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.
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.
·
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.
·
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.
·
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.
·
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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