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HISTORY AND EPIDEMIOLOGY

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Sodium monofluoroacetate (SMFA) occurs naturally in plants native to Brazil, Australia, and South and West Africa (eg, gifblaar {Dichapetalum cymosum}).11 The highest concentration (8.0 mg/g) is found in the seeds of a South African plant, Dichapetalum braunii.11 In the 1940s, SMFA was released as a rodenticide (CAS No. 62-74-8) and assigned the compound number 1080, which was registered as its trade name. Fluoroacetamide, a similar pesticide, is known as Compound 1081. These compounds are widely effective as poisons against most mammals and some amphibians.26 Both products were banned in the United States in 1972, except to protect sheep and cattle from coyotes. Collars embedded with SMFA are placed around the neck of livestock, the typical point of attack for coyotes.

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Sodium monofluoroacetate is used extensively in New Zealand and Australia to control the possum population and other animal species considered pests that have no natural predators. Its continued use is extremely controversial, but following a recent review of the ramifications of the use of the compound, the government of New Zealand retained both the aerosolized and collar applications. Reported cases of human poisoning with SMFA are uncommon and the epidemiology is poorly understood. There have been only 65 reported cases from 1999 to 2010 with no deaths in the National Poisoning Database System of the American Association of Poison Control Centers (Chap. 136).

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TOXICOKINETICS AND TOXICODYNAMICS

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Sodium monofluoroacetate is an odorless and tasteless white powder with the consistency of flour. When it is dissolved in water, it is said to have a vinegarlike taste. Sodium monofluoroacetate and fluoroacetamide (CAS No. 640-19-7) are well absorbed by the oral and inhalational routes.10,11,12,27 Detailed toxicokinetic data are lacking in humans, but in sheep, up to 33% of an ingested dose is excreted unchanged in the urine over 48 hours. Glucuronide and glutathione conjugates have been isolated.11 Substantial defluorination is not thought to occur in vivo. The serum half-life is estimated to be 6.6 to 13.3 hours in sheep.10 Sodium monofluoroacetate has an LD50 of 0.07 mg/kg in dogs.19 The oral dose thought to be lethal to humans is 2 to 10 mg/kg.3

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PATHOPHYSIOLOGY

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Sodium monofluoroacetate, a structural analog of acetic acid (Fig. 115–1), is an irreversible inhibitor of the tricarboxylic acid cycle (Fig. 13–3). Monofluoroacetic acid enters the mitochondria, where it is converted to monofluoroacetyl-coenzyme A (CoA) by acetate thiokinase. Mitochondrial citrate synthase is then joined with the monofluoroacetyl-CoA complex with oxaloacetate to form fluorocitrate. Fluorocitrate then covalently binds aconitase, preventing the enzyme from any further metabolic activity in the tricarboxylic acid cycle.17 Thus, fluorocitrate acts as a “suicide inhibitor” of aconitase, producing a biochemical dead end. The net toxicity caused by fluorocitrate results from the increase in tricarboxylic acid cycle ...

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