causes nausea, vomiting, and a feeling of generalized malaise. For this reason, it is called a vomiting agent.
Except for those produced by DM, the biological effects from these agents begin seconds after exposure and continue for 15 minutes or so after one exits the contamination to fresh, clean air. The effects from DM begin two to four minutes after the onset of exposure and may last an hour or two. (This is advantageous militarily, as an individual unaware of the agent will continue to inhale it for several minutes and absorb a larger dose. He may then vomit, requiring mask removal, which leads to continued inhalation of agent.)
Usually the circumstances of exposure make the diagnosis obvious. The history and the few physical signs (conjunctival injection with normal pupils, tearing, etc.) are usually adequate. On a battlefield, the sudden onset of burning pain and irritation might lead one to consider Lewisite or phosgene oxime exposure, but the signs and symptoms of riot-control agents gradually recede, whereas those from the vesicants worsen.
There are no specific laboratory tests that will confirm the diagnosis. Complications, e.g., infection of a skin lesion, will produce the laboratory findings characteristic of the complication.
The effects of exposure to these agents under the usual field conditions generally are self-limiting and require no specific therapy. Most will disappear in 15 to 30 minutes, although erythema may persist for an hour or longer.
The following section discusses potential complications occurring only under exceptional circumstances, such as exposure to a very large amount of agent (as in an enclosed space), exposure in adverse weather, or experimental studies in humans or animals. They are not to be expected with normal use of these agents.
Less than 1% of exposed people will have effects severe or prolonged enough to cause them to seek medical care. Those who do probably will have eye, airway, or skin complaints. Because there is no antidote for these agents, treatment consists of symptomatic management.
Eyes: The eye should be carefully flushed with water or saline, and impacted particles should be sought. General care consists of a topical solution (many are available) to relieve the irritation and topical antibiotics. An ophthalmologist should be consulted for further evaluation and care.
Pulmonary: These agents may exacerbate chronic disease or unmask latent disease (although there is little evidence of this). Bronchospasm with wheezing and mild distress continuing hours after exposure may occur in a latent asthmatic. More severe effects and respiratory distress may occur in one with chronic bronchitis or emphysema. Management includes oxygen administration (with assisted ventilation, if necessary), bronchodilators if bronchospasm is present, and specific antibiotics dictated by the results of sputum studies (Gram stains of smears followed by culture). A specialist skilled in the treatment of inhalation injury should be consulted early. Animal studies and very limited human data indicate that maximal effects occur 12 hours after exposure.
Skin: The early erythema requires reassurance, but no specific therapy unless severe and prolonged more than an hour or two. The later onset erythema precipitated by a larger exposure in a hot and humid atmosphere is usually more severe and less likely to resolve quickly. It may require the use of soothing compounds such as calamine, camphor, and mentholated creams. Small vesicles should be left intact, but larger ones will ultimately break and should be drained. Irrigation of denuded areas several times a day should be followed by the application of a topical antibiotic. Large, oozing areas have responded to compresses containing substances such as colloidal oatmeal, Burrow's solution, and other dermatologic preparations.
A person exposed to the usual field concentrations of riot-control agents will probably not be seen at a triage area. Those presenting with complications should be triaged according to the nature of their injuries.
Because the effects of field concentrations clear within minutes, the casualty should be returned to duty as soon as possible. Casualties with complications may require evacuation and further medical treatment before returning to duty.
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Introduction |
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