ATrain Education

 

Continuing Education for Health Professionals

NV: Bioterrorism and Weapons of Mass Destruction

Module 3

Chemical Weapons

Chemical weapons agents are classified as either nonpersistent or persistent. Nonpersistent agents dissipate within a few hours and are most threatening to the lungs. Persistent agents may take up to one month to dissipate if they have been deposited on soil, vegetation, or objects. They are most threatening to the skin.

Scientists often categorize hazardous chemicals by the type of chemical or by the effects a chemical would have on people exposed to it. The categories/types used by CDC are as follows:

Biotoxins

Poisons that come from plants or animals

  • Abrin, Brevetoxin, Colchicine, Digitalis, Nicotine, Ricin, Saxitoxin, Strychnine, Tetrodotoxin, Trichothecene

Blister Agents/Vesicants

Chemicals that severely blister the eyes, respiratory tract, and skin on contact

  • Mustards
    • Mustard gas (H) (sulfur mustard)
    • Mustard/lewisite (HL)
    • Nitrogen mustard (HN-1, HN-2, HN-3)
    • Sesqui mustard
    • Sulfur mustard (H) (mustard gas)
  • Lewisites/chloroarsine agents
    • Lewisite (L, L-1, L-2, L-3)
    • Mustard/lewisite (HL)
  • Phosgene oxime (CX)

Blood Agents

Poisons that affect the body by being absorbed into the blood

  • Arsine (SA)
  • Carbon Monoxide
  • Cyanide
    • Cyanogen chloride (CK)
    • Hydrogen cyanide (AC)
    • Potassium cyanide (KCN)
    • Sodium cyanide (NaCN)
  • Sodium monofluoroacetate (compound 1080)

Caustics (Acids)

Chemicals that burn or corrode people’s skin, eyes, and mucus membranes (lining of the nose, mouth, throat, and lungs) on contact

  • Hydrofluoric acid (hydrogen fluoride)
  • Hydrogen chloride

Choking/Lung/Pulmonary Agents

Chemicals that cause severe irritation or swelling of the respiratory tract (lining of the nose, throat, and lungs)

  • Ammonia
  • Bromine (CA)
  • Chlorine (CL)
  • Hydrogen chloride
  • Methyl bromide
  • Methyl isocyanate
  • Osmium tetroxide
  • Phosgene
    • Diphosgene (DP)
    • Phosgene (CG)
  • Phosphine
  • Phosphorus, elemental, white or yellow
  • Sulfuryl fluoride

Incapacitating Agents

Drugs that make people unable to think clearly or that cause an altered state of consciousness (possibly unconsciousness)

  • BZ
  • Fentanyls and other opioids

Long-Acting Anticoagulants

Poisons that prevent blood from clotting properly, which can lead to uncontrolled bleeding

  • Super warfarin

Metals

Agents that consist of metallic poisons

  • Arsenic
  • Barium
  • Mercury
  • Thallium

Nerve Agents

Highly poisonous chemicals that work by preventing the nervous system from working properly

  • G agents
    • Sarin (GB)
    • Soman (GD)
    • Tabun (GA)
  • V agents
    • VX

Organic Solvents

Agents that damage the tissues of living things by dissolving fats and oils

  • Benzene

Riot Control Agents/Tear Gas

Highly irritating agents normally used by law enforcement for crowd control or by individuals for protection (eg, mace)

  • Bromobenzylcyanide (CA)
  • Chloroacetophenone (CN)
  • Chlorobenzylidenemalononitrile (CS)
  • Chloropicrin (PS)
  • Dibenzoxazepine (CR)

Toxic Alcohols

Poisonous alcohols that can damage the heart, kidneys, and nervous system

  • Ethylene glycol

Vomiting Agents

Chemicals that cause nausea and vomiting

  • Adamsite (DM) (CDC, 2016b)

Covert Chemical Release

Since September 11, 2001, concern has increased about potential terrorist attacks involving the use of chemical agents. In addition, cases since then involving intentional or inadvertent contamination of food with chemicals highlighted the need for healthcare providers and public health officials to be alert for patients in their communities who have signs and symptoms consistent with chemical exposures (CDC, 2003).

Intentional release of chemical agents may be an overt event, one whose nature reveals itself, such as release of a nerve agent in a subway or a large explosion of a chemical container. On the other hand, a chemical release might be a covert event, an unrecognized release in which the presence of sick people could be the first sign of an exposure; this could include deliberate contamination of food, water, or a consumer product.

To increase the likelihood that healthcare providers recognize a chemical release–related illness, and that public health authorities will implement the appropriate emergency response and public health actions, the CDC has identified examples of chemical-induced illness (see table below under “Identifying Chemical Agents”) and created appropriate guidance for healthcare providers and public health personnel (CDC, 2003).

The CDC recognizes that the covert release of a chemical agent might not be easily identified, for at least five reasons:

  • Symptoms of exposure to some chemical agents (eg, ricin) might be similar to those of common diseases (eg, gastroenteritis).
  • Immediate symptoms of certain chemical exposures might be nonexistent or mild despite the risk for long-term effects (eg, neurocognitive impairment from dimethyl mercury, teratogenicity from isotretinoin, or cancer from aflatoxin).
  • Exposure to contaminated food, water, or consumer products might result in reports of illness to healthcare providers over a long period and in various locations.
  • People exposed to two or more agents might have symptoms not suggestive of any one chemical agent (ie, a mixed clinical presentation).
  • Healthcare providers might be less familiar with clinical presentations suggesting exposure to chemical agents than they are with illnesses that are treated frequently (CDC, 2003).

Epidemiologic Clues

Identifying a covert release of a chemical agent may depend on alert healthcare professionals as they begin to see victims of the release. First receivers (eg, hospital-based emergency staff), may be in the best position to observe epidemiologic clues that suggest such a release. These clues include:

  1. An unusual increase in the number of patients seeking care for potential chemical release–related illness
  2. Unexplained deaths among young or healthy persons
  3. Emission of unexplained odors by patients
  4. Clusters of illness in persons who have common characteristics, such as drinking water from the same source
  5. Rapid onset of symptoms after an exposure to a potentially contaminated medium (eg, parasthesias and vomiting within minutes of eating a meal)
  6. Unexplained death of plants, fish, or animals (domestic or wild)
  7. A syndrome (ie, a constellation of clinical signs and symptoms in patients) suggesting a disease associated commonly with a known chemical exposure (eg, neurologic signs or pinpoint pupils in eyes of patients with a gastroenteritis-like syndrome or acidosis in patients with altered mental status) (CDC, 2003)

Identifying Chemical Agents

Because various chemical agents could be used as covert weapons, the actual clinical syndrome varies depending on the type of agent, the amount and concentration of the chemical, and the route of the exposure. However, some clinical presentations may be more common with a covert chemical release. Certain syndromes are associated with groups of chemical agents with similar toxic properties that have been used previously, have high toxicity, or are easily available (see table) (CDC, 2003).

 

*Not intended as a complete differential diagnosis for each syndrome or as a list of all chemicals that might be used in a covert chemical release.
**Potential agents for a covert chemical release based on historic use (ie, intentional or inadvertent use), high toxicity, and/or ease of availability.
***Unreliable sign.
Source: CDC, 2003.

Clinical Syndromes and Potential Chemical Etiologies*

Category

Clinical syndrome

Potential chemical etiology

Cholinergic crisis

  • Salivation, diarrhea, lacrimation, bronchorrhea, diaphoresis, and/or urination
  • Miosis, fasciculations, weakness, bradycardia or tachycardia, hypotension or hypertension, altered mental status, and/or seizures
  • Nicotine
  • Organophosphate insecticides**—decreased acetylcholinesterase activity
  • Carbamate insecticides
  • Medicinal carbamates (eg, physostigmine)

Generalized muscle rigidity

Seizure-like, generalized muscle contractions or painful spasms (neck and limbs) and, usually, tachycardia and hypertension

Strychnine—intact sensorium

Oropharyngeal pain and ulcerations

Lip, mouth, and pharyngeal ulcerations and burning pain

  • araquat**—dyspnea and hemoptysis secondary to pulmonary edema or hemorrhage; can progress to pulmonary fibrosis over days to weeks
  • Diquat
  • Caustics (acids, alkalis)
  • Inorganic mercuric salts
  • Mustards (sulfur)

Cellular hypoxia

  • Mild: nausea, vomiting, and headache
  • Severe: altered mental status, dyspnea, hypotension, seizures, and metabolic acidosis
  • Cyanide** (hydrogen cyanide gas, sodium cyanide)—bitter almond odor
  • Sodium monofluoroacetate (SMFA)**—hypocalcemia or hypokalemia
  • Carbon monoxide
  • Hydrogen sulfide
  • Sodium azide
  • Methemoglobin-causing agents

Peripheral neuropathy and/or neurocognitive effects

  • Peripheral neuropathy signs and symptoms: muscle weakness and atrophy, “glove and stocking” sensory loss, and depressed or absent deep-tendon reflexes
  • Neurocognitive effects: memory loss, delirium, ataxia, and/or encephalopathy
  • Mercury (organic)**—visual disturbances, paresthesias, and/or ataxia
  • Arsenic (inorganic)**—delirium and/or peripheral neuropathy
  • Thallium—delirium and/or peripheral neuropathy
  • Lead—encephalopathy
  • Acrylamide—encephalopathy and/or peripheral neuropathy

Severe gastrointestinal illness, dehydration

Abdominal pain, vomiting, profuse diarrhea (possibly bloody), and hypotension, possibly followed by multisystem organ failure

  • Arsenic**
  • Ricin**—inhalation an additional route of exposure; severe respiratory illness possible
  • Colchicine
  • Barium—hypokalemia common

 

As noted above, it is likely that a covert chemical release would be first recognized by healthcare providers, public health agencies, and poison control centers as they become aware of patterns while assessing illness and treating patients. Familiarity of healthcare professionals with the general characteristics of a covert chemical release, plus recognition of epidemiologic clues and related clinical syndromes, could reduce morbidity and mortality as these workers implement the appropriate emergency response.

Public health agencies and healthcare providers might render the most appropriate, timely, and clinically relevant treatment possible by using treatment modalities based on syndromic categories (eg, burns, respiratory depression, neurologic damage, shock). Because of the hundreds of new chemicals introduced globally each month, it is more pragmatic to treat exposed persons by clinical syndrome rather than specific agent (CDC, 2003; CDC, 2000).

Recognizing Specific Chemical Agents

The Centers for Disease Control and Prevention (CDC) provide many reference materials for recognizing and treating the effects of all types of chemical compounds. These include “reference cards” for dozens of individual chemical compounds that outline essential information for emergency and hospital personnel, including the type of personal protective clothing and equipment (PPE) needed when treating victims. While PPE is necessary for treating virtually anyone who has been exposed to a chemical agent, specifics vary according to the agent involved. It is critical to have this information on hand and for staff to be trained to consult it.

Following are the CDC guidelines for two of the common categories of chemical agents—vesicants and nerve agents. These guidelines provide information on recognizing signs and symptoms, initial treatment, and alternative diagnoses. Remember that the details will differ for other agents and you should always know how to access reference materials quickly at your facility.

Vesicant (Blister Agent) Poisoning

Vesicants, also referred to as “blister agents,” were the most commonly used chemical warfare agents during World War I. Likely routes of exposure are inhalation, dermal contact, and ocular contact. Vesicants are highly reactive chemicals that combine with proteins, DNA, and other cellular components to result in cellular changes immediately after exposure.

Depending on the vesicant, clinical effects may occur immediately (as with phosgene oxime, lewisite) or may be delayed for 2 to 24 hours (as with mustards). Following exposure, the most commonly encountered clinical effects include dermal (skin erythema, blistering), respiratory (pharyngitis, cough, dyspnea), ocular (conjunctivitis, burns), and gastrointestinal (nausea, vomiting).

The amount and route of exposure to the vesicant, the type of vesicant, and the premorbid condition of the person exposed contribute to the time of onset and the severity of illness. For example, ingestion of a vesicant leads to gastrointestinal symptoms more prominent than those that would result from inhalation exposure to the same dose and type of vesicant (CDC, 2013ca).

Signs and Symptoms

The following is a more comprehensive list of signs and symptoms that may be encountered in a person exposed to a vesicant. Signs and symptoms are not listed in order of presentation or specificity. Also, partial presentations (an absence of some of the following signs/symptoms) do not necessarily imply less severe disease.

Respiratory signs and symptoms include:

  • Chest tightness
  • Clear rhinorrhea
  • Cough
  • Dyspnea (shortness of breath)
  • Hemoptysis
  • Nasal irritation/pain
  • Sore throat
  • Tachypnea

Dermal signs and symptoms include:

  • Blisters (within 1 hour with phosgene oxime, delayed for 2 to 12 hours with lewisite, delayed for 2 to 24 hours with mustards)
  • Erythema (immediate with lewisite and phosgene oxime, may be delayed for 2 to 24 hours with mustards)
  • Immediate blanching (phosgene oxime)
  • Itching
  • Necrosis and eschar (over a period of 7 to 10 days)

Ocular signs and symptoms include:

  • Blindness
  • Blurred vision
  • Corneal ulceration
  • Conjunctivitis
  • Eyelid edema
  • Eye pain/burning
  • Lacrimation
  • Photophobia

Cardiovascular signs include:

  • Atrioventricular block and cardiac arrest (with high-dose exposure)
  • Hypotension (with high-dose exposure to lewisite)

Gastrointestinal signs and symptoms (prominent if ingestion is a route of exposure) include:

  • Abdominal pain
  • Diarrhea (sometimes bloody)
  • Hematemesis
  • Nausea and vomiting

Central nervous system signs and symptoms (with exposure to high doses) include:

  • Ataxia
  • Coma
  • Convulsions
  • Tremors

Hematologic signs and symptoms:

  • Anemia
  • Bleeding/hemorrhage
  • Bone marrow suppression
  • Increased susceptibility to infection
  • Leukocytopenia
  • Thrombocytopenia (CDC, 2013ca)
Laboratory Findings

Although it is a nonspecific finding, leukopenia can indicate vesicant exposure. It usually begins 3 to 5 days after exposure. With a white blood cell count <500, the prognosis is poor.

Differential Diagnosis
  • Barbiturates
  • Bullous pemphigoid
  • Chemotherapeutic agents
  • Carbon monoxide
  • Other chemical burns (eg, with strong acids, bases, corrosives)
  • Pemphigus vulgaris
  • Stevens-Johnson syndrome
  • Staphylococcus scalded skin syndrome
  • Toxic epidermal necrolysis

Note: The actual clinical manifestations of a vesicant exposure may be more variable than the syndrome described above (CDC, 2013ca).

Nerve Agents and Organophosphate (OP) Pesticide Poisoning

Nerve agents are chemical warfare agents that have the same mechanism of action as organophosphate (OP) pesticides. They are potent inhibitors of acetylcholinesterase. Inhibition of acetylcholinesterase leads to an accumulation of acetylcholine in the central and peripheral nervous system. Excess acetylcholine produces a predictable cholinergic syndrome consisting of copious respiratory and oral secretions, diarrhea and vomiting, sweating, altered mental status, autonomic instability, and generalized weakness that can progress to paralysis and respiratory arrest.

The amount and route of exposure to the nerve agent or OP pesticide, the type of nerve agent or pesticide, and the premorbid condition of the exposed person contribute to the time of onset and the severity of illness. For example, inhalation of a nerve agent or an OP pesticide leads to a quicker onset of poisoning with more severe symptoms than dermal exposure, given the same amount of agent (CDC, 2013cb).

Signs and Symptoms

The following are more comprehensive lists of signs and symptoms that may be encountered in a person exposed to a nerve agent or OP pesticide. Signs and symptoms are not listed in order of presentation or specificity. Also, partial presentations (an absence of some of the following signs/symptoms) do not necessarily imply less severe disease.

Central nervous system signs and symptoms include:

  • Miosis (unilateral or bilateral)
  • Headache
  • Restlessness
  • Convulsions
  • Loss of consciousness
  • Coma

Respiratory signs and symptoms include:

  • Rhinorrhea (perfuse watery runny nose)
  • Bronchorrhea (excessive bronchial secretions)
  • Wheezing
  • Dyspnea (shortness of breath)
  • Chest tightness
  • Hyperpnea (increased respiratory rate/depth)—early
  • Bradypnea (decreased respiratory rate)—late

Cardiovascular signs include:

  • Tachycardia (increased heart rate)—early
  • Hypertension (high blood pressure)—early
  • Bradycardia (decreased heart rate)—late
  • Hypotension (low blood pressure)—late
  • Arrhythmias Dysrhythmias (prolonged QT on EKG, ventricular tachycardia)

Gastrointestinal signs and symptoms include:

  • Abdominal pain
  • Nausea and vomiting
  • Diarrhea
  • Urinary incontinence, frequency

Musculoskeletal signs and symptoms include:

  • Weakness (may progress to paralysis)
  • Fasciculations (local or generalized)

Skin and mucous membrane signs and symptoms include:

  • Profuse sweating (local or generalized)
  • Lacrimation (tear formation)
  • Conjunctival injection
Laboratory Findings
  • Decreased plasma or red blood cell (RBC) cholinesterase activity.

Limitations:

  • Wide normal range for enzyme activity makes interpretation difficult without a baseline measurement.
  • Cholinesterase activity correlates poorly with severity of local effects after vapor exposures.
  • Plasma or RBC cholinesterase may be disproportionately inhibited depending on the particular nerve agent, amount of exposure, and time interval since exposure.

Interpreting cholinesterase activity:

Plasma cholinesterase

  • Usually declines faster than RBC cholinesterase
  • Is easier to assay than RBC cholinesterase
  • Regenerates faster than RBC cholinesterase
  • May have a day-to-day variation in enzyme activity as high as 20%
  • Is less specific than RBC cholinesterase
  • Can show false depression from liver disease, malnutrition, pregnancy, genetic deficiency, or drugs (eg, codeine, morphine, cocaine, succinylcholine)

Red blood cell cholinesterase

  • Is a better reflection of CNS cholinesterase activity
  • Is more specific test than plasma cholinesterase
  • May have a day-to-day variation in enzyme activity as high as 10%
  • Can show false depression from antimalarial therapy or pernicious anemia
Differential Diagnosis
  • Carbamate insecticides
  • Medicinal carbamates (eg, pyridostigmine, neostigmine, physostigmine)
  • Cholinomimetic compounds (eg, pilocarpine, methacholine, bethanechol)
  • Nicotine alkaloids (eg, nicotine, coniine)
  • Muscarine-containing mushrooms
  • Neuromuscular blocking drugs (eg, atracurium, vecuronium)

Note: The actual clinical manifestations of an exposure to a nerve agent or an OP pesticide may be more variable than the syndrome described in this document (CDC, 2013cb).

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