SODIUM CYANIDE
(Strongly Suspected)
SODIUM CYANIDE
CASRN: 143-33-9
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAuiaaFb:1
Human Health Effects:
Human Toxicity Excerpts:
SYMPTOMATOLOGY: 1. Massive doses may produce,
without warning, sudden loss of consciousness and prompt death from respiratory
arrest. With smaller but still lethal doses, the illness may be prolonged for 1
or more hours. 2. Upon ingestion, a bitter, acrid, burning taste is sometimes
noted, followed by a feeling of constriction or numbness in the throat.
Salivation, nausea and vomiting are not unusual ... 3. Anxiety, confusion,
vertigo, giddiness, and often a sensation of stiffness in the lower jaw. 4.
Hyperpnea and dyspnea. Respirations become very rapid and then slow and
irregular. Inspiration is characteristically short while expiration is greatly
prolonged. 5. The odor of bitter almonds may be noted on the breath or vomitus
... 6. In the early phases of poisoning, an increase in vasoconstrictor tone
causes a rise in blood pressure and reflex slowing of the heart rate.
Thereafter, the pulse becomes rapid, weak, and sometimes irregular. ... A bright
pink coloration of the skin due to high concentrations of oxyhemoglobin in the
venous return may be confused with that of carbon monoxide poisoning. /Cyanide/
SYMPTOMATOLOGY: 7. Unconsciousness, followed
promptly by violent convulsions, epileptiform or tonic, sometimes localized but
usually generalized. Opisthotonos and trismus may develop. Involuntary
micturition and defecation occur. 8. Paralysis follows the convulsive stage. The
skin is covered with sweat. The eyeballs protrude, and the pupils are dilated
and unreactive. The mouth is covered with foam, which is sometimes bloodstained.
... The skin color may be brick red. Cyanosis is not prominent in spite of weak
and irregular gasping. In the unconscious patient, bradycardia and the absence
of cyanosis may be key diagnostic signs. 9. Death from respiratory arrest.
/Cyanide/
MOST SPECIFIC PATHOLOGICAL FINDING IN ACUTE
CASES /OF CYANIDE POISONING/ IS BRIGHT RED COLOR OF VENOUS BLOOD. THIS IS
STRIKING, VISIBLE EVIDENCE OF INABILITY OF TISSUE CELLS TO UTILIZE OXYGEN ...
VENOUS BLOOD IS ONLY ABOUT 1 VOL % LOWER IN OXYGEN CONTENT THAN ARTERIAL BLOOD
... /CYANIDES/
WORKERS IN ELECTROPLATING INDUST HAVE SHOWN
DERMATITIS TO BE A PROBLEM. ALSO REPORTED WERE ITCHING, SCARLET RASH, PAPULES
... IRRITATION OF NOSE, LEADING TO OBSTRUCTION, BLEEDING, SLOUGHS, AND IN SOME
CASES PERFORATION OF SEPTUM. /CYANIDES/
... ENLARGED THYROID GLANDS /WERE REPORTED/ IN
WORKERS EXPOSED TO CYANIDE SALTS IN HEAT TREATMENT OF METALS. IT WAS SUGGESTED
THAT ABSORPTION OF CYANIDE DUST & HYDROGEN CYANIDE PRODUCED BY HYDROLYSIS OF
CYANIDE SALTS, WAS FOLLOWED BY METABOLISM TO THIOCYANATE, & THAT FAILURE TO
ELIMINATE THIS ... CAUSED GOITROGENIC EFFECT. /CYANIDE SALTS/
... IT IS POSSIBLE FOR CYANIDE TO CAUSE
BLINDNESS & TO DAMAGE OPTIC NERVES & RETINA. /CYANIDE/
A STUDY WAS UNDERTAKEN TO ASSESS THE HEALTH
STATUS OF WORKERS EXPOSED TO CYANIDE FUMES & AEROSOLS IN A FACTORY. CYANIDE
LEVELS WERE MEASURED IN THE WORK ENVIRONMENT & IN BLOOD & URINE. SMOKERS
HAD HIGHER CONCENTRATIONS THAN NON-SMOKERS. THE HIGHEST LEVELS WERE 0.8 &
0.2 MG/CU M IN BREATHING ZONE & GENERAL WORKROOM ATMOSPHERE, RESPECTIVELY.
THE WORKERS COMPLAINED OF TYPICAL CYANIDE POISONING IN SPITE OF THE LOW CONCN.
... /CYANIDES/
THE TLV FOR ALKALI CYANIDES ... IS BASED ON
ADDED IRRITATION CAUSED BY ALKALINITY, SUFFICIENT TO RESULT IN EPISTAXIS
(NOSEBLEED) & NASAL ULCERATION. AIR CONCN OF CYANIDE FROM ALKALI CYANIDES
PRODUCING THIS EFFECT (NOSEBLEED) DID NOT GREATLY EXCEED 5 PPM. /ALKALI
CYANIDES/
Cyanides are absorbed from the skin &
mucosal surfaces and are ... dangerous when inhaled because toxic amt are ...
absorbed through bronchial mucosa & alveoli. Symptoms, which /may/ occur ...
are giddiness, headache, palpitation, dyspnea, & unconsciousness. There may
be some evidence of local irritation from the salts & nausea & vomiting.
... Central nervous depression. ... Early electrocardiographic changes may
include atrial fibrillation, ectopic ventricular beats, and abnormal QRS complex
with T wave originating high on the R wave. Sinus bradycardia is a common
presenting sign. As cyanide levels in the blood rise, ataxia develops & is
followed by coma, convulsions, & death. /Cyanides/
Signs & symptoms of acute cyanide
poisoning reflect cellular hypoxia & are often nonspecific. Onset of
symptoms depends on dose, route, & duration of exposure. Inhalation produces
... flushing, headache, tachypnea, & dizziness ... irregular stridulous
breathing, coma, seizure, & death ... /Cyanide/
WHEN ABSORBED, /CYANIDE/ ... REACTS READILY
WITH ... CYTOCHROME OXIDASE IN MITOCHONDRIA; CELLULAR RESPIRATION IS THUS
INHIBITED & CYTOTOXIC HYPOXIA RESULTS. ... RESPIRATION IS /INITIALLY/
STIMULATED ... A TRANSIENT STAGE OF CNS STIMULATION WITH HYPERPNEA AND HEADACHE
IS OBSERVED; FINALLY THERE ARE HYPOXIC CONVULSIONS AND DEATH DUE TO RESPIRATORY
ARREST. /CYANIDE/
SODIUM CYANIDE PRODUCES
ALL TYPICAL SYMPTOMS OF OTHER SOURCES OF CYANIDE ION. IT CAN PRODUCE ACUTE
SYMPTOMS BY INHALATION & BY SKIN ABSORPTION AS WELL AS BY INGESTION. FATAL
DOSAGE BY ORAL INGESTION WILL VARY CONSIDERABLY DEPENDING ON WHETHER OR NOT FOOD
IS PRESENT IN STOMACH, ETC. IT IS PROBABLY ON ORDER OF 1-2 MG/KG ...
VOLATILE CYANIDES /SRP: AND ALL AIRBORNE
CYANIDE SALTS/ RESEMBLE HYDROCYANIC ACID PHYSIOLOGICALLY, INHIBITING TISSUE
OXIDN & CAUSING DEATH THROUGH ASPHYXIA. CYANOGEN IS PROBABLY AS TOXIC AS
HYDROCYANIC ACID ... /CYANIDES/
In minimal lethal doses, cyanide affects
primarily the central nervous system. Cyanide initially stimulates the
peripheral chemoreceptors, causing increased respirations. It also promotes
slowing of the heart by stimulating the carotid body receptors. The electrical
activity of the brain may stop while the heart is still beating. /Cyanide/
The most common symptoms of a long-term
cyanide exposure that has exceeded current standards have been headache,
dizziness, nausea or vomiting, and a bitter or almond taste. Mild abnormalities
of vitamin B12, folate, and thyroid function have been noted, but symptoms did
not correlate with these changes. Other excessive exposures to cyanide have
resulted in psychosis and thyroid enlargement without symptoms of thyroid
dysfunction. Several clinical syndromes have been associated with chronic
cyanide toxicity ... . These diseases may be due to high cyanide levels,
impaired cyanide detoxification mechanisms, nutritional deficiencies, or some
combination of these factors. /Cyanide/
In serious poisonings, the skin is cold,
clammy, and diaphoretic. Cyanosis may be a late finding, since poor tissue
utilization of oxygen results in elevated venous oxygen levels. Retinal veins
and arteries may appear similar in color because of the elevated venous oxygen
level. /Cyanide/
Depression of the cardiovascular system
requires cyanide doses higher than those necessary for depression of the CNS.
Initial tachycardia occurs followed by bradycardia.. Dysrhythmias and
hypotension often precede peripheral vascular collapse. The ECG may display
striking ischemic changes; pulmonary edema may complicate severe intoxications.
/Cyanide/
The CNS is the most sensitive target organ of
cyanide poisoning, with early stimulation followed by CNS depression. Early
symptoms include lightheadedness, giddiness, tachypnea, nausea, vomiting,
feeling of neck constriction and suffocation, confusion, restlessness, and
anxiety. Initial tachypnea results from direct stimulation of carotid body
chemoreceptors followed by respiratory depression. Severe cyanide poisonings
progress to stupor, coma, opisthotonus, convulsions, fixed dilated pupils, and
death. /Cyanide/
Workers, such as electroplaters and picklers,
who are daily exposed to cyanide solutions may develop a "cyanide"
rash, characterized by itching and by mascular, papular, and vesicular
eruptions.
Exposure to small amounts of cyanide compounds
over long periods of time is reported to cause loss of appetite, headache,
weakness, nausea, dizziness, and symptoms of irritation of the upper respiratory
tract and eyes.
Because cyanide salts are rapidly absorbed
from mucous membranes, symptoms following acute inhalation of or mucous membrane
contact with toxic concentrations of cyanide salts may begin within seconds to a
few minutes after exposure.
Skin, Eye and Respiratory Irritations:
Irritating to skin, eyes, and respiratory
system.
Medical Surveillance:
Preplacement and annual medical examinations
shall include: An initial or interim work and medical history with special
attention to skin disorders and those non-specific symptoms, such as headache,
nausea, vomiting, dizziness or weakness, that may be associated with chronic
exposure. A physical examination giving particular attention to skin, thyroid,
and the cardiovascular and upper respiratory systems. ... Two physicians
treatment kits shall be immediately available to trained medical personnel at
each plant where there is a potential for the release of, accidental or
otherwise, or for contact with, hydrogen cyanide or cyanide salts. ... First-aid
kits shall be immediately available at workplaces where there is potential for
the release, accidental or otherwise, of hydrogen cyanide or a potential for
exposure to cyanide salts. ... Pertinent medical records shall be maintained for
5 years following the last exposure to hydrogen cyanide or cyanide salts.
/Cyanide salts/
Initial medical examination /should include/:
a complete history and physical examination ... to detect existing conditions
that might place the exposed employee at incr risk & to establish a baseline
for future health monitoring. ... Examination of cardiovascular, nervous, &
upper resp systems, & thyroid should be stressed. The skin should be exam
for evidence of chronic disorders. ... The aforementioned medical exam should be
repeated on an annual basis. ... /Cyanides/
Pre-placement and periodic examinations should
include the cardiovascular and central nervous systems, liver and kidney
function, blood, history of fainting and dizzy spells. Blood cyanide levels may
be useful during acute intoxication. Urinary thiocyanate levels have been used
but are nonspecific and are elevated in smokers. /Cyanides/
Arterial Blood Gases: Arterial blood gases may
be useful for monitoring of metabolic acidosis that can occur from cyanide
poisoning. /Cyanide/
EKG Measurement: EKG monitoring may be useful
since changes have been found with cyanide exposure. /Cyanide/
The assessment of cyanide exposure can be
accomplished through measurement of cyanide. Most information found in the
literature regarding monitoring for absorption of cyanide preferred the
measurement of blood cyanide. ... Blood Reference Ranges: Normal - non-smokers,
<0.02 ug/ml; smokers, average 0.041 ug/ml; Exposed - Levels of <0.2 ug/ml
have been found to be non-toxic; however, levels of 0.5 - 1.0 ug/ml have been
associated with tachycardia and flushing. Toxic - Levels of 1.0 - 2.5 ug/ml have
been associated with obtundation; coma and respiratory depression with levels
greater than 2.5 ug/ml; death with values greater than 3 ug/ml. Serum or Plasma
Reference Ranges: Normal - cyanide: nonsmoker, 0.004 ug/ml; smoker, 0.006 ug/ml;
Exposed - not established; Toxic - cyanide; greater than 0.1 ug/ml. Urine
Reference Ranges: Normal - not established; Exposed - not established; Toxic -
not established. /Cyanide/
Respiratory Symptom Questionnaires:
Questionnaires have been published by the American Thoracic Society and the
British Medical Research Council. These questionnaires have been found to be
useful in identification of people with chronic bronchitis, however certain
pulmonary function tests such as FEV1 have been found to be better predictors of
chronic airflow obstruction. /Cyanide/
Chest Radiography: This test is widely used
for assessing pulmonary disease. Chest radiographs have been found to be useful
for detection of early lung cancer in asymptomatic people, especially for
detection of peripheral tumors such as adenocarcinomas. However, even though
OSHA mandates this test for exposure to some toxicants such as asbestos, there
are conflicting views on its efficacy in detection of pulmonary disease.
/Cyanide/
Pulmonary Function Tests: The tests that have
been found to be practical for population monitoring include: Spirometry and
expiratory flow-volume curves; Determination of lung volumes; Diffusing capacity
for carbon monoxide; Single-breath nitrogen washout; Inhalation challenge tests;
Serial measurements of peak expiratory flow; Exercise testing. /Cyanide/
Evaluation of Peripheral Neuropathy: Nerve
conduction study; Electromyography; Quantitative sensory testing; Thermography.
/Cyanide/
Evaluation of Central Nervous System Effects:
Evaluation of CNS effects can be performed through neuropsychological
assessment, which consists of a clinical interview and administration of
standardized personality and neuropsychological tests. The areas that the
neuropsychology test batteries focus on include the domains of memory and
attention; visuoperceptual, visual scanning, visuospatial, and visual memory;
and motor speed and reaction time. There is limited data on which components of
the test batteries are best indicators of early CNS effects. /Cyanide/
Evaluation of Cranial Neuropathies: Evaluation
of cranial nerve damage, as evidenced by symptoms such as loss of balance,
visual function, smell, taste, or sensation on the face, can be accomplished
through a physical examination focusing on tests such as: Smell Assessment ...
Visual Assessment ... Facial and Trigeminal Nerve Assessment ... Vestibular
Assessment ... Hearing Assessment. /Cyanide/
Populations at Special Risk:
WORKERS WITH CHRONIC DISEASES OF KIDNEYS,
RESPIRATORY TRACT, SKIN OR THYROID ARE AT GREATER RISK OF DEVELOPING TOXIC
CYANIDE EFFECTS THAN ARE HEALTHY WORKERS. /CYANIDES/
Probable Routes of Human Exposure:
/IN ELECTROPLATING/ ... SODIUM BATH CONTAINS SODIUM
CYANIDE ... ...
... SYMPTOMS OF CHRONIC DISEASE ... REPORTED
IN ELECTROPLATERS & SILVER POLISHERS AFTER SEVERAL YEARS OF EXPOSURE.
/CYANIDES/
AMONG FUMIGATORS ... CYANIDE POISONING IS
RECOGNIZED ... /CYANIDES/
DERMATITIS ... IN WORKERS CHRONICALLY EXPOSED
TO CYANIDE SOLN. ELECTROPLATERS SUFFER FROM SUCH IRRITATION. /CYANIDE SOLN/
Body Burden:
Cyanide is present in normal healthy human
organs at concentrations ranging up to 0.5 mg/kg. /Cyanide/
Antidote and Emergency Treatment:
Basic Treatment: Establish a patent airway.
Suction if necessary. Watch for signs of respiratory insufficiency and assist
ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15
l/min. Administer amyl nitrite ampules as per protocol and physician order ... .
Monitor for shock and treat if necessary ... . Monitor for pulmonary edema and
treat if ... . Anticipate seizures and treat if necessary ... . For eye
contamination, flush eyes immediately with water. Irrigate each eye continuously
with normal saline during transport ... . Do not use emetics. For ingestion,
rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the
patient can swallow, has a strong gag reflex, and does not drool ... . /Cyanide
and related compounds/
Advanced Treatment: Consider orotracheal or
nasotracheal intubation for airway control in the patient who is unconscious or
in respiratory arrest. Positive pressure ventilation techniques with a bag valve
mask device may be beneficial. Start an IV with D5W /SRP: "To keep
open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia
are present. Watch for signs of fluid overload. Administer cyanide antidote kit
as per protocol and physician order ... . Monitor and treat cardiac arrhythmias
if necessary ... . Consider vasopressors to treat hypotension without signs of
hypovolemia ... . Consider drug therapy for pulmonary edema ... . Treat seizures
with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye
irrigation ... . /Cyanide and related compounds/
Although a variety of agents are effective
antidotes in the experimental animal (nitrites, dimethylaminophenol, cobalt EDTA,
hydroxocobalamin, stroma-free methemoglobin solutions, pyruvate, thiosulfate,
sulfur sulfanes, mercaptopyruvate, oxygen) only the three-step Eli-Lilly cyanide
kit is approved in the US. /Cyanide/
/SRP: For patients treated with nitrites:/
Measurement of methemoglobin may be useful for assessing exposure. However,
methemoglobin levels may be artificially low if not analyzed within a few hours
after drawing the blood. Methemoglobin levels have been found to correlate with
clinical symptoms in most cases. /Cyanide/
The use of the combination consisting of 4 g
of hydroxoycobalamin and 8 g of sodium thiosulfate as an antidote in cases of
cyanide poisoning is reviewed. The antidote, which has been used in France since
1970, has proved to be nontoxic and therefore can be given in cases where the
diagnosis of cyanide poisoning is not absolutely certain. On the other hand, the
Lilly Cyanide Antidote Kit, which has been approved for use in the USA for the
same purpose, has been shown to be toxic and its use requires caution. The
antidotal effectiveness of the association of hydroxoycobalamin and sodium
thiosulfate has been demonstrated in mice and other animal species poisoned with
cyanide. Most animal studies reveal a strong antidotal synergism between the two
agents. In France, the efficacy of the antidotal combination has been proved in
patients who have ingested as much as 1.5 g of potassium cyanide and have blood
cyanide levels on the order of 15 ug/ml. In the USA, the antidotal combination
is designated as an orphan drug by the FDA and studies have been started to
validate its safety and efficacy before being approved for use in this country.
/Cyanide/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
CYANIDES SUCH AS ... HYDROGEN CYANIDE,
POTASSIUM CYANIDE AND SODIUM CYANIDE ARE ACUTELY
POISONOUS, INTERFERING WITH METABOLIC PROCESSES & CAUSING RAPID DEATH. IN
SEVERE POISONING, PUPILS ARE CHARACTERISTICALLY WIDELY DILATED.
Acute systemic toxicity of hydrogen cyanide, sodium
cyanide, and potassium cyanide by instillation into the inferior
conjunctival sac was investigated in rabbits. LD50 value of hydrogen cyanide was
0.103 mmol/kg. Signs of toxicity appeared rapidly & death occurred within 3
to 12 min after instillation of cyanide into the conjunctival sac of the rabbit.
Thus, following ocular instillation, cyanides may be absorbed across the
conjunctival blood vessels in amounts sufficient to produce systemic toxicity.
THE TERATOGENIC POTENTIAL OF SODIUM
CYANIDE WAS EVALUATED IN THE GOLDEN HAMSTER. INFUSION WAS BY MEANS OF SC
IMPLANTED OSMOTIC MINIPUMPS BETWEEN DAYS 6 AND 9 OF GESTATION. INFUSION OF SODIUM
CYANIDE AT DOSE RATES OF 0.126, 0.1275, AND 0.1295 MMOL/KG/HR PRODUCED
HIGH INCIDENCES OF MALFORMATIONS AND RESORPTIONS IN THE OFFSPRING. MOST COMMON
ANOMALIES WERE NEURAL TUBE DEFECTS, INCLUDING EXENCEPHALY AND ENCEPHALOCELE.
OTHERS OCCURRED LESS FREQUENTLY AND INCLUDED HYDROPERICARDIUM AND CROOKED TAIL.
A TOTAL DOSE EQUIVALENT TO 30-40 TIMES THE ACUTE SC LD50 DOSE WAS ADMIN BY
INFUSION TO THESE ANIMALS BEFORE SIGNS OF MATERNAL TOXICITY APPEARED.
WILD COYOTES WERE TESTED IN ACUTE ORAL
TOXICITY TESTS AND TOXIC-COLLAR TESTS USING THE COMPOUNDS SODIUM
CYANIDE AND DIPHACINONE. FIVE COYOTES RECEIVED 4, 8, 16, 32, OR 64 MG/KG SODIUM
CYANIDE BY ORAL SYRINGE IN THE ACUTE TEST. RESULTS SHOWED SURVIVAL OF THE
ONE ANIMAL GIVEN 4 MG/KG; THE OTHERS DIED WITHIN 2 MINUTES AFTER DOSING. IN
TOXIC-COLLAR EXPERIMENTS 6 COYOTES WERE ALLOWED TO ATTACK SHEEP FITTED WITH
COLLAR CONTAINING EITHER DIPHACINONE OR SODIUM CYANIDE. ONLY
1 OF THE COYOTES THAT PUNCTURED A SODIUM CYANIDE COLLAR
INGESTED A LETHAL DOSE OF THE POISON, WHEREAS 3 COYOTES THAT PUNCTURED
DIPHACINONE COLLARS ALL RECEIVED LETHAL AMOUNTS OF THE ANTICOAGULANT.
IN EXPTL ANIMALS, DEMONSTRATION OF EFFECTS OF
CYANIDE POISONING ON RETINA & OPTIC NERVE HAS BEEN SUCCESSFUL PRINCIPALLY
WITH ACUTE SEVERE, NEAR-LETHAL OR LETHAL POISONINGS. /CYANIDES/
IN RABBITS, AFTER SUBLETHAL DOSES OF CYANIDE,
CHANGES IN ELECTRORETINOGRAM HAVE BEEN OBSERVED. /CYANIDE/
The significance of various physiological
factors contributing to the pathogenesis of experimental cyanide encephalopathy,
such as the systemic atrial blood pressure, venous pressure, common carotid
blood flow, and local blood flow of the cerebral grey and white matters, and
blood gas including pH, is examined. The histology and topography of the brain
damage was also analyzed. Twenty-one cats were divided into four groups. The
animals in groups 1, 2, and 3 were subject to continuous infusion of 0.2% sodium
cyanide soln and to the ensuing hypotension below 100 mm Hg by
administering a ganglion-blocking drug and by respiratory arrest. Severe damage
developed in the deep cerebral white matter, corpus callosum, pallidum, and
substantia nigra, but the damage of the cerebral cortex and hippocampus was not
remarkable. The animals in group 4 that were subject to sodium
cyanide infusion without significant hypotension (>100 mm Hg), but to
the same degree of acidosis as that of the other groups, had similar
morphological changes, but to a lesser degree. Apparently, the
pathophysiological factors of tissue hypoxia and subsequent hypotension operated
in cyanide leucoencephalopathy. The topography selectivity related to the
characteristic cerebral vascular system, and the severity of the white matter
lesions, was related to the intensity of both hypoxia and hypotension during
cyanide infusion, but not to the extent of acidosis, total dose of cyanide, or
duration of its infusion. ...
... The acute toxicity of 11 chemicals to
rainbow trout (Salmo gairdneri) fry (average weight 1 g) that had been reared
for about 8 wk on 1 of 5 diets. Chemicals tested against the fish included sodium
cyanide. Responses of the fish to the chemicals were consistent in all 5
groups. No group demonstrated superior resistance to these chemicals. Diet
appears to have little influence on the sensitivity of young rainbow trout to
chemicals in acute toxicity tests.
Intact neutrophils killed opsonized
Actinobacillus actinomycetemcomitans under aerobic and anaerobic conditions, and
the kinetics of these reactions indicated that both oxidative and nonoxidative
mechanisms were operative. Oxidative mechanisms contributed significantly, and
most of the killing attributable to oxidative mechanisms was inhibited by sodium
cyanide, which suggested that the myeloperoxidase-hydrogen
peroxide-chloride system participated in the oxidative process.
The participation of afferents from carotid
and aortic bodies in the hyperventilation caused by cytotoxic hypoxia was
assessed in pentobarbitone-anesthetized cats. Dose-response curves for the
ventilatory effects induced by iv injections of sodium cyanide
were obtained before and after successive denervations of peripheral
chemoreceptors, in different sequences. Bilateral aortic neurotomy or unilateral
carotid neurotomy did not affect significantly the minimal sensitivity to the
drug, although maximal reactivity was reduced in some cats. After bilateral
carotid neurotomy, with preservation of aortic nerves, sensitivity was reduced,
but hyperventilation was still provoked by large doses of cyanide. Bilateral
aortic neurotomy and bilateral carotid neurotomy abolished the ventilatory
responses to the drug. In cats with bilateral aortic neurotomy and unilateral
carotid neurotomy, ventilatory responses had a high degree of correlation with
increases of carotid chemosensory discharges in the range between approximately
200% of control and the gasping threshold. Thus, the aortic bodies of the cat
play a significant role in the hyperventilation produced by cytotoxic hypoxia,
although it is less marked than that induced through the carotid bodies.
In 6 animals breathing spontaneously through
the intact upper airway, iv administration of respiratory stimulants (sodium
cyanide or nicotine) produced a dose-related decrease in upper airway
resistance. In 9 animals, upper airway resistance was measured across the
isolated upper airway. The stimulants produced a dose-related decrease in upper
airway resistance. In both preparations inspiratory resistance fell at lower
doses than expiratory resistance. Eventually a dose could be given which
resulted in comparable, minimal values of resistance during both inspiration and
expiration. Pharmacological challenge resulted in a change in the route of
airflow (from nose only to nose-and-mouth breathing) as well a change in caliber
of the airway at the level of the naso-pharynx and hyoid appendage. In
anesthetized dogs, respiratory stimulants will decrease upper airway resistance
by increasing activation of upper airway muscles which may enlarge the airway,
change the route of flow, and thus overcoming collapsing forces produced by
increased chest wall muscle activation.
The renal vasodilatory effects of cholinergic
drugs, and the relation between hemodynamic and natriuretic changes, were
investigated by comparing intrarenal infusions of sodium
cyanide to that of acetylcholine in 5 mongrel dogs. Infusion of /each/
compound resulted in immediate and ipsilateral increases in the fractional
excretion of sodium, potassium, calcium and magnesium. Each agent increased the
renal plasma flow to the same extent. Regression plots of the relation between
changes in sodium excretion and changes in renal plasma flow were similar for
both agents.
In cats, reflex hyperpnea produced by sodium
cyanide was mediated by both carotid and aortic nerves and the response
was greater when both carotid nerves were intact than when only 1 was intact.
... In explanted chick embryos ... sodium
cyanide above a concn of 5x10-3 M inhibited development of the central
nervous system with less effect on heart development.
Toxic effects of zinc cyanide complexes were
similar to those of sodium cyanide, whereas adult
Leptomysis Mediterranean was less sensitive to sodium cyanide
(LC50 88 ug cyanide/l) and zinc cyanide complexes than to cadmium cyanide
complexes. This may be due to toxic effects of cadmium besides those of cyanide.
The invertebrates are more sensitive to cyanide than fish which are used at
present as standard aqueous indicator organisms.
IF ... ANIMALS ... HAVE EATEN CYANOGENIC
PLANTS, CLINICAL SIGNS MAY VARY FROM MILD TACHYPNEA & APPARENT ANXIETY TO
SEVERE PANTING, GASPING, & BEHAVIORAL ALARM. OTHER SIGNS INCL SALIVATION,
MUSCLE TREMORS, LACRIMATION, URINATION & DEFECATION, SEVERE COLIC, EMESIS,
PROSTRATION, ... CLONIC CONVULSIONS, MYDRIASIS, & RAPID DEATH. ... MUCOUS
MEMBRANES ARE ... PINK & BLOOD IS CHERRY RED & MAY NOT CLOT. RED COLOR
IS DUE TO HYPEROXYGENATION THAT OCCURS WHILE THE ANIMAL IS DYING. THERE MAY BE
AGONAL HEMORRHAGES ON HEART. GI TRACT & LUNG MAY HAVE CONGESTION &
PETECHIAL HEMORRHAGES. /CYANOGENIC PLANTS/
IN THE CASE OF HYDROCYANIC ACID AND CYANIDES
/IN VERY HIGH DOSES/, DEATH USUALLY OCCURS /IN ANIMALS/ WITHIN A FEW SECONDS:
THERE MAY BE CONVULSIONS, PARALYSIS, STUPOR, & CESSATION OF RESPIRATION
BEFORE THAT OF HEARTBEATS. /CYANIDES/
Except for the more sensitive invertebrate
species, such as Daphnia pulex and Gammarus pseudolimnaeus, invertebrate species
are usually more tolerant of cyanide than are freshwater fish species, which
have most acute values clustered between 50 to 200 ug/l. A long-term survival
and two life cycle test with fish gave chronic values of 7.9, 14, and 16 ug/l,
respectively, with Gammarus pseudolimnaeus being comparable to fish in
sensitivity and isopods being considerably more tolerant. /Free cyanide: HCN and
CN-/
... /THERE IS A/ COMBINED EFFECT OF PULMONARY
EDEMA AND THE INTERFERENCE OF CELLULAR METABOLISM BY THE CYANIDE RADICAL.
/CYANIDE ION/
The LD50s of sodium cyanide for
black vulture (Coragyps atratus), American kestrel (Falco sparverius), Japanese
quail (Coturnix japonica), domestic chicken (Gallus domesticus), eastern screech
owl (Otus asio), and European starling (Sturnus vulgaris) were 4.8, 4.0, 9.4,
21, 8.6, and 17 mg/kg, respectively. The LD50s for the flesh eating birds
(vulture, kestrel, and owl) were lower (4.0-8.6 mg/kg) than LD50s for birds
(quail, chicken, starling) that feed predominantly on plant material (9.4-21
mg/kg).
Salmonella typhimurium strain (OASS positive)
synthesize a toxic but non mutagenic metabolite from cyanide and O-acetylserine.
Salmonella typhimurium mutant DW379 (OASS deficient) is neither able to carry
out this reaction in vitro nor produce the toxic metabolite in vivo. L-Cysteine
reverses the cyanide metabolite mediated inhibition and thus allows OASS
positive strains to grow in medium containing cyanide and O-acetylserine. The
toxic metabolite is ninhydrin-positive, adheres strongly to the cation-exchange
column, and migrates in thin layer chromatography to an Rf value similar to that
of beta-cyanoalanine.
The major detoxification pathway for cyanide (CN)
in many species is a biotransformation to the less toxic thiocyanate (SCN).
Hepatic thiosulfate: cyanide sulfurtransferase (rhodanese) is the principal
enzyme demonstrating in vitro catalytic activity. Despite the assumed importance
of the hepatic enzyme for cyanide detoxification in vivo, the effects of liver
damage (surgical or chemical) on cyanide lethality in animals have not been
examined previously. Male CD-1 mice were pretreated with carbon tetrachloride
(CCl4, 1 ml/kg, ip) 24 hr prior to the administration of sodium
cyanide (NaCN). In other experiments, carbon tetrachloride was given in
the same doses at both 48 hr and 24 hr prior to sodium
cyanide. Hepatotoxicity was documented by elevated serum glutamicpyruvic
transaminase (SGPT) activity, by histologic evaluation of the extent of cellular
necrosis, by electron microscopy of the mitochondrial fraction, and by the
increased duration of zoxazolamine-induced paralysis. Lethality was not changed
by carbon tetrachloride pretreatments when sodium cyanide was
given alone in doses of 4 or 6 mg/kg or at a dose of 10.7 mg/kg following sodium
thiosulfate (1 g/kg, ip). A statistically significant protective effect was
exhibited by carbon tetrachloride when sodium cyanide was
given at a dose of 16 mg/kg following the administration of sodium thiosulfate.
Rhodanese activity as measured in mitochondrial preparations fractionated from
the livers of mice pretreated with carbon tetrachloride was not different from
that in animals given the corn oil vehicle even though electron micrographs
showed extensive mitochondrial damage. No difference in cyanide lethality was
evident between sham operated mice and partially (2/3) hepatectomized mice at 24
hr post-surgery.
In cats, a dose of 1.2 mg/kg was fatal; Dogs a
dose of 2.25 mg/kg caused death in 48 hours. In monkeys a dose of 0.8 mg/kg
altered ECG patterns, similar to humans.
Glomus cells of the rabbit excised carotid
body were slightly depolarized by sodium cyanide, a
response that occurred slowly and with a gradual onset. In contrast, dopamine
and acetylcholine strongly depolarized the cells. The membrane potential
responses to sodium cyanide appeared to be indirect.
The swimming performance of guinea pigs was
degraded following administration of sodium cyanide at
doses which were not lethal for individual animals. Decrements in performance
were observed two minutes following subcutaneous administration of sodium
chloride, were maximal at 8-16 min and, at the highest dose tested, did not
return to control levels until 64-128 min. Pretreatment with p-aminopropiophenone
at a dose inducing 7-15% methemoglobinemia, 15-19 minutes after administration,
protected animals against the effects of sodium cyanide upon
swimming performance. However, the protection decreased as the interval between
p-aminopropiophenone and NaCN was increased from 15 to 75 minutes.
Non-Human Toxicity Values:
Inorganic cyanides are acutely toxic
compounds, for example, the LD50 in the rat is 15 mg/kg for sodium
cyanide ...
LD50 Rat oral 6440 ug/kg
LD50 Rat ip 4300 ug/kg
LD50 Mouse ip 5881 ug/kg
LD50 Mouse sc 3660 ug/kg
LD50 Mouse un 10 mg/kg
LD50 Rabbit intramuscular 1666 ug/kg
LD50 Rabbit ocular routes 5048 ug/kg
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
OPOSSUMS WERE DOSED WITH SODIUM
CYANIDE BY ... STOMACH TUBE. ... ANALYSIS INDICATED THAT MAJOR ROUTE OF
DETOXICATION ... WAS BY CONVERSION TO THIOCYANATE, WHICH WAS EXCRETED IN URINE.
TRACES OF 2-IMINO-4-THIAZOLIDINE CARBOXYLIC ACID WERE OBSERVED IN CRUDE
CONCENTRATED EXTRACT OF URINE.
... CYANIDE ION IS CONJUGATED WITH SULFUR TO
FORM THIOCYANATE. ... CONJUGATION IS CATALYZED BY THE ENZYME RHODANESE WHICH IS
WIDELY DISTRIBUTED IN MOST ANIMAL TISSUES EXCEPT BLOOD, LIVER BEING PARTICULARLY
ACTIVE. ... THE RHODANESE MECHANISM IS CAPABLE OF DETOXICATING ONLY LIMITED AMT
OF CYANIDE, SUCH AS ARE FORMED DURING NORMAL METAB. /ANOTHER SULFUR DONOR IS
3-MERCAPTOPYRUVATE. THE ENZYME, MERCAPTOSULFUR TRANSFERASE IS LOCALIZED IN
CYTOSOL./ /CYANIDE/
Salmonella typhimurium strain (OASS positive)
(OASS, O-acetylserine sulfhydrylase) synthesize a toxic but non-mutagenic
metabolite from cyanide and O-acetylserine. Salmonella typhimurium mutant DW379
(OASS deficient) is neither able to carry out this reaction in vitro nor produce
the toxic metabolite in vivo. L-Cysteine reverses the cyanide metabolite
mediated inhibition and thus allows OASS positive strains to grow in medium
containing cyanide and O-acetylserine. The results suggest that the enzyme O-acetylserine
sulfhydrylase catalyzes the reaction of cyanide and O-acetylserine to form the
toxic metabolite. This metabolite from ninhydrin-positive, adheres strongly to
the cation-exchange column, and migrates in thin layer chromatography to an Rf
value similar to that of beta-cyanoalanine.
/ONE OF/ THE MAJOR MECHANISMS FOR REMOVING
CYANIDE FROM THE BODY IS ITS ENZYMATIC CONVERSION, BY THE MITOCHONDRIAL ENZYME
RHODANESE (TRANSSULFURASE), TO THIOCYANATE, WHICH IS RELATIVELY ... /LESS
TOXIC/. /CYANIDE/
FACTORS THAT INCR LIKELIHOOD OF HYDROGEN
CYANIDE POISONING FROM INGESTION OF CYANOGENIC PLANTS INCLUDE: (1) LARGE AMT OF
FREE HYDROGEN CYANIDE & CYANOGENIC GLYCOSIDE IN PLANT, (2) RAPID INGESTION;
(3) INGESTION OF A LARGE AMT OF PLANT, & (4) RUMINAL PH & MICROFLORA
THAT CONTINUE TO HYDROLYZE GLYCOSIDE /SRP: TO RELEASE HYDROGEN CYANIDE/ RAPID
INTAKE OF PLANT ... EQUIV TO ABOUT 4 MG HYDROGEN CYANIDE/KG OF BODY WT IS
CONSIDERED TO BE LETHAL AMOUNT OF PLANT MATERIAL. ... /CYANOGENIC PLANTS/
RUMINANTS ARE MORE SUSCEPTIBLE TO POISONING BY
CYANOGENIC PLANTS /SRP: WHICH RELEASE HYDROGEN CYANIDE/ THAN ARE HORSES &
PIGS ... /CYANOGENIC PLANTS/
Absorption, Distribution & Excretion:
IN 30 DAYS, 72% OF (14)C FROM AN IP DOSE OF
(14)C-CYANIDE TO MICE WAS EXCRETED IN URINE AND FECES, 25% IN EXPIRED AIR AND 3%
WAS RETAINED IN ANIMALS. PEAK EXCRETION OCCURRED WITHIN 10 MIN IN EXPIRED AIR
AND WITHIN 6-24 HR IN URINE AND FECES. /CYANIDE/
CYANIDES ARE RAPIDLY ABSORBED FROM SKIN &
ALL MUCOSAL SURFACES & ARE MOST DANGEROUS WHEN INHALED, BECAUSE TOXIC AMT
ARE ABSORBED THROUGH BRONCHIAL MUCOSA & ALVEOLI. /CYANIDES/
THE CYANIDE ION IS READILY ABSORBED AFTER ORAL
OR PARENTERAL ADMIN. PROLONGED LOCAL CONTACT WITH CYANIDE SOLN ... MAY RESULT IN
ABSORPTION OF TOXIC AMT THROUGH SKIN. PART OF ABSORBED CYANIDE IS EXCRETED
UNCHANGED BY THE LUNG. LARGER PORTION ... IS CONVERTED BY SULFURTRANSFERASE
RELATIVELY NONTOXIC TO THIOCYANATE ION. /CYANIDE/
As estimated in rats given 30 mg sodium
cyanide intraperitoneally over a period of 8 days, 80 percent of the
total cyanide is excreted in the urine in the form of thiocyanate.
Cyanide is distributed to all organs and
tissues via the blood, where its concn in red cells is greater than that in
plasma by a factor of two or three. /Cyanides/
Once absorbed into the body, cyanide can form
complexes with heavy metal ions. /Cyanide/
Acute systemic toxicity of hydrogen cyanide, sodium
cyanide, and potassium cyanide by instillation into the inferior
conjunctival sac was investigated in rabbits. LD50 value of hydrogen cyanide was
0.103 mmol/kg. Signs of toxicity appeared rapidly & death occurred within 3
to 12 min after instillation of cyanide into the conjunctival sac of the rabbit.
Thus, following ocular instillation, cyanides may be absorbed across the
conjunctival blood vessels in amounts sufficient to produce systemic toxicity.
Inhalation of cyanide salt dusts is dangerous
because the cyanide will dissolve on contact with moist mucous membranes and be
absorbed into the bloodstream. /Cyanide salts/
Cyanide is concentrated in red blood cells at
a RBC/plasma ratio is 100/l. The volume of distribution of cyanide ion is
approximately 1.5 l/kg. About 60% if CN- in plasma is protein bound. /Cyanide/
Biological Half-Life:
Half-life for the conversion of cyanide to
thiocyanate from a non-lethal dose in man is between 20 min and 1 hr. /Cyanide/
Mechanism of Action:
CYANIDE HAS A VERY HIGH AFFINITY FOR IRON IN
THE FERRIC STATE. WHEN ABSORBED, /CYANIDE/ ... REACTS READILY WITH TRIVALENT
IRON OF CYTOCHROME OXIDASE IN MITTCHONDRIA; CELLULAR RESPIRATION IS THUS
INHIBITED & CYTOTOXIC HYPOXIA RESULTS. SINCE UTILIZATION OF OXYGEN IS
BLOCKED, VENOUS BLOOD IS OXYGENATED AND IS ALMOST AS BRIGHT RED AS ARTERIAL
BLOOD. RESPIRATION IS STIMULATED BECAUSE CHEMORECEPTIVE CELLS RESPOND AS THEY DO
TO DECREASED OXYGEN. A TRANSIENT STAGE OF CNS STIMULATION WITH HYPERPNEA AND
HEADACHE IS OBSERVED; FINALLY THERE ARE HYPOXIC CONVULSIONS AND DEATH DUE TO
RESPIRATORY ARREST. /CYANIDE/
SINGLE DOSES OF CYANIDE PRODUCE ALTERATIONS IN
PATTERN OF BRAIN METABOLITES CONSISTENT WITH DECR IN OXIDATIVE METABOLISM &
INCR IN GLYCOLYSIS. DECR IN BRAIN GAMMA-AMINOBUTYRIC ACID ... HAVE BEEN ASCRIBED
TO CYANIDE INHIBITION OF GLUTAMIC ACID DECARBOXYLASE. /CYANIDE/
THE CORTICAL GRAY MATTER, HIPPOCAMPUS (H1),
CORPORA STRIATA, & SUBSTANTIA NIGRA ARE COMMONLY AFFECTED. ... CYANIDE ALSO
HAS PROPENSITY FOR DAMAGING WHITE MATTER, PARTICULARLY CORPUS CALLOSUM. CYANIDE
INHIBITS CYTOCHROME OXIDASE & PRODUCES CYTOTOXIC ANOXIA, BUT ALSO CAUSES
HYPOTENSION THROUGH ITS EFFECTS ON HEART. /CYANIDE/
Evoked release of transmitter at the squid
giant synapse was examined under conditions where the calcium ion concentration
in the presynaptic terminal was manipulated by inhibitors of calcium
sequestration. Simultaneous intracellular recordings of presynaptic and
postsynaptic resting action potentials were made during bath application of
various metabolic inhibitors including sodium cyanide. Cyanide
reversibly depressed the post-synaptic potential. The progressive reduction of
post-synaptic potential amplitude was accompanied by a reversible increase in
synaptic delay. The time course of block of the post-synaptic potential was
similar for different agents and dependant on the rate of presynaptic activity
(30-40 min at 0.01 Hz). Recovery of the post-synaptic action potential following
block by cyanide was obtained within 40 min. Synaptic depression by the
metabolic inhibitors does not result from changes in the presynaptic resting or
action potentials, nor from a change in post-synaptic receptor sensitivity. The
post-synaptic response to local ionophoresis of L-glutamate was unchanged
following the inhibition of evoked release of transmitter by cyanide. Injections
of EDTA into presynaptic terminals poisoned by cyanide produced transient
increases in post-synaptic potential amplitude, suggesting that cyanide is
having its effect through raising intracellular calcium rather than lowering
ATP. Control experiments injecting EDTA into unpoisoned nerve terminals showed
no apparent effect on evoked transmitter release.
The effects of carotid body chemoreceptor
stimulation by sodium cyanide on respiration and
phrenic nerve activity were studied in intact and vagotomized rabbits. In intact
animals an intracarotid injection of 30 ug of sodium cyanide resulted
in an elevation of phrenic nerve activity and a rapid onset of respiratory
excitation associated with an increase in respiratory rate and the response was
markedly potentiated after vagotomy. The change in respiratory rate was
primarily due to a decrease in expiration time in intact animals, whereas it
resulted from a pronounced decrease in inspiration time in vagotomized animals.
Apparently, a suppressive effect of the vagus nerve on carotid body
chemoreceptor reflex occurred. An induction of a continuous increase in phrenic
nerve activity accompanied by apneustic respiration by intracarotid dopamine was
another evidence to support the /observation/.
The major detoxification pathway for cyanide
in many species is a biotransformation to the less toxic thiocyanate. Hepatic
thiosulfate: cyanide sulfurtransferase (rhodanese) is the principal enzyme
demonstrating in vitro catalytic activity. Despite the assumed importance of the
hepatic enzyme for cyanide detoxification in vivo, the effects of liver damage
(surgical or chemical) on cyanide lethality in animals have not been examined
previously. Male CD-1 mice pretreated with carbon tetrachloride (CCl4, 1 mg/kg,
ip 24 hr prior to the administration of sodium cyanide. In
other experiments carbon tetrachloride was given in the same doses at both 48 hr
and 24 hr prior to sodium cyanide. Hepatotoxicity was
documented by elevated serum glutamic pyruvic transaminase (SGPT) activity, by
histologic evaluation of the extent of cellular necrosis, by electron microscopy
of the mitochondrial fraction, and by the increased duration of zoxazolamine-induced
paralysis. Lethality was not changed by carbon tetrachloride pretreatments when sodium
cyanide was given alone in doses of 4 or 6 mg/kg or at a dose of 10.7
mg/kg following sodium thiosulfate (sodium sulfide, 1 g/kg, ip). A small but
statistically ... protective effect was exhibited by CCl4 when sodium
cyanide was given at a dose of 16 mg/kg following the administration of
sodium sulfide. Rhodanese activity as measured in mitochrondrial preparations
fractionated from the livers of mice pretreated with carbon tetrachloride was
not different from that in animals given the corn oil vehicle even through
electron micrographs showed extensive mitochondrial damage. No difference in
cyanide lethality was evident between sham-operated mice and partially (2/3)
hepatectomized mice at 24 hr post-surgery. An intact healthy liver does not
appear to be essential for cyanide detoxification in mice whether or not
thiosulfate is also given. Because rhodanese activity was slightly but ...
higher in mitochondria lysed by Triton X-100 than in intact mitochondria, the
mitochondrial membrane may constitute a barrier to sodium sulfide.
Presumably, the accumulation of cyanide in
erythrocytes is a reflection of its binding to methemoglobin.
The cyanide ion (CN-) ... forms complexes with
a number of other chemicals (eg, in tissues) and has a strong affinity for
cobalt. /Cyanide ion/
Human lymphocytes were irradiated by (60)Co
gamma-rays after 0, 10, 20, 35, 45, 48, and 49.5 hr of incubation. Immediately
after irradiation sodium cyanide, sodium fluoride, or
monoiodoacetic acid was given for 2.5 hr. Non irradiated cells were subject to
the same treatments. Chromosomal aberrations were analyzed in metaphase cells of
the first mitosis. When administered alone, all chemicals increased the
frequency of chromatid aberrations. The special analysis showed that these
chemicals were not mutagens in a strict sense, as the observed increase of
aberration frequency was due to inhibition of repair process, which increased
the probability of manifestation of spontaneous changes (so-called "pseudomutagenesis").
The same chemicals increased the frequency of radiation-induced aberrations
during two periods of mitotic cycle, namely, in the end of the G1 stage and in
the G2 stage.
/CYANIDE/ ... REACTS ... WITH TRIVALENT IRON
OF CYTOCHROME OXIDASE IN MITOCHONDRIA TO FORM THE CYTOCHROME OXIDASE-CN COMPLEX
... THE CYTOCHROME-OXIDASE-CN COMPLEX IS DISSOCIABLE; THE MITOCHONDRIAL ENZYME
SULFURTRANSFERASE ... MEDIATES TRANSFER OF SULFUR FROM THIOSULFATE TO CYANIDE
ION. THUS, THIOCYANATE IS FORMED ... KINETIC STUDIES INDICATE THAT THE CLEAVAGE
OF THE THIOSULFATE SULFUR-SULFUR BOND IS THE RATE-LIMITING STEP IN THIS
REACTION. RELATIVELY MINOR PATHWAYS INCL COMBINATION WITH CYSTINE TO FORM
2-IMINO-THIAZOLIDINE-4-CARBOXYLIC ACID, OXIDATION TO CARBON DIOXIDE &
FORMATE, & FORMATION OF CYANOCOBALAMIN. /CYANIDE/
Interactions:
FASTED MONGREL DOGS WERE SUBJECTED TO SODIUM
THIOSULFATE INFUSION FOLLOWED BY SODIUM CYANIDE ADMIN
(1 MG/KG) 30 MIN LATER. A PHARMACOKINETIC MODEL SHOWED THAT SODIUM THIOSULFATE
INCREASED THE RATE OF CONVERSION OF CYANIDE TO THIOCYANATE BY A FACTOR OF 36.5;
ALSO, IT REDUCED THE APPARENT VOLUME OF DISTRIBUTION OF CYANIDE.
ATTEMPTS WERE MADE TO EVALUATE THE EFFECTS OF
PRETREATMENT WITH AIR AND OXYGEN EITHER ALONE OR IN VARIOUS COMBINATIONS WITH
SODIUM NITRITE AND/OR SODIUM THIOSULFATE ON THE PHYSIOLOGIC DISPOSITION OF
SODIUM (14)C-CYANIDE IN MICE. OXYGEN EITHER ALONE OR IN COMBINATION WITH SODIUM
THIOSULFATE ... ENHANCED THE RESPIRATORY EXCRETION WHEN COMPARED WITH AIR.
SODIUM THIOSULFATE ACCELERATED THE INITIAL RATE, BUT NOT THE TOTAL AMOUNT OF
RADIOACTIVITY EXCRETED. THE CUMULATIVE RECOVERY OF RADIOACTIVE GASES WAS ...
GREATER WITH GROUPS RECEIVING OXYGEN EITHER ALONE OR WITH SODIUM THIOSULFATE. NO
SIGNIFICANT DIFFERENCES BETWEEN VARIOUS EXPERIMENTAL GROUPS WERE NOTED IN THE
TOTAL AMOUNT OF URINARY RADIOACTIVITY EXCRETED OR THE TOTAL BODY RETENTION OF
RADIOACTIVITY.
Previous reports indicated that prophylactic
protection against cyanide intoxication in mice can be enhanced by
administration of chlorpromazine when it is given with sodium thiosulfate. The
mechanism of potentiation of sodium thiosulfate by chlorpromazine was studied
alone and in combination with sodium nitrite. Although chlorpromazine was found
to induce a hypothermic response, the mechanism of enhancement of the antagonism
of cyanide by chlorpromazine does not correlate with the hypothermia produced.
Various other possible mechanisms were investigated, such as rate of
methemoglobin formation, enzymatic activity of rhodanese and cytochrome oxidase,
and alpha-adrenergic blockade. The alpha-adrenergic blocking properties of
chlorpromazine may provide a basis for its antidotal effect, since this
protective effect can be reversed with an alpha-antagonist, methoxamine.
/Cyanide/
The effects of tribuyltin and sodium
cyanide on hemolysis in human erythrocytes are described. Tributyltin has
a sharp cut take off concentration for induction of hemolysis. A 5 uM
concentration of tributyltin induces hemolysis and 1 uM or less does not in
erythrocyte suspensions with lysis are sigmoidal indicating a complex molecular
mechanism leading to lysis. Ten mM sodium cyanide plus
1 uM tributyltin does not stimulate hemolysis rates above levels observed with
10 mM sodium cyanide alone. Five nM sodium
cyanide plus hemolytic concentrations of tributyltin stimulates hemolysis
rates synergistically compared with either cyanide or tributyltin alone.
Ultrastructurally, hemolytic concentrations of tribuyltin can be visualized in
the electron microscope by osmium staining during fixation as electron dense
spheres penetrating the lipid bilayer of the erythrocyte plasma membrane. Ten mM
sodium cyanide plus 25 uM tributyltin increases
slightly the size of osmiophilic structures in erythrocyte membranes compared
with those spheres seen in cells exposed to 25 uM tribuyltin alone. Sodium
cyanide is the only compound tested that stimulates tributyltin induced
hemolysis.
Pharmacology:
Interactions:
FASTED MONGREL DOGS WERE SUBJECTED TO SODIUM
THIOSULFATE INFUSION FOLLOWED BY SODIUM CYANIDE ADMIN
(1 MG/KG) 30 MIN LATER. A PHARMACOKINETIC MODEL SHOWED THAT SODIUM THIOSULFATE
INCREASED THE RATE OF CONVERSION OF CYANIDE TO THIOCYANATE BY A FACTOR OF 36.5;
ALSO, IT REDUCED THE APPARENT VOLUME OF DISTRIBUTION OF CYANIDE.
ATTEMPTS WERE MADE TO EVALUATE THE EFFECTS OF
PRETREATMENT WITH AIR AND OXYGEN EITHER ALONE OR IN VARIOUS COMBINATIONS WITH
SODIUM NITRITE AND/OR SODIUM THIOSULFATE ON THE PHYSIOLOGIC DISPOSITION OF
SODIUM (14)C-CYANIDE IN MICE. OXYGEN EITHER ALONE OR IN COMBINATION WITH SODIUM
THIOSULFATE ... ENHANCED THE RESPIRATORY EXCRETION WHEN COMPARED WITH AIR.
SODIUM THIOSULFATE ACCELERATED THE INITIAL RATE, BUT NOT THE TOTAL AMOUNT OF
RADIOACTIVITY EXCRETED. THE CUMULATIVE RECOVERY OF RADIOACTIVE GASES WAS ...
GREATER WITH GROUPS RECEIVING OXYGEN EITHER ALONE OR WITH SODIUM THIOSULFATE. NO
SIGNIFICANT DIFFERENCES BETWEEN VARIOUS EXPERIMENTAL GROUPS WERE NOTED IN THE
TOTAL AMOUNT OF URINARY RADIOACTIVITY EXCRETED OR THE TOTAL BODY RETENTION OF
RADIOACTIVITY.
Previous reports indicated that prophylactic
protection against cyanide intoxication in mice can be enhanced by
administration of chlorpromazine when it is given with sodium thiosulfate. The
mechanism of potentiation of sodium thiosulfate by chlorpromazine was studied
alone and in combination with sodium nitrite. Although chlorpromazine was found
to induce a hypothermic response, the mechanism of enhancement of the antagonism
of cyanide by chlorpromazine does not correlate with the hypothermia produced.
Various other possible mechanisms were investigated, such as rate of
methemoglobin formation, enzymatic activity of rhodanese and cytochrome oxidase,
and alpha-adrenergic blockade. The alpha-adrenergic blocking properties of
chlorpromazine may provide a basis for its antidotal effect, since this
protective effect can be reversed with an alpha-antagonist, methoxamine.
/Cyanide/
The effects of tribuyltin and sodium
cyanide on hemolysis in human erythrocytes are described. Tributyltin has
a sharp cut take off concentration for induction of hemolysis. A 5 uM
concentration of tributyltin induces hemolysis and 1 uM or less does not in
erythrocyte suspensions with lysis are sigmoidal indicating a complex molecular
mechanism leading to lysis. Ten mM sodium cyanide plus
1 uM tributyltin does not stimulate hemolysis rates above levels observed with
10 mM sodium cyanide alone. Five nM sodium
cyanide plus hemolytic concentrations of tributyltin stimulates hemolysis
rates synergistically compared with either cyanide or tributyltin alone.
Ultrastructurally, hemolytic concentrations of tribuyltin can be visualized in
the electron microscope by osmium staining during fixation as electron dense
spheres penetrating the lipid bilayer of the erythrocyte plasma membrane. Ten mM
sodium cyanide plus 25 uM tributyltin increases
slightly the size of osmiophilic structures in erythrocyte membranes compared
with those spheres seen in cells exposed to 25 uM tribuyltin alone. Sodium
cyanide is the only compound tested that stimulates tributyltin induced
hemolysis.
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
/IN ELECTROPLATING/ ... SODIUM BATH CONTAINS SODIUM
CYANIDE ... ...
... SYMPTOMS OF CHRONIC DISEASE ... REPORTED
IN ELECTROPLATERS & SILVER POLISHERS AFTER SEVERAL YEARS OF EXPOSURE.
/CYANIDES/
AMONG FUMIGATORS ... CYANIDE POISONING IS
RECOGNIZED ... /CYANIDES/
DERMATITIS ... IN WORKERS CHRONICALLY EXPOSED
TO CYANIDE SOLN. ELECTROPLATERS SUFFER FROM SUCH IRRITATION. /CYANIDE SOLN/
Body Burden:
Cyanide is present in normal healthy human
organs at concentrations ranging up to 0.5 mg/kg. /Cyanide/
Natural Pollution Sources:
In bacteria, cyanide production has been
observed in Chromobacterium violaceum and certain species of Pseudomonas.
/Cyanide/
Artificial Pollution Sources:
Material containing cyanide compounds disposed
of on land may lead to elevated levels of cyanide in underlying strata and in
groundwater. /Cyanides/
Environmental Fate:
Aquatic Fate: The alkali metal salts are very
soluble in water, and as a result, they readily dissociate into their respective
anions and cations upon release to water. The resulting cyanide ion may then
form hydrogen cyanide or react with various metals present in natural water. If
the cyanide ion is present in excess, complex metallocyanides may form; however,
if metals are prevalent, simple metal cyanides may form.
Environmental Standards & Regulations:
FIFRA Requirements:
As the federal pesticide law FIFRA directs,
EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their future use.
Under this pesticide reregistration program, EPA examines health and safety data
for pesticide active ingredients initially registered before November 1, 1984,
and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act
of 1996. Pesticides for which EPA had not issued Registration Standards prior to
the effective date of FIFRA 1988 were divided into three lists based upon their
potential for human exposure and other factors, with List B containing
pesticides of greater concern and List D pesticides of less concern. Sodium
cyanide is found on List C. Case No: 3086; Pesticide type: rodenticide;
Case Status: Reregistration Eligibility Decision Approved 9/94, PB95-173514 -
OPP has made a decision that some/all uses of the pesticide are eligible for
reregistration, as reflected in a Reregistration Eligibility Decision (RED)
document.; Active ingredient (AI): sodium cyanide; Data
Call-in (DCI) Date(s): 9/30/92; AI Status: Reregistration Eligibility Decision
Completed - OPP has completed a Reregistration Eligibility document for the
case/AI.
TSCA Requirements:
Section 8(a) of TSCA requires manufacturers of
this chemical substance to report preliminary assessment information concerned
with production, use, and exposure to EPA as cited in the preamble in 51 FR
41329.
Pursuant to section 8(d) of TSCA, EPA
promulgated a model Health and Safety Data Reporting Rule. The section 8(d)
model rule requires manufacturers, importers, and processors of listed chemical
substances and mixtures to submit to EPA copies and lists of unpublished health
and safety studies. Sodium cyanide is included on this
list.
Manufacturers and processors of sodium
cyanide are required to conduct chemical fate and terrestrial effects
tests under TSCA section 4.
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
Releases of CERCLA hazardous substances are
subject to the release reporting requirement of CERCLA section 103, codified at
40 CFR part 302, in addition to the requirements of 40 CFR part 355. Sodium
cyanide is an extremely hazardous substance (EHS) subject to reporting
requirements when stored in amounts in excess of its threshold planning quantity
(TPQ) of 100 lbs.
RCRA Requirements:
P106; As stipulated in 40 CFR 261.33, when sodium
cyanide, as a commercial chemical product or manufacturing chemical
intermediate or an off-specification commercial chemical product or a
manufacturing chemical intermediate, becomes a waste, it must be managed
according to federal and/or state hazardous waste regulations. Also defined as a
hazardous waste is any container or inner liner used to hold this waste or any
residue, contaminated soil, water, or other debris resulting from the cleanup of
a spill, into water or on dry land, of this waste. Generators of small
quantities of this waste may qualify for partial exclusion from hazardous waste
regulations (40 CFR 261.5(e)).
/SRP:/ D003; A solid waste containing sodium
cyanide may become characterized as a hazardous waste when subjected to
testing for reactivity as stipulated in 40 CFR 261.23, and if so characterized,
must be managed as a hazardous waste.
Clean Water Act Requirements:
Sodium cyanide is
designated as a hazardous substance under section 311(b)(2)(A) of the Federal
Water Pollution Control Act and further regulated by the Clean Water Act
Amendments of 1977 and 1978. These regulations apply to discharges of this
substance. This designation includes any isomers and hydrates, as well as any
solutions and mixtures containing this substance.
Federal Drinking Water Standards:
EPA 200 ug/l /Cyanide ion/
Federal Drinking Water Guidelines:
EPA 200 ug/l /Cyanide ion/
State Drinking Water Guidelines:
(AZ) ARIZONA 220 ug/l /Cyanide ion/
(ME) MAINE 154 ug/l /Cyanide ion/
(MN) MINNESOTA 100 ug/l /Cyanide ion/
Chemical/Physical Properties:
Molecular Formula:
C-N-Na
Molecular Weight:
49.0
Color/Form:
White cubic crystals
WHITE SOLID IN FORM OF GRANULES, FLAKES, OR
EGGS (RESEMBLING CHICKEN EGGS)
White, granular or crystalline solid.
Odor:
Odorless when perfectly dry, emits odor of
hydrogen cyanide when damp
Faint odor of bitter almonds
Faint almond-like odor.
Boiling Point:
1496 deg C
Melting Point:
563 deg C
Corrosivity:
Corrosive to aluminum.
Density/Specific Gravity:
1.595 g/cu cm @ 20 deg C
Heat of Vaporization:
3041 J/g
pH:
Aq soln strongly alkaline
Solubilities:
48 G/100 CC WATER @ 10 DEG C
82 G/100 CC WATER @ 35 DEG C
Slightly sol in alcohol
Spectral Properties:
INDEX OF REFRACTION: 1.452
Vapor Pressure:
1 mm Hg @ 817 deg C; 10 mm Hg @ 983 deg C
Viscosity:
4 cP @ 30 deg C (26% aqueous soln)
Other Chemical/Physical Properties:
Soln readily dissolves gold and silver in
presence of air
DELIQUESCES
Absorbs water from the air forming a syrup
Heat of capacity: 1.40 @ 25-72 deg C; heat of
fusion: 179 J/g; heat of formation: -89.9X10+3 J/mole (exothermic); heat of
solution: -1548 J/mole; hydrolysis constant: 2.51X10-5 @ 25 deg C
When heated in a dry carbon dioxide
atmosphere, sodium cyanide fuses without much
decomposition. Thermal dissociation of sodium cyanide has
been studied in an atm of helium at 600-1050 deg C and in an atm of nitrogen at
1050-1255 deg C. It has been shown that vapor phase over melt contains
decomposition products.
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: TOXIC; inhalation, ingestion or
contact (skin, eyes) with vapors, dusts or substance may cause severe injury,
burns, or death. Reaction with water or moist air will release toxic, corrosive
or flammable gases. Reaction with water may generate much heat which will
increase the concentration of fumes in the air. Fire will produce irritating,
corrosive and/or toxic gases. Runoff from fire control or dilution water may be
corrosive and/or toxic and cause pollution.
Fire or explosion: Non-combustible, substance
itself does not burn but may decompose upon heating to produce corrosive and/or
toxic fumes. Vapors may accumulate in confined areas (basement, tanks,
hopper/tank cars etc.). Substance will react with water (some violently),
releasing corrosive and/or toxic gases. Reaction with water may generate much
heat which will increase the concentration of fumes in the air. Contact with
metals may evolve flammable hydrogen gas. Containers may explode when heated or
contaminated with water.
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 50 to
100 meters (160 to 330 feet) in all directions. Keep unauthorized personnel
away. Stay upwind. Keep out of low areas. Ventilate enclosed areas.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. Structural firefighters'
protective clothing is recommended for fire situations ONLY; it is not effective
in spill situations.
Evacuation: Spill: Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: Note: Most foams will react with the
material and release corrosive/toxic gases. Small fires: CO2 (except for
Cyanides), dry chemical, dry sand, alcohol-resistant foam. Large fires: Water
spray, fog or alcohol-resistant foam. Move containers from fire area if you can
do it without risk. Do not use straight streams. Dike fire control water for
later disposal; do not scatter the material. Fire involving tanks or car/trailer
loads: Fight fire from maximum distance or use unmanned hose holders or monitor
nozzles. Do not get water inside containers. Cool containers with flooding
quantities of water until well after fire is out. Withdraw immediately in case
of rising sound from venting safety devices or discoloration of tank. ALWAYS
stay away from the ends of tanks.
Spill or leak: ELIMINATE all ignition sources
(no smoking, flares, sparks or flames in immediate area). All equipment used
when handling the product must be grounded. Do not touch damaged containers or
spilled material unless wearing appropriate protective clothing. Stop leak if
you can do it without risk. A vapor suppressing foam may be used to reduce
vapors. DO NOT GET WATER INSIDE CONTAINERS. Use water spray to reduce vapors or
divert vapor cloud drift. Prevent entry into waterways, sewers, basements or
confined areas. Small spills: Cover with DRY earth, DRY sand, or other
non-combustible material followed with plastic sheet to minimize spreading or
contact with rain. Use clean non-sparking tools to collect material and place it
into loosely covered plastic containers for later disposal.
First aid: Move victim to fresh air. Call
emergency medical care. Apply artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance;
induce artificial respiration with the aid of a pocket mask equipped with a
one-way valve or other proper respiratory medical device. Administer oxygen if
breathing is difficult. Remove and isolate contaminated clothing and shoes. In
case of contact with substance, immediately flush skin or eyes with running
water for at least 20 minutes. For minor skin contact, avoid spreading material
on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation,
ingestion or skin contact) to substance may be delayed. Ensure that medical
personnel are aware of the material(s) involved, and take precautions to protect
themselves.
List of Dangerous Water-Reactive Materials:
Materials Which Create Large Amounts of Toxic (PIH) Vapor When Spilled in Water
(Dangerous From 0.5 to 10 km (0.3 to 6.0 miles) Downwind) Name of Material: Sodium
cyanide, Toxic Vapor (PIH) Produced: hydrogen cyanide.
If material involved in fire: Extinguish fire
using agent suitable for type of surrounding fire. (Material itself does not
burn or burns with difficulty.) Use water in flooding quantities as fog. Cool
all affected containers with flooding quantities of water. Use foam, dry
chemical, or carbon dioxide. Use water spray to knock-down vapors.
Skin, Eye and Respiratory Irritations:
Irritating to skin, eyes, and respiratory
system.
NFPA Hazard Classification:
Health: 3. 3= Materials that, on short
exposure, could cause serious temporary or residual injury, including those
requiring protection from all bodily contact. Fire fighters may enter the area
only if they are protected from all contact with the material. Full protective
clothing, including self-contained breathing apparatus, coat, pants, gloves,
boots, and bands around legs, arms, and waist, should be provided. No skin
surface should be exposed.
Flammability: 0. 0= This degree includes any
material that will not burn.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Fire Fighting Procedures:
Carbon dioxide fire extinguishers must not be
used where cyanide salts are present. /Cyanide salts/
Wear chemical protective suit with
self-contained breathing apparatus.
Avoid carbon dioxide extinguishers. Extinguish
fire using agent suitable for surrounding fire. Use water spray to keep
fire-exposed containers cool.
If material involved in fire: Extinguish fire
using agent suitable for type of surrounding fire. (Material itself does not
burn or burns with difficulty.) Use water in flooding quantities as fog. Cool
all affected containers with flooding quantities of water. Use foam, dry
chemical, or carbon dioxide. Use water spray to knock-down vapors. /Sodium
cyanide solution/
If material involved in fire: Extinguish fire
using agent suitable for type of surrounding fire. (Material itself does not
burn or burns with difficulty.) Use foam, dry chemical, or carbon dioxide. Do
not use water on material itself. If large quantities of combustibles are
involved, use water in flooding quantities as spray and fog. Use water spray to
knock-down vapors. /Sodium cyandie, solid/
Toxic Combustion Products:
Toxic oxides of nitrogen are produced in fires
involving this material. /Sodium cyanide solution; sodium
cyanide, solid/
Firefighting Hazards:
Not combustible, but if involved in a fire
decomposes to produce hydrogen cyanide & oxides of nitrogen.
Explosive Limits & Potential:
Explodes if melted with nitrite or chlorate at
about 450 deg C.
Hazardous Reactivities & Incompatibilities:
Violent reaction with fluorine /gas/,
magnesium, nitrates, nitric acid ...
Hydrogen cyanide and mercury (II) cyanide: The
cyanide, /mercury(II) cyanide/, is a friction-and impact-sensitive explosive and
may initiate detonation of liquid hydrogen cyanide. Other metal cyanides are
similar. /Metal cyanides/
Dangerous; on contact with acid, acid fumes,
water, or steam ... will produce toxic and flammable vapors of CN- and sodium
oxide.
Cyanide may react with carbon dioxide in
ordinary air to form toxic hydrogen cyanide gas. /Cyanide/
Fusion of mixtures of metal cyanides with
metal chlorates, perchlorates, or nitrates ... causes a violent explosion.
/Metal cyanides/
Contact with acids and acid salts causes
immediate formation of toxic and flammable hydrogen cyanide gas. ... /Cyanides/
Strong oxidizers (such as acids, acid salts,
chlorates & nitrates) [Note: Absorbs moisture from the air forming a syrup].
Hazardous Decomposition:
... If involved in a fire decomposes to
produce hydrogen cyanide and oxides of nitrogen.
Immediately Dangerous to Life or Health:
25 mg/cu m (as CN)
Protective Equipment & Clothing:
WHERE SKIN CAN BE EXPOSED ... PROTECTIVE
CLOTHING, INCLUDING IMPERVIOUS HAND PROTECTION SHOULD BE PROVIDED. ...
/CYANIDES/
Wear special protective clothing and positive
pressure self-contained breathing apparatus.
Respirator Selection: Less than or equal to 25
mg/cu m: (1) Filter type respirators, approved for toxic dust, with half-mask
(not applicable for calcium cyanide). (2) Chemical cartridge respirators with
replaceable cartridge for toxic dusts and acid gases; With half-mask. Maximum
service life 4 hr. Less than or equal to 50 mg/cu m: (1) Full-face gas mask,
chest or back mounted type, with industrial size canister for toxic dust and
hydrocyanic acid gas. Maximum service life 2 hr. (2) Type C supplied
air-respirator, continuous-flow or pressure-demand type (positive pressure) with
full facepiece. (3) Type A supplied-air respirator, (hose mask with blower) with
full facepiece. Greater than 50 mg/cu m: (1) Self-contained breathing apparatus
with positive pressure in full facepiece. (2) Combination supplied-air
respirator pressure-demand type with auxiliary self-contained air supply.
Emergency (no concentration limit): (1) Self-contained breathing apparatus with
positive pressure in facepiece. (2) Combination supplied-air respirator,
pressure-demand type, with auxiliary self-contained air supply. Evacuation or
Escape (no concentration limit): (1) Self-contained breathing apparatus in
demand or pressure-demand mode (negative or positive pressure). (2) Full-face
gas mask, front or back mount type with industrial size canister for toxic dust
and hydrocyanic acid gas. /Cyanide salts/
Chemical safety goggles shall be worn by
employees engaged in any operation wherein there is danger or likelihood that
dusts or solutions of cyanide salts will come into contact with the eye.
Full-length face shields with forehead protection shall be worn by employees
engaged in any operation wherein there is danger or likelihood that dusts,
molten salts, or solutions of cyanide salts may contact the face. /Cyanide
salts/
... Rubber gloves /should be worn/ when
handling cyanide solutions ...
Wear appropriate personal protective clothing
to prevent skin contact.
Wear appropriate eye protection to prevent eye
contact.
Eyewash fountains should be provided in areas
where there is any possibility that workers could be exposed to the substance;
this is irrespective of the recommendation involving the wearing of eye
protection.
Facilities for quickly drenching the body
should be provided within the immediate work area for emergency use where there
is a possibility of exposure. [Note: It is intended that these facilities
provide a sufficient quantity or flow of water to quickly remove the substance
from any body areas likely to be exposed. The actual determination of what
constitutes an adequate quick drench facility depends on the specific
circumstances. In certain instances, a deluge shower should be readily
available, whereas in others, the availability of water from a sink or hose
could be considered adequate.]
Recommendations for respirator selection. Max
concn for use: 25 mg/cu m. Respirator Class(es): Any supplied-air respirator.
Any self-contained breathing apparatus with a full facepiece.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive pressure mode.
Any supplied-air respirator that has a full face piece and is operated in
pressure-demand or other positive pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other positive
pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a
chin-style, front- or back-mounted canister /SRP: rebreather or oxygen
generating/ providing protection against the compound of concern and having a
high-efficiency particulate filter. Any appropriate escape-type, self-contained
breathing apparatus.
Preventive Measures:
If material not involved in fire: Keep sparks,
flames, and other sources of ignition away. Keep material out of water sources
and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if
without undue personnel hazard. Use water spray to knock-down vapors. /Sodium
cyanide solution/
If material not involved in fire: Keep sparks,
flames, and other sources of ignition away. Keep material out of water sources
and sewers. Use water spray to knock-down vapors. Do not use water on material
itself. /Sodium cyanide, solid/
Personnel protection: ... If contact with the
material anticipated, wear appropriate chemical protective clothing. /Sodium
cyanide, solid/
Personnel protection: Avoid breathing vapors.
Keep upwind. ... Avoid bodily contact with the material. ... Do not handle
broken packages unless wearing appropriate personal protective equipment. Wash
away any material which may have contacted the body with copious amounts of
water or soap and water. /Sodium cyanide solution; sodium
cyanide, solid/
When cyanide salts are used in fused salt
baths, mechanical local exhaust ventilation should be provided to control any
cyanide emissions. /Cyanide salts/
Eyewash facilities and emergency showers shall
be provided in areas where contact with ... cyanide salts as either solids or
solutions is likely. Work clothing which has been contaminated by absorption of,
or contact with, cyanide shall be thoroughly laundered before it is worn again.
/Hydrogen cyanide and cyanide salts/
If the clothing is to be laundered or
otherwise cleaned to remove the cyanide, the person performing the operation
should be informed of cyanide's hazardous properties. /Cyanides/
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers.
PERSONS WHO WORK WITH & AROUND CYANIDE
PREPN SHOULD BE GIVEN SPECIFIC DETAILED INSTRUCTIONS ON MANAGEMENT OF CYANIDE
POISONING. /CYANIDES/
Food storage, preparation, and eating shall be
prohibited in areas where HCN is used. Smoking and the carrying of tobacco and
other smoking materials shall also be prohibited in these areas. Clean and
sanitary lunchroom facilities, if provided, must be in non-exposure areas. ...
Clothing-change and locker-room facilities shall be provided in a non-exposure
area. Workers should be encouraged to shower after work and to change work
clothing frequently. Showers and basin washing facilities shall be located in
the locker-room area. /Hydrogen cyanide or cyanide salts/
ATTENTION TO ... VENTILATION IS NECESSARY. ...
BECAUSE OF THE LOW PERMISSIBLE EXPOSURE LEVEL ... COMPLETE ENCLOSURE OF PROCESS
IS RECOMMENDED. ... THOSE WORKING WITH CYANIDE SALTS SHOULD BE INSTRUCTED THAT
CONTACT WITH ACIDS WILL RELEASE HYDROGEN CYANIDE. WHERE EXPOSURE POTENTIAL
EXISTS, WORKERS SHOULD BE TRAINED TO RECOGNIZE THE ODOR OF HYDROGEN CYANIDE
& WHEN ... DETECTED, WORK AREA SHOULD BE EVACUATED IMMEDIATELY. /CYANIDES/
Contact lenses should not be worn when working
with this chemical.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet or
significantly contaminated should be removed and replaced.
Workers whose clothing may have become
contaminated should change into uncontaminated clothing before leaving the work
premises.
ALL CONTAINERS ... SHOULD BE KEPT COVERED OR
IN EXHAUSTED HOOD WHEN NOT IN USE. ANY PROCESS THAT MAY RELEASE HYDROGEN CYANIDE
SHOULD BE MECHANICALLY EXHAUSTED, WITH PROVISION FOR HIGHER RATE DURING
EMERGENCIES. DIRECT READING INSTRUMENTS FOR DETERMINATION OF HYDROCYANIC ACID
ARE AVAILABLE. /CYANIDES/
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
Two physician's treatment kits shall be
immediately available to trained medical personnel at each plant where there is
a potential for the release of, accidental or otherwise, or for contact with,
hydrogen cyanide or cyanide salts. ... First-aid kits shall be immediately
available at workplaces where there is potential for the release, accidental or
otherwise, of hydrogen cyanide or a potential for exposure to cyanide salts. ...
Pertinent medical records shall be maintained ... /SRP: for the duraton of
employment plus 50 years [29 CFR 1910.1020]/ following the last exposure to
hydrogen cyanide or cyanide salts. /Hydrogen cyanide and cyanide salts/
Stability/Shelf Life:
AQ SOLN ... RAPIDLY DECOMPOSES ON STANDING.
Aqueous solutions of sodium
cyanide are slightly hydrolyzed (Kh= 2.5X10-5) at ordinary temperatures
to produce hydrogen cyanide.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
Storage Conditions:
Store in a cool, dry, well-ventilated
location. Separate from water, acids, carbon dioxide.
Cyanide salts as solids must be stored in
sealed or tightly closed containers. No hooks should be used in handling cyanide
containers. ... Storage areas must be adequately ventilated to ensure that
cyanide concentrations do not exceed the recommended workplace environmental
limits. /Cyanide salts/
ALL CONTAINERS OF CYANIDE SALTS SHOULD BE KEPT
COVERED OR IN EXHAUST HOOD WHEN NOT IN USE. /CYANIDES/
Cyanide salts as solids or solutions must be
... protected from corrosion or damage. They should be stored so there is no
contact with nitrate-nitrite mixtures or peroxides. /Cyanide salts/
Cleanup Methods:
WASTE CYANIDE SALTS FROM CASE HARDENING OF
STEEL ARE DESTROYED BY REACTING THE SALTS AT 650-700 DEG C WITH WASTE FERRIC
HYDROXIDE SLUDGES FROM VARIOUS SOURCES. /CYANIDE SALTS/
Environmental considerations - Land spill: Dig
a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP:
If time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Cover solids with a plastic
sheet to prevent dissolving in rain or fire fighting water. /Sodium
cyanide, solid/
Environmental considerations - Land spill: Dig
a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP:
If time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Dike surface flow using
soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid
with fly ash or cement powder. Cover solids with a plastic sheet to prevent
dissolving in rain or fire fighting water. /Sodium cyanide solution/
Environmental considerations - Air spill:
Apply water spray or mist to knock down vapors. Vapor knock down water is
corrosive or toxic and should be diked for containment. /Sodium
cyanide solution; sodium cyanide, solid/
Environmental considerations - Water spill:
Add dilute caustic soda (sodium hydroxide). Add calcium hypochlorite ... Adjust
pH to neutral (pH= 7). /Sodium cyanide solution; sodium
cyanide, solid/
Spills of sodium cyanide ...
solids may be shoveled carefully into containers, with care being taken
that cyanide dust is not dispersed into the air. The residue after shoveling, or
small spills, may be removed by dry vacuuming or flushing with a liberal
quantity of water.
The electrodialysis through polyethylene
membranes is used by the Legrand Copper Plating Co at Limoges, France to recover
3000 kg copper and 3400 kg sodium cyanide annually from
wastewaters.
If cyanide is spilled ... 1. Ventilate area of
spill. 2. Collect spilled material in the most convenient and safe manner for
reclamation or for treatment in a cyanide disposal system.
POON CP C; MANAGE CONTROL HEAVY MET ENVIRON,
INT CONF 572-75 (1979)] REMOVAL OF COPPER, NICKEL, ZINC, CADMIUM AND CYANIDE
FROM PLATING WASTEWATER BY ELECTROFLOTATION IS DISCUSSED. /CYANIDES/
Keep water away from release. Avoid contact
with dust, mist, or solution. Do not create dust. Prompt cleanup and removal are
necessary. Shovel into suitable dry container. Control runoff and isolate
discharged material for proper disposal.
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number D003; P106,
must conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Cyanide salts should not be flushed into any
drain which may contain or subsequently receive acid waste. ... Cyanide process
waste solutions and flushings from spills should be passed through a cyanide
waste disposal system. /Cyanide salts/
Sodium cyanide is a
poor candidate for incineration.
SMALL AMOUNTS OF AMMONIUM CHLORIDE-BUFFERED,
AQUEOUS SODIUM CYANIDE WERE DECONTAMINATED WITH CALCIUM
HYPOCHLORITE AT LESS THAN OR EQUAL TO 12 DEGREES, WHILE LARGER AMOUNTS OF
CYANIDE WASTE WERE TREATED WITH HYPOCHLORITE FROM ANY SOURCE AT PH 10 TO CONVERT
CYANIDE ION TO CYANATE ION.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time-Weighted Avg: 5 mg/cu m). Skin Designation. /Cyanides, as CN/
Threshold Limit Values:
Ceiling limit 5 mg/cu m, skin
NIOSH Recommendations:
Recommended Exposure Limit: 10 Min Ceiling
Value: 4.7 ppm (5 mg/cu m).
Immediately Dangerous to Life or Health:
25 mg/cu m (as CN)
Other Occupational Permissible Levels:
Inorganic cyanide standards: Bulgaria 0.3
mg/cu m; Czechoslovakia 3-15 mg/cu m; Finland 7 mg/cu m; Federal Republic of
Germany 5 mg/cu m; Hungary 0.3 mg/cu m; Poland 0.3 mg/cu m; Romania 0.3 mg/cu m;
USSR 0.3 mg/cu m; and Yugoslavia 5 mg/cu m. /Calcium, potassium, sodium,
Cyanide salts/
Manufacturing/Use Information:
Major Uses:
/Former use/ Fumigating citrus and other fruit
trees, ships, railway cars, warehouses
/FORMER USE/ AS RODENTICIDE
Cleaning metals; mfr of dyes and pigments,
nylon int, chelating cmpd; extracting gold and silver from ores.
For rabbit, rat burrows and holes; termite
nests
COMPONENT OF ELECTROPLATING SOLUTIONS, EG, FOR
ZINC; COMPONENT OF SALTS FOR CASE HARDENING OF STEEL; AGENT FOR EXTRACTION OF
GOLD & SILVER FROM ORES; DEPRESSANT IN FROTH FLOTATION SEPARATION OF ORES;
CHEM INT FOR PHENYLGLYCINE
Manufacture of hydrocyanic acid and many other
cyanides
Chemical uses are in 5 general categories:
dyes, including optical brighteners; agricultural chemicals; pharmaceuticals;
chelating or sequestering agents; and specialties, preparation of nitriles,
carbylamines, cyano fatty acids, and heavy metal cyanides, misc uses include
heat-treating, metal stripping, and compounds for clearing smut
Used as a single and multidose poison on
pastures, range land, and forest lands for coyote, fox and wild dog. /M-44
cyanide capsules/
Used as an insecticide and miticide for
postharvest application for non-stored commodity of citrus or fumigation of
trucks (feed/food-full). /Sodium cyanide, crystalline/
Manufacturers:
Cyanco Co., P.O. Box 1999, Winnemucca, NV
89446 (702)623-1214; Production site: Winnemucca, NV 89446
Degussa-Huls, Corp., 65 Challenger Rd.,
Ridgefield Park, NJ 07660, (201)641-6100; Production site: Theodore, AL 36590
DuPont, Hq, 1007 Market St., Wilmington, DE
19898, (302)774-1000; DuPont Specialty Chemicals, DuPont Performance, Specialty,
and Fine Chemicals; Production site: Memphis, TN 38127
FMC Corp., 200 East Randolph Dr., Chicago, IL
60601, (312)861-6000; Chemical Products Group; Alkali Chemicals Division;
Production site: Green River, WY
Sterling Chemicals, Inc., Hq, 1200 Smith St.,
Suite 1800, Houston, TX 77002, (713) 650-3700; Production site: Texas City, TX
77590
Methods of Manufacturing:
Sodium cyanide can be
prepared by heating sodium amide with carbon, by melting sodium chloride and
calcium cyanamide together in an electric furnace ...
Molten sodium, ammonia and charcoal react to
give a high grade (98%) sodium cyanide
General Manufacturing Information:
U.S.: For use only by trained persons with
permit or license.
Formulations/Preparations:
Powder
Grades: 30% soln; 73-75%; 96-98%; reagent;
technical; briquettes granular.
The cyanide of commerce is 95-98% pure.
Mixtures of sodium cyanide with
sodium chloride or carbonate for special uses are also marketed.
M-44 cyanide capsules; Pelletted/tabletted;
88.78% sodium cyanide (74002)
Sodium cyanide; crystalline;
99% sodium cyanide (74002)
U. S. Production:
(1977) AT LEAST 1.14X10+11 G
U. S. Imports:
(1978) 7.01X10+9 G
(1982) 7.45X10+9 G
(1985) 8.32X10+9 g
(1986) 2.77x10+7 lb
U. S. Exports:
(1978) 9.66X10+9 G
(1982) 9.96X10+9 G
(1985) 1.23X10+10 g
(1987) 9,031,377 lb
Laboratory Methods:
Clinical Laboratory Methods:
CYANIDE MAY BE LIBERATED FROM BIOLOGICAL
FLUIDS /BLOOD, URINE/ BY ACIDIFICATION. THE EVOLVED CYANIDE IS ABSORBED IN
ALKALI AND SODIUM CYANIDE THUS FORMED IS QUANTITATIVELY
DETERMINED BY MEASURING THE ABSORBANCE OF CHROMOPHORES FORMED BY INTERACTION OF
THE CYANIDE ION WITH SUITABLE REAGENTS ... /ANOTHER/ PROCEDURE PRESENTS A
SENISITIVE GAS CHROMATOGRAPHIC METHOD FOR DETERMINATION OF CYANIDE IN BIOLOGICAL
SPECIMENTS, BASED ON ITS CONVERSION TO CYANOGEN CHLORIDE USING CHLORAMINE-T.
/TOTAL CYANIDE/
A FLUOROMETRIC MICRODIFFUSION METHOD IS
DESCRIBED FOR DETERMINING CYANIDE IN BIOLOGICAL FLUIDS. THIS DETECTION IS BASED
ON THE PRODUCTION OF FLUORESCENCE BY THE TREATMENT OF CN WITH P-BENZOQUINONE.
/TOTAL CYANIDE/
GAS CHROMATOGRAPHIC DETERMINATION OF CYANIDES
IN BIOLOGICAL SPECIMENS BASED UPON ITS CONVERSION TO CYANOGEN CHLORIDE USING
CHLORAMINE-T (SODIUM P-TOLUENE SULFONCHLORAMIDE) IS DISCUSSED. /TOTAL CYANIDE/
Analytic Laboratory Methods:
ION SELECTIVE ELECTRODE: FRANK, ROSE &
RISEMAN; ANAL CHEM (44) 2227 (1972); FLUOROMETRY: DANCHIK & BOLTZ; ANAL CHIM
ACTA (49) 567 (1970); GAS CHROMATOGRAPHY: VALENTOUR, AGGARWAL & SUNSHINE;
ANAL CHEM (46) 924 (1974); ION SELECTIVE ELECTRODE, FLUOROMETRY, AND
CHROMATOGRAPHY USED TO DETERMINE SODIUM CYANIDE.
A GAS CHROMATOGRAPHIC METHOD FOR DETERMINING
RESIDUES OF SODIUM CYANIDE IN VEGETATION AND SOIL IS
PRESENTED. SOIL PLOTS WERE TREATED WITH 0.88 G OF SODIUM
CYANIDE. VERY SMALL AMOUNTS WERE FOUND IN THE VEGETABLE AND SOIL SAMPLES
TAKEN 2 DAYS AFTER TREATMENT INDICATING THE CONTAMINATION OF THE ENVIRONMENT
FROM THE USE OF M-44 CARTRIDGES WHICH CONTAIN SODIUM CYANIDE IS
NOT LIKELY TO OCCUR.
Color reaction: Oxidation of hemoglobin to
methemoglobin, which reacts with cyanide to form cyanomethemoglobin. This
compound has a characteristic red color and a characteristic absorption
spectrum. /Total Cyanide/
Colorimetric method: Pyridine-pyrazolone.
/Total Cyanide/
Seven methods for the analysis of simple
cyanides have been investigated including: 1) An ion-exchange procedure; 2) A
continuous flow distillation; 3) An EDTA electrode method; 4) The AISI aeration
method; 5) An EDTA aeration method; 6) The modified Roberts-Jackson method; and
7) The EPA method for Cyanides Amenable to Chlorination. Of all the seven
procedures studied, the modified Roberts-Jackson method is the best. It gives
complete recovery for all but one of the simple cyanides without decomposing the
complex cyanides. ... It has the unique ability to perform accurately in the
presence of both sulfide and thiocyanate. A lower limit of 2 ppb + or - 1 ppb is
possible with a precision of + or - 10% above 10 ppb. ... The ligand-exchange
procedure appears to be the most advantageous method of analysis of total
cyanides. /Total Cyanides/
EPA Method 9010: Colorimetric, Manual. Method
9010 is used to determine the concentration of inorganic cyanide in an aqueous
waste or leachate. The method detects inorganic cyanides that are present as
either simple soluble salts or complex radicals. It is used to determine values
for both total cyanide and cyanide amenable to chlorination; it is not intended
to determine if a waste is hazardous by the characteristic of reactivity. The
cyanide, as hydrocyanic acid, is released by refluxing the sample with strong
acid and distillation of the hydrogen cyanide into an absorber-scrubber
containing sodium hydroxide solution. The cyanide ion in the absorbing solution
is then manually determined colorimetrically by converting the cyanide to
cyanogen chloride by reaction with chloramine-T at a pH less than 8 without
hydrolyzing the cyanate. ... Color is formed on addition of the pyridine-barbituric
acid reagent. In a single laboratory, using mixed domestic and industrial waste
samples at concentrations of 0.06, 0.13, 0.28, and 0.62 mg cyanide/l, the
standard deviations were + or - 0.005, + or - 0.007, + or - 0.031, and + or -
0.094, respectively. In a single laboratory, using mixed industrial and domestic
waste samples at concentrations of 0.28 and 0.62 mg cyanide/l, recoveries were
85% and 102%, respectively. /Total and Amenable Cyanide/
REVIEW WHICH DISCUSSES THE METHODS & LIMIT
OF DETECTIONS OF CYANIDE IN NATURAL & TREATED WATERS, INDUST EFFLUENTS,
BIOLOGIC FLUIDS & SOLIDS: GAS CHROMATOGRAPHY (25 NG/ML), FLUOROMETRY (1
PPB), ION-SELECTIVE ELECTRODES (25 UG/L) & ABSORPTION SPECTROPHOTOMETRY (1-5
UG/L). /TOTAL CYANIDE/
Indirect atomic absorption spectrometric
analysis: (1) The complex dicyano-bis-(1,10-phenanthroline)-iron (II) is formed
and then extracted into chloroform. The chloroform is evaporated and the residue
is taken up in ethanol. The ethanol solution is aspirated directly into the
flame, and iron equivalent to a known amount of cyanide is then determined. (2)
The second method is based on precipitating silver cyanide, then determining the
excess silver ion in the supernatant by atomic absorption spectrometry. /Total
Cyanide/
Sampling Procedures:
Analyte: Sodium; Matrix: air; Sampler: filter
(0.8 um cellulose membrane); Flow rate: 1-4 l/min; Vol: min: 13 l, max: 2000 l;
Stability: stable /Elements, Sodium/
Special References:
Special Reports:
NIOSH; Criteria Document: Hydrogen Cyanide and
Cyanide Salts (1976) DHEW Pub. NIOSH 77-108
Nat'l Research Council Canada; Effects of
Cyanides on Aquatic Organisms with Emphasis Upon Fresh Water Fishes (1982) NRCC
No.19246
Health Effects Assessment for Sodium
Cyanide Report; Iss EPA/540/1-86/012
Sodium cyanide; potassium
cyanide: Cahiers de notes documentaries 118: 133-138 (1985)
DHHS/ATSDR; Toxicological Profile for Cyanide
(Update) TP-92/09 (1993)
USEPA; Ambient Water Quality Criteria Doc:
Cyanide (1984) EPA 440/5-84-028
USEPA; Ambient Water Quality Criteria Doc:
Cyanides (1980) EPA 440/5-80-037
DHHS/NTP; NTP Technical Report on Toxicity
Studies of Sodium Cyanide Administered in Drinking
Water to F344/N Rats and B6C3F1 Mice Rpt No. 37 (1993) NIH Publication No.
94-3386
Synonyms and Identifiers:
Synonyms:
M-44 cyanide capsules
**PEER REVIEWED**
Caswell No 758
**PEER REVIEWED**
CIANURO DI SODIO (ITALIAN)
**PEER REVIEWED**
CYANIDE OF SODIUM
**PEER REVIEWED**
CYANOGRAN
**PEER REVIEWED**
CYANURE DE SODIUM (FRENCH)
**PEER REVIEWED**
CYMAG
**PEER REVIEWED**
EPA Pesticide Chemical Code 074002
**PEER REVIEWED**
HYDROCYANIC ACID, SODIUM SALT
**PEER REVIEWED**
KYANID SODNY (CZECH)
**PEER REVIEWED**
Associated Chemicals:
Cyanide ion;57-12-5
Formulations/Preparations:
Powder
Grades: 30% soln; 73-75%; 96-98%; reagent;
technical; briquettes granular.
The cyanide of commerce is 95-98% pure.
Mixtures of sodium cyanide with
sodium chloride or carbonate for special uses are also marketed.
M-44 cyanide capsules; Pelletted/tabletted;
88.78% sodium cyanide (74002)
Sodium cyanide; crystalline;
99% sodium cyanide (74002)
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1689; Sodium cyanide, solid
or solution
IMO 6.1; Sodium cyanide, solid
or solution
Standard Transportation Number:
49 232 27; Sodium cyanide solution
49 232 28; Sodium cyanide, solid
EPA Hazardous Waste Number:
P106; An acute hazardous waste when a
discarded commercial chemical product or manufacturing chemical intermediate or
an off-specification commercial chemical product or a manufacturing chemical
intermediate.
D003; /SRP:/ A waste containing sodium
cyanide may (or may not) be characterized a hazardous waste following
testing for the reactivity characteristics as prescribed by the Resource
Conservation and Recovery Act (RCRA) regulations.
RTECS Number:
NIOSH/VZ7530000
Administrative Information:
Hazardous Substances Databank Number: 734
Last Revision Date: 20020213
Last Review Date: Reviewed by SRP on 5/6/2000