Parathion

CAS RN:56-38-2

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for parathion, but could potentially occur in individual cases.
    • B) USES: Parathion is an organophosphate acaracide and insecticide. The use of parathion is severely restricted or banned in many countries. Since October 2003, production, importation, or application of parathion in the US is illegal.
    • C) TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop.
    • D) EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
    • E) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
      • 2) SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
      • 3) DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to parathion. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete.
      • 4) CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
      • 5) INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) Vital sign changes can include bradycardia or tachycardia, hypotension or hypertension, tachypnea, respiratory paralysis or fever.
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Miosis, lacrimation, blurred vision and salivation are common; mydriasis may occur in severe poisonings.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) Bradycardia, hypotension, and chest pain may occur. Tachycardia and hypertension are also common. Dysrhythmias and conduction defects may occur in severe poisonings.
    • B) One case of pericarditis has occurred with otherwise typical symptoms.
0.2.6 RESPIRATORY
  • 0.2.6.1 ACUTE EXPOSURE
    • A) Dyspnea, rales, bronchorrhea, or tachypnea may be noted. Pulmonary edema may occur in severe cases.
    • B) Bronchospasm may occur in asthmatics or as a pharmacological muscarinic effect.
    • C) Acute respiratory insufficiency is the main cause of death in acute poisonings.
    • D) Delayed respiratory effects may occur 2 to 3 weeks after acute exposure.
0.2.7 NEUROLOGIC
  • 0.2.7.1 ACUTE EXPOSURE
    • A) Headache, dizziness, muscle spasms, and profound weakness are common. Altered level of consciousness, seizures, and coma may occur. Seizures may be more common in children.
    • B) Delayed polyneuropathy of the mixed sensory-motor type may occur 6 to 21 days after acute exposure. Recovery may be slow or incomplete.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Vomiting, diarrhea, fecal incontinence, pancreatitis and abdominal pain may occur, especially from percutaneous and inhalation exposures.
0.2.9 HEPATIC
  • 0.2.9.1 ACUTE EXPOSURE
    • A) Liver function may be disturbed.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Increased urinary frequency or, in severe cases, urinary incontinence has occurred.
0.2.11 ACID-BASE
  • 0.2.11.1 ACUTE EXPOSURE
    • A) Metabolic acidosis has occurred in several severe poisonings.
0.2.13 HEMATOLOGIC
  • 0.2.13.1 ACUTE EXPOSURE
    • A) Alteration in prothrombin time and/or tendency to bleeding may occur.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) Sweating is a consistent but not universal sign.
    • B) Dermal sensitization may occur.
0.2.15 MUSCULOSKELETAL
  • 0.2.15.1 ACUTE EXPOSURE
    • A) Myopathic changes were seen in the diaphragm on autopsy in one case.
0.2.16 ENDOCRINE
  • 0.2.16.1 ACUTE EXPOSURE
    • A) Both hypoglycemia and hyperglycemia have occurred with organophosphate poisoning; cholinergic agents stimulate secretion of insulin by the islets of Langerhans.
    • B) Hyperglycemia and glycosuria, with or without ketosis, may occur in severe poisoning.
0.2.17 METABOLISM
  • 0.2.17.1 ACUTE EXPOSURE
    • A) Inhibition of plasma and/or red blood cell cholinesterase is the clinical hallmark of organophosphate toxicity.
0.2.18 PSYCHIATRIC
  • 0.2.18.1 ACUTE EXPOSURE
    • A) Decreased vigilance, defects in expressive language and cognitive function, impaired memory, depression, anxiety or irritability and psychosis have been reported, more commonly in persons having other clinical signs of organophosphate poisoning.
    • B) Visual and auditory hallucinations have occurred with parathion poisoning.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Parathion has been fetotoxic in laboratory animals.
  • B) No reports were available on possible reproductive effects of parathion in humans; however, methyl parathion, a closely related compound, has been linked with human birth defects.
  • C) Pregnant MICE were more sensitive to parathion than nonpregnant ones.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS56-38-2 (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) IARC Classification
        • a) Listed as: Parathion
        • b) Carcinogen Rating: 2B
      • 1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Parathion has been classified as possibly carcinogenic to humans (Group
    • 2B) by IARC following a systematic review and evaluation.
0.2.22 GENOTOXICITY
  • A) Parathion has induced DNA damage in rodents, mutations in Salmonella and sister chromatid exchanges in vitro (RTECS , 1991).
  • B) Parathion was not mutagenic in bacterial mutagenesis tests. However, DNA and chromosomal damage were observed in human cells in vitro (Guyton et al, 2015).
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