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 - sulphur mustard (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 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.

• 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 odour. This exposure does not effect 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 sulphur 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 is 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 oedema 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 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.

• Liquid arsenical vesicants cause severe damage to the eye. On contact, pain and blepharospasm occur instantly. Oedema 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 oedema 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 vapours of arsenical vesicants are so irritating to the respiratory tract that conscious casualties will immediately put on a mask to avoid the vapour. 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.

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.