Sodium fluoroacetate

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Sodium fluoroacetate
Names
IUPAC name
Sodium 2-fluoroacetate
Other names
1080
SFA
Sodium monofluoroacetate, compound 1080, 1080
Identifiers
3D model (JSmol)
ChemSpider
ECHA InfoCard 100.000.499 Edit this at Wikidata
KEGG
RTECS number
  • AH9100000
  • InChI=1S/C2H3FO2.Na/c3-1-2(4)5;/h1H2,(H,4,5);/q;+1/p-1 checkY
    Key: JGFYQVQAXANWJU-UHFFFAOYSA-M checkY
  • InChI=1/C2H3FO2.Na/c3-1-2(4)5;/h1H2,(H,4,5);/q;+1/p-1
    Key: JGFYQVQAXANWJU-REWHXWOFAP
  • [Na+].[O-]C(=O)CF
Properties
NaFC2H2O2
Molar mass 100.0 g/mol
Appearance Fluffy, colorless to white powder
Melting point 200 °C (325.15 K)
Boiling point Decomposes
soluble
Hazards
Occupational safety and health (OHS/OSH):
Main hazards
 Toxic, Flammable
Flash point ?
Lethal dose or concentration (LD, LC):
0.1–5.0 mg/kg (oral in various species of rats and mice)[1]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Sodium fluoroacetate is the organofluorine chemical compound with the formula FCH2CO2Na. This colourless salt is used as a metabolic poison. It occurs naturally as an anti-herbivore metabolite in various plants but can also be produced synthetically. It is a derivative of fluoroacetic acid, a carboxylic acid. The more common fluorinated acetic acid trifluoroacetic acid and its derivatives are far less toxic.

History and production

The effectiveness of sodium fluoroacetate as a rodenticide was reported in 1942.[1] The name "1080" refers to the catalogue number of the poison, which became its brand name.[2]

The salt is synthesized by treating sodium chloroacetate with potassium fluoride.[3] Production has declined because the salt is banned in many countries.

Occurrence

Sodium fluoroacetate occurs naturally in at least 40 plants in Australia, Brazil, and Africa. It was first identified in the poison leaf Dichapetalum cymosum by Marais in 1944.[4][5] As early as 1904, colonists in Sierra Leone used extracts of Chailletia toxicaria which also contains fluoroacetic acid or its salts to poison rats.[6][7] It is believed that the compound is even present in tea leaves in tiny amounts.[8] The Australian pea family Gastrolobium (“poison peas”), is only one of several native Australian plant genera which contain the toxin: others include Gompholobium, Oxylobium, Nemcia and Acacia. The presence of such plants in the fields of farmers in Western Australia has often forced these farmers to 'scalp' their land, that is remove the top soil and any poison pea seed which it may contain, and replace it with a new poison pea-free top soil sourced from elsewhere in which to sow crops.[citation needed]

Toxicology

Fluoroacetate is highly toxic to mammals and insects.[2] The oral dose of fluoroacetate sufficient to be lethal in humans is 2–10 mg/kg.[9]

The toxicity varies with species. The New Zealand Food Safety Authority established lethal doses for a number of species. Dogs, cats and pigs appear to be most susceptible to poisoning.[10]

The enzyme fluoroacetate dehydrogenase has been discovered in a soil bacterium, which can detoxify fluoroacetate in the surrounding medium.

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, which reacts with citrate synthase to produce fluorocitrate. A metabolite of fluorocitrate binds very tightly to aconitase, thereby halting the citric acid cycle. This inhibition results in an accumulation of citrate in the blood which deprives cells of energy.[2]

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 normally due to Ventricular arrhythmias, progressive hypotension unresponsive to treatment, and secondary lung infections.[2]

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.[11]

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.[12]

Treatment

Effective antidotes are unknown. Research in monkeys has shown that the use of glyceryl monoacetate can prevent problems if given after ingestion of sodium fluoroacetate, and this therapy has been tested in domestic animals with some positive results. In theory, glyceryl monoacetate supplies acetate ions to allow continuation of cellular respiration which the sodium fluoroacetate had disrupted.[13]

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.[14]

Uses

Common Brushtail Possum, an invasive pest in New Zealand whose population is controlled with sodium fluoroacetate.
See also: 1080 usage in New Zealand

Sodium fluoroacetate is used as a pesticide, especially for mammalian pest species. 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 and rats.[15] In the United States, it is used to kill coyotes.[16] Prior to 1972 when the EPA cancelled all uses, sodium fluoroacetate was used much more widely as a cheap[17] predacide and rodenticide; in 1985, the restricted-use "toxic collar" approval was finalized.[18] Other countries using 1080 include Australia, Mexico, and Israel.[2]

Western Shield is a project to boost populations of endangered mammals in south-west Australia conducted by the DEC. The project entails distributing fluoroacetate baited meat from the air to kill predators. Wild dogs and foxes will readily eat the baited meat. Cats pose a greater difficulty as they are not interested in scavenging.[citation needed] However, an Australian RSPCA commissioned study criticized 1080, calling it an inhumane killer.[19] Some Western Australian herbivores have, by natural selection, developed partial immunity to the effects of fluoroacetate,[20] so that its use as a poison has the advantage of reduced collateral damage to native herbivores.

Environmental impact

Since 1080 is highly water soluble, it will be dispersed and diluted in the environment by rain and stream water. Some micro-organisms in the soil, such as Pseudomonas species, may defluorinate 1080. Sodium monofluoroacetate at the concentrations found in the environment after standard baiting operations will break down in natural water containing living organisms, such as aquatic plants or micro-organisms. It is stable in sterile water. Water-monitoring surveys, conducted during the 1990s, have confirmed that significant contamination of waterways following aerial application of 1080 bait is unlikely. [21]


Food chain

  • Trials show that 1080 is rapidly biodegraded by aquatic and land plants, and by micro-organisms in water and soils.24
  • Trials also show that animals ingesting sub-lethal doses of 1080 rapidly excrete the poison or metabolise it into non-toxic products. All traces of the poison in live animals are gone within 10 days.25
  • Fish were fed 1080 baits in separate studies in the United States and New Zealand. Of the fish tested in both trials, 100 percent survived and none showed any ill effects.
  • Sausages containing levels of 1080 comparable to those found in a 1080-poisoned possum carcass were also fed to eels in the New Zealand study. After eating all of the sausages, all of the eels survived and none became ill. The eels rapidly eliminated the toxin from their bodies.

Bird populations

  • DOC monitors bird populations and bush health following 1080 applications in many parts of the country. Long-term assessments demonstrate that native bird populations are not damaged by 1080, and indeed that most native bird species show net benefits, especially from the impact of the 'triple predator' by-kill effect of aerial 1080, referred to above. The benefits for native bird populations of effectively taking out three major predators at once are in some cases spectacular.28
  • Some inadvertent by-kill of native birds has been recorded, but is more than made up for by the subsequent increase in populations. Kea deaths recorded on the West Coast in 2008 are, however, of real concern, and the Department of Conservation is working with the Kea Conservation Trust on extensive research to determine how to prevent this recurring in future.29

Insect populations

  • Monitoring of ground-based insect populations show minimal loss of insect life from 1080, and increase after aerial 1080 targeting as a result of reduced insect predation from introduced mammalian predators.

References

  1. ^ a b Kalmbach ER (1945). "Ten-Eighty, a War-Produced Rodenticide". Science. 102 (2644): 232–3. doi:10.1126/science.102.2644.232. PMID 17778513.
  2. ^ a b c d e Proudfoot AT, Bradberry SM, Vale JA (2006). "Sodium fluoroacetate poisoning". Toxicol Rev. 25 (4): 213–9. doi:10.2165/00139709-200625040-00002. PMID 17288493.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Aigueperse, Jean (2005). "Ullmann's Encyclopedia of Industrial Chemistry" (Document). Weinheim: Wiley-VCH. doi:10.1002/14356007.a11_307. {{cite document}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |contribution= ignored (help)
  4. ^ Marais JCS (1943). "The isolation of the toxic principle "K cymonate" from "Gifblaar", Dichapetalum cymosum". Onderstepoort Jour. Vet. Sci. Animal Ind. 18: 203.
  5. ^ Marais JCS (1944). "Monofluoroacetic acid, the toxic principle of "gifblaar" Dichapetalum cymosum". Onderstepoort Jour. Vet. Sci. Animal Ind. 20: 67.
  6. ^ Renner (1904). "Chemical and Physiological Examination of the Fruit of Chailletia Toxicaria". Jour African Soc.: 109.
  7. ^ Power FB, Tutin F (1906). "C hemical and Physiological Examination of the Fruit of Chailletia Toxicaria". J. Am. Chem. Soc. 28: 1170. doi:10.1021/ja01975a007.
  8. ^ Vartiainen T, Kauranen P (1984). "The determination of traces of fluoroacetic acid by extractive alkylation, pentafluorobenzylation and capillary gas chromatography-mass spectrometry". Anal Chim Acta. 157 (1): 91–7. doi:10.1016/S0003-2670(00)83609-0.
  9. ^ Beasley, Michael (2002). "Guidelines for the safe use of sodium fluoroacetate (1080)" (PDF). New Zealand Occupational Safety & Health Service. Retrieved 2007-12-17. {{cite web}}: Unknown parameter |month= ignored (help)
  10. ^ "Controlled Pesticides: Sodium Fluoroacetate (1080) in Pest Control" (PDF). Agricultural Compounds and Veterinary Medicines Group. Retrieved 2007-12-17.
  11. ^ Gupta, Ramesh (2007). Veterinary Toxicology: Basic and Clinical Principles. Amsterdam: Elsevier. p. 556. ISBN 0-12-370467-7. Retrieved 2010 Jul 28. {{cite book}}: Check date values in: |accessdate= (help)
  12. ^ Eason (1993 October 28). King, Carolyn (ed.). "Sodium monofluoroacetate and alternative toxins for possum control". New Zealand Journal of Zoology. 20 (3). Wellington, New Zealand: The Royal Society of New Zealand: 330. ISSN 0301-4223. Retrieved 2010 Jul 2. Sodium monofluoroacetate was readily absorbed and rapidly eliminated in all species: only traces were detectable in sheep muscle after 72-96 h {{cite journal}}: Check date values in: |accessdate= and |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  13. ^ Brent, Jeffrey (2005). Critical care toxicology: diagnosis and management of the critically poisoned patient. St. Louis: Mosby. p. 970. ISBN 0-8151-4387-7. Retrieved 2010 Jul 28. Glycerol monoacetate, 0.1 to 0.5 mL/kg/hr, as a Krebs cycle substrate replacement, has prolonged survival in a primate model, but it also may aggravate toxicity and seems to be effective only early in the course. {{cite book}}: Check date values in: |accessdate= (help)
  14. ^ Rippe, James M.; Irwin, Richard S. (2008). Irwin and Rippe's intensive care medicine. Philadelphia: Wolters Kluwer Health / Lippincott Williams & Wilkins. pp. 1666–1667. ISBN 0-7817-9153-7. Retrieved 2010 Jul 28. General supportive measures are paramount and aimed at maintaining the airway, breathing, and circulation. Activated charcoal should be administered in all suspected ingestions presenting within 1 to 2 hours after ingestion. Seizures should be treated with benzodiazepines or barbiturates. Hypocalcemia and prolonged QTc intervals may require calcium and magnesium supplementation. Various treatments have been tested in animals [149,161-163]. The most useful agent appears to be glyceryl monoacetate, which provides excess acetate as a substrate for the TCA cycle. The clinical use of glyceryl monoacetate remains unproven, however. {{cite book}}: Check date values in: |accessdate= (help)CS1 maint: multiple names: authors list (link)
  15. ^ Green W (July 2004). "The use of 1080 for pest control" (pdf). The Animal Health Board and The Department of Conservation. Retrieved 2008-12-16.
  16. ^ "Wildlife Services Factsheet May 2010: The Livestock Protection Collar" (PDF). U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS). Retrieved 2010 Jul 30. Coyotes are the leading cause of predation losses for sheep and goat producers. ... The LPC is registered by the Environmental Protection Agency (EPA) as a restricted use product. {{cite web}}: Check date values in: |accessdate= (help)
  17. ^ Leydet, François (1988). The coyote: defiant songdog of the West. Norman: University of Oklahoma Press. p. 110. ISBN 0-8061-2123-8. Retrieved 2010 Jul 30. So it was not humaneness that convinced PARC that Compound 1080 was the ideal tool for coyote control. Sodium monofluoroacetate had other attractions. It was cheap, and tiny amounts were effective: all you needed was sixteen grams, costing twenty-eight cents, to treat 1000 pounds of horsemeat, or enough, theoretically, to kill 11,428 coyotes at 1.4 ounces of bait meat per lethal dose. {{cite book}}: Check date values in: |accessdate= (help)
  18. ^ "Sodium Fluoroacetate: Reregistration Eligibility Decision (RED) Fact Sheet" (PDF). Environmental Protection Agency. Retrieved 2010 Jul 30. Sodium fluoroacetate is an acute toxicant predacide which is used against coyotes which prey on sheep and goats. ... Sodium fluoroacetate is a restricted use pesticide which may be used only by trained, certified applicators and which is only registered for use in livestock protection collars. Sodium fluoroacetate will retain the restricted use classification imposed by the Agency in 1978 due to its high acute toxicity and the need for highly specialized applicator training. ... Development and use of sodium fluoroacetate as a predacide and rodenticide in the U.S. began in the 1940s prior to the 1947 enactment of the Federal Insecticide, Fungicide, and Rodenticide Act by which requirements for federal registration of pesticide products were instituted. In 1964 and again in 1971, the use of poisons to control predatory mammals were reviewed by selected committees. In 1972, EPA cancelled all registered predator control uses of sodium fluoroacetate, sodium cyanide, and strychnine. In 1977, the US Department of the Interior (USDI) applied for an Experimental Use Permit (EUP) to investigate the potential risks and benefits associated with the use of sodium fluoroacetate in "toxic collars" which would be placed on the necks of sheep and goats. ... In 1981, EPA was petitioned by the USDI and livestock interests to revisit the 1972 predacide cancellation decision with respect to sodium fluoroacetate. ... In 1985, EPA granted a registration to USDI for a toxic collar product which was transferred in 1986 to the Animal and Plant Health Inspection Service (APHIS) of the US Department of Agriculture (USDA). ... The rodenticide uses of sodium fluoroacetate were cancelled due to lack of supporting data. In 1989, all "special local needs" registrations issued under § 24(c) of FIFRA were cancelled, and all pending applications for Federal registration were denied by August 1990. {{cite web}}: Check date values in: |accessdate= (help)
  19. ^ Speechley, Jane (15 November 2007). "1080 is not a humane poison: International journal publishes RSPCA paper". RSPCA. Archived from the original on 2007-11-18. Retrieved 2007-12-17.
  20. ^ L. E. Twigg and D. R. King, OIKOS 61, 412 (1991)
  21. ^ Eason, C.T.; Powlesland (2002). Technical Review of Sodium Monofluoroacetate (1080) Toxicology. ISBN 0-478-09346-2. Retrieved 2011-07-13. {{cite book}}: Check |url= value (help)

http://www.1080facts.co.nz/

Further reading

External links

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