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Chapter: Modern Medical Toxicology: Hydrocarbons and Pesticides: Pesticides

Chlorophenoxy Compounds - Herbicides (Weedicides)

Chlorophenoxyacetate herbicides include the following: ■■ MCPA (4-chloro-2-methylphenoxyacetic acid) ■■ MCPP (2-methyl-4-chlorophenoxypropionic acid) ■■ DCPP (2,4-dichlorophenoxypropionic acid) ■■ 2,4D (2,4-dichlorophenoxyacetic acid) ■■ 2,4,5-T (2,4,5-trichlorophenoxyacetic acid)

Chlorophenoxy Compounds

Chlorophenoxyacetate herbicides include the following:

■■  MCPA (4-chloro-2-methylphenoxyacetic acid)

■■  MCPP (2-methyl-4-chlorophenoxypropionic acid)

■■  DCPP (2,4-dichlorophenoxypropionic acid)

■■  2,4D (2,4-dichlorophenoxyacetic acid)

■■  2,4,5-T (2,4,5-trichlorophenoxyacetic acid)

These herbicides are used to kill broad-leaved weeds in cereal crops, grassland parks and gardens, and weeds in ponds, lakes, and irrigation canals.


2,4D: Fennoxone, Weednash.


Rapid and complete absorption of chlorophenoxy compounds from the GI tract has been reported. Dermal absorption is limited. Chief organs of deposition are kidneys, liver, central and peripheral nervous systems, and the gastrointestinal tract. They are highly protein bound. Phenoxy acid esters and salts are primarily metabolised by acid hydrolysis; a minor amount is conjugated. They are primarily eliminated unchanged (90%) by the kidneys via the renal organic anion secretory system.

Clinical Features


o     Nausea, vomiting, diarrhoea, miosis, fever, hypotension, emesis, tachycardia, bradycardia, ECG abnormalities, pulmonary oedema, muscle rigidity, rhabdomyolysis, muscle weakness, peripheral neuropathy, hyperthermia, acidaemia and coma.

o     Hypocalcaemia, hyperkalaemia, and hypophosphataemia.

o     Ingestions involving high concentrations, or exposures of long duration may produce burning in the mouth, oesophagus and stomach.

o     Vertigo, headache, malaise and paraesthesias can occur.

o     Thrombocytopenia and leukopenia have also been reported.

·      Allegations of human birth defects related to 2,4-D and/or 2,4,5-T have not been confirmed. However, some evidence from a report on Vietnam veteran’s children shows a limited or suggestive level of evidence between exposure to 2,4-D and/or 2,4,5-T and spina bifida. A major limitation of the report was the inability to quantify levels of herbicide exposure in individual troops.

·      The causal relationship between chlorophenoxy herbicides and cancer remains controversial. Some studies have suggested a relationship between chlorophenoxy herbicides and both soft tissue sarcoma and non-Hodgkin’s lymphoma, while others have not.

·      A mixture of 2,4-D and 2,4,5-T (Agent Orange) has been alleged to have caused cancer, birth defects, and many other illnesses in Vietnam veterans. It is however more likely that contaminant (2,3,7,8-tetrachlorodibenzodioxin or TCDD) caused these effects.



·              Monitor CPK levels and serum myoglobin levels.

·              Monitor liver and kidney function tests.

·              Monitor CBC and platelet count.


·              Monitor urine for pH, protein, RBC’s, myoglobin, and urine output.

·              Chlorophenoxy compound urine analysis may be useful as a confirmatory test. Limited data suggest that urinary 2,4-D levels may be useful in monitoring workers with industrial and commercial exposure.

Radiographic Studies: Monitor the chest X-ray in patientswith significant exposure.

Laboratory Methods:

·              GC/MS—A method using acid hydrolysis, diazoethane derivatisation, and silica gel column chromatography for sample preparation followed by combined capillary gas chromatography and mass spectrometry in the selective ionisation modes of positive and negative chemical ioni-sation was successful in improving the detection limit to 1 ppb for urine samples. This method is designed for use in large epidemiologic studies to document exposure to chlorophenoxy herbicides.

·              HPLC—Can be used by utilising methanolic hydro-chloric acid extraction and resolution with a phenyls-ilyl-modified silica column/aqueous buffer acetonitrile eluent, to partially quantify a variety of chlorophenoxy compounds in biological samples of acutely poisoned patients. The limit of detection is said to be 20 mg/L. 2,4-D can be quantitated in human autopsy material.

·              Visceral samples are acidified, and blood and plasma deproteinised with methanol, followed by acidifica-tion, extraction with diethyl ether, and analysis using HPLC.

·              Urinary levels of 2,4-D can be detected with gas chro-matography with mass selective detection (GC/MSD) with a lower limit of detection of 5 ppb.

·              Ultraviolet Spectrometry—This is an older and non-selective method which does not differentiate between chlorophenoxy and benzonitrile herbicides. These two herbicide types are often combined in commercial products. Published values using this method are of dubious value.

·              A direct enzyme immunoassay can detect urinary levels as low as 19 ppm and has been validated in 2,4-D-exposed workers.


·            Decontamination: Activated charcoal, gastric lavage, etc.,can be considered if no more than 4 hours have elapsed since ingestion.

·            Manage respiratory depression if present. Assisted venti-lation may be required.

·            Hypotension: Infuse 10 to 20 ml/kg of isotonic fluid and place in Trendelenburg position. If hypotension persists, administer dopamine or noradrenaline. Consider central venous pressure monitoring to guide further fluid therapy.

·            Maintain adequate urine flow with intravenous fluids if the victim is dehydrated. Monitor fluid and electrolyte balance and replace as required.

·            Manage hyperthermia with sponge baths.

·            Induce alkaline diuresis if myoglobinuria, coma, or severe metabolic acidosis is present.

·            Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disturbances (particularly hypokalaemia, hypocalcaemia, and hypomagnesaemia). Lignocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Sotalol is a good alternative. Unstable rhythms require cardioversion. Atropine may be used when severe brady-cardia is present.

For inhalation exposure:

·              Move patient from the toxic environment to fresh air.

·              Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respira-tory tract irritation, bronchitis, or pneumonitis.

·              Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required.

·              Administer inhaled beta adrenergic agonists if bron-chospasm develops.

·              Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases. Maintain adequate ventilation and oxygena-tion with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 ml/kg) is preferred if ARDS develops. The pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output.

For dermal exposure:

·              Remove contaminated clothing and jewellery; wash skin, hair and nails vigorously with repeated soap washings. Leather absorbs pesticides; all contami-nated leather should be discarded.

·              Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

·            Haemodialysis is not effective; alkaline diuresis may be useful, particularly if begun soon (vide supra). Plasmapheresis may be effective for late treatment of poisoning.

Autopsy Features

·      Apart from non-specific signs, evidence of disseminated muscle cell necrosis was discovered in myocardial fibres, focal with reactive cellular infiltration, in one case of fatal ingestion. The man died within 12 hours of the ingestion.

·              Significant erosion of the stomach lining was also observed.

·              There was in addition, massive haemostasis of the lungs in all capillaries, and severe alveolar oedema

·      Fluid filled lungs with large quantities of oedema fluid expressible from cut surfaces were described at autopsy in another fatal ingestion case. In this case, the abdominal and thoracic cavities contained a thin reddish watery fluid.

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