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

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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 veryvolatile, 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 Flammability: Flammable at temperatures > -18 EC

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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:

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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:

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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.

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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.

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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.

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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.

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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.

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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 adirect 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

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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).

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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.

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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 ventilationBecause 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 thecyanide 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

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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.com4. RMIT, health and safety manual.5. ATSDR.com6. CDC.com

TYPES OFHAZARD/ EXPOSURE

ACUTE HAZARDS/CLINICAL SIGNS/SYMPTOMS

PREVENTION/PERSONAL PROTECTIVE EQUIPMENT

FIRST AID/FIRE FIGHTING

FIRE Extremely flammable. Gives off irritating or toxic gases in a fire.

NO open flames, NO sparks, and NO smoking.

Shut off supply; if not possible and 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, explosion-proof electrical equipment and lighting.

In case of fire: keep cylinder cool by spraying with water. Combat fire from a sheltered position.

ROUTE OFEXPOSURE

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Synopsis:

May be absorbed through skin and eyes.

AVOID ALL CONTACT! IN ALL CASES refer for medical attention!

Triage procedures and medical management guidelines - see ATSDR medical management guidelines for Hydrogen Cyanide.

Inhalation: Headache Dizziness Confusion Nausea Shortness of breath Convulsions Vomiting Weakness Anxiety Irregular heart beat Tightness in the

chest Unconsciousness

Effects may be delayed.

Ventilation, local exhaust, or breathing protection.

Gas mask with HC (Hydrogen Cyanide) canister (escape).

Pressure demand, self-contained breathing apparatus (SCBA) (SCBA CBRN, if available) is recommended in response to non-routine emergency situations

CBRN, Full Facepiece APR (when available) is recommended in non-routine, emergency situation environments less than IDLH but above REL or PEL levels.

Fresh air, rest. Half-upright position. Avoid mouth to mouth resuscitation, administer oxygen by trained personnel.

Seek medical attention immediately.(See Notes.)

Triage procedures and medical management guidelines - see ATSDR medical management guidelines for Hydrogen Cyanide.

Skin: MAY BE ABSORBED!

(See Inhalation for other symptoms.)

Butyl rubber gloves. Teflon, Responder, or Tychem Protective clothing. See NIOSH Protective Clothing.

Remove contaminated clothes. Rinse skin with plenty of water or shower. Wear protective gloves when administering first aid.

Seek medical attention immediately.

Eyes: VAPOR WILL BE ABSORBED! Redness.

(See Inhalation for other symptoms.)

Safety goggles, face shield, or eye protection in combination with breathing protection.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then seek medical attention immediately.

Ingestion:

Burning sensation.

(See Inhalation for other symptoms.)

Do not eat, drink, or smoke during work. Wash hands before eating.

Rinse mouth. See inhalation. Do NOT induce vomiting.

Seek medical attention immediately. (See Notes.)

OCCUPATIONAL EXPOSURE LIMITS (OELs): OSHA PEL: TWA 10 ppm (11 mg/m3) skin

NIOSH REL: ST (short term) 4.7 ppm (5 mg/m3) skin 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 ANALYTICAL METHODS:

NIOSH 6010 (HYDROGEN CYANIDE)NIOSH 7904 (CYANIDES, aerosol and gas)

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.)

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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.

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

PHYSICALPROPERTIES

Melting Point: 8.6°F (-13°C)

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

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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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