Chemical Agents of Opportunity for Terrorism: TICs & TIMs

Chemical Agents of Opportunity for Terrorism
Training Support Package
Participant Guide
Module Four Summary
Cyanide and fumigants constitute a threat to the general population because they are widely
available, easily weaponized, and can be highly toxic if inhaled. In a 2003 bulletin, the US
Department of Homeland Security warned of the possible use of cyanide gas as a weapon and
the threat of its introduction into forced air ventilation systems. Fumigants, while more tightly
controlled, could easily be used in a similar fashion.
Cyanide is an extremely toxic and rapidly acting poison. Discovered in 1782 by the noted
Swedish chemist Carl Wilhelm Scheele [1742 – 1786], prussic acid (hydrogen cyanide) was
found to have numerous industrial applications. During WWI and II, cyanide gas was employed
as a chemical warfare agent and, under the name Zyklon B, used as part of Hitler’s “Final
Solution”. Popular conceptions of cyanide have been shaped by its frequent appearance as a
murder weapon in detective fiction and by tragic real-world mass poisonings.
Given its abundant legitimate uses, cyanide can be easily purchased in a variety of forms –
most commonly sodium cyanide, potassium cyanide, and calcium cyanide. Using a simple
chemical reaction, cyanide salts can be mixed with an acid to produce hydrogen cyanide gas.
The dose of cyanide required to produce toxicity varies with type of exposure. About 200 mg of
potassium cyanide is lethal if ingested, whereas airborne concentrations of >110ppm for 30
minutes are generally considered fatal.
Cyanide acts by inhibiting specific enzymes – predominantly cytochrome aa3 in the
mitochondrial electron transport chain – resulting in the complete arrest of cellular respiration
and chemical asphyxiation of cells. The heart and CNS system, being the most oxygensensitive
organs in the human body, are most affected by cyanide poisoning. Cyanide may also
impact myocardial cells but this effect is, as yet, not well established.
The clinical effects of cyanide poisoning include: gasping, syncope, and cardiac arrest. There is
no specific constellation of signs and symptoms; no toxidrome. The oft-discussed bitter almond
scent is not a reliable indicator of the presence of cyanide gas. Cyanide poisoning should be
suspected whenever a group of people seem to have collapsed following an unknown inhalation
exposure.
The clinical laboratory can be useful in making the diagnosis of cyanide poisoning. Anion gap
metabolic acidosis is usually present and it is due to the presence of large amounts of lactate
(L-lactate). Arteriolization (i.e., inability of peripheral tissues to use oxygen) of the venous blood
gas may be present. This leads to a very poor oxygen extraction ratio and a very high content of
oxyhemoglobin in the venous blood. Oxygen saturations of >80% in venous blood are highly
suggestive of arteriolization phenomenon. Blood cyanide levels can also be obtained but these
are usually performed outside the hospital setting and have a 2-3 day turnaround time.
The treatment of cyanide poisoning starts with oxygenation and supportive care. Intubation and
ventilation are often required. Specific antidotal therapies exist and need to be applied as soon
as possible after exposure. Currently two different antidote kits are available in the US: the
traditional 3-step (“Eli Lilly”) kit or the more recently approved one-step Cyanokit® (Merck).
The first and oldest antidote is the 3-step cyanide antidote kit, still affectionately still referred to
as the Eli Lilly kit. The first step involves the insufflation of amyl nitrite capsules in the nares of
the victim to induce a methemoglobinemia. Step two involves intravenous administration of
sodium nitrite another methemoglobin inducer. Methemoglobin can bind cyanide to form
cyanomethemoglobin. The third and last step involves the intravenous administration of sodium
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