Dicrotophos

CAS RN:141-66-2

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Dicrotophos is registered for use as an insecticide or acaricide in the US.
    • B) TOXICOLOGY: Competitively inhibits 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 to organophosphates is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
    • D) 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 dicrotophos. 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 SIGNS0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Miosis, lacrimation, and blurred vision are common; mydriasis may occur in severe poisonings. Opsoclonus has occurred rarely.
    • B) Excessive salivation commonly occurs.
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 poisonings.
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 previously sensitized asthmatics or as a pharmacological 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. Alterations of the level of consciousness, seizures, and coma may occur. Seizures may be more common in children.
    • B) Peripheral neuropathy of the mixed sensory-motor type may be delayed in onset by 6 to 21 days. Recovery may be slow or incomplete.
      • 1) Dicrotophos did not induce delayed neurotoxicity in the standard hen assay.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Vomiting, diarrhea, fecal incontinence, abdominal pain and pancreatitis may occur.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Increased urinary frequency and urinary incontinence have occurred.
    • B) Immune-complex nephropathy with proteinuria and/or amorphous crystalluria may be seen.
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) The hallmark of organophosphate poisoning is inhibition of plasma pseudocholinesterase and erythrocyte acetylcholinesterase.
    • B) 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) Muscle weakness, fatigability, and fasciculations are common findings, and may be delayed in onset by several days. Paralysis may supervene.
    • B) The magnitude of the muscle response to a given neural stimulation was not affected in rats given dicrotophos in the diet.
0.2.16 ENDOCRINE
  • 0.2.16.1 ACUTE EXPOSURE
    • A) Hyperglycemia and glycosuria have been observed.
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, 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) Some organophosphates are sensitizers.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Dicrotophos was not teratogenic in mice, but was teratogenic in birds.
  • B) Most organophosphates have not been teratogenic in experimental animals, but some have caused lower fetal or birth weights and/or higher neonatal mortality.
  • C) Sporadic reports of human birth defects related to organophosphates have not been verified.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS141-66-2 (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) Not Listed
    • B) IARC Carcinogenicity Ratings for CAS18250-63-0 (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
    • C) IARC Carcinogenicity Ratings for CAS3735-78-2 (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) Not Listed
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Dicrotophos was not carcinogenic in feeding studies in rats or dogs.
    • B) Most organophosphates are thought NOT to be carcinogenic; however, some controversy exists.
0.2.22 GENOTOXICITY
  • A) Mutations have been observed in microorganisms. Sister chromatid exchanges were noted in hamster ovary cells. Gene conversion/mitotic recombination was observed in S. cerevisiae.
0.2.23 OTHER
  • 0.2.23.1 ACUTE EXPOSURE
    • A) Delayed symptoms have occurred from acute exposure to dicrotophos.
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