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HYDROGEN CYANIDE Human Health Effects:
See Occupational Exposure Standards Human Toxicity Excerpts:
SYMPTOMS OF ... POISONING APPEAR WITHIN ... SECONDS TO MIN AFTER INGESTION OR BREATHING VAPORS ... THEY CONSIST OF GIDDINESS, HYPERPNEA, HEADACHE, PALPITATION CYANOSIS, & UNCONSCIOUSNESS. ASPHYXIAL CONVULSIONS MAY PRECEDE DEATH.
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. As long as the heart beat continues, prompt and vigorous treatment offers some promise of survival. /Cyanide/
... ONLY OCCASIONALLY HAS REFERENCE BEEN MADE TO IRRITATION OF EYE, CONJUNCTIVITIS, OR SUPERFICIAL KERATITIS DEVELOPING AFTER CHRONIC EXPOSURE TO HYDROGEN CYANIDE GAS.
... WORKERS EXPOSED FOR PERIODS OF ... 7 YEARS AT CONCN BETWEEN 4 & 12 PPM ... /SHOWED/ INCREASE IN SUBJECTIVE SYMPTOMS SUCH AS HEADACHE, WEAKNESS, CHANGES IN TASTE & SMELL, IRRITATION OF THROAT, VOMITING, EFFORT DYSPNEA, LACRIMATION, ABDOMINAL COLIC, PRECORDIAL PAIN & NERVOUS INSTABILITY.
ENLARGEMENT OF THYROID GLAND, ATTRIBUTED POSSIBLY TO EFFECTS OF THIOCYANATE, CHIEF METABOLITE OF CYANIDE, WAS REPORTED ... /IN WORKERS EXPOSED OVER A PERIOD OF YEARS TO LOW CONCENTRATION IN AIR/.
Two episodes of cyanide poisoning occurred children who exhibited typical signs and symptoms of cyanide poisoning 2 hr after ingestion of a large amount of apricot kernels; 7 children recovered and 1 died soon after admission. The second episode involved 16 children who had eaten a sweet prepared from kernels. Symptoms and signs were identical to those in the first group but appeared 0.5 hr after ingestion and were more severe. Thirteen children recovered, 2 died shortly after admission and a third child died 2 hr later. Apricot kernals contain a cyanogenic substance called amygdalin, which after hydrolysis, liberates hydrocyanic acid. This activation usually only occurs after ingestion. In the second episode hydrolysis probably occurred during the preparation of the sweets, explaining the short interval between ingestion and appearance of the signs of poisoning.
Chronic exposure may cause fatigue, weakness.
Liquid hydrogen cyanide ran over the bare hand of a worker wearing a fresh air respirator. Cyanide inhalation was prevented, but the worker collapsed into deep unconsciousness within five minutes, suggesting significant percutaneous absorption. /Liquid hydrogen cyanide/
Two signs associated with cyanide poisoning in man: ... (1) the failure to utilize molecular oxygen in peripheral tissues results in abnormally high concn of oxyhemoglobin in the venous return, which accounts for a flush or brick-red skin; And (2) attempts to compensate for the inhibition of oxidative metabolism leads to increased demands on glycolysis, which accounts for a metabolic (lactic) acidosis.
An outbreak of spastic paraparesis, which mostly affected women and children, occurred in a northern province of Mozambique in 1981. The epidemic was related to chronic cyanide intoxication associated with a diet consisting almost exclusively of cassava. A prolonged drought in the area had exhausted all food resources except cassava, especially the bitter varieties. A nutritional, toxicological, and botanical investigation was carried out in 2 of the 5 districts affected. The main findings were that cyanide levels were unusually high in the cassava plant as a consequence of the drought with daily intakes estimated at 15-31.5 mg hydrogen cyanide. Detoxification of the bitter varieties by sun-drying was inadequate because of the general food shortage and metabolic detoxification was probably reduced owing to the absence of sulfur-containing amino acids in the women and children. The nutritional status of the population, however, was not very poor and symptoms of advanced undernutrition were rarely seen.
A STUDY WAS UNDERTAKEN TO ASSESS THE HEALTH STATUS OF WORKERS EXPOSED TO CYANIDE FUMES & AEROSOLS IN A FACTORY DURING ELECTROPLATING AND CASEHARDENING JOBS. 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/
A case of overexposure to hydrogen cyanide inside a 3500 gal tank which had contained a slurry of hydrazodiisobutyronitrile (which decomposed with water to give some hydrogen cyanide & acetone) is presented. This case is unusual in that survival without sequelae occurred despite exposure to HCN in the order of 500 mg/cu m for a six minute exposure, especially as treatment was not initiated until approximately 1 hr after exposure. Thus, survival with minimal sequelae can occur.
... IT IS POSSIBLE FOR CYANIDE TO CAUSE BLINDNESS & TO DAMAGE OPTIC NERVES & RETINA. /CYANIDE/
Blood cyanide (HCN) or plasma thiocyanate (SCN) ... concentrations, or both, were measured in 30 patients (ages 11 months - 72 years) receiving Na nitroprusside (SNP) ... for 12 - 314 hr. Sequential measurements in 3 of these patients (infused 5, 12 and 13 days) showed that HCN concentrations varied with dose rate, while thiocyanate concentrations increased linearly with increasing Na nitroprusside dose. The accumulated data confirmed that the rate of administration (0.3 - 6.5 ug/kg/min) determined the plasma HCN concentrations (0 - 3.8 umol/l). Thus, if prolonged ... plasma HCN concentrations > 1 umol/l are to be avoided, the maximum safe sustained dose rate of Na nitroprusside will ... /be/ near ... 4 ug/kg/min.
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/
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 giddness, 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/
... HYDROGEN CYANIDE APPEARS TO BE LESS SELECTIVE THAN HYDROGEN SULFIDE IN TOXICITY TO THE CORNEAL EPITHELIUM, YET THESE SUBSTANCES ARE OTHERWISE ABOUT EQUALLY TOXIC ... HYDROGEN SULFIDE HAS BECOME ... HIGHLY SELECTIVE TOXICITY TO THE CORNEAL EPITHELIUM, BUT ONLY OCCASIONALLY HAS REFERENCE BEEN MADE TO IRRITATION OF EYE, CONJUNCTIVITIS, OR SUPERFICIAL KERATITIS DEVELOPING AFTER CHRONIC EXPOSURE TO HYDROGEN CYANIDE GAS.
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/
... 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/
HIGH CONCN PRODUCES TACHYPNEA (CAUSING INCREASED INTAKE OF CYANIDE); THEN DYSPNEA, PARALYSIS, UNCONSCIOUSNESS, CONVULSIONS, & RESPIRATORY ARREST. HEADACHE, VERTIGO, NAUSEA & VOMITING MAY OCCUR WITH LESSER CONCN. CHRONIC EXPOSURE ... MAY CAUSE FATIGUE, WEAKNESS.
Vapor (Gas) Irritant Characteristics: Vapor is not very irritating but is extremely poisonous; Liquid or Solid Irritant Characteristics: Liquid is not /very/ irritating but is extremely poisonous if absorbed through lung, skin, or eyes.
Both Laetrile and amygdalin-containing fruit pits /cherries, peaches, apricots, apples, and pears/ have been implicated as causes of acute cyanide poisoning in humans.
Points of attack: Liver, kidneys, cardiovascular system, central nervous system.
VOLATILE /SRP: AIRBORNE/ CYANIDES RESEMBLE HYDROCYANIC ACID PHYSIOLOGICALLY, INHIBITING TISSUE OXIDN & CAUSING DEATH THROUGH ASPHYXIA. CYANOGEN IS PROBABLY AS TOXIC AS HYDROCYANIC ACID ... /CYANIDES/
Chemicals responsible for tissue hypoxia include carbon monoxide, hydrogen sulfide, and hydrogen cyanide. The major concern is the development of atherosclerosis followed by ischemic changes in vital organs such as the brain or heart. It is frequently difficult to prove that occupational factors are responsible for an individual illness, partly because the cardiovascular symptoms related to occupational exposures are often brought on by an underlying pathology which is not related to the job. However, it is sometimes possible to demonstrate a relationship between an increased occurrence of cardiovascular disorders and occupational factors among groups of workers. Cardiac disorders include coronary heart disease, cardiac arrhythmias, sudden death, chronic cor pulmonale, and disorders of the peripheral blood vessels such as secondary Raynaud's phenomenon. Careful questioning about the pattern of principal symptoms including chest pain, dyspnea, palpitation, syncope, cough, edema, and fatigue is the primary manner in which information about cardiovascular disorders is obtained. Information is frequently taken from a 12 lead electrocardiogram. (Ordinary chest radiographs may provide information concerning the presence of certain diseases of the heart and great vessels, but these are not generally useful in early detection).
The excretion of hydrogen cyanide in breath and blood concentrations of cyanide were measured in eight normal subjects. There was no correlation between breath and blood levels of cyanide. Furthermore, breath cyanide concentrations calculated from blood values were much lower than measured values. When saliva was incubated at 37 deg C, hydrogen cyanide was formed in the presence of air but not in a nitrogen atmosphere. No hydrogen cyanide was formed with boiled saliva and the production of hydrogen cyanide from saliva was inhibited by catalase and by 6-N-phopyl-thiouracil. Centrifugation of saliva resulted in a supernatant and a sediment, which were both required for the formation of hydrogen cyanide. Dialysis of the supernatant abolished its cyanide forming ability, which could be restored by addition of thiocyanate.
Five patients with smoke inhalation from house fires presented to the hospital in a comatose state. Carboxyhemoglobin levels were elevated in all five patients, mean= 32% + or - 6. Arterial blood gases revealed the following means: pH 7.16 + or - 0.06; partial pressure of carbon dioxide 35 mm HG + or - 10.5; carbonate 12.6 mEq/l + or - 0.07; base excess -16 mEq/l + or - 1.58; partial pressure of oxygen 353 mm Hg + or - 149; oxygen saturation 66% 5.5. The patients were presumed to have both cyanide and carbon monoxide intoxication and were treated with the cyanide antidote kit and hyperbaric oxygen (HBO). Four of five patients awoke within 15 minutes of reaching maximum pressure and remained neurologically intact thereafter. The fifth patient died one week later. Cyanide blood levels drawn prior to treatment revealed a mean of 1.62 + or - 1.44 ug/ml. The highest blood cyanide level was 3.9 ug/ml (the death) and the lowest 0.35 ug/ml.
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 poisoning results in weakness, headache, confusion, and nausea and vomiting. Long term effects may include neurasthenia with autonomic nervous system involvement, psychic alterations, precordial pains, breathlessness on exertion, bradycardia, arterial hypotonia, polycythemia, dyspepsia, hepatic impairment, and thyroidal hypofuction.
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/
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/
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/
Cyanide is a potent oral poison producing symptoms in minutes and death in minutes to hours. One teaspoon of 29% liquid hydrogen cyanide has been fatal.
The release of excessive amounts of HCN gas into the breathing zone of workers can result in collapse and death within seconds to minutes.
The toxicologic differential diagnosis of cyanide poisoning includes methemoglobinemia ..., asphyxia ..., and poisonings ...
Hydrogen cyanide poisoning is marked by abrupt onset of profound toxic effects that may include syncope, seizures, coma gasping respirations, and cardiovascular collapse, causing death within minutes.
Acute cyanide poisoning is rapidly fatal. Less acute cases may produce symptoms such as headache, dizziness, nausea, and so on.
Symptoms of acute cyanide poisoning are headache, giddiness, and a sense of sinking; palpitations; dyspnea with inadequate ventilation; and unconsciousness. When convulsions occur they are typically associated with brain hypoxia related to terminal respiratory arrest. Chronic manifestations of toxicity include skin disorders ... nasal irritation and drainage, headaches and neurologic problems such as tremor.
Human Toxicity Values:
Lethal adult dose of hydrogen cyanide is 50 mg.
Skin, Eye and Respiratory Irritations:
Hydrogen cyanide is a mild upper respiratory irritant and may cause slight irritation of the nose and throat. There may also be irritation from skin and eye contact with the liquid.
Medical Surveillance:
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.
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/
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:
Inhalation of vapor or aerosol, percutaneous absorption of liquid and concn vapor, ingestion and eye and skin contact.
... Hydrogen cyanide can be absorbed through the skin ...
EXPOSURE ... OCCURS ... WITH FUMIGATION OF SHIPS, WORKSHOPS, & DWELLINGS ... IN FUMIGATION INTENDED TO KILL AGRICULTURAL PARASITES, IN CHEM LABORATORIES, IN BLAST-FURNACE GAS, IN MFR OF ILLUMINATING GAS, & IN GAS FROM BURNING NITROCELLULOSE. INDUST PROCESSES ... WITH ... DANGER OF HCN ... EXPOSURE ARE PREPN OF CYANIDES & DECOMP OF CYANIDES BY EXPOSURE TO AIR & BY WEAK ACIDS & EXTRACTION OF PHOSPHORIC ACID FROM BONES. PRESENCE OF HCN IN VARIOUS INDUST GASES RESULTS FROM INCOMPLETE COMBUSTION OF NITROGEN-CONTAINING ORG CMPD ...
HYDROGEN CYANIDE AIR CONTENTS IN THE WORKPLACE WITH PROTECTION MEASURES FOR BRIQUETTING OF FERROSILICON ARE 0.5-5.0 PPM. THE URINARY THIOCYANATES CONTENT IN EXPOSED WORKERS IS GIVEN.
Occupational diseases caused by exposure to the asphyxiants carbon monoxide, hydrogen cyanide, or hydrogen sulfide were reveiwed. Exposure to hydrogen cyanide may occur involved in the chemical maufacture of monomers.
Some common furnishing fabrics and padding materials that give rise to smoke and acutely toxic substances on combustion were subjected to chemical and biological testing. Materials were cotton, cotton-rayon, rayon, wool, poly(vinyl alc)-poly(vinyl chloride), modacrylic, polyurethane foam, polyester wadding, and neoprene foam. The products were selected for the type of fire-resistant finishes used. Samples were heated at 500 and 700 degrees C in air, in accordance with the procedures of DIN 53446. Hydrogen cyanide was detected in the smoke gases. The changes in composition of the smoke gases with time and heavy components in the smoke were examined qualitatively. Particulates and liquids in the smoke were trapped in an ice trap for analysis. The toxicity of the smoke and smoke gases to rats was also measured. The carbon monoxide binding in rat blood was detected via carboxyhemoglobin measurement. Frequently, the fireproofing additives gave rise to a higher heat of combustion, but even at lower heats the smoke contained toxic gases. ... In a room lethal amounts of hydrogen cyanide are formed from modacrylics and Flamentin-flameproof cotton at the lower temp and from wool at the higher temp.
The toxicology of gases, vapors, mists, and fumes which workers may be exposed to in an occupational setting are reviewed. Included are the asphyxiant gases carbon dioxide, nitrogen, methane, carbon monoxide, hydrogen cyanide, and hydrogen sulfide, and the irritant gases ammonia, chlorine, ozone, phosgene, sulfur dioxide, and oxides of nitrogen. Industries whose workers may be at at risk of being exposed to these agents are numerous. They include various industries involving chemical refining, welding, mining, degreasing, electoplating, bleaching, sewage treatment industries.
NIOSH (NOES Survey 1981-1983) has statistically estimated that 3,780 workers (254 of these are female) are potentially exposed to hydrogen cyanide in the US(1). Occupational exposure to hydrogen cyanide may occur through inhalation and dermal contact with this compound at workplaces where hydrogen cyanide is produced or used(SRC). The general population may be exposed to hydrogen cyanide from automobile exhaust and waste incinerators(SRC).
Body Burden:
Hydrogen cyanide is present in human being's blood(1). People who smoke or consume vegetables having a relatively high hydrogen cyanide content may have slightly higher blood levels(1).
Minimum Fatal Dose Level:
The lethal oral dose of HCN is estimated to be about 50 milligrams in an adult.
Emergency Medical Treatment:
Emergency Medical Treatment:
[Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO, 2004; CCIS Volume 122, edition expires Nov, 2004. Hall AH & Rumack BH (Eds): TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2004; CCIS Volume 122, edition expires Nov, 2004.]**PEER REVIEWED**
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/
... The two main antidotal strategies ... are the induction of methemoglobinemia with amyl nitrite or sodium nitrite and the enhancement of conversion of cyanide to thiocyanate by the administration of sodium thiosulfate.
/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:
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/
... 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 & LUNGS MAY HAVE CONGESTION & PETECHIAL HEMORRHAGES. /CYANOGENIC PLANTS/
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 HCN was 0.039 mmol/kg. Signs of toxicity appeared rapidly & death occurred within 3 to 12 min after instillation of hydrogen 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.
Effects of sublethal hydrogen cyanide exposure on exogenous yolk production by liver was examined in sexually maturing female rainbow trout at onset of vitellogenesis. Fish were exposed to 0.01, 0.02 & 0.03 mg/l for 7 days at 12.5 deg C. Serum calcium & phosphoprotein phosphorus levels were measured & hepatosomatic indexes calculated as indicators of exogenous yolk production. Serum calcium levels were reduced at 0.01 mg/l in males & females. There was no apparent effect upon serum phosphoprotein phosphorus levels or hepatosomatic indexes at this concn. Serum calcium levels in females were reduced & hepatosomatic indexes declined at 0.02 mg/l. The implication of reduced serum calcium during early vitellogenesis upon secondary yolk production & reproduction in females is discussed.
There is an apparent relation between the degree of swimming inhibition caused by cyanide and temperature, the effect being more pronounced at lower temperatures. For example, /rainbow trout in a Blawzka type swimming chamber exhibited the following measurements/, at 45 ug/l hydrogen cyanide and 18 deg C, swimming performance was reduced by about 26% but at 30 ug/l and 12 deg C this reduction was 71%. At 15 ug/l and 6 deg C the trout suffered a 90% reduction of swimming stamina. The effects of cyanide on swimming are immediate and may last long after the fish have been returned to clean water. Even though immediate improvement of swimming after return of the fish to cyanide free water occurs, full recovery of chronically exposed salmonoids is not complete 15-20 days after their removal from cyanide containing water.
No reproduction occurred among adult bluegills when exposed for 289 days to 5.2 ug of hydrogen cyanide/l. During this period, however, only a total of 13 spawnings occurred in two controls and no dose response relationship was observed.
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-/
Toxicologic evaluation of smoke produced during smoldering chair tests was undertaken by exposing mice to smoke emitted prior to, as well as following, flaming ignition of the chairs. By exposing several groups of mice to undiluted smoke from the room containing the chairs, as well as various dilutions of the smoke, different levels of acute lethality were obtained. Chairs constructed with polyurethane foam were found to create higher toxic atmospheres than chairs constructed with polyester or cotton fiber cushions. ... Sensory irritation monitored in mice during the smoldering tests indicated that an intense level of irritation was present long before large amounts of smoke were generated and long before flaming ignition occurred. The phenomenon of eye, nose and throat irritation would, therefore, be the first effect impeding escape attempts of individuals in a fire situation. Sensory irritation was followed by asphyxiation as evolution of carbon monoxide or hydrogen cyanide, or both, occurred.
It is suspected that hydrogen cyanide may be an important factor in incapacitating fire victims, but the effects of sublethal exposures are not well characterized. Also, the incapacitating effects of fire atmospheres result from exposure to a mixture of toxic products so that the contribution from each component is difficult to determine. The mechanisms of incapacitation in monkeys exposed to the pyrolysis products of polyacrylonitrile were compared to those resulting from low level hydrogen cyanide gas exposures. The physiological effects of the polyacrylonitrile atmospheres were almost identical to those of hydrogen cyanide gas alone. They consisted of hyperventilation, followed by loss of consciousness after 1-5 min, bradycardia with arrhythmias and T-wave abnormalities, and were followed by a rapid recovery after exposure. Hydrogen cyanide is considered to be the major toxic product formed by the pyrolysis of polycrylonitrile. It is suggested that hydrogen cyanide may produce rapid incapacitation at low blood levels of cyanide in fires.
PHYTOTOXIC BUT USUALLY NOT AT VAPOR CONCN FATAL TO INSECTS; AVOID USE ON TREES BEARING COPPER SPRAY RESIDUES OR TREATED FOR CORRECTION OF COPPER DEFICIENCY.
Some common furnishing fabrics and padding materials that give rise to smoke and acutely toxic substances on combustion were subjected to chemical and biological testing. Materials were cotton, cotton-rayon, rayon, wool, poly(vinyl alc)-poly(vinyl chloride), modacrylic, polyurethane foam, polyester wadding, and neoprene foam. The products were selected for the type of fire-resistant finishes used. Samples were heated at 500 and 700 degrees C in air, in accordance with the procedures of DIN 53446. Hydrogen cyanide was detected in the smoke gases. The changes in composition of the smoke gases with time and heavy components in the smoke were examined qualitatively. Particulates and liquids in the smoke were trapped in an ice trap for analysis. The toxicity of the smoke and smoke gases to rats was also measured. The carbon monoxide binding in rat blood was detected via carboxyhemoglobin measurement. Frequently, the fireproofing additives gave rise to a higher heat of combustion, but even at lower heats the smoke contained toxic gases. ... In a room lethal amounts of hydrogen cyanide are formed from modacrylics and Flamentin-flameproof cotton at the lower temp and from wool at the higher temp.
IN THE CASE OF HYDROCYANIC ACID AND CYANIDES /IN VERY HIGH DOSES/, DEATH USUALLY OCCURS /IN ANIMALS/ WITHIN FEW SECONDS: THERE MAY BE CONVULSIONS, PARALYSIS, STUPOR, & CESSATION OF RESPIRATION BEFORE THAT OF HEARTBEATS. /CYANIDES/
Male and female mice and rats were subjected in an exposure chamber (30 cu m) to the products of thermal degradation of polyurethane foam, linen, or acrylics, and the concentrations of toxic gases (CO, CO2, HCN, and NOx) were determined and their single and combined effects were related to mortality rate. Death of the animals was observed after 30 minute exposure to these toxic gases and the dead animals showed epithelial and pulmonary lesions, acute lung edema, and the presence of C-rich particles in the lung. Mice were more sensitive to these toxic gases than rats. These gases were not toxic to the liver or kidney following 15 days exposure.
Toxicity of combustion products from ... polyurethane foam was examined in mice at 25 deg and at 19 vol % oxygen, and in a medium with higher temp (35 deg C and 45 deg C) and reduced oxygen level (16% and 11%). The exposure was for 30 min. ... polyurethane foam toxic effects were especially noticeable at 35 deg C and 16% oxygen level. The toxic effect of polyurethane foam also increased with increasing temp and reduced oxygen content.
Chemical composition and the toxicity (rats) of the airborne combustion products (500-700 deg C) of certain Finish textiles and upholstery materials, which were either treated with fire retardants or untreated, were investigated. ... Relatively high concentrations of HCN (>100 ppm) were generated from modacrylic, wool, Flamentin (fire retardant; a mixture or ammonium salts) treated cotton, etc. ... Most of deaths in rats occurred during the 30 min exposure. At 500 deg C, the most toxic materials were modacrylic, Flamentin-cotton and polyester fiber retardant fiber fill. At 700 deg C, modacrylic, wool, Flamentin-cotton, had the strongest toxic effects, in decreasing order. Toxic effects were attributed to HCN and carbon monoxide. No toxic effect was linked to hydrogen chloride despite ... high concentrations.
Combustion of a polyamide fiberglass for 5 min at air flow rates of 0.5, 1, or 2 l/min, generated 5.34, 3.25 and 0.122 mg HCN/l respectively. Carbon monoxide content also decreased with increasing air rate. ... A 5 min inhalation of combustion gases evolving at 0.5 l air/min, killed 50% of mice, whereas the offgases evolving at 1-2 l/min were nonlethal. Exposure to gases evolved at 0.5-2 l air/min during 1-, 2-, or 3- min combustion induced a 48.7, 32.3, and 19.2%, respectively, transformation of Hb into COHb.
A series of experiments were performed in mice to evaluate the toxicity of carbon monoxide, hydrogen cyanide (HCN) and low oxide atm. The results for both carbon monoxide and HCN for the time concn relationships to produce asphyxiation and death indicate that the asphyxiation end-point did not offer advantages over the measurement of acute lethality. Percentage escape activity measurement for carbon monoxide was not a good measure since it occurred just prior to asphyxiation or death. Depression of central nervous system (CNS), measured by depression of resp rate, occurred at concentrations lower than the LC50 by about a factor of 3. Such an effect can be detected at even lower concentrations, & unlike asphyxiation or disappearance of escape activity, this effect is not followed immediately by death which was generally the case with other 2 endpoints. At low concentrations of oxygen, just above concn which caused death, a very small decrease in resp rate followed by recovery was observed; with both carbon monoxide and HCN, however, a severe resp depression was observed at concentrations below those inducing death and while recovery was fairly rapid with HCN, it was very slow with carbon monoxide.
Groups of adult rats were repeatedly exposed to the pyrolysis products either of a rigid polyurethane foam or of hemlock, to which was added 0 or 200 ppm hydrogen cyanide (HCN) under conditions that did not result in depletion of oxygen in the exposure atmosphere. Other groups were exposed to HCN in air or in air + carbon monoxide Some of the HCN exposed groups were presented with a chlorpromazine/thiosulfate combination protective against cyanide toxicity. Exposure to HCN without protective pretreatment was associated with mild cardiotoxicity as measured by the magnitude of release of cardiac-specific creatine phosphokinase activity and by the number of ectopic heart beats induced by norepinephrine injection. Much of the difference in the cardiotoxicities of polyurethane and hemlock smokes could be related to their different contents of HCN. However, the prevalence of focal histopathological lesions in the rat hearts did not correlate well with the other 2 measures of cardiotoxicity.
Carbon monoxide, hydrogen cyanide (HCN), and hydrochloric acid are the major gaseous toxicants encountered in the atmosphere during fires. Experimental intoxications increased protein content in lavage pulmonary fluid indicating pulmonary subedema or edema. Expected for hydrochloric acid this occurrence was not so predictable for HCN and carbon monoxide; ... The increase of neutral sugars, sialic acid, and fucose ... contents revealed the irritating effect of HCN and hydrochloric acid.
-o CYANIDES SUCH AS ... HYDROGEN CYANIDE, POTASSIUM CYANIDE AND SODIUM CYANIDE ARE S, INTERFERING WITH METABOLIC PROCESSES & CAUSING RAPID DEATH. RE POISONING, PUPILS ARE CHARACTERISTICALLY WIDELY DILATED.
The lethal toxicity (96 hr LC50) of cyanide (HCN) to juvenile rainbow trout (Salmo gairdneri) varied seasonally and with exercise (swimming at one body length/sec). The trout were acclimated to the 12 deg C test temperature for 3-4 weeks, under a 12 hr photoperiod before being tested at different times of the year. In summer, there was no significant difference of sensitivity between exercised and non exercised trout. From summer to winter, the 96 hr LC50 for exercised trout remained unchanged at 0.052 mg/l HCN, while the LC50 of the non-exercised trout dropped significantly to 0.043 mg/l HCN. The median survival times of the two groups of trout were the same in the summer, but in the winter the exercised fish survived twice as long as the non-exercised fish.
Larval fathead minnows (Pimephales promelas) were exposed for 96 hr to several concentrations of hydrogen cyanide. The range of safe concentrations determined from 96 hr macromolecular content (RNA, DNA & protein) & growth was within or near the range of safe concentrations determined by concomitant longer term exposure. RNA, DNA & protein content/larva & RNA/DNA ratio were sensitive to toxicant stress & followed a log-linear dose response. Larval RNA content appeared to be at the 96 hr measurement most responsive to toxicant exposure.
Growth of fathead minnow yolk sac larvae was characterized from changes in dry weight and total content and concentrations of RNA, DNA and protein in fish exposed to a sublethal level of HCN (hydrogen cyanide) (58 ug/l) and in age matched controls. Cyanide toxicosis occurred within 24 hr of exposure as evidenced by significant reductions in protein and RNA content and RNA/DNA ratio of larvae. After 96 hr exposure to HCN, larvae exhibited the same growth rate and protein synthetic rate (RNA/DNA) as control fish. HCN toxicosis and recovery is rapid and at least partial tolerance to HCN develops within 96 hr of exposure in larval fathead minnows.
Cyanide markedly affected growth and resting metabolic rate while causing degenerative hepatic necrosis in juvenile rainbow trout (Salmo gairdneri). ... In continuously renewed water at 12.5 deg C, fish were exposed to cyanide concn of 0.00, 0.01, 0.02, or 0.03 mg/l hydrogen cyanide (HCN) for 18 days. At 0.02 and 0.03 mg/l HCN, growth was reduced by 40 to 95% after 18 days. At all concn, cyanide caused a severe initial repression of specific growth rate, followed by a highly significant increase which was insufficient to compensate for the original repression. Previous exposure to cyanide promoted a higher resting metabolic rate during the six days following exposure, the effect increasing with cyanide concn. At all concn tested, widespread cyanide-induced degenerative necrosis of hepatocytes was observed.
Non-Human Toxicity Values:
LC50 Rat inhalation 142 ppm/30 min
LC50 Mouse inhalation 169 ppm/30 min
LC50 Dog inhalation 300 ppm/3 min
LD50 Rat subcutaneous 3700 ug/kg
LCLo Rabbit inhalation 600 mg/cu m/2 min
LDLo Groundhog subcutaneous 100 ug/kg
LD50 Rabbit im 486 ug/kg
LD50 Rabbit ocular routes 1040 ug/kg
LD50 Rat iv 810 ug/kg
LD50 Mouse oral 3700 ug/kg
LD50 Mouse ip 2990 ug/kg
LD50 Mouse iv 990 ug/kg
LD50 Mouse im 2700 ug/kg
LD50 Dog iv 1340 ug/kg
Ecotoxicity Values:
Daphnia: 50% immobilization after 48 hr at 1.8 mg/l. /Conditions of bioassay not specified/
LC50 Asellus communis 2.29 mg/l/96 hr /Conditions of bioassay not specified/
LC50 Gammarus pseudolimnaeous 0.17 mg/l/96 hr /Conditions of bioassay not specified/
TLm Pinperch 0.069 mg/l/24 hr /Conditions of bioassay not specified/
TLm Lepomis humilis (sunfish) 0.18 mg/l/24 hr /Conditions of bioassay not specified/
TLm Pinperch 0.05 mg/l/24 hr (in seawater) /Conditions of bioassay not specified/
LTC Lepomis macrochirus (bluegill eggs) 535-693 ug/l/96 hr, flow-through bioassay
LC50 Lepomis macrochirus (bluegill swim up fry) 232-365 ug/l/96 hr, flow-through bioassay
LC50 Lepomis macrochirus (bluegill, juvenile) 75-125 ug/l/96 hr, flow-through bioassay
LC50 Perca flavescens (yellow perch eggs) >276-389 ug/l/96 hr, flow-through bioassay
LC50 Perca flavescens (yellow perch, juvenile) 76-108 ug/l/96 hr, flow-through bioassay
LC50 Salvelinus fontinalis (brook trout eggs) >212 to >242 ug/l/96 hr, flow-through bioassay
LC50 Salvelinus fontinalis (brook trout, sac fry) 108-518 ug/l/96 hr, flow-through bioassay
LC50 Salvelinus fontinalis (brook trout, swim up fry) 56-106 ug/l/96 hr, flow-through bioassay
LC50 Salvelinus fontinalis (brook trout, juvenile) 53-143 ug/l/96 hr, flow-through bioassay
LC50 Salmo gairdnerii (rainbow trout) 57 ug/l/96 hr, flow-through bioassay
LC50 Pimephales promelas (fathead minnow eggs) 121-352 ug/l/96 hr, flow-through bioassay
LC50 Pimephales promelas (fathead minnow, swim up fry) 82-122 ug/l/hr, flow-through bioassay
LC50 Pimephales promelas (fathead minnow, juvenile) 82-137 ug/l/96 hr, flow-through bioassay
LC50 Pimephales promelas (fathead minnow, juvenile, wild stock) 157-191 ug/l/96 hr, flow-through bioassay
LC50 Goniobasis livescens (snail) 760,000 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Lymnaea emarginata (snail) 3,300 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Lymnaea sp, (snail, embryo) 51,900 ug/l/96 hr
LC50 Physa integra (snail) 1,350 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Stemonema rubrum (mayfly) 500 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Hyfropsyche sp (caddisfly) 2,000 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Salmo gairdneri (rainbow trout) 68 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnow) 240 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnow, juvenile) 120 ug/l/5 days /Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnow, juvenile) 123 ug/l/96 hr /Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill, juvenile) 134 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill, juvenile) 154 ug/l/72 hr /Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill) 160 ug/l/48 hr /Conditions of bioassay not specified/
LC50 Perca flavescens (yellow perch, embryo) 281 ug/l/96 hr /Conditions of bioassay not specified/
TSCA Test Submissions:
Hydrocyanic acid (CAS # 74-90-8) was evaluated for subacute inhalation toxicity in Sprague-Dawley rats (5/sex/group) administered whole-body exposures to a mean analytical concentration of 67.8 +/- 7.0 ppm for 6 hours on 3 consecutive days under dynamic conditions (2060-2200 L/min). An initial exposure was associated with hypoactivity, rapid shallow breathing, anoxia/hypoxia signs, and convulsions, followed by chromorhinorrhea, convulsions and varied signs of labored breathing. Survivors of 2 exposures exhibited rapid breathing and reduced mean bodyweight with a solitary male rat exhibiting arching of the back. Signs of toxicity associated with a third exposure were limited to hypoactivity and quick shallow breathing; mean daily bodyweight gains were restored. Mortality occurred either during or following an initial exposure in 1 and 2 males, respectively. Necropsy of these study decedents revealed cyanosis of the extremities, hemorrhagic lungs, lung and tracheal edema, blanching of the liver, chromorhinorrhea, urine-filled bladder, gaseous distention of the gastro-intestinal tract, and a solitary incidence of blood engorgement of the heart and surrounding vasculature. On terminal necropsy of study survivors, females exhibited slight to moderate hemorrhage (3/5) and grey discoloration (2/5) of the lung.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
LARGER PORTION /OF ABSORBED CYANIDE/ ... IS CONVERTED BY ... SULFURTRANSFERASE/S/ TO ... THIOCYANATE ION. ... MINOR METABOLIC PATHWAYS INCL COMBINATION WITH CYSTINE TO FORM 2-IMINO-THIAZOLIDINE-4-CARBOXYLIC ACID, OXIDATION TO CARBON DIOXIDE & FORMATE, & CONVERSION TO CYANOCOBALAMIN.
The enzymatic decomposition of thiocyanate into cyanide by a thiocyanate oxidase has been found in mammals, but only in erythrocytes.
A very small fraction of the total cyanide is bound by hydroxocobalamin, probably less than 1 percent.
Because the liver contains the highest activity of rhodanese, it is possible that existing liver disease might slow the rate of cyanide metabolism.
Cyanide is converted to products which enter metabolic pathways for one-carbon compounds and is converted to formate and to carbon dioxide.
Hydrogen cyanide reacts with acetaldehyde followed by hydrolysis to produce lactic acid
... CYANIDE ION IS CONJUGATED WITH SULFUR TO FORM THIOCYANATE. ... CONJUGATION IS CATALYZED BY ... RHODANESE WHICH IS WIDELY DISTRIBUTED IN MOST ANIMAL TISSUES ... /LIVER/ PARTICULARLY ACTIVE. ... 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/
Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.
/ONE OF/ THE MAJOR MECHANISM/S/ FOR REMOVING CYANIDE FROM THE BODY IS ITS ENZYMATIC CONVERSION, BY THE MITOCHONDRIAL ENZYME RHODANESE (TRANSSULFURASE), TO THIOCYANATE, WHICH IS RELATIVELY ... /LESS TOXIC/. /CYANIDE/
RUMINANTS ARE MORE SUSCEPTIBLE TO POISONING BY CYANOGENIC PLANTS /SRP: WHICH RELEASE HYDROGEN CYANIDE/ THAN ARE HORSES & PIGS ... /CYANOGENIC PLANTS/
FACTORS THAT INCR LIKELIHOOD OF HCN POISONING FROM INGESTION OF CYANOGENIC PLANTS INCLUDE: (1) LARGE AMT OF FREE HCN & 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 HCN/KG OF BODY WT IS CONSIDERED TO BE LETHAL AMOUNT OF PLANT MATERIAL. ... /CYANOGENIC PLANTS/
Aliphatic nitriles have been postulated to manifest their toxicity through cyanide (CN) liberation. The signs of toxicity and effect of equitoxic LD50 doses of saturated and unsaturated aliphatic mono- and dinitriles on tissue and blood CN levels, tissue glutathione levels and cytochrome c oxidase activities were studied in rats. Signs of toxicity were classified into cholinomimetic effects observed with unsaturated nitriles and CNS effects observed with saturated potassium cyanide. Hepatic and blood CN levels 1 hr after treatment were highest following malononitrile and decreased in the order of propionitrile > potassium cyanide > butyronitrile > acrylonitrile > allylcyanide > fumaronitrile > acetonitrile. The order differed in brain where potassium cyanide preceded malononitrile and PCN. Hepatic and cytochrome c oxidase were significantly inhibited and corresponded to their CN levels. No significant inhibition of cytochrome c oxidase was observed in vitro. Acrylonitrile was the only nitrile which significantly reduced tissue GSH levels. Toxic expression of aliphatic nitriles depended on CN release and their degree of unsaturation. With unsaturated aliphatic nitriles CN release played a minimal role in their toxicity. /Cyanides/
Acute toxicity and metabolism of 7 dinitriles in mice was studied in relation to the chemical structures. The oral LD50 for each nitrile was detected under different conditions for mice pretreated with either carbon tetrachloride (CCl4) or olive oil. All test nitriles were metabolized into cyanide in vivo and in vitro. The cyanide level was variable among the compounds (0.35-0.74 ug cyanide/g brain) at death in the brains of mice, the level from malononitrile and adiponitrile being comparable to that found in mice killed by dosing with potassium cyanide. After receiving each nitrile, the mean survival time of mice pretreated with CCl4 was prolonged and their brain cyanide level decreased when compared with the corresponding control. With malononitrile, the former did not significantly change and the latter decreased slightly. Brain cyanide levels of control mice at death showed a peak at the lower log P region, whereas those of CCl4 pretreated animals remained lower independently of log P, with the exception of malononitrile. Microsomal metabolism of nitriles to cyanide was greatly inhibited when microsomes were prepared from livers of mice pretreated with CCl4. The relationship between log (1/LD50-CCl4), LD50 in mice pretreated with CCl4, and log P fits a parabolic plot. /Cyanides/
Humans detoxify cyanide by transferring sulfane sulfur to cyanide, thus converting it to thiocyanate (SCN). Thiocyanate is excreted in the urine ... Two main enzymes ... rhodanese ... and ... beta-mercaptopyruvate-cyanide sulfurtransferase.
Cyanide is rapidly taken up and sequestered by red blood cells. Such action does not appear to enhance the metabolism of cyanide, but might act to partially lessen toxicity by preventing the diffusion of cyanide out of blood into tissues.
Absorption, Distribution & Excretion:
IN 30 DAYS, 72% OF (14)C FROM IP DOSE OF (14)C-CYANIDE TO MICE WAS EXCRETED IN URINE & FECES, 25% IN EXPIRED AIR, & 3% WAS RETAINED ... PEAK EXCRETION OCCURRED WITHIN 10 MIN IN EXPIRED AIR & WITHIN 6-24 HR IN URINE & FECES.
THE CYANIDE ION IS READILY ABSORBED AFTER ORAL OR PARENTERAL ADMIN. PROLONGED LOCAL CONTACT WITH ... HCN MAY RESULT IN ABSORPTION OF TOXIC AMT THROUGH SKIN. PART OF ABSORBED CYANIDE IS EXCRETED UNCHANGED BY THE LUNG. LARGER PORTION ... CONVERTED BY ... SULFURTRANSFERASE TO RELATIVELY NONTOXIC THIOCYANATE ION. /CYANIDE/
Hydrogen cyanide vapor is absorbed rapidly through the lung. Because HCN has a pKa of 9.2 and exists primarily as the acid under biological conditions, absorption across the alveolar membrane should be rapid. Human inhalation of 270 ppm HCN vapor brings death immediately, while 135 ppm is fatal after 30 minutes.
Hydrogen cyanide, in either liquid or vapor form, is absorbed through the skin. Absorption is probably increased if the skin is cut, abraded, or moist.
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. Presumably, the accumulation of cyanide in erythrocytes is a reflection of its binding to methemoglobin. /Cyanides/
A significant difference between the amount of cyanide in the whole blood of smokers and non-smokers could not be detected, but, the plasma thiocyanate levels of the smokers were significantly elevated. A ratio of cyanide to thiocyanate in body fluids was about 1 to 1000. A more reliable index of cyanide exposure may be measurement of plasma thiocyanate rather than determination of whole blood cyanide.
The acute systemic toxicity of hydrogen cyanide, sodium cyanide and potassium cyanide by instillation into the inferior conjunctival sac was investigated. In the rabbit, the LD50 values in mmol/kg were 0.039 for HCN, 0.103 for sodium cyanide, and 0.121 for potassium cyanide. The acute lethal toxicity of sodium cyanide was not significantly different when applied as a solution or solid, and mixing the solid with an inert powder (kaolin) did not modify the toxicity. For all preparations, signs of toxicity appeared rapidly and death occurred within 3 to 12 min of the eye being contaminated. Cyanide concns in blood, serum, and various tissues were measured, and the results found compatible with a diagnosis of death from acute cyanide poisoning. Thus, following their instillation into the conjunctival sac, cyanides may be absorbed across conjunctival blood vessels in amounts sufficient to produce systemic toxicity. Contamination of the eye with cyanide could be a hazardous route of exposure.
Hydrogen cyanide (HCN) was significantly more toxic than sodium cyanide or potassium cyanide by im and transocular routes, and potassium cyanide significantly less toxic than HCN or sodium cyanide by skin penetration. Acute inhalation studies indicated a proportionately longer time to cause death at the lower concn, and thus larger total doses of HCN are required to cause death by low-concn than by high-concn exposure. Following death by acute cyanide poisoning, whole blood concn are high and diagnostic significance; serum levels are 1/3-1/2 those in whole blood. Blood cyanide concn vary with the route, being lowest by inhalation and skin penetration. For a given exposure route, blood concn are similar for different species. Cyanide concn in certain specific tissues vary markedly with exposure route.
CN- FORMS COMPLEXES WITH A NUMBER OF OTHER CHEMICALS (EG IN TISSUES) & HAS STRONG AFFINITY FOR COBALT. /CYANIDE ION/
CYANIDES ARE RAPIDLY ABSORBED FROM SKIN & ALL MUCOSAL SURFACES & ARE MOST DANGEROUS WHEN INHALED, BECAUSE TOXIC AMT ARE ABSORBED THROUGH BRONCHIAL MUCOSA & ALVEOLI. /CYANIDES/
Once absorbed into the body, cyanide can form complexes with heavy metal ions. /Cyanide/
Liquid hydrogen cyanide ran over the bare hand of a worker wearing a fresh air respirator. Cyanide inhalation was prevented, but the worker collapsed into deep unconsciousness within five minutes, suggesting significant percutaneous absorption. /Liquid hydrogen cyanide/
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/
... Cyanide salts are absorbed rapidly from mucous membranes ...By inhalation ...
Substantial absorption can occur through intact skin if vapor concentration is high.
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:
The acute mode of action of hydrogen cyanide is limited to binding those porphyrins that contain iron III, such as cytochrome oxidase, hyperoxidases, and methemoglobin.
The inhibition of cytochrome oxidase is noncompetitive and hence, is independent of the relative proportions of toxicant and substrate with which the enzyme reacts. Thus, the acute toxicity of cyanide will be determined almost completely by the concn of cyanide (in the mitochondrial matrix) surrounding the structure on which cytochrome oxidase is thought to be located (oxysomes of the mitochondrial cristae). Differences in sensitivity to cyanide may occur between different animal species, and many plant mitochondria contain electron transport chains which are insensitive to cyanide.
While the concn of cytochrome oxidase in fish mitochondria apparently does not vary with ambient temperature, the activity of the enzyme is greater in mitochondria from cold-associated individuals. Therefore, one would expect fish to be more sensitive to cyanide when acclimated to lower temperatures.
When cyanide stops the production of ATP associated with the electron transport chain, another metabolic pathway is activated and ATP is synthesized via the degradation of glucose to lactic acid, or an equivalent end product. Degradation of glucose, commonly referred to as glycolysis, does not utilize oxygen but does not produce sufficient ATP to sustain organisms that are relatively active.
The mitochondrial electron transport system may also be seriously disturbed by cyanide through the inhibition of succinate dehydrogenase, which is a nonheme flavin-containing iron-sulfur protein which passes electrons to the cytochrome system. The peculiarity of this enzyme is its sulfur linkages which are of the persulfide or sulfane type, favoring a "labile sulfur" condition that is essential for activity. Cyanide is a strong thiophile reacting with the "labile" sulfur thus breaking the persulfide bond.
Hydroperoxidases consist of two classes of enzymes, catalases and peroxidases, both of which utilize hydrogen peroxide as a substrate. The ferro-heme group is strongly inhibited by cyanide, although the physiological significance at sublethal levels remains obscure. ... One tissue that could be seriously affected by the inhibition of catalase by cyanide is the blood, where the formation of hydrogen dioxide would lead to the oxidation of hemoglobin Fe(2+) into methemoglobin Fe(3+), thus reducing the oxygen carrying capacity of the organism.
During chronic cyanide exposure the precursers of Vitamin B12 may react with cyanide, thereby reducing the amount of available Vitamin B12.
The cyanide ion produces acute anoxia of the central nervous system by inactivating the cytochrome oxidase enzyme system necessary for tissue respiration. Death in acute cases occurs within a few seconds.
CYANIDE HAS A VERY HIGH AFFINITY FOR IRON IN FERRIC STATE. WHEN ABSORBED IT REACTS READILY WITH ... IRON OF CYTOCHROME OXIDASE IN MITOCHONDRIA; 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 /BY CYANIDE/. ... 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/
The cyanide ion (CN-) ... has a strong affinity for cobalt. /Cyanide ion/
The objective was to ascertain whether cyanide shares the properties of methylene blue as a selective inhibitor of vascular smooth muscle relaxation elicited by agents that stimulate the formation of cyclic GMP. Experiments were performed with endothelium-intact rings prepared from bovine intrapulmonary artery. Methylene blue, a good inhibitor of soluble guanylate cyclase, antagonized both arterial relaxation and cyclic GMP accumulation in response to sodium nitroprusside, glyceryl trinitrate, S-nitroso-N-acetylpenicillamine and acetylcholine. In contrast, cyanide inhibited only the responses to sodium nitroprusside. ... Contractile responses to phenylephrine, potassium, and U46619 were potentiated by methylene blue but not by cyanide. Cyanide does not share the properties of methylene blue as an inhibitor of arterial relaxation elicited by vasodilators that stimulate cyclic GMP formation.
/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:
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/
Mathematical modeling methods for the intoxication of rats by carbon monoxide and hydrogen cyanide are extended to accommodate combined atmospheres of these fire gas toxicants. Predictions using the Fractional ED model for both incapacitation and lethality show no significant differences from animal bioassay data. Use of the model is suggested as a substitute for live animal testing for the toxicity of smoke produced from burning materials.
Acute toxicity at single and combined exposures of carbon monoxide and hydrogen cyanide (HCN) was studied on rats in terms of concentration-time product (ppm/min) necessary to kill animals (lethal concentration time). ... After exposure, blood sample was withdrawn from the right side of the heart. Carbon monoxide concentrations in the gas and blood were determined gas chromatographically. HCN in the gas sample was measured spectrophotometrically, after being absorbed into sodium hydroxide solution ... At single exposures, mean lethal concentration time for carbon monoxide was 78,000 + or - 22,000 and for HCN was 4,700 + or - 940. In combined exposure, various combinations of carbon monoxide and HCN were used. A fractional concentration time, defined as a ration of concentration time to lethal concentration time, multiplied by 100, was calculated for each gas. A linear relationship between fractional concentration times averaged 100 + or - 26. On the other hand, linear relation was not observed between blood levels of the two toxicants at death.
Cysteine, a sulfur-containing amino acid, is required to metabolize ascorbic acid (as ascorbate sulfate) and detoxify cyanide (to thiocyanate). In guinea pigs, conjoint use of laetrile (a cyanogenic glycoside) and ascorbic acid (in large doses) decreases the detoxification of cyanide derived from laetrile through diminishing the availability of cysteine, but not impairing hepatic rhodanese activity, which is involved in the detoxification of cyanide to thiocyanate.
... Solids that can release a toxic gas on reacting with water ... chemicals are nonselective, highly reactive, and cytotoxic.
Pharmacology:
Interactions:
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/
Mathematical modeling methods for the intoxication of rats by carbon monoxide and hydrogen cyanide are extended to accommodate combined atmospheres of these fire gas toxicants. Predictions using the Fractional ED model for both incapacitation and lethality show no significant differences from animal bioassay data. Use of the model is suggested as a substitute for live animal testing for the toxicity of smoke produced from burning materials.
Acute toxicity at single and combined exposures of carbon monoxide and hydrogen cyanide (HCN) was studied on rats in terms of concentration-time product (ppm/min) necessary to kill animals (lethal concentration time). ... After exposure, blood sample was withdrawn from the right side of the heart. Carbon monoxide concentrations in the gas and blood were determined gas chromatographically. HCN in the gas sample was measured spectrophotometrically, after being absorbed into sodium hydroxide solution ... At single exposures, mean lethal concentration time for carbon monoxide was 78,000 + or - 22,000 and for HCN was 4,700 + or - 940. In combined exposure, various combinations of carbon monoxide and HCN were used. A fractional concentration time, defined as a ration of concentration time to lethal concentration time, multiplied by 100, was calculated for each gas. A linear relationship between fractional concentration times averaged 100 + or - 26. On the other hand, linear relation was not observed between blood levels of the two toxicants at death.
Cysteine, a sulfur-containing amino acid, is required to metabolize ascorbic acid (as ascorbate sulfate) and detoxify cyanide (to thiocyanate). In guinea pigs, conjoint use of laetrile (a cyanogenic glycoside) and ascorbic acid (in large doses) decreases the detoxification of cyanide derived from laetrile through diminishing the availability of cysteine, but not impairing hepatic rhodanese activity, which is involved in the detoxification of cyanide to thiocyanate.
... Solids that can release a toxic gas on reacting with water ... chemicals are nonselective, highly reactive, and cytotoxic.
Minimum Fatal Dose Level:
The lethal oral dose of HCN is estimated to be about 50 milligrams in an adult.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Hydrogen cyanide's production and use as a starting material in the manufacture of acrylates, cyanide salts, herbicides and dyes as well as its former use as a fumigant resulted in its release to the environment through various waste streams. If released to air, a vapor pressure of 742 mm Hg at 25 deg C indicates hydrogen cyanide will exist solely as a vapor in the ambient atmosphere. Vapor-phase hydrogen cyanide will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 535 days. If released to soil, hydrogen cyanide is expected to have very high mobility. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 1.33X10-4 atm-cu m/mole. Hydrogen cyanide may volatilize from dry soil surfaces based upon its vapor pressure. Hydrogen cyanide can be biodegraded by acclimated microbial cultures and sludges, but is usually toxic at high concentrations to unacclimated microbial systems. If released into water, hydrogen cyanide is not expected to adsorb to suspended solids and sediment in water. Volatilization from water surfaces is expected to be an important fate process based upon this compound's estimated Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 3 hours and 3 days, respectively. A pKa of 9.2 indicates that the dissociated form may exist at high pH. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic organisms is low. Occupational exposure to hydrogen cyanide may occur through inhalation and dermal contact with this compound at workplaces where hydrogen cyanide is produced or used. The general population may be exposed to hydrogen cyanide from automobile exhaust and waste incinerators. (SRC)
Probable Routes of Human Exposure:
Inhalation of vapor or aerosol, percutaneous absorption of liquid and concn vapor, ingestion and eye and skin contact.
... Hydrogen cyanide can be absorbed through the skin ... EXPOSURE ... OCCURS ... WITH FUMIGATION OF SHIPS, WORKSHOPS, & DWELLINGS ... IN FUMIGATION INTENDED TO KILL AGRICULTURAL PARASITES, IN CHEM LABORATORIES, IN BLAST-FURNACE GAS, IN MFR OF ILLUMINATING GAS, & IN GAS FROM BURNING NITROCELLULOSE. INDUST PROCESSES ... WITH ... DANGER OF HCN ... EXPOSURE ARE PREPN OF CYANIDES & DECOMP OF CYANIDES BY EXPOSURE TO AIR & |