Sodium Cyanide

CAS RN: 143-33-9

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) Sodium cyanide exposure may produce death within minutes. Signs and symptoms following non-lethal, subacute, or chronic exposure may include syncope, weight loss, headache, dizziness, nausea, vomiting, palpitations, confusion, deep inspiratory gasps followed by hyperpnea, hyperventilation, anxiety, and vertigo.
    • B) Cyanosis is generally a late finding and usually does not occur until circulatory collapse and apnea are evident; particularly at the premorbid stage of cyanide toxicity. Initially the patient may experience flushing, tachycardia, tachypnea, headache, and dizziness. This may progress to agitation, stupor, coma, apnea, seizures, metabolic acidosis, pulmonary edema, bradycardia, hypotension, and death.
    • C) Sodium cyanide exposure may produce death within minutes. IMMEDIATELY BEGIN ADMINISTERING 100% OXYGEN. OBTAIN THE CYANIDE ANTIDOTE KIT AND PREPARE IT FOR USE. Non-lethal, subacute, or chronic exposure may produce headache, dizziness, nausea, vomiting, palpitations, confusion, deep inspiratory gasps followed by hyperpnea, hyperventilation, anxiety, and vertigo. Severe signs of hypoxia in the absence of cyanosis suggest cyanide poisoning. Patients have reportedly survived potentially lethal ingestions with only supportive care. The absence of a rapidly deteriorating course does not exclude cyanide poisoning.
  • 0.2.1.2 CHRONIC EXPOSURE
    • A) Functional changes in hearing, loss of appetite, headache, weakness, nausea, dizziness, upper respiratory tract irritation, and dermatoses have been described in chronically exposed workers.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) Tachycardia, deep inspiratory gasps followed by hyperpnea, tachypnea, hypertension may be early findings after acute cyanide poisoning, followed by hypotension, bradycardia, dyspnea, apnea, and asystole.
      • 1) Tachycardia and hypertension may be seen in the initial phases of cyanide poisoning (Vogel et al, 1981).
      • 2) Bradycardia and hypotension are seen in the late phases of cyanide poisoning (Stewart, 1974; Hall & Rumack, 1986).
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Dilated pupils are common in severe poisoning; corneal edema, conjunctivitis, and keratitis may occur. Retinal arteries and veins may appear equally red on funduscopic examination.
    • B) Transient blindness has been reported in rare instances. Damaged optic nerves have been observed in experimental animals. A burning sensation in the nose, mouth, and throat may occur.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) Tachycardia, bradycardia, hypertension, hypotension, cardiac dysrhythmias, EKG changes, and asystole may be observed.
0.2.6 RESPIRATORY
  • 0.2.6.1 ACUTE EXPOSURE
    • A) Tachypnea, deep inspiratory gasps followed by hyperpnea, apnea, noncardiogenic pulmonary edema may be apparent.
0.2.7 NEUROLOGIC
  • 0.2.7.1 ACUTE EXPOSURE
    • A) Symptoms following acute cyanide exposure include syncope, headache or CNS stimulation, agitation, dizziness, and vertigo followed by coma, seizures, and death. Sequelae may be paralysis and a Parkinsonian syndrome.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Nausea, vomiting, and abdominal pain may occur.
0.2.11 ACID-BASE
  • 0.2.11.1 ACUTE EXPOSURE
    • A) Anion gap metabolic acidosis and lactic acidosis are evident following cyanide toxicity.
0.2.13 HEMATOLOGIC
  • 0.2.13.1 ACUTE EXPOSURE
    • A) Venous blood may have a bright red color. Anemia has also been reported.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) Cyanide has been said to be absorbed through intact skin. Itching, irritation, rash, and dermatitis may occur.
    • B) Cyanosis may be evident particularly at the premorbid stage of cyanide toxicity.
0.2.15 MUSCULOSKELETAL
  • 0.2.15.2 CHRONIC EXPOSURE
    • A) Permanent motor impairment may occur.
0.2.16 ENDOCRINE
  • 0.2.16.1 ACUTE EXPOSURE
    • A) Enlarged thyroid glands may occur. Thyroid dysfunction has been reported from chronic occupational exposure to cyanide.
0.2.18 PSYCHIATRIC
  • 0.2.18.2 CHRONIC EXPOSURE
    • A) Permanent mental impairment may occur following severe acute poisoning.
0.2.20 REPRODUCTIVE HAZARDS
  • A) ANIMAL STUDIES - Sodium cyanide administered to pregnant rats has produced an increased incidence of resorptions and congenital malformations in the offspring, consisting of neural tube defects including exencephaly and encephalocele (Doherty et al, 1982). Concomitant administration of sodium thiosulfate prevented these teratogenic effects (Doherty et al, 1982). Post-implantation mortality was observed in the hamster.
  • B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
  • C) No information about possible male reproductive effects was found in available references at the time of this review.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS143-33-9 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
  • 0.2.21.2 HUMAN OVERVIEW
    • A) At the time of this review, no studies were found on the possible carcinogenic activity of sodium cyanide in humans.
  • 0.2.21.3 ANIMAL OVERVIEW
    • A) At the time of this review, no studies were found on the possible carcinogenic activity of sodium cyanide in experimental animals.
0.2.22 GENOTOXICITY
  • A) Sodium cyanide caused sex chromosome loss/nondisjunction in D. melanogaster.
0.2.23 OTHER
  • 0.2.23.1 ACUTE EXPOSURE
    • A) The odor of bitter almonds in expired breath or gastric contents of patients may not be detected by a significant portion of the population.
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