Mustard Agents: An Overview of the Sulfur and Nitrogen Mustard Agents
NOTICE: TO ALL CONCERNED Certain text files and messages contained on this site deal with activities and devices which would be in violation of various Federal, State, and local laws if actually carried out or constructed. The webmasters of this site do not advocate the breaking of any law. Our text files and message bases are for informational purposes only. We recommend that you contact your local law enforcement officials before undertaking any project based upon any information obtained from this or any other web site. We do not guarantee that any of the information contained on this system is correct, workable, or factual. We are not responsible for, nor do we assume any liability for, damages resulting from the use of any information on this site.
Mustard Agents: An overview of the sulfur and nitrogen mustard agents
Mustard Agents
Source: A FOA Briefing Book on Chemical Weapons
Mustard agents are usually classified as "blistering agents" owing to
the similarity of the wounds caused by these substances resembling
burns and blisters. However, since mustard agents also cause severe
damage to the eyes, respiratory system and internal organs, they
should preferably be described as "blistering and tissue-injuring
agents". Normal mustard agent, bis-(2-chloroethyl)sulphide, reacts
with a large number of biological molecules. The effect of mustard
agent is delayed and the first symptoms do not occur until between
2-24 hours after exposure.
Mustard agent was produced for the first time in 1822 but its
harmful effects were not discovered until 1860. Mustard agent was
first used as a CW agent during the latter part of the First World
War and caused lung and eye injuries to a very large number of
soldiers. Many of them still suffered pain 30-40 years after they had
been exposed, mainly as a result of injuries to the eyes and chronic
respiratory disorders.
Towards the end of the Second World War a large number of
soldiers and sailors were injured during a German attack on the
Italian port of Bari. A cargoship loaded with mustard agent
ammunition was hit and large amounts of mustard agent became
mixed with the water. The victims swam around in the contaminated
water but it was not realized until too late that a large number of
people had been injured by mustard agent. The Bari Incident served
as a macabre illustration of the delayed effect of mustard agent.
During the war between Iran and Iraq in 1979-88, Iraq used large
quantities of chemical agents. About 5 000 Iranian soldiers have
been reported killed, 10-20 per cent by mustard agent. In addition,
there were 40 000 to 50 000 injured. A typical result of warfare with
mustard agent is that the medical system is loaded with numerous
injured who require long and demanding care.
Incidents are still occurring annually in the neighbourhood of
Sweden where people risk injury from mustard agent. This largely
involves fishermen who are exposed to mustard agent brought to the
surface by fishing nets. The background is found in the dumping of
chemical weapons after the Second World War in waters off the
Danish and Swedish coasts. Many fishing ports in south Sweden
and Denmark have resources to care for injured people and to
decontaminate equipment contaminated by mustard agent. Certain
resources are also available on the fishing vessels.
Mustard agent is very simple to manufacture and can therefore be a
"first choice" when a country decides to build up a capacity for
chemical warfare.
Apart from mustard agent, there are also several other closely related
compounds which have been used as chemical weapons. During the
1930's, several reports were published on the synthesis of nitrogen
mustard agent and its remarkable blistering effect. The mechanism of
action and symptoms largely agree with those described for mustard
agent. Germans and Americans started the military production of
nitrogen mustard agent in 1941 and 1943, respectively, whereas the
development in England was abandoned following an explosion.
There is no verified use of nitrogen mustard agents as chemical
weapons and their usefulness is restricted by these types of agents
being unsuitable for storage.
Physical and Chemical Properties
In its pure state, mustard agent is colourless and almost odourless.
The name was given to mustard agent as a result of an earlier
production method which yielded an impure mustard-smelling
product. Mustard agent is also claimed to have a characteristic smell
similar to rotten onions. However, the sense of smell is dulled after
only a few breaths so that the smell can no longer be distinguished.
In addition, mustard agent can cause injury to the respiratory system
in concentrations which are so low that the human sense of smell
cannot distinguish them.
At room temperature, mustard agent is a liquid with low volatility
and is very stable during storage. The melting-point for pure mustard
agent is 14.4 oC. In order to be able to effectively use mustard agent
at lower temperatures, it has been mixed with lewisite in some types
of ammunition in a ratio of 2:3. This mixture has a freezing-point of
-26 oC. During the Second World War, a form of mustard agent with
high viscosity was manufactured by means of the addition of a
polymer. This is the first known example of a thickened CW agent.
Mustard agent can easily be dissolved in most organic solvents but
has negligible solubility in water. In aqueous solutions, mustard
agent decomposes into non-poisonous products by means of
hydrolysis. This reaction is catalyzed by alkali. However, only
dissolved mustard agent reacts, which means that the decomposition
proceeds very slowly. Bleaching-powder and chloramines, however,
react violently with mustard agent, whereupon non-poisonous
oxidation products are formed. Consequently, these substances are
used for the decontamination of mustard agent.
Mechanism of Action
The toxic effects of mustard agent depend on its ability to covalently
bind to other substances. The chlorine atom is spiked off the ethyl
group and the mustard agent is transferred to a reactive sulphonium
ion. This ion can bind to a large number of different biological
molecules. Most of all it binds to nucleophiles such as nitrogen in
the base components of nucleic acids and sulphur in SH-groups in
proteins and peptides. Since mustard agent contains two "reactive
groups", it can also form a bridge between or within molecules.
Mustard agent can destroy a large number of different substances in
the cell by means of alkylation and thereby influence numerous
processes in living tissue.
Symptoms
In the form of gas or liquid, mustard agent attacks the skin, eyes,
lungs and gastro-intestinal tract. Internal organs may also be injured,
mainly blood-generating organs, as a result of mustard agent being
taken up through the skin or lungs and transported into the body.
The delayed effect is a characteristic of mustard agent. Mustard
agent gives no immediate symptoms upon contact and consequently
a delay of between two and twenty-four hours may occur before pain
is felt and the victim becomes aware of what has happened. By then
cell damage has already been caused.
Symptoms of mustard agent poisoning extend over a wide range.
Mild injuries consist of aching eyes with abundant flow of tears,
inflammation of the skin, irritation of the mucous membrane,
hoarseness, coughing and sneezing. Normally, these injuries do not
require medical treatment. Severe injuries which are incapacitating
and require medical care may involve eye injuries with loss of sight,
the formation of blisters on the skin, nausea, vomiting and diarrhoea
together with severe respiration difficulty.
Acute mortality arising from exposure to mustard agent is low. The
dose needed to directly kill a person upon inhalation is, e.g., about
50 times larger than the dose giving acute mortality upon poisoning
with the nerve agent soman. People who die after exposure to
mustard agent usually do so after a few days up to one or more
weeks.
Minor skin damage may be caused by mustard agent in the gaseous
state whereas the most severe injuries are caused after contact with
liquid mustard agent. Skin damage first appears as a painful
inflammation. Depending on the level of exposure, the injury may
develop into pigmentation, which flakes-off after a couple of weeks,
small surface blisters or deep liquid-filled blisters with subsequent
skin necrosis. In extreme cases, the skin necrosis may be so
comprehensive that no blisters occur. Skin injuries are more severe
in humid and warm climates. Similarly, the injuries will be more
severe where the skin is moist and warm, e.g., in the groin and
armpits.
Experience has shown that even extremely extensive skin damage,
80-90 %, can be cured if the patient is kept free of infection.
However, injuries to the skin require a very long period of
recuperation, much longer than thermal burns, and may require care
and plastic surgery over a period of several months.
Injury to the eyes appear initially as irritation with eye inflammation
and a strong flow of tears. Depending on exposure, the symptoms
thereafter may successively develop to sensitivity to light, swollen
eyelids, and injury to the cornea. Severe damage to the eye may lead
to the total loss of vision. Victims suffering damage to the eyes may
encounter problems persisting up to 30-40 years following exposure.
The most common cause of death as a result of mustard agent
poisoning is complications after lung injury caused by inhalation of
mustard agent. Lung injuries become apparent some hours after
exposure and will first appear as a pressure across the chest,
sneezing and hoarseness. Severe coughing and respiration
difficulties caused by pulmonary oedema will gradually occur and
after a couple of days, a "chemical pneumonia" may develop. Most
of the chronic and late effects are also caused by lung injuries.
The effect on inner organs which is most pronounced is injury to the
bone marrow, spleen and lymphatic tissue. This may cause a drastic
reduction in the number of white blood cells 5-10 days after
exposure, a condition very similar to that after exposure to radiation.
This reduction of the immune defence will complicate the already
large risk of infection in people with severe skin and lung injuries.
Antidotes and Methods of Treatment
There is no treatment or antidote which can affect the basic cause of
mustard agent injury. Instead, efforts must be made to treat the
symptoms. By far the most important measure is to rapidly and
thoroughly decontaminate the patient and thereby prevent further
exposure. This decontamination will also decrease the risk of
exposure to staff. Clothes are removed, the skin is decontaminated
with a suitable decontaminant and washed with soap and water. If
hair is suspected to be contaminated then it must be shaved off. Eyes
are rinsed with water or a physiological salt solution for at least five
minutes.
In medical treatment, efforts are made to control infections by means
of antibiotics. Pain can be eased by local anesthetics. After skin
injuries have healed, it may be necessary to introduce plastic
surgery. Lung injuries are treated with bronchodilatory treatment.
Medicine to relieve coughing and also cortisone preparations may be
used. Eye injuries are treated locally with painkillers and with
antibiotics if required. Despite treatment, inflammation and light
sensitivity may remain for long periods.
Modern knowledge on the mechanisms behind mustard agent
injuries may lead mainly to new ways of treatment. The first step,
alkylation, takes place extremely rapidly and is probably very
difficult to influence. Future treatment may concentrate on
suppressing and alleviating the development of symptoms and
thereby improve the opportunities for good recovery.
Types of Injury Caused by Mustard Agent
It is impossible to identify a single mechanism for the damage
caused by mustard agent. However, two possible important
mechanisms can be mentioned where the first step in both is the
formation of a reactive sulphonium ion. One such mechanism is the
bonding of mustard agent to the base compounds in DNA
(alkylation). The bonding may induce breakages of strands and the
formation of bridges between the two strands in the DNA molecule.
Bridges of this kind prevent DNA from functioning normally during
cell division which may lead to severe injury and possibly cell
mortality. Damage to the DNA may also lead to mutations and
disturbance to the natural repair mechanisms of DNA. The influence
on DNA can cause the increased frequency of cancer observed after
exposure to mustard agent.
The other mechanism of action is interaction between mustard agent
and intracellular glutathion. Glutathion is a small peptide molecule
which, among other things, takes care of the free radicals formed
during cell respiration. If too large an amount of glutathion is bound
by mustard agent, then the regulation of these free radicals no longer
functions. Since free radicals are extremely toxic, this may lead to a
number of processes in the cell being severely disturbed.
Mustard agent can also bind to different proteins in the cell.
However, it is not known how much this contributes to the injuries
caused. The binding takes place at the functional groups, e.g., the
sulphydryl or amino groups. If the binding is made to, for example,
the active site of enzymes, then their activity is inhibited which
could lead to metabolic disorders. If, on the other hand, membrane
proteins are bound, the result can be a modified uptake of
substances and the inner environment of the cell will become
disturbed.
Physical Properties of Mustard Agent
Molecular weight, Dalton159.1
Density, g/cm31.27
Boiling-point oC217
Melting-point oC14
Vapour pressure mm Hg at 25oC0.11
Volatility mg/m3 at 25 oC900
Solubility in water % at 20oC0,06
Toxicity of Mustard Agent
Inhalation: LCt50 1 500 mg*min/m3
Skin exposure: LCt50 10 000 mg*min/m3
Smallest blister-causing dose on skin: 0,02 mg
|