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; Bai Cao Ku.
3D model (JSmol)
CompTox Dashboard (EPA)
|Molar mass||257.16 g·mol−1|
|Melting point||175 to 180 °C (347 to 356 °F; 448 to 453 K)|
|Boiling point||> 300 °C (572 °F; 573 K)|
|Vapor pressure||<0.0000001 mmHg (20 °C)|
|Main hazards||Toxic, environmental hazard|
|Safety data sheet||Aldrich MSDS|
|H301, H311, H315, H319, H330, H335, H372, H410|
|P260, P273, P280, P284, P301+310, P305+351+338|
|Lethal dose or concentration (LD, LC):|
LD50 (median dose)
|57 mg/kg (rat, oral)|
120 mg/kg (mouse, oral)
25 mg/kg (dog, oral)
22 mg/kg (guinea pig, oral)
LC50 (median concentration)
|3 mg/m3 (mouse, 30 min respirable dust)|
3 mg/m3 (guinea pig, 30 min respirable dust)
LCLo (lowest published)
|1 mg/m3 (rat, respirable dust, 6 h)|
6400 mg/m3 (rat, nonrespirable dust, 4 h)
|NIOSH (US health exposure limits):|
|TWA 0.5 mg/m3 (resp) [skin]|
|TWA 0.1 mg/m3 (resp) [skin]|
IDLH (Immediate danger)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Paraquat (trivial name; //), or N,N′-dimethyl-4,4′-bipyridinium dichloride (systematic name), also known as Methyl Viologen, is an organic compound with the chemical formula [(C6H7N)2]Cl2. It is classified as a viologen, a family of redox-active heterocycles of similar structure. Paraquat was manufactured by Chevron. This salt is one of the most widely used herbicides. It is quick-acting and non-selective, killing green plant tissue on contact. It is also toxic to human beings and animals due to its redox activity, which produces superoxide anions. It has been linked to the development of Parkinson's disease and is banned in several countries.
Pyridine is coupled by treatment with sodium in ammonia followed by oxidation to give 4,4′-bipyridine. This chemical is then dimethylated with chloromethane to give the final product as the dichloride salt.
Although first synthesized in 1882, paraquat's herbicidal properties were not recognized until 1955 in the Imperial Chemical Industries (ICI) laboratories at Jealott's Hill. Paraquat was first manufactured and sold by ICI in early 1962 under the trade name Gramoxone, and is today among the most commonly used herbicides.
Paraquat is classified as a non-selective contact herbicide. The key characteristics that distinguish it from other agents used in plant protection products are:
- It kills a wide range of annual grasses and broad-leaved weeds and the tips 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.
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. Thus, Paraquat has been banned in the European Union since 2007.
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.
There is an ongoing international campaign for a global ban, but the cheap and therefore popular paraquat continues to be unrestricted in most developing countries. A small group of countries, including India and Guatemala and supported by manufacturers, have blocked the listing of paraquat as a hazardous chemical for the purposes of the Rotterdam Convention.
Reactivity and mode of action
Paraquat is an oxidant that interferes with electron transfer, a process that is common to all life. Addition of one electron gives the radical cation:
- [paraquat]2+ + e− [paraquat]+.
The radical cation is also susceptible to further reduction to the neutral [paraquat]0:
- [paraquat]+. + e− [paraquat]0
As an herbicide, paraquat acts by inhibiting photosynthesis. In light-exposed plants, it accepts electrons from photosystem I (more specifically ferredoxin, 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 restart the cycle.
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.
Weed resistance management
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.
One example is the "double knock" system used in Australia. 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 widely relied upon by farmers as a resistance management strategy. Nevertheless, herbicide resistance has been seen for both herbicides in Western Australia.
A computer simulation showed that with alternating annual use 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. 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.
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 have been some successful cases of using cyclophosphamide to treat paraquat poisoning. Oxygen should not be administered unless SpO2 levels are below 92%, as high concentrations of oxygen intensify the toxic effects. 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.
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 (400–800 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.
The alveolar epithelial cells of the lung selectively concentrates paraquat. Even a single swig, immediately spat out, can cause death from fibrous tissue developing in the lungs, leading to asphyxiation.
One of the characters in the infamous British public information film Apaches (1977) dies hours after accidentally swallowing a small amount; the paraquat in the film is contained in a receptacle similar to a whisky bottle.
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. Accidental deaths and suicides from paraquat ingestion are relatively common. For example, there are more than 5,000 deaths in China from paraquat poisoning every year. 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.
During the late 1970s, a controversial program sponsored by the US government sprayed paraquat on cannabis fields in Mexico. Following Mexican efforts to eradicate marijuana and poppy fields in 1975, the United States government helped by sending helicopters and other technological assistance. Helicopters were used to spray the herbicides paraquat and 2,4-D on the fields; marijuana contaminated with these substances began to show up in US markets, leading to debate about the program. Perhaps in an attempt to deter people from using cannabis, representatives of the program warned that spraying rendered the crop unsafe to smoke.
Whether any injury came about due to the inhalation of paraquat-contaminated marijuana is uncertain. A 1995 study found that "no lung or other injury in cannabis users has ever been attributed to paraquat contamination". 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."
In a study by Imperial Chemical Industries, rats who inhaled paraquat showed development of squamous metaplasia in their respiratory tracts after a couple of weeks. This study was included in a report given to the State Department by the Mitre Corporation. The U.S. Public Health Service stated that "this study should not be used to calculate the safe inhalation dose of paraquat in humans."
Use in suicide and murder
A large majority (93 percent) of fatalities from paraquat poisoning are suicides, which occur mostly in developing countries. For instance, in Samoa from 1979–2001, 70 percent of suicides were by paraquat poisoning. Trinidad and Tobago is particularly well known for its incidence of suicides involving the use of Gramoxone (commercial name of paraquat). In southern Trinidad, particularly in Penal, Debe from 1996–1997, 76 percent of suicides were by paraquat, 96 percent of which involved the over-consumption of alcohol such as rum. Fashion celebrity Isabella Blow committed suicide using paraquat in 2007. Paraquat is widely used as a suicide agent in third-world countries because it is widely available at low cost. Further, the toxic dose is low (10 mL or 2 teaspoons is enough to kill). Campaigns exist to control or even ban paraquat, and there are moves to restrict its availability by requiring user education and the locking up of paraquat stores. When a 2011 South Korean law completely banned paraquat in the country, death by pesticide plummeted 46%, contributing to the decrease of the overall suicide rate.
In 2011, a US National Institutes of Health study showed a link between paraquat use and Parkinson's disease in farm workers. 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. Paraquat-induced toxicity in rats has also been linked to Parkinson's-like neurological degenerative mechanisms. A study by the Buck Institute for Research on Aging showed a connection between exposure to paraquat and iron in infancy and mid-life Parkinson's in laboratory mice. A 2013 meta-analysis published in Neurology found that 'exposure to paraquat ... was associated with about a 2-fold increase in risk' of Parkinson's disease.
Paraquat is structurally similar to MPP+, a known fast-acting inducer of Parkinson's disease in primate brains. The chloride of MPP+ was sold under the trade name Cyperquat.
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.
- NIOSH Pocket Guide to Chemical Hazards. "#0478". National Institute for Occupational Safety and Health (NIOSH).
- "Paraquat dichloride". International Programme on Chemical Safety. October 2001.
- Sigma-Aldrich Co., 1,1′-Dimethyl-4,4′-bipyridinium dichloride hydrate. Retrieved on 2015-03-29.
- "Paraquat". Immediately Dangerous to Life and Health Concentrations (IDLH). National Institute for Occupational Safety and Health (NIOSH).
- In 1932, the German-American chemist Leonor Michaelis (1875–1949) named paraquat "methyl viologen" and used it as an indicator in redox reactions. See:
- Michaelis, L. (1932). "Ein Reduktions-Indikator im Potentialbereich der Wasserstoffüberspannung" [A reduction indicator in the voltage range of hydrogen overpotential]. Biochemische Zeitschrift (in German). 250: 564–567.
- See also: Michaelis, L.; Hill, Edgar S. (1933). "The viologen indicators" (PDF). The Journal of General Physiology. 16 (6): 859–873.
- "Two pesticides—rotenone and paraquat—linked to Parkinson's disease, study suggests". Science Daily. 2011. Retrieved October 25, 2011.
- Kamel, F. (2013). "Paths from Pesticides to Parkinson's" (Submitted manuscript). Science. 341 (6147): 722–723. doi:10.1126/science.1243619. PMID 23950519.
- "Paraquat and Diquat". IPCS INCHEM.
- Weidel, H.; Russo, M. (1882). "Studien über das Pyridin" [Studies of pyridine]. Monatshefte für Chemie (in German). 3: 850–885. The Austrian chemist Hugo Weidel and his student M. Russo synthesized the iodide salt of paraquat (which they called Dimethyldipyridyljodid) by reacting 4,4'-bipyridine (γ-Dipyridyl) with methyl iodide (Jodmethyl). The synthesis is described on pages 863–864 and the molecule's structure is proposed on p. 867.
- Calderbank, A.; et al. (1978). "Chapter 9: Bipyridylium herbicides". In Peacock, F.C. (ed.). Jealott's Hill: Fifty years of Agricultural Research 1928-1978. Imperial Chemical Industries Ltd. pp. 67–86. ISBN 0901747017.
- "Paraquat". Pesticides News. 32: 20–21. 1996.
- Coats, G. E.; Funderburk, Jr., H. H.; Lawrence, J. M.; Davis, D. E. (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.
- Revkin, A. C. (1983). "Paraquat: A potent weed killer is killing people". Science Digest. 91 (6): 36–38.
- Hood A. E. M.; Jameson H. R.; Cotterell R. (1963). "This technique involved destruction of pastures by herbicides such as paraquat as a substitute for ploughing". Nature. 197 (4869): 381.
- Hood A. E. M. (1965). Ploughless farming using "Gramoxone". Outlook on Agriculture IV, 6, 286–294
- Huggins D R & Reganold J. P. (2008). No-Till: the Quiet Revolution. Scientific American, July 2008, pp 70–77
- COURT OF FIRST INSTANCE OF THE EUROPEAN COMMUNITIES, PRESS RELEASE No° 45/07
- Wesseling, C., Corriols, M., Bravo, V., (2005), Acute pesticide poisoning and pesticide registration in Central America, Toxicology and Applied Pharmacology, 207, 697-705.
- Hakim, Danny (20 December 2016). "This Pesticide Is Prohibited in Britain. Why Is It Still Being Exported?". New York Times. Retrieved 21 December 2016.
- Bockman T. M.; Kochi J. K. (1990). "Isolation and oxidation-reduction of methylviologen cation radicals. Novel disproportionation in charge-transfer salts by X-ray crystallography". J. Org. Chem. 55 (13): 4127–4135. doi:10.1021/jo00300a033.
- Summers L.A. (1980) The Bipyridinium Herbicides. Academic Press, New York, NY.
- Bus; Gibson, JE; et al. (1984). "Paraquat: model for oxidant-initiated toxicity". Environmental Health Perspectives. 55: 37–46. doi:10.1289/ehp.845537. PMC 1568364. PMID 6329674.
- Beckie, H. J. (2011). "Herbicide-resistant weed management: Focus on glyphosate". Pest Management Science. 67 (9): 1037–48. doi:10.1002/ps.2195. PMID 21548004.
- 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: 16–21. doi:10.1614/WT-07-038.1.
- 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 (3): 265–271. doi:10.1071/ar05373.
- Walsh, M. J.; Powles, S. B. (2007). "Management Strategies for Herbicide-resistant Weed Populations in Australian Dryland Crop Production Systems". Weed Technology. 21 (2): 332–338. doi:10.1614/WT-06-086.1.
- in ryegrass
- 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): 418–427. doi:10.1046/j.0043-1737.2003.00356.x.
- Newstead CG (1996). "Cyclophosphamide treatment of paraquat poisoning". Thorax. 51 (7): 659–60. doi:10.1136/thx.51.7.659. PMC 472483. PMID 8882068.
- "Clinical Practice Guidelines 2017 (Updated February 2018) - Emergency Medical Technician". [Irish] Pre-Hospital Emergency Care Council. February 2018. Archived from the original on 15 August 2018.
- Pratt, I. S.; Keeling, P. L.; Smith, L. L. (1980). "The effect of high concentrations of oxygen on paraquat and diquat toxicity in rats". Archives of Toxicology. Supplement. 4: 415–418. ISSN 0171-9750. PMID 6933951.
- Paraquat Dichloride, United States Environmental Protection Agency, accessed 16 August 2007.
- Kliegman (2011). Nelson's Textbook of Pediatrics (19 ed.). Elsevier. ISBN 978-1-4377-0755-7.
- Buzik, Shirley C.; Schiefer, H. Bruno; Irvine, Donald G. (1997). Understanding Toxicology: Chemicals, Their Benefits and Risks. Boca Raton: CRC Press. p. 31. ISBN 978-0-8493-2686-8.
- Centers for Disease Control, Facts about Paraquat Archived 2005-12-23 at the Wayback Machine, accessed 13 October 2006.
- Panic over Paraquat, Time Magazine, May 1, 1978
- "Drug Survival News". 6 (5). March 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
- "Paraquat". High Times. 1 (91). 1983.
- Dinham, B. (1996). "Active Ingredient fact sheet, Paraquat". Pesticide News. 32: 20–21.
- Paraquat and Suicide, Pestizid Aktions-Netzwerk e.V. (PAN Germany).
- Premack, Rachel (2018-06-09). "South Korea has the highest rate of deaths by suicide in the developed world — but a 2011 law helped decrease rates by 15%". Business Insider. Retrieved 2019-04-08.
- Emsley, John. Molecules of Murder: Criminal Molecules and Classic Cases. Royal Society of Chemistry Publishing, 2008, p.195
- 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.
- 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.
- "Combined Exposure to Environmental Toxics Accelerates Age-related Development of Parkinson's Disease in Mice" (Press release). Buck Institute for Aging Research. June 2007.
- Pezzoli, Gianni; Cereda, Emanuele (2013). "Exposure to pesticides or solvents and risk of Parkinson disease". Neurology. 80 (22): 2035–2041. doi:10.1212/wnl.0b013e318294b3c8. PMID 23713084.
- T.Z. Rzezniczak; L.A. Douglas; J.H. Watterson; T.J.S. Merritt (2011). "Paraquat administration in Drosophila for use in metabolic studies of oxidative stress". Analytical Biochemistry. 419 (2): 345–347. doi:10.1016/j.ab.2011.08.023. PMID 21910964.
- Slade, P. (1966). "The Fate of Paraquat Applied to Plants". Weed Research. 6 (2): 158–167. doi:10.1111/j.1365-3180.1966.tb00876.x.
- Smith, S. N.; Lyon, A. J. E.; Sahid, Ismail BIN (1976). "The Breakdown of Paraquat and Diquat by Soil Fungi". New Phytologist. 77 (3): 735–740. doi:10.1111/j.1469-8137.1976.tb04668.x.
- "Stop Paraquat". Erklärung von Bern. Archived from the original on 2007-06-08.
- "The Paraquat Information Center". Syngenta Crop Protection AG.
- "NIOSH Pocket Guide to Chemical Hazards". Centers for Disease Control and Prevention.
- Paraquat in the Pesticide Properties DataBase (PPDB)
- Paraquat dichloride in the Pesticide Properties DataBase (PPDB)