Weapons of Mass Destruction

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Weapons of Mass Destruction

• The Chemical Agents

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Stevan Cordas DO MPH

• Consultant Bioterrorism - Chemical WMD - Texas
  Department of Health
• Local Emergency Planning Committee - Tarrant
  county (toxicology)
• Medical Reserve Corps oversight committee.
• Clinical Associate Professor TCOM
• Certified internal medicine, allergy immunology,
  occupational medicine

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Nerve Agents

• Are related to organophosphate pesticides.
• Are lethal in small amounts.
• Act as cholinesterase inhibitors at receptor
  sites.
• 5 nerve agents are currently recognized GA or
  tabun, GB or sarin, GD or soman, GF and VX.

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Organophosphates and Carbamyl Agents

• Diazinon (Spectracide)
• Malathion
• Parathion
• Chlorfenviphos
• Dimethoate
• Ronnel
• Nerve Gas Agents

• Pyridostigmine (Mestinon)
• Physostigmine (Antilirium)
• Neostigmine (Prostigmine)
• Cognex and others
• Sevin Dust, Carbaryl and many others

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History of Nerve Gas

• First organophosphate 1854
• Tabun (GA) - Schroeder discovered 1936
• Sarin (GB) Schroeder discovered 1937
• Military production of tabun nazi 1942
• 30,000 tons of tabun produced 1942-45
• Soman (GD) discovered 1944

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History of Nerve Gas

• GF discovered Schroeder 1944
• VX discovered Port Down, England 1955
• Russians captured tabun factories and start their
  own production-1946
• United states and England start their own
  production. Edgewood chemical and biologic
  center. 1950-1970

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History of Nerve Gas

• President Nixon orders all chemical and biologic
  agents destroyed. 1969.
• Chemical stockpiles partially destroyed in the
  United States.
• Soviet union continued production 1946-91 -
  developed Novilchek agents - current production
  status uncertain.

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History of Nerve Gas

• Iraq develops tabun and uses it against Iran
  1982-1985 . Iraq also used tabun against Kurdish
  dissidents.
• Iraq admits to placing sarin in scuds and
  artillery 1991- operation desert storm.
• Large amounts of chemical containers destroyed by
  U.S. forces 1991 98,900 low level exposures.
  Gulf war syndrome emerges.

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History of Nerve Gas

• 1994 - First attack by Japanese cult using sarin
  gas 7 dead and 200 injured.
• 1995 Second attack same cult using sarin in
  Tokyo subways 12 dead and 6000 injured.
• 1998 Traces of VX found in Iraqi warheads.
• 2001-London police find sarin plans thwart
  attack.
• 2001- Insecticide bomb found on terrorist in
  Israel.

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Sarin

• Also known as GB phosphonofluoridic acid,
  methyl, isopropyl ester Isoproposmethylphosphonyl
  fluoride
• Odorless and colorless
• Heavier than air hovers near the ground
• More lethal in higher temperature
• Degrades faster with rise in humidity
• 26 times more deadly than cyanide gas

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Basic Mechanism

• Nerve gases bind to an esterase (ChE) that breaks
  down acetylcholine after it is released from the
  nerve end plate.
• After a period of time this binding undergoes
  complex changes and cannot not be reversed this
  is called aging.
• This results in an excess acetylcholine (ACh)
  syndrome which affects the muscarinic and
  nicotinic receptors.

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The ACh Goes to Muscarinic and Nicotinic Receptor
Sites.
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Signs and symptoms of Nerve Gas

• Miosis, dim vision, pain in eyes
• Severe rhinorrhea, lacrymation
• Bronchorrhea
• Nausea, Vomiting
• Diaphoresis
• Memory, fatigue, anxious, impaired judgment

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Signs and symptoms of Nerve Gas

• Increased airways resistance.
• Diarrhea and involuntary micturition.
• Local or generalized muscle fasciculations.
• Muscle fatigue then flaccid paralysis.
• Convulsions and Coma.
• DUMBELS

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Clinical Picture When Exposed to Nerve Gas Vapor

• In mild cases, miosis, rhinorrhea, slight
  tightness in chest or bronchospasm,slight
  dyspnea, increased secretions, ocular pain and
  frontal headaches.
• In moderate cases. An exaggeration of the above
  symptoms with marked dyspnea, nausea and vomiting.

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Clinical Picture

• In severe cases the same symptoms as for moderate
  but also confusion, unconsciousness, muscular
  fasciculations (generalized), involuntary
  micturition and defecation, apnea, flaccid
  paralysis, convulsions, arrhythmias.

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Case 1

• 27 year old male exposed to unknown substance
  that was lethal to others in the area.
• Subjective Anxiety, nausea, rhinorrhea, mild
  chest tightness.
• Objective Miosis, diaphoresis, elevated BP,
  regular heart rate, short onset time, seems
  stable. RBC cholinesterase 30 of normal.

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Hazard to Health Professionals

• Persons whose skin or clothing is contaminated
  with nerve agent can contaminate rescuers by
  direct contact or through off-gassing vapor.
  Persons whose skin is exposed only to nerve agent
  vapor pose no risk of secondary contamination
  however, clothing can trap vapor.

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Protect Yourself

• Nerve agent vapor is readily absorbed by
  inhalation and ocular contact and produces rapid
  local and systemic effects. The liquid is readily
  absorbed thorough the skin however, effects may
  be delayed for several minutes to up to18 hours.

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• Respiratory Protection Pressure-demand,
  self-contained breathing apparatus (SCBA) is
  recommended in response situations that involve
  exposure to any nerve agent vapor or liquid.
• Skin Protection Chemical-protective clothing and
  butyl rubber gloves are recommended when skin
  contact is possible because nerve agent liquid is
  rapidly absorbed through the skin and may cause
  systemic toxicity.

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• Chemical casualty triage is based on walking
  feasibility, respiratory status, age, and
  additional conventional injuries. The triage
  officer must know the natural course of a given
  injury, the medical resources immediately
  available, the current and likely casualty flow,
  and the medical evacuation capabilities.

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Treat ABC

• Quickly ensure that the victim has a patent
  airway. Maintain adequate circulation. If trauma
  is suspected, maintain cervical immobilization
  manually and apply a decontaminable cervical
  collar and a backboard when feasible. Apply
  direct pressure to stop arterial bleeding, if
  present.

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General Principles of Triage for Chemical Exposure

• Check triage tag/card for any previous treatment
  or triage.
• Survey for evidence of associated traumatic/blast
  injuries.
• Observe for sweating, labored breathing,
  coughing/vomiting, secretions.
• Severe casualty triaged as immediate if assisted
  breathing is required.

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General Principles of Triage for Chemical Exposure

• Blast injuries or other trauma, where there is
  question whether there is chemical exposure,
  victims must be tagged as immediate in most
  cases. Blast victims evidence delayed effects
  such as ARDS, etc.
• Mild/moderate casualty self/buddy aid, triaged
  as delayed or minimal and release is based on
  strict follow up and instructions.

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Treatment of Nerve Gas Agents

• Hold your breath.
• Get fresh air as soon as possible.
• If you have a respirator, put it on.
• In the military there are three kits use them
  all.

• In the civilian sector the same first three rules
  apply. If the patient only has miosis 5 or 10
  minutes after removal from agent, they probably
  dont need treatment.

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Mark I Kit

• If the military Mark I kits containing
  autoinjectors are available, they provide the
  best way to administer the antidotes. One
  autoinjector automatically delivers 2 mg atropine
  and the other automatically delivers 600 mg 2-PAM
  Cl.

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Decontaminate as a Priority

• Rapid decontamination is critical to prevent
  further absorption by the patient and to prevent
  exposure to others. Decontaminable gurneys and
  back boards should be used if possible when
  managing casualties in a contaminated area.
  Decontaminable gurneys are made of a monofilament
  polypropylene fabric that allows drainage of
  liquids, does not absorb chemical agents, and is
  easily decontaminated.

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• If water supplies are limited, and showers are
  not available, an alternative form of
  decontamination is to use 0.5 sodium
  hypochlorite solution, or absorbent powders such
  as flour, talcum powder, or Fuller's earth If
  exposure to vapor only is certain, remove outer
  clothing and wash exposed skin with soap and
  water or 0.5 sodium hypochlorite. Place
  contaminated clothes and personal belongings in a
  sealed double bag.

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Specific Therapy for Nerve Gas

• Give atropine sulfate 2mg IV and 2 mg IM stat.
  Manage Airways, breathing and circulation. Early
  intubation and ventilatory support with
  oxygenation. Repeat atropine 2mg IM every 5 or 10
  minutes and watch for return of copious
  secretions and increasing dyspnea. For severe sx,
  6 mg is given initially.
• Follow atropine with Pralidoxime (2-PAM) Protopam
  in I g vials. 15 to 25 mg/kg or given over 15
  minutes IV.
• 15 mg/kg IM for mild to moderate cases

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2 PAM

• 2-PAM Cl solution needs to be prepared from the
  ampoule containing 1 gram of desiccated 2-PAM Cl
  inject 3 ml of saline, 5 distilled or sterile
  water into ampoule and shake well. Resulting
  solution is 3.3 ml of 300 mg/ml. Mild/Moderate
  symptoms include localized sweating, muscle
  fasciculations, nausea, vomiting, weakness,
  dyspnea.
• Severe symptoms include unconsciousness,
  convulsions, apnea, flaccid paralysis.

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Effect of Atropine
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Treatment (contd.)

• Little effect of 2 PAM treatment on Soman (GD)
  due to rapid aging.
• Pyridostigmine pretreatment is most helpful here
  and has some value with GA. Given orally 30mg
  every 8 hours.
• If the individual is alive 5 minutes after
  inhaling the vapor they probably can make it with
  your help.

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RBC Cholinesterase Levels

• With minor adverse effects there is no
  correlation with RBC-ChE levels.
• With vomiting one can suspect that at least
  inhibition of 50 to 90 of the baseline ChE has
  occurred.
• Often used to verify organophosphate poisonings.
  Only decreased by pernicious anemia.

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Late effects of Nerve Gas Attacks

• Generally no serious adverse effects 6 months
  late.
• With convulsions and apnea, inability to learn
  new tasks, memory impairment and retrograde
  amnesia has occurred.
• No clear evidence of peripheral neuropathy or
  intermediate syndrome.

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Resource for more information

• Agency for Toxic Substances and Disease Registry
  Division of Toxicology1600 Clifton Road NE,
  Mailstop F-32Atlanta, GA 30333 Phone
  1-888-42-ATSDR (1-888-422-8737)FAX
    (770)-488-4178Email ATSDRIC_at_cdc.gov
•  

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Blister Gases

• HD, H, HN2, HN3, CX, L

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Sulfur Mustard, 2,2, - Di (Chloro-ethyl)-sulfide
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H and HD

• Pure Mustard Gas is HD, impure is H.
• Sulfur Mustard is a vesicant and a respiratory
  irritant. It was the most effective chemical
  agent in WWI accounting for 85 of the chemical
  injuries.
• Besides being a severe respiratory irritant, it
  affected the skin like a burn with painful
  blisters,. The eyes, axilla and scrotum were
  especially sensitive.

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History of Blister Gas

• 1822- First discovered.
• 1860- Ability to produce burns and vesicles
  proven.
• 1917 Used by Germans for the first time at
  Ypres, France. Called Yperite by French. Lost by
  Germans.
• Called yellow cross by the allies and later H and
  HD. H stood for Hun. HD produced 85 of chemical
  casualties in WWI.

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History of Blister Gas

• French quickly followed as did English. The US
  troops used French blister canisters and shells.
• Captain Lewis team discovers lewisite 1918.
• US production after WWI begins Pine Bluff and
  Aberdeen Proving Ground as chemical warfare
  department under war department forms in latter
  days of WWI. Especially from 1950 to 1969.

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History of Blister Gases

• No use in WWII, Korea or Viet Nam of blister
  gases. Bari incident Dec 2 1943.
• 1981 Iraq uses HD against Iran.
• 1984 Iraq uses HD against Kurds.
• 1991 Iraq deploys HD but doesnt have a chance to
  use them.

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WWI Mustard Casualties and Death
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Physical Properties

• Thick oily amber to brown liquid which
  freezes/melts at 58 F.
• Heavier than air (vapor) or water (liquid).
• Persistent.
• Penetrates skin in 2 minutes.
• Causes cellular damage in 5 minutes.
• Delayed onset of clinical effects. 2-48 hours.

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Diagnosis

• Delayed onset of clinical symptoms.
• Urinary thiodiglycol levels elevated.
• Possible chemical pneumonia manifestations on
  x-ray.
• Mainly a clinical diagnosis depending on the
  circumstances.
• M8, M9 ( paper if liquid Mustard).
• CAM.

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• 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 lt 500, the prognosis is poor.

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Effects of Mustard

• Mustard enter the skin rapidly and convert to
  cyclic agents that are alkylating agents.
• They are mutagenic, teratogenic, cytotoxic, and
  ultimately carcinogenic.
• DNA adducts are formed and cross linkage damage
  occurs.
• The incidence of lung cancer is increased
  slightly in Mustard survivors than controls.

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Clinical Aspects of Mustard

• Mild cases the eyes will develop an irritating
  conjunctivitis that lasts approximately two
  weeks. Respiratory symptoms do not occur. The
  skin will turn reddish and itch or burn.
• There is always a latent period of 4 to 12 hours
  before clinical symptoms occur with Mustard even
  though the damage occurs quickly.
• In slightly more severe cases the skin will look
  like scarlet fever.

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Clinical Aspects of Mustard

• High doses will increase mortality, usually from
  delayed toxic pulmonary edema.
• CNS effects including convulsions occur.
• Severe neutropenia and thrombocytopenia can
  occur.
• Those who recover are often hospitalized for
  months even in the more recent poisonings.

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Differential diagnosis

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

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Treatment of Mustard Gas Casualties

• Decontaminate the eyes with water, saline or a
  weak sodium bicarbonate solution.
• Remove clothes and bag properly.
• Decontaminate the skin with 0.5 (1 to 10
  dilution) Clorox. Wash this off after 4 or 5
  minutes with soap and water.
• Antibacterial eye drops.
• Systemic narcotics prn.

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Management

• Eyes Avoid topical anesthetics or analgesics.
• Use mydriatics, topical antibiotics.
• Vaseline on lids (Dont use eye patch.
• Sunglasses.

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Skin

• Unroof blisters. Fluid is non-toxic.
• Debridement of burns.
• Soothing lotions.
• Frequent irrigations.
• Systemic analgesics.
• Electrolyte and fluid replacement but not like
  that for burns.

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Airways

• Steam, Cough suppressants.
• Oxygen.
• Bronchodilators, Steroids.
• Early intubation may be required.
• Specific antibiotic administration. Avoid
  prophylactic antibiotics,
• Assisted ventilation.

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Marrow

• May need to use
• Reverse isolation.
• Hormonal therapy.
• Marrow transplants.
• Cellular replacement i.e. platelet transfusions
  etc.

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Death

• Usually pulmonary with higher exposure
  concentrations.
• Secondary infection common and can be fatal.
• Radiomimetic effect of HD depresses immunity.

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Lewisite

• Lewisite or L (NATO) an immediate reacting
  vesicant that closes the eyes with blepharospasm
  quickly and produces vesicles. And respiratory
  effects including pulmonary edema circulatory
  effects and death can result from this agent.

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Treatment of Lewisite Poisoning

• Decontamination is critical and must be performed
  rapidly as the number one priority. Remove form
  the agent, Remove the clothes, Make sure you
  decontaminate the hair.
• Give BAL, DMPS or DMSA to act as an antidote to
  this agent.

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Phosgene Oxime

• Dichlorformoxime is a colorless powder that is
  not a vesicant but an urticant. It commonly
  produces deep necrosis of the skin and muscle as
  well and is one of the most severe irritants
  known. It is termed CX by NATO.
• It will vaporize at room temperatures.
• Can cause pulmonary edema and death.

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As a review of signs and symptoms as pertain to
different vesicants the following slides are
offered as a review of systems.
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Respiratory signs and symptoms

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

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Dermal signs and symptoms

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

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Ocular signs and symptoms

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

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• Cardiovascular signs
• Hypotension (with high-dose exposure to lewisite)
  
• Atrioventricular block and cardiac arrest (with
  high-dose exposure)
• Gastrointestinal signs and symptoms (prominent if
  ingestion is a route of exposure)
• Abdominal pain
• Nausea and vomiting
• Hematemesis
• Diarrhea (sometimes bloody)

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

• Tremors
• Convulsions
• Ataxia
• Coma

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• Because no antidote exists for mustard exposure,
  the best thing to do is avoid it. If the nitrogen
  mustard release was indoors, get out of the
  building. If the release was outdoors, move away
  from the area of the release, stay upwind if
  possible, and seek higher ground. Quickly moving
  to an area where fresh air is available is highly
  effective in reducing the possibility of death
  from exposure to nitrogen mustard.

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Remove Clothing

• If you think you may have been exposed, you
  should remove your clothing, rapidly wash your
  entire body with soap and water, and get medical
  care as quickly as possible.
• Quickly take off clothing that has nitrogen
  mustard on it. Any clothing that has to be pulled
  over the head should be cut off the body instead
  of pulled over the head.

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Washing yourself

• As quickly as possible, wash any nitrogen mustard
  from your skin with large amounts of soap and
  water. Washing with soap and water will help
  protect people from any chemicals on their
  bodies.
• If your eyes are burning or your vision is
  blurred, rinse your eyes with plain water for 10
  to 15 minutes. If you wear contacts, remove them
  and put them with the contaminated clothing. Do
  not put the contacts back in your eyes (even if
  they are not disposable contacts). If you wear
  eyeglasses, wash them with soap and water.

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Dispose

• Place your clothing inside a plastic bag. Avoid
  touching contaminated areas of the clothing. If
  you can't avoid touching contaminated areas, or
  you aren't sure where the contaminated areas are,
  wear rubber gloves or put the clothing in the bag
  using tongs, tool handles, sticks, or similar
  objects. Anything that touches the contaminated
  clothing should also be placed in the bag.

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Cyanogens

• Cyanogen chloride (CK)
• and hydrogen cyanide (AC)

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Sources of Cyanide

• Available without a prescription
• Rodenticides, Insecticides
• Silver and metal polishing solutions
• Fumigating products
• Photographic development solutions
• Tanning and electroplating industries
• Metallurgy - jewelers

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History of Cyanides

• Used as a potion to kill friends and enemies
  since ancient Rome.
• Isolated and identified by Sheele 1784.
• Continues to be used in the gas chamber as
  potassium cyanide dropped into dilute sulfuric
  acid. Still popular in murder and suicide.
• Used by France 1915-16 as hydrogen cyanide gas.
  Called AC by military.

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History of Cyanide

• Cyanogen chloride, also called CK by the
  military, introduced September 1916.
• Austrians tried cyanogen bromide about the same
  time.
• In WWII millions of civilians and captured
  soldiers died from hydrocyanic acid adsorbed on a
  dispersible base (Zyklon B), a rodenticide.
• Aum Shinrikyo 1995 attempt to kill more in Tokyo.

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History of Cyanide

• Iraq felt to have used cyanide against Iran, the
  Kurds and a village in Syria in 1981-85.
• 7 killed from poisoned Tylenol -1982.
• A major cause of death from fires is cyanide from
  the combustion products of plastics and other man
  made material.
• Cassava, low grade CN poisoning, causes tropical
  ataxic neuropathy.

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Additional History

• Who will forget the Jonestown massacre or the
  Tylenol deaths?
• Cause of toxic amblyopia for tobacco originated
  cyanide.
• Congenital flaw in cyanide metabolism lead to
  Lebers Optic Atrophy.

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Facts About Cyanides

• 50 mg of the gas and 500mg of the sodium or
  potassium salts is lethal.
• Cigarette smoke contains 0.041 ?g/ml whole blood.
  0.016 ?g/ml in Controls.
• Inhalation of gas kills in seconds. Longer period
  with the soluble gt insolublegt cyanogen salts.
  Skin absorption is possible with this agent.
• Italian authorities arrested a Al Quaeda Cell it
  Italy with 9 lbs of potassium cyanide intending
  to poison the water of the US Embassy.

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Pathophysiology

• Rapidly enters the blood through breath,
  intestine or skin.
• Cases histotoxic hypoxia by interfering with the
  respiratory cytochrome oxidase system. Greatest
  affinity for oxidized Iron at the cytochrome a-a3
  complex.
• TWA 8 hours in US is 10 ppm. 100 ppm will kill in
  one hour. 300 ppm will kill in minutes.
• CN is an important killer in fires.

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Clinical Aspects of Cyanide Poisoning

• If not fatal, we see weakness of the legs,
  vertigo, headache and nausea.
• This may be followed by convulsions and death. At
  a high Ct, death will occur in 20 seconds. It is
  unlikely that you will encounter any of those
  cases. The survivors should be observed and if
  symptomatic treated.

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Clinical Manifestations of Cyanide Poisoning

• Gasping for air, hypertensive, bradycardic.
• Bulging eyes.
• Odor of bitter almonds - faint. 20-40 cant
  smell it.
• Cold clammy skin May have cherry red skin.
  Cyanosis late.
• Venous blood the same color as arterial blood
  bright red or cherry pink.
• May look inebriated, confused, dizzy, nauseated.
  Chest pain.

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Diagnosis of Cyanide Poisoning

• Clinical diagnosis mainly. CYANTOSNO paper.
• Blood cyanide of 0.2 ?g/ml Clinical toxicity
  begins.
• Blood cyanide of 1.0 to 2.5 ?g/ml stupor and
  agitation. Levels over 2.5 ?g/ml potentially
  fatal.
• Pulse oximetry not useful.
• Draw arterial and venous oxygen saturation. If
  less than 10 mm Hg suspect cyanide.
• Look for elevated lactate and metabolic acidosis.
  Plasma lactate gt 6 mmol/L.

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Treatment of Cyanide Poisoning

• Use Lilly cyanide antidote kit.
• Manage ABC of emergency care.
• Remove from agent and remove any liquid cyanide
  that is present. But skin contamination is not
  required for the gas.

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Treatment of Cyanide Poisoning

• First you must rapidly bind or fixate the cyanide
  ion either by creating methemoglobin or fixing it
  with cobalt compounds. Any person who is
  conscious and breathing normally more than 5
  minutes after being exposed to and removed from
  cyanide agents will recover without any treatment
  as this substance is rapidly detoxified by the
  body.

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Treatment of Cyanide Poisoning

• Amyl nitrite is often used if there is a
  respiratory positive pressure present. Do not use
  amyl nitrate with oxygen as an explosion may
  occur. Follow this with sodium thiosulphate. In
  the military, amyl nitrate is used less than in
  the civilian sector. More meaningful and
  predictable levels of methemoglobin can be
  produced by sodium nitrate.

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Treatment of Cyanide Poisoning

• If there is impairment with breathing, IV sodium
  nitrate should be used (10 cc of a 3 solution,
  300mg over 3 minutes). This will produce
  methemoglobin, which binds the cyanide. Keep the
  patient flat or their blood pressure will fall
  from the nitrite. Try to obtain a little cyanosis
  to indicate methemoglobinemia.

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Treatment of Cyanide Poisoning

• Administer the sodium thiosulphate at a dose of
  12.5 Gms (50 cc of a 50 solution over a 10
  minute period of time.
• Remember that methemoglobin levels higher than
  10 usually indicate that further nitrates are
  not needed. Cardiac complications with higher
  doses.

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Treatment of Cyanide Poisoning

• Remember that sodium thiosulphate must always be
  given to complete the medical detoxification of
  cyanate by converting the free and bound cyanide
  to thiocyanates under the influence of the enzyme
  rhodenase. The relatively nontoxic thiocyanates
  can be metabolized.

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Summary of Cyanides

• There is generally a favorable prognosis for
  survivors of a cyanide attack who have residual
  symptoms.
• Aggressive care is required to ensure a good
  outcome including cobaltous agents or nitrates
  followed by sodium thiocyanate.

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Odors of Some Chemical Weapons

• Nerve gas None to fruity or paint-like.
• Mustard Garlic or Horseradish.
• Lewisite Fruity to germanium.
• Phosgene New mown hay or green corn.
• Cyanide Bitter almond (faint).

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If In Doubt

• Regional poison control center (1-800-222-1222)
• Centers for Disease Control and Prevention
• Public Response Hotline (CDC)
• English [phone]
• Español [phone]
• TTY [phone]

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