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

Riot Control AgentsCN for years. In 1941 Queen and Stander 149 reported thecase of a 43-year-old military recruit who spent 5 minutesexposed to an atmosphere of CN while masked.After removing the mask and leaving the chamber hedeveloped a severe allergic reaction. Within 5 minutesof exiting the chamber, he complained of generalizeditching, which progressively worsened until by 4 hourshe had developed a diffuse and intense erythema overhis entire body, except for his feet and the part of hisface that was covered by the mask. His temperaturewas 38.9°C (102°F), which rose to 39.4°C (103°F) bythe next day. By 48 hours postexposure, vesication andsevere subcutaneous edema had strikingly altered hisfacial appearance. This was accompanied by severegeneralized itching. These signs subsided over thenext 4 days, and the desquamation which was profuseat day 6 gradually decreased. This recruit had beenexposed to a similar CN exercise 17 years previouslyand developed itching, but had not been exposed inthe interim. 149Another case of cutaneous hypersensitivity wasreported by Madden in 1951, 150 in which a police officerreceived an initial exposure to CN, and 5 years later onrepeated exposure developed recurrent attacks of whatwas probably allergic contact dermatitis. The sourceof the repeated exposures was unrecognized until thepolice officer realized that he was using outdated CNbombs for eradication of rodents on his property. Hedeveloped a severe dermatitis on his legs with eachuse over a period of 5 years. When a small area of oneleg was intentionally exposed to CN, an acute contactdermatitis appeared and subsided within 8 hours. 150Holland and White 141 studied the skin reactions inhumans following CN application. Irritation beganwithin 10 minutes and became more severe when theagent was left in place. By 60 minutes, 0.5 mg CN hadproduced irritation and erythema on the skin of all thepeople tested. These effects disappeared when the CNwas removed, but recurred transiently when the areaswere washed during the subsequent 12 hours. In allcases, diffuse redness appeared in an area up to threetimes the original contact area. At doses of over 2 mg,localized edema occurred but subsided after 24 hours.When applied dry in doses of 0.5 to 2 mg, the rednessdisappeared within 72 hours. At higher doses and atall doses applied moist, the redness became raisedand papular. The papules coalesced to form a ring ofvesicles at about 48 hours. Two weeks later, the lesionswere evident as faint areas of hyperpigmentation.These effects contrasted to those of CS also evaluatedin these studies. CS at doses under 20 mg caused noirritation or erythema, and no vesiculation resultedfrom CS at doses of 30 mg or less. Thus CN is a morepotent primary irritant on the skin than CS.Ophthalmologic effects. The irritation caused byCN in the eye signals avoidance and, by causing lacrimationand blepharospasm, initiates a defense mechanism.3 High levels of CN can produce chemical injuryto the eyes characterized as corneal and conjunctivaledema, chemosis, and loss of corneal epithelium. 136Physical injuries may also occur following dispersionvia grenade-type tear gas devices. 135,136 More lasting orpermanent effects may occur when CN is released atclose range (within a few meters), particularly if thedose is from a forceful blast from a cartridge, bomb,pistol, or spray.Using records from the files of the Armed ForcesInstitute of Pathology in Washington, DC, Levineand Stahl 151 reviewed eye injuries caused by tear gasweapons. Although many of the histories were incomplete,in about half of the cases the injuries were selfinflicted or accidental. In the other cases, the injurieswere caused by a second person firing a weapon atclose range with intent to injure the patient. In someinstances, particles of agglomerated agent were driveninto the eye tissues by the force of the blast, and a possiblechemical reaction caused damage over monthsor years. In other instances, the injury was probablycaused by the blast or other foreign particles ratherthan by CN. The authors carefully pointed out thatfeatures of the weapon, such as the blast force, thepropellant charge, the wadding, and the age of thecartridge (in older cartridges, the powder agglomeratesand forms larger particles) should be consideredin evaluating eye damage from CN. 151Rengstorff 152 also concluded that traumatic effects ofblast are a considerable factor that must be consideredwhen determining the cause of permanent eye injuryin CN exposures. Although permanent eye damagehas been reported from the use of CN weapons at closerange, separating the effects of the weapon from thoseof the compound is difficult. There is no evidence thatCN at harassing or normal field concentrations causespermanent damage to the eye. 3Other physiological responses. The 1984 NationalResearch Council study 60 reported histopathologicalchanges following CN exposures including hemorrhage,perivascular edema, congestion of the alveolarcapillaries, occluded bronchioles, and alveolitis.Renal histopathology demonstrated congestion andcoagulative necrosis in the cortical renal tubules inCN exposed mice. Hepatic histopathology consisted ofcloudy swelling and lobular and centrolobular necrosisof hepatocytes. 60Long-term effects and severe medical complications.Between 1958 and 1972, 99 human subjectsunderwent experimental exposures to CN at EdgewoodArsenal. Of these, 69 were exposed by aerosol463