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Nerve Agents.
Nerve agents are organophosphate ester derivatives of
phosphoric acid. They are generally divided into the Gagents,
which in the unmodified state are volatile, and the
V-agents, which tend to be more persistent. Even G-agents
are capable of being thickened with various substances to
increase the persistence and penetration of the intact skin.
The principal nerve agents are Tabun (GA), Sarin (GB),
Soman (GD), and VX. (In some countries the V-agents are
known as A-agents.)
The G-agents are fluorine- or cyanide-containing organophosphates.
In pure form they are colorless liquids.
Their solubility in water ranges from complete miscibility
for GB to almost total insolubility for GD. They have a
weakly fruity odor but in field concentrations are odorless.
Clothing gives off G-agents for about 30 minutes after
contact with vapor; consider this fact before unmasking.
The V-agents are sulfur-containing organophosphorous
compounds. They are oily liquids with high boiling points,
low volatility, and resultant high persistency. They are
primarily contact hazards. They are exceptionally toxic; the
limited amount of vapor they produce is sufficient to be an
inhalation hazard. They have very limited volubility in
water and are hydrolyzed only minimally. V-agents affect
the body in essentially the same manner as G-agents.
The nerve agents are all viscous liquids, not nerve gas
per se. However, the vapor pressures of the G-series nerve
agents are sufficiently high for the vapors to be lethal
rapidly. The volatility is a physical factor of most importance.
GB is so volatile that small droplets sprayed from a
plane or released from a shell exploding in the air may
never reach the ground. This total volatilization means that
GB is largely a vapor hazard. At the other extreme agent
VX is of such low volatility that it is mainly a liquid contact
hazard. Toxicity can occur from the spray falling on one’s
skin or clothes and from touching surfaces on which the
spray has fallen. GD is also mainly a vapor hazard, while
GA can be expected to contaminate surfaces for a sufficiently
long time to provide a relevant contact hazard.
Thickeners added to GD increase persistence in the
field. The thickened agents form large droplets that provide
a greater concentration reaching the ground and a
greater contact hazard than the unthickened forms.
The relative volubility of these compounds in water and
soil is of significance because it relates to their disposition.
The ability of GB and GA to mix with water means that
water could wash them off surfaces, that these agents can
easily contaminate water sources, and that they will not
penetrate skin as readily as the more fat-soluble agents VX
and GD. G-agents spread rapidly on surfaces, such as skin;
VX spreads less rapidly, and the thickened agents very
slowly. The moist surfaces in the lungs absorb all the agents
very well.
Both the G- and V-agents have the same physiological
action on humans. They are potent inhibitors of the enzyme
acetylcholinesterase (AChE), which is required for the
function of many nerves and muscles in nearly every multicellular
animal. Normally, AChE prevents the accumulation
of acetylcholine after its release in the nervous system.
Acetylcholine plays a vital role in stimulating voluntary
muscles and nerve endings of the autonomic nervous system
and many structures within the central nervous system.
Thus, nerve agents that are cholinesterase inhibitors permit
acetylcholine to accumulate at those sites, mimicking
the effects of a massive release of acetylcholine. The major
effects will be on skeletal muscles, parasympathetic end
organs, and the central nervous system.
Individuals poisoned by nerve agents may display the
following symptoms:
Difficulty in breathing.
Drooling and excessive sweating.
Nausea.
Vomiting, cramps, and loss of bladder/bowel control.
Twitching, jerking, and staggering.
Headache, confusion, drowsiness, coma, and convulsion.
The number and severity of symptoms depend on the
quantity and route of entry of the nerve agent into the body.
When the agent is inhaled, a prominent symptom is pinpointing
of the pupils of the eyes and dimness of vision
because of the reduced amount of light entering. However,
if exposure has been through the skin or by ingestion of a
nerve agent, the pupils may be normal or only slightly to
moderately reduced in size. In this event, diagnosis must
rely upon the symptoms of nerve agent poisoning other
than its effects on the pupils.
Exposure through the eyes produces a very rapid onset
of symptoms (usually less than 2 to 3 minutes). Respiratory
exposure usually results in onset of symptoms in 2 to 5 minutes; lethal doses kill in less than 15 minutes. Liquid in
the eye kills nearly as rapidly as respiratory exposure.
Symptoms appear much more slowly from skin absorption.
Skin absorption great enough to cause death may
occur in one to two hours. Respiratory lethal dosages kill
in one to ten minutes, and liquid in the eye kills nearly as
rapidly. Very small skin dosages sometimes cause local
sweating and tremors but little other effects. Nerve agents
are cumulative poisons. Repeated exposure to low concentrations,
if not too far apart, will produce symptoms.
Treatment of nerve agent poisoning includes use of the
nerve agent antidote (atropine and 2-PAM chloride).
Atropine blocks acetylcholine; 2-PAM Cl, reactivates the
enzyme AChE. As time passes without treatment the binding
of nerve agents to AChE “ages” and the 2-PAM Cl can
no longer remove the agent. Certain agents, such as GD,
that age rapidly may resist treatment if it is not prompt.
Therefore, an antidote enhancer, pyridostigmine bromide
(PB), is available to US forces in active theaters of operation.
PB pretreatment increases the victim’s survivability
when the antidote is used after exposure to nerve agents