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Paraquat (trivial name; ), or N, N′-dimethyl-4,4′-bipyridinium dichloride (systematic name), also known as methyl viologen, is a toxic organic compound with the chemical formula (C6H7N)2Cl2. It is classified as a viologen, a family of redox-active heterocycles of similar structure.In 1932, the German-American chemist Leonor Michaelis (1875–1949) named paraquat "methyl viologen" and used it as an indicator in redox reactions. See:
This salt is one of the most widely used worldwide. It is quick-acting and non-selective, killing green plant tissue on contact.
Paraquat is highly toxic to humans and other animals. The toxicity and lethality depends on the dose and how the herbicide is absorbed by the body. In humans, paraquat damages the mouth, stomach, and intestines if it is ingested orally. Once absorbed in the body, paraquat causes particular damage to the lungs, kidneys, and liver. Paraquat's lethality is attributed to its enhancing production of superoxide anions and human lung cells can accumulate paraquat. Paraquat exposure has been strongly linked to the development of Parkinson's disease.
Paraquat may be in the form of salt with chloride or other anions; quantities of the substance are sometimes expressed by cation mass alone (paraquat cation, paraquat ion). The name is derived from the para positions of the quaternary nitrogens.
Use of other methylating agents gives the bispyridinium with alternate . For example, Hugo Weidel's original synthesis used methyl iodide to produce the diiodide.
Paraquat is classified as a non-selective contact herbicide. The key characteristics that distinguish it from other agents used in plant protection products are:
These properties led to paraquat being used in the development of no-till farming.
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.Court of first instance of the European Communities, Press Release No° 45/07 Thus, paraquat has been banned in the European Union since 2007.
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In the United States, paraquat is available primarily as a solution in various strengths. It is classified as a restricted use pesticide, which means that it can be used by licensed applicators only. According to an October 2021 estimate, the use of paraquat in US agriculture as mapped by the US Geological Survey showed a doubling from 2013 to 2018, reaching annually, up from in 1974.
There is an ongoing international campaign for a global ban, but the cheap and popular paraquat continues to be unrestricted in most developing countries. The Chemical Review Committee (CRC) of the Rotterdam Convention recommended to the Conference of the Parties (COP) paraquat dichloride formulations for inclusion in Annex III to the Convention in 2011. A small group of countries, including India and Guatemala and supported by manufacturers, have since blocked the listing of paraquat as a hazardous chemical for the purposes of the Rotterdam Convention.
In Australia, paraquat is used as a herbicide to control annual grasses, broadleaf weeds and Lolium in crops of , Faba beans, Pea, Lupinus, and Vicia. Aerial spraying is forbidden, as is harvesting within 2 weeks of application in some crops.
In India, Paraquat dichloride 24% SL is widely used for broad-spectrum control of weeds on potato, cotton, rubber, wheat, tea, maize, rice, grapes, apple and aquatic weeds.
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 (ROS) 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.L. A. (Lindsay Anderson) Summers (1980). 9780126764505, London; New York : Academic Press. . ISBN 9780126764505 This induces necrosis, and unlike with some mechanisms of necrosis, does not produce double-stranded breaks. Target weeds die within 4 days; symptoms can show after as little as a few hours.
Paraquat is often used in science to catalyze the formation of 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.
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 a vineyard in Western Australia – though this singular report gives no indication of what regimen was being followed, particularly if the two herbicides were being used in a "double knock" tandem.
A computer simulation reported in the scientific journal Weed Research 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.
Paraquat is also toxic when inhaled and is in the Toxicity Category I (the highest of four levels) for acute inhalation effects. For agricultural uses, the United States Environmental Protection Agency (EPA) determined that particles used in agricultural practices (400–800 μm) are not in the respirable range. Paraquat also causes moderate to severe irritation of the eye and skin. Diluted paraquat used for spraying is less toxic; thus, the greatest risk of accidental poisoning is during mixing and loading paraquat for use.
The standard treatment for paraquat poisoning is first to remove as much as possible by pumping the stomach. Fuller's earth or activated charcoal may also improve outcomes depending on the timing. Haemodialysis, haemofiltration, haemoperfusion, or antioxidant therapy may also be suggested. Immunosuppressive therapy to reduce the inflammation is an approach suggested by some, however only low certainty evidence supports using medications such as with cyclophosphamide in addition to the standard care to reduce mortality. It is also unknown if adding glucocorticoid with cyclophosphamide to the standard care has unwanted side effects such as increasing the risk of infection. Oxygen should not be administered unless SpO2 levels are below 92%, as high concentrations of oxygen intensify the toxic effects. (1980). 9783540101918 ISBN 9783540101918
Death may occur up to 30 days after ingestion.
Lung injury is a main feature of poisoning. Liver, heart, lung, and kidney failure can occur within several days to 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.Centers for Disease Control, Facts about Paraquat , accessed 13 October 2006. The mechanism underlying paraquat's toxic damage to humans is still unknown. The severe inflammation is thought to be caused by the generation of highly reactive oxygen species and nitrite species that results in oxidative stress. The oxidative stress may result in mitochondrial toxicity and the Apoptosis and lipid peroxidation which may be responsible for the organ damage. It is known that the alveolar epithelial cells of the lung selectively concentrate paraquat. (2025). 9781437707557, Elsevier. ISBN 9781437707557 It has been reported that a small dose, even if removed from the stomach or spat out, can still cause death from fibrous tissue developing in the lungs, leading to . (1997). 9780849326868, CRC Press. ISBN 9780849326868
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 in part leading to China's ban in 2017. 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.
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".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. 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 Pyrolysis during smoking to dipyridyl, which is a product of combustion of the leaf material itself (including cannabis) and presents little toxic hazard."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
In a study by Imperial Chemical Industries, rats that 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."
The indiscriminate paraquat murders, which occurred in Japan in 1985, were carried out using paraquat as a poison. Paraquat was used in the UK in 1981 by a woman who poisoned her husband. American serial killer Steven David Catlin killed two of his wives and his adoptive mother with paraquat between 1976 and 1984. In 2022, a 22-year-old woman, Greeshma Raj, was found guilty of using paraquat for murdering her boyfriend, Sharon Raj, in Kerala, India.
In the UK, the use of paraquat was banned in 2007, but the manufacture and export of the herbicide is still permitted. In April 2022, the BBC reported that some UK farmers had called for a ban on British production of paraquat, and stated that "There is no scientific consensus and many conflicting studies on any possible association between Paraquat and Parkinson's". In the US, a class action lawsuit against Syngenta is ongoing; the company rejects the claims but has paid £187.5 million into a settlement fund. As of August 2024, more than 5,700 cases against Syngenta (manufacturer of Gramoxone) and Chevron (the former distributor) are pending in the paraquat multidistrict litigation in the US; the first of 10 bellwether trials will start in 2024. On April 15, 2025, attorneys representing plaintiffs in the multidistrict litigation entered into a settlement agreement. The settlement came as the first bellwether trial was six months away.
In August 2024, the British Columbia Supreme Court certified a class-action lawsuit against Syngenta on behalf of at least two plaintiffs who were diagnosed with Parkinson's after exposure to paraquat.
According to the NIEHS, pesticide exposure has consistently been associated with the onset of Parkinson's disease.
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