Protecting yourself against chemical weapons

October 25th, 1998

In order to assist tourists in KL, may I present the following tips? They will also be of use to medical personal treating such casualties, and to the general public who may be curious about such things.

"Riot" control practices may provide discomfort to those observing gatherings, so the following notes explain how to identify and protect yourself against unintended discomfort.


Irritant agents (lachrymators) are local irritants which in very low concentrations act primarily on the eyes, causing intense pain and lacrimation. Higher concentrations irritate the upper respiratory tract and the skin and sometimes cause nausea and vomiting. These agents may be dispersed as fine particulate smoke (aerosols) or in solutions as droplet aerosols. Examples of irritant agents are O-chlorobenzylidene malononitrile (CS), chloroacetophenone (CN), chloroacetophenone in chloroform (CNC), bromobenzylcyanide (CA), and dibenz-(b,f)-1,4-oxazepine (CR).

At present, CS is being used in KL in the form of grenades. CR and CS may be in use with water cannons. The tourist can generally expect not to be targeted by water cannon or grenades, but may well be affected by accidental exposure to CS. CN and CA appear not to be in use.


a. Protection against field concentrations of irritant agents is provided by protective masks and ordinary clothing secured at the neck, wrists, and ankles. Masks are unlikely to be available, but any cartridge style mask will protect against respiratory complications. A wet mask of the type used to protect against the effects of haze will provide a limited degree of protection. Goggles which are air tight will also protect, but are likely to be exceedingly uncomfortable to wear.

b. Following exposure, clothing and individual equipment should be inspected for agent residue. If a residue is found, individuals should change or decontaminate the clothing to protect themselves and other unmasked persons. Decontaminate CS-contaminated clothing by airing for a few minutes.


a. Agent CS. Agent CS is a white crystalline solid which melts at 90°C and is stable under ordinary storage conditions. It has a pungent, pepper-like odour. A CS cloud is white at the point of release and for several seconds after release. Agent CS is disseminated by burning, exploding, and forming an aerosol. It may also be used in liquid form in an appropriate solvent. This agent is faster-acting, about 10 times more potent, and less toxic than CN.

b. Agent CR. Agent CR is a pale yellow crystalline solid which melts at 73°C and is stable in organic solutions. It has limited solubility in water and is not hydrolysed in aqueous solutions. It has a pepper-like odour. The agent is currently used only in solution for dissemination in liquid dispensers. The solution in the dispensers contains 0.1 percent CR in 80 parts propylene glycol and 20 parts water. In organic solutions, CR is an eye irritant at concentrations of 0.0025 percent or even lower. Agent CR differs from CS in being less toxic when inhaled but skin effects are more pronounced and longer lasting. It is more persistent in the environment and on clothing.

c. Agents CN and CA. Agent CN is a white crystalline solid, boiling at 248°C and freezing at 54°C. Agent CA is usually a liquid, boiling at 242°C and freezing at 25°C. Agent CN may also be used in liquid form in appropriate solvents. The odour of CN is like that of apple blossoms. The odour of CA is like that of sour fruit. These agents may appear as a bluish-white cloud at the point of release. A solid agent is dispersed as fine particulate smoke and as vapour from burning munitions, such as lachrymator candles and grenades. Liquid agents may be dispersed from airplane spray or bursting munitions.

CN and CA do not appear to be in use at present.


a. Agent CS.

(1) Eyes and respiratory tract. When an unmasked person enters a cloud of CS, the effects are felt almost immediately. Incapacitation begins in 20 to 60 seconds, depending upon the degree of agent concentration. The effects last for 5 to 10 minutes after removal to fresh air. There is marked burning pain in the eyes with copious lacrimation and blepharospasm, thin mucous nasal discharge, coughing, and dyspnea. Following heavy exposures, there may be nausea and vomiting. Exposure to extremely high concentrations in an enclosed space may cause tracheitis and bronchitis. Even if that happens, permanent damage is very unlikely.

(2) Skin.

(a) Warm, moist skin (especially on the face, neck, ears, and body folds) is susceptible to irritation by CS. A stinging sensation may occur promptly, even at moderately low concentrations. Higher concentrations may cause an irritant dermatitis with erythema and, rarely, blisters on the same body regions. Stinging subsides after 5 to 10 minutes, even with continued exposure. An increase in the stinging is noted upon the individual's removal to fresh air. Repeated exposures may cause delayed hypersensitivity with allergic contact dermatitis. Inflammation and blistering similar to sunburn may occur after a heavy or prolonged exposure, especially if the individual's skin is fair.

(b) The following solution can be applied as a wash or spray to cleanse unbroken skin of a CS affected person. (If this is painful in the eyes or in wounds, normal saline should be used instead.) To make the solution, add 100 gm of sodium bicarbonate, 50 gm of sodium carbonate, and 15 ml of 10 percent benzalkonium chloride solution to 1,500 ml of distilled water. The solution is stable and should be prepared in advance of need.

b. Agent CR. Agent CR is similar in effect to CS, but the minimal effective concentration is lower and the lethal concentration (LCt) is higher. Symptoms and treatment are similar to those of CS.

c. Agents CN and CA.

(1) Eyes and respiratory tract. The vapours or smokes of these agents cause basically the same reactions as does CS. However, their toxicities are generally higher and their effectiveness as lachrymators are generally lower than CS; that is, higher concentrations of CN or CA are required to produce an irritant effect equivalent to that of CS. Recovery is quick if exposure is brief, but prolonged exposure may cause conjunctivitis and photophobia. Extremely high concentrations of these agents in enclosed spaces may cause tracheitis, bronchitis, pulmonary oedema, or cerebral oedema. Exposures of this magnitude are rare.

(2) Skin. Stinging of the skin and, with higher concentrations, irritant dermatitis may occur in warm, humid weather. These agents are potential skin sensitisers although apparently less so than CS. Droplets of liquid or particles of solid lachrymators in the eyes may be corrosive and produce burns like those of a strong acid.


a. Agent CS. Diagnosis of exposure to CS is made from the pepper-like odour, the presence of intense eye effects, dyspnea, coughing, and mucous rhinorrhea.

b. Agent CR. Diagnosis of exposure to CR is similar to the diagnosis of CS. CR produces a burning sensation in the nose and sinuses.

c. Agents CN and CA. Diagnosis of exposure to these agents is made from their odours and from the marked coughing and dyspnea, in addition to the eye effects described above. Also, headache and mental depression may appear as late effects of CN exposure.


Put on a protective mask, clear it, and keep your eyes open as much as possible (if eyes are protected by the mask or goggles). Move out of the contaminated environment, if possible. When your vision clears, go on with your tourism. When it is safe to do so, remove the mask and blot away the tears. DO NOT rub the eyes. If drops or particles have entered the eye, try to forcibly open it and flush it with copious amounts of water. Chest discomfort usually can be relieved merely by talking. If exposure has been heavy, significant cutaneous reaction may develop. The cutaneous reaction can be prevented by immediately flushing the skin with copious amounts of water.


a. Eyes. Ordinarily, the effects on the eyes are self-limiting and do not require treatment. If large particles or droplets of the agent are in the eye, treatment as for corrosive materials may be required. This is much less likely in CS exposure than in CA or CN exposure. Prompt irrigation of the eye with copious amounts of water is essential. Impacted particles of the agent may be removed mechanically. After complete decontamination, an ophthalmic corticosteroid ointment may be used. Patients heavily exposed to CN or CA must be observed closely for development of corneal opacity and iritis. If either condition develops, promptly refer the patient for definitive ophthalmologic treatment.

b. Skin. Ordinarily, early (up to 1 hour) erythema and stinging sensation are transient and do not require treatment. Delayed erythema (irritant dermatitis) may be treated with a bland shake lotion (such as calamine lotion) or a topical corticosteroid (0.10 percent triamcinolone acetonide, 0.025 percent fluocinolone acetonide, 0.05 percent flurandrenolone), depending upon severity. Cases with blisters should be managed as a second degree burn. Treat oozing acute contact dermatitis with a wet dressing of 1 to 40 Burow's solution or colloidal oatmeal for 30 minutes, three times daily. The topical steroid should follow the wet dressing immediately. Secondary infections are treated with appropriate antibiotics. If significant pruritus occurs, an oral antihistamine should be used.

c. Pulmonary. In the rare event of pulmonary effects following massive exposure, evacuation for hospital care is required. Treatment is basically the same as for lung-damaging agents. (Refer below)


Most persons affected by irritant agents require no medical attention. Casualties are rare. Severe reactions of the eyes or the skin may take days or weeks to heal, depending upon their severity.

Treatment for lung damaging agents:-

a. Rest and Warmth. A casualty exposed to a lung-damaging agent should be kept at rest until the danger of pulmonary oedema is past. Tightness of the chest and coughing should be treated with immediate rest and comfortable warmth. The casualty should be evacuated in a semi seated position if dyspnea or orthopnea make a supine posture impractical. Mandatory evacuation by litter in cases of significant respiratory involvement has been advocated.

b. Sedation. Sedation should be used sparingly. Codeine in doses of 30 to 60 mg may be effective for cough. Restlessness may be a manifestation of hypoxia; therefore, only cautious use of sedatives is advised. Use of sedatives should be withheld until adequate oxygenation is assured and facilities for possible respiratory assistance are available. Barbiturates, atropine, analeptics, and antihistamines are all contraindicated.

c. Oxygen. Hypoxemia may be controlled by oxygen supplementation. Early administration of positive airway pressure (intermittent positive pressure breathing (IPPB), positive end-expiratory pressure (PEEP) mask ("PEEP mask"), or, if necessary, intubation with or without a ventilator) may delay and/or minimise the pulmonary oedema and reduce the degree of hypoxemia.

d. Antibiotics. Antimicrobial therapy should be reserved for acquired bacterial bronchitis/pneumonitis. Prophylactic therapy is not indicated.

e. Steroids. After exposure to a sufficiently high dose of CS or similar agent, pulmonary oedema will follow. Administration of corticosteroids has been recommended, but proof of their beneficial effects is lacking. It has been suggested that, when steroid treatment is initiated within a very short time of the exposure, this therapy may lessen the severity of the oedema. Rest, warmth, sedation, and oxygen are also of great importance, as indicated above. Doses of steroids used are much greater than those used in asthma. Treatment for exposure to a lung-damaging agent or similar compound should be judged on the basis of precautionary treatment for what seems a mild but possibly dangerous exposure, and definitive treatment for an exposure which is definitely expected to endanger life. Two regimes are in use: one using dexamethasone-sodium phosphate and the other using beclomethasone dipropionate or betamethasone valerate. In either case, treatment should be started as soon as possible, ideally within 15 minutes of exposure.

(1) Using dexamethasone-sodium phosphate, the procedure is as follows:

(a) Treatment should start at the earliest possible moment with the inhalation of the steroid from an inhaler. Four puffs (or strokes) should be inhaled at once. This should be followed by 1 puff every 3 minutes until any sense of irritation is overcome. After this, 5 puffs should be inhaled every 15 minutes until a total of 150 puffs have been inhaled (that is, the entire contents of one standard inhaler are finished). When this stage has been reached, 1 puff should be inhaled hourly during the day, and, as a preparation for sleep, 5 puffs should be inhaled every 15 minutes until a total of 30 puffs have been reached. This regimen should be repeated each day for at least 5 days or longer if there are any abnormalities, including indications of pulmonary oedema or infiltrates on the chest x-ray, after which treatment may be withdrawn. If recovery is slow, the dosage may be reduced to 6 puffs a day and continued until recovery is complete.

(b) Definitive treatment for exposures which definitely endanger life should include the above regime of inhaled steroid treatment, supplemented by systemic steroids as follows:

•Day 1 1,000 mg prednisolone, IV
•Day 2 and 3 800 mg prednisolone, IV
•Day 4 and 5 700 mg prednisolone, IV

Beginning with day 6, the dose of systemic steroids should be reduced as soon as possible, provided that the chest x-ray remains clear. If further early systematic treatment is necessary, adrenaline may be given in the acute stage of bronchial spasm and oxygen may be necessary. Treatment of severe cases is very difficult because of tissue damage. Absolute rest and administration of oxygen are fundamental. Expectorants may also be used. Bronchopneumonia is treated by antibiotics.

(2) Using beclomethasone dipropionate or betamethasone dipropionate, the procedure is as follows: (The differences occur due to the various absorption characteristics of these steroids. Limited systemic therapy is necessary, even for precautionary treatment.)

(a) Treatment should commence as soon as possible with the inhalation of 10 puffs of the steroid from an inhaler. Five puffs should be given each hour for the next 10 hours. Then 1 puff should be given hourly for the next 24 hours for as long as inhalational therapy is considered necessary (at least 5 days). Systemic therapy is needed even for precautionary treatment during the first 24 hours and should commence as soon as possible with the IV injection of 20 mg of betamethasone or the equivalent dose of another systemic steroid. This dose should be repeated IV or IM every 6 hours for at least the first 24 hours. During the next 5 days, inhalation therapy should be continued but systemic therapy may be reduced based on clinical response and chest x-ray improvement.

(b) Definitive treatment may call for longer periods of systemic therapy.

(c) Prednisolone, betamethasone, or methylprednisolone are preferred to other steroids for systemic use, as there is evidence that these steroids do not interfere with collagen metabolism. Antibiotic coverage should be considered with these high doses of steroids in patients predisposed to pulmonary infection complications. Side effects of high steroid dosages should be accepted provided they do not themselves endanger life. Any indication of pulmonary fibrosis will necessitate antifibrotic treatment.

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