Handout - Chemical Agents (EMPRC)

Chemical Agents
Clinicians Course/ Version 1

Student Handout
7Apr 2009
Terminal Learning Objective: Identify the various types of chemical agents, their signs and symptoms,
and treatment options, in accordance with referenced materials.
Enabling Learning Objectives:
A. Given a possible CBRNE event, Name various types, signs and symptoms for exposure to Pulmonary
Agents
B. Name various types, signs and symptoms for exposure to Cyanide Compounds (Blood Agents)
C. Name various types, signs and symptoms for exposure to Nerve Agents
D. Name various types, signs and symptoms for exposure to Vesicants (Blister Agents)
E. Name various types, signs and symptoms for exposure to Riot control and incapacitating agents
I. Identify the types of pulmonary agents

1. Pulmonary (Choking) agents
a. The term "pulmonary agents" is sometimes used in a general way to apply to chemical compounds
that produce local toxic inhalational injury in any part of the respiratory tract. In the U.S. Army, the
term is usually restricted to pulmonary-edematogenic agents, that is, those chemicals that affect the
small or peripheral airways and cause pulmonary edema. A vesicant, or blister agent can also
damage the airways (i.e. hydrochloric acid sulfur dioxide, acetic acid, and ammonia).
b. Agents that fall into this general category include:
• Sulfur mustard
• Heated particle matter (i.e. most smokes)
• Strong mineral and organic acids and bases
c. Primary Pulmonary Agents: Most pulmonary (choking) agents are gases at ambient temperatures.
Some are liquids that evaporate rapidly, and others are chilled and compressed to form liquids for
transport. Both the gases and the liquids (especially if extremely cold) may in some cases irritate and
damage exposed eyes and skin, but their most prominent effects are usually from inhalation of vapors
or gases.
The main target tissues are the large airways (including the nose, mouth, larynx, trachea, and
large bronchi) and the small airways (including respiratory bronchioles, air sacs, and alveoli) in the
respiratory tract. Although systemic distribution in the bloodstream may occur, this module will focus
on the local effects (especially on the respiratory tract) of pulmonary agents.
1) Phosgene (CG): John Davy developed phosgene in 1812. It was first used as a weapon by
Germany in 1917 during World War I. Phosgene was responsible for thousands of deaths during
the war because of its action on the peripheral compartment (small airways) and its effectiveness
in producing pulmonary edema in those exposed who are unmasked. CG was used both alone
and in combination with chlorine. Deaths have occurred after the inhalation of only a few breaths
of high concentrations of phosgene.
2) Diphosgene (DP): Diphosgene is a liquid at usual temperatures but produces a vapor with a
suffocating odor. It was synthesized in an attempt to penetrate protective mask filters designed to
protect against phosgene. At high temperatures, it decomposes to release phosgene.
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3) Chlorine: Initially proposed as a chemical agent during the American Civil War, chlorine gas
was first used in WW I, with an estimated production of 93,800 tons. The Germans first used
chlorine gas successfully in Ypres, Belgium. In this one engagement, there were over 10,000
casualties among the unprotected French and Algerian troops. Chlorine is still a terrorist threat
today.
II. Outline Behavior and Risk for each agent

2. Pulmonary (Choking) Agents: Behavior and Risk
a. Behavior: Pulmonary (choking) agents act on the respiratory tract. They allow fluid to leak into
the lungs.
1) Cause damage to the respiratory system
A. Mild irritation and coughing paroxysma

B. Shortness of breath and feeling of chest tightness, pulmonary edema
2) Death
b. Risk: Effects include shortness of breath, difficulty breathing, sudden laryngeal spasm, pulmonary
edema, vomiting, abnormally low blood pressure, and possible death.
III. Identify physiological affects and characteristics for each agent.
3. Pulmonary (Choking) Agents. Pulmonary agents attack the tissue of the airways and lungs.
a. Acute Toxic-Inhalational Injury: Although some pulmonary agents may irritate eyes and mucous
membranes, their primary toxicity is to the airways and follows inhalation of smoke particles, vapors,
or gases. A critical aspect of dealing with acute toxic-inhalational casualties is to determine the
compartment or compartments affected and then to treat the compartmental damage rather than to
adhere to a specific treatment protocol for each agent.
b. The following agents can cause varying degrees of acute toxic inhalational injury:
1) Smokes, in general: Smokes are aerosols composed of fine particles suspended in the
atmosphere and have many of the properties associated with other aerosols (dusts, mists, and
fogs). Smoke particles from fires and from most military smokes are too large to reach the small,
peripheral airways, and direct damage (including thermal injury) from these particles is usually
limited to the central airway. However, a wide variety of gases and vapors may be adsorbed
onto, or adhere to, smoke particles; and these particles may therefore introduce these gases into
the upper airways and allow them easier access to the smaller, peripheral, airways.
Most heat damage from smoke inhalation is not due to heated air (which transfers heat very
poorly to tissues) but rather from inhaled smoke particles. Military smokes (with their assigned
NATO codes in parentheses when applicable) include the following:
●Sulfur trioxide-chlorosulfonic acid (FS)

●Titanium tetrachloride (FM)
●White phosphorus (WP) (also used as an incendiary agent)
●Red phosphorus (RP)
●Colored smokes
●Petroleum oil, or fog oil (SGF)
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These agents are all predominantly centrally acting pulmonary agents and not pulmonary agents
in the restricted military sense of peripherally acting compounds. Standard white military
obscurant smoke, or HC smoke is an exception in that it releases compounds that can reach the
peripheral airways as vapors or gases and that can produce pulmonary edema; see "Standard
white military obscurant smoke (HC, or HC smoke).“
2) Sulfur mustard (H, HD): Sulfur mustard is referred to as H when impure and as HD when
distilled, or pure (neat). HD is a solid below 14°C (58°F) and boils at 217°C 423°F). It is
traditionally classified as a vesicating, or blister, agent but also has local effects on the respiratory
tract when it is inhaled. Sulfur mustard dissolves only slowly in water but upon dissolving forms
an incredibly reactive compound that chiefly attacks the central, or large-airways, compartment of
the respiratory tract. In large doses, sulfur mustard can also cause peripheral damage
(pulmonary edema), but in low to moderate doses sulfur mustard is the prototypical centrally
acting respiratory toxicant. (Associate the s sound at the beginning of "sulfur mustard" with the
sound at the beginning of "centrally acting”.)
3) Lewisite (L): Lewisite, which freezes (depending upon its purity) at -18°to 0°C (~0° to 32°F)
and boils at 190°C (347°F), is another vesicant with effects on the airways. However, by reason
of the arsenic atom in this compound, its mechanism and sites of action differ somewhat from
those of sulfur mustard. Lewisite affects the central airways directly, but arsenic-induced damage
to the small capillaries surrounding alveoli may also occur even in low to moderate doses and
result in leakage of fluid into airways and in pulmonary edema. Thus, Lewisite, which you could
remember as a leaky compound, is a combination agent, with effects on both compartments even
in low to moderate doses.
4) Chlorine: Chlorine, which boils at -34°C (-29°F), has been used as a chemical-warfare agent
and because of its extensive industrial use and easy availability (preformed or by synthesis) is
also a terrorist weapon of opportunity. Simply opening the valve on a chlorine or phosgene tank
car near a large metropolitan area could produce mass casualties. Household combination of
basic hypochlorite solutions (bleach) with acids and bases generates chlorine and chloramines,
respectively. Both chlorine and chloramines are intermediate in aqueous solubility and in
chemical reactivity. Think of chlorine as the prototypical combination respiratory agent, with
effects on both compartments even in low to moderate doses.
5) Phosgene (CG): Phosgene, like chlorine, has been used as a chemical-warfare agent and
also is widely used and readily available industrially. Both compounds are used as precursors for
more complex chlorinated hydrocarbons, the primary components of modern plastics and dyes.
Thousands of tons of phosgene are produced, stored, and transported each year in this country,
creating the potential for a large-scale release from an industrial accident, sabotage, or terrorist
event. Phosgene boils at -7°C (19°F). It is relatively insoluble in water and relatively slows to
react chemically, and by reason of these characteristics, it affects primarily the smaller airways.
Think of phosgene as the prototypical peripherally acting pulmonary agent.
6) Perfluoroisobutylene (PFIB): Organofluoride polymers are valued by the chemical industry

for their desirable chemical and physical properties. Polymers such as polytetrafluoroethylene
(Teflon®), are used extensively in military aircraft and vehicles because of their lubricating and
insulating properties. When organofluoride polymers are burned or pyrolyzed (thermally
degraded) at relatively low temperatures (about 450°C, or about 850°F), a self-limited flu like
syndrome called polymer fume fever results. However, during combustion or degradation at
higher temperatures (above about 850°F, or above about 1,500°F), several very toxic byproducts
are produced. Perfluorisobutylene (PFIB) is the most studied of these byproducts, and inhalation
of PFIB or its related compounds produces the same effects on the peripheral airways as does
phosgene.
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7) Oxides of nitrogen (NO2): Nitrogen combines with oxygen in different proportions to form a
variety of oxides, collectively referred to as oxides of nitrogen, or NOx, which are all gases at
usual environmental temperatures. They include the colorless gas nitric oxide (NO), the brown-
red gas nitrogen dioxide (NO2, which gives photochemical smog its brown color), and the yellow
gas nitrogen tetroxide (N2O4). Oxides of nitrogen can be generated from nitrous acid in silage,
from high-temperature welding, from combustion or pyrolysis of nitrogen-containing compounds,
from diesel-engine exhaust, and from the discharge of the nitrate-based explosives found in
small-arms rounds, artillery shells, and other munitions. Exposure to high levels of nitrogen
oxides, particularly in enclosed spaces, can produce peripheral-airway injury leading to
pulmonary edema. A characteristic that oxides of nitrogen share with HC smoke is the ability to
cause late-onset pulmonary fibrosis (organizing pneumonia). This process is probably
immunologically mediated and therefore may be amenable to steroid treatment during the acute
phase of pulmonary edema.
8) Toxic industrial chemicals (TICS)/toxic industrial materials (TIMS): Toxic industrial

chemicals, or TICs, are according to the North Atlantic Treaty Organization (NATO) chemicals
that are at least as poisonous as ammonia (that is, with LCt50s less than 100,000 mg-min/m³)
and that are produced in large quantities industrially. A broader definition would be any industrial
chemical that could be released in sufficient quantities to produce mass casualties either on or off
the battlefield. The list of such chemicals is far too long to reproduce here, but a general
prediction of the compartment or compartments likely to be affected by a given chemical can be
made on the basis of the aqueous solubility, the chemical reactivity, and the dose of the chemical.
Since the evaluation of a pulmonary-agent casualty should focus on the type of damage, knowing
the identity of the specific TIC or TICs released, while helpful, is not always necessary. Clinical
recognition of damage to the central compartment, the peripheral compartment, or both should be
sufficient to guide therapy in the absence of identification of specific chemicals.
9) Cyanide compounds (AC, CK) and nerve agents: A variety of other chemicals, including
chemical-warfare agents and certain toxic industrial chemicals, can affect the airways. However,
because they do not produce localized toxic inhalational injury specifically targeted to the
respiratory tract and because when pulmonary injury results from these compounds it arises from
different mechanisms of action and causes different kinds of damage, these other compounds are
generally not considered to be pulmonary agents even in a general sense. Hydrogen cyanide
(AC) is a systemic agent, causing hypoxic damage to all cells in the body (and with no specific
predilection for the lung). In addition to cyanide-related systemic effects, cyanogen chloride (CK)
also has both central and peripheral pulmonary effects, but only by reason of the chlorine that it
releases. Nerve agents cause cholinergic crisis, which can lead to constriction of bronchi and
increased bronchial secretions. However, effects in the lung do not arise from direct damage to
respiratory epithelium and are a special case of cholinergic crisis occurring throughout the rest of
the body. Paraquat is an herbicide that can cause severe and fatal pulmonary fibrosis, but after
ingestion rather than by inhalation.
10) Standard white military obscurant smoke (HC smoke): Standard white military
obscurant smoke (HC) is often called HC smoke. It is composed of hexachloroethane (hence,
the NATO code, HC), zinc oxide, aluminum, and traces of heavy metals but upon heating
releases zinc chloride, phosgene, carbon tetrachloride, ethyl tetrachloride, hexachlorobenzene,
chlorine, hydrogen chloride, and carbon monoxide. It can thus have a variety of effects in both
compartments of the respiratory tract, but it is most toxic to the peripheral airways and can cause
pulmonary edema. A characteristic that HC smoke shares with oxides of nitrogen is the ability to
cause late-onset pulmonary fibrosis (organizing pneumonia). This process is probably
immunologically mediated and therefore may be amenable to steroid treatment during the acute
phase of pulmonary edema.
c. Properties and Toxicities Chlorine and Phosgene: Military dispersion of chlorine and phosgene
during World War I followed either the release of these agents as gases from liquid-filled cylinders or the
explosion of liquid-filled shells. There was subsequent rapid volatilization or boiling of the agent with
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frequent formation of a white cloud due to temperature-induced condensation of atmospheric water vapor
into clouds. The released chlorine was a dense green-yellow gas with a characteristic pungent and acrid
odor; phosgene spontaneously converted to a colorless, low-lying vapor or gas four times as dense as
air. Phosgene was often mixed with other substances.
1) Chlorine:
a. Often described as having pungent and acrid odor - The characteristic odor of chlorine is
readily detected even at nontoxic concentrations, although olfactory accommodation does
occur to very low concentrations of the gas. Only half as much phosgene is required to kill
half of an exposed group, phosgene is thus twice as potent as chlorine. Perfluoroisobutylene
may be up to ten times more toxic than phosgene.
b. Green-yellow in color
2) Phosgene:
a. Described as having the smell of newly mown or musty hay, or green corn - Because the
odor of phosgene may be faint or lost after accommodation, olfactory detection of the classic
odor of newly mown hay, musty hay, or green corn is not a reliable indicator of phosgene
exposure. The eye irritation, coughing, sneezing, hoarseness, and other central respiratory
effects seen after exposure to high concentrations are also unreliable guides to phosgene
exposure. Moreover, even a single breath or two of a sufficiently high concentration of
phosgene can be fatal.
b. Twice as potent as chlorine
c. A single breath of a sufficiently high concentration can be fatal
d. Colorless
IV. List clinical signs and symptoms associated with each agent
4. Clinical Effects of Acute Pulmonary Toxicants:
a. Sulfur Mustard (H, HD) Inhalation (Vapor) with Rapid Onset of Symptoms:
Because sulfur mustard does not readily dissolve in water to form, an acid, initial irritation is usually
absent. There may be no sneezing, coughing, hoarseness, or laryngospasm acutely, and if the odor
of sulfur mustard is not recognized or distinguished from other odors in the environment, exposure
may not be recognized by the victim. Sulfur mustard begins acting immediately, but the signs of
turbulent airflow in the central compartment of the respiratory tract typically do not become apparent
until after a latent period of hours. (Like the latent period for peripherally acting pulmonary agents,
the latent period for sulfur mustard is inversely correlated with dose.) These effects will include noise
and also irritation from the developing inflammation. Also, in high doses, sulfur mustard can damage
to the peripheral compartment.
1). Low to Moderate Doses
A. Central effects (noise: Sneezing, coughing, wheezing, irritation) after a dose-related

latent period, usually of several hours.
B. No peripheral effects expected.
2) High Doses
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latent period, usually of several hours but shorter than that seen with low to moderate doses.
B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.
b. Lewisite (L) Inhalation (Vapor) with Rapid Onset of Symptoms: Because Lewisite acts like sulfur
mustard to damage the central airways but also acts via arsenic to damage the peripheral airways via
a separate mechanism, even low to moderate doses of Lewisite can cause both central and
peripheral clinical effects involving the respiratory tract.

latent period, usually of several hours.
2). High Doses

latent period, usually of several hours but shorter than that seen with low to moderate doses.
B. Peripheral effects: Late-onset shortness of breath (but occurring earlier than after low to
moderate doses) progressing to pulmonary edema with accompanying hypotension and
circulatory collapse ("Lewisite shock").
c. Chlorine Inhalation (Vapor) with Rapid Onset of Symptoms: Even relatively low concentrations of
chlorine are usually detectable by odor and by reason of irritation of the nasopharynx and
oropharynx. Because of its intermediate aqueous solubility and intermediate chemical reactivity,
chlorine produces clinical effects referable to both the central and peripheral compartment in
approximately equal measure, although not simultaneously.
1) Massive Doses: Exposure to massively supralethal concentrations of chlorine can lead to

immediate collapse, apnea, and sudden cardiac death. The mechanism appears to be
immediate and extensive coagulation of blood in both the pulmonary and also the systemic
circulations by large amounts of generated acid.
2). Low to Moderate Dose
A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately

and either resolving or persisting (depending upon the dose and the extent of injury).
3). High Doses

and often persisting.
moderate doses) progressing to pulmonary edema.
d. Phosgene (CG) Inhalation (Vapor) with Rapid Onset of Symptoms: The victim of a low to
moderate dose of phosgene may or may not notice an unusual odor; exposure, even to a dangerous
amount, is often unapparent. Because phosgene is primarily a peripherally acting agent at low to
moderate doses, no effects at all may be seen until the victim develops shortness of breath some
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time after exposure. However, exposure to high concentrations of phosgene may produce central-
compartment effects that may either persist or resolve but that in this setting indicate a high dose.
1). Massive Doses: Exposure to massively supralethal concentrations of phosgene can lead to
immediate collapse, apnea, and sudden cardiac death. As in the case of massive doses of
chlorine, the mechanism appears to be immediate and extensive coagulation of blood in both the
pulmonary and also the systemic circulations by generated acid.
A. No central effects expected.
3). High Doses
A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately and
either resolving or persisting (depending upon the dose and the extent of injury).
e. Perfluoroisobutylene (PFIB) Inhalation (Vapor) with Rapid Onset of Symptoms: PFIB is a

peripherally acting agent with effects similar to those of phosgene but with a typically shorter latent
period than that of phosgene.
1) Low to Moderate Doses
2). High Doses
A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately and
either resolving or persisting (depending upon the dose and the extent of injury).
f. Oxides of Nitrogen (NO2) Inhalation (Vapor) with Rapid Onset of Symptoms: The acute course of
exposure to oxides of nitrogen is similar to that of exposure to phosgene or PFIB. However, after a
symptom-free apparent recovery of days to weeks, a relapse may be heralded by shortness of
breath, this time from the development of interstitial pulmonary fibrosis rather than simply from the
acute accumulation of fluid in the airways. Probably because the late-onset fibrosis is
immunologically activated, the initial inhaled dose does not appear to be correlated with the risk of
development of fibrosis.
C. Late-onset effects: In few cases, shortness of breath and decrease in pulmonary function
(often irreversible) following an apparent recovery from the acute effects.
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2). High Doses

and either resolving or persisting (depending upon the dose and the extent of injury).
C. Late-onset effects: In a low percentage of cases, shortness of breath and decrease in

pulmonary function (often irreversible) following an apparent recovery from the acute effects.
V. Describe methods for diagnosis of pulmonary agents

5. Diagnosis
a. History characteristically different from most trauma victims.
b. May be a latent period of a few hours to several days.
c. Severe exposure may produce central-compartment symptoms, which could rapidly become fatal.
d. Primary objective is NOT to determine the specific agent(s) – determine the type of compartmental
injury or injuries.
e. Casualties with toxic inhalation injuries present with a history that is characteristically different from
that of most trauma victims, and the cause-effect relationship may be particularly difficult to assess
when the exposure is unapparent or is to a low concentration over a prolonged period of time.
Depending on the agent and intensity of exposure, there may be a latent period of a few hours to
several days. There is also normally a further delay between the onset of symptoms and the
appearance of objective clinical signs. While a latent period is typical, severe exposure can also
produce central-compartment symptoms, such as laryngospasm or bronchospasm, which could
rapidly become fatal. In the case of pulmonary agents, the primary objective is not to determine
the specific agent or agents but rather to determine the type of injury to the central compartment,
peripheral compartment, or both.
f. Ancillary Diagnosis
1) Chest radiography may detect pulmonary edema
2) In general, laboratory and radiological tests for pulmonary edema are most useful for
monitoring the clinical course
VI. Name specific treatment for casualties affected by each agent
6. Treatment:
a. General principles applicable to both central and peripheral compartment damage are as follows:
1) Protect yourself from exposure!
2) Use detectors and personal protective equipment as indicated.
3) Terminate the exposure to the agent by doing as many as possible of the following:
A. Eliminate the source of exposure.
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B. Protect the casualty in place (for example, by masking).
C. Remove the casualty from the site of exposure.
D. Consider the ABCDDs of immediate chemical-casualty care!
4) Recognize and treat the DAMAGE, not the agent!
b. Central-Compartment Damage: The following guidelines particularly applicable to central-

compartment damage should be followed:
1) Treat local irritative effects on the skin and eyes.
2) Consider early intubation, especially if soot is present around the nose or mouth.
3) Administer warm, moist (humidified) oxygen (or warm, moist air with supplemental oxygen).
4) Consider aggressive pulmonary toilet (positioning, percussion, and drainage) to help mobilize
and remove airway debris and secretions.
5) Consider bronchoscopy for not only diagnostic confirmation of damage to central airways but
also for removal of pseudomembranes and other debris.
6) Consider bronchodilators as indicated for bronchoconstriction and bronchospasm.
7) Consider anti-inflammatory agents (including nonsteroidal agents and, as clinically indicated,

steroids) to manage airway edema and other indicators of acute inflammation.
8) Monitor the patient carefully for infection, but do not administer antibiotics prophylactically;
instead, choose antibiotics after isolating an organism and determining its antibiotic-sensitivity
profile.
9) Always consider the potential for concomitant peripheral-compartment damage, especially in

patients with transient irritation or coughing that then resolves.
10) Consider the potential for the future development of reactive-airway dysfunction syndrome
(RADS), or irritant-induced asthma.
11) Recognize and treat the DAMAGE, not the agent!
c. Peripheral-Compartment Damage: The following guidelines particularly applicable to peripheral-

compartment damage should be followed:
1) Maintain a high index of suspicion for peripheral-compartment damage and monitor the patient
for shortness of breath.
2) Monitor suspected victims of peripheral-compartment damage for at least 12 hours if they

remain asymptomatic and for at least 24 hours if symptoms develop.
3) Maintain suspected victims of peripheral-compartment damage at strict bed rest during

monitoring.
4) Consider early evacuation to a pulmonary intensive-care unit for all victims suspected of
significant peripheral-compartment damage.
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5) Administer warm, moist (humidified) supplemental oxygen.
6) Carefully apply positive pressure ventilation (PPV), with, for example, continuous positive
airway pressure (CPAP) in a conscious patient or positive end-expiratory pressure (PEEP) in an
intubated patient.
7) Pay careful attention to the balance between removing adequate fluid from the respiratory
tract and removing too much fluid from the systemic circulation; place a central line to monitor
intravascular pressures in the pulmonary and systemic circulations.
8) Remove sufficient fluid from the respiratory tract to treat the pulmonary edema while at the
same time maintaining enough fluid in the systemic circulation to support adequate tissue
perfusion.
9) Consider administering steroids to decrease the risk of late-onset cryptogenic organizing

pneumonia for those with possible exposure to NOx or HC smoke.
10) Do not administer antibiotics until isolating an organism and determining its antibiotic-
sensitivity profile.
d. Treatment of Specific Agents
1) Smokes, in general - Smokes may cause either thermal or chemical damage to the central
compartment. In addition, some vapors or gases associated with smokes may reach the
peripheral compartment to cause damage there (an example is HC smoke). Treat the central-
compartment damage as described under general treatment and under treatment of central-
compartment damage and be alert for the development of shortness of breath or other indicators
of injury to the peripheral compartment.
2) Lewisite (L) - In its actions on the respiratory tract, Lewisite creates immediate pain and
irritation with eventual inflammatory changes (including erythema and edema) and necrosis of
epithelium in central airways. However, it also produces delayed-onset pulmonary edema by
means of arsenic-induced damage to pulmonary capillary endothelium. Clinically, it acts as a
combination agent, and treatment of its pulmonary effects thus involves a combination of the
measures described for general treatment, for treatment of central-compartment damage, and for
peripheral-compartment damage. The initial absence of shortness of breath should not blind the
treating clinician to the likelihood of the eventual development of pulmonary edema with
concomitant systemic hypotension (so-called "Lewisite shock"). The specific antidote (British
Anti-Lewisite [BAL], or dimercaprol) could be considered for subcutaneous or intramuscular
administration for systemic absorption, but the use of BAL has not been systematically evaluated
or the treatment of the pulmonary effects of Lewisite.
3) Chlorine - Chlorine is the classical combination agent in terms of its causing approximately
equal damage to the central compartment and to the peripheral compartment in both low and
high doses. Treatment should be directed to the initial central-compartment damage and to
monitoring for the possible appearance of pulmonary edema. An almost characteristic initial
complaint of chlorine exposure is that of suffocation-the sensation of inability to get enough air.
Individuals who survive a single, acute exposure generally demonstrate few or no long-term
pathological or physiological sequelae. Individuals with underlying cardiopulmonary disease or
those who suffer complications (such as pneumonia) during therapy are at risk for developing
chronic bronchitis or (very rarely) a gradual and progressive organizing pneumonia. Assessment
of these individuals suggests that chronic or progressive illness is more likely to have resulted
from a combination of inadequately treated complicating infections and cigarette smoking than
from the destructive effects of a single, acute exposure to chlorine. The mechanism does not
appear to be immunological in nature. Most deaths occur within the first 24 hours and are caused
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by respiratory failure. Generally, the patient gradually recovers from the acute injury in 36 to 72
hours, depending on the degree of exposure.
4) Phosgene (CG) - Phosgene exposure produces predominantly peripheral-compartment

damage in low to moderate doses, although damage from released acid at high concentrations
can produce central-compartment effects. However, central-compartment effects are typically
transient even at high doses, and the chief therapeutic challenge is pulmonary edema and its
complications (such as infection). Follow the general principles of treatment for acute pulmonary
toxicants and the guidelines for the treatment of peripheral-compartment damages. These
guidelines include monitoring, enforced bed rest, and administration of supplemental oxygen.
When pulmonary edema ensues, intubation and positive pressure ventilation with PEEP may be
necessary to maintain adequate oxygenation. Recovery in survivors is usually without serious
sequelae.
5) Perfluoroisobutylene (PFIB) - Inhalation of PFIB, like that of other peripheral-compartment

agents, is followed by a very rapid toxic effect on the pulmonary tissues, with microscopic
changes of perivascular edema evident within five minutes. However, the clinical presentation is
the typical one of pulmonary edema heralded by delayed-onset shortness of breath.
Management is identical to that for phosgene exposure. Treatment of the pulmonary edema
produced by PFIB exposure follows the same principles as treatment of phosgene
exposure. Just as with phosgene inhalation, exercise after exposure exacerbates the symptoms
and worsens the outcome. The patient with PFIB exposure should be placed at rest and
observed for at least 6 hours. Maintenance of adequate oxygenation in patients with frank
pulmonary edema will likely require positive pressure ventilation with PEEP.
6) Oxides of nitrogen (NO2) - Exposure to oxides of nitrogen may be unapparent to the victim but
mainly causes direct peripheral-compartment damage (with ensuing pulmonary edema) and also,
in a small % of patients, immunological damage leading to late-onset pulmonary fibrosis.
Treatment of the acute episode should be as for phosgene exposure but with the possible
addition of steroids in an effort to reduce the risk of late-onset pulmonary fibrosis (organizing
pneumonia). At NOx concentrations of 0.5 parts per million (ppm) or less, individuals with
preexisting airway disease show no clinical effects post exposure. At 0.5 ppm to approximately
1.5 ppm, individuals with asthma may note minor airway irritation. Concentrations of 1.5 ppm
may produce changes in pulmonary function measurements in normal individuals, including
airway-narrowing, reduction of diffusing capacity of the lung, and widening of the alveolar-arterial
difference in the partial pressure of oxygen (PAO2-PaO2 gradient). Standard therapy for
pulmonary edema may be supplemented with acute steroid therapy to minimize fibrotic changes
that lead to persistent airway obstruction. Pneumonitis appears to complicate the initial
pulmonary edema relatively early; nevertheless, the use of prophylactic antibiotics is not
indicated.
7) Standard white military obscurant smoke (HC smoke) - Exposure to HC smoke causes
irritation of the nasopharynx and central airways by reason of smoke particles and other products
of combustion or pyrolysis. Nevertheless, the chief concern with HC smoke is, as with oxides of
nitrogen, direct peripheral-compartment damage (with ensuing pulmonary edema) and also, in a
small percentage of patients, immunological damage leading to late-onset pulmonary fibrosis.
Treatment of the acute episode should be as for phosgene exposure but with the possible
addition of steroids in an effort to reduce the risk of late-onset pulmonary fibrosis (organizing
pneumonia).
ELO B: Name various types, signs and symptoms for exposure to Cyanide Compounds (Blood
Agents)
I. Recognize the behavior and risks associated with each compound
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1. Cyanide Compounds (Blood Agents)
a. Introduction: Cyanide compounds are historically known as blood agents. However, they do not
actually act primarily in the blood; these compounds are rapidly acting cellular poisons. Antidotes
must be administered within minutes of exposure to be maximally effective.
b. Behavior
1) Rapidly transported throughout the body by the blood and affects the cells of the body.
2) Combines with the enzymes in the cells throughout the body so that they are unable to use
oxygen (anaerobic metabolism).
3) Results in cell death especially in the sensitive cells of the brain and heart.
c. Risk
1) Without the enzymes functioning, the cell suffocates.
2) If sufficient cells are affected, the victim dies, even with adequate levels of oxygen available in
the ambient environment and being carried by red blood cells.
d. Cyanide Compounds are substances that can kill a person by interfering with the ability of the
cells of the body to utilize oxygen, causing rapid cell death. Therefore, the brain, heart, and liver are
severely affected. Examples include Hydrogen cyanide (AC) and Cyanogen chloride (CK)
II. Identify types of cyanide compounds
2. Cyanide Compounds
a. Cyanide is:
1) Found in nature: Cyanide is found in the seeds of more than 300 plants, including cherry
and peach pits. The unapproved and ineffective anti-cancer remedy laetrile, made from peach
pits, can release cyanide following ingestion. Other plants also contain compounds (cyanogenic
glycosides) that can release cyanide. Our body has processes that metabolize low levels of
cyanide daily. Cyanide antidotes work to enhance this process.
2) A product of burning: Burning plastics, wood, and silk release cyanide causing its presence
to be a major player in smoke from house fires. Tobacco smoke also contains cyanide.
3) A tool for murder and suicide: During World War II, the Nazis used hydrogen cyanide in the
form of Zyklon B to kill millions of prisoners in the gas chambers in death camps. Adolph Hitler
and several of his top lieutenants committed suicide with cyanide-filled glass capsules. More
recent cyanide incidents include the following:
A. In 1978, cyanide-laced Kool-Aid killed 913 members of the Jonestown,Guyana People's

Temple cult
B. In 1982, seven died in Chicago from cyanide-tainted Tylenol capsules, which led to
tamper-resistant packaging.
4) Widely used in industry: Cyanide is used in a wide variety of industrial processes including
plastics production, gold and silver extraction during mining, and hide tanning. It is transported
12
on highways and railways for industry. In 2000, Romania saw a catastrophic release of cyanide
from a cyanide wastewater storage lake used in mining operations. The cyanide killed millions of
fish in the Danube River.
5) A chemical-warfare agent: The French military used cyanide-laced artillery shells during the
opening days of World War I.
6) A potential terrorist weapon: Since 2000, U.S. and British intelligence have reported
planned use of cyanide in the British subways and in United States Embassy water supplies in
Rome. It was deployed, without success, in Tokyo subway restrooms by the Aum Shumrikyo cult
several weeks after the sarin attacks in the 1980s. It is the chemical weapon most considered in
planning by terrorists, though it has not yet been effectively deployed in terrorist attacks.
b. Cyanide compounds as chemical-warfare agents are:
1) Hydrogen cyanide (AC): Isolated by Wilhelm Scheele in 1782, who later died by inhaling the
vapors from a broken flask, AC was first used in munitions in 1915 during World War I. The
lethal vapor dispersed quickly and was not deployed in amounts large enough to be effective on
the open battlefield.
2) Cyanogen chloride (CK): The French developed CK in 1916. It combines cyanogens with
chloride, forming a vapor that stays low to the ground and evaporates at a slower rate than AC. It
is highly irritating to the lungs if inhaled, and in high concentrations, it can kill rapidly by
paralyzing the respiratory system's nerve center.
III. List the clinical signs and symptoms associated with cyanide compounds
3. Signs and Symptoms for exposure to Cyanide Compounds
a. Symptom Development
1) Inhalation
15 sec - Gasping (hyperpnea)

30 sec - Loss of consciousness
60 sec - Convulsions
3 to 5 min - Breathing cessation (apnea)
5 to 8 min - Asystole (cardiac arrest) and death
2) Ingestion
7 min - Rapid deep breathing/dizziness

10 min - Anxiety/cramps/vomiting
15 min - Weakness
20 min - Loss of consciousness/convulsions
25 min - Breathing cessation, aystole (cardiac arrest), and death
b. Initial symptoms
1) Tachypnea and tachycardia

2) Dizziness
3) Headache
4) Vomiting
5) Weakness and restlessness
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c. Exposure to large quantities
1) Lung injury
2) Loss of consciousness
3) Respiratory failure
4) Convulsions
5) Hypotension and bradycardia
6) Death
d. Central Nervous System
1) Signs
A. Inhalation: Initial hyperpnea can occur suddenly with high concentrations and progress
within seconds to convulsions and loss of consciousness.
B. Ingestion: Signs are similar to those from inhalation but are delayed up to several minutes
and may also include vomiting.
2) Symptoms
A. Inhalation: Initial symptoms at low concentrations may be nonspecific headaches,

dizziness, a feeling of doom); as exposure continues, or at high doses, gasping and loss of
consciousness can occur within seconds.
B. Ingestion: Symptoms are as for inhalation but are usually delayed by several minutes. A
metallic taste and epigastric pain may also be noted, along with nausea and vomiting in some
cases.
e. Ocular
1) Signs: In some cases, bright red coloration of retinal veins on funduscopic examination; in
addition, possible chemical conjunctivitis with cyanogen chloride. Hypoxic pupillary dilution may
be seen shortly before death.
2) Symptoms: Headache or blurred vision; in addition, irritation and eye pain with cyanogen
chloride (CK).
f. Dermal
1) Signs: Normal skin coloration or flushing, from higher-than-normal levels of oxygen in the
venous circulation. Cyanosis is not part of the classically described presentation but may be seen
in up to 50% of cases, especially as the patient approaches death.
2) Symptoms: Possible flushing sensation; in addition, possible skin irritation due to CK.
g. Cardiovascular
1) Signs
A. Inhaled: Initial hypertension, followed by hypotension, weak and irregular pulse,

bradycardia, cardiac dysrhythmias, and asystole (cardiac arrest).
B. Ingested: Same signs as with inhalation, but delayed in onset.
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2) Symptoms: Palpitations, possible chest pain, and lightheadedness progressing rapidly at high
concentrations, to loss of consciousness.
h. Respiratory
1) Signs
A. Inhaled: At high concentrations, initial hyperpnea from reflex involving the carotid bodies
and the respiratory center of the medulla; eventually, shallow breathing and apnea. Signs of
pulmonary edema may also occur, especially but not exclusively with cyanogen chloride
(CK).
B. Ingestion: Same signs as for inhalation, but delayed in onset.
2) Symptoms
A. Inhaled: Air hunger, gasping, and occasionally chest pain before collapse; in addition,
upper-airway irritation with cyanogen chloride (CK).
B. Ingested: Same respiratory symptoms as with inhalation, but delayed.
i. Gastrointestinal
1) Signs: Ingested: Vomiting possible after ingestion.
2) Symptoms
A. Inhalation: Possible nausea if collapse is not immediate.
B. Ingestion: Metallic taste in mouth, epigastric distress, and possible nausea and vomiting.
IV. State the methods of diagnosis and treatment for exposure to cyanide compounds
4. Diagnosis
a. Recognition and management of cyanide poisoning depends upon a high index of suspicion.
There is not time to wait for the results of definitive laboratory testing.
b. Victims may or may not report an odd smell, so odor is not a reliable warning of cyanide exposure.
From 40% to 60% of the population lacks the gene needed to detect this odor, and even if the odor is
detected, rapid olfactory accommodation may occur. Also, not all who can detect the odor of cyanide
compare it to the classical description of "bitter almonds“.
c. Try to clarify the circumstances of exposure. Was there an odd smell? Was cyanide known to be
present in the area? Is there the possibility of contamination of food or drink by cyanide? Was a tank,
a sprayer, or another dissemination device seen? Are the signs and symptoms consistent with
cyanide exposure?
d. An initial diagnosis can be made by examining signs and questioning those who observed the
victim when they were exposed. An initial diagnosis can be made by examining signs and
questioning those who observed the victim when they were exposed. For example, the individual, or
those who were with them, recall a musty smell of bitter almonds. Ask if the individual works in an
area where cyanide is present, if others were affected by vapors, or if the person drank something in
the past 30 minutes that might cause this. Routine toxicology analyses do not specifically test for
15
cyanide. Whole blood should be sent immediately for confirmatory cyanide testing even though
treatment should not wait for results, which may take some time.
e. Whole blood should be sent immediately for confirmatory cyanide testing even though treatment
should not wait for results, which may take some time. Blood cyanide levels greater than 0.5 mcg/mL
suggest cyanide toxicity, and levels of 2.5 to 3.0 mcg/mL are associated with severe symptoms and
death. Cyanide poisoning causes lactic acidosis, and an elevated anion gap and high lactate levels
are consistent with significant exposure. Because cells poisoned by cells are unable to extract oxygen
from the blood, venous oxygenation will be higher than usual; and a decreased arterio-venous
oxygen difference is highly suggestive of cyanide intoxication.
5. Treatment
a. In the event that cyanide vapor is released:
1) Protect yourself by donning your mask.
2) Terminate exposure in the victim by moving him or her to fresh air or masking the victim, or
both.
3) Provide immediate supportive care, including specific antidotes.
b. Immediate supportive care:
1) Secure the airway, intubate if necessary, and provide artificial ventilation (beware unprotected
mouth-to-mouth rescue breathing) with 100% oxygen.
2) Obtain intravenous access and begin cardiac monitoring.
3) Consider gastric lavage and activated charcoal if less than two hours have elapsed since
ingestion.
4) Correct significant acidemia (pH < 7.15) by administration of sodium bicarbonate.
5) Promptly begin administration of specific cyanide antidotes.
c. Cyanide Antidote Kits: Use either the nitrite/thiosulfate-containing cyanide antidote kit or the
hydroxocobalamin-containing CyanoKit.
1) Cyanide antidote kit:
A. Administer amyl nitrite by crushing an ampoule in gauze and holding near face (or
putting inside mask) for 30 seconds out of every minute.
B. Infuse intravenously the contents of a 10-mL vial of a 3% solution (300 mg) of sodium
nitrite at a rate of 2 to 5 mL/min for adults.
C. Immediately after the completion of the dose of sodium nitrite, infuse intravenously
the contents of a 50-mL bottle of a 25% solution (12.5 g) of sodium thiosulfate in adults
over a ten-minute period.
V. Outline the course and outcome for cyanide compound exposure
6. Outcome
a. General supportive therapy combined with specific antidotal therapy is very effective in cases of
cyanide poisoning and can be lifesaving even after breathing has stopped.
b. Even if specific antidotes are not available, many patients will survive with attention to airway,
16
breathing, circulation, and immediate decontamination.
c. Recovery of patients can be rapid after treatment.
d. Some severely exposed patients can have residual effects relating either to effects of cyanide
on the brain or to prolonged hypoxia, but most patients will recover without sequelae.
ELO C: Name various types, signs and symptoms for exposure to Nerve Agents
I. Identify the types of Nerve agents
1. Introduction: Nerve agents are considered the primary agents of threat to the U.S. military because of
their high toxicity and effectiveness through multiple routes of entry (respiratory tract, skin, and eyes).
The biological effects from nerve-agent exposure occur as nerve-agent molecules bind to and inactivate
certain enzymes in the body. Immediate and accurate diagnosis and treatment are imperative for patient
recovery.
2. Types of Nerve Agents: Nerve agents, organophosphate (OP) insecticides, and carbamate
compounds all act by inhibiting a crucial enzyme called acetylcholinesterase (AChE), or just
cholinesterase (ChE) for short. Chemicals that poison this enzyme are called anticholinesterases.
a. Tabun (GA): The Nazis synthesized the G agents (GA, GB, GD, and GF) during World War II.
There is evidence that they were tested in concentration camps.
b. Sarin (GB): The religious cult Aum Shinrikyo released GB in the Tokyo subway system in 1995,
killing 12, poisoning 1,000, and sending 5,500 to the hospital for medical attention. The Iraqi military
used GB against Kurdish villagers in 1988 and against Iranian military and civilians during the Iraq-
Iran War.
c. Soman (GD): GD has an irreversible effect within a few minutes. Immediate application of the
antidote pralidoxime chloride (2-PAM Cl) is critical. The pretreatment pyridostigmine bromide (PB)
was primarily developed to increase survival against GD.
d. VX: VX was first synthesized in the 1950s by British industry and was produced by the U.S. in the
1960s. The U.S. demilitarized it in the 1970s. VX is stockpiled in the former Soviet Union and is
possibly produced by other countries. It is the most persistent nerve agent.
II. Recognize the Behavior and risks associated with nerve agents
3. Behavior and Risk
a. Behavior: Nerve agents inhibit an enzyme in the body called acetylcholinesterase (AcHE). This
enzyme metabolizes acetylcholine, which is one of the major neurotransmitters in the body.
b. Risk
1) Inhibition of AcHE allows acetylcholine to accumulate.
2) Instead of producing normal muscle contraction, gland secretion, and nerve-to-nerve
conduction, hyperactivity occurs.
3) First responders are at risk from handling victims contaminated with liquid agents as well as
the vapors that may be trapped in victims clothing or on the victim's skin before they are
decontaminated.
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III. Identify the characteristics of the various nerve agents
4. Characteristics
a. Non-persistent: G agents tend to be non-persistent and are usually gone within hours. Some of
their specific properties include:
1) All watery liquids at usual temperatures
2) All relatively volatile
3) Vapors 5-6 times heavier than air; vapor hazard is usually greater than liquid hazard
4) Toxicity: GD > GB > GA
b. Persistent: VX persists in the environment for days. These persistent agents have the following
characteristics:
1) Liquid with consistency of motor oil
2) Low volatility, but vapors may be generated under certain conditions
3) Primarily liquid or aerosol hazard
4) More potent than G agents
IV. List the clinical signs and symptoms for nerve agent exposure
5. Signs and Symptoms
a. Miosis (pinpoint pupils), with visual pain and blurring
b. Excess secretions in the mouth, lungs, and gastrointestinal tract
c. Excessive sweating
d. Nausea and vomiting
e. Generalized seizures
f. Mental status changes
g. Coma and ultimately death
6. Diagnosis
a. Diaphoresis
b. Urination
c. Miosis
d. Bronchospasm
e. Bronchorrhea
f. Emesis
g. Lacrimation
h. Loose stools
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i. Salivation
V. State the methods and tests used for diagnosis of nerve agent exposure
7. Laboratory Testing:
a. Generally non-specific, with the exceptions of tests to measure the activity of the following
enzymes:
1) Erythrocyte anticholinersterase (RBC-ChE, true cholinesterase)
2) Plasma cholinesterase (pseudocholinesterase, butyrycholinesterease, BuChE)
b. Test-Mate Organophosphate Pesticide Exposure Kit: The Test-mate Organophosphate

Pesticide Exposure Kit was developed for field-hospital laboratories to analyze blood and plasma
cholinesterase activity for workers exposed to OP insecticides. Low ChE activities from a potential
nerve-agent casualty support the diagnosis of exposure, but because of individual variation in RBC-
ChE baselines, a normal or minimally depressed activity with this kit does not exclude mild exposure.
c: Do NOT delay treatment while waiting for lab results!: Initially, clinically based, management
of a suspected nerve-agent casualty should not be delayed until the receipt of results from laboratory
testing. The major role for laboratory testing in cases of suspected nerve-agent exposure is for
confirmation of the clinical diagnosis.
VI. List the pretreatment options for casualties affected by nerve agents
8. Pretreatment – Pyridostigmine Bromide (PB)
a. Pyridostigmine bromide (PB) is a carbamate. You recall that carbamates, unlike OP compounds
such as nerve agents, bind reversibly to AChE. Why would we need such a compound, and how could
it help?
1) Why we need PB: For most nerve agents, standard post-exposure antidotes work well.
However, remember soman (GD), the "super glue" of nerve agents? Because of the extremely
rapid aging of soman, one of the post-exposure antidotes (the oxime) is relatively ineffective
unless given in the first ten minutes after exposure. Therefore, we need an additional medical
countermeasure that PB provides. PB when used in this way should really be called a "pre-
exposure antidotal enhancer” rather than a true "pretreatment”.
2) How PB works: PB works by temporarily binding to less than 20% of the body's AChE. This
creates a small serve of life-sustaining AChE enzyme that is not available for nerve agent
attachment. It ties up only a small amount of AChE at any one time and after a few hours
releases itself. This allows someone who was exposed to GD to have a chance of survival.
3) When PB is effective: PB is maximally effective when taken regularly before GD exposure

so that it can tie up the AChE. It is not effective if taken during or after exposure. After a GD
exposure, standard nerve agent treatments are still needed. PB must be refrigerated when
stored prior to troop distribution or it begins to lose its effectiveness.
4) Side effects of PB: PB may have some temporary side effects, including diarrhea, flatus,
loose stools, abdominal cramps, and urinary urgency. These typically subside in a few days.
5) Who can order its administration: Only senior unit commanders can order members to take
PB. This should be with the advice of the unit physician and following theater commander
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directives. PPB is not currently approved to be taken for more than 21 consecutive days but can
be reissued after a short wait period.
VII. Describe the general approaches for treatment
9. Buddy Care/Self-Care
a. In a pre-hospital environment, three drugs are available as auto injectors: Atropine Sulfate,
Pralidoxime Chloride (2-PAM chloride), Diazepam/CANA (Convulsant Antidote, Nerve Agent ).
b. MARK I vs. ATNAA

Two of them (atropine sulfate and 2-Pralidoxine Chloride) are often packaged together in a kit that is
known as the Nerve Agent Antidote Kit (NAAK), or the Mark I Kit.
1) Atropine Sulfate: Atropine sulfate blocks the effects of excessive ACh, but only at
muscarinic receptors. Each atropine auto-injector contains 2 mg of antidote. One to three
atropine auto-injectors, each followed by an auto-injector on 2-PAM chloride, are given depending
upon the initial condition of the victim. After three sets of 2-PAM chloride auto-injectors have
been given, atropine may be repeated until the effects of muscarinic over stimulation resolve.
Intramuscular (IM) injection can be lifesaving, especially before intravenous (IV) access is
obtained. Atropine absorption is even faster after IV administration or administration via an
endotracheal tube. However, there is a small risk of serious heart-rhythm abnormalities if a large
bolus of atropine is given IV to a hypoxic or hypovolemic patient. Because airway resistance may
be so great that ventilation may be difficult, atropine should be given even before intubation and
attempts at mechanical ventilation. Although workers poisoned by OP insecticides can require a
total of up to 1 to 2 grams of atropine, the muscarinic effects of nerve agents are usually
abolished by a total of 20 mg of atropine as long as an oxime is also given. In the absence of 2-
PAM chloride, the total required dose of atropine may be doubled. However, the decision to stop
giving atropine is made on the basis of control of secretions and airway resistance and not on a
given total dose.
2) Pralidoxime Chloride (2-PAM chloride): Pralidoxime chloride (2-PAM chloride) is one of a

group of chemicals called oximes. Oximes are used with atropine to treat poisoning by nerve
agents and by OP insecticides (but not in cases of poisoning by carbamate insecticides). Oximes
do not act at cholinergic receptors. Instead, they break the bond that attaches a nerve-agent to
AChE (as long as the bond has not already aged). However, their major clinical effects are to
decrease twitching and to restore strength in skeletal muscles. Each auto-injector contains 600
mg of 2-PAM chloride, and after each of the first three-atropine injections, a corresponding
injection of 2-PAM chloride is given. However, although atropine can be given repeatedly after
the first three doses, an interval of an hour is recommended after the first three doses of 2-PAM
chloride and the next does. Like atropine, it can be given IM or IV. The usual IV does is 1,000
mg given slowly over 20 to 30 minutes.
3) Diazepam: Benzodiazepines such as diazepam and midazolam do not act directly on nerve
agents or at cholinergic receptors but act on different receptors in the brain to raise the seizure
threshold, that is, to make it more difficult to seize. Other anticonvulsants such as phenytoin or
phenobarbital are not effective against nerve-agent seizures. Diazepam should be given as soon
as seizures are observed but also in any victim who is seriously enough affected to require the
administration of three Mark I kits (three atropine auto-injectors and three 2-PAM chloride auto-
injectors) at once, because victims who are this severely poisoned are at a high risk of seizing.
Not that a flaccid (limp) nerve-agent casualty may still have abnormal electrical activity, seizures
in the brain even though paralysis of skeletal muscles may prevent the casualty from showing
large, rhythmic movements (convulsions).
10. Decontamination
20
a. The first D in ABCDD
b. Immediate, as needed
c. Timeliness
VIII. Describe the symptoms and outcome for nerve agent exposures
11. Inhalation (Vapor) - rapid onset of symptoms
a. Mild: Signs/Symptoms
1) Miosis with or without rhinorrhea

2) Mild chest tightness, slight dyspnea
b. Treatment
1) One Mark 1 kit or one ATNAA

2) Observation
3) Diazepam if seizures present
c. Moderate: Signs/Symptoms
1) Miosis
2) Rhinorrhea
A. Moderate-to-marked dyspnea (bronchorrhea and/or bronchoconstriction

B. Nausea
C. Vomiting
d. Treatment
1) Two or three Mark 1 kits or ATNAAs

2) 2-PAM Cl, as needed
3) Standby ventilatory support
e. Severe: Signs/Symptoms
2) Convulsions
3) Flaccid paralysis
4) Apnea
f. Treatment
1) Three Mark 1 kits or ATNAAs and diazepam

2) Standby ventilatory support, suction
3) IV fluids
4) Additional atropine, 2-PAM Cl, and/or diazepam, as needed
5) Monitoring of secretions, BP (if situation allows), and respiration
12. Inhalation (Liquid on Skin) – onset may be delayed
21
a. Mild: Signs/Symptoms
1) Localized sweating
2) Fasciculations at site of liquid contact
b. Treatment
1) One Mark I kit or one ATNAA

2) Observation
c. Moderate: Signs/Symptoms
1) Vomiting
2) Diarrhea
A. Nausea
B. Dyspnea
C. Generalized weakness
D. Localized sweating and fasciculation at site
d. Treatment
1) Two or three Mark 1 kits or ATNAAs

2) Standby ventilatory support
e. Severe: Signs/Symptoms
2) Convulsions
3) Flaccid paralysis
4) Apnea
f. Treatment
1) Three Mark 1 kits or ATNAAs and diazepam

2) Standby ventilatory support, suction
3) IV fluids
4) Additional atropine, 2-PAM Cl, and/or diazepam, as needed
5) Monitoring of secretions, BP (if situation allows), and respiration
13. Outcome: If treatment is adequate and timely, patients will most likely recover. However, victims
may experience difficulties in concentration, coordination, alertness, and display other subtle
neuropsychiatric and cognitive impairments for months after exposure. Many victims with severe
exposure may die in a mass casualty setting.
ELO D: Name various types, signs and symptoms for exposure to Vesicants (Blister Agents)
I. Outline behavior and risks for each agent
1. Vesicants (Blister Agents): Vesicants, or blister agents, were first used in World War I in which they
resulted in numerous casualties (with primary injury to the lungs and eyes) but comparably fewer deaths.
They constitute both a vapor threat and a liquid threat. They can penetrate street clothing. Prompt
decontamination is the only way to reduce damage once the agent has contacted the skin.
22
a. Behavior
1) Destroy internal structures within the cells.
2) Have their greatest effects on cells with which the agents come in direct contact such as skin
or mucous membranes (primarily of the eyes and lungs).
3) Mustard agents are systemically absorbed, where they affect the bone marrow and blood cell
components.
4) Mustard has a delayed effect, whereas Lewisite creates an immediate burning sensation.
b. Risk: Exposure can result in long-term increased cancer risk among survivors.
II. Identify the characteristics for the various blister agents
3. Characteristics
a. Man-made poisons that can inflict serious illness or injury on persons with exposure to minute
quantities.
b. Rapid acting (Mustard takes longer to appear, however).
c. Burn/blister skin, mucous membranes, airways, and GI tract.
d. May cause systemic changes.
III. State the types of blister agents
4. Types
a. Sulfur Mustard (HD): (odor – garlic, onion, mustard, tar, or asphalt) and Nitrogen Mustard (HN)
(odor – maybe be odorless or fishy). Both sulfur mustard and nitrogen mustards have a great
deal of persistence and stability in cold and temperate climates. In liquid form, sulfur mustard
(HD) usually has an oily consistency.
b. Nitrogen mustards (HN1, HN2, and HN3) were developed as chemical warfare agents but were
never extensively used on the battlefield. HN is used in treatment regimens for Hodgkin's disease
and some forms of non-Hodgkin's lymphoma. It is given intravenously (IV) under controlled
conditions and
disrupts cell division. Rapidly proliferating cells, such as some cancer cells, are very sensitive to
HN. Skin Exposure Reduction Paste Against Chemical Warfare Agents (SERPACWA) is
approved for skin application with the wearing of Personal Protective Equipment (PPE). Applying
this paste to the skin before exposure provides a protective barrier that will prevent the
penetration of liquid mustard agents.
c. Lewisite (L): (odor – geranium-like). Lewisite contains trivalent arsenic. At 70 to 90°F, it will
persist for 18 to 36 hours. Between 40 and 60°F, it will persist for 48 to 72 hours. More volatile
than sulfur mustard (HD) at colder climates, Lewisite can be mixed with HD to lower the freezing
point.
This mixture is called HL.
d. Phosgene Oxime (CX): (odor – irritating or disagreeable): The vapor pressure of CX is high
enough to produce symptoms below 95°F. CX is highly corrosive to most metals or tissue.
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IV. Determine the signs and symptoms associated with each vesicant
a. Blepharospasm
b. Skin
1) Erythema from exposure to Sulfur Mustard (HD) is delayed 1 to 24 hours, and usually appears
between 4 and 8 hours. Exposure to Lewisite results in pain on contact with human skin and the
development of erythema within 15 to 30 minutes.
2) Small vesicles; later coalesce
3) Blisters/bulla
4) Possible coagulation necrosis with liquefaction
c. Airway
1) Upper: nose sinuses, pharynx (epistaxis, sore throat, hacking cough)
2) Mid: Larynx (hoarseness)
3) Lower: Bronchioles (dyspnea, productive cough)
4) Pulmonary edema is rare
d. Gastrointestinal Injury
1) Nausea and vomiting, within 24 hours
2) Tissue destruction, after 3 to 5 days
V. State diagnosis options based on exposure to various vesticants
6. Diagnosis: Mustard Exposure
a. Dermal
1) Skin exposed (even through clothing) to liquid or vapor mustard will develop a sunburn-like
warmth, itching, stinging, and redness usually beginning 4 to 8 hours after exposure.
2) Blisters form within 2 to 24 hours (on average) and peak within days.
3) Severely affected skin may bypass blister formation and turn first red and then black as the
skin dies. Extensive skin sloughing may be seen.
4) Although a ring of blisters may surround a central clear area, blisters may also be irregularly
distributed, without any central clearing.
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b. Ocular
1) Mild - Redness and severe itching after several hours
2) Moderate - Eye irritation may begin between 4 and 12 hours after exposure and may progress
to reddening and swelling of the conjunctiva and to pain severe enough to prevent the victim from
opening his or her eyes
3) Severe - Severe pain, possible miosis (pinpoint pupils), and, with high-dose liquid exposure,
possible perforation and loss of the eyeball
c. Pulmonary
1) Congestion of nose, throat, trachea, large bronchi, and membranes.
2) Burning sensation in the throat.
3) Hoarseness.
4) Dry, nonproductive cough that later becomes productive.
d. Gastrointestinal
1) Possible nausea and vomiting with high doses.
2) With severe exposure, there may be bloody diarrhea as GI tract tissue is destroyed.
e. Other
1) There is an initial rise in white blood cell count (leukocytosis).
2) With high exposures, white blood cell count eventually drops (leukopenia).
3) A white blood cell count less than 200 indicates a grave prognosis.
4) High doses will eventually suppress all types of blood cells (pancytopenia).
7. Diagnosis: Lewisite Exposure
a. Dermal
1) Pain, irritation, and stinging of skin and mucous membranes occur within 1 to 2 minutes after
exposure.
2) After approximately 5 minutes of contact, an area of necrotic tissue and sloughing may
develop, followed by a blistering process that reaches its peak in 18 hours.
3) Blisters often develop outward from a central point.
4) Burns are often deeper than with HD.
5) Itching can occur for several days after exposure.
25
b. Ocular
1) Immediate pain/stinging on vapor contact, causing reflex lid closure (blepharospasm), a

protective reflex. Because of severe pain, the victims keep their eyes closed.
2) Causes lid and conjunctiva edema.
3) If a small amount of agent contacts the eye, it can cause tissue perforation, cornea edema,
miosis (with temporary blindness), and possible corneal abrasion after a few hours.
4) Less likely to cause long-term effects like HD does, such as delayed Keratitis.
c. Pulmonary
1) Pain within a minute or so of contact with liquid or vapor
2) Pronounced irritation to nasal mucosa
3) Severe tissue destruction
4) Lung inflammation
5) Large quantities of frothy sputum
6) Bronchopneumonia
7) Pulmonary edema and hypotension (Lewisite shock)
d. Gastrointestinal: Large amounts can cause severe systemic symptoms:
1) Vomiting
2) Bloody diarrhea
e. Other
1) After exposure to small amounts of Lewisite, fluid loss from leaking capillaries can cause
decreased renal function and hypotension (low blood pressure).
2) Severe exposure (skin or inhaled) can result in shock, liver and kidney necrosis, and death.
3) Arsenic-induced fluid leakage into the lungs from exposure to Lewisite vapor or liquid can lead
to Lewisite shock, characterized by pulmonary edema, hypotension with decreased hepatic and
renal perfusion, and vascular collapse.
8. Diagnosis: Phosgene Oxime Exposure
a. Dermal
1) Immediate pain and burning lasting several days.
2) CX is the most damaging of the vesicants, causing skin damage similar to that of acid burns.
3) Within minutes, a blanched area within an erythematous ring develops.
4) Subsequent development of wheal reaction (a hive or welt) occurs in 30 minutes.
26
5) Tissue necrosis follows within several hours.
b. Ocular
1) Immediate pain, severe irritation.
2) Conjunctivitis and keratitis.
3) Corneal scarring may develop.
c. Pulmonary
1) Immediate pain and burning is present.
2) CX affects both large and small airways.
3) Pulmonary edema is particularly prominent and results from high doses, even if applied only to
the skin.
9. Laboratory Diagnosis
a. No specific common laboratory test exists to confirm mustard agent, Lewisite, or phosgene oxime.
b. Leukocytosis may be initially found, but if significant bone marrow involvement is present, a
pancytopenia may rapidly ensue.
c. Thiodiglycol, a urinary metabolite of sulfur mustard, can be measured at more sophisticated

laboratories.
d. Careful monitoring of leukocyte (white blood cell) counts can help to confirm the onset of bone
marrow depression after severe exposures.
VI. Discuss treatment options and potential outcome for exposure to vesicants
10. Treatment: Decontamination Methods
a. Remove clothes, immediately (preferably within two minutes, but as soon as possible) remove any
liquid visible on the skin and flush affected eyes with water or saline for at least five minutes.
b. Wash effected hair with soap and water, or cut affected hair.
c. Remove all gross contamination (soaked clothing, agent globs) with gauze, the M291 Skin
Decontamination Kit, or field expedients (e.g., gloved hands, leaves, and sticks) and wash the skin
gently but thoroughly with soap and water.
d. Do not use chlorine bleach. It will further damage the skin.
11. Treatment: Mustard
a. Skin
1) Decontaminate the skin.

2) Calamine reduces burning and itching for mild cases.
3) Blisters larger than 2 cm should be unroofed.
27
4) Practice infection prevention.
5) Removing dead tissue will speed healing process.
b. Systemic
1) Use antiemetics and fluid replacements for nausea and vomiting.

2) Severe diarrhea or low white blood count (less than 200 cells per cubic millimeter) suggests
high exposure and poor prognosis.
3) Manage pancytopenia with transfusions, isolation, strict hygiene, and possibly colony-
stimulating factors (CSF).
c. Eyes
1) Irrigate eyes to remove agent and debris.
2) For mild lesions, use soothing eye solution.
3) For more severe cases, apply topical antibiotics.
4) To keep the pupil open, apply topical mydriatic eye drops.
5) Prevent eyelid adhesion by using topical antibiotic ointment.
6) Ease eye pain by systemic or local analgesics.
7) Consult ophthalmologist for moderate to serve cases.
d. Pulmonary
1) Mild airway problems - Keep patient comfortable.
2) More severe - Maintain adequate oxygenation.
3) Treat with bronchodilators if necessary.
4) Maintain airway patency by early intubation if the risk of laryngospasms is high and by
pulmonary toilet (percussion and drainage).
5) Consider tracheotomy if airway obstruction present.
6) Bronchoscopy may be indicated to remove debris.
7) After positive cultures, treat pneumonia with antibiotic.
12. Treatment: Lewisite - There is an antidote, dimercaprol, also called British Anti-Lewisite
(BAL). It binds to the arsenic of Lewisite, displacing it from cellular receptor sites. However, BAL may not
be available.
a. BAL applied topically to the skin immediately after exposure will decrease lesion severity.
b. If effects are systemic or pulmonary symptoms are present, BAL can be injected intramuscularly
(IM):
1) BAL 0.5 mL per 25 pounds IM every 4 hours three times; maximum of 4 mL

2) If poisoning is severe, IM injections can be shortened to every 2 hours.
3) BAL side effects include hypertension and tachycardia.
28
13 Treatment: Phosgene Oxime
a. Skin
1) Decontaminate the skin.
2) Healing may still be incomplete after 6 months.
b Pulmonary
1) Treat large and small airway effects, especially pulmonary edema.
14. Treatment: Phosgene Oxime
a. Eyes
1) Irrigate eyes to remove agent and debris
2) For mild lesions, use soothing eye solution
3) For more severe cases, apply topical antibiotics
4) To keep the pupil open, apply topical mydriatic eye drops (atropine/homatoatropine)
5) Vaseline® or similar material can keep eyelids from sticking and reduce scarring of eye under
lid
6) Eye pain may be eased by systemic or local analgesics.
15. Outcome: Deaths from sulfur mustard tend to occur in three waves, each with its own predominant
mechanism:
a. Deaths within the first 24 hours are usually from airway obstruction either from sloughing of
respiratory epithelium or from reflex laryngospasm.
b. Deaths within 24 and 96 hours are usually from secondary bacterial pneumonia.
c. Deaths in the second week after exposure are usually from septic pneumonia secondary to bone-
marrow suppression.
ELO E: Name various types, signs and symptoms for exposure to Riot control and incapacitating
agents
I. Outline the behavior and risk with incapacitating agents
1. Introduction to Riot Control & Incapacitating Agents: It is important to develop an understanding of the
various types of agents and their effects on the human body due to their probable use in civilian settings,
such as riots, hostage situations, or warfare. Riot control and incapacitating agents work in different ways
and were developed for different purposes.
a. Riot control agents are a specific class of agents, commonly known as irritants, tear gas, and
vomiting agents. They cause temporary incapacitation by irritating body tissues, including the skin,
eyes, and respiratory tract. Many are regularly used by police departments, and occasionally by the
military, for crowd control and for tunnel clearing operations.
29
b. Incapacitating agents are a specific class of agents once designed by the military to cause non-
lethal incapacitation of individuals and interfere with their job performance. The effects of these
chemical compounds were to last several days and affect the brain and nervous system. The U.S.
military no longer uses these agents. However, the former Soviet Union stockpiled similar agents,
and other nations have the capability to produce these agents.
a. Behavior
1) Produce biological effects by inhibiting an enzyme in the body.
2) This under stimulates the nerve impulses in the brain.
b. Risk: Effects include confusion, illusions, hallucinations, rapid heartbeat, and blurred vision.
II. List the types of incapacitating agents
3. Anticholinergic Compounds: 3-Quinuclidinyl Benzilate (BZ) is an anticholinergic glycolate compound

no longer used by the U.S. military. However, other countries may have developed BZ or similar
compounds.
a. Related to atropine, scopolamine, and hyoscyamine

b. Odorless
c. A persistent solid with a high melting point (it can be dispersed by heat-producing munitions)
d. Can be dissolved in non-polar solvents
e. Half-life of 3 to 4 weeks in moist air
f. Extremely persistent in soil, water, and on most surfaces for several weeks
III. Determine the signs and symptoms associated with exposure to incapacitating agents
a. Central Nervous System

1) Stupor
2) Confusion
3) Confabulation with concrete and panoramic illusions and hallucinations
4) Victims may regress to automatic behaviors (i.e., plucking and disrobing)
b. Cardiovascular: Variable with initial tachycardia, which returns to normal or bradycardia over time
c. Eyes
1) Blurred vision
2) Capillary dilation
d. Dry mouth
e. The patient may demonstrate an elevated temperature
f. Peripheral Effects: Just remember: "Blind as a bat, dry as a bone, hot as hare, red as a beet, and
mad as a hatter”.
g. Body Temperature: (Patients may demonstrate an elevated temperature, as they are not able to
sweat. “. . .hot as Hades . . . "
30
h. Ocular: Signs and symptoms of eye involvement may include mydriasis (dilated pupils), blurred
vision, and inability to accommodate or focus the eyes. "...blind as a bat..."
i. Face and Skin: A flushed face occurs as blood rushes to the skin surface to try to cool the body
that cannot sweat, “. . . red as a beet . . . “
j. Mouth: The patient may exhibit a dry mouth (xerostomia). The skin is also very dry as the sweat
glands are not functioning, “. . . dry as a bone . . .”
k. Cardiovascular: This variable effect causes resting tachycardia (for the first few days), returning to
normal or bradycardia heart rate thereafter.
l. Effects in the Brain: The effects of blocking muscarinic receptors in the brain are the following:
1) Attention and memory deficits, including short-term distractibility
2) Deficits of expression and comprehension, including slurred speech, monotonous tone of
voice, and handwriting deterioration
3) Sleepwalking-like behavior, with disrobing, mumbling, and picking ("woolgathering," or
"phantom behaviors")
4) Concrete, easily describable illusions and hallucinations, often decreasing in size over time
("Lilliputian hallucinations")
5) A gradual decrease in the level of consciousness, beginning with lethargy and progressing
through stupor to coma
IV. Determine the methods to diagnosis exposure to incapacitating agents
5. BZ Diagnosis: However BZ exhibits anticholinergic effects that aid in the diagnosis of the patient.
These include a flushed face, hot and dry skin, confused thinking, and panoramic hallucinations based on
real objects (e.g., patient may see clouds and think they are ducks in flight, or may see a few insects and
think they are a swarm, the panoramic nature of these decreases over time). You will see these effects in
a group of casualties who were in the same exposure area.
a. Indoles and Schizophrenic Psychosis: Patients may smile or laugh. They may express
irrational fear, be easily distracted, and have difficulty expressing themselves. Patients may
demonstrate perceptual disorientation and variable increase in pupil size, heart rate, and blood
pressure. They may have stomach cramps and may vomit. Differing characteristics: BZ
hallucinations based on real object, schizophrenic may not. BZ patients have hot red skin, dry mouth,
difficulty urinating, constipated. BZ intoxicated speech very slurred, speech of other diagnosis may
not be.
b. Cannabinoid: Cannabinoid effects include euphoria, relaxation, daydreaming, unconcerned

attitude, easy laughter, hypotension, and dizziness on sudden standing. Differing characteristics: BZ
lethargic, slurred speech. Persons with cannabinoid intoxication may be more alert. BZ patients
have hot red skin, dry mouth, difficulty urinating, and may be constipated. BZ patients have specific
hallucinations related to the size and quantity of real objects in their environment.
c. Anxiety Reactions: Patients demonstrating anxiety reactions may visible tremble, cling, plead,
and cry. Conversion reactions such as blindness and paralysis may occur. They may show a
decrease in disturbance with reassurance. This reaction may be more prominent in individuals
previously exposed to trauma. Differing characteristics: BZ lethargic, slurred speech. Persons with
anxiety reactions will probably be more active. BZ patients have hot red skin, dry mouth, difficulty
urinating, and constipation. BZ patients have specific hallucinations related to the size and quality of
real objects in their environment.
d. Heat Intolerance/Exhaustion: Heat intolerance/exhaustion effects include flushed red skin,

moving from sweating to lack of sweating, dry skin, low-grade fever, disorientation, and slurred
31
speech. Differing characteristics: This may be more difficult to differentiate and may coexist with BZ
intoxication. A BZ casualty will not recover with re-hydration and heat management alone. Evaluate
the quality of the hallucination. Determine if others in the area have similar symptoms.
V. List treatment options and outcome for incapacitating agent exposure
6. BZ Treatment:
a. General supportive management of the patient includes:
1) Observation
2) Decontamination of skin and clothes with soap and water
3) Physical restraint as necessary
4) Confiscation of weapons and related items
5) Prevention and, as indicated, treatment, of hyperthermia
6) Evacuation of the patient to a higher-level medical facility as needed.
b. Management includes treatment of heat injuries; disarming, restraining, and evacuating the
patient; and possible administration of an antidote.
7. BZ Antidote
a. Carbamate compound known as physostigmine.
b. Does not shorten the clinical course of BZ poisoning
c. Reduces the effects of BZ.
d. Relapses will occur if treatment ends prematurely.
e. Carbamate compound known as physostigmine

1) Injection- Intramuscularly (IM): 45 mcg/kg in adults (20 mcg/kg in children). Effects from a
single IM injection last only about 60 minutes, necessitating frequent re-dosing. This is the safest
way to administer the dose, especially initially.
2) Oral - Mix 60 mcg/kg with juice, as it is bitter tasting. This is the safest way to administer
subsequent doses of the medication if the patient will take it in this form.
3) Intravenous (IV) Administer 30 mcg/kg, or less, slowly (1 mg/min). This requires close
monitoring to watch for nerve agent-like symptoms in the event of an overdose.
f. Does not shorten the clinical course of BZ poisoning
g. Reduces the effects of BZ
h. Relapses will occur if treatment ends prematurely
8. Outcome
a. Riot Control Agents: Individuals exposed to riot control agents usually require only supportive
care and recover within a few hours.
b. Incapacitating Agents: Individuals exposed to incapacitating agents usually require observation

and care to ensure safety and prevent a heat injury. They typically recover in 1 to 4 days.
32
VI. Outline the behavior and risks with riot control agents
a. Behavior: Cause temporary, but intense, pain and discomfort to the skin, mucous membranes,
and eyes.
b. Risk
1) With prolonged exposure to extreme amounts, some of these agents may cause skin redness
and blistering.
2) All these agents have only temporary effects and a high safety profile/record.
VII. List the types of riot control agents
10. Types of Riot Control Agents: Five compounds are in use as riot control agents:
a. Diphenylaminearsine (DM or Adamsite)

1) Nonpersistent vomiting agent
2) Yellow to green crystalline substance
3) Relatively odorless
4) Dispersed by aerosol in a cloud
5) In high concentrations, the cloud is a canary yellow color
b. 1-chloroacetopenone (CN or Mace®)

1) Often used for individual self-protection
2) Clear, yellow-brown solid
3) Odor of apple blossoms
4) Usually dispensed in a liquid spray or foam spray
c. Ortho-chlorobenzilidene-malononitrile (CS)
1) Commonly known as tear gas
2) Replaced CN for large-scale riot control use because it takes a lower dose to cause irritation
3) White, crystalline, solid substance
4) Pepper-like odor
5) Usually dispersed as an aerosol
6) Although the smoke is non-persistent, CS powder may stick to rough surfaces, such as
clothes
d. Dibenzl (b,f)-1:4-oxazepine (CR)

1) Pale yellow, crystalline solid
2) Release may occur as an aerosolized smoke or a liquid suspension
3) May also be released via grenade
4) More potent and less toxic than CS
e. Oleoresin of capsaicin (OC, or pepper spray)

1) Made from the fatty oil resin in the cayenne pepper plant.
2) Currently in use by many police forces, by individuals for protection, and as a replacement for
CN and CS.
3) Typically released as a stream of liquid spray or sticky foam material - that adheres to the
individual.
4) Can be processed as a powder or used in a fogger.
5) Causes pain by binding to VR1 (vanilloid receptor subtype 1) receptors in neurons.
33
VIII. Determine the signs and symptoms associated with exposure to riot control agents
a. Eyes
1) Excessive tearing
2) Burning
3) Blepharospasm
4) Redness
b. Skin
1) Burning
2) Erythema
c. Airways
1) Burning
2) Coughing
3) Dyspnea (difficulty breathing)
4) Increased secretions
5) Bronchi spasm
IX. Determine the methods to diagnosis exposure to incapacitating agents
12. Diagnosis
a. Eyes: Signs and symptoms of eye exposure include burning, irritation, conjunctival injection,
tearing, blepharospasm (reflex eyelid closure), and photophobia (sensitivity to light).
b. Lungs: Involvement of the airway produces sneezing, coughing, tightness in the chest, and
irritating secretions. Nasal effects include rhinorrhea and burning.
c. Stomach: Gastrointestinal tract effects may include gagging, retching, and vomiting.
d. Skin: Signs and symptoms of skin exposure may include redness of the skin, pain, and, in severe
cases, blistering.
34
X. Identify the agent specific symptoms of the various riot control agents
13. Agent-Specific Effects:
a. Diphenylaminearsine (DM or Adamsite): Three major differences from other riot control agents:
1) Effects are not immediate, but rather delayed for several minutes, causing individuals who
delay donning their masks to remove the mask due to pain (demasking effect).
2) Effects may last for several hours.
3) Causes nausea and vomiting as well as, onoccasion, headache, depression, malaise, and
chills.
b. 1-Chloroacetophenone (CN)
1) Tearing of the eyes
2) Nasal discharge as body attempts to clear the CN
3) Blepharospasm
4) Irritation of the tissues, nose, mouth, eyes
5) Inflammation of the throat and lung tissues
6) Feeling of chest tightness, difficulty breathing
7) Itching and skin redness
8) Blistering with high-dose exposure
9) Increased skin tingling and burning sensation on moist skin
May cause temporary vomiting with exposure to large amounts.
c. Ortho-chlorobenzylidene-malononitrile (CS): Most effects disappear within 30 minutes.

2) Nasal discharge as the body attempts to clear the CS
3) Blepharospasm (reflex eyelid closure)
4) Irritation of the tissues, nose, mouth, eyes
7) Itching and skin redness with high-dose exposure
8) Headache
d. Dibenzl (b, f)-1:4-oxazepine (CR): Within seconds of exposure:

2) Rhinorrhea (nasal discharge) as the body attempts to clear the agent
3) Blepharospasm (reflex eye closure)
4) Irritation of the nose, mouth, eyes
5) Eyelid inflammation that can last up to 6 hours
8) Itching and skin redness with high-dose exposure
9) Increased skin tingling and burning sensation on moist skin
10) Possible temporary increase blood pressure due to discomfort
11) Fewer effects in small airways than CS
e. Oleoresin of Capsaicin (OC or pepper spray)

1) Immediate and intense pain on contact with skin, particularly at the eyes, nose, and mouth
3) Blepharospasm
4) Temporary respiratory difficulty
5) Panic reaction from intense pain
6) Lightheadedness from difficulty breathing
D-1
XI. List treatment options for riot control agent exposure
14. Treatment
a. The effects of riot control agents are transient in nature.
b. Treatment consists of symptomatic management.
c. There are no antidotes for riot control agents.
D-2

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Chemical Agents

Clinicians Course/ Version 1

Enabling Learning Objectives:

I. Identify the types of pulmonary agents

b. Agents that fall into this general category include:

II. Outline Behavior and Risk for each agent

1) Cause damage to the respiratory system

A. Mild irritation and coughing paroxysma

III. Identify physiological affects and characteristics for each agent.

●Sulfur trioxide-chlorosulfonic acid (FS)

6) Perfluoroisobutylene (PFIB): Organofluoride polymers are valued by the chemical industry

8) Toxic industrial chemicals (TICS)/toxic industrial materials (TIMS): Toxic industrial

b. Twice as potent as chlorine

c. A single breath of a sufficiently high concentration can be fatal

4. Clinical Effects of Acute Pulmonary Toxicants:

1). Low to Moderate Doses

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) after a dose-related

B. No peripheral effects expected.

B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.

1). Low to Moderate Doses

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) after a dose-related

B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.

2). High Doses

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) after a dose-related

1) Massive Doses: Exposure to massively supralethal concentrations of chlorine can lead to

2). Low to Moderate Dose

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately

3). High Doses

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately

2). Low to Moderate Doses

A. No central effects expected.

B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.

3). High Doses

e. Perfluoroisobutylene (PFIB) Inhalation (Vapor) with Rapid Onset of Symptoms: PFIB is a

1) Low to Moderate Doses

A. No central effects expected.

B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.

2). High Doses

1). Low to Moderate Doses

A. No central effects expected.

B. Peripheral effects: Late-onset shortness of breath progressing to pulmonary edema.

A. Central effects (noise: Sneezing, coughing, wheezing, irritation) occurring immediately

C. Late-onset effects: In a low percentage of cases, shortness of breath and decrease in

V. Describe methods for diagnosis of pulmonary agents

a. History characteristically different from most trauma victims.

b. May be a latent period of a few hours to several days.

VI. Name specific treatment for casualties affected by each agent

1) Protect yourself from exposure!

2) Use detectors and personal protective equipment as indicated.

A. Eliminate the source of exposure.

C. Remove the casualty from the site of exposure.

D. Consider the ABCDDs of immediate chemical-casualty care!

4) Recognize and treat the DAMAGE, not the agent!

b. Central-Compartment Damage: The following guidelines particularly applicable to central-

1) Treat local irritative effects on the skin and eyes.

6) Consider bronchodilators as indicated for bronchoconstriction and bronchospasm.

7) Consider anti-inflammatory agents (including nonsteroidal agents and, as clinically indicated,

9) Always consider the potential for concomitant peripheral-compartment damage, especially in