Chapter 12
Physical Characteristics
Clinical Effects

Physical Characteristics
Clinical Effects

DM (Diphenylaminearsine)
CR (Dibenz(b,f)
CA (Bromobenzylcyanide)

Respiratory Tract
Cardiovascular System

*Formerly, Chief, Chemical Casualty Care Office, and Director, Medical Management of Chemical Casualties Course, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010-5425; currently, Chemical Casualty Consultant, 14Brooks Road, Bel Air, Maryland 21014 Medical Aspects of Chemical and Biological Warfare INTRODUCTION
Riot control agents are compounds that cause organs affected. The eyes, nose, and respiratory tract temporary incapacitation by irritation of the eyes are the primary organs affected, although the skin (tearing and blepharospasm), causing them to close, is also often involved. The compounds produce and irritation of the upper respiratory tract. They temporary disability because the extreme eye irri- are often called irritants, irritating agents, and ha- tation and blepharospasm cause the eyes to close rassing agents; the general public usually calls them temporarily, and the irritation of the airways causes tear gas. Like most of the other chemical agents dis- coughing, shortness of breath, and sometimes retch- cussed in this textbook, riot control agents are ing or vomiting. One of these compounds, DM, is known by two-initial designators that are neither noted for also causing vomiting and malaise.
abbreviations nor acronyms of their chemical names The United States does not recognize riot con- but are most akin to code names. Hence an expla- trol agents as chemical warfare agents as defined nation of the derivations of the names is usually in the Geneva Convention of 1925. The Geneva Gas Protocol of 1925 was ratified by the United States Three types of riot control agents are recognized: on 22 January 1975. At that time, the United States lacrimators, which primarily cause lacrimation and interpreted the protocol as prohibiting the first use eye irritation; sternutators, which mainly cause of lethal chemicals, but not of nonlethal ones such sneezing and irritation of the upper respiratory as riot control agents or herbicides.
tract; and vomiting agents, which additionally During the Vietnam War, before the protocol rati- cause vomiting. Because these compounds—CS, fication, the United States had used the riot control CN, DM, CR, and CA—have a number of charac- agent CS (o-chlorobenzylidene malononitrile) exten- teristics in common, they are grouped together as sively. On 8 April 1975, President Ford signed Ex- riot control agents in this chapter. The small dis- ecutive Order 11850, which unilaterally renounced tinctions among them are noted in the discussion first use of riot control agents in armed conflict, with of each agent. Table 12-1 lists the chemical, physi- specified exceptions. These exceptions include first cal, environmental, and biological properties of the use for riot control in areas under direct U.S. mili- three major agents: CS, CN, and DM. Characteris- tary control (including control of rioting prisoners tics common to all compounds in this category are of war), use in rescue operations, use in situationsin which civilians screen or mask attacks, and use • a rapid time of onset of effects (seconds to in rear echelons to protect convoys from terrorists or similar groups. Presidential approval is required • a relatively brief duration of effects (15–30 in advance for either first or retaliatory use of riot min) once the victim has escaped the con- Of all the compounds discussed in this book, riot control agents are perhaps the most scrutinized by the public. In civilian life, law enforcement agen- • a high safety ratio (the ratio of the lethal cies use riot control agents in civil disturbances, dose [estimated] to the effective dose).
riots, or to avoid using deadly force. The militarycommonly uses them in training. The symptoms Riot control agents all produce effects by sensory described below, therefore, will be familiar to most irritation, causing extreme discomfort or pain in the Irritant compounds were allegedly used by Modern use probably began in the 1910–1914 pe- Marcus Fulvius against the Ambracians in the sec- riod, when ethylbromoacetate was employed against ond century BC. The Byzantines apparently knew criminals by French police. At the beginning of World of the efficacy of using irritant substances to harass War I, some of these former policemen, who were then the enemy. Plutarch described a Roman general who in the French army, began to use some of these muni- used an irritant agent cloud in Spain to drive the tions on the battlefield with some degree of success.
enemy out of concealment in caves,1 a use similar to Although the German use of chlorine at Ypres, Bel-
that of the United States in Vietnam 2,000 years later.
gium, on 22 April 1915 is generally heralded as the TABLE 12-1
Malononitrile (CS)
0.0041 mm Hg at approx 20°C 4.5 x 10-11 mm Hg at 25°C Fragrant (like apple blossoms) Yellow-green, odorless, *Compared with the density of airLCt50: the concentration • time (Ct) that is lethal to 50% of the population exposed ICt50: the Ct that incapacitates 50% of the population exposed beginning of chemical warfare on the modern battle- a riot control agent was widely used in the Vietnam War.
field, irritating substances had already been in use for Riot control agents gained some notoriety when about a year. During World War I, approximately 30 they were used in civil disturbances in Paris, France, different compounds were tried for their irritant ef- in 1968; in Londonderry, Northern Ireland, in fects, usually without much success.2 As noted above, 1969; in several protest demonstrations in the Medical Aspects of Chemical and Biological Warfare United States in the late 1960s; and in prison riots.
many years and is commercially available in devices More recently, riot control agents were used in an for self-protection under its proprietary name, Mace unsuccessful attempt to drive the Branch Davidians (the chemical, not the devices, is manufactured by from their compound near Waco, Texas, in Febru- General Ordnance Equipment Corp., Pittsburgh, Pa.). CS is the compound that is used by the mili- Probably the best known of these compounds is tary in most countries and almost exclusively by CN (1-chloroacetophenone); it has been used for law enforcement agencies throughout the world.
ing the mid 1960s, hydrophobic formulations of CS, CS1 and CS2, were developed. The former is a mi- cronized powder with 5% hydrophobic silica aero- gel; the latter is a siliconized, microencapsulated form of CS1. CS1 and CS2 last for several weeksand are a persistent hazard during military opera- tions. Because of their persistence, they have notbeen used for civil disturbances.
The riot control agent known as CS (o-chloro- Clinical Effects
benzylidene malononitrile) was first synthesized in1928 by Corson and Stoughton (hence its code Clinical effects common to all of these riot con- name). It replaced CN as the standard riot control trol agents are listed in Exhibit 12-1. In the eye, an or irritant agent in the U.S. Army in 1959. In the initial burning feeling or irritation progresses to late 1950s, CS was also adopted by most U.S. law pain accompanied by blepharospasm, lacrimation, enforcement agencies and by the military and law and conjunctival injection. The intense blepharo- enforcement agencies of other countries, because CS spasm causes the eyes to close. Photophobia is of- is more effective than CN (it causes effects at lower ten present and may linger for an hour. The mu- doses) and is less toxic (ie, its LCt50, the vapor or cous membranes of the mouth, including the tongue aerosol exposure [concentration • time] that is le- and palate, have a sensation of discomfort or burn- thal to 50% of the exposed population, is higher).
ing, with excess salivation. Rhinorrhea is accompa- nied by pain inside the nose and perhaps around Physical Characteristics
the external nares. When inhaled, these compoundscause a burning sensation or a feeling of tightness CS is a white, crystalline solid with a low vapor in the chest, with coughing, sneezing, and increased pressure. It is almost insoluble in water and only secretions. On unprotected skin, especially if the air slightly soluble in ethyl alcohol and carbon tetra- is warm and moist (see skin effects of CS), these chloride. Because of these physical characteristics, agents cause tingling or burning; within a few min- decontaminating buildings, furniture, and other utes, erythema may develop at the exposed sites.
material after CS use in urban riots is difficult. Dis-semination of CS can be by explosive dispersion of Tolerance to Exposure
a powder or solution, by dispersion of the powderin a fine state, by spraying a solution, or by releas- Typically, effects appear within seconds of expo- ing as smoke from a pyrotechnic mixture.3 The sure to an aerosolized compound and worsen as method of dissemination may influence the sever- long as one remains in the cloud. Most effects slowly ity of the injury (see eye injury for CN). The Mate- dissipate, starting within a few minutes after one rial Safety Data Sheet, which the manufacturer in-
leaves the contaminated area. By 30 minutes, most cludes in each package, assigns it a flammability effects have completely abated, although the usu- rating of 4 (on a scale of 0 to 4). The agent was a ally mild erythema may persist for 1 to 2 hours. If large contributor in the conflagration that burned one does not leave shortly after the onset of irrita- the Branch Davidian compound and its inhabitants tion, the effects might become more severe, with marked coughing, gagging, retching, and vomiting.
CS tends to agglomerate when used and resists Most individuals note marked harassment at a weathering poorly (losing its effectiveness). Dur- concentration of 3 to 5 mg/m3 and leave the area ing, but voluntarily returned for the remainder of EXHIBIT 12-1
the period). Individuals did not develop toleranceto the compound after ten exposures of 1 to 13 mg/ CLINICAL EFFECTS OF RIOT CONTROL
Duration of tolerance was reduced in exercising individuals, presumably because of deeper breath- ing and deeper penetration of the particles into thelung, and chest symptoms were more pronounced than when the subjects were exposed while resting.
An increase in tolerance was noted when the tem- perature was low (–18°C; 0°F); a slight decrease in tolerance occurred in a hot environment (36°C). Skin symptoms (such as a burning sensation) were more prominent at the hot temperature than at moderate One might expect that personality and mental set could determine tolerance to CS; a dedicated hijacker, for example, might be able to resist its effects. To test for a correlation between personality and tol- Gastrointestinal Tract
erance to an irritant compound, a group of men were exposed to CS, then tested on the Minnesota Multiphasic Personality Inventory (MMPI).6 Those individuals with less tolerance to CS were charac- terized by the MMPI by greater use of denial, re- pression, and somatic complaints than the moretolerant group. Furthermore, the more tolerantgroup had a higher mean general intelligence score(127 compared with 100 for the less tolerant group).
as soon as possible.4 Tolerance develops, however, In a similar study,7 subjects with high scores clas- in those who have been in close contact with CS for sified as abnormal on certain MMPI scales tolerated a period of time, such as production or laboratory less CS than did subjects with normal scores. After workers. Those who have developed tolerance can the administration of diazepam, the tolerance to CS stay in their accustomed concentration of CS and was significantly increased in the group with ab- the discomfort does not increase, and, in fact, may normal scores, but not in the group with normal decrease. Those who work in a CS environment and scores. This result suggests that anxiety, which was get CS on their clothing often become so accus- reduced more by diazepam in the group with ab- tomed to its effects that they wear the clothing out normal scores, plays a role in tolerance.
of the area without remembering, only to have oth-ers complain.
Respiratory Tract Effects
Tolerance was examined experimentally in an early study5 in which men were placed in a concen- Inasmuch as CS is usually disseminated as an tration of 0.43 mg/m3; the concentration was slowly aerosol (powder or in solution), the most common increased to 2.0 mg/m3 over 60 minutes. If the men route of absorption is by inhalation. In an LCt50 were able to withstand the initial effects, they could study,8 four species (rat, rabbit, guinea pig, and remain at the higher concentration. During this time, mouse) were exposed to aerosolized CS powder for some subjects played cards and two attempted to read.
5 to 60 minutes. The LCt50 values (based on mor- In a similar study,4 when four subjects were ex- tality within 14 d) ranged from 50,010 mg•min/m3 posed to a low concentration that was increased to (in the mouse) to 88,480 mg•min/m3 (in the rat).
6 mg/m3 over 10 minutes, three subjects left before No animal died during exposure; most of those that the time was up. In contrast, when the same sub- died afterwards did so within 2 days. The lungs of jects were exposed to the same low concentration those dying were congested and edematous, and that was slowly increased to 6 mg/m3 over a 30- many had hemorrhages. The trachea was congested minute period, three remained for 30 more minutes with moderate amounts of mucus. On microscopi- (the fourth subject left after 2 min because of cough- cal examination, moderate to marked congestion of Medical Aspects of Chemical and Biological Warfare alveolar capillaries and intrapulmonary veins, in- 48 animals) within 48 hours in the 750-mg/m 3 ter- and intraalveolar hemorrhages, and excess se- group, and only two deaths (in 240 animals) oc- cretions in the smaller airways were seen. Animals curred in the 150-mg/m3 group. In these animals that died after 48 hours also had evidence of early and in those sacrificed at 24 hours and onward, bronchopneumonia. Those that survived for 14 days had normal lungs on gross and microscopic exami- In a continuation of this study,9 rats were exposed to CS at 1,000 to 2,000 mg/m3 for 5 minutes per day Pyrotechnically dispersed smoke from a CS gre- for 5 days. None of the rats died. Minimal patho- nade was used in a similar study design with the logical changes were found on sacrifice of the ani- same four species.9 At high concentrations and ex- mals, but 5 of 56 had bronchopneumonia. A group posure times of 5 to 20 minutes, the LCt50 values of 50 rats was exposed to a concentration of 12 to (based on mortality within 14 days) ranged from 15 mg/m3 for 80 minutes daily for 9 days.9 Five rats 35,000 mg•min/m3 (in the guinea pig) to 76,000 died from bronchopneumonia and on sacrifice, 5 of mg•min/m3 (in the mouse). No animal died dur- the remaining 45 rats were found to have broncho- ing exposure, and only two died within 12 hours of removal from the chamber. With concentrations In a long-term study,10 mice were exposed to 3 or ranging from 31.9 to 56.4 mg/m3 and a 5-hour per 30 mg/m3 of CS for 60 minutes per day for 55 ex- day exposure for 1 to 7 days, the LCt50 values (14- posures and then observed for 6 months longer. A day mortality) were from 25,000 mg•min/m3 (rat) daily exposure of 192 mg/m3 for 60 minutes per day was stopped after three exposures because of The lungs of animals that died before 14 days deaths. Rats and mice were also exposed to these were edematous and congested, with areas of hem- doses daily for 120 days; daily exposure at 236 mg/ orrhage and excessive amounts of mucus in the tra- m3 was stopped after 5 days. At the two low con- chea and bronchi. The alveolar capillaries and in- centrations (3 and 30 mg/m3), the number of deaths trapulmonary veins were congested, with areas of over the year of study did not exceed the number alveolar hemorrhages and hemorrhagic atelectasis.
of deaths in control groups, which were exposed to A few had edema, but no inflammatory cell infil- air in the exposure chamber daily. After a year, mice tration was noted. In addition, most animals had evi- receiving 30 mg/m3 had a statistically significant dence of circulatory failure, with dilated right ven- increase in chronic laryngitis and tracheitis, but oth- tricles and enlarged livers, kidneys, and spleens.9 erwise the pathological findings for these animals Animals that survived 14 days had no abnormali- were not different from those of the control group.
ties on pathological examination. The investigators In particular, no relationship was found between pointed out that the presence of pulmonary edema specific tumors and the total dose of CS.
and hemorrhages in the absence of inflammatorycell infiltration suggests that the smoke caused di- Dermatological Effects
rect injury to the pulmonary capillary endotheliumand that the main cause of death was pulmonary CS is a primary irritant to the skin. In addition, damage. They also commented that, because of the individuals may develop allergic contact dermati- agglomeration of the smoke particles and subse- tis after an initial, uneventful exposure to it.
quent precipitation of the compound, concentra- Typically, several minutes after an acute expo- tions as high as those used could not be maintained sure to a low concentration of CS, a prickly feeling or burning is felt in exposed areas of skin. This sen- Two hundred sixty-four rats and 250 hamsters sation is more noticeable if the skin is wet or freshly were exposed to CS concentrations of 750, 480, or abraded (eg, after shaving). The sensation may be 150 mg/m3 for 30, 60, or 120 minutes, respectively accompanied or followed by erythema, which usu- (the calculated Ct values were 22,500, 28,800, and ally persists for an hour or less. Under certain cir- 18,000 mg•min/m3, respectively). Only one animal cumstances—involving the amount of CS, the tem- died in the first 6 hours after exposure; 33 died perature, and the humidity—a more intense within 48 hours, and 31 of these were in the 480- erythema may follow about 2 hours later. If the mg/m3 (60-min) group. Those dying within 48 amount of CS, the temperature, and the humidity hours had moderately severe congestion in the are all high, the erythema becomes even more se- lungs, with alveolar hemorrhage and edema in vere, and edema and vesication appear hours later.
some. Acute tubular necrosis was present in some The time course is the same as that for the skin dam- of the animals. In contrast, no deaths occurred (in To test the effects of CS on human skin, the arms tive humidity), all four subjects had minimal de- of volunteers were exposed to high concentrations layed erythema at Ct values of 26,025 or 30,240 of CS thermally generated from an M7 grenade.11 mg•min/m3. In contrast, at the tropical conditions, The exposure was at a temperature of 36°C and the effective Ct for producing delayed erythema humidity of 100%; the average concentration was 300 mg/m3, and exposure times ranged from 15 to The authors of the study pointed out that many 60 minutes. All subjects noted stinging about 5 min- variables make it difficult to predict which indi- utes after onset of exposure. After being withdrawn viduals might be more sensitive than others. Among from the apparatus, the arms were rinsed with cold, these variables are skin pigmentation, eye color, running water to remove the powder that clung to complexion, and susceptibility to sunburn.12 hairs; this procedure caused the stinging to increase.
Although the conditions of these studies were Ct values of 4,440 and 9,480 mg•min/m3 caused severe, serious skin reactions can occur under an immediate skin response: a patchy, vascular milder, more common conditions. First- and second- erythema, which subsided after 30 minutes with no U.S. Army Chemical Corps officers on a field exer- Ct values of 14,040 and 17,700 mg•min/m 3 cise.13 Temperature and humidity were high, it had caused a more severe initial dermal response, which been raining heavily, and their uniforms were required 3 hours to disappear. After 12 to 24 hours, soaked through. The officers, who were wearing a delayed reaction, consisting of first- and second- fatigues, ponchos, and M17 protective masks, were degree burns, appeared. Blistering occurred in four hit with a cloud of micropulverized CS1 from a dis- of the eight subjects (Figure 12-1). With treatment perser; soon afterwards, they noted burning of their (discussed below), these lesions resolved in 10 to unprotected skin. About 2 hours later, some of the 14 days; by 6 weeks later, a small amount of post- men hosed off and some changed clothes, but most did neither. About 14 to 16 hours after exposure, By means of a sleeve with removable patches, blistering began, and all of the men who had not arms of volunteers in another study12 were exposed hosed off or changed clothes eventually developed to CS thermally generated from an M7 grenade. The patches were removed at appropriate times to give Firemen in Washington, D. C., were frequently Ct exposures of 1,550 to 33,120 mg•min/m3 at tropi- exposed to CS during the riots of April 1968; in ad- cal conditions (37°C; 98% relative humidity) or at dition, they were exposed to CS as they entered one of three temperate conditions (14°C and 41% buildings in which CS had been disseminated. The relative humidity; 20°C and 95% relative humidity; CS on floors or furniture was reaerosolized both by 22°C and 72% relative humidity). No subjects at their movement and by the force of water from their 14°C or 22°C had the delayed erythema at Ct val- hoses. They later developed erythema and edema ues of up to 25,560 mg•min/m3. At 20°C (95% rela- of periorbital skin and other exposed areas.14 Fig. 12-1. (a) Erythema 25 hours after exposure to a high Ct (the product of concentration of vapor or aerosol • time
of exposure; in this instance, 14,040 mg•min/m3) of CS at 97°F and 100% humidity. (b) The same skin lesions at 45
hours, with vesication. Reprinted from Hellreich A, Goldman RH, Bottiglieri NG, Weimer JT. The Effects of Thermally-
Generated CS Aerosols on Human Skin.
Edgewood Arsenal, Md: Medical Research Laboratories; 1967: 19. Technical
Report 4075.
Medical Aspects of Chemical and Biological Warfare Earlier investigators reported vesication after CS with the solution and least severe with the smoke.
patch testing.4 They also mixed CS with sodium After exposure to the smoke, the eyes had a tran- hypochlorite (household bleach) and found that in sient, slight excess of lacrimation and congestion all subjects tested, the product caused a reaction that of conjunctival vessels lasting 24 hours; the tissues was much more severe than that produced by CS were normal when examined 7 days later.
alone. For that reason, hypochlorite is not recom- The solid (0.5–5.0 mg) caused lacrimation at all mended for decontamination of CS on skin. (A hypo- doses, blepharitis that increased with dose and chlorite is successfully used as a decontaminant for lasted up to a week, and chemosis at 5 mg, which was mild and lasted 3 days. Minimal iritis and CS is a primary irritant and causes contact der- keratitis, of 24 hours’ duration, were seen in two of matitis, typically in workers in CS-manufacturing five animals receiving 5 mg. At concentrations of or -packing plants. A reaction is more common in 1% and higher, CS in solution caused conjunctivitis warm weather and high humidity or in sweating and iritis, chemosis, keratitis, and corneal vascu- subjects. The lesion begins some hours after expo- larization; the lesion was more severe and lasted sure as an erythema, with burning and stinging; the longer with the higher doses. Histological examina- area becomes edematous at about 24 hours, then tion indicated patchy denudation of corneal epithe- vesicles or bullae may appear. Common sites are lium and a neutrophilic infiltration of the cornea.17 those of partial occlusion, such as the areas under Reports of severe eye injuries from riot control the cuff or glove and under the shirt collar.
agents have involved the agent CN. They are dis- CS is also a sensitizer and can cause allergic con- tact dermatitis, which is the result of a delayed hy-persensitivity reaction. An initial exposure may not Gastrointestinal Tract Disturbances
cause a reaction, but a later exposure to even a smallamount produces an often severe dermatitis, with A handful of instances in which an individual erythema, edema, vesication, and, in severe in- ate CS are known. In all but two cases, children were the victims. Typically, they were playing in an old Differentiation of the two reactions—primary impact area on a military installation and came irritant dermatitis and allergic contact dermatitis— across some shells containing a powdery substance, is often difficult clinically and usually requires which they ate. One adult ingestion was an attempt at suicide by an otherwise healthy young man; theother was an individual who ate a CS pellet (820 Ophthalmological Effects
mg) after a friend told him it was a vitamin pill.18 The oral LD50 (dose that is lethal to 50% of the The eye is a sensitive target organ of riot control exposed population) of CS was found to be 143 mg/ agents. In studies14,15 on humans, CS (0.1% or 0.25% kg in the female rabbit, the most sensitive of three CS in water; 1.0% CS in trioctyl phosphate), when species studied (the rat, about 1,300 mg/kg; the placed or sprayed into the eyes, caused inability to guinea pig, 212 mg/kg; and the male rabbit, 231 open the eyes for 10 to 135 seconds. A transient con- mg/kg).8 The animals that died had multiple, ex- junctivitis but no corneal damage as assessed by tensive hemorrhagic erosions of the gastric mucosa, with perforation of the wall, and a few had in- In another study,16 subjects were exposed to CS2 creased peritoneal fluid. In those surviving for sev- (powder dispersal) or CS powder (thermally dis- eral days, intraabdominal adhesions were found.
seminated) at 0.1 to 6.7 mg•min/m3 for 20 seconds After male rats and female guinea pigs received 0.5 to 10 minutes. Their visual acuity was tested at in- LD50 of CS by stomach tube, and male rabbits re- tervals during and after the exposure. Subjects who ceived 0.3 LD50 by this route, the incidence of wet could keep their eyes open during the exposure to or runny stools was no greater than that for the con- read the chart had minimally impaired visual acu- trol vehicle, polyethylene glycol 300 (PEG300).19 The ity, and no appreciable change in acuity from investigators concluded that diarrhea is not an effect of ingested CS. They also suggested that riot- In an investigation of the ophthalmic toxicity of ers would not have diarrhea from CS exposure, CS,17 rabbit eyes were contaminated with CS in so- since they would be unlikely to swallow this much, lution (0.5%–10% in polyethylene glycol), as a solid, but that an intensely emotional experience such as and as a pyrotechnically generated smoke (15 min- being in a riot may itself be a cause of disturbed utes at 6,000 mg/m3). The effects were most severe bowel function. In another study,20 the oral LD50 varied widely in rats (178–358 mg/kg), depending than the lethal Ct do not die during exposure or on the solvent used. After death, moderate to severe immediately afterwards, but many die hours later, gastroenteritis was noted on gross examination.
in contrast to the usually rapid death caused by cya- No deaths or severe complications in humans nide. Moreover, the lung damage found on patho- from ingestion of CS are known. The young man logical examination is adequate to explain death.8,9 mentioned above who had attempted suicide by CS In addressing this issue, a British report3 suggests ingestion was given large amounts of what were that whereas cyanide might be a causative factor in described as “saline cathartics” and over the next the rapid deaths occurring after intravenous admin- 24 hours had repeated episodes of severe abdomi- istration, it is not a factor in death after aerosol ad- nal cramps and diarrhea; whether these symptoms ministration. If one were to absorb completely all were due to the illness or the treatment is unknown.
the CS during a 1-minute exposure at 10 mg/m3, A surgical team examined the patient early and and if both cyanides on the molecule were liberated— stood by during the acute phase. The patient recov- and evidence suggests that only one is liberated—the ered uneventfully. The adult who ate a CS pellet total amount of cyanide received would be equiva- was given liquid antiacid and viscous lidocaine lent to that received from two puffs of a cigarette.
orally and droperidol intravenously. He vomitedtwice, had six voluminous watery bowel move- Other Physiological Responses
ments without blood, and otherwise recovered un-eventfully. Blood cyanide was less than 1 µg/dL 18 When subjects were exposed to CS concentra- hours after ingestion (see section on metabolism).18 tions of 1 to 13 mg/m3 daily for 10 days, their air-way resistances, measured 2 to 4 minutes after the Metabolic Effects
fourth and tenth exposures, were unchanged fromthe preexposure values.4 Tidal volume, vital capac- Both in vivo and, in water, in vitro, CS ( o- ity, and peak flow in 36 subjects also were un- chlorobenzylidene malononitrile) is hydrolyzed to changed when they were measured immediately 2-chlorobenzaldehyde and malononitrile. Malono- nitrile contains two cyanide moieties, and it is Heart rates of subjects were lower immediately thought that at least one of these is liberated and after exposure compared with preexposure values.4 attaches to sulfur via the enzyme rhodanese to form Subjects entered a chamber of CS with masks on; thiocyanate, which is excreted in the urine.
immediately on removing their masks, their mean Some authors have suggested that cyanide con- blood pressure increased by 20 mm Hg systolic and tributes to mortality in CS-caused deaths.21,22 In dogs 11 mm Hg diastolic. After they had remained in the given CS by the aerosol or intravenous routes, the CS for 20 minutes, however, their blood pressures plasma concentrations of thiocyanate increased over were comparable to the preexposure values.4 The the following 24 to 48 hours, presumably because of blood pressures of subjects drenched with dilute transformation of the liberated cyanide to thiocyan- solutions of CS were transiently elevated to about ate by combination with endogenous sulfur.21 Af- ter CS was given intraperitoneally, the mortality After daily exposures to CS for 10 days, seven was markedly decreased by the intravenous admin- subjects had no alterations in blood sodium, potas- istration of thiosulfate, which may have provided sium, alkaline phosphatase, or bromsulfophthalein; additional sulfur for the transformation of cyanide to one of the seven had an increase in thymol turbid- thiocyanate.21 Also, after intravenous administration ity. No chest radiograph or urinary changes were of CS or malononitrile, the signs and the times to death seen. 4 In another study, 5 although significant were similar (15–60 min), suggesting that both caused changes were seen in some blood chemistries after effects by the same mechanism.22 In this report, the exposure, all values were within the normal range.
authors also noted the similarities of signs and times Pregnant rats and rabbits were exposed to CS of death for these two compounds, compared with aerosols at concentrations of 6, 20, or 60 mg/m3 for 5 minutes on days 6 to 15 and 6 to 18 of gestation, One author of the latter report, however, clearly respectively. In addition, rats were given CS (20 notes in a later communication23 that the mode and mg/kg) intraperitoneally on days 6, 8, 10, 12, and time of death differ depending on whether CS is 14 of gestation. No embryolethality or teratogenic- administered by the intravenous route or by aero- sol. As noted earlier in the discussion of respira- CS and some of its metabolites were found not tory effects for CS, animals exposed to far greater to have mutagenic effects in the Ames Salmonella Medical Aspects of Chemical and Biological Warfare typhimurium assay with microsome supplement- row erythrocytes of mice exposed to CS. 27 The ation.26 In addition, no mutagenic effects were authors of another study28 of rats and Salmonella found in assays for reverse mutations in S typhim- concluded that CS did not induce point mutations urium after exposure to CS, in assays for sex-linked, or carcinogenic processes mediated by DNA bind- recessive lethal mutations in sperm cells after Dro- ing. However, CS did give a positive response in the sophila were fed CS, or in chromosomes of bone mar- forward mutation assay in mouse lymphoma cells.29 CN (1-CHLOROACETOPHENONE)
trachea, bronchi, and bronchioles; and more evi-dence of early bronchopneumonia.
Dermatological Effects
A textbook published in 1925 states that CN in Physical Characteristics
field concentrations does not damage human skin;however, the powder might produce burning: Like CS, the riot control agent known as CN (1- “slight rubefaction, and sometimes small vesicles chloroacetophenone) is a solid or powder and can appear.” 31(p171) Early cases of CN dermatitis—one of be disseminated as a smoke generated from a gre- primary irritant dermatitis in a soldier and three in nade or other device, or in powder or liquid for- civilian employees who probably had allergic der- mulations. Under the trade name Mace, it is in most matitis from working around CN for years—were devices sold for self-protection, although today it is commonly mixed with or is being replaced by A severe allergic reaction to CN developed after a 43-year-old military recruit went through the CN was first synthesized by Graebe in 1871 and CN training chamber routine (ie, an individual was used in World War I. Before the late 1950s, it spends 5 min in the chamber masked, then re- was the standard tear gas used by the military and moves the mask and exits the chamber). Within 5 minutes after exiting, the patient complained of The harassing concentration for CN is about 10 generalized itching, which became progressively mg/m3, compared with about 4 mg/m3 for CS. It is worse over the following hours. Four hours after more toxic than CS, and the human LCt exiting, he had a diffuse and intense erythema over lethal Ct) has been estimated to be 7,000 mg•min/ his entire body except his feet and the portion of m3 for pure aerosol and 14,000 mg•min/m3 for a his face covered by the mask. His temperature was 38.9°C (102°F) and rose to 39.4°C (103°F) the nextday. By 48 hours after exposure, he had vesication Clinical Effects
and later developed severe subcutaneous edemathat “strikingly altered the appearance of the In general, the clinical effects caused by CN are face”33(p1879) and severe generalized itching. Over the the same as those caused by CS. The harassing dose next 4 days, the signs subsided, and desquamation, is higher and CN is more toxic and more likely to which was profuse at day 6, gradually decreased.
cause serious effects, particularly in skin and eyes The patient had developed itching during a tear gas (see below). Most effects from exposures to a low exercise 17 years previously but had not been ex- concentration will disappear within 20 to 30 minutes.
A police officer received an initial exposure to Respiratory Tract Effects
CN and 5 years later, on repeated exposure, devel-oped recurrent attacks of what was probably aller- In studies parallel to those described above for gic contact dermatitis. The source of the repeated CS, CN was found to be 3- to 10-fold more toxic exposures was unrecognized until he realized that he had been using outdated CN bombs for eradica- 50) than CS in rats, rabbits, guinea pigs, and mice.8 In addition, the pathological findings in the lungs were more severe, with more edema; CN (0.5 mg), when left in place for 60 minutes, patchy acute inflammatory cell infiltration of the caused irritation and erythema on the skin of all humans tested in one study,35 whereas CS caused weapon from close range with intent to injure the no effects in amounts less than 20 mg. When the patient. In some instances, particles of agglomer- CN was moist, 0.5 mg caused vesication in most ated agent were driven into the eye tissues by the subjects, whereas vesication was not seen after ex- force of the blast; the authors of the study suggested that a chemical reaction caused damage over In addition to being a more potent primary irri- months or years. In other instances, the injury was tant on the skin than CS, CN is also a more potent probably caused by the blast or other foreign par- skin sensitizer.36 Several people developed allergic ticles rather than by CN. The authors carefully contact sensitivity to CN after patch testing.37 Be- pointed out that features of the weapon, such as the cause of the high incidence of sensitization in test blast force, the propellant charge, the wadding, and subjects, CN should be considered a potent allergic the age of the cartridge (in older cartridges, the sensitizer, and those who are frequently exposed powder agglomerates and forms larger particles) should be aware of the high likelihood of develop- should be considered in evaluating eye damage due The author of another review41 came to the same Ophthalmological Effects
conclusion: the traumatic effect of the blast is a con-siderable factor, and one cannot always be sure that The irritation caused by CN in the eye signals CN per se is the cause of permanent injury.
avoidance and, by causing lacrimation and bleph- In a study20 comparing the effects of CN and CS arospasm, initiates a defense mechanism. High con- in the eyes of rabbits, CN at a concentration of 10% centrations of CN sprayed into the eyes from a dis- (wt/vol) caused iritis and conjunctivitis lasting tance have caused edema of the corneal epithelium longer than 7 days and corneal opacity lasting and conjunctiva and many minute epithelial defects longer than 55 days. In contrast, CS, at the same in the cornea.39 Healing was rapid, however.
concentration, caused moderate conjunctivitis but More lasting or permanent effects may occur no iritis or corneal opacities; all eyes were normal when CN is released at close range (within a at 7 days. Other evidence30 indicates that when CN few meters), particularly if it is from a forceful is applied directly to the eye in powder form or is blast from a cartridge, bomb, pistol, or spray. One sprayed at close range, a more severe reaction than study 40 based on case records from the files of the Armed Forces Institute of Pathology in Washing- Although permanent eye damage has been re- ton, D. C., reviewed eye injuries from tear gas; un- ported from the use of CN weapons at close range, fortunately, many of the histories were incomplete.
separating the effects of the weapon from those of In about half the cases, the injuries were self- the compound is difficult. There is no evidence that inflicted and accidental; in the other half, the CN at harassing or normal field concentrations injuries were caused by a second person firing a SEVERE MEDICAL COMPLICATIONS FROM THE USE OF CS AND CN
The indiscriminate use of large amounts of CN he had an episode of cyanosis, which cleared with in confined spaces has caused injuries requiring suctioning. On examination, he was in respiratory medical attention and death. An incident of injury distress with suprasternal retraction, wheezes, and to an infant from CS has also been reported.
rales bilaterally. The chest radiograph was clear.
A 4-month-old infant was in a house into which Antibiotics, high-dose steroids, and positive-pres- police fired CS tear gas canisters for 2 to 3 hours to sure breathing were started. He slowly improved subdue a disturbed adult. Immediately on being until the seventh hospital day, when his tempera- removed from the house, the infant was taken to a ture rose to 40.4°C (104.4°F) and coughing in- hospital, where he was observed to have copious creased. An infiltrate was noted on the chest radio- secretions of the nose and mouth and frequent graph. Physical findings were unremarkable except sneezing and coughing. He required frequent for coarse breath sounds throughout the lungs. He suctioning to relieve upper airway obstruction.
improved with further antibiotic and ventilatory Physical examination was unremarkable except for therapy and was discharged on day 12, only to be the secretions, slight conjunctival injection, and readmitted on day 13 with an increasing cough and rapid heart rate and respirations. On the second day, a progression of the infiltrate. With more antibiot- Medical Aspects of Chemical and Biological Warfare ics and other therapy, he gradually recovered and grees of illness, and at least three received medical was discharged after 28 days in the hospital.42 treatment (the authors carefully pointed out that In a prison incident, 44 inmates were in a cell block sprayed with CN; 28 inmates later sought A prisoner was found dead under his bunk 46 medical attention, and 8 were hospitalized. All eight hours later. Other prisoners reported that he had complained of malaise, lethargy, and anorexia. Five had “red eyes,” had vomited “bloody” material, and had pharyngitis, three of whom developed pseudo- had sought medical attention on several occasions.
membranous exudates several days later. Three also On autopsy, he was noted to have rigor mortis, cy- developed tracheobronchitis with purulent sputum, anosis of the face and head, and no evidence of but no infiltrates on chest radiograph. Four patients physical injury. His lungs had subpleural petechiae, had facial burns, and three had bullae on the legs; hyperemia, mild edema, and patchy areas of con- the most severely affected had first- and second- solidation; microscopic examination showed bron- degree burns over 25% of his body. One patient was chopneumonia clustered around exudate-filled admitted 5 days after the incident with a papuloves- bronchioles. His larynx and tracheobronchial tree icular rash of his face, scalp, and trunk, which had were lined with an exudative pseudomembrane; appeared 2 days earlier. Ten prisoners were treated microscopic examination showed this was a fibrin- as outpatients for first- and second-degree burns, rich exudate containing polymorphonuclear leuko- and six had localized papulovesicular rashes. Ten cytes and their degenerating forms. There was no had conjunctivitis with edema of the conjunctiva, evidence of gastrointestinal hemorrhage; other or- and in some the eyelids were closed by the swell- ing, but no patient had corneal injuries or perma- Another individual had an altercation with the nent eye damage. The patients with laryngotracheo- police and locked himself into a room in his house.
bronchitis were given bronchodilators, postural A single CN grenade (128 g) was thrown into the drainage, and positive-pressure exercises. Two were room (approximately 27 m3), where the patient re- given short-term, high-dose steroids, but none re- mained for 30 more minutes (128,000 mg • 30 min ceived antibiotics. One required bronchodilator ÷ 27 m3 provides an estimated Ct of about 142,500 therapy 3 months later, but the others made prompt mg•min/m3, or an exposure 10-fold higher than the The skin lesions were treated with debridement On admission to the hospital, his respirations were and applications of silver sulfadiazine and, in some 24 per minute, his conjunctiva were suffused, his pu- cases, with topical steroids and antihistamines. Skin pils were small and unreactive, mucoid discharge color was almost normal 3 months later. Topical ste- from his nose and mouth was abundant, his lungs roids caused the conjunctival edema to begin to re- were clear, and an occasional premature ventricular solve in 48 hours. The only estimate of the amount contraction was evident on the electrocardiogram. He of CN used was obtained from the prisoners, each remained “in a semicomatose condition for approxi- of whom claimed to have been sprayed multiple mately 12 hours and then suddenly developed pul- times. Although the first- and third-floor windows monary edema and died.”45(p375) Relevant findings on were open, the exhaust system was off during the autopsy included cyanosis, frothy fluid in the mouth and nose, acute necrosis of the mucosa of the respira- In another prison incident, the windows and tory tree with pseudomembrane formation, desqua- doors were closed and ventilation was off during mation of the lining of the bronchioles with edema what was described as a “prolonged gassing” of and inflammation of the walls, and a protein-rich fluid inmates confined to individual cells. It was later in most of the alveolar spaces. Foci of early broncho- estimated that the incident lasted 110 minutes.
Among the dispensers used were at least six ther- Information on three other cases of death from mal grenades of CN, fourteen 100-g projectiles of CN, which the authors obtained from other medi- CN, and more than 500 mL of an 8% CS solution.
cal examiners, are summarized in the same report.45 Using only the amount in the CN projectiles, the Details were scanty, but the autopsy findings were authors of the report calculated that the prisoners similar; in each case, the individual was confined were exposed to a Ct of 41,000 mg•min/m3. The in a relatively small space. Exposure was for 10 total number of prisoners exposed was not noted.
minutes in one instance and for hours in the others Afterward, some had coughing with varying de- OTHER RIOT CONTROL COMPOUNDS
DM (Diphenylaminearsine)
which last for several hours after exposure. DM andrelated compounds are known as vomiting agents,but the incidence of vomiting and the amount of compound necessary to cause it are not known with certainty. In studies dating from 1922 to 1958,46 hu-mans were exposed to Cts ranging from 4.6 to 144mg•min/m3; nausea was noted in fewer than 10% of the subjects. Because of the lack of data, the Ctnecessary to cause nausea and vomiting has not been established,46 but has been estimated to beabout 370 mg•min/m3.24 The riot control agent known as DM (diphenyl- One death has been reported46 from DM inhala- aminearsine) is one of a group of compounds that tion (the information on this fatality is incomplete).
are known as vomiting agents. The others, which A DM generator was operated in a barrack, expos- are of much less military importance, are the agents ing 22 sleeping men. The estimated concentration DA (diphenylchlorarsine) and DC (diphenylcyano- was 1,130 to 2,260 mg/m3, and the duration of ex- arsine). DM was first synthesized by the German posure was estimated to be 5 minutes (by one chemist Wieland in 1915 and, independently, by the source) or 30 minutes (by a second source). For a 5- U.S. chemist Adams in 1918. DM is also known as minute exposure, the estimated Ct would be 5,650 to 11,300 mg•min/m3; for a 30-minute exposure, 33,900 DM is a yellow-green, odorless, crystalline sub- to 67,800 mg•min/m3. One individual died; the post- stance that is not very volatile. It is insoluble in mortem findings were severe airway and lung dam- water and relatively insoluble in organic solvents.
age, similar to those seen after death from CN.
Its primary action is on the upper respiratory tract, Another source47 reported severe pulmonary injury causing irritation of the nasal mucosa and nasal si- and death after accidental exposure to high concen- nuses, burning in the throat, tightness and pain in trations of DM in confined spaces, but no details the chest, and uncontrollable coughing and sneez- ing. It also causes eye irritation and burning, how-ever, with tearing, blepharospasm, and injected con- CR (Dibenz(b,f) -1:4-oxazepine)
DM is more toxic than other riot control agents; 11,000 mg•min/m3.46 The amount that is intoler-able for humans has been estimated by some to be 22 mg•min/m3 and by others to be 150 mg•min/ m3.46 The threshold for irritation in humans is about 1 mg/m3, but men have tolerated Ct exposures of100 to 150 mg•min/m3.
Two characteristics make this class of compounds The riot control agent known as CR (dibenz(b,f)- unique among the riot control agents. The first is 1:4-oxazepine) is a relatively new compound, first that the effects do not appear immediately on ex- synthesized in 1962 by Higginbottom and Suschitzkey.
posure or seconds afterwards, but several minutes CR is more potent and less toxic than CS. Because later. In the absence of symptoms, a soldier will not of the low vapor pressure of CR solution, no respi- mask immediately; by the time he masks, he will ratory tract effects are anticipated from its use. The have absorbed a significant amount. The effects may LCt50 for animals exposed to grenade-generated smokes was found to be 167,500 mg•min/m3. The The second characteristic of these compounds is estimated LCt50 for humans is probably higher than that there may be more prolonged systemic effects, such as headache, mental depression, chills, nau- CR is sparingly soluble in water, and a cosolvent sea, abdominal cramps, vomiting, and diarrhea, (PEG300 is frequently used) is necessary when it is Medical Aspects of Chemical and Biological Warfare dispersed in solution. Since CR does not degrade to cause effects—and it appears to be much safer, in water, it resists weathering and persists in the as judged from the higher LCt50 and the lack of In humans, the effects caused by CR are qualita- tively similar to those caused by CS, but there is an CA (Bromobenzylcyanide)
approximately 5-fold difference in potency. A splashof a solution in the range of 0.01% to 0.1% causesimmediate eye pain, blepharospasm, and lacrima- tion, which persist for 15 to 30 minutes, and con- junctival injection and minimal edema of lid mar- gins, which last for 3 to 6 hours. A solution splashedin the mouth causes burning of the tongue and pal- ate and salivation for 5 to 10 minutes. If a splashenters the nose, it causes irritation and rhinorrhea.
The riot control agent known as CA (bromo- Skin exposure causes burning within a few minutes, benzylcyanide) was the last irritating agent intro- which persists for 15 to 30 minutes, and an erythema duced by the Allies in World War I, and it was the lasting for 1 to 2 hours. A blood pressure increase most potent. It corrodes iron and steel, is not chemi- may accompany the subjective discomfort; this is cally stable in storage, and is sensitive to heat, all thought to be caused by the stress of the irritation, characteristics that made it unsuitable for storage since the amount of CR that could be absorbed is much too small to cause a pharmacological effect.24 CA irritates the eyes and causes lacrimation at A transient erythema (1–2 h) occurs, but CR does concentrations of 0.15 and 0.3 mg/m3; the LCt50 not induce inflammatory cell infiltration, vesication, was estimated to be 27,000 mg•min/m3.50 More or contact sensitization, and it does not delay the recent studies indicate that the estimated LCt50 for healing of skin injuries.24,48 The potential for eye humans is 11,000 mg•min/m3,51 indicating that it damage is also significantly less than it is from CS is among the more toxic riot control agents. The or CN.24 CR was neither teratogenic nor embryo- health effects caused by CA are very similar to those lethal in one study49 when given as an aerosol or CA is rarely used and is a relatively unimpor- Compared with other riot control agents, CR is tant agent of this class. The compound is included relatively new; no data from its use exist. Experi- here primarily because it is discussed in Treatment mental studies indicate that its effects are similar of Chemical Agent Casualties and Conventional Mili- to those of CS except that it causes almost no ef- tary Chemical Casualties,52–54 field manuals published fects in the lower airways and lungs. It is much more by the Department of Defense for use by the U.S.
potent than CS—a smaller concentration is needed MEDICAL CARE
The effects from riot control agents are usually to bring prompt relief of symptoms and to hydro- self-limiting, and medical attention is usually not lyze the agent.13 No form of hypochlorite should be required. Exiting the contaminated area should bring some measure of relief in 15 to 30 minutes orsooner. In rare circumstances, complications may occur on the skin, in the eyes, or in the airways.
For dermatitis, a topical steroid preparation (eg, Decontamination
triamcinolone acetonide, fluocinolone acetonide,flurandrenolone, or betamethasone-17-valerate) is The use of water on the skin may result in tran- the principal therapeutic agent. Oozing lesions sient worsening of the burning sensation. Soap and should be treated with wet dressings (moistened water may be more effective but may also cause with fluids such as 1:40 Burow’s solution). Appro- a momentary increase in the symptoms. CS rapid- priate antibiotics should be given for secondary ly hydrolyzes in an alkaline solution; a solution infection, and oral antihistamines for itching.13 Vesi- containing 6% sodium bicarbonate, 3% sodium car- cating lesions have been successfully treated with bonate, and 1% benzalkonium chloride was found compresses of a cold silver nitrate solution (1:1,000) for 1 hour, applied six times daily.11 One person with tory effects may not become manifest until 12 to 24 severe lesions and marked discomfort was given a hours after exposure. An individual who has pro- short course of an oral steroid. An antibiotic oint- longed dyspnea or objective signs should be hospi- ment was applied locally, but systemic antibiotics talized under careful observation. Further care should be as described in Chapter 9, Toxic Inhala-tional Injury. Although people with chronic bron- chitis have been exposed to riot control agents with-out untoward effects, any underlying lung disease A local anesthetic might be applied once for se- (eg, asthma, which affects one person in six in the vere pain, but continued use should be restricted.
general, or the military, population) might be exac- The eye should be thoroughly flushed to remove any particles of the agent. If the lesion is severe,the patient should be sent to an ophthalmologist.
Cardiovascular System
Respiratory Tract
Transient hypertension has been noted after ex- posure to riot control agents, primarily because of Usually, the cough, chest discomfort, and mild the anxiety or pain of exposure rather than a phar- dyspnea are gone 30 minutes after exposure to clean macological effect of the compound. Whatever the air. However, both the animal data (detailed in the cause, adverse effects may be seen in individuals section on CS) and the clinical experience with the with hypertension, cardiovascular disease, or an an- infant exposed to CS suggest that severe respira- FUTURE USE
More research is needed to illuminate the full areas and under the circumstances in which the use health consequences of riot control agents, as one of CS or CN has apparently been abused (eg, the report55 has suggested. Information gaps in this West Bank and the Gaza Strip in the Middle East, chapter indicate areas that might fruitfully be ex- and Seoul, South Korea). Public opinion and the plored, although funding for such research is prob- Geneva Protocol did not dissuade Iraq from using lematic. The limited resources of the military pro- several types of chemical weapons in the conflict gram in chemical defense are probably more wisely with Iran, or prevent Libya from constructing a spent on investigating better defense against and large manufacturing facility at Rabta, apparently for medical care for victims of agents that cause more the manufacture of chemical weapons. Despite the severe consequences and are more likely to be used concern about the loss of innocent lives and injury on a battlefield. Law enforcement agencies gener- among innocent bystanders, there is serious doubt ally have few funds for these purposes. Manufac- that a prohibition of the use of riot control agents turers probably do not have a large interest in this topic; it is unlikely that their profits from these com- While it is true that in some instances dialogue pounds are large enough to support such an effort.
and negotiation should precede the use of riot con- Federal medical funding is generally concerned trol agents, one wonders how this suggestion might with more serious diseases affecting larger seg- have been received by the desperate refugees. Al- though CS allegedly caused injury, the amount of Other concerns discussed in the report55 were the injury was probably small compared to what might “pattern of use” of these compounds. Are there cir- have been inflicted if CS had not been available and cumstances in which the use of riot control agents more extreme measures had been used. Possibly, the can, or cannot, be condoned? The “pattern of use” use of CS is sometimes the most benign solution in might be difficult to regulate, particularly in the Riot control agents are intended to harass or to Much evidence suggests that riot control agents cause temporary incapacitation. Their intended tar- are safe if they are used as intended and if the re- get might be the foe in an armed conflict—with the limi- sponse is as intended. When they are not used as tations outlined above—or rioters in a civil disturbance.
intended, and the response is not as intended, how- Medical Aspects of Chemical and Biological Warfare ever, there may be devastating consequences (eg, the deaths of the Branch Davidians at Waco, Tex.).
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Source: http://posa.org.au/wp-content/uploads/2010/08/Riot-Control-Agents.pdf

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