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Chemical Warfare Agents

A chemical agent is a substance which is intended for use in military operations to kill, seriously injure or incapacitate people because of its physiological effects. Excluded from this definition are riot control agents, herbicides, smoke and flame.

Nerve Agents

The nerve agents are a group of particularly toxic chemical warfare agents. They were developed just before and during World War II and are related chemically to the organophosphorus insecticides. The principle agents in this group are:

The "G" agents tend to be non-persistent whereas the "V" agents are persistent. Some "G" agents may be thickened with various substances in order to increase their persistence, and therefore the total amount penetrating intact skin. At room temperature GB is a comparatively volatile liquid and therefore non-persistent. GD is also significantly volatile, as is GA though to a lesser extent. VX is a relatively non-volatile liquid and therefore persistent. It is regarded as presenting little vapour hazard to people exposed to it. In the pure state nerve agents are colorless and mobile liquids. In an impure state nerve agents may be encountered as yellowish to brown liquids. Some nerve agents have a faint fruity odour.

TOXICOLOGICAL DATA

Route

ocular

inhalation

inhalation (15 1/min)

inhalation (15 1/min)

percutaneous

Form

vapor

vapor

vapor

vapor

liquid

Effect

miosis

runny nose

incapacitation

death

death

Type

ECt50

ECt50

ICt50

LCt50

LD50

GA

--

--

--

135

4,000

GB

<2

<2

35

70

1700

GD

<2

<2

35

70

350

VX

< 0.09

< 0.09

25

30

10

Dosage

mg-min/m3

mg-min/m3

mg-min/m3

mg-min/m3

mg/70 kg man

The values are estimates of the doses which have lethal effects on man. LD50 expresses the dose at which 50 per cent of the exposed population will die as a result of their injuries. A different measure is used for inhalation, the product of the concentration (C) and the length of exposure (t). Again, L stands for lethal and 50 for 50 per cent effect. Effective dosages for vapor are estimated for exposure durations of 2-10 minutes.

The effects of the nerve agents are mainly due to their ability to inhibit acetylcholinesterase throughout the body. Since the normal function of this enzyme is to hydrolyse acetylcholine wherever it is released, such inhibition results in the accumulation of excessive concentrations of acetylcholine at its various sites of action. These sites include the endings of the parasympathetic nerves to the smooth muscle of the iris, ciliary body, bronchial tree, gastrointestinal tract, bladder and blood vessels; to the salivary glands and secretory glands of the gastrointestinal tract and respiratory tract; and to the cardiac muscle and endings of sympathetic nerves to the sweat glands.

The sequence of symptoms varies with the route of exposure. While respiratory symptoms are generally the first to appear after inhalation of nerve agent vapour, gastrointestinal symptoms are usually the first after ingestion. Tightness in the chest is an early local symptom of respiratory exposure. This symptom progressively increases as the nerve agent is absorbed into the systemic circulation, whatever the route of exposure. Following comparable degrees of exposure, respiratory manifestations are most severe after inhalation, and gastrointestinal symptoms may be most severe after ingestion.

The lungs and the eyes absorb nerve agents rapidly. In high vapour concentrations, the nerve agent is carried from the lungs throughout the circulatory system; widespread systemic effects may appear in less than 1 minute. Nerve agent poisoning may be identified from the characteristic signs and symptoms. If exposure to vapour has occurred, the pupils will be very small, usually pin-pointed. If exposure has been cutaneous or has followed ingestion of a nerve agent in contaminated food or water, the pupils may be normal or, in the presence of severe systemic symptoms, slightly to moderately reduced in size. In this event, the other manifestations of nerve agent poisoning must be relied on to establish the diagnosis. No other known chemical agent produces muscular twitching and fasciculations, rapidly developing pin-point pupils, or the characteristic train of muscarinic, nicotinic and central nervous system manifestations.

The rapid action of nerve agents call for immediate self treatment. Unexplained nasal secretion, salivation, tightness of the chest, shortness of breath, constriction of pupils, muscular twitching, or nausea and abdominal cramps call for the immediate intramuscular injection of 2 mg of atropine, combined if possible with oxime.

Blister or vesicant agents

Blister or vesicant agents are likely to be used both to produce casualties and to force opposing troops to wear full protective equipment thus degrading fighting efficiency, rather than to kill, although exposure to such agents can be fatal. Blister agents can be thickened in order to contaminate terrain, ships, aircraft, vehicles or equipment with a persistent hazard.

Vesicants burn and blister the skin or any other part of the body they contact. They act on the eyes, mucous membranes, lungs, skin and blood-forming organs. They damage the respiratory tract when inhaled and cause vomiting and diarrhoea when ingested.

The vesicant agents include:

HD and HN are the most feared vesicants historically, because of their chemical stability, their persistency in the field, the insidious character of their effects by attacking skin as well as eyes and respiratory tract, and because no effective therapy is yet available for countering their effects. Since 1917, mustard has continued to worry military personnel with the many problems it poses in the fields of protection, decontamination and treatment. It should be noted that the ease with which mustard can be manufactured and its great possibilities for acting as a vapour would suggest that in a possible future chemical war HD will be preferred to HN.

Due to their physical properties, mustards are very persistent in cold and temperate climates. It is possible to increase the persistency by dissolving them in non-volatile solvents. In this way thickened mustards are obtained that are very difficult to remove by decontaminating processes.

Exposure to mustard is not always noticed immediately because of the latent and sign-free period that may occur after skin exposure. This may result in delayed decontamination or failure to decontaminate at all. Whatever means is used has to be efficient and quick acting. Within 2 minutes contact time, a drop of mustard on the skin can cause serious damage. Chemical inactivation using chlorination is effective against mustard and Lewisite, less so against HN, and is ineffective against phosgene oxime.

The great majority of mustard gas casualties survive. There is no practical drug treatment available for preventing the effects of mustard. Infection is the most important complicating factor in the healing of mustard burns. There is no consensus on the optimum form of treatment.

Protection against these agents can only be achieved by a full protective ensemble. The respirator alone protects against eye and lung damage and gives some protection against systemic effects. No drug is available for the prevention of the effects of mustard on the skin and the mucous membranes caused by mustards. It is possible to protect the skin against very low doses of mustard by covering it with a paste containing a chlorinating agent, e.g., chloramine. The only practical prophylactic method is physical protection such as is given by the protective respirator and special clothing.

In a pure form lewisite is a colorless and odourless liquid, but usually contains small amounts of impurities that give it a brownish colour and an odour resembling geranium oil. It is heavier than mustard, poorly soluble in water but soluble in organic solvents. L is a vesicant (blister agent), also, it acts as a systemic poison, causing pulmonary edema, diarrhea, restlessness, weakness, subnormal temperature, and low blood pressure. In order of severity and appearance of symptoms, it is: a blister agent, a toxic lung irritant, absorbed in tissues, and a systemic poison. When inhaled in high concentrations, may be fatal in as short a time as 10 minutes.

An antidote for lewisite is Dimercaprol (British Anti-Lewisite (BAL)). This ointment may be applied to skin exposed to lewisite before actual vesication has begun. Some blistering is inevitable in most arsenical vesicant cases. The treatment of the erythema, blisters and denuded areas is identical with that for similar mustard lesions. Burns severe enough to cause shock and systemic poisoning are life-threatening. Even if the patient survives the acute effects, the prognosis must be guarded for several weeks.

CX - Phosgene oxime

Phosgene oxime [CX] is a white crystalline powder. It melts between 39-40 C, and boils at 129 C.By the addition of certain compounds it is possible to liquify phosgene oxime at room temperature. It is fairly soluble in water and in organic solvents. In aqueous solution phosgene oxime is hydrolyses fairly rapidly, especially in the presence of alkali. It has a high vapour pressure, its odour is very unpleasant and irritating. Even as a dry solid, phosgene oxime decomposes spontaneously and has to be stored at low temperatures.

In low concentrations, phosgene oxime severely irritates the eyes and respiratory organs. In high concentrations, it also attacks the skin. A few milligrams applied to the skin cause severe irritation, intense pain, and subsequently a necrotising wound. Very few compounds are as painful and destructive to the tissues.

Phosgene oxime also affects the eyes, causing corneal lesions and blindness and may affect the respiratory tract causing pulmonary oedema. The action on the skin is immediate: phosgene oxime provokes irritation resembling that caused by a stinging nettle. A few milligrams cause intense pain which radiates from the point of application, within a minute the affected area turns white and is surrounded by a zone of erythema (skin reddening) which resembles a wagon wheel in appearance. In 1 hour the area becomes swollen and within 24 hours the lesion turns yellow and blisters appear. Recovery takes 1 to 3 months.

CHOKING AGENTS

Chemical agents which attack lung tissue, primarily causing pulmonary oedema, are classed as lung damaging agents. To this group belong: The toxic action of phosgene is typical of a certain group of lung damaging agents. Phosgene is the most dangerous member of this group and the only one considered likely to be used in the future. Phosgene was used for the first time in 1915, and it accounted for 80% of all chemical fatalities during World War I.

Phosgene is a colorless gas under ordinary conditions of temperature and pressure. Its boiling point is 8.2C, making it an extremely volatile and non-persistent agent. Its vapour density is 3.4 times that of air. It may therefore remain for long periods of time in trenches and other low lying areas. In low concentrations it has a smell resembling new mown hay.

The outstanding feature of phosgene poisoning is massive pulmonary oedema. With exposure to very high concentrations death may occur within several hours; in most fatal cases pulmonary oedema reaches a maximum in 12 hours followed by death in 24-48 hours. If the casualty survives, resolution commences within 48 hours and, in the absence of complicating infection, there may be little or no residual damage.

During and immediately after exposure, there is likely to be coughing, choking, a feeling of tightness in the chest, nausea, and occasionally vomiting, headache and lachrymation. The presence or absence of these symptoms is of little value in immediate prognosis. Some patients with severe coughs fail to develop serious lung injury, while others with little sign of early respiratory tract irritation develop fatal pulmonary oedema. A period follows during which abnormal chest signs are absent and the patient may be symptom-free. This interval commonly lasts 2 to 24 hours but may be shorter. It is terminated by the signs and symptoms of pulmonary oedema. These begin with cough (occasionally substernally painful), dyspnoea, rapid shallow breathing and cyanosis. Nausea and vomiting may appear. As the oedema progresses, discomfort, apprehension and dyspnoea increase and frothy sputum develops. The patient may develop shock-like symptoms, with pale, clammy skin, low blood pressure and feeble, rapid heartbeat. During the acute phase, casualties may have minimal signs and symptoms and the prognosis should be guarded. Casualties may very rapidly develop severe pulmonary oedema. If casualties survive more than 48 hours they usually recover.

Sources and Methods



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