Paraquat

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Paraquat
Paraquat-3D-balls.png
Paraquat.svg
Identifiers
CAS number 1910-42-5 YesY
PubChem 15938
ChemSpider 15146 YesY
UNII 2KZ83GSS73 YesY
ChEBI CHEBI:28786 N
ChEMBL CHEMBL458019 YesY
Jmol-3D images Image 1
Properties
Molecular formula C12H14Cl2N2
Molar mass 257.16 g mol−1
Appearance White powder
Density 1.25 g/cm3
Melting point 175-180 °C[1]
Boiling point >300 °C[1]
Solubility in water High
Hazards
MSDS Oxford MSDS
Main hazards Toxic
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
 N (verify) (what is: YesY/N?)
Infobox references

Paraquat is the trade name for N,N′-dimethyl-4,4′-bipyridinium dichloride, one of the most widely used herbicides in the world. Paraquat, a viologen, is quick-acting and non-selective, killing green plant tissue on contact. It is also toxic to human beings and animals. Research has shown that it is linked to development of Parkinson's disease.[2][3] The name is derived from the para positions of the quaternary nitrogens.

Production[edit]

Pyridine is coupled with sodium in anhydrous ammonia to give 4,4'-bipyridine, which is then methylated with chloromethane to give the desired compound:[4]

Synthesis of paraquat.png

History[edit]

Although first synthesized in 1882, paraquat's herbicidal properties were not recognized until 1955.[5] Paraquat was first manufactured and sold by ICI in early 1962, and is today among the most commonly used herbicides.

The European Union approved the use of paraquat in 2004 but Sweden, supported by Denmark, Austria, and Finland, appealed this decision. In 2007, the court annulled the directive authorizing paraquat as an active plant protection substance stating that the 2004 decision was wrong in finding that there were no indications of neurotoxicity associated with paraquat and that the studies about the link between paraquat and Parkinson's disease should have been considered.[6]

Herbicide use[edit]

Paraquat is used as a quaternary ammonium herbicide, one of the most widely used herbicides in the world. It is quick-acting, non-selective, and kills green plant tissue on contact. It is redistributed within the plant, but does not harm mature bark.

The key characteristics that distinguish the non-selective contact herbicide paraquat from other active ingredients used in plant protection products are:

  • It is non-selective, which means it kills a wide range of annual grasses and broad-leaved weeds and the tops of established perennial weeds.
  • It is very fast-acting.
  • It is rain-fast within minutes of application.
  • It is partially inactivated upon contact with soil.[7][8]

These properties led to paraquat being used in the development of no-till farming.[9][10][11] Current research into no-till farming using mulching techniques as a substitute for herbicide application are producing good results[12]

In the United States, paraquat is available primarily as a solution in various strengths. It is classified as "restricted use," which means that it can be used by licensed applicators only. In the European Union, paraquat has been forbidden since 2007.[6]

Reactivity and mode of action[edit]

Paraquat reacts as an electron acceptor in redox and radical reactions.

As an herbicide, paraquat acts by inhibiting photosynthesis. In light-exposed plants, it accepts electrons from photosystem I (more specifically Fd, which is presented with electrons from PS I) and transfers them to molecular oxygen. In this manner, destructive reactive oxygen species are produced. In forming these reactive oxygen species, the oxidized form of paraquat is regenerated, and is again available to shunt electrons from photosystem I to start the cycle again.[13]

Paraquat is often used in science to catalyze the formation of reactive oxygen species (ROS), more specifically, the superoxide free radical. Paraquat will undergo redox cycling in vivo, being reduced by an electron donor such as NADPH, before being oxidized by an electron receptor such as dioxygen to produce superoxide, a major ROS.[14]

Weed resistance management[edit]

Problems with herbicide resistant weeds may be addressed by applying herbicides with different modes of action, along with cultural methods such as crop rotation, in integrated weed management (IWM) systems. Paraquat, with its distinctive mode of action, is one of few chemical options that can be used to prevent and mitigate problems with weeds that have become resistant to the very widely used non-selective herbicide glyphosate.[15][16]

One example is the "Double Knock" system used in Australia.[17] Before planting a crop, weeds are sprayed with glyphosate first, then followed seven to ten days later by a paraquat herbicide. Although twice as expensive as using a single glyphosate spray, the "Double Knock" system is an important resistance management strategy widely relied upon by farmers.[18] Although herbicide resistance has been seen for both herbicides in Western Australia in ryegrass

A computer simulation conducted by researchers at the Western Australian Herbicide Research Initiative (WAHRI) calculated that if the herbicide used in land preparation was alternated annually between glyphosate and paraquat, only one field in five would be expected to have glyphosate resistant annual ryegrass (Lolium rigidum) after 30 years, compared to nearly 90% of fields sprayed only with glyphosate.[19] A "Double Knock" regime with paraquat cleaning-up after glyphosate was predicted to keep all fields free of glyphosate resistant ryegrass for at least 30 years.

"Paraquat pot"[edit]

During the late 1970s, a controversial program sponsored by the US government sprayed paraquat on cannabis fields in Mexico.[20] Since much of this cannabis was subsequently smoked by Americans, the US government's "Paraquat Pot" program stirred much debate. Perhaps in an attempt to deter people from using cannabis, representatives of the program warned that spraying rendered the crop unsafe to smoke.

However, independent bodies have studied paraquat in this use. A 1995 study found that "no lung or other injury in cannabis users has ever been attributed to paraquat contamination".[21] Also a United States Environmental Protection Agency manual states: "... toxic effects caused by this mechanism have been either very rare or nonexistent. Most paraquat that contaminates cannabis is pyrolyzed during smoking to dipyridyl, which is a product of combustion of the leaf material itself (including cannabis) and presents little toxic hazard."[22]

Use in suicide and murder[edit]

A large majority (93%) of fatalities from paraquat poisoning are suicides, which occur mostly in developing countries.[23] For instance, in Samoa from 1979–2001, 70% of suicides were by paraquat poisoning. Trinidad and Tobago is particularly well known for its incidence of suicides involving the use of gramoxone. In southern Trinidad, particularly in Penal, Debe from 1996–1997, 76% of suicides were by paraquat, 96% of which involve the over-consumption of alcohol such as rum.[24] Fashion celebrity Isabella Blow committed suicide using paraquat in 2007.

The reason paraquat is such a widely used suicide agent in third-world countries is due to its widespread availability, low toxic dose (10 mL or 2 teaspoons is enough to kill) and relative low cost. There are campaigns to control or even ban paraquat outright, and there are moves to restrict its availability by requiring user education and the locking up of paraquat stores.

The indiscriminate paraquat murders, which occurred in Japan in 1985, were carried out using paraquat as a poison.

Paraquat, as the weedkiller Gramoxone, was used in the UK in 1981 by Susan Barber to poison the gravy of her husband Michael's pie. She was convicted of murder in November 1982, maintaining throughout that she had not intended to kill him.[25]

Toxicity[edit]

Pure paraquat, when ingested, is highly toxic to mammals, including humans; potentially leading to acute respiratory distress syndrome (ARDS). Although there are no specific antidotes, fuller's earth or activated charcoal is an effective treatment if taken in time. There were also some successful cases of using cyclophosphamide (Endoxan) to treat Paraquat poisoning.[26] Death may occur up to 30 days after ingestion. Diluted paraquat used for spraying is less toxic; thus, the greatest risk of accidental poisoning is during mixing and loading paraquat for use.[5]

In acute toxicity studies using laboratory animals, paraquat has been shown to be highly toxic by the inhalation route and has been placed in Toxicity Category I (the highest of four levels) for acute inhalation effects. However, the EPA has determined that particles used in agricultural practices (400 to 800 μm) are well beyond the respirable range and therefore inhalation toxicity is not a toxicological endpoint of concern. Paraquat is toxic (Category II) by the oral route and moderately toxic (Category III) by the dermal route. Paraquat will cause moderate to severe eye irritation and minimal dermal irritation, and has been placed in Toxicity Categories II and IV (slightly toxic) respectively for these effects.[27]

Even a single swig, immediately spat out, can cause death from fibrous tissue developing in the lungs, leading to asphyxiation.[28]

According to the Centers for Disease Control, ingesting paraquat causes symptoms such as liver, lung, heart, and kidney failure within several days to several weeks that can lead to death up to 30 days after ingestion. Those who suffer large exposures are unlikely to survive. Chronic exposure can lead to lung damage, kidney failure, heart failure, and oesophageal strictures.[29] Accidental deaths and suicides from paraquat ingestion are relatively common. For example, there have been 18 deaths in Australia from paraquat poisoning since 2000.[30] Long term exposures to paraquat would most likely cause lung and eye damage, but reproductive/fertility damage was not found by the United States Environmental Protection Agency (EPA) in their review.

Parkinson's disease[edit]

In 2011, a US National Institutes of Health study showed a link between paraquat use and Parkinson's disease in farm workers.[31] A co-author of the paper said that paraquat increases production of certain oxygen derivatives that may harm cellular structures, and that people who used paraquat, or other pesticides with a similar mechanism of action, were more likely to develop Parkinson's.[2] Paraquat-induced toxicity in rats has also been linked to Parkinson's-like neurological degenerative mechanisms.[32] A study by the Buck Institute showed a connection between exposure to paraquat and iron in infancy and mid-life Parkinson's in laboratory mice.[33]

Paraquat also induces oxidative stress in invertebrates such as Drosophila melanogaster. Paraquat-fed flies suffer early-onset mortality, and significant increases in superoxide dismutase activity.[34]

References[edit]

  1. ^ a b "Paraquat dichloride". International Programme on Chemical Safety. October 2001. 
  2. ^ a b "Two pesticides -- rotenone and paraquat -- linked to Parkinson's disease, study suggests". sciencedaily.com. 2011. Retrieved October 25, 2011. 
  3. ^ Kamel, F. (2013). "Paths from Pesticides to Parkinson's". Science 341 (6147): 722–723. doi:10.1126/science.1243619. PMID 23950519. 
  4. ^ "Paraquat and Diquat". IPCS INCHEM. 
  5. ^ a b "Paraquat". Pesticides News 32: 20–21. 1996. 
  6. ^ a b COURT OF FIRST INSTANCE OF THE EUROPEAN COMMUNITIES, PRESS RELEASE No° 45/07
  7. ^ Coats, G. E.; G. E. Coats, H. H. Funderburk Jr, J. M. Lawrence, D. E. Davis (28 July 2006). "Factors Affecting Persistence and Inactivation of Diquat and Paraquat". Weed Research 6 (1): 58–66. doi:10.1111/j.1365-3180.1966.tb00867.x. Retrieved 3 April 2014. 
  8. ^ Revkin, A. C. (1983). "Paraquat: A potent weed killer is killing people". Science Digest 91 (6): 36–38. 
  9. ^ Hood A. E. M., Jameson H. R. and Cotterell R. (1963). This technique involved destruction of pastures by herbicides such as paraquat as a substitute for ploughing. Nature, 197, 4869, 381
  10. ^ Hood A. E. M. (1965). Ploughless farming using "Gramoxone". Outlook on Agriculture IV, 6, 286–294
  11. ^ Huggins D R & Reganold J. P. (2008). No-Till: the Quiet Revolution. Scientific American, July 2008, pp 70–77
  12. ^ Halde, Caroline. "How to make organic no-till work for field crops in Southern Manitoba". natural systems agriculture. University of Manitoba. Retrieved 3 April 2014. 
  13. ^ Summers L.A. (1980) The Bipyridinium Herbicides. Academic Press, New York, NY.
  14. ^ Bus et al.; Gibson, JE (1984). "Paraquat: model for oxidant-initiated toxicity". Environmental Health Perspectives 55: 37–46. doi:10.1289/ehp.845537. PMC 1568364. PMID 6329674. 
  15. ^ Beckie, H. J. (2011). "Herbicide-resistant weed management: Focus on glyphosate". Pest Management Science: n/a. doi:10.1002/ps.2195.  edit
  16. ^ Eubank, T. W.; Poston, D. H.; Nandula, V. K.; Koger, C. H.; Shaw, D. R.; Reynolds, D. B. (2008). "Glyphosate-resistant Horseweed (Conyza canadensis) Control Using Glyphosate-, Paraquat-, and Glufosinate-Based Herbicide Programs". Weed Technology 22: 16. doi:10.1614/WT-07-038.1.  edit
  17. ^ Borger C.P. & Hashem A. (2007). Evaluating the double knockdown technique: sequence, application interval, and annual ryegrass growth stage. Australian Journal of Agricultural Research, 58, 265–271
  18. ^ Walsh, M. J.; Powles, S. B. (2007). "Management Strategies for Herbicide-resistant Weed Populations in Australian Dryland Crop Production Systems". Weed Technology 21 (2): 332. doi:10.1614/WT-06-086.1.  edit
  19. ^ Neve, P.; Diggle, A. J.; Smith, F. P.; Powles, S. B. (2003). "Simulating evolution of glyphosate resistance in Lolium rigidum II: Past, present and future glyphosate use in Australian cropping". Weed Research 43 (6): 418. doi:10.1046/j.0043-1737.2003.00356.x.  edit
  20. ^ Panic over Paraquat, Time Magazine, May 1, 1978
  21. ^ Pronczuk de Garbino J, Epidemiology of paraquat poisoning, in: Bismuth C, and Hall AH (eds), Paraquat Poisoning: Mechanisms, Prevention, Treatment, pp. 37-51, New York: Marcel Dekker, 1995.
  22. ^ Reigart, J. Routt and Roberts, James R. Recognition and Management of Pesticide Poisonings, 5th edition. Washington, DC: United States Environmental Protection Agency, 1999. Book available online
  23. ^ Dinham, B. (1996). "Active Ingredient fact sheet, Paraquat". Pesticide News 32: 20–21. 
  24. ^ Paraquat and Suicide, Pestizid Aktions-Netzwerk e.V. (PAN Germany).
  25. ^ Emsley, John. Molecules of Murder: Criminal Molecules and Classic Cases. Royal Society of Chemistry Publishing, 2008, p.195
  26. ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC472483/
  27. ^ Paraquat Dichloride, United States Environmental Protection Agency, accessed 16 August 2007.
  28. ^ Buzik, Shirley C.; Schiefer, H. Bruno; Irvine, Donald G. (1997). Understanding Toxicology: Chemicals, Their Benefits and Risks. Boca Raton: CRC Press. p. 31. ISBN 0-8493-2686-9. 
  29. ^ Centers for Disease Control, Facts about Paraquat, accessed 13 October 2006.
  30. ^ "Poisoned Latrobe," Gary Stevens, Valley Express Feb. 8, 2008.
  31. ^ Tanner, C. M.; Kamel, F. et al. (2011). "Rotenone, Paraquat, and Parkinson's Disease". Environmental Health Perspectives 119 (6): 866–872. doi:10.1289/ehp.1002839. PMC 3114824. PMID 21269927.  edit
  32. ^ Ossowska, K.; Smiałowska, M. et al. (2006). "Degeneration of dopaminergic mesocortical neurons and activation of compensatory processes induced by a long-term paraquat administration in rats: Implications for Parkinson's disease". Neuroscience 141 (4): 2155–2165. doi:10.1016/j.neuroscience.2006.05.039. PMID 16797138.  edit
  33. ^ "Combined Exposure to Environmental Toxics Accelerates Age-related Development of Parkinson's Disease in Mice" (Press release). Buck Institute for Aging Research. June 2007. 
  34. ^ T.Z. Rzezniczak, L.A. Douglas, J.H. Watterson, and T.J.S. Merritt (2011). "Paraquat administration in Drosophila for use in metabolic studies of oxidative stress". Analytical Biochemistry (journal) 419 (2): 345–347. doi:10.1016/j.ab.2011.08.023. PMID 21910964. 

Further reading[edit]

External links[edit]