CAS RN:333-41-5

Health Effects

    • A) USES: Used for pest control in industrial agriculture (tends to be more toxic agents), organophosphates of low to intermediate toxicity are used to control ectoparasites on farm and companion animals, and humans (head lice), and for home and garden pest control. Poisoning occasionally occurs from ingestion of contaminated crops or food.
    • B) 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 develop.
    • C) EPIDEMIOLOGY: Exposure is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
      • 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, acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia 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 development of delayed peripheral neuropathy. Manifestations can include inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, 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. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases 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.
  • A) Most organophosphates are not teratogenic in animals, but some cause lower fetal birth weights and/or higher neonatal mortality.
  • B) Sporadic reports of human birth defects related to organophosphates have not been fully verified.
    • A) Refer to individual documents for information about carcinogenic effects of organophosphates. TETRACHLORVINPHOS has been classified as possibly carcinogenic to humans (Group
    • 2B) by IARC following a systematic review and evaluation.
  • A) Cytogenetic studies of organophosphate-exposed workers have suggested possible increases in frequencies of chromosome aberrations (Van Bao et al, 1974), but the evidence is not compelling.
  • B) TETRACHLORVINPHOS: Tetrachlorvinphos was not mutagenic in bacterial mutagenesis tests, but genotoxicity in some assays (chromosomal damage) and increased cell proliferation (hyperplasia) were observed in animals and/or in vitro studies (Guyton et al, 2015).
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