Dimethoate

CAS RN: 60-51-5

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) The following are general effects due to organophosphates, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for dimethoate, but could potentially occur in individual cases.
    • B) USES: Dimethoate, an organophosphate compound, is used as a systemic and contact insecticide. It is registered for use in the US and other countries; however it is not available for residential use in the US.
    • 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 dimethoate. 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, and 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. Opsoclonus has occurred rarely.
    • B) Acute glaucoma has been reported from dimethoate poisoning.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) Bradycardia, hypotension, and chest pain may occur. Tachycardia is also common. Dysrhythmias and conduction defects may occur in severe cases.
0.2.6 RESPIRATORY
  • 0.2.6.1 ACUTE EXPOSURE
    • A) Dyspnea, rales, bronchorrhea, or tachypnea may occur; with pulmonary edema in severe cases.
    • B) Bronchospasm may occur in previously sensitized asthmatics or as a muscarinic effect.
    • C) Acute respiratory insufficiency is the main cause of death in acute poisonings.
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) Muscle weakness, fatigability, and fasciculations are common findings and may be delayed in onset by several days. Paralysis may supervene.
    • C) Peripheral neuropathy (mixed sensory-motor type) may be delayed in onset by 6 to 21 days. Recovery may be slow or incomplete.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Vomiting, diarrhea, fecal incontinence and abdominal pain may occur.
    • B) Acute pancreatitis has been reported from dimethoate poisoning.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Increased urinary frequency or, in severe cases, urinary incontinence has occurred.
    • B) Acute renal failure is a rare complication of severe poisoning.
0.2.11 ACID-BASE
  • 0.2.11.1 ACUTE EXPOSURE
    • A) Metabolic acidosis has occurred in severe cases.
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.
0.2.16 ENDOCRINE
  • 0.2.16.1 ACUTE EXPOSURE
    • A) Hyperglycemia and glycosuria with or without ketosis may occur in severe poisoning.
0.2.17 METABOLISM
  • 0.2.17.1 ACUTE EXPOSURE
    • A) The hallmark of dimethoate poisoning is inhibition of plasma pseudocholinesterase or erythrocyte acetylcholinesterase, or both.
0.2.18 PSYCHIATRIC
  • 0.2.18.1 ACUTE EXPOSURE
    • A) Decreased vigilance, hallucinations, 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.
0.2.19 IMMUNOLOGIC
  • 0.2.19.1 ACUTE EXPOSURE
    • A) Dermal sensitization may occur.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Sporadic reports of human birth defects related to organophosphates have not been fully verified.
  • B) One case of spontaneous delivery after acute dimethoate poisoning has been reported.
  • C) Dimethoate was teratogenic in rats and cats and embryotoxic in mice.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS60-51-5 (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 dimethoate in humans.
  • 0.2.21.3 ANIMAL OVERVIEW
    • A) Dimethoate has been carcinogenic in rats by the oral route but was not carcinogenic in mice.
0.2.22 GENOTOXICITY
  • A) Dimethoate has induced DNA damage, unscheduled DNA synthesis, mutations, chromosome aberrations, sister chromatid exchanges, and other genotoxic events at the chromosomal level in a variety of short-term test systems in vitro or in vivo (RTECS , 1991).
  • B) There are some equivocal studies suggesting increased chromosome aberrations from occupational exposure. No increase in chromosome aberration frequency was found in lymphocytes of two women after acute suicidal dimethoate ingestion. Inheritance of an amplified CHE gene or inducibility of the gene on chromosome 3 was suggested in a chronically exposed family (Van Bao et al, 1974; Prody et al, 1989).
0.2.23 OTHER
  • 0.2.23.1 ACUTE EXPOSURE
    • A) Delayed toxicity can occur from acute exposure to dimethoate.
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