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This story was printed from Biological and
Chemical Agents,
located at /27393/dreamwvr/agents/sarin1.htm
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SARIN
INTRODUCTION
Sarin (GB) was entitled after its four pioneers(Schrader, Ambros,
Rüdriger, and van der Linde). In June 1939, formula for Sarin was
given to ChemWarfare section of the Army Weapons Office at Berlin-Spandau along
with a sample of the chemical compound. All synthetic routes for Sarin studied
at that time required use of hydrogen fluoride(HF), that caused severe corrosion
problems that necessitated use of quartz- and silver-lined components.
Pilot plants were built at Spandau, Münster Lager, on Lüneberg heath, and
pilot manufacture of Sarin was carried out in Building 144 in Dyernfurth.
Dyernfurth Sarin plant was variously listed as possessing a capacity of 40 or
100 tons per month. A 500-ton per month production plant was under construction
at Falkenhagen, southeast of Berlin, at the end of World War II. Estimates vary
for the total Sarin production from 500 kg to 10 tons.
The US started producing Sarin in early 1950s and ended regular production in
1956. NATO accepted it as standard chemical warfare agent in early 1950s. Iraq
used Sarin in the 1980-88 war with Iran and had large stocks available in the
1990-91 Gulf War. The Japanese Aum Shinrikyo religious sect released an impure
form of Sarin in Matsumoto in 1994 and in the Tokyo underground in 1995.Aum
Shinrikyo Cult was said to have used the nerve agent in a Tokyo subway. We can
only link this to the fact that Japan and Nazi Germany were axis allies, and the
latter may have shared such chemical warfare technology, but it never seemed
that Japan went ahead with the production of Sarin nerve gas. This incident
gives some clues as to the new roles that nerve agents play, as tools of
terrorists instead of powerful countries.
Sarin belongs to a group of toxic organo-phosphorus compounds inhibiting
cholinesterase, that are stable, effortlessly dispersed, highly poisonous and
have rapid effects both when absorbed through the skin and through respiration.
It is a colorless and odorless gas, that is soluble in water and has a lethal
dose of 0.5 milligram for an adult. It is 26 times more deadly than cyanide gas
and is 20 times more lethal than potassium cyanide. Just 0.01 milligram per
kilogram of body weight a pinprick sized droplet will kill a human.
The vapor is slightly heavier than air, so it drifts close to ground. Under wet
and humid weather conditions Sarin disintegrates swiftly, but as temperature
rises up to a certain point, Sarin’s lethal duration rises, despite humidity.
Colorless, non-persistent liquid, that gives off no odor when vaporizing. The
vapour is colorless. Sarin evaporates 36 times as quickly as Tabun. It can be
made more persistent through the addition of certain oils or petroleum products.
MECHANISM OF ACTION
A property of Sarin is that it is tremendously toxic and has very
prompt effect. It enters the body through inhalation or through the skin.
Poisoning may also occur through consumption of liquids or foods contaminated
with Sarin.
Route for entering the body is of significance for the period required for Sarin
to begin having effect. It also influences the symptoms developed and, to some
extent, the sequence of the different symptoms. Generally, the poisoning works
faster when the agent is absorbed through the respiratory system than via other
routes as the lungs contain many blood vessels and inhaled Sarin can therefore
rapidly diffuse into blood circulation and reach the target organs.
Among these organs, the respiratory system is one of the most significant. If a
person is exposed to a high concentration of Sarin, e.g., 200-mg Sarin/m3
death may occur within a couple of minutes.
Poisoning takes longer when the Sarin enters the body through the skin. Sarin is
fat-soluble and penetrates outer layers of the skin. However, it takes some time
before the poison reaches deeper blood vessels. Consequently, the first symptoms
do not occur until 20-30 minutes after the initial exposure but subsequently the
poisoning process may be rapid if the total dose of Sarin is high.
The toxic effect of Sarin depends on it becoming bound to an enzyme,
acetylcholinesterase, and thereby inhibits this vital enzyme's normal biological
activity in the cholinergic nervous system. When such an enzyme is inhibited,
the active site loses its specificity and will not be able to accommodate the
complementary substrate (acetylcholine), form an ES-COMPLEX and break it down
into simpler products.
CAUSE OF DEATH
In the lack of treatment, death is caused by anoxia due to airway
obstruction, weakness of muscles of respiration and central depression of
respiration.
Airway obstruction is due to pharyngeal muscular collapse, upper airway and
bronchial secretions, bronchial constriction and occasionally laryngospasm and
paralysis of respiratory muscles.
Respiration is shallow, laboured, and rapid and the casualty may gasp and
struggle for air. Cyanosis increases. Finally, respiration becomes slow and then
ceases.
Unconsciousness ensues. Blood pressure (which may have been transitorily
elevated) falls. Cardiac rhythm may become irregular and death may follow.
If aided ventilation is commenced through cricothyroidotomy or endotracheal tube
and airway secretions are taken out by postural drainage and suction and
diminished by the administration of atropine, the individual may survive several
lethal doses of a nerve agent. However, 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 sequence of symptoms.
PROTECTION
To prevent inhalation of an incapacitating or lethal dose it is
critical that breath is held and the respirator put on at the first warning of
the presence, or suspected presence, of a nerve agent.
Normal clothing is penetrated by these agents whether contact is with liquid or
vapour and specialised clothing including a respirator, nuclear, biological, and
chemical (NBC) suit, gloves and overboots are required for protection when
liquid agent is present. Respirator shields eyes, mouth and respiratory tract
against nerve agent spray vapour and aerosol. Nerve agent vapour in field
concentrations is absorbed through the skin very slowly, if at all, so that
where a vapour hazard exists alone, the respirator may provide adequate
protection without the use of an nuclear-biological-chemical(NBC) suit.
DECONTAMINATION
Significance of early decontamination can not be over-emphasised.
Decontamination of the skin should be achieved rapidly if it is to be fully
effective. Liquid agent may be removed by fullers' earth or chemically
inactivated by the use of reactive decontaminants. Decontamination personnel
should use a respirator and full protective equipment whilst decontamination is
performed.
Once victim is decontaminated, or agent fully absorbed, no further risk of
contamination exists. The victim's body fluids, urine or faeces do not present a
chemical warfare (CW) hazard.
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