Chemical Agents Fact Sheet

Hydrofluoric Acid

A.  Summary of Agent Effects

Hydrofluoric acid (HF) is one of the strongest inorganic acids. HF is a
clear, colorless liquid, and, when exposed to air, concentrated
solutions and anhydrous HF produce pungent fumes. HF is a caustic acid
and can produce severe tissue damage either as the water solution, or in
the anhydrous form (hydrogen fluoride). The fluoride ion in HF can also
rapidly penetrate the skin and cause systemic effects, especially
cardiac arrhythmias.

B.  Clinical Effects

**Immediate.** HF concentrations \>50 percent are immediately apparent.
Concentrations of 20 to 50 percent may appear within 1 to 8 hours, and
concentrations of 0 to 20 percent may appear in up to 24 hours.

**Skin.** The initial signs of HF burn are redness, edema, and
blistering. The initial exposure to HF may not look like a typical acid
burn. Skin may only appear red and may not be painful at first. Damage
to skin may happen during several hours or days, and deep, painful
wounds may develop. Strong acid concentrations (more than 50 percent)
cause immediate, severe, burning pain and a whitish discoloration of the
skin that usually proceeds to blister formation. Exposure to HF vapors
can also result in similar burns. Skin contact with acid concentrations
in the 20- to 50‑percent range may not produce clinical signs or
symptoms for 1 to 8 hours.

**Eyes.** HF can cause severe eye burns. Initial signs are instant pain,
stinging, tearing, red­ness, and swelling of the eyelids, followed by
destruction or opacification of the cornea. Blindness may result from
severe or untreated exposures.

**Respiratory.** A mild exposure to HF can cause irritation to the nose,
throat, and respira­tory system. Onset of symptoms may be delayed for
several hours. Severe exposure can cause nose and throat burns, lung
inflammation, tracheobronchitis, and pulmonary hemorrhagic edema (fluid
in the lungs). HF fumes may cause larynospasm, laryngeal edema,
bronchospasm and/or acute pulmonary edema. Acute symptoms may include
coughing, choking, chest tightness, chills, fever, and cyanosis.

**Ingestion.** If HF is ingested, severe burns to the mouth, esophagus,
and stomach may occur. Symptoms may include severe stomach and
intestinal irritation (nausea, vomiting, diarrhea), abdominal pain,
vomiting of blood, collapse of blood pressure, and shock.

**Systemic.** Significant amounts of fluoride ion may be absorbed by
skin contact, inhalation, or by ingestion. If systemic absorption of
fluoride occurs, hypocalcemia (depletion of calcium in the body),
hypomagnesemia, hyperkalema, cardiac arrhythmias, and altered pulmonary
hemodynamics may also occur.

C.  Medical Management

**Skin Contact.** Immediately flush contaminated skin with large
quantities of cold water for at least 15 minutes. Speed and thoroughness
in washing off the acid is of primary impor­tance. Begin flushing even
before removing clothing. Remove all contaminated clothing while
continuing to flush with water. Rinse with large amounts of running
water. If 0.13 percent benzalkoniumchloride (Zephiran) solution or
2.5 percent calcium gluconate gel are available, the rinsing may be
limited to 5 minutes, with the soaks or gel applied as soon as the
rinsing is stopped. Begin soaking the affected areas in iced
0.13 percent benzalkonim chloride (Zephiran) solution. Use ice cubes,
not shaved ice, to prevent frostbite. If immersion is not practical,
towels should be soaked with iced 0.13 percent benzalkonium chloride
(Zephiran) solution and used as compresses for the burned area.
Compresses should be changed every 2 to 4 minutes. Benzalkonium chloride
(Zephiran) soaks or compresses should be continued until pain is
relieved or until more definitive medical treatment is provided. Start
massaging 2.5 percent calcium gluconate gel into the burn site. Calcium
gluconate gel can be prepared by mixing a 10‑milliliter ampule of
calcium cluconate with a 2‑ounce tube of K‑Y Jelly^^. Apply gel
frequently and massage continuously until pain and/or redness disappear
or until more definitive medical care is given. It is advisable for the
individual applying the calcium gluconate gel to wear surgical gloves to
prevent a possible secondary HF burn. If benzalkonium chloride
(Zephiran) or calcium gluconate gel is not available, use an iced
saturated water solution of magnesium sulfate (Epsom Salts), iced 70
percent alcohol, or iced 0.2 percent water solution of Hyamine 1622.

**Eye Contact.** Immediately flush the eyes for at least 15 minutes with
large amounts of gently flowing water. Hold eyelids open and away from
the eye during irrigation to allow thorough flushing of the eyes. Do not
use benzalkonium chloride (Zephiran) solution for burns of the eyes. If
sterile 1 percent calcium gluconate solution is available, washing may
be limited to 5 minutes, after which the 1 percent calcium gluconate
solution should be used repeatedly to irrigate the eye using a syringe
or eye irrigator. If a physician is not immediately available, apply one
or two drops of 0.5 percent tetracaine hydrochloride, 0.5 percent
proparacaine, or other aqueous, topical ophthalmic anesthetic and
continue irrigation.

**Respiratory.** Immediately move victim to fresh air. Oxygen should be
administered as soon as possible. A nebulized solution of 2.5 percent
calcium gluconate may be adminis­tered with oxygen inhalation.

**Ingestion.** Have the victim drink large amounts of water as quickly
as possible to dilute the acid. Do not induce vomiting. Do not give
emetics or baking soda. Give several glasses of milk or several ounces
of milk of magnesia, Mylanta, Maalox, or grind up and administer up to
30 Tums, Caltrate, or other antacid tablets with water. The calcium or
magnesium in these compounds may act as an antidote.

**Systemic.** If systemic absorption of fluoride occurs, hypocalcemia
(depletion of calcium in the body), hypomagnesemia, hyperkalema, cardiac
arrhythmias, and altered pulmonary hemodynamics may also occur. Cardiac
monitoring, monitoring serum calcium, magnesium, and electrolytes should
be examined and the administration of intravenous (IV) calcium
gluconate, correcting magnesium and electrolyte imbalance, and, in
extreme cases, hemodialysis should be instituted.

Table 4-1. Agent Exposure

  ---------------- ------------------------------------------------------
  **Eyes**         Instant pain, stinging, tearing, redness, and swelling
                   of the eyelids.

  **Skin**         Initial signs are redness, edema, and blistering.
                   Strong acid concentrations (more than 50 percent)
                   cause immediate, severe, burning pain and a whitish
                   discoloration of the skin that usually proceeds to
                   blister formation.

  **Respiratory    Mild exposure can irritate nose, throat, and
  Tract**          respiratory system. Severe exposure can cause nose and
                   throat burns, lung inflammation, tracheo­bronchitis,
                   and pulmonary hemorrhagic edema (fluid in the lungs).
                   HF fumes may cause larynospasm, laryngeal edema,
                   bronchospasm, and/or acute pulmonary edema. Acute
                   symptoms may include coughing, choking, chest
                   tightness, chills, fever, and cyanosis.

  **Ingestion**    Severe burns to the mouth, esophagus, and stomach,
                   including severe stomach and intestinal irritation
                   (nausea, vomiting, diarrhea), abdominal pain, vomiting
                   of blood, collapse of blood pressure, and shock.

  **Systemic       Hypocalcemia (depletion of calcium in the body),
  Effects**        hypomagnesemia, hyperkalema, cardiac arrhythmias, and
                   altered pulmonary hemodynamics.

  **Time of        HF concentrations \>50 percent are immediately
  Onset**          apparent. Concentrations of 20 to 50 percent are 1 to
                   8 hours, and concentrations of 0 to 20 percent are up
                   to 24 hours.

  **Chronic        Chronic toxicity and skeletal fluorosis.
  Exposure**       
  ---------------- ------------------------------------------------------

Lewisite

A.  Summary of Agent Effects

Lewisite is a vesicant that damages the eyes, skin, and airways by
direct contact. After absorption, it causes an increase in capillary
permeability to produce hypovolemia, shock, and organ damage. Exposure
to lewisite causes immediate pain or irritation, although lesions
require hours to become full blown. Management of a lewisite casualty is
similar to management of a mustard casualty, although a specific
antidote, British Anti-Lewisite (BAL: \[dimercaprol\]) will alleviate
some effects.

Lewisite presents a vapor and liquid hazard and may damage the eyes,
skin, respiratory tract, and circulatory system. Exposure to lewisite
causes immediate (within 30 seconds) irritation or pain. The skin
absorbs lewisite within 3 to 5 minutes.

The vapor may be inhaled into the respiratory tract, causing the
immediate onset of burning pain, irritation of the nose, reflex
coughing, and chest tightness.

The vapor also affects the eyes, with the immediate onset of pain,
redness, uncontrollable blinking, and swelling of the eyelids.

The vapor or a liquid splash of lewisite on the skin may cause immediate
stinging pain and destruction of tissue, followed by blistering within
12 hours.

Lewisite is an oily, colorless liquid, and impure lewisite is amber to
brown and black in color, with the characteristic odor of geraniums. It
is more volatile than mustard.

D.  Clinical Effects

There is almost no data on humans exposed to lewisite; the following is
based on animal investigations.

**Immediate.** A person with a droplet of lewisite on his or her skin
will note the burning and will immediately take steps to try to remove
it. The vapor is so irritating that a person will attempt to leave the
contaminated area if possible. Because this warning causes a person
exposed to take immediate steps to decontaminate, the lewisite lesion
will probably not be as severe as the lesion from mustard, since
exposure to mustard is often undetected and decontamination is not done.

**Skin.** Within about 5 minutes after contact, liquid lewisite will
produce a grayish area of dead skin. Inflammation and blister formation
follow more rapidly than in a similar lesion from mustard, although the
full lesion does not develop for 12 to 18 hours. The lewisite lesion has
more dead tissue and tissue sloughing than does a mustard lesion.

**Eyes.** Lewisite causes pain and inflammation of the edges of the
eyelids on contact. Swelling of the conjunctiva and lids follows, and
the eyes may be swollen shut within an hour. Inflammation of the iris
and corneal damage may follow if the dose is high. Liquid lewisite
causes severe eye damage within minutes of contact.

**Respiratory.** The extreme irritancy of lewisite to the nasal area and
upper airways causes the person to attempt to leave the area. Scanty
data indicates that lewisite causes the same airway signs and symptoms
as does mustard. The airway mucosa is the primary target and damage
progresses down the airways in the dose-dependent manner. Pseudomembrane
formation is prominent. Pulmonary edema, which occurs rarely and usually
only to a minimal degree after mustard exposure, may complicate exposure
to lewisite.

**Other.** Available data suggest lewisite causes an increase in
permeability of systemic capillaries with resulting intravascular fluid
loss, hypovolemia, shock, and organ conges­tion. This may lead to liver
or kidney failure with more prominent gastrointestinal (GI) effects
(including vomiting and diarrhea) than after mustard exposure.

E.  Medical Management

Early decontamination is the only way of preventing or lessening
lewisite damage. BAL was developed as an antidote for lewisite. There is
evidence that BAL in oil, given intra­muscularly, will reduce the
systemic effects of lewisite. However, BAL itself causes some toxicity,
and the user should read the package insert carefully. BAL skin ointment
and BAL ophthalmic ointment decrease the severity of skin and eye
lesions when applied immediately after early decontamination.

Table 4-1. Agent Exposure

  ---------------- ------------------------------------------------------
  **Eyes**         Instant pain, conjunctivitis, and swelling of the
                   eyelids, followed by corneal scarring and iritis.
                   Permanent blindness is possible within 1 minute of
                   exposure.

  **Skin**         Immediate stinging pain that increases in severity
                   with time. Skin redden­ing appears within 30 minutes
                   after exposure accompanied by pain with itching and
                   irritation for 24 hours. Blisters appear within
                   12 hours after exposure with more pain, which
                   diminishes after 2 to 3 days.

  **Respiratory    Irritating to nasal passages. Produces a burning
  Tract**          sensation followed by a profuse nasal secretion and
                   violent sneezing. Prolonged exposure causes coughing
                   and production of large quantities of frothy mucus.

  **Systemic       Lewisite on the skin and inhaled vapors are absorbed
  Effects**        and may cause systemic poisoning. A manifestation of
                   this is a change in capillary perme­ability, which
                   permits loss of sufficient fluid from the blood stream
                   to cause hemoconcentration, shock, and death. Acute
                   systematic poisoning from large skin burns causes
                   pulmonary edema, diarrhea, restlessness, weak­ness,
                   subnormal temperature, and low blood pressure in
                   animals.

  **Time of        Immediate (within 30 seconds).
  Onset**          

  **Chronic        Lewisite can cause sensitization and chronic lung
  Exposure**       impairment. Some evidence suggests lewisite might also
                   be a carcinogen.
  ---------------- ------------------------------------------------------

Malathion

A.  General Facts

Malathion is a broad spectrum, organophosphate pesticide with very high
mammalian toxicity. It may be absorbed through the skin, by inhalation,
and via the GI tract. Malathion is most commonly used to control insects
and mites, and it has a wide range of applications on many crops against
numerous insect species. Malathion is available in dust, emulsion
concentrate, granular, ultra-low volume (ULV) liquid, and wettable
powder formulations. Malathion is one of a class of insecticides
referred to as organophospates. These chemicals act by interfering with
the activities of cholinesterase, an enzyme essential for the proper
working of the nervous systems of both humans and insects.

Anticholinesterase agents work by blocking the enzyme the body uses to
destroy one of its nerve signal transmitters after it has done its job.
This has two effects: one is that control is lost over the affected part
of the nervous system; the other is that large concentrations of the
chemical transmitter rapidly build up within the body, and the chemical
is itself a powerful poison. The body is first incapacitated and then
forced to poison itself, which can happen rapidly. After exposure to a
lethal dose of nerve agent, severe convulsion will set in, followed
closely by collapse, paralysis, and death.

Malathion, in concentration, is a lethal, deep brown to yellow liquid
with a garlic odor. It is a volatile liquid and, therefore,
nonpersistent, which means it will readily evaporate from the skin
surface. It is most easily absorbed through the respiratory system, but
is appreciably absorbed through the skin or eyes, however, there is an
increased lethality, especially through the skin, at higher
temperatures. The onset of clinical symptoms may be rapid (within
several minutes) or gradual (within a few hours), depending on the
amount of exposure. Typical symptoms for low-concentration exposure are
miosis (causing pinpoint pupils), headache, increased salivation,
increased nasal secretion, and bronchoconstriction. For higher
concentration exposure, the symptoms include coughing, difficulty
breathing, increased perspiration, GI effects (e.g., nausea, vomiting,
colic, diarrhea), effects on skeletal musculature, and, eventually,
death by suffocation due to effects on respiratory musculature and the
central nervous system (CNS). First aid techniques include artificial
respiration plus oxygen and administering atropine-oxime.

F.  Clinical Effects

The initial effects of exposure to an organophosphate depend on the dose
and route of exposure. The initial effects from a sublethal amount of
agent by vapor exposure are different from the initial effects from a
similar amount of liquid agent on the skin. Exposure to a small amount
of nerve agent vapor causes effects in the eyes, nose, and airways.
These effects are from local contact of the vapor with the organ and do
not indicate systemic absorption of the agent. In this circumstance, the
erythrocyte-ChE may be normal or depressed. A small amount of liquid
agent on the skin causes systemic effects initially in the GI tract.
Lethal amounts of vapor or liquid cause a rapid cascade of events
culminating within a minute or two with loss of consciousness and
convulsive activity followed by apnea and muscular flaccidity within
several more minutes.

Effects from nerve agent vapor begin within seconds to several minutes
after exposure. Loss of consciousness and onset of seizure activity have
occurred within a minute of exposure to a high concentration. After
exposure to a very low concentration, miosis and other effects may not
begin for several minutes, and miosis may not be complete for 15 to 30
minutes after removal from the vapor. There is no latent period or delay
in onset from vapor exposure. Effects may continue to progress for a
period of time, but maximal effects usually occur within minutes after
exposure stops. A large amount of liquid on the skin causes effects
within minutes. Commonly, there is an asymptomatic period of from 1 to
30 minutes and then the sudden onset of a cascade of events, possibly
including loss of consciousness, seizure activity, apnea, and muscular
flaccidity. After small amounts of liquid agent on the skin, the onset
of effects has been delayed for as long as 18 hours after contact. These
are initially GI effects and are usually not life-threatening.
Generally, the longer the interval, the less severe the effects are.

**Eyes.** Miosis is a characteristic sign of exposure to nerve agent
vapor. It occurs as a result of direct contact of vapor with the eye.
Liquid agent on the skin will not cause miosis if the amount of liquid
is small; a moderate amount of liquid may or may not cause miosis; a
lethal or near-lethal amount of agent usually causes miosis. A droplet
of liquid in or near the eye will also cause miosis. Miosis will begin
within seconds or minutes after the onset of exposure to agent vapor,
but it may not be complete for many minutes if the vapor concentration
is low. Miosis is bilateral in an unprotected individual. Miosis is
often accompanied by complaints of pain, dim vision, blurred vision,
conjunctival infection, nausea, and, occasionally, vomiting. The pain
may be sharp or dull in or around the eyeball, but more often is a dull
ache in the frontal part of the head. Dim vision is due in part to the
small pupil, and cholinergic mechanisms in the visual pathways also
contribute. The complaint of blurred vision is less easily explained, as
objective testing usually indicates an improvement in visual acuity
because of the "pinhole" effect. Conjunctival infection may be mild or
severe and, occasionally, subconjunctival hemorrhage is present. Nausea
(and sometimes vomiting) is part of a generalized complaint of not
feeling well. Topical homatropine or atropine in the eye can relieve
miosis, pain, dim vision, and nausea.

**Nose.** Rhinorrhea may be the first indication of nerve agent vapor
exposure. Its severity is dose-dependent.

**Airway.** Nerve agent vapor causes bronchoconstriction and increased
secretions of the glands in the airways in a dose-related manner. The
exposed person may feel a slight tightness in his or her chest after a
small amount of agent and may be in severe distress after a large amount
of agent. Cessation of respiration occurs within minutes after the onset
of effects from exposure to a large amount of nerve agent. This apnea is
probably mediated through the CNS, although peripheral factors such as
skeletal muscle weakness (e.g., the intercostal muscles) and
bronchoconstriction may contribute.

**Gastrointestinal Tract.** After they are absorbed, nerve agents cause
an increase in the motility of the GI tract and an increase in
secretions by the glands in the wall of the GI tract. Nausea and
vomiting are early signs of liquid exposure on the skin. Diarrhea may
occur with large amounts of agent.

**Glands.** Nerve agent vapor causes increases in secretions from the
glands it contacts, such as the lacrimal, nasal, salivary, and bronchial
glands. Localized sweating around the site of liquid agent on the skin
is common, and generalized sweating after a large liquid or vapor
exposure is common. Increased secretions of the glands of the GI tract
occur after systemic absorption of the agent by either route.

**Skeletal Muscle.** The first effect of nerve agents on skeletal muscle
is stimulation producing muscular fasciculation and twitching. After a
large amount of agent, fatigue and weakness of muscles are rapidly
followed by muscular flaccidity. Fasciculation is sometimes seen early
at the site of a droplet of liquid agent on the skin, and generalized
fasciculation is common after a large exposure. These may remain long
after most of the other acute signs decrease.

**Central Nervous System.** The acute CNS signs of exposure to a large
amount of nerve agent are loss of consciousness, seizure activity, and
apnea. These begin within a minute after exposure to a large amount of
agent vapor and may be preceded by an asymptomatic period of from 1 to
30 minutes after contact of liquid with the skin. After exposure to
smaller amounts of nerve agent, CNS effects vary and are nonspecific.
They may include forgetfulness, an inability to concentrate fully,
insomnia, bad dreams, irritability, impaired judgment, and depression.
They do not include frank confusion and misperceptions (i.e.,
hallucinations). These may occur in the absence of physical signs or
other symptoms of exposure. After a severe exposure these symptoms occur
upon recovery from the acute severe effects. In either case, they may
persist for as long as 4 to 6 weeks.

**Cardiovascular.** The heart rate may be decreased because of
stimulation by the vagus nerve, but it is often increased because of
other factors, such as fright, hypoxia, and the influence of adrenergic
stimulation secondary to ganglionic stimulation. Thus, the heart rate
may be high, low, or in the normal range. Bradyarrhythmias, such as
first-, second-, or third-degree heart block may occur. The blood
pressure may be elevated from adrenergic factors, but is generally
normal until the terminal decline.

G.  Diagnosis and Treatment

**General Information.** An organophosphorus pesticide of very high
acute toxicity is easily absorbed through the intact skin as well as by
inhalation and via the GI tract. It is converted in vivo to the oxygen
analogue paraoxon, which then inhibits acetyl cholinester­ase. Continued
exposure to low amounts may inhibit blood cholinesterase to dangerous
levels.

**Signs and Symptoms.** Initial symptoms of poisoning may include
excessive sweating, headache, weakness, giddiness, nausea, vomiting,
stomach pains, blurred vision, slurred speech, and muscle twitching.
More advanced symptoms of poisoning may be convul­sions, coma, loss of
reflexes, and loss of sphincter control.

**Laboratory.** The most important laboratory finding is reduction in
activity of blood cholinesterases.

**Treatment.** Atropine and pralidoxime are specific antidotes and
repeated doses may be necessary. If the pesticide has been ingested,
unless the patient is vomiting, rapid gastric lavage should be performed
using 5 percent sodium bicarbonate if available. For skin contact, the
skin should be washed with soap and water. If the compound has entered
the eyes, they should be washed with isotonic saline.

Persons without signs of respiratory inefficiency but with manifest
peripheral symptoms should be treated with 2 to 4 mg of atropine sulfate
and additionally with 1000 to 2000 mg of pralidoxime chloride or 250 mg
of toxogonin (adult dose) by slow intravenous injection. More atropine
may be given as needed. Persons with severe intoxication with
respiratory difficulties, convulsions, and unconsciousness should
immediately be given atropine and a reactivator. In such severe cases, 4
to 8 mg of atropine sulfate should be given initially, followed by
repeated doses of 2 mg at 5- to 10-minute intervals. The patient's
condition, including respiration, blood pressure, pulse frequency,
salivation, and convulsions should be carefully observed as a guide to
further administration of atropine. If the patient is cyanotic,
artificial respiration should be given at the same time as atropine.

The airways should be kept free and artificial respiration should be
applied, if required, preferably by mechanical means. If necessary,
intubation should be performed.

Contraindications are morphine, barbituates, phenothiazine
tranquillizers, and central stimulants of all kinds.

If the acute toxic effect is survived and adequate artificial
respiration has been given if needed, the chances of complete recovery
are good. However, in very severe cases, particularly if artificial
respiration has been inadequate, prolonged hypoxia may give rise to
permanent brain damage.

H.  Decontamination

Decontamination is the reduction or removal of chemical agents.
Decontamination may be accomplished by removing these agents by physical
means or by chemical neutralization or detoxification. Decontamination
of skin is the primary concern, but decontamination of eyes and wounds
must also be done when necessary.

The most important and effective decontamination of any chemical
exposure is that decon­tamination done within the first minute or two
after exposure.

Decontamination of casualties is an enormous task. The process requires
dedication of large numbers of personnel and large amounts of time. Even
with appropriate planning and training, the requirement demands a
significant contribution of resources.

Liquids and solids are the only substances that can be effectively
removed from the skin. It is generally impossible and unnecessary to
decontaminate vapor. Removal from the atmosphere containing the vapor is
all that is required.

Many substances have been evaluated for their usefulness in skin
decontamina­tion. The most common problems with potential decontaminates
are irritation of the skin, toxicity, ineffectiveness, or high cost. An
ideal decontaminate will rapidly and completely decontaminate all known
chemical and biological (C/B) warfare agents. Furthermore, a suitable
skin decontaminate must have certain properties that are not
requirements for decontaminates for equipment. Recognized desirable
traits of a skin decontaminate include neutralization of all agents,
safety (compound to be both nontoxic and noncorrosive), ease of
application by hand, availability, rapid action, nonproduction of toxic
end products, stability in long-term storage, short-term stability
(after issue to unit/individual), affordability, nonenhancement of
percutaneous agent absorption, no irritability, hypoallergenicity, and
ease of disposal.

Decontamination issues have been explored since the beginning of modern
chemical warfare. After years of research worldwide, simple principles,
which consistently produce good results, still apply. The first, which
is without equal, is timely physical removal of the agent. To remove the
substance by the best means available is the primary objective. Chemical
destruction (detoxification) of the offending agent is a desirable
secondary objective. Physical removal is imperative because none of the
chemical means of destroying these agents do so instantaneously.
Although decontamination preparations, such as fresh hypochlorite, react
rapidly with some agents (e.g., the half time for destruction of VX by
hypochlorite at a pH of 10 is 1.5 minutes), the half times of
destruction of other agents, such as mustard, are much longer. If a
large amount of agent is present initially, a longer time is needed to
completely neutralize the agent to a harmless substance. Timely use of
water, soap and water, or flour followed by wet tissue wipes may work in
many cases.

I.  Summary

Malathion is an organophosphorus compound that inhibits cholinesterase.
It is a very toxic substance. Contact with the skin, inhalation of dust
or spray, or swallowing may be fatal. Wear protective gloves, clean
protective clothing, and a respirator of the organic-vapor type when
handling this material. Bathe immediately after work. Ensure containers
are stored under lock and key. Empty containers must be disposed of in
such a way to prevent all possibility of accidental contact with them.
Keep the material out of reach of children and well away from
foodstuffs, animal feed, and their containers. In case of contact,
immediately remove contaminated clothing and wash the skin thoroughly
with soap and water; for eyes, flush with water for 15 minutes.

If poisoning occurs, call a physician. Atropine and pralidoxime are
specific antidotes and repeated doses may be necessary. Artificial
respiration may be needed.

Mustard

J.  Summary of Agent Effects

> An individual exposed to mustard will feel very little pain and will
> not notice symptoms for quite some time. However, the longer the
> exposure without removal of the mustard agent, the more severe will be
> the damage to affected areas of the body. Mustard is a blister agent
> that affects the eyes, lung, and skin. The eyes are very susceptible,
> reacting to very low concentration from mustard. Exposure to mustard
> on the skin can range from redness and inflammation to severe blisters
> and extreme soreness. Inhalation of the agent will cause irritation of
> the throat, tightness of chest, hoarseness and coughing. If medical
> treatment is not received in the early stages of contamination, severe
> bronchopneumonia with accompanying high fever can occur.
>
> Mustard is an oily liquid with a color ranging from a light yellow to
> brown. Its odor is that of garlic, onion, or mustard, but because of
> accommodation of smell, odor should not be relied on for detection.
> Under temperature conditions mustard evaporates slowly and is
> primarily a liquid hazard, but its vapor hazard increases with
> increasing temperature. At 100 degrees Farenheit or above, it is a
> definite vapor hazard.

# B. Clinical Effects

> **Immediate.** Mustard binds irreversibly to tissue within several
> minutes after contact. If decontamination is not done immediately
> after exposure there is no way to prevent injury, although later
> decontamination might prevent a more severe lesion.
>
> **Skin.** Mustard causes tissue damage within several minutes after
> contact, without causing any concomitant clinical effects. Skin is red
> and develops blisters within 2-24 hours.
>
> **Eyes.** Mustard causes tearing, itchy, burning and a gritty feeling
> to the eyes. The onset of the first effect is 4-12 hours.
>
> **Respiratory.** The extreme irritancy of mustard causes mild to
> severe shortness of breath within 2-4 hours. A mild irritancy can
> cause a runny nose, sneezing, nosebleed, hoarseness, and a hacking
> cough. This occurs within 12-24 hours.

# C. Medical Management

> There is no known antidote for mustard exposure; the process of
> cellular destruction is irreversible. Therefore, it is very important
> to remove the mustard as quickly as possible. The best means of
> removal is by flushing with water and 5 percent solution of sodium
> hypochlorite or liquid household bleach within one minute, or washing
> with soap and water after using an absorber of mustard, such as flour.
>
> Mustard's effects are delayed, appearing hours after exposure. Organs
> most commonly affected are the skin, eyes, and airways. Following
> exposure to large quantities of mustard, presursor cells of the bone
> marrow are damaged, leading to pancytopenia and increased
> susceptibility to infection. The gastrointestinal tract may be
> damaged, and there are sometimes central nervous system signs. There
> is no specific antidote, and management is symptomatic therapy.
> Decontamination immediately after exposure is the only way to reduce
> damage. Mustard reacts with tissue within minutes of entering the body
> and is no longer an intact molecule. Blood, tissue, and blister fluid
> do not contain mustard, and one cannot become exposed to mustard by
> contact with body fluids or tissues.

Agent Exposure

+---------------+------------------------------------------------------+
| **Eyes**      | Irritation, conjunctivitis and corneal opacity and   |
|               | damage in the eyes.                                  |
+---------------+------------------------------------------------------+
| **Skin**      | Mild exposure resembles sunburn, and is associated   |
|               | with a burning, stinging pain. Erythema and blisters |
|               | on the skin.                                         |
+---------------+------------------------------------------------------+
| **Respiratory | Mild upper respiratory signs to marked airways.      |
| Tract**       |                                                      |
|               | Pulmonary edema is not usually present unless the    |
|               | damage is severe and then it usually is hemorrhagic. |
+---------------+------------------------------------------------------+
| **Systemic    | Lewisite has gastrointestinal effects and bone       |
| Effects**     | marrow stem cell suppression.                        |
+---------------+------------------------------------------------------+
| **Gas         | The gastrointestinal tract is very susceptible to    |
| trointestinal | mustard damage, either from systemic absorption or   |
| Tract**       | ingestion of the agent. Even a small amount, will    |
|               | often cause nausea with or without vomiting lasting  |
|               | 24 hours or less.                                    |
+---------------+------------------------------------------------------+
| **Time of     | Asymptomatic latent period (within hours).           |
| Onset**       |                                                      |
+---------------+------------------------------------------------------+
| **Chronic     | The cause of mustard poisoning is commonly           |
| Exposure**    | respiratory failure. Deaths can occur from the third |
|               | to the sixth day after exposure from secondary       |
|               | bacterial pneumonia caused by bacterial invasion.    |
+---------------+------------------------------------------------------+

Parathion

A.  Summary of Agent Effects

Parathion is a broad spectrum, organophosphate pesticide with very high
mammalian toxicity. It may be absorbed through the skin, by inhalation,
and via the gastrointestinal (GI) tract. Parathion is most commonly used
to control insects and mites, and it has a wide range of applications on
many crops against numerous insect species. Parathion is available in
dust, emulsion concentrate, granular, ULV liquid, and wettable powder
formulations. Parathion is one of a class of insecticides referred to as
organophospates. These chemicals act by interfering with the activities
of cholinesterase, an enzyme essential for the proper working of the
nervous systems of humans and insects.

K.  Selected Properties

**Physical Characteristics.** When pure, a colorless almost odorless
liquid m.p. 6.1 °C, b.p. 157 °C to 162 °C at 0.6 torr. The technical
material is a yellow to dark brown liquid with a pungent garlic-like
odor.

**Solubility.** Water at 25 °C, very slightly soluble (24 mg/l).
Miscible with most organic solvents, slightly soluble in petroleum oils.

**Stability.** Fairly stable at neutral or slightly acid pH. At pH 5 to
6, 1 percent is hydrolyzed in 62 days at 25 °C. Rapidly hydrolyzed in
alkali. Isomerizes on heating to the O,S-diethyl isomer. Darkens with
exposure to sunlight.

**Vapor Pressure (Volatility).** 3.78 x 10-5 torr at 20 °C. In a number
of fatal cases of human poisoning, the dosage victims received orally
was exactly 900 mg. In another case, death resulted from 120 mg.
Children 5 to 6 years old have been killed by ingestion of 2 mg of
parathion (about 0.1 mg/kg).

**General.** Parathion is an organophosphorus compound that inhibits
cholinesterase. It is a very toxic substance. Contact with the skin,
inhalation of dust or spray, or swallowing may be fatal. Wear protective
gloves, clean protective clothing, and a respirator of the
organic-vapour type when handling this material. Bathe immediately after
work. Ensure containers are stored under lock and key. Empty containers
must be disposed of in such a way that prevents all possibility of
accidental contact with them. Keep the material out of reach of children
and well away from foodstuffs, animal feed, and their containers. In
case of contact, immediately remove contaminated clothing and wash the
skin thoroughly with soap and water; for eyes, flush with water for
15 minutes.

If poisoning occurs, call a physician. Atropine and pralidoxime are
specific antidotes and repeated doses may be necessary. Artificial
respiration may be needed.

L.  Emergency Aid

**Early Symptoms of Poisoning.** Early symptoms of poisoning may include
excessive sweating, headache, weakness, giddiness, nausea, vomiting,
stomach pains, blurred vision, slurred speech, and muscle twitching.
Later, there may be convulsions, coma, loss of reflexes, and loss of
sphincter control.

**Treatment Before Person Is Seen by Physician.** If these symptoms
appear following exposure, the person should stop work immediately,
remove contaminated clothing, and wash the affected skin with water and
soap, if available, and flush the area with large quantities of water.
If swallowed, and the person is conscious, vomiting should be induced.
In the event of collapse, artificial respiration should be given,
bearing in mind that if mouth-to-mouth resuscitation is used, vomit may
contain toxic amounts of parathion.

M.  Diagnosis and Treatment

**General Information.** Parathion is an organophosphorus pesticide of
very high acute toxicity that is easily absorbed through the intact skin
as well as by inhalation and via the GI tract. It is converted in vivo
to the oxygen analogue paraoxon, which then inhibits acetyl
cholinesterase. Continued exposure to low amounts may inhibit blood
cholinesterase to dangerous levels.

**Signs and Symptoms.** Initial symptoms of poisoning may include
excessive sweating, headache, weakness, giddiness, nausea, vomiting,
stomach pains, blurred vision, slurred speech, and muscle twitching.
More advanced symptoms of poisoning may be convulsions, coma, loss of
reflexes, and loss of sphincter control.

**Laboratory.** The most important laboratory finding is reduction in
activity of blood cholinesterases. Other findings are raised urinary
levels of 2‑nitrophenol.

**Treatment.** If the pesticide has been ingested, unless the patient is
vomiting, rapid gastric lavage should be performed using 5 percent
sodium bicarbonate if available. For skin contact, the skin should be
washed with soap and water. If the compound has entered the eyes, they
should be washed with isotonic saline.

Persons without signs of respiratory inefficiency but with manifest
peripheral symptoms should be treated with 2 to 4 mg of atropine sulfate
and additionally with 1000 to 2000 mg of pralidoxime chloride or 250 mg
of toxogonin (adult dose) by slow intravenous injection. More atropine
may be given as needed. Persons with severe intoxication with
respiratory difficulties, convulsions, and unconsciousness should
immediately be given atropine and a reactivator. In such severe cases, 4
to 8 mg of atropine sulfate should be given initially, followed by
repeated doses of 2 mg at 5‑ to 10‑minute intervals. The patient's
condition, including respiration, blood pressure, pulse frequency,
salivation, and convulsions, should be carefully observed as a guide to
further administration of atropine. If the patient is cyanotic,
artificial respiration should be given at the same time as atropine.

The airways should be kept free and artificial respiration should be
applied, if required, preferably by mechanical means. If necessary,
intubation should be performed.

Contraindications are morphine, barbituates, phenothiazine
tranquillizers, and central stimulants of all kinds.

**Prognosis.** If the acute toxic effect is survived and adequate
artificial respiration has been given, if needed, the chances of
complete recovery are good. However, in very severe cases, particularly
if artificial respiration has been inadequate, prolonged hypoxia may
cause permanent brain damage.

Sarin

A.  Summary of Agent Effects

Nerve agents are anticholinesterase agents that work by blocking the
enzyme the body uses to destroy one of its nerve signal transmitters
after it has done its job. This has two effects: one is that control is
lost over the affected part of the nervous system; the other is that
large concentrations of the chemical transmitter rapidly build up within
the body, and the chemical is itself a powerful poison. The body is
first incapacitated and then forced to poison itself, which can happen
rapidly. After exposure to a lethal dose of nerve agent, severe
convulsions will set in, followed closely by collapse, paralysis, and
death.

Sarin (GB) is a highly lethal, colorless, odorless liquid. It is a
volatile liquid and, therefore, nonpersistent, which means it will
readily evaporate from most surfaces. It is most easily absorbed through
the respiratory system and is not appreciably absorbed through the skin
or eyes; however, there is an increased lethality, especially through
the skin, at higher temperatures. The onset of clinical symptoms may be
rapid (within several minutes) or gradual (within a few hours),
depending on the amount of exposure. Typical symptoms of a
low-concentration exposure are miosis, headache, increased salivation,
increased nasal secretion, and bronchoconstriction. For higher
concentration exposures, the symptoms include coughing, difficulty
breathing, increased perspiration, gastrointestinal (GI) effects
(e.g., nausea, vomiting, colic, diarrhea), effects on skeletal
musculature and, eventually, death by suffocation due to effects on
respiratory musculature and the central nervous system (CNS). First aid
techniques include artificial respiration plus oxygen and administering
appropriate antidotes.

N.  Clinical Effects

The initial effects of exposure to a nerve agent depend on the dose and
route of exposure. The initial effects from a sublethal amount of agent
by vapor exposure are different from the initial effects from a similar
amount of liquid agent on the skin. Exposure to a small amount of nerve
agent vapor causes effects in the eyes, nose, and airways. These effects
are from local contact of the vapor with the organ and do not indicate
systemic absorption of the agent. In this circumstance, the
erythrocyte-ChE may be normal or depressed. A small amount of liquid
agent on the skin causes systemic effects initially in the GI tract.
Lethal amounts of vapor or liquid cause a rapid cascade of events
culminating within a minute or two, with loss of consciousness and
convulsive activity followed by apnea and muscular flaccidity within
several more minutes.

Effects from nerve agent vapor begin within seconds to several minutes
after exposure. Loss of consciousness and onset of seizure activity have
occurred within a minute of exposure to a high concentration. After
exposure to a very low concentration, miosis and other effects may not
begin for several minutes, and miosis may not be complete for 15 to
30 minutes after removal from the vapor. There is no latent period or
delay in onset from vapor exposure. Effects may continue to progress for
a period of time, but maximal effects usually occur within minutes after
exposure stops. A large amount of liquid on the skin causes effects
within minutes. Commonly, there is an asymptomatic period of from 1 to
30 minutes and then the sudden onset of an overwhelming cascade of
events, including loss of consciousness, seizure activity, apnea, and
muscular flaccidity. After small amounts of liquid agent on the skin,
the onset of effects has been delayed for as long as 18 hours after
contact. These are initially GI effects and are usually not
life-threatening. Generally, the longer the interval, the less severe
the effects.

**Eyes.** Miosis, constriction of the pupils, is a characteristic sign
of exposure to nerve agent vapor. It occurs as a result of direct
contact of vapor with the eye. Liquid agent on the skin will not cause
miosis if the amount of liquid is small; a moderate amount of liquid may
or may not cause miosis; a lethal or near-lethal amount of agent usually
causes miosis. A droplet of liquid in or near the eye will also cause
miosis. Miosis will begin within seconds or minutes after the onset of
exposure to agent vapor, but it may not be complete for many minutes if
the vapor concentration is low. Miosis is bilateral in an unprotected
individual. Miosis is often accompanied by complaints of pain, dim
vision, blurred vision, conjunctival infection, nausea, and occasionally
vomiting. The pain may be sharp or dull in or around the eyeball, but
more often is a dull ache in the frontal part of the head. Dim vision is
due in part to the small pupil, and cholinergic mechanisms in the visual
pathways also contrib­ute. The complaint of blurred vision is less easily
explained, as objective testing usually indicates an improvement in
visual acuity because of the "pinhole" effect. Conjunctival infection
may be mild or severe, and occasionally subconjunctival hemorrhage is
present. Topical homatropine or atropine in the eye can relieve miosis,
pain, dim vision, and nausea.

**Nose.** Rhinorrhea, excessive secretions from the nose, may be the
first indication of nerve agent vapor exposure. Its severity is
dose-dependent.

**Airway.** Nerve agent vapor causes bronchoconstriction and increased
secretions of the glands in the airways in a dose-related manner. The
exposed person may feel a slight tight­ness in his or her chest after a
small amount of agent and may be in severe distress after a large amount
of agent. Apnea, cessation of respiration, occurs within minutes after
the onset of effects from exposure to a large amount of nerve agent.
This apnea is probably mediated through the CNS, although peripheral
factors such as skeletal muscle weakness (e.g., the intercostal muscles)
and bronchoconstriction may contribute.

**Gastrointestinal Tract.** After they are absorbed, nerve agents cause
an increase in the motility of the GI tract and an increase in
secretions by the glands in the wall of the GI tract. Nausea and
vomiting are early signs of liquid exposure on the skin. Diarrhea may
occur with large amounts of agent.

**Glands.** Nerve agent vapor causes increased secretions from the
glands it contacts, such as the lacrimal, nasal, salivary, and bronchial
glands. Localized sweating around the site of liquid agent on the skin
is common, and generalized sweating after a large liquid or vapor
exposure is common. Increased secretions in the glands of the GI tract
occur after systemic absorption of the agent by either route.

**Skeletal Muscle.** The first effect of nerve agents on skeletal muscle
is stimulation producing muscular fasciculation and twitching. After a
large amount of agent, fatigue\
and weakness of muscles are rapidly followed by muscular flaccidity.
Fasciculation is sometimes seen early at the site of a droplet of liquid
agent on the skin, and generalized fasciculation is common after a large
exposure. This may remain long after most other acute signs decrease.

**Central Nervous System.** The acute CNS signs of exposure to a large
amount of nerve agent are loss of consciousness, seizure activity, and
apnea. These begin within a minute after exposure to a large amount of
agent vapor and may be preceded by an asymptomatic period of from 1 to
30 minutes after contact of liquid with the skin. After exposure to
smaller amounts of nerve agent, CNS effects vary and are nonspecific.
They may include forgetfulness, an inability to concentrate fully,
insomnia, bad dreams, irritability, impaired judgment, and depression.
They do not include frank confusion and misperceptions (i.e.,
hallucinations). These may occur in the absence of physical signs or
other symptoms of exposure. After severe exposure, these symptoms occur
upon recovery from the acute severe effects. In either case, they may
persist for as long as 4 to 6 weeks.

**Cardiovascular.** The heart rate may be decreased because of
stimulation by the vagus nerve, but it is often increased because of
other factors, such as fright, hypoxia, and the influence of adrenergic
stimulation secondary to ganglionic stimulation. Thus, the heart rate
may be high, low, or in the normal range. Bradyarrhythmias, such as
first-, second-, or third-degree heart block may occur. The blood
pressure may be elevated from adrenergic factors, but is generally
normal until the terminal decline.

Table 4-1. Agent Exposure

+--------------------------------+---+---+-------------------------------------+
| ##### Vapor Exposure           |   |   |                                     |
+--------------------------------+---+---+-------------------------------------+
| **Mild**                       | # |   |                                     |
|                                | # |   |                                     |
|                                | # |   |                                     |
|                                | # |   |                                     |
|                                | # |   |                                     |
|                                |   |   |                                     |
|                                | S |   |                                     |
|                                | e |   |                                     |
|                                | v |   |                                     |
|                                | e |   |                                     |
|                                | r |   |                                     |
|                                | e |   |                                     |
+--------------------------------+---+---+-------------------------------------+
| **Eyes:** Miosis, dim vision,  | * |   |                                     |
| headache.                      | A |   |                                     |
|                                | l |   |                                     |
| **Nose:** Rhinorrhea.          | l |   |                                     |
|                                | t |   |                                     |
| **Mouth:** Salivation.         | h |   |                                     |
|                                | o |   |                                     |
| **Lungs:** Dyspnea ("tightness | s |   |                                     |
| in the chest").                | e |   |                                     |
|                                | l |   |                                     |
| **Time of Onset:** Seconds to  | i |   |                                     |
| minutes after exposure.        | s |   |                                     |
|                                | t |   |                                     |
| **Treatment:** 1 MARK I (see   | e |   |                                     |
| insert box for definition of   | d |   |                                     |
| MARK I Nerve Agent Antidote    | u |   |                                     |
| Kit).                          | n |   |                                     |
|                                | d |   |                                     |
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|                                | . |   |                                     |
+--------------------------------+---+---+-------------------------------------+
| ##### Liquid on Skin           |   |   |                                     |
+--------------------------------+---+---+-------------------------------------+
| **Mild/Moderate**              |   |   | **Severe**                          |
+--------------------------------+---+---+-------------------------------------+
| Muscle twitching at site of    |   | * |                                     |
| exposure.                      |   | A |                                     |
|                                |   | l |                                     |
| Sweating at site of exposure.  |   | l |                                     |
|                                |   | t |                                     |
| Nausea, vomiting.              |   | h |                                     |
|                                |   | o |                                     |
| Feeling of weakness.           |   | s |                                     |
|                                |   | e |                                     |
| **Time of Onset:** 10 minutes  |   | l |                                     |
| to 18 hours after exposure.    |   | i |                                     |
|                                |   | s |                                     |
| **Treatment:** 1 to 2 MARK Is, |   | t |                                     |
| depending on severity of       |   | e |                                     |
| symptoms.                      |   | d |                                     |
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|                                |   | . |                                     |
+--------------------------------+---+---+-------------------------------------+

O.  Medical Management

Management of a casualty with nerve agent intoxication consists of
decon­tamination, ventilation, administration of the antidotes, and
supportive therapy. The condition of the patient dictates the need for
each of these and the order in which they are done.

Skin decontamination is not necessary after exposure to vapor alone, but
clothing should be removed because it may contain "trapped" vapor.

The need for ventilation will be obvious, and the means of ventilation
will depend on available equipment. Airway resis­tance is high (50 to 70
cm of water) because of bronchoconstriction and secretions, and initial
ventilation is difficult. The resistance decreases after atropine
administration, after which ventilation will be easier. The copious
secretions, which may be thickened by atropine, also impede ventilatory
efforts and require frequent suctioning. In reported cases of severe
nerve agent exposure, ventilation has been required from 0.5 to 3 hours.

Three drugs are used to treat nerve agent exposure. These three
therapeutic drugs are atropine, pralidoxime chloride (2-PAM Cl), and
diazepam. Atropine is a cholinergic blocking, or anticholinergic,
compound. It is extremely effective in blocking the effects of excess
acetylcholine at peripheral muscarinic sites. When small amounts (2 mg)
are given to normal individuals without nerve agent intoxication,
atropine causes mydriasis, a decrease in secretions (including a
decrease in sweating), mild sedation, a decrease in GI motility, and
tachycardia. In people not exposed to nerve agents, amounts of 10 mg or
higher may cause delirium. Potentially, the most hazardous effect of
inadvertent use of atropine (2 mg, i.m.) in a young person not exposed
to a cholinesterase-inhibiting com­pound in a warm or hot atmosphere is
inhibition of sweating, which may lead to heat injury. Pralidoxime
chloride (600 mg) is used along with the atropine (2 mg). Atropine and
pralidoxime chloride autoinjectors are packaged together in a MARK I kit
(see insert box). Pralidoxime chloride (Protopam chloride; 2-PAM Cl) is
an oxime. Oximes attach to the nerve agent that is inhibiting the
cholinesterase and break the agent-enzyme bond to restore the normal
activity of the enzyme. Abnormal activity in skeletal muscle decreases
and normal strength returns. Oximes do not cause a decrease in
secretions. Diazepam is an anticonvulsant drug used to decrease
convulsive activity and reduce brain damage caused by prolonged seizure
activity.

P.  Decontamination

Decontamination is the reduction or removal of chemical agents.
Decontamination may be accomplished by removal of these agents by
physical means or by chemical neutralization or detoxification.
Decontamination of skin is the primary concern, but decontamination of
eyes and wounds must also be done when necessary.

The most important and effective decontamination of any chemical
exposure is that decontamination done within the first minute or two
after exposure.

Decontamination of casualties is an enormous task. The process requires
dedication of large numbers of personnel and large amounts of time. Even
with appropriate planning and training, the requirement demands a
significant contribution of resources.

Liquids and solids are the only substances that can be effectively
removed from the skin. It is generally impossible and unnecessary to
decontaminate vapor. Removal from the atmos­phere containing the vapor is
all that is required.

Many substances have been evaluated for their usefulness in skin
decontamination. The most common problems with potential decontaminates
are irritation of the skin, toxicity, ineffectiveness, or high cost. An
ideal decontaminate will rapidly and completely decon­taminate all known
chemical and biological (C/B) warfare agents. Furthermore, a suitable
skin decontaminate must have certain properties that are not
requirements for decontami­nates of equipment. Recognized desirable
traits of a skin decontaminate include neutrali­zation of all agents,
safety (compound to be nontoxic and noncorrosive), ease of application
by hand, availability, rapid action, nonproduction of toxic end
products, stability in long-term storage, short-term stability (after
issue to unit/individual), affordability, nonenhance­ment of percutaneous
agent absorption, no irritability, hypoallergenicity, and ease of
disposal.

Decontamination issues have been explored since the beginning of modern
chemical warfare. After years of research worldwide, simple principles,
which consistently produce good results, still apply. The first, which
is without equal, is timely physical removal of the agent. To remove the
substance by the best means available is the primary objective. Chemical
destruction (detoxification) of the offending agent is a desirable
secondary objec­tive. Physical removal is imperative because none of the
chemical means of destroying these agents do so instantaneously.
Although decontamination preparations, such as fresh hypochlorite, react
rapidly with some agents (e.g., the half time for destruction of VX by
hypochlorite at a pH of 10 is 1.5 minutes), the half times of
destruction of other agents, such as mustard, are much longer. If a
large amount of agent is present initially, a longer time is needed to
completely neutralize the agent to a harmless substance. Timely use of
water, soap and water, or flour followed by wet tissue wipes may work in
many cases.

VX

A.  Summary of Agent Effects

The nerve agents are anticholinesterase agents, working by blocking the
enzyme the body uses to destroy one of its nerve signal transmitters
after it has done its job. This has two effects: one is that control is
lost over the affected part of the nervous system; the other is that
large concentrations of the chemical transmitter rapidly build up within
the body, and the chemical itself is a powerful poison. The body is
first incapacitated and then forced to poison itself, which can happen
rapidly. After exposure to a lethal dose of nerve agent, severe
convulsion will set in, followed closely by collapse, paralysis, and
death.

VX is an odorless, colorless to straw-colored liquid, similar in
appearance to motor oil. As a lethal cholinesterase inhibitor, doses
that are potentially life threatening may be only slightly larger than
those producing mild effects. Death usually occurs within 15 minutes
after absorption of a fatal dosage.

Q.  Clinical Effects

Symptoms of overexposure may occur within minutes or hours, depending on
the dose. They include miosis (constriction of pupils) and visual
effects, headaches and pressure sensation, runny nose and nasal
congestion, salivation, tightness in the chest, nausea, vomiting,
giddiness, anxiety, difficulty in thinking, difficulty sleeping,
nightmares, muscle twitches, tremors, weakness, abdominal cramps,
diarrhea, and involuntary urination and defecation. In severe exposure,
symptoms progress to convulsions and respiratory failure.

**Eyes.** Miosis (pinpoint pupils) is a characteristic sign of exposure
to nerve agent vapor. It occurs as a result of direct contact of vapor
with the eye. Liquid agent on the skin will not cause miosis if the
amount of liquid is small; a moderate amount of liquid may or may not
cause miosis; a lethal or near-lethal amount of agent usually causes
miosis. A droplet of liquid in or near the eye will also cause miosis.
Miosis will begin within seconds or minutes after the onset of exposure
to agent vapor, but it may not be complete for many minutes if the vapor
concentration is low. Miosis is bilateral in an unprotected individual.
Miosis is often accompanied by complaints of pain, dim vision, blurred
vision, conjunctival infection, nausea, and, occasionally, vomiting. The
pain may be sharp or dull in or around the eyeball, but more often is a
dull ache in the frontal part of the head. Dim vision is due in part to
the small pupil, and cholinergic mechanisms in the visual pathways also
con­tribute. The complaint of blurred vision is less easily explained, as
objective testing usually indicates an improvement in visual acuity
because of the "pinhole" effect. Con­junctival infection may be mild or
severe and, occasionally, subconjunctival hemorrhage is present. Nausea
(and sometimes vomiting) is part of a generalized complaint of not
feeling well. Topical homatropine or atropine in the eye can relieve
miosis, pain, dim vision, and nausea.

**Nose.** Rhinorrhea (runny nose) may be the first indication of nerve
agent vapor exposure. Its severity is dose dependent.

**Airway.** Nerve agent vapor causes bronchoconstriction and increased
secretions of the glands in the airways in a dose-related manner. The
exposed person may feel a slight tight­ness in his or her chest after a
small amount of agent and may be in severe distress after a large amount
of agent. Cessation of respiration occurs within minutes after the onset
of effects from exposure to a large amount of nerve agent. This apnea is
probably mediated through the central nervous system (CNS), although
peripheral factors such as skeletal muscle weakness (e.g., the
intercostal muscles) and bronchoconstriction may contribute.

**Gastrointestinal Tract.** After they are absorbed, nerve agents cause
an increase in the motility of the gastrointestinal (GI) tract and an
increase in secretions by the glands in the wall of the GI tract. Nausea
and vomiting are early signs of liquid exposure on the skin. Diarrhea
may occur with large amounts of agent.

**Glands.** Nerve agent vapor causes increases in secretions from the
glands it contacts, such as the lacrimal, nasal, salivary, and bronchial
glands. Localized sweating around the site of liquid agent on the skin
is common, and generalized sweating after a large liquid or vapor
exposure is common. Increased secretions of the glands of the GI tract
occur after systemic absorption of the agent by either route.

**Skeletal Muscle.** The first effect of nerve agents on skeletal muscle
is stimulation pro­ducing muscular fasciculation and twitching. After a
large amount of agent, fatigue and weakness of muscles are rapidly
followed by muscular flaccidity. Fasciculation is sometimes seen early
at the site of a droplet of liquid agent on the skin, and generalized
fasciculation is common after a large exposure. This may remain long
after most other acute signs decrease.

**Central Nervous System.** The acute CNS signs of exposure to a large
amount of nerve agent are loss of consciousness, seizure activity, and
apnea. These begin within a minute after exposure to a large amount of
agent vapor and may be preceded by an asymptomatic period of from 1 to
30 minutes after contact of liquid with the skin. After exposure to
smaller amounts of nerve agent, CNS effects vary and are nonspecific.
They may include forgetfulness, an inability to concentrate fully,
insomnia, bad dreams, irritability, impaired judgment, and depression.
They do not include frank confusion and misperceptions (i.e.,
hallucinations). These may occur in the absence of physical signs or
other symptoms of exposure. After severe exposure, these symptoms occur
upon recovery from the acute severe effects. In either case, they may
persist for as long as 4 to 6 weeks.

**Cardiovascular.** The heart rate may be decreased because of
stimulation by the vagus nerve, but it is often increased because of
other factors, such as fright, hypoxia, and the influence of adrenergic
stimulation secondary to ganglionic stimulation. Thus, the heart rate
may be high, low, or in the normal range. Bradyarrhythmias, such as
first-, second-, or third-degree heart block may occur. The blood
pressure may be elevated from adrenergic factors, but is generally
normal until the terminal decline.

Table 4-1. Agent Exposure

+----------------+-------+-----------------+-------+-----------------+
| **Route**      | **F   | **Effect**      | **T   | **Dosage**      |
|                | orm** |                 | ype** |                 |
+----------------+-------+-----------------+-------+-----------------+
| Ocular         | Vapor | Miosis          | ECt50 | \< 0.09         |
|                |       |                 |       | mg-min/m^3^     |
| Inhalation     | Vapor | Runny nose      | ECt50 |                 |
|                |       |                 |       | \< 0.09         |
| Inhalation (15 | Vapor | Severe          | ICt50 | mg-min/m^3^     |
| 1/min)         |       | incapacitation  |       |                 |
|                | Vapor |                 | LCt50 | 25 mg-min/m^3^  |
| Inhalation (15 |       | Death           |       |                 |
| 1/min)         | L     |                 | LD50  | 30 mg-min/m^3^  |
|                | iquid | Death           |       |                 |
| Percutaneous   |       |                 |       | 10 mg/70 kg man |
+----------------+-------+-----------------+-------+-----------------+

> Effective dosages for vapor are estimated for exposure durations of 2
> to 10 minutes.

R.  Medical Management

Management of a casualty with nerve agent intoxication consists of
decontamination, venti­lation, administration of the antidotes, and
supportive therapy. The condition of the patient dictates the need for
each of these and the order in which they are done.

> **Inhalation.** If severe signs of agent exposure appear (i.e., chest
> tightens, pupil constric­tion, incoordination), immediately administer,
> in rapid succession, all three Nerve Agent Antidote Kits (NAAKs),
> MARK I injectors (or atropine if directed by physician). Injec­tions
> using the MARK I kit injectors may be repeated at 5‑ to 20‑minute
> intervals if signs and symptoms are progressing, until three series of
> injections have been administered. No more injections will be given
> unless directed by medical personnel. In addition, a record will be
> maintained of all injections given. If breathing stops, give
> artificial respiration. Mouth-to-mouth resuscitation should be used
> when approved mask-bag or oxygen delivery systems are unavailable. Do
> not use mouth-to-mouth resuscitation when facial contamina­tion exists.
> If breathing is difficult, administer oxygen.

**Eye Contact.** Immediately flush eyes with water for 10 to 15 minutes.
Although miosis (pinpointing of the pupils) may be an early sign of
agent exposure, an injection should not be administered when miosis is
the only sign present. Instead, the individual should be immediately
taken to a medical treatment facility for observation.

**Skin Contact.** Remove victims from the contaminated area into fresh
air and take off clothing. Immediately wash contaminated skin with
copious amounts of soap and water, 10 percent sodium carbonate solution,
or 5 percent liquid household bleach. Rinse well with water to remove
excess decontaminant. Administer NAAK, MARK I, only if localized
sweating and muscular twitching symptoms are observed.

**Ingestion.** Do not induce vomiting. First symptoms are likely to be
in the GI tract. Immediately administer NAAK, MARK I.

Three drugs are used to treat nerve agent exposure and another is used
as pretreatment for potential nerve agent exposure. The three
therapeutic drugs are atropine, pralidoxime chloride, and diazepam.
Atropine is a cholinergic blocking, or anticholinergic, compound. It is
extremely effective in blocking the effects of excess acetylcholine at
peripheral muscarinic sites. Under experimental conditions, very large
amounts may block some cholinergic effects at nicotinic sites, but these
antinicotinic effects are not evident even at high clinical doses. When
small amounts (2 mg) are given to normal individuals without nerve agent
intoxi­cation, atropine causes mydriasis, a decrease in secretions
(including a decrease in sweating), mild sedation, a decrease in GI
motility, and tachycardia. In people not exposed to nerve agents,
amounts of 10 mg or higher may cause delirium. Potentially, the most
hazardous effect of inadvertent use of atropine (2 mg, i.m.) in a young
person not exposed to a cholinesterase inhibiting compound in a warm or
hot atmosphere is inhibition of sweating, which may lead to heat injury.
Prali­doxime chloride (600 mg) is in an autoinjector for use along with
the atropine injector (2 mg). These atropine and pralidoxime chloride
autoinjectors are packaged together in a MARK I kit (see insert box).
Pralidoxime chloride (Protopam chloride; 2-PAM Cl) is an oxime. Oximes
attach to the nerve agent that is inhibiting the cholinesterase and
break the agent-enzyme bond to restore the normal activity of the
enzyme. Abnormal activity in skeletal muscle decreases and normal
strength returns. Oximes do not cause a decrease in secretions. Diazepam
is an anticonvulsant drug used to decrease convulsive activity and
reduce brain damage caused by prolonged seizure activity.

S.  Decontamination

> Decontamination is the reduction or removal of chemical agents.
> Decontamination may be accomplished by removal of these agents by
> physical means or by chemical neutralization or detoxification.
> Decontamination of skin is the primary concern, but decontamination of
> eyes and wounds must also be done when necessary. Skin decontamination
> is not neces­sary after exposure to vapor alone, but clothing should be
> removed because it may contain "trapped" vapor. The most important and
> effective decontamination of any chemical exposure is that
> decontamination done within the first minute or two after exposure.
>
> Decontamination of casualties is an enormous task. The process
> requires dedication of large numbers of personnel and large amounts of
> time. Even with appropriate planning\
> and training, the requirement demands a significant contribution of
> resources.
>
> Liquids and solids are the only substances that can be effectively
> removed from the skin.\
> It is generally not possible or necessary to decontaminate vapor.
> Removal from the atmos­phere containing the vapor is all that is
> required.
>
> Many substances have been evaluated for their usefulness in skin
> decontamination. The most common problems with potential
> decontaminates are irritation of the skin, toxicity, ineffectiveness,
> or high cost. An ideal decontaminate will rapidly and completely
> decon­taminate all known chemical and biological (C/B) warfare agents.
> Furthermore, a suitable skin decontaminate must have certain
> properties that are not requirements for decontami­nates of equipment.
> Recognized desirable traits of a skin decontaminate include
> neutraliza­tion of all agents, safety (compound to be nontoxic and
> noncorrosive), ease of application by hand, availability, rapid
> action, nonproduction of toxic end products, stability in long-term
> storage, short-term stability (after issue to unit/individual),
> affordability, nonenhance­ment of percutaneous agent absorption, no
> irritability, hypoallergenicity, and ease of disposal.
>
> Decontamination issues have been explored since the beginning of
> modern chemical warfare. After years of research worldwide, simple
> principles, which consistently produce good results, still apply. The
> first, which is without equal, is timely physical removal of the
> agent. To remove the substance by the best means available is the
> primary objective. Chemical destruction (detoxification) of the
> offending agent is a desirable secondary objec­tive. Physical removal
> is imperative because none of the chemical means of destroying these
> agents do so instantaneously. Decontamination preparations, such as
> fresh hypo­chlorite, react rapidly with some agents (e.g., the half
> time for destruction of VX by hypochlorite at a pH of 10 is
> 1.5 minutes); the half times of destruction of other agents, such as
> mustard, are much longer. If a large amount of agent is present
> initially, a longer time is needed to completely neutralize the agent
> to a harmless substance. Timely use of water, soap and water, or flour
> followed by wet tissue wipes may work in many cases.