ENVIRONMENTAL SCIENCE FOR CYANIDE

1. Berikut merupakan kutipan ilmiah yang bermanfaat sehingga disusun dan digunakan
sebagai referensi pribadi.
Cyanide poisoning occurs when a living organism is exposed to a compound that
produces cyanide ions (CN−) when dissolved in water. Common poisonous cyanide
compounds include hydrogen cyanide gas and the crystalline solidspotassium
cyanide and sodium cyanide. The cyanide ion halts cellular respiration by inhibiting
the enzyme cytochrome c oxidase found in the mitochondria.
Cyanide poisoning is a form of histotoxic hypoxia because the cells of an organism
are unable to use oxygen, primarily through the inhibition of cytochrome c oxidase.
Acute hydrogen cyanide poisoning can result from inhalation of fumes from burning
polymer products that use nitrile in their production, such as polyurethane, or
vinyl.[1] It can also be caused by breakdown of nitroprusside into nitric oxide and
cyanide during treatment of hypertensive crisis.[specify]
If cyanide is inhaled it causes a coma with seizures, apnea, and cardiac arrest, with
death following in a matter of seconds. At lower doses, loss of consciousness may
be preceded by general weakness, giddiness, headaches, vertigo, confusion, and
perceived difficulty in breathing. At the first stages of unconsciousness, breathing is
often sufficient or even rapid, although the state of the victim progresses towards a
deep coma, sometimes accompanied by pulmonary edema, and finally cardiac
arrest. A cherry red skin color that changes to dark may be present as the result of
increased venous hemoglobin oxygen saturation. Cyanide does not directly
cause cyanosis. A fatal dose for humans can be as low as 1.5 mg/kg body weight.[2]
In addition to its uses as a pesticide and insecticide, cyanide is contained in tobacco
smoke and smoke from building fires, and is present in some foods such
asalmonds, apricot kernel, apple seeds, orange seeds, cassava (also known as yuca
or manioc), and bamboo shoots. Vitamin B12, in the form of hydroxocobalamin(also
spelled hydroxycobalamin), may reduce the negative effects of chronic exposure,
and a deficiency can lead to negative health effects following exposure.[3]
Exposure to lower levels of cyanide over a long period (e.g., after use of improperly
processed cassava roots as a primary food source in tropical Africa) results in

2. increased blood cyanide levels, which can result in weakness and a variety of
symptoms, including permanent paralysis, nervous lesions,[4][5][6] hypothyroidism,[5
]and miscarriages.[7][8] Other effects include mild liver and kidney damage.[9][10]
Cyanide has the potential to be bioremediated. Among the enzyme families which
degrade cyanide are nitrogenases, rhodanese, and the nitrilases. Cyanide
hydratases, part of the lyase enzyme family that convert cyanide are present in
certain species of fungi hydrolyze cyanide to formamide, Cyanide dihydratases
convert it directly to formate and ammonia, end products that pose far less toxicity.[11]
The United States standard cyanide antidote kit first uses a small inhaled dose
of amyl nitrite, followed by intravenous sodium nitrite, followed by
intravenous sodium thiosulfate.[12] Hydroxocobalamin is newly approved in the US
and is available in Cyanokit antidote kits.[13] Sulfanegen TEA, which could be
delivered to the body through an intra-muscular (IM) injection, detoxifies cyanide and
converts the cyanide into thiocyanate, a less toxic substance.[14] Alternative methods
of treating cyanide intoxication are used in other countries.
Agent Description
Nitrites
The nitrites oxidize some of the hemoglobin's iron from
the ferrous state to the ferric state, converting the
hemoglobin into methemoglobin.
Cyanide binds avidly to methemoglobin, forming
cyanmethemoglobin, thus releasing cyanide from
cytochrome oxidase.[15] Treatment withnitrites is not
innocuous as methemoglobin cannot carry oxygen, and
severe methemoglobinemia may need to be treated in
turn withmethylene blue.[note 1]
Thiosulfate
The evidence for sodium thiosulfate's use is based on
animal studies and case reports: the small quantities of
cyanide present in dietary sources and in cigarette
smoke are normally metabolized to relatively harmless

3. thiocyanate by the mitochondrial
enzyme rhodanese(thiosulfate cyanide
sulfurtransferase), which uses thiosulfate as a
substrate. However, this reaction occurs too slowly in
the body for thiosulfate to be adequate by itself in acute
cyanide poisoning. Thiosulfate must therefore be used
in combination with nitrites.[15]
Hydroxocobalamin
Hydroxocobalamin, a form (or vitamer) of vitamin
B12 made by bacteria, and sometimes denoted vitamin
B12a, is used to bind cyanide to form the
harmless cyanocobalamin form of vitamin B12.
4-Dimethylaminophenol
4-Dimethylaminophenol (4-DMAP) has been
proposed[by whom?] in Germany as a more rapid antidote
than nitrites with (reportedly) lower toxicity. 4-DMAP is
used currently by the German military and by the
civilian population. In humans, intravenous injection of
3 mg/kg of 4-DMAP produces 35 percent
methemoglobin levels within 1 minute. Reportedly, 4-
DMAP is part of the US Cyanokit, while it is not part of
the German Cyanokit due to side effects (e.
g. hemolysis).
Dicobalt edetate
Cobalt ions, being chemically similar to iron ions, can
also bind cyanide. One current cobalt-based antidote
available in Europe is dicobalt edetate or dicobalt-
EDTA, sold as Kelocyanor. This agent chelates cyanide
as the cobalticyanide. This drug provides an antidote
effect more quickly than formation of methemoglobin,
but a clear superiority to methemoglobin formation has
not been demonstrated. Cobaltcomplexes are quite
toxic, and there have been accidents reported in the UK
where patients have been given dicobalt-EDTA by
mistake based on a false diagnosis of cyanide

4. poisoning. Because of its side effects, it should be
reserved only for patients with the most severe degree
of exposure to cyanide; otherwise, nitrite/thiosulfate is
preferred.[18]
Glucose
Evidence from animal experiments suggests that
coadministration of glucose protects against cobalt
toxicity associated with the antidote agent dicobalt
edetate. For this reason, glucose is often administered
alongside this agent (e.g. in the formulation
'Kelocyanor').
It has also been anecdotally suggested that glucose is
itself an effective counteragent to cyanide, reacting with
it to form less toxic compounds that can be eliminated
by the body. One theory on the apparent immunity
of Grigory Rasputin to cyanide was that his killers put
the poison in sweet pastries and madeira wine, both of
which are rich in sugar; thus, Rasputin would have
been administered the poison together with massive
quantities of antidote. One study found a reduction in
cyanide toxicity in mice when the cyanide was first
mixed with glucose.[19] However, as yet glucose on its
own is not an officially acknowledged antidote to
cyanide poisoning.
3-
Mercaptopyruvateprodrugs
The most widely studied cyanide-metabolizing pathway
involves utilization of thiosulfate by the
enzyme rhodanese, as stated above. In humans,
however, rhodanese is concentrated in the kidneys
(0.96 units/mg protein) and liver (0.15 u/mg), with
concentrations in lung, brain, muscle and stomach not
exceeding 0.03 U/ml.[20] In all these tissues, it is found
in the mitochondrial matrix, a site of low accessibility for
ionized, inorganic species, such as thiosulfate. This

5. compartmentalization of rhodanese in mammalian
tissues leaves major targets of cyanide lethality,
namely, the heart and central nervous system,
unprotected. (Rhodanese is also found in red blood
cells, but its relative importance has not been
clarified.[21][22])
A different cyanide-metabolizing pathway, 3-
mercaptopyruvate sulfurtransferase (3-
MPST, EC 2.8.1.2), which is more widely distributed in
mammalian tissues than rhodanese, is being explored.
3-MPST converts cyanide to thiocyanate, using the
cysteine catabolite, 3-mercaptopyruvate (3-MP).
However, 3-MP is extremely unstable chemically.
Therefore, a prodrug, sulfanegen sodium (2, 5-
dihydroxy-1,4-dithiane-2,5-dicarboxylic acid disodium
salt), which hydrolyzes into 2 molecules of 3-MP after
being administered orally or parenterally, is being
evaluated in animal models.[23][24]
Oxygen therapy
Oxygen therapy is not a cure in its own right. However,
the human liver is capable of metabolizing cyanide
quickly in low doses (smokers breathe in hydrogen
cyanide, but it is such a small amount and metabolized
so fast that it does not accumulate).
The International Programme on Chemical
Safety issued a survey (IPCS/CEC Evaluation of
Antidotes Series) that lists the following antidotal agents
and their effects: oxygen, sodium thiosulfate, amyl
nitrite, sodium nitrite, 4-dimethylaminophenol,
hydroxocobalamin, and dicobalt edetate ('Kelocyanor'),
as well as several others.[25] Other commonly-
recommended antidotes are 'solutions A and B' (a
solution offerrous sulfate in aqueous citric acid, and

6. aqueous sodium carbonate, respectively) and amyl
nitrite.
The UK Health and Safety Executive (HSE) has
recommended against the use of solutions A and B
because of their limited shelf life, potential to cause iron
poisoning, and limited applicability (effective only in
cases of cyanide ingestion, whereas the main modes of
poisoning are inhalation and skin contact). The HSE
has also questioned the usefulness of amyl nitrite due
to storage/availability problems, risk of abuse, and lack
of evidence of significant benefits. It also states that the
availability of Kelocyanor at the workplace may mislead
doctors into treating a patient for cyanide poisoning
when this is an erroneous diagnosis. The HSE no
longer recommends a particular cyanide
antidote.[26] Qualified UK first aiders are now only
permitted to apply oxygen therapy using a bag valve
mask, providing they have been trained in its usage.
1. Jump up^ Methylene blue has historically been used as an antidote to
cyanide poisoning,[16] but is not a preferred therapy due to its theoretical risk
of worsening of cyanide symptoms by displacement of cyanide from
methemoglobin, allowing the toxin to bind to tissue electron transport
chains.[17]
2. On December 5, 2009, a fire in the night club Lame Horse (Khromaya
Loshad) in the Russian city of Perm took the lives of 156 people. 111 people
died on the spot and 45 later in hospitals. One of the main causes of death
was poisoning from cyanide and other toxic gases released by the burning of
plastic andpolystyrene foam used in the construction of club interiors. Taking
into account the number of deaths, this was the largest fire in post-Soviet
Russia.[citation needed][when?]
3. On January 27, 2013, a fire at the Kiss nightclub in the city of Santa Maria, in
the south of Brazil, caused the poisoning of hundreds of young people by

7. cyanide released by the combustion of soundproofing foam made
with polyurethane. By March 2013, 241 fatalities were confirmed.[27][28]
4. Hydrogen cyanide in the form of Zyklon B was used in German extermination
camps during World War II, and especially from March 1942 onwards, when it
was first used experimentally to murder Russian prisoners of war
at Auschwitz. Use of the poison was scaled up rapidly until custom-built gas
chambers (holding up to about 2000 victims) were constructed as part of the
new crematoria complex at Auschwitz-Birkenau. There was also a large
undressing room next to the gas chamber, and the victims were told to
undress and leave their clothes on a numbered peg for collection later. They
were told that they would receive a hot shower, and false shower heads were
fitted in the ceilings of the gas chambers, so as to maintain the deception. The
gas chambers were sealed hermetically to prevent gas leakage. The Zyklon B
pellets were then dropped into the chamber via small openings in the roof.
When the pellets were exposed to moisture and human heat (as in a closed
chamber), they gave off gaseous HCN, which then killed the victims. Workers
in theSonderkommando were employed to remove the corpses from the gas
chamber and strip them of any valuables, such as gold teeth, before the
bodies were cremated. The gas was used mainly at Auschwitz and Majdanek,
but theextermination camps such as Treblinka built earlier used engine
exhaust gas, in which carbon monoxide was the toxic component. The gas
chambers were either mobile lorries as at Chelmno or specially built
chambers as at Sobibor andBelzec. The victims included prisoners of
war, Jews from across Europe, Romani gypsies, Poles, ill and disabled
peopleof all nationalities, as well as political
prisoners, homosexuals, Jehovah's witnesses and anyone who opposed the
Nazis.
5. Hydrogen cyanide gas has also been used for judicial execution in some
states of the United States, where cyanide was generated by reaction
between potassium cyanide (or sodium cyanide[29][30]) dropped into a
compartment containingsulfuric acid, directly below the chair in the gas
chamber.[31]

8. Cyanide was stockpiled in chemical weapons arsenals in both the Soviet Union and
the United States in the 1950s and 1960s.[citation needed] However, as a military agent,
hydrogen cyanide was not considered very effective, since it is lighter than air and
needs a significant dose to incapacitate or kill.
Cyanide salts are sometimes used as fast-acting suicide devices. Cyanide reacts at
a higher level with high stomach acidity.
 In February 1937, the Uruguayan short story writer Horacio Quiroga committed
suicide by drinking cyanide in a hospital at Buenos Aires.
 In 1937, polymer chemist Wallace Carothers committed suicide by cyanide.
 In the 1943 Operation Gunnerside to destroy the Vemork Heavy Water Plant in
World War II (an attempt to stop or slow German atomic bomb progress), the
commandos were given cyanide tablets (cyanide enclosed in rubber) kept in the
mouth and were instructed to bite into them in case of German capture. The
tablets ensured death within three minutes.[32]
 Cyanide, in the form of pure liquid prussic acid (a historical name for hydrogen
cyanide), was the favored suicide agent of the Third Reich. It was used to commit
suicide by Erwin Rommel (1944), after being accused of conspiring against
Hitler; Adolf Hitler's wife, Eva Braun (1945); and by Nazi leaders Heinrich
Himmler(1945), possibly Martin Bormann (1945), and Hermann Göring (1946).
 It is speculated that, in 1954, Alan Turing used an apple that had been injected
with a solution of cyanide to commit suicide after being convicted of having a
homosexual relationship—illegal at the time in the UK—and forced to undergo
hormonal castration.
 Members of the Sri Lankan LTTE (Liberation Tigers of Tamil Eelam,
whose insurgency lasted from 1983 to 2009), used to wear cyanide vials around
their necks with the intention of committing suicide if captured by the government
forces.
 On June 6, 1985, serial killer Leonard Lake died in custody after having ingested
cyanide pills he had sewn into his clothes.
 On June 28, 2012, Wall Street trader Michael Marin ingested a cyanide pill
seconds after a guilty verdict was read in his arson trial in Phoenix, AZ; he died
minutes after.[33]

9.  In 2000, a spill at Baia Mare, Romania resulted in the worst environmental
disaster in Europe since Chernobyl.[34]
 In 2000, Allen Elias,[35] CEO of Evergreen Resources was convicted of
knowing endangerment for his role in the cyanide poisoning of employee
Scott Dominguez.[36][37] This was one of the first successful criminal
prosecutions of a corporate executive by the Environmental Protection
Agency.
 John Tawell, a murderer who in 1845 became the first person to be arrested
as the result of telecommunications technology
 Grigori Rasputin (1916; attempted, later killed by gunshot)
 Goebbels children (1945)
 Chicago Tylenol murders (1982)
 Ronald Clark O'Bryan (1944–1984)
 Richard Kuklinski (1935–2006)
 Jonestown, Guyana, was the site of a large mass murder-suicide,[38] in which
over 900 members of the Peoples Temple drank potassium cyanide–
laced Flavor Aid in 1978.
 In 1995, a device was discovered in a restroom in the Kayabacho Tokyo
subway station, consisting of bags of sodium cyanide and sulfuric acid with a
remote controlled motor to rupture them in what was believed to be an
attempt by the Aum Shinrikyo cult to produce toxic amounts of hydrogen
cyanide gas.[39]
 In 2003, Al Qaeda reportedly planned to release cyanide gas into the New
York City Subway system. The attack was supposedly aborted because there
would not be enough casualties.[40]
Homicide[edit]
 The Detective Conan manga/anime series has a large number of cases in which
the victims are killed by cyanide, with all or most mentioning an 'almond scent' to
describe it.
 Raymond Chandler uses "a little potassium hydrocyanide" against private
detective Philip Marlowe in The Little Sister – "merely relaxing".

10.  In Agatha Christie's And Then There Were None, the first death occurs from
cyanide poisoning.
 In Agatha Christie's Sparkling Cyanide (also entitled Remembered Death), based
upon her Hercule Poirot short story entitled "Yellow Iris", Rosemary and George
Barton are poisoned by cyanide crystals.
 In Ngaio Marsh's Death At The Bar, Luke Watchman, a top London barrister and
King's Counsel dies of potassium cyanide poisoning after a freak dart throwing
accident whilst holidaying in Devon.
 In Hit Man: A Technical Manual for Independent Contractors by "Rex Feral", the
use of cyanide to poison a mark is explained in detail.
 In the Joseph Kesselring play Arsenic and Old Lace, two old ladies mix wine
with arsenic, cyanide and strychnine to use to kill old men.
 In Roald Dahl's short story "The Landlady", a landlady poisons a young boy
named Billy Weaver staying in her Bed and Breakfast with tea that was said to
taste suspiciously like cyanide (described as tasting like "bitter almonds"),
presumably to stuff him.
 In the film "The Little Girl Who Lives Down the Lane", Rynn Jacobs (Jodie Foster)
poisons Frank Hallet (Martin Sheen) with cyanide-tainted tea, serving him
almond cookies to mask the taste.
 Bishop Lilliman was killed by 'V', forcing the bishop to swallow a communion
wafer poisoned with cyanide in Alan Moore and David Lloyd's comic book
series, V for Vendetta.
 In the manga Battle Royale, Yuko Sakaki's assigned weapon is hydrocyanic acid.
She uses it to poison food intended for Shuuya Nanahara, but it ends up being
ingested by Yuka Nakagawa.
 In Phoenix Wright: Ace Attorney: Trials and Tribulations game, the third case
solved by the player involves a programmer who is murdered when potassium
cyanide is slipped into his coffee at a restaurant.
 In the game Hitman: Contracts, the player can assassinate people using cyanide.
 In the 1999 Midsomer Murders episode "Judgement Day", the second murder
victim is poisoned by cyanide mixed in a glass of wine.
 In the 2008 Doctor Who episode "The Unicorn and the Wasp", the Doctor is
nearly poisoned by cyanide, but manages to metabolize it and detoxify himself

11. using a combination of proteins, salt, and a shock, plus the advantage of his non-
human physiology.
 In the Assassin's Creed video game series, Alan Turing was revealed to have
been killed by Templars who laced an apple (which he would later eat) with
cyanide in an attempt to make it look as if he had committed suicide.
 In the film Irrational Man, cyanide is used to kill a judge.
 In Agatha Christie's novel The Hollow, a woman called Gerda Christow kills
herself when she gets caught by murder of her husband.
 In Agatha Christie's novel The Secret Adversary, the villain "Mr Brown"
commits suicide using cyanide concealed in a signet ring.
 In Robert Louis Stevenson's Strange Case of Dr Jekyll and Mr Hyde, Dr.
Jekyll kills himself with cyanide, deduced as the smell of kernels (almonds) is
evident.
 In Ian Fleming's James Bond stories and the movies based on them, 00
agents are issued cyanide capsules for use in the event of capture by the
enemy. James Bond is described as having thrown his away.
 Gabriel García Márquez's novel Love in the Time of Cholera begins with
Jeremiah de Saint-Amour's suicide by cyanide poisoning.
 Australian author Nevil Shute's 1957 novel about life after nuclear war, On the
Beach, gives the scenario of the Australian government giving survivors free
cyanide tablets to commit suicide rather than face death from radiation
poisoning.
 In the James Bond film Dr. No (1962), James Bond believes that his cab
driver is an enemy agent, and after a fight scene, begins to interrogate the
driver, who proceeds to poison and kill himself with cyanide embedded in a
cigarette.
 In William Styron's 1979 novel Sophie's Choice and the movie based on the
book, Sophie and Nathan commit suicide by ingesting a cyanide pill.
 In Ford Maddox Ford's novel The Good Soldier one of the main characters,
Florence, commits suicide by drinking her phial of "prussic acid" after learning
that her lover is having an affair with another woman.
 In Japanese author Koushun Takami's 1999 novel Battle Royale and the
film Battle Royale based on the book, Yuko Sakaki is given a small bottle

12. of potassium cyanide (KCN) as a "special bonus" in addition to the weapon
provided in her day pack.
 In the second season of the US TV series 24, several of the terrorists keep
cyanide pills immediately on their person so they can swallow them
immediately to avoid capture.
 In the Kannada film Cyanide (2006), which is about the incidents that
occurred in the peripheries of Bangalore after the assassination of the former
Indian Prime Minister Rajiv Gandhi, the killers of the Prime Minister use
cyanide vials to commit suicide to avoid being captured by the police.
 In the film Unknown (2011), Jürgen commits suicide by emptying a bag of
sodium cyanide into his coffee, disguised as a packet of sugar.
 In the film Captain America: The First Avenger (2011), Heinz Kruger commits
suicide by cyanide tablet upon being caught.
 In the James Bond film Skyfall (2012), Javier Bardem's character, Silva,
discusses his failed attempt to commit suicide using a hydrogen cyanide
capsule whilst under interrogation. Rather than kill him, the hydrogen cyanide
burned his body internally, forcing him to wear a prosthetic face plate to hide
his disfigurement.
 In the song To The End by My Chemical Romance, the bride in the album's
story drinks cyanide on her wedding day.
Cyanide poisoning can be difficult to detect. The effects of cyanide ingestion are very
similar to the effects of suffocation; because cyanide stops the cells of the body from
being able to use oxygen, which all cells need to survive. The symptoms of cyanide
poisoning are similar to those experienced when hiking or climbing at high altitudes.
 General weakness, confusion, bizarre behavior, excessive sleepiness, coma,
shortness of breath, headache,dizziness, and seizures can all present with
cyanide poisoning.
 Typically, an acute ingestion will have a dramatic, rapid onset, immediately
affecting the heart and causing sudden collapse. It can also immediately affect
the brain and cause a seizure or coma.

13.  Chronic poisoning (over a long period of time) from ingestion or environmental
poisoning will have a more gradual onset.
 The skin of a cyanide-poisoned person can sometimes be unusually pink or
cherry-red because oxygen will stay in the blood and not get into the cells. The
person may also breathe very fast and have either a very fast or very slow
heartbeat. Sometimes the person's breath can smell like bitter almonds, though
this can be difficult to detect.
 Perhaps most important is the setting, rather than the signs or symptoms.
o A person who works in a laboratory or plastics factory has a higher risk of
cyanide poisoning.
o Home, RV, boat, or building fires always include the additional concern of
cyanide exposure.
o If you know someone has been depressed or has substance abuse problems
and you find him or her with any of the signs or symptoms of cyanide
poisoning, then a suicide attempt is possible.
Cyanide toxicity is generally considered to be a rare form of poisoning. However,
cyanide exposure occurs relatively frequently in patients with smoke inhalation from
residential or industrial fires. In addition, intensive treatment with sodium
nitroprusside or long-term consumption of cyanide-containing foods is a possible
source of cyanide poisoning. Historically, cyanide has been used as a chemical
warfare agent, and it could potentially be an agent for a terrorist attack.[1, 2]
Cyanide exists in gaseous, liquid, and solid forms. Hydrogen cyanide (HCN, also
known as prussic acid) is a volatile liquid that boils at 25.6° C (78.1° F). Potassium
and sodium cyanide salts are water soluble, whereas mercury, copper, gold, and
silver cyanide salts are poorly water soluble.
In addition, a number of cyanide-containing compounds, known as cyanogens, may
release cyanide during metabolism. These include, but are not limited to, cyanogen
chloride and cyanogen bromide (gases with potent pulmonary irritant effects), nitriles
(R-CN), and the vasodilator nitroprusside sodium, which may produce iatrogenic
cyanide poisoning during prolonged or high-dose intravenous (IV) therapy (>10
mcg/kg/min). (See Etiology.)

14. Industry widely uses nitriles as solvents and in the manufacturing of plastics. Nitriles
may release HCN during burning or when metabolized after absorption by the skin or
gastrointestinal tract. A number of synthesized and natural compounds produce HCN
when burned. These combustion gases likely contribute to the morbidity and
mortality from smoke inhalation. Finally, long-term consumption of cyanide-
containing foods, such as cassava root or apricot seeds,[3] may lead to cyanide
poisoning.
Depending on its form, cyanide may cause toxicity through inhalation, ingestion,
dermal absorption, or parenteral administration. Clinical manifestations vary widely,
depending on the dose and route of exposure, and may range from minor upper
airway irritation to cardiovascular collapse and death within minutes. (See Clinical
Presentation.) In severe cases, rapid, aggressive therapy consisting of supportive
care and antidote administration can be lifesaving. (See Treatment andMedication.)
Cyanide as a chemical weapon
HCN (North Atlantic Treaty Organization [NATO] designation AC) is one of two
cyanide chemical warfare agents[4, 5, 6] ; the other is cyanogen chloride (NATO
designation CK). Cyanide is a rapidly lethal agent when used in enclosed spaces
where high concentrations can be achieved easily.[7, 8, 9, 10] In addition, because of the
extensive use of cyanide in industry in the United States, this agent presents a
credible threat for terrorist use.[5]
Cyanide was first used as a chemical weapon in the form of gaseous HCN in World
War I. Starting in 1915, the French military used approximately 4000 tons of cyanide,
without notable success. The failure of this measure was probably attributable to the
high volatility of cyanide and the inability of the 1- to 2-lb munitions used to deliver
the amounts of chemical required for biologic effects.[5, 6]
The introduction of cyanogen chloride by the French in 1916 made available a
compound that, being both more toxic and less volatile, was a more effective
chemical agent. Other alleged military uses of cyanide include Japanese attacks on
China before and during World War II and Iraqi attacks on Kurds in the 1980s.

15. Administer a cyanide antidote if the diagnosis of cyanide toxicity is strongly
suspected, without waiting for laboratory confirmation. Available antidotes are
hydroxocobalamin (Cyanokit) and sodium thiosulfate and sodium nitrite (Nithiodote).
Both are given intravenously.
Patients who present with more than minimal symptoms that resolve without
treatment should be admitted for observation and supportive care. In patients with
acute poisoning from hydrogen cyanide (HCN) gas or soluble salts, the principal
acute care concerns are hemodynamic instability and cerebral edema. The
continuous cardiac monitoring, respiratory and cardiovascular support, and frequent
neurologic evaluation these patients require is generally best provided in an
intensive care unit.
Conversely, acute poisoning from cyanogens (nitriles) or poorly soluble salts may not
manifest or become life-threatening for several hours after exposure. These patients
require a 24-hour observation period.[23, 24]
Oxygenation should be optimized and continuous cardiac monitoring provided.
Depending on the severity of symptoms, endotracheal intubation may be necessary
to optimize oxygen delivery and protect the airway. Serum lactate concentrations,
chemistries, and arterial or venous blood gases should be monitored.
Patients should be reevaluated 7-10 days after discharge from the
hospital.[25]Delayed onset of Parkinson-like syndrome or neuropsychiatric sequelae
may be noted on followup.
Special concerns in pregnancy
Fetal demise is possible in cyanide poisoning. Aggressive support and antidotal
treatment of the mother is paramount. An obstetric evaluation following stabilization
of the mother is essential. Therapeutic abortion may be indicated in the presence of
fetal demise.
Murder mysteries and spy novels often feature cyanide as a fast-acting poison, but
you can be exposed to this toxin from everyday chemicals and even common foods.

16. Have you ever wondered how cyanide poisons and kills people, how much it takes
before it's toxic, and whether there is a cure? Here's what you need to know.
What Is Cyanide?
The term "cyanide" refers to any chemical containing a carbon-nitrogen (CN) bond.
Many substances contain cyanide, but not all of them are deadly poisons. Sodium
cyanide (NaCN), potassium cyanide (KCN), hydrogen cyanide (HCN), and cyanogen
chloride (CNCl) are lethal, but thousands of compounds called nitriles contain the
cyanide group yet aren't as toxic. In fact, you can find cyanide in nitriles used as
pharmaceuticals, such as citalopram (celexa) and cimetidine (Tagamet). Nitriles
aren't as dangerous because they don't readily release the CN- ion, which is the
group that acts as a metabolic poison.
How Cyanide Poisons
In a nutshell, cyanide prevents cells from using oxygen to make energy molecules.
The cyanide ion, CN-, binds to the iron atom in cytochrome C oxidase in the
mitochondria of cells. It acts as an irreversible enzyme inhibitor, preventing
cytochrome C oxidase from doing its job, which is to transport electrons to oxygen in
the electron transport chain of aerobic cellular respiration. Without the ability to use
oxygen, mitochondria can't produce the energy carrier adenosine triphosphate
(ATP). Tissues that require this form of energy, such as heart muscle cells and nerve
cells, quickly expend all their energy and start to die. When a large enough number
of critical cells die, you die.
Exposure To Cyanide
Cyanide can be used as a poison or chemical warfare agent, but most people are
exposed to it unintentionally. Some ways to be exposed to cyanide include:
 eating cassava, lima beans, yucca, or almonds
 eating apple seeds, cherry stones, apricot pits, or peach pits

17.  smoking cigarettes
 burning plastic
 burning coal
 inhaling smoke from a house fire
 ingesting acetonitrile-based products are used to remove artificial nails
 drinking water, eating food, touching soil, or inhaling air that has been contaminated
 exposure to rodenticide or other cyanide-containing pesticide
Many industrial processes involve compounds that contain cyanide or can react with
water or air to produce it. Paper, textile, photochemical, plastics, mining, and
metallurgy industries all may deal with cyanide. Some people report an odor of bitter
almonds associated with cyanide, but not all toxic compounds produce the scent and
not all people can smell it. Cyanide gas is less dense than air, so it will rise.
Symptoms of Cyanide Poisoning
Inhaling a high dose of cyanide gas rapidly causes unconsciousness and often
death. Lower doses may be survivable, especially if immediate aid is provided. The
symptoms of cyanide poisoning are similar to those displayed by other conditions or
exposure to any of a number of chemicals, so don't assume cyanide is the cause. Do
remove yourself from the cause of exposure and seek immediate medical attention!
Immediate Symptoms
 headache
 dizziness
 weakness
 confusion
 fatigue
 lack of coordination
Symptoms from Larger Doses or Longer Exposure

18.  low blood pressure
 unconsciousness
 convulsions
 slow heart rate
 lung damage
 respiratory failure
 coma
Death from poisoning usually results from respiratory failure or heart failure. A
person exposed to cyanide may have cherry-red skin from high oxygen levels or a
dark or blue coloring, from Prussian blue (iron binding to the cyanide ion). Also, skin
and body fluids may give off an odor of almonds.
How Much Cyanide Is Lethal?
How much cyanide is too much depends on the route of exposure, the dose, and
duration of exposure. Inhaled cyanide presents a greater risk than ingested cyanide.
Skin contact is not as much of a concern (unless it has been mixed with DMSO),
except touching the compound could lead to accidentally swallowing some of it. As a
rough estimate, since lethal dose depends on the exact compound and several other
factors, about half a gram of ingested cyanide will kill a 160-lb adult.
Unconsciousness, followed by death, could occur within several seconds of inhaling
a high dose of cyanide, but lower doses and ingested cyanide may allow a few hours
to a couple of days for treatment. Emergency medical attention is critical.
Is there a Treatment for Cyanide Poisoning?
Because it's a relatively common toxin in the environment, the body can detoxify a
small amount of cyanide. For example, you can eat the seeds of an apple or
withstand cyanide from cigarette smoke without dying.

19. When cyanide is used as a poison or a chemical weapon, treatment depends on the
dose. A high dose of inhaled cyanide is lethal too quickly for any treatment to take
effect. Initial first aid for inhaled cyanide is getting the victim to fresh air. Ingested
cyanide or lower doses of inhaled cyanide may be countered by administering
antidotes that detoxify cyanide or bind to it. For example, natural vitamin
B12, hydroxocobalamin, reacts with cyanide to form cyanocobalamin, which is
excreted in urine.
Inhalation of amyl nitrite may aid breathing in victims of cyanide and also carbon
monoxide poisoning, although few first aid kits contain these ampules anymore.
Depending on the conditions, complete recovery may be possible, although
paralysis, liver damage, kidney damage, and hypothyroidism are possible.