Know your pesticide: Paraquat

by Dr. Mohd. Isa Abd. Majid
The Sun, May 3, 1997

OVER THE PAST 10 YEARS, PARAQUAT has been the source of nearly 700 poisoning cases in Malaysia. Out of these, about 73% were due to suicide while the reminder were a result of accidental and occupational exposures. The reason for such a high incidence of poisoning with paraquat is somewhat difficult to determine but efforts have been made by the relevant agencies to reduce the number of registered products containing paraquat.

The ingestion of commercial paraquat formulations in all suicidal causes in variably fatal (about 60% death rate) and the resulting clinical features can be seen in a course of three to four weeks, depending on the quantity of paraquat ingested.

Commercial preparations of paraquat are normally sold in the form of liquid concentrate with a concentration ranging from 20% w/w to 42% w/w. These solutions are available for agricultural use as dichloride salts, which are water-soluble.

Besides being supplied in the form of a single active ingredient, there are products in the market containing paraquat in combinations with other herbicides such as sodium chlorate and 2,4-dimethylamine. From 1992-94, there were 92 registered products containing paraquat in Malaysia. Most of these products were supplied to farmers in the form of aqueous solutions ranging from 13% w/w to 25% w/w.

Besides the low-concentration products, paraquat is also supplied in bulk, normally referred to as tehcnical grade, to large scale plantations. The normal concentration of paraquat for the technical grade products is 42% w/w. Currently, there are about 20 products containing paraquat approved to be used in the agriculture sector. The following are some important points concerning paraquat.

How does paraquat act on weeds?

In terms of its action on weeds, paraquat interferes with the intracellular electron transfer systems, thus inhibiting the reduction of an enzyme during photosynthesis. This will then result in the accumulation of superoxide radicals which cause destruction of lipid cell membranes of the leaves.

What are the clinical manifestations of paraquat poisoning?

The symptoms of paraquat poisoning depends on the amount and route of absorption into the body. Exposure to paraquat through brief dermal contact or inhalation of spray mist procedures mild symptoms consisting of local skin irritation, reversible irregularities in nail morphology and occasional epistaxis. Following exposure to the eye, corneal injury, lacrimation and corrosion of the lens may result.

The major symptoms from paraquat ingestion are seen in the mouth and the oesophagus. They may include ulcers on the lips, burning and ulceration of the tongue and pharynx. In some massive ingestion cases, oesophageal ulceration may occur.

This may proceed to oesophageal perforation. Following ingestion of greater than 50ml of the liquid concentrate, the patient may develop pulmonary oedema, cardiac failure, renal failure, liver failure and also convulsions caused by central nervous system involvement. Under these circumstances, death may occur within several hours to a few days as a result of multiple organ failure.

Ingestion of a smaller volume (10 ml to 20 ml) of the concentrate produces the same symptoms with the exception that the development of renal failure occurs within two to six days after ingestion. The major effect of poisoning at this volume is the accumulation of high concentrations of paraquat in the lung. In the lung, the paraquat ion undergoes a continuous reduction-oxidation process to form free radicals capable of reacting with oxygen. This reaction leads to the production of a reactive oxygen also known as superoxide onion and the regeneration of the paraquat ions.

The superoxide anoin is then converted into hydrogen peroxide by the enzymes superoxide dismutase. The continous generation of the superoxide anion under the depletion of an enzyme and hydrogen peroxide will then attact the polyunsaturated lipids present in the lung membranes to produce lipid hydroporoxides (a form of lipid-free radical) which in turn can react with further unsaturated lipids to form more lipid-free radicals, thereby perpetuating the system.

The resulting cellular membrane damage reduces the functional intefrity of the lung cells, affects efficient gas transport and exchange and results in respiratory impairment. The development of pulmonary lesions as a result of cellular lipid peroxidation can be divided into two distinct phases.

The first phase, which occurs within one to three days after ingestion, is characterised by the destruction of the alveolar epithelial cells. This leads to alveolitis, characterised by pulmonary oedema and infiltration of the air spaces of the lungs and the intestinal tissues with neutrophil polymorphs.

The second phase involves the development of extensive fibrosis as a response to the acute alveolitis occurring in the first phase. During this stage, the proliferation of the fribroblasts and deposition on collagen will further reduce the effectiveness of gaseous exchange. The consequence is death resulting from severe anoxia.

In summary, as the lung function begins to deteriorate, the patient will suffer from breathlessness, tachypnoea, widespread crepitations and central cyanosis. These changes continue over a period of five to seven days before the patient finally develops respiratory failure.

How is paraquat poisoning managed?

There is no specific antidote for paraquat poisoning, In such poisoning, treatment from confirmed ingestion of paraquat ingestion is largely supportive and aimed at interrupting the pathway of paraquat toxicity. Its management is primarily directed at removing paraquat from the site of absorption such as the gastrointestinal tract, increasing its excretion from blood and adopting measures aimed at preventing lung damage.

It should be noted that hospitalisation is required in all cases of suspected paraquat poisoning.

  • Prevention of absorption
    Gastric lavage should be performed immediately if possible within two hours after ingesting paraquat. This is to reduce further absorption of paraquat into the bloodstream. Following gastric emptying, the adminisyration of mineral absorbents such as Fuller's Earth, bentonite or activated charcoal is initiated to remove any unabsorbed paraquat remaining in the gastrointestinal tract. In some cases, cathartics, for example magnesium sulphate, magnesium citrate or sorbitol, may be given every four hours either concurrently or separately with the absorbents.
  • Enhancement of elimination
    A variety of techniques has been used in an attempt to enhance the elimination of paraquat from the body. The recommended regimen for increased paraquat excretion from the blood is haemoperfusion, which has been shown to increase the chance of survival among poisoned patients. Using this approach, the haemoperfusion may be repeated until the paraquat level remains below a certain value, normally 0.01 mg/ml.
  • Prevention of pulmonary damage
    Paraquat is known to accumulate selectively in lung tissues and destruction of the tissues is exacerbated by the administration of oxygen. Thus it is suggested that the minimal oxygen is given to the patient to reduce the damage caused by the oxygen.

The writer is a pharmacist and head of the Toxicology Laboratory at the National Poison Centre, Universiti Sains Malaysia, 11800 Minden, Penang.


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