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Types of Chemical Weapons 

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 Blister Agents Choking Agents
  • GA - Tabun
  • GB - Sarin
  • GD - Soman
  • GF - Cyclosarin
  • VX - Methylphosphonothioic Acid
  • HD - Sulfur Mustard (Yperite)
  • HN - Nitrogen Mustard
  • L - Lewisite
  • CX - Phosgene Oximine
  • CG - Phosgene
  • DP - Diphosgene
  • Cl - Chlorine
  • PS - Chloropicrin

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:

  • GA - tabun
  • GB - sarin
  • GD - soman
  • GF - cyclosarin
  • VX - methylphosphonothioic acid

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 vapor 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 odor.

  • GB and VX doses which are potentially life-threatening may be only slightly larger than those producing least effects. Death usually occurs within 15 minutes after absorption of a fatal VX dosage.
  • Although only about half as toxic as GB by inhalation, GA in low concentrations is more irritating to the eyes than GB. Symptoms appear much more slowly from a skin dosage than from a respiratory dosage. Although skin absorption great enough to cause death may occur in 1 to 2 minutes, death may be delayed for 1 to 2 hours. Respiratory lethal dosages kill in 1 to 10 minutes, and liquid in the eye kills almost as rapidly.

Toxicological Data

Route Form Effect Type GA GB GD VX Doasge
Ocular Vapor Miosis ECt50 -- <2 <2 <0.09 mg•min/m3
Inhalation at RMV = 15 1/min Vapor Runny Nose ECt50 -- <2 <2 <0.09 mg•min/m3
Inhalation at RMV = 15 liters/min Vapor Incapacitation ICt50 -- 35 35 25 mg•min/m3
Inhalation at RMV = 15 liters/min Vapor Death LCt50 135 70 70 30 mg•min/m3
Percutaneous Liquid Death LD50 4,000 1,700 350 10 mg

Ct (Concentration time; mg•min/m3) - A measure of exposure to a gas, the effective vapor exposure, determined by the concentration of the gas (mg/m3) and the length of exposure (min).
ECt50 (Effective Concentration Time; mg•min/m3) - The Ct at which a gas debilitates 50% of the exposed population in a specific way.
ICt50 (Incapacitating Concentration Time; mg•min/m3) - The Ct at which a gas incapacitates 50% of the exposed population.
LCt50 (Lethal concentration time; mg•min/m3) - The Ct at which a gas kills 50% of the exposed population.
LD50 (Lethal dose; mg) - The dose or amount at which a substance kills 50% of the exposed population.
RMV (Respiratory minute volume; liters/min) - Volume of air inhaled per minute.

The values are estimates of the doses which have lethal effects on a 70kg man. Effective dosages of 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 vapor, 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 vapor concentrations, the nerve agent is carried from the lungs throughout the circulatory system; widespread systemic effects may appear in less than 1 minute.

  • The earliest ocular effect which follows minimal symptomatic exposure to vapor is miosis. The pupillary constriction may be different in each eye. Within a few minutes after the onset of exposure, there also occurs redness of the eyes. Following minimal exposure, the earliest effects on the respiratory tract are a watery nasal discharge, nasal hyperaemia, sensation of tightness in the chest and occasionally prolonged wheezing
  • Exposure to a level of a nerve agent vapor slightly above the minimal symptomatic dose results in miosis, pain in and behind the eyes and frontal headache. Some twitching of the eyelids may occur. Occasionally there is nausea and vomiting.
  • In mild exposures, the systemic manifestations of nerve agent poisoning usually include tension, anxiety, jitteriness, restlessness, emotional lability, and giddiness. There may be insomnia or excessive dreaming, occasionally with nightmares.
  • If the exposure is more marked, the following symptoms may be evident: headache, tremor, drowsiness, difficulty in concentration, impairment of memory with slow recall of recent events, and slowing of reactions. In some casualties there is apathy, withdrawal and depression.
  • With the appearance of moderate systemic effects, the casualty begins to have increased fatiguability and mild generalised weakness which is increased by exertion. This is followed by involuntary muscular twitching, scattered muscular fasciculations and occasional muscle cramps. The skin may be pale due to vasoconstriction and blood pressure moderately elevated.
  • If the exposure has been severe, the cardiovascular symptoms will dominate and twitching (which usually appear first in the eyelids and in the facial and calf muscles) becomes generalised. Many rippling movements are seen under the skin and twitching movements appear in all parts of the body. This is followed by severe generalised muscular weakness, including the muscles of respiration. The respiratory movements become more laboured, shallow and rapid; then they become slow and finally intermittent.
  • After moderate or severe exposure, excessive bronchial and upper airway secretions occur and may become very profuse, causing coughing, airway obstruction and respiratory distress. Bronchial secretion and salivation may be so profuse that watery secretions run out of the sides of the mouth. The secretions may be thick and tenacious. If the exposure is not so overwhelming as to cause death within a few minutes, other effects appear. These include sweating, anorexia, nausea and heartburn. If absorption of nerve agent has been great enough, there may follow abdominal cramps, vomiting, diarrhea, and urinary frequency. The casualty perspires profusely, may have involuntary defecation and urination and may go into cardiorespiratory arrest followed by death.
  • If absorption of nerve agent has been great enough, the casualty becomes confused and ataxic. The casualty may have changes in speech, consisting of slurring, difficulty in forming words, and multiple repetition of the last syllable. The casualty may then become comatose, reflexes may disappear and generalised convulsions may ensue. With the appearance of severe central nervous system symptoms, central respiratory depression will occur and may progress to respiratory arrest.
  • After severe exposure the casualty may lose consciousness and convulse within a minute without other obvious symptoms. Death is usually due to respiratory arrest requires prompt initiation of assisted ventilation to prevent death. If assisted ventilation is initiated , the individual may survive several lethal doses of a nerve agent.
  • If the exposure has been overwhelming, amounting to many times the lethal dose, death may occur despite treatment as a result of respiratory arrest and cardiac arrhythmia. When overwhelming doses of the agent are absorbed quickly, death occurs rapidly without orderly progression of symptoms.
Nerve agent poisoning may be identified from the characteristic signs and symptoms. If exposure to vapor 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 diarrhea when ingested.

The vesicant agents include:
  • HD - sulfur mustard, or yperite
  • HN - nitrogen mustard
  • L - lewisite (arsenical vesicants may be used in a mixture with HD)
  • CX - phosgene (properties and effects are very different from other vesicants)

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 vapor 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.

  • In a single exposure the eyes are more susceptible to mustard than either the respiratory tract or the skin. The effects of mustard on the eyes are very painful. Conjunctivitis follows exposure of about 1 hour to concentrations barely perceptible by odor. This exposure does not affect the respiratory tract significantly. A latent period of 4 to 12 hours follows mild exposure, after which there is lachrymation and a sensation of grit in the eyes. The conjunctival and the lids become red. Heavy exposure irritates the eyes after 1 to 3 hours and produces severe lesions.
  • The hallmark of sulfur mustard exposure is the occurrence of a latent symptom and sign free period of some hours post exposure. The duration of this period and the severity of the lesions are dependent upon the mode of exposure, environmental temperature and probably on the individual himself. High temperature and wet skin are associated with more severe lesions and shorter latent periods.
  • If only a small dose is applied to the skin, the skin turns red and itches intensely. At higher doses blister formation starts, generally between 4 and 24 hours after contact, and this blistering can go on for several days before reaching its maximum. The blisters are fragile and usually rupture spontaneously giving way to a suppurating and necrotic wound. The necrosis of the epidermal cells is extended to the underlying tissues, especially to the dermis. The damaged tissues are covered with slough and are extremely susceptible to infection. The regeneration of these tissues is very slow, taking from several weeks to several months.
  • Mustard attacks all the mucous membranes of the respiratory tract. After a latent period of 4 to 6 hours, it irritates and congests the mucous membranes of the nasal cavity and the throat, as well as the trachea and large bronchi. Symptoms start with burning pain in the throat and hoarseness of the voice. A dry cough gives way to copious expectoration. Airway secretions and fragments of necrotic epitheliums may obstruct the lungs. The damaged lower airways become infected easily, predisposing to pneumonia after approximately 48 hours. If the inhaled dose has been sufficiently high the victim dies in a few days, either from pulmonary edema or mechanical asphyxia due to fragments of necrotic tissue obstructing the trachea or bronchi, or from superimposed bacterial infection, facilitated by an impaired immune response.

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 odorless liquid, but usually contains small amounts of impurities that give it a brownish color and an odor 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.

  • Liquid arsenical vesicants cause severe damage to the eye. On contact, pain and blepharospasm occur instantly. Edema of the conjunctival and lids follow rapidly and close the eye within an hour. Inflammation of the iris usually is evident by this time. After a few hours, the edema of the lids begins to subside, while haziness of the cornea develops.
  • Liquid arsenical vesicants produce more severe lesions of the skin than liquid mustard. Stinging pain is felt usually in 10 to 20 seconds after contact with liquid arsenical vesicants. The pain increases in severity with penetration and in a few minutes becomes a deep, aching pain. Contamination of the skin is followed shortly by erythema, then by vesication which tends to cover the entire area of erythema. There is deeper injury to the connective tissue and muscle, greater vascular damage, and more severe inflammatory reaction than is exhibited in mustard burns. In large, deep, arsenical vesicant burns, there may be considerable necrosis of tissue, gangrene and slough.
  • The vapors of arsenical vesicants are so irritating to the respiratory tract that conscious casualties will immediately put on a mask to avoid the vapor. No severe respiratory injuries are likely to occur except among the wounded who cannot put on masks and the careless, who are caught without masks. Lewisite is irritating to nasal passages and produces a burning sensation followed by profuse nasal secretion and violent sneezing. Prolonged exposure causes coughing and production of large quantities of froth mucus. Injury to respiratory tracts, due to vapor exposure is similar to mustard's; however, edema of the lung is more marked and frequently accompanied by pleural fluid.

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.

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 vapor pressure and its odor 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 necrotizing 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 edema. 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 edema, are classed as lung damaging agents. To this group belong:

  • CG - phosgene
  • DP - diphosgene
  • Cl - chlorine
  • PS - chloropicrin

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 8.2°C, making it an extremely volatile and non-persistent agent. Its vapor 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 edema. With exposure to very high concentrations death may occur within several hours; in most fatal cases pulmonary edema 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 edema. 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 edema. These begin with cough (occasionally substernally painful), dyspnea, rapid shallow breathing and cyanosis. Nausea and vomiting may appear. As the edema progresses, discomfort, apprehension and dyspnea 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 edema. If casualties survive more than 48 hours they usually recover.