Paraquat

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For the British military operation to recapture South Georgia, see Operation Paraquat.
Paraquat
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200px
IUPAC name 1,1'-dimethyl-4,4'-bipyridinium dichloride
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 1910-42-5
SMILES [Cl-].[Cl-].C[n+]1ccc(cc1)c2cc[n+](C)cc2
InChI InChI=1/C12H14N2.2ClH/c1-
13-7-3-11(4-8-13)12-
5-9-14(2)10-6-12;;/
h3-10H,1-2H3;2*1H/
q+2;;/p-2/fC12H14N2.2Cl/
h;2*1h/qm;2*-1
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
Main hazards Toxic
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references

Paraquat is the trade name for N,N'-Dimethyl-4,4'-bipyridinium dichloride, a viologen. Paraquat is used as a quaternary ammonium herbicide. It is dangerously poisonous to humans if swallowed. Other members of this class include diquat, cyperquat, diethamquat, difenzoquat, and morfamquat. All of these are easily reduced to the radical ion, which generates superoxide radical that reacts with unsaturated membrane lipids.

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.[2]

Herbicide use

The compound is 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:

  • Paraquat is non-selective, which means it kills a wide range of annual grasses and broad-leaved weeds and the tops of established perennial weeds.
  • Paraquat is very fast-acting.
  • Paraquat is rain-fast within minutes of application.
  • Paraquat becomes biologically inactive upon contact with soil.[3]

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 10th 2007.

Health risks

Pure paraquat ingested is highly toxic to mammals and humans, and there are no specific antidotes. However, fuller's earth or activated charcoal is an effective treatment, if taken in time. Death may be 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.[4]

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.[5]

Even a single swig immediately spat out can cause death from fibrous tissue developing in the lungs leading to asphyxiation.[6]

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 could 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.[7]

Paraquat-induced toxicity in rats has also been linked to Parkinson's-like pathological degenerative mechanisms.[8] 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.[9]

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.

Emergency care

Persons exposed to or contaminated by paraquat, with any suspected ingestion or absorption, should be treated by emergency medical services immediately. Prehospital care should follow these guidelines: [10]

  • Remove patient from further contact with substance.
  • Decontaminate with large volumes of water; remove patient's clothing.
  • Avoid secondary contamination by contact either with substance or runoff from decontamination efforts.
  • Establish and maintain a patent airway.
  • The administration of supplemental oxygen is advised against; however, prudent patient care dictates that oxygen should not be withheld from persons exhibiting clinical signs and symptoms of hypoxia. Emergency medical services personnel should consult with their medical control physician for specific case-by-case guidance.
  • Provide supportive treatment as indicated.
  • Consider evacuation to an appropriate hospital by helicopter; if air evacuation is not available, expedite transport by ground ambulance.
  • In the case of contamination of the eye, irrigate the affected eye with normal saline solution for at least 15 minutes.

Paraquat Pot

During the late 1960s, a controversial program sponsored by the US government sprayed paraquat on marijuana fields in South America. 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, [11] 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". [12]

References

  1. 1.0 1.1 Paraquat dichloride. International Programme on Chemical Safety (October 2001).
  2. COURT OF FIRST INSTANCE OF THE EUROPEAN COMMUNITIES, PRESS RELEASE No° 45/07
  3. Revkin, A. C. 1983. Paraquat: A potent weed killer is killing people. Science Digest 91(6):36-38, 42, 100-104.
  4. PAN UK, Paraquat, accessed 13 October 2006.
  5. EPA, [1], accessed 16 August 2007.
  6. Buzik, Shirley C.; Schiefer, H. Bruno; Irvine, Donald G. (1997). Understanding Toxicology: Chemicals, Their Benefits and Risks. Boca Raton: CRC Press, 31. ISBN 0-8493-2686-9. 
  7. Center for Disease Control, Facts about Paraquat, accessed 13 October 2006.
  8. 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:10.1016/j.neuroscience.2006.05.039.
  9. Buck Institute for Aging Research (June 2007). Combined Exposure to Environmental Toxics Accelerates Age-related Development of Parkinson's Disease in Mice. Press release.
  10. Halpin, Ted; Eric Hallman, Ellen Abend, Tonya Van Slyke (2005). Cornell Farmedic Training Program Student Manual. Ithaca, NY: Cornell University Press. 
  11. 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.
  12. 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

External links

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