Paraquat
From Wikipedia, the free encyclopedia
| Paraquat | |
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| IUPAC name |
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| Other names | paraquat dichloride; methyl viologen dichloride; Crisquat; Dexuron; Esgram; Gramuron; Ortho Paraquat CL; Para-col; Pillarxone; Tota-col; Toxer Total; PP148; Cyclone; Gramixel; Gramoxone; Pathclear; AH 501. |
| Identifiers | |
| CAS number | [] |
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| Properties | |
| Molecular formula | C12H14Cl2N2 |
| Molar mass | 257.16 g/mol |
| Appearance | off-white powder |
| Density | 1.25 g/cm3, solid |
| 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, 100 kPa) Infobox references |
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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 when swallowed.
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[edit] Production
Pyridine is coupled with sodium in anhydrous ammonia to give 4,4'-bipyridine, which is then methylated with chloromethane to give the desired compound:[2]
[edit] History
Paraquat was first produced for commercial purposes in 1961 by ICI (now Syngenta) and is today among the most commonly used herbicides.
The European Union allowed paraquat in 2004. Sweden, supported by Denmark, Austria, and Finland, brought the European Union commission to court. On 11 July 2007 the court annulled the directive authorising Paraquat as an active plant protection substance.[3]
[edit] Herbicide use
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. Being a herbicide, paraquat protects crops by controlling a wide range of annual and certain perennial weeds that reduce crop yield and quality by competing with the crop for water, nutrients, and light.
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 becomes biologically inactive upon contact with soil.[4]
In the United States, paraquat is available primarily as a liquid in various strengths. It is classified as "restricted use," which means that it can be used only by licensed applicators. As with many chemicals, caution must be exercised during use. In the European Union, paraquat has been forbidden since July 11th 2007.
[edit] Scientific use
Paraquat is often used in science to catalyze the formation of reactive oxygen species (ROS). Paraquat will under go redox cycling in vivo, being reduced by an electron donor such NADPH, before being oxidized by an electron receptor such as dioxygen to produce superoxide, a major ROS. [5]
[edit] "Paraquat pot"
During the late 1970s, a controversial program sponsored by the US government sprayed paraquat on marijuana fields in Mexico.[6] Since much of this marijuana was subsequently smoked by Americans, the US government's "Paraquat Pot" program stirred much debate. Perhaps in an attempt to deter people from using marijuana, representatives of the program warned that spraying rendered the crop unsafe to smoke.
However, independent bodies have studied paraquat in this use. Jenny Pronczuk de Garbino, [7] stated: "no lung or other injury in marijuana users has ever been attributed to paraquat contamination". On this topic, D.P. Morgan states in a United States Environmental Protection Agency publication that: "Smoking Paraquat-contaminated marijuana does not result in lung damage as the herbicide is pyrolyzed to dipyridyl (which does not present a toxic hazard) during smoking". [8]
[edit] In suicide
A large majority (93%) of fatalities from paraquat poisoning are cases of intentional self-administration, ie, suicides. In third world countries, paraquat is a "major suicide agent".[9] For instance, in Samoa from 1979-2001, 70% of suicides were by Paraquat poisoning. In Southern Trinidad from 1996-1997, 76% of suicides were by paraquat.[10]
The reason paraquat is such a widely used suicide agent in third-world countries is due to its widespread availability, low toxic dose (10 mLs or 2 teaspoons is enough to kill) and relative cheapness. 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.
[edit] Safety
Pure paraquat ingested is highly toxic to mammals and humans potentially leading to acute respiratory distress syndrome (ARDS), and there are no specific antidotes. However, fuller's earth or activated charcoal is an effective treatment, if taken in time. Death may occur up to 30 days after ingestion. Diluted paraquat used for spraying is less so, thus the greatest risk of accidental poisoning is during mixing and loading Paraquat for use.[11]
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) for these effects.[12]
Even a single swig, immediately spat out, can cause death from fibrous tissue developing in the lungs leading to asphyxiation.[13]
According to the Center 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.[14] Accidental deaths and suicides from paraquat ingestion are relatively common. For example, there have been 18 deaths in Australia from paraquat poisoning since 2000.[15]
Paraquat-induced toxicity in rats has also been linked to Parkinson's-like pathological degenerative mechanisms.[16] A study by the Buck Institute shows a connection between exposure to paraquat and iron in infancy and mid-life Parkinson's in laboratory mice.[17]
Long term exposures to paraquat would most likely cause lung and eye damage, but reproductive/fertility damage was not found by the EPA in their review. Some suspect a possible link to a greater incidence of Parkinson's disease.
[edit] References
- ^ a b "Paraquat dichloride". International Programme on Chemical Safety. October 2001. http://www.inchem.org/documents/icsc/icsc/eics0005.htm.
- ^ "Paraquat and Diquat". IPCS INCHEM. http://www.inchem.org/documents/ehc/ehc/ehc39.htm.
- ^ COURT OF FIRST INSTANCE OF THE EUROPEAN COMMUNITIES, PRESS RELEASE No° 45/07
- ^ Revkin, A. C. 1983. Paraquat: A potent weed killer is killing people. Science Digest 91(6):36-38, 42, 100-104.
- ^ Bus et al. Paraquat: model for oxidant-initiated toxicity. Environmental Health Perspectives (1984) vol. 55 pp. 37-46
- ^ Panic over Paraquat, Time Magazine, Monday, May 1, 1978
- ^ 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.
- ^ 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
- ^ Dinham, B. 1996: Active Ingredient fact sheet, Paraquat, in: PAN UK: Pesticide News No. 32, p. 20-1: [1], 24.06.2003
- ^ http://www.pan-germany.org/download/fact_paraquat2.pdf
- ^ PAN UK, Paraquat, accessed 13 October 2006.
- ^ United States Environmental Protection Agency, [2], accessed 16 August 2007.
- ^ 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.
- ^ Center for Disease Control, Facts about Paraquat, accessed 13 October 2006.
- ^ "Poisoned Latrobe," Gary Stevens, Valley Express Feb. 8, 2008.
- ^ K. Ossowska, M. S'Mialowska, K. Kuter, J. Wieron'ska, B. Zieba, J. Wardas, P. Nowak, J. Dabrowska, A. Bortel, I. Biedka, G. Schulze and H. Rommelspacher (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:.
- ^ Buck Institute for Aging Research (June 2007). Combined Exposure to Environmental Toxics Accelerates Age-related Development of Parkinson's Disease in Mice. Press release. http://www.buckinstitute.org/site/index.php?option=com_content&task=view&id=428.
[edit] External links
- "Stop Paraquat". The Berne Declaration. http://www.evb.ch/en/f25000087.html.
- "The Paraquat Information Center". Syngenta Crop Protection AG. http://www.paraquat.com.
[edit] Further reading
- Slade, P. (1966). "The Fate of Paraquat Applied to Plants". Weed Research 6: 158. doi:.
- Smith, S. N. (1976). "The Breakdown of Paraquat and Diquat by Soil Fungi". New Phytologist 77: 735. doi:.
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