Medical Aspects of Chemical Warfare (2008) - The Black Vault

Medical Aspects of Chemical WarfareINTRODUCTIONThe 1993 Chemical Weapons Convention treatydefines riot control agents (RCAs) as agents that canrapidly produce sensory irritation or disabling physicaleffects in humans that disappear within a short timefollowing termination of exposure. 1 More specifically,these are chemical agents that are designed to causetemporary incapacitation of the individual throughintense irritation of tissues and the creation of a strongsensation of discomfort, including difficulty breathingand pain, without causing long-term disabilityor death. These disabling physiological effects occurwhen RCAs come into contact with the sensory nervereceptors at the site of contamination, resulting in localpain and discomfort with associated reflexes.RCAs include chemicals from the following pharmacologicalclasses: irritants, lachrymators, sternutators,emetics, sedatives, hypnotics, serotonin antagonists,hypotensives, thermoregulatory disruptors, nauseants,vision disruptors, neuromuscular blockers, andmalodorous substances. 2 They are considered harassingagents, nonlethal or less than lethal agents, and althoughnot gases, they are usually referred to as tear gas. 3 RCAsare relatively safe to use, especially when used in theopen air, but have been known to cause death on occasion,particularly when used in close confines with inadequateventilation or when the exposed individual waspredisposed to cardiorespiratory compromise throughdisease or heavy intoxication with drugs or alcohol.Like other chemical agents, RCAs are designated withNorth Atlantic Treaty Organization (NATO) letter codesto label and help distinguish them. The agents coveredin this chapter are those that have been used, or allegedlyused, since World War II; their chemical names andrespective NATO codes are o-chlorobenzylidene malononitrile(CS); oleoresin capsicum (OC); chloropicrin(PS); 1-chloroacetophenone (CN), diphenylaminearsine(DM), and dibenz(b,f)(1,4)oxazepine (CR).Characteristics common to all of the agents discussedin this chapter are• a rapid time of onset of effects (seconds to afew minutes);• a relatively brief duration of effects (15–30minutes) in most cases, once the exposedindividual exits the contaminated area and isdecontaminated (ie, the material is removedfrom the victim’s clothing and skin); and• a high safety ratio, that is, a relatively lowdose of these agents is needed to cause tissueirritation or pain (effective dose or effectiveconcentration), but a significantly larger doseis required to cause death (lethal dose or lethalconcentration, LCt 50). 2–4This chapter will cover only RCAs that have beenpurposefully or allegedly used in recent history. Becauseof their prevalent use, CS and OC will be coveredin greater detail than other agents.Although the effects differ slightly among thevarious agents, all RCAs cause some form of eye irritationinvolving lacrimation and blepharospasm,which causes the eyes to close temporarily, renderingvictims unable to see and dramatically reducingtheir ability to resist. PS, CN, CS, CR, DM, and OCalso cause irritation to airways resulting in coughing,shortness of breath, and retching or vomiting. 3 DM ineffective doses causes significant vomiting with resultingmental depression and malaise. These agentscause some degree of pain sensation either throughirritation of peripheral nerve endings in tissue, suchas the mucous membranes and skin (PS, CN, CS, CR),or by causing the sudden release of neurotransmitters,such as bradykinin or substance P, which signal thesensation of intense pain (OC). 2The reflex most associated with death from theinhalation exposure of irritants is the Kratschmer reflex,first reported in 1870 as the immediate responseof apnea or cessation of respiration in rabbits followingexposure to chemical irritants such as chloroformand carbon dioxide. 5 The response is a protectivereflex or defense mechanism to prevent or reducethe amount of noxious chemical reaching the lowerrespiratory tract and maintain homeostasis. Accompaniedby bradycardia and a biphasic fall and rise inaortic blood pressure, the reflex is mediated by theolfactory (I), trigeminal (V), and glossopharyngeal(IX) cranial nerves. It has also occurred in rodent andcanine experiments following exposure to volatilesolvents and was demonstrated to occur in humans. 6The cardiopulmonary receptors involved in the reflexprevent the absorption and distribution of the inhaledirritant to the vital organs, as well as facilitating theexpulsion of the irritant, and the extracardiopulmonarymechanisms promote metabolism and excretion of theabsorbed chemical. These effects have been describedby Aviado and Salem and by Aviado and Aviado. 7–9During apnea or cessation of respiration, blood levelsof carbon dioxide increase and drive the respiratorycenter to restart breathing. Individuals with compromisedimmune systems, nervous system depressionas a result of alcohol or illicit drug consumption, or acombination of these, may not be able to restart respirationand die from asphyxia. The Kratschmer reflexmay be responsible in part for some in-custody deathsattributed by law enforcement agencies to positionalasphyxia following the initial use of pepper sprays inthe United States in the early 1990s. 2442