Cyanide gas toxicity

This paper is dedicated to highlight some facts on cyanide gas toxicity including; possible
sources, physical nature, chemical nature, pathophysiology, clinical presentation of a case
and management.

Table of contents:
Title Page
Introduction 2
Physical and chemical nature 2
Possible sources 3
Routes of exposure 4
Pathophysiology, toxicokinetics 5
Pathophysiology, toxicodynamics 8
Clinical picture 9
Differential diagnosis of cyanide gas toxicity 10
Recommended laboratory investigations 11
Treatment and management 14
References 15
Appendix 1-table summarizing general information about HCN 15

1
Introduction:
Cyanides are the salts of hydrocyanic acid and are among the most poisonous
substances known. Sodium and potassium cyanides are solids, but are often used in
solution with water. The most dangerous compounds are hydrogen cyanides (also known
as hydrocyanic acid or prussic acid) and cyanogen, which are stored under pressure as
liquids but which are used as gases. Hydrocyanic acid gas is liberated from solid cyanides
by the action of acids, water or even water vapor.
Cyanide is a rapidly acting, potentially deadly chemical that can exist in various
forms.
• Cyanide can be a colorless gas, such as hydrogen cyanide (HCN) or cyanogen
chloride (CNCl), or a crystal form such as sodium cyanide (NaCN) or potassium
cyanide (KCN).
• Cyanide sometimes is described as having a bitter almond smell, but it does not
always give off an odor, and not everyone can detect this odor.
• Cyanide is also known by the military designations AN (for hydrogen cyanide)
and CK (for cyanogen chloride).
• Exposure of cyanides to strong oxidizers such as nitrates and chlorates may cause
fires and explosions.

Physical and chemical nature:

Hydrogen cyanide is a colorless or pale-blue liquid at room temperature. It is very

volatile, readily producing flammable and toxic concentrations at room temperature.
Hydrogen cyanide gas mixes well with air, and explosive mixtures are easily formed.
At temperatures below 25.50c, hydrogen cyanide is a colorless or pale-blue liquid
(hydrocyanic acid); at higher temperatures, it is a colorless gas. Hydrogen cyanide is very
volatile, producing potentially lethal concentrations at room temperature. The vapor is
flammable and potentially explosive. Hydrogen cyanide has a faint, bitter almond odor
and a bitter, burning taste. It is soluble in water and is often used as a 96% aqueous
solution.
• Molecular weight: 27.03 Daltons
• Boiling point (760 mm Hg): 25.6 EC
• Freezing point: -13.4 EC
• Specific gravity: 0.69 (water = 1)
• Vapor pressure: 630 mm Hg 20 EC
• Gas density: 0.94 (air = 1)
• Water solubility: Miscible with water

2
 • Flammability: Flammable at temperatures > -18 EC
• Flammable range: 5.6% to 40% (concentration in air)

Cyanide is a chemical group consisting of one atom of carbon connected to one

atom of nitrogen by three molecular bonds (C≡N) and cyanides are compounds
(substances formed by the joining of two or more atoms) that contain a cyanide group
(typically shown as CN). Cyanides can both occur naturally or be man-made and many
are powerful and rapid-acting poisons. Hydrogen cyanide (HCN), which is a gas, and the
simple cyanide salts (sodium cyanide and potassium cyanide) are common examples of
cyanide compounds.

NaCN + H2O → HCN + NaOH

KCN + H2O → HCN + KOH
Hydrogen cyanide reacts with amines, oxidizers, acids, sodium hydroxide, calcium
hydroxide, sodium carbonate, caustic substances, and ammonia. Hydrogen cyanide may
polymerize at 500cto 600c.

Cyanides form strong complexes with many metals, particularly those of the
transition series. One example of such complex formation is the reaction of cyanide with
iron in the formation of ferrocyanide and ferricyanide complexes. Solutions of
ferrocyanides and ferricyanides can form hydrogen cyanide and cyanide ions when
exposed to sunlight or ultraviolet radiation. Cyanogenic glycosides are cyanide
compounds produced naturally in many plants. These glycosides produce hydrogen
cyanide when hydrolyzed or digested. For example, in the human gut, the cyanogenic
glycoside amygdaline, which is found in bitter almonds and in apricot pits and is the
active ingredient in the drug Laetrile, undergoes two enzymatically catalyzed hydrolysis
steps. The first step involves the removal of one of the two β-D-glucopyranosyl groups
from amygdaline through the action of beta-glucosidase to form the cyanogenic
glycoside, prunasin. The enzyme, emulsion, then hydrolyzes prunasin to form hydrogen
cyanide, glucose, and benzaldehyde.

Hydrogen cyanide has a pKa of 9.2; therefore, solutions of cyanide compounds in

water (such as from sodium cyanide and potassium cyanide) can form hydrogen cyanide
at acid and neutral pHs. Alkaline solutions with pH >12 are practical for preventing
significant outgassing of hydrogen cyanide. At neutral pH, cyanogen undergoes a slow
hydrolysis to form hydrogen cyanide, cyanic acid (HOCN), and other products. At
alkaline pH, CNCl hydrolyzes to CNO–, which has only limited toxicity. Alkaline
chlorination of water containing cyanide produces cyanogen chloride. Thiocyanate
(SCN–) is an oxidation product of the cyanide anion (CN–), produced in the presence of a
sulfur donor.

• Other names for HCN: hydrocyanic acid, prussic acid, formonitrile, formic
anammonide, carbon hydride nitride, cyanane, and cyclone.

Possible sources:

3
 Cyanide is generally considered to be a rare source of poisoning; however,
cyanide exposure occurs relatively frequently in patients with smoke inhalation from
residential or industrial fires. Cyanide poisoning also may occur in industry, particularly
in the metal trades, mining, electroplating, jewelry manufacturing, and x-ray film
recovery. It is also encountered in fumigation of ships, warehouses, and other structures.
Cyanides are also used as suicidal agents, particularly among healthcare and laboratory
workers.
Industry widely uses nitrites as solvents and in the manufacturing of plastics.
Nitrites may release HCN during burning or when metabolized following absorption by
the skin or gastrointestinal tract. A number of synthesized (e.g., polyacrylonitrile,
polyurethane, polyamide, urea-formaldehyde, melamine) and natural (e.g., wool, silk)
compounds produce HCN when burned. These combustion gases likely contribute to the
morbidity and mortality of smoke inhalation.
In manufacturing, cyanide is used to make paper, textiles, and plastics. It is present in the
chemicals used to develop photographs.

Cyanide is used in tempering steel, dyeing, explosives, engraving, the

production of acrylic resin plastic, and other organic chemical products (eg: historically:
formic acid). The less toxic ethyl acetate (C4H8O2) has now largely replaced the use of
cyanide in insect killing jars. Hydrogen Cyanide is also being used for capital punishment
in gas chambers in six US states, all of which have other options available.
Chronic consumption of cyanide-containing foods, such as cassava, may lead to cyanide
poisoning.

Thiocyanates are a group of compounds formed from a combination of sulfur,

carbon, and nitrogen. Thiocyanates are found in various foods and plants; they are
produced primarily from the reaction of free cyanide with sulfur. This reaction occurs in
the environment (for example, in industrial waste streams that contain cyanide) and in the
human body after cyanide is swallowed or absorbed. Thiocyanate is the major product
formed from cyanide that passes into the body as the body attempts to rid itself of
cyanide. Although thiocyanates are less harmful than cyanide in humans, they are known
to affect the thyroid glands, reducing the ability of the gland to produce hormones that are
necessary for the normal function of the body.

Ammonium thiocyanate is used in antibiotic preparations, pesticides, liquid

rocket fuels, adhesives, and matches. It also is used in photographic processes, to
improve the strength of silks, and as a weed killer.

Thiocyanates are present in water primarily because of discharges from coal processing,
extraction of gold and silver, and mining industries. Thiocyanates in soil result from direct
application of herbicides (weed killers), insecticides, and rodenticides and from disposal of
byproducts from industrial processes. Less important sources include release from damaged
or decaying tissues of certain plants, such as mustard, kale, and cabbage.

Routes of exposure:

4
 • Someone could come into contact with cyanide by breathing air, drinking water,
eating food or touching soil that contains the chemical.
• Cyanide enters water, soil or air as a result of both natural processes and industrial
activities. In air, cyanide is present mainly as the gas hydrogen cyanide.
• Smoking cigarettes is one of the major sources of cyanide exposure for people
who do not work in industries in which cyanide is used.
• Cyanide gas can even cause poisoning when it contacts the skin, also cyanide dust
can be absorbed from the skin provided that it is dissolved in sweat or other moist
surfaces.
• Cyanide gas cause eye affection when it contacts the eye.
• Ingestion can occur when cyanide gas become dissolved in drinking water or
absorbed by foods.

Pathophysiology:

Toxicokinetics:

Following inhalation, cyanide is rapidly distributed throughout the body, with

measurable levels detected in all organs studied to date. Cyanide can be distributed in the
body within seconds and death can occur within minutes.
• Absorption:
Cyanide as hydrogen cyanide is rapidly absorbed (within seconds) following
inhalation exposure. Humans retained 58% of hydrogen cyanide in the lungs after
inhaling the gas through normal breathing.

Hydrogen cyanide is moderately lipid-soluble, which, along with its small size,
allows it to rapidly cross mucous membranes and to be taken up instantly across the
alveolar epithelium of the lung after inhalation; penetration across the epidermis is less
rapid.
• Distribution:
Once cyanide is absorbed, it is rapidly distributed by the blood throughout the
body. Tissue levels of hydrogen cyanide were 0.75, 0.42, 0.41, 0.33, and 0.32 mg/100 g of
tissue in the lung, heart, blood, kidney, and brain, respectively, in a man who died
following inhalation exposure to hydrogen cyanide gas.
In one case of death due to cyanide oral exposure, it was estimated that 30 mg of
hydrogen cyanide had been ingested and that 3 hours had elapsed before death. In another
case, tissue cyanide levels from a man who died from inhalation of hydrogen cyanide
were reported as 0.5 mg per 100 mL of blood and 0.11, 0.07, and 0.03 mg/100 g in the
kidney, brain, and liver, respectively. Urinary cyanide levels were reported as 0.2 mg/100
mL, and 0.03 mg/100 g were found in the gastric contents. Following chronic
occupational exposure to 0.19–0.75 ppm hydrogen cyanide,
56.0 and 18.3 μg CN–/100 mL were found in the blood of smokers and nonsmokers,
respectively. The cyanide levels in control groups were 4.8 μg/mL for smokers and 3.2
μg/mL for nonsmokers.

5
Cyanide is rapidly distributed by the blood throughout the body. In a study using orally
administered radioactively labeled potassium cyanide, radioactivity detected in whole
blood or plasma decreased rapidly within 6 hours. Of the low levels of radioactivity
detected in the red blood cells, about 94% of the radioactivity recovered was found in the
hemolysate; of which 70% was detected in the heme fraction, 14–25% in globin, and only
5–10% in cell membranes. It was determined that the pattern of distribution of cyanide
did not vary with the concentration used. Ballantyne observed higher cyanide levels in
whole blood than in serum in rabbits exposed dermally to hydrogen cyanide, potassium
cyanide, and sodium cyanide.

• Metabolism:

Reports of ingestion of cyanides by humans and reports of occupational exposure indicate

that cyanide is transformed into thiocyanate. A plasma half-life of 20 minutes to 1 hour
has been estimated for cyanides in humans after nonlethal exposures.

(1) the major pathway, conversion to thiocyanate by either rhodanese or 3-

mercaptopyruvate sulfur transferase;
(2) conversion to 2-aminothiazoline-4-carboxylic acid;
(3) incorporation into a 1-carbon metabolic pool; or
(4) combining with hydroxocobalamin to form cyanocobalamin (vitamin B12).
Thiocyanate has been shown to account for 60–80% of an administered cyanide dose
while 2-aminothiazoline-4-carboxylic acid accounts for about 15% of the dose. The
conversion of cyanide to thiocyanate was first demonstrated in 1894. Conversion of
cyanide to thiocyanate is enhanced when cyanide poisoning is treated by intravenous
administration of a sulfur donor. The sulfur donor must have a sulfane sulfur, a sulfur
bonded to another sulfur (e.g., sodium thiosulfate). During conversion by rhodanese, a
sulfur atom is transferred from the donor to the enzyme, forming a persulfide
intermediate. The persulfide sulfur is then transferred from the enzyme to cyanide,
yielding thiocyanate. Thiocyanate is then readily excreted in the urine as the major
metabolite. Once thiocyanate is formed, it is not converted back to cyanide.

6
 • Elimination and excretion:
Following chronic occupational exposure to 0.19–0.75 ppm hydrogen cyanide,
24-hour urinary levels of thiocyanate were 6.23 (smokers) and 5.4 μg/mL (nonsmokers)
in exposed workers as compared with 3.2 (smokers) and 2.15 μg/mL (nonsmokers) in
the controls. Further data about routes of elimination could be analyzed from the
previous figure.
The severity of neurological effects in humans and animals after acute oral
exposure to cyanide is dose-related. Central nervous system effects have been observed
following acute-duration exposures and chronic-duration exposures, via the inhalation
and oral routes. Necrosis is the most prevalent central nervous system effect following
acute-duration exposure to high concentrations of cyanide, whereas demyelination is
observed in animals that survive repeated exposure protocols.

N.B.Route-Dependent Toxicity. A great similarity exists among cyanide-induced effects following inhalation, oral,
and dermal exposure. Signs of toxicity in target organs from acute cyanide exposure (primarily central nervous
system and heart), and chronic exposure (including central nervous system and thyroid gland), are similar in both
humans and animals regardless of route. In general, the latency of effects is shortest by the inhalation route, similar
for the oral route, but longer for the dermal route, since the skin is a thicker barrier to penetration. The rate of cyanide
absorption and, therefore, latency of toxic effects is decreased in fasting animals.

7
Toxicodynamics:

Cyanide compounds are very toxic to humans, and inhalation exposure can be
rapidly fatal. Cyanide compounds prevent the transfer of oxygen from the blood to body
tissues as a result of selective inhibition of respiratory enzymes. The heart and central
nervous system are particularly prone to rapid damage. They act as cellular asphyxiant.
Cyanide affects virtually all body tissues, attaching itself to ubiquitous
metalloenzymes and rendering them inactive. Its principal toxicity results from
inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial
oxidative phosphorylation and inhibiting cellular respiration, even in the presence of
adequate oxygen stores. Cellular metabolism shifts from aerobic to anaerobic, with the
consequent production of lactic acid. Consequently, the tissues with the highest oxygen
requirements (brain and heart) are the most profoundly affected by acute cyanide
poisoning.

Cyanide (as hydrogen cyanide), originating in vivo by dissociation of potassium

cyanide, sodium cyanide, and other cyanogenic compounds or arising from catabolism of
cyanogenic glycosides, exerts its acute toxic effects by complexion with the ferric iron
atom in metalloenzymes, resulting in histotoxic anoxia through inhibition of cytochrome
c oxidase, metalloenzymes that function as the terminal oxidase of the inner
mitochondrial membrane respiratory chain. A two-step process has been proposed:
cyanide as hydrogen cyanide first penetrates a protein crevice of cytochrome c oxidase
and binds to the protein. Hydrogen cyanide then binds to the trivalent iron ion of the
enzyme, forming a relatively stable (but reversible) coordination complex. One mole of
hydrogen cyanide is bound to one mole of cytochrome c oxidase. As a result, the enzyme
becomes unable to catalyze the reactions in which electrons would be transferred from
reduced cytochrome to oxygen. Cellular oxygen utilization is thus impaired, with
resultant reduction in or cessation of aerobic metabolism. Glucose catabolism then shifts
from the aerobic pathway to anaerobic metabolism including the pentose phosphate
pathway, resulting in increased blood glucose, pyruvic acid, lactic acid, and nicotinamide
adenine dinucleotide (NADPH) levels, and a decrease in the adenosine
triphosphate/adenosine diphosphate (ATP/ADP) ratio. Wilson et al. (1994) suggest that it
is the binding of cyanide to oxidized CuB, the copper ion that is part of the dioxygen
binding-site that leads to the inhibition of cytochrome c oxidase.

The inhibition of oxygen use by cells (termed histoxic hypoxia) causes oxygen
tensions to rise in peripheral tissues. This results in a decrease in the unloading gradient
for oxyhemoglobin; thus, oxyhemoglobin is carried in the venous blood. Inhibition of
oxygen utilization is thought to occur rapidly after cyanide exposure. Tadic (1992)
determined that inhibition of cytochrome c oxidase activity in rat brains was most
pronounced between 15 and 20 minutes after administration of sodium cyanide (12 mg/kg
or 1.3xLD50). In addition to binding to cytochrome c oxidase, cyanide also binds to
catalase, peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase,
ascorbic acid oxidase, xanthine oxidase, and succinic dehydrogenase. These reactions
may also contribute to the classic signs of cyanide toxicity.

8
Clinical picture:
A history of recent depression in the patient with sudden collapse or altered mental status,
acidosis, and tachyphylaxis in the ICU patient on nitroprusside should evoke suspicion of
the diagnosis.

• General weakness, malaise, and collapse

• Neurologic symptoms (reflect progressive hypoxia)

o Headache, vertigo, dizziness

o Giddiness, inebriation, confusion

o Generalized seizures

o Coma

• Gastrointestinal symptoms - Abdominal pain, nausea, vomiting

• Cardiopulmonary symptoms

o Shortness of breath, possibly associated with chest pain

o Apnea

The effects of cyanide on specific systems in case of acute poisoning are as follows:
Inhaled cyanide gas causes laryngospasm with stridors and wheezes giving the
characteristic cyanide cry.
CNS CNS signs and symptoms usually develop rapidly. Initial symptoms are
nonspecific and include excitement, dizziness, nausea, vomiting, headache, and
weakness. As poisoning progresses, drowsiness, tetanic spasm, lockjaw, convulsions,
hallucinations, loss of consciousness and coma may occur. Acute exposure of humans to
fatal levels of hydrogen cyanide causes a brief stage of central nervous system stimulation
followed by depression, convulsions, coma with abolished deep reflexes and dilated
pupils, paralysis, and in some cases, death.

9
Cardiovascular Abnormal heartbeat can occur in cases of severe poisoning. Slow
heartbeat, intractable low blood pressure, and death may result. High blood pressure and a
rapid heartbeat may be early, transient findings. Palpitations and hypotension were the
most frequently reported cardiovascular effects in patients after accidental inhalation
poisoning with cyanide

Respiratory After systemic poisoning begins, victims may complain of shortness of

breath and chest tightness. Pulmonary findings may include rapid breathing (tachypnea)
and increased depth of respirations. As poisoning progresses, respirations become slow
and gasping; a bluish skin color may or may not be present. Accumulation of fluid in the
lungs may develop. Children may be more vulnerable to gas exposure because of
relatively increased minute ventilation per kg and failure to evacuate an area promptly
when exposed.

Metabolic An anion-gap, metabolic acidosis occurs in severe poisoning from

increased blood levels of lactic acid. Because of their higher metabolic rates, children
may be more vulnerable to toxicants interfering with basic metabolism.

Dermal Dermal absorption can occur, leading to systemic toxicity. Absorption

occurs more readily at high ambient temperature and relative humidity. Because of their
relatively larger surface area: body weight ratio, children are more vulnerable to toxicants
absorbed through the skin. Initially there is hyperthermia followed by hypothermia.

Ocular When splashed in the eye, hydrogen cyanide can cause eye irritation and
swelling. Eye contact with cyanide salts has produced systemic symptoms in
experimental animals.

Potential Squeal Survivors of severe exposure may suffer brain damage due to a
direct action on neurons, or to lack of oxygen, or possibly due to insufficient blood
circulation. Cases of neurological sequel such as personality changes, memory deficits,
disturbances in voluntary muscle movements, and the appearance of involuntary
movements (i.e., extra pyramidal syndromes) have been reported.

Death occurs from 2-10 minutes from cerebral or myocardial anoxia.

Differential diagnosis of cyanide toxicity:

• Acute Coronary Syndrome ,Anaphylaxis
• Anxiety, Encephalitis, Herpes Simplex Encephalitis, Lactic Acidosis, Mesenteric
Ischemia, Metabolic Acidosis, Methemoglobinemia, Myocardial Infarction,
Pediatrics, Apnea Pediatrics, Gastroenteritis Pediatrics, Headache Pediatrics,
Meningitis and Encephalitis Pediatrics, Tachycardia.
• Plant Poisoning, Hemlock -Pulmonary Embolism -Sedation -Shock, Cardiogenic
-Smoke Inhalation -Stroke, Ischemic -Toxicity, Carbon Monoxide -Toxicity,
Hydrogen Sulfide- Toxicity, Iron- Toxicity, Isoniazid- Toxicity, Nonsteroidal Anti-
inflammatory Agents

10
 Recommended laboratory investigations:
N.B. treatment should be started in diagnosis without waiting for the laboratory investigations.

Lab Studies:

• Arterial and venous blood gases

o Metabolic acidosis, often severe, combined with reduced arterial-venous

oxygen saturation difference (<10 mm Hg) suggests diagnosis.

o Apnea may result in combined metabolic and respiratory acidosis.

• Blood lactate level

o A plasma lactate concentration greater than 10 mmol/L in smoke

inhalation or greater than 6 mmol/L after reported or strongly suspected
pure cyanide poisoning suggests significant cyanide exposure.

• Red blood cell and plasma cyanide concentration

o Cyanide blood concentrations are not generally available in time to aid in

the treatment of acute poisoning.

o In cyanogen exposures, these tests provide documentation for therapeutic

use, which may last several days.

o Blood cyanide concentrations may artificially increase after sodium nitrite

administration because of in vitro release of cyanide from
cyanomethemoglobin during the analytical procedure by strong acid used
in analysis.

• Carboxyhemoglobin (HbCO) or blood carbon monoxide concentration (by

infrared spectroscopy) may be obtained in patients with smoke inhalation to rule
out concurrent exposure.

• Blood concentrations of methanol, ethylene glycol, iron, ketones, and salicylates

may be useful in evaluation of unexplained metabolic acidosis. Pending results
should not delay the treatment if cyanide exposure is suspected.

• Methemoglobin concentrations provide a guide for continued therapy after use of

methemoglobin-inducing antidotes such as sodium nitrite.

o Presence of methemoglobin suggests little or no free cyanide for binding

because methemoglobin vigorously binds cyanide to form
cyanomethemoglobin (not measured as methemoglobin).

11
 o Elevated levels of methemoglobin (>10%) indicate that further nitrite
therapy is not indicated and, in fact, may be dangerous.

Imaging Studies:

• No imaging studies are indicated acutely.

• MRI may be useful during evaluation of postexposure neurologic sequelae.

Other Tests:

• ECG may show nonspecific changes.

o Atrioventricular (AV) blocks

o Supraventricular or ventricular arrhythmias

o Ischemic ECG changes and eventual asystole

In the following page, an example of the performed tests is provided.

12
13
Treatment and management:
1. First aid measures:
· remove the patient from the source of contamination - to fresh air if hydrogen cyanide
gas (HCN) is present;
· If the patient is not breathing, do not use mouth to mouth or mouth to nose ventilation
Because of the danger to the rescuer, use a resuscitation bag and mask instead;
· If pulse is absent, start external cardiac massage;
· give 100 per cent oxygen by mask if available;
· remove all contaminated clothing; wash the affected areas with soap and copious
amount of water; and
· arrange for the urgent transfer of the patient, accompanied by an attendant with the
cyanide emergency kit, to medical professionals.

2. Decontamination:

o Remove clothing.
 Then, quickly take off clothing that may have cyanide on it. If
possible, any clothing that has to be pulled over the head should be
cut off the body instead so the chemical does not get near the eyes,
mouth or nose. If helping other people remove their clothing, try to
avoid touching any contaminated areas.
o Wash affected areas.
 As quickly as possible, wash any cyanide from the skin with lots of
soap and water.
 If the eyes are burning or vision is blurred, rinse your eyes with
plain water for 10 to 15 minutes.
 If contact lenses are worn, remove them and put them with the
contaminated clothing. Do not put the contacts back in. If
eyeglasses are worn, wash them with soap and water. Eyeglasses
can be put back on after they are washed.
 If you are wearing jewelry that you can wash with soap and water,
wash it and put it back on. If it cannot be washed, put it with the
contaminated clothing.
o Discard contaminated items.
 Place the clothing and any other contaminated items 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 use tongs,
sticks or similar objects. Anything that touches the contaminated
clothing should also be placed in the bag.
 Seal the bag, and then seal that bag inside another plastic bag.
 Call the local county health department right away. (Visit
www.idph.state.il.us//local/alpha.htm for a listing of all county
health departments in Illinois or check your local phone book.)
 When the local or state health department or emergency personnel
arrive, tell them what you did with your clothes. The health

14
 department or emergency personnel will arrange for further
disposal. Do not handle the plastic bags yourself.
o Gastric lavage with an oxidizing agent as potassium permengnate could be
used to get rid of any ingested cyanide, the oxidizing agent help cyanide to
transform to cyanate to decrease its absorption.

3. Cyanide antidotes (life saving measure in case of cyanide toxicity):

• Nitrite Thiosulfates:
 Amyl nitrite inhalation: to form met-Hb, this can bind CN.
 Sodium nitrite: also to form met-Hb but it is used because it can be
given in IV form and allows free oxygenation.
 Sodium Thiosulfates: acts as sulfur donor, helping conversion of N
to thiocyanate to be easily excreted and metabolized.

The met-Hb could be restored to the normal state by using methylene blue or vitamin C

• Other antidotes:
 Hydroxycobolamin: to form cyanocobolamin to help remove CN
from Hb and allow further absorption of CN from tissues by Hb.
 Kelocyanol (cobalt EDTA): chelates cyanide forming stable
compounds which could be excreted by the kidney.

References:
1. Gold’s Frank manual of toxicological emergencies.
2. Principles of toxicology, Shine and Brown, second edition.
3. emedicine.com
4. RMIT, health and safety manual.
5. ATSDR.com
6. CDC.com
TYPES OF ACUTE HAZARDS/ PREVENTION/ FIRST AID/
HAZARD/ CLINICAL SIGNS/ PERSONAL PROTECTIVE FIRE FIGHTING
EXPOSURE SYMPTOMS EQUIPMENT
FIRE Extremely flammable. Gives off NO open flames, NO sparks, and Shut off supply; if not possible and
irritating or toxic gases in a fire. NO smoking. no risk to surroundings, let the fire
burn itself out; in other cases
extinguish with powder, water
spray, foam, carbon dioxide.
EXPLOSION Gas/air mixtures are explosive. Closed system, ventilation, In case of fire: keep cylinder cool
explosion-proof electrical by spraying with water. Combat
equipment and lighting. fire from a sheltered position.
ROUTE OF
EXPOSURE
Synopsis: May be absorbed through skin AVOID ALL CONTACT! IN ALL CASES refer for
and eyes. medical attention!

Triage procedures and medical

15
 management guidelines - see
ATSDR medical management
guidelines for Hydrogen Cyanide.

• Headache
Inhalation: Ventilation, local exhaust, or Fresh air, rest. Half-upright
breathing protection. position. Avoid mouth to mouth
• Dizziness resuscitation, administer oxygen
• Confusion Gas mask with HC (Hydrogen
by trained personnel.
• Nausea Cyanide) canister (escape).
Seek medical attention
• Shortness of breath
immediately.(See Notes.)
• Convulsions Pressure demand, self-contained
breathing apparatus (SCBA)
• Vomiting (SCBA CBRN, if available) is
• Weakness recommended in response to non-
routine emergency situations Triage procedures and medical
• Anxiety management guidelines - see
• Irregular heart beat
CBRN, Full Facepiece APR
ATSDR medical management
• Tightness in the chest guidelines for Hydrogen Cyanide.
(when available) is recommended
• Unconsciousness in non-routine, emergency
situation environments less than
IDLH but above REL or PEL
• Effects may be delayed. levels.

Skin: MAY BE ABSORBED!
(See Inhalation for other
symptoms.)
Butyl rubber gloves. Teflon, Remove contaminated clothes.
Responder, or Tychem Protective Rinse skin with plenty of water or
clothing. See NIOSH Protective shower. Wear protective gloves
Clothing. when administering first aid.

Seek medical attention

immediately.
Eyes: VAPOR WILL BE ABSORBED! Safety goggles, face shield, or eye First rinse with plenty of water for
Redness. protection in combination with several minutes (remove contact
breathing protection. lenses if easily possible), then seek
medical attention immediately.
(See Inhalation for other
symptoms.)
Ingestion: Burning sensation. Do not eat, drink, or smoke during Rinse mouth. See inhalation. Do
work. Wash hands before eating. NOT induce vomiting.
(See Inhalation for other
symptoms.)
Seek medical attention
immediately. (See Notes.)
OCCUPATIONAL OSHA PEL: TWA 10 ppm (11 mg/m3) skin
EXPOSURE LIMITS NIOSH REL: ST (short term) 4.7 ppm (5 mg/m3) skin
(OELs): ACGIH TLV : 4.7 ppm; 5 mg/m3 (ceiling value) (skin) (ACGIH 2002).
NIOSH IDLH: 50 ppm
(See Acute Exposure Guideline levels below.)
SAMPLING AND NIOSH 6010 (HYDROGEN CYANIDE)
ANALYTICAL NIOSH 7904 (CYANIDES, aerosol and gas)
METHODS:
DECONTAMINATION Patients/victims: Wet contaminated clothing should be removed and the underlying skin washed with
soap and water or water alone for 2-3 minutes.

Equipment: N/A

Environment: (See Spillage Disposal.)

SPILLAGE DISPOSAL Evacuate danger area immediately! Consult an expert! Ventilation. Absorb remaining liquid in sand or
inert absorbent and remove to safe place. Do NOT wash away into sewer. NEVER direct water jet on
liquid. Prevent from entering confined spaces. Do NOT let this chemical enter the environment.

Extra personal protection: gas-tight chemical protection suit including self-contained breathing
apparatus.

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 STORAGE: Fireproof. Separated from food and feedstuffs. Cool. Store only if stabilized.
PACKAGING &
LABELLING UN# 1051 (Guide 117)(anhydrous or greater than 20% solution)
UN# 1613 (Guide 154) (less than 20% solution)
Marine pollutant.
F+ symbol
T+ symbol
R: 12-26
S: 1/2-7/9-16-36/37-38-45
Hazard Class: 6.1
Subsidiary Risks: 3
Packing Group: I
NFPA 704 Signal:
Health - 4
Flammability - 4
Reactivity - 2
Special -
IMPORTANT DATA PHYSICAL STATE; APPEARANCE:
Colorless Gas or Liquid, with characteristic odor.

PHYSICAL DANGERS:
The gas mixes well with air, explosive mixtures are easily formed.

CHEMICAL DANGERS:
The substance may polymerize due to warming, under the influence of base(s), over 2% water, or
temperatures above 184°C, or if not chemically stabilized, with fire or explosion hazard. On
combustion, forms toxic and corrosive gases, including nitrogen oxides. The solution in water is a weak
acid. Reacts violently with oxidants, hydrogen chloride in alcoholic mixtures, causing fire and explosion
hazard.

ROUTES OF EXPOSURE:
The substance can be absorbed into the body by inhalation, through the skin and by ingestion.

INHALATION RISK:
A harmful contamination of the air can be reached very quickly on evaporation of this substance at
20°C.

EFFECTS OF SHORT-TERM EXPOSURE:

The substance irritates the eyes and the respiratory tract. Cyanides poison the vital organs of the body
(for example the lungs and heart) including areas of the brain that regulate proper functioning of those
organs. Exposure may result in convulsions, unconsciousness and in death. (See Notes.)

EFFECTS OF LONG-TERM OR REPEATED EXPOSURE:

N/A
PHYSICAL Melting Point: 8.6°F (-13°C)
PROPERTIES Boiling Point: 78.8°F (26°C)
Vapor Pressure (20°C): 618.7 mm Hg
Relative vapor density (air = 1): 0.94
Volatility: N/A
Relative vapor density (water = 1): 0.69
Aqueous Solubility(20°C): miscible
estimated log Kow: N/A
Flashpoint: -0.4°F (-18°C) c.c
Flammability: N/A
Auto-ignition temperature: 1000.4°F (538°C)

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