Definitions

Sodium_fluoroacetate

Sodium fluoroacetate

[floor-oh-as-i-teyt, flawr-oh-, flohr-oh-]
| Section8 = }} Sodium fluoroacetate (also known as sodium monofluoroacetate, compound 1080 or 1080) is a potent metabolic poison that occurs naturally as an anti-herbivore metabolite in various plants. It works by interfering with the citric acid cycle, and is used primarily to control mammalian pests, including invasive species. The existence of this chemical was first noted in the Second World War.

Uses

Sodium fluoroacetate is used as a rodenticide. Farmers and graziers use the poison to protect pastures and crops from various herbivorous mammals. It is used in New Zealand to control the Common Brushtail Possum , while in the United States it is used to kill coyotes. Other countries using 1080 include Australia, Mexico and Israel.

Western Shield is a recent project to boost populations of endangered mammals in south-west Australia. The project is to drop Sodium fluoroacetate baited meat from helicopters or light aircraft to kill predators. Wild dogs and foxes will readily eat the baited meat. Cats pose a greater difficulty as cats aren’t interested in already dead animals. Recently a pilot tried putting small sound generators inside the baits with significant positive results. However, an Australian RSPCA commissioned study criticized 1080 calling it an inhumane killer.

History

Sodium fluoroacetate was discovered by German military chemists in World War II. The chemical was highly potent — but it was difficult to deliver, requiring ingestion or injection for optimal effect. As such, it was largely overlooked until it was independently rediscovered by American chemists researching pesticides. The name "1080" refers to the catalogue number of the poison, which became its brand name.

Occurrence

Sodium fluoroacetate occurs naturally in at least 40 plants in Australia, Brazil and Africa. It was first identified as the poison of poison leaf Dichapetalum cymosum by Marais in 1944, although it had been reported as early as 1904 that colonists in Sierra Leone used extracts of Chailletia toxicaria which also contains fluoroacetic acid or its salts to poison rats. It is believed that the compound is even present in tea leaves in tiny amounts. The Australian pea family Gastrolobium (“poison peas”), have sodium fluoroacetate in the leaf tips and seeds. This forces livestock farmers in Western Australia to hand-weed out all the plants from their paddocks. It also means that some Western Australian herbivores have, by natural selection, developed partial immunity to the effects of fluoroacetate; this has been used for an advantage in DEC’s wildlife conservation project named Western Shield.

Toxicology

Fluoroacetate is highly toxic to mammals and insects. The oral dose of fluoroacetate sufficient to be lethal in humans is 2–10 mg/kg.

Species have different susceptibility to sodium fluoroacetate due to metabolic differences. The New Zealand Food Authority established lethal doses for a number of species. Dogs, cats and pigs appear to be the species most susceptable to poisoning.

Mechanism of action

Fluoroacetate is similar to acetate, which has a pivotal role in cellular metabolism. Fluoroacetate disrupts the citric acid cycle (also known as the Krebs cycle) by combining with coenzyme A to form fluoroacetyl CoA. This is then substituted for acetyl CoA in the citric acid cycle and reacts with citrate synthase to produce fluorocitrate. A metabolite of fluorocitrate binds very tightly to aconitase, thereby halting the citric acid cycle. This results in an accumulation of citrate in the blood which deprives cells of energy.

Symptoms

In humans the symptoms of poisoning normally appear between 30 minutes and three hours after exposure. Initial symptoms typically include nausea, vomiting and abdominal pain; sweating, confusion and agitation follow. In significant poisoning cardiac abnormalities including tachycardia or bradycardia, hypotension and ECG changes develop. Neurological effects include muscle twitching and seizures; Consciousness becomes progressively impaired after a few hours leading to coma. Death is generally due to Ventricular arrhythmias, progressive hypotension unresponsive to treatment, and secondary lung infections.

Symptoms in domestic animals vary: dogs tend to show nervous system signs such as convulsions and uncontrollable running, whilst large herbivores such as cattle and sheep more predominantly show cardiac signs.

Sub-lethal doses of sodium fluoroacetate may cause damage to tissues with high energy needs — in particular, the brain, gonads, heart, lungs and fetus. Sub-lethal doses are typically completely metabolised and excreted within four days.

Treatment

Because of the biochemical interference in the TCA or Krebs Cycle, sodium fluoroacetate poisoning is very difficult to treat, as once clinical symptoms are shown, the Krebs Cycle has shut down. There is no known effective antidote. Research in monkeys has shown that the use of glyceryl monoacetate can prevent problems if given after ingestion of sodium fluoroacetate, and this has been done in domestic animals with some positive results. The theory of using glyceryl monoacetate is that it will supply acetate ions to allow continuation of the cellular respiration process which the sodium fluoroacetate has disrupted.

In clinical cases, use of muscle relaxants, anti-convulsants, mechanical ventilation and other supportive measures may all be required. Few animals or people have been treated successfully after significant sodium fluoroacetate ingestions.

References

Further reading

  • Klingensmith CW (1945). "The Natural Occurrence of Fluoroacetic Acid, the Acid of the New Rodenticide 1080". Science 102 622–623.

External links

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