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| Names | |
|---|---|
| Preferred IUPAC name 1,1′-Dimethyl[4,4′-bipyridine]-1,1′-diium dichloride | |
| Other names Paraquat dichloride; Methyl viologen dichloride; MVCl2; Crisquat; Dexuron; Esgram; Gramuron; Ortho Paraquat CL; Para-col; Pillarxone; Tota-col; Toxer Total; PP148; Cyclone; Gramixel; Gramoxone; Pathclear; AH 501; Bai Cao Ku. | |
| Identifiers | |
3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider |
|
| ECHA InfoCard | 100.016.015 |
| UNII | |
| |
| |
| Properties | |
| C12H14Cl2N2 | |
| Molar mass | 257.16 g·mol−1 |
| Appearance | Yellow solid[1] |
| Odor | faint, ammonia-like[1] |
| Density | 1.25 g/cm3 |
| Melting point | 175 to 180 °C (347 to 356 °F; 448 to 453 K)[2] |
| Boiling point | > 300 °C (572 °F; 573 K)[2] |
| High | |
| Vapor pressure | <0.0000001 mmHg (20 °C)[1] |
| Hazards | |
| Occupational safety and health (OHS/OSH): | |
Main hazards | Toxic, environmental hazard |
| GHS labelling: | |
   | |
| H301,H311,H315,H319,H330,H335,H372,H410[3] | |
| P260,P273,P280,P284,P301+P310,P305+P351+P338 | |
| 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)[4] |
LC50 (median concentration) | 3 mg/m3 (mouse, 30 min respirable dust) 3 mg/m3 (guinea pig, 30 min respirable dust)[4] |
LCLo (lowest published) | 1 mg/m3 (rat, respirable dust, 6 h) 6400 mg/m3 (rat, nonrespirable dust, 4 h)[4] |
| NIOSH (US health exposure limits): | |
PEL (Permissible) | TWA 0.5 mg/m3 (resp) [skin][1] |
REL (Recommended) | TWA 0.1 mg/m3 (resp) [skin][1] |
IDLH (Immediate danger) | 1 mg/m3[1] |
| Safety data sheet (SDS) | Aldrich MSDS |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Paraquat (trivial name;/ˈpærəkwɒt/), orN,N′-dimethyl-4,4′-bipyridinium dichloride (systematic name), also known asmethyl viologen, is a toxicorganic compound with thechemical formula [(C6H7N)2]Cl2. It is classified as aviologen, a family ofredox-active heterocycles of similar structure.[5] It is one of the most widely usedherbicides 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.[6] Once absorbed in the body, paraquat causes particular damage to the lungs, kidneys, and liver.[6] Paraquat's lethality is attributed to its enhancing production ofsuperoxide anions and human lung cells can accumulate paraquat. Paraquat exposure has been strongly linked to the development ofParkinson's disease.[7]
Paraquat may be in the form ofsalt withchloride or otheranions; quantities of the substance are sometimes expressed by cation mass alone (paraquat cation, paraquat ion). The name is derived from thepara positions of thequaternary nitrogens.
Pyridine is coupled by treatment withsodium inammonia followed by oxidation to give4,4′-bipyridine. This chemical is then dimethylated withchloromethane (its discoverers Austrian chemistHugo Weidel and his student M. Russo usediodomethane) to give the final product as the dichloride salt.[8]
Use of other methylating agents gives the bispyridinium with alternatecounterions. For example,Hugo Weidel's original synthesis usedmethyl iodide to produce the diiodide.[9]
Although first synthesized by Weidel and Russo in 1882,[9] paraquat's herbicidal properties were not recognized until 1955 in theImperial Chemical Industries (ICI) laboratories atJealott's Hill, Berkshire, England.[10][11] Paraquat was first manufactured and sold by ICI in early 1962 under thetrade nameGramoxone, 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:
These properties led to paraquat being used in the development ofno-till farming.[14][15][16]
The European Union approved the use of paraquat in 2004 but Sweden, supported by Denmark, Austria, and Finland, appealed this decision.[17] 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 andParkinson's disease should have been considered.[18][19] Thus, paraquat has been banned in theEuropean Union since 2007.[20]
China also banned the domestic use of Paraquat in 2017; Thailand followed soon after in 2019 and Brazil, Chile, Malaysia, Peru and Taiwan between 2020 and 2022.[21] India banned it in Odisha in 2023, and temporarily banned it in Kerala in 2011, though the pesticide is still widely used throughout the majority of the country.[22].
China, the United Kingdom, and Switzerland are responsible for the production of the majority of paraquat for worldwide usage, despite the fact that they each have banned its usage domestically.[23]
In the United States, paraquat is available primarily as a solution in various strengths. It is classified as arestricted 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 10,000,000 pounds (4,500,000 kg) annually,[24] up from 1,054,000 pounds (478,000 kg) in 1974.[25]
There is an ongoing international campaign for a global ban, but the cheap and popular paraquat continues to be unrestricted in most developing countries.[26] The Chemical Review Committee (CRC) of theRotterdam Convention recommended to the Conference of the Parties (COP) paraquat dichloride formulations for inclusion in Annex III to the Convention in 2011.[27] 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.[28]
In Australia, paraquat is used as a herbicide to control annual grasses, broadleaf weeds andryegrass in crops ofChickpeas,Faba beans,field peas,lupins,lentils andvetch. Aerial spraying is forbidden, as is harvesting within 2 weeks of application in some crops.[29]
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.[30]
In the United States the registry for paraquat began in 1964 and did not complete registration until 1997. Paraquat then had a registry review in 2011.[31] in 2016 to minimize exposure the EPA required that applicators be certified after completing new training requirements. They also created a new closed package system that prevents spills and new warning labels.[32] During the review era, the EPA released a draft for human health and ecological assessment in for public comment in October 2019.[33]They then released the proposed interim draft in October 2020 and after reviewing comments from other various organizations.[34] Once they had reviewed the various public comments; the EPA released their finalized Interim decision in July 2021. Which was designed to have many different stricter measures to mitigate exposure to paraquat.[35] With most of them revolving around the use of respirators, time of use, level of use and proper licensing to use along with many other stringent measures.[36]
Paraquat is an oxidant that interferes withelectron transfer, a process that is common to all life. Addition of one electron gives the radical cation:
The radical cation is also susceptible to further reduction to the neutral [paraquat]0:[37]
As an herbicide, paraquat acts by inhibiting photosynthesis. In light-exposed plants, it accepts electrons fromphotosystem I (more specificallyferredoxin, which is presented with electrons from PS I) and transfers them to molecular oxygen. In this manner, destructivereactive 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.[38] This inducesnecrosis, and unlike with some mechanisms of necrosis, does not producedouble-stranded breaks.[39] Target weeds die within 4 days; symptoms can show after as little as a few hours.[29]
Paraquat is often used in science to catalyze the formation of ROS, more specifically, thesuperoxide free radical. Paraquat will undergo redox cyclingin vivo, being reduced by an electron donor such asNADPH, before being oxidized by an electron receptor such asdioxygen to producesuperoxide, a major ROS.[40]
Problems withherbicide resistant weeds may be addressed by applying herbicides with different modes of action, along with cultural methods such ascrop rotation, inintegrated weed management (IWM) systems.[41] 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 herbicideglyphosate.[42][43] Paraquat is a Group L (Aus), D (global), 22 (numeric)resistance class herbicide, which it shares withdiquat andcyperquat.[44]
One example is the "double knock" system used in Australia.[45] 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.[46] Nevertheless, herbicide resistance has been seen for both herbicides in a vineyard in Western Australia[47] – 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.[48]
A computer simulation reported in the scientific journalWeed 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.[49] 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 toxic to humans (Category II) by theoral route and moderately toxic (Category III) through the skin.[50] Pure paraquat, when ingested, is highly toxic to mammals, including humans, causing severeinflammation and potentially leading to severe lung damage (e.g., irreversiblepulmonary fibrosis, also known as 'paraquat lung'), acute respiratory distress syndrome (ARDS), and death.[51][52] The mortality rate is estimated between 60% and 90%.[51]
Exposure to Paraquat can cause a wide range of serious health effects, including confusion, acute kidney failure, liver failure, increased blood pressure or heart rate, damage to the heart, damage to the lungs leading to fluid-filled lungs and respiratory failure, weak muscles, extreme fatigue and lethargy, nausea or vomiting, diarrhea, and in severe cases, coma.[53]
Paraquat is also toxic when inhaled and is in theToxicity Category I (the highest of four levels) for acute inhalation effects.[50] For agricultural uses, theUnited States Environmental Protection Agency (EPA) determined that particles used in agricultural practices (400–800 μm) are not in the respirable range.[50] Paraquat also causes moderate to severe irritation of the eye and skin.[50] Diluted paraquat used for spraying is less toxic; thus, the greatest risk of accidental poisoning is during mixing and loading paraquat for use.[11]
The standard treatment for paraquat poisoning is first to remove as much as possible by pumping the stomach.[54]Fuller's earth oractivated charcoal may also improve outcomes depending on the timing. Haemodialysis, haemofiltration, haemoperfusion, or antioxidant therapy may also be suggested.[51] Immunosuppressive therapy to reduce the inflammation is an approach suggested by some, however only low certainty evidence supports using medications such asglucocorticoids withcyclophosphamide in addition to the standard care to reduce mortality.[51] It is also unknown if adding glucocorticoid with cyclophosphamide to the standard care has unwanted side effects such as increasing the risk of infection.[51] Oxygen should not be administered unlessSpO2 levels are below 92%, as high concentrations of oxygen intensify the toxic effects.[55][56]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, andoesophageal strictures.[57] The mechanism underlying paraquat's toxic damage to humans is still unknown. The severe inflammation is thought to be caused by the generation of highlyreactive oxygen species andnitrite species that results inoxidative stress. The oxidative stress may result inmitochondrial toxicity and theinduction of apoptosis andlipid peroxidation which may be responsible for the organ damage.[51] It is known that thealveolarepithelial cells of the lung selectively concentrate paraquat.[58] 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 toasphyxiation.[59]
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[60] in part leading to China's ban in 2017.[21] 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.
During the late 1970s, a controversial program sponsored by the US government sprayed paraquat oncannabis fields in Mexico.[61] 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 and2,4-D on the fields; marijuana contaminated with these substances began to show up in US markets, leading to debate about the program.[62]
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".[63] Also aUnited States Environmental Protection Agency manual states: "... toxic effects caused by this mechanism have been either very rare or nonexistent. Most paraquat that contaminates cannabis ispyrolyzed during smoking todipyridyl, which is a product of combustion of the leaf material itself (including cannabis) and presents little toxic hazard."[64]
A large majority (93 percent) of fatalities from paraquat poisoning aresuicides, which occur mostly indeveloping countries.[65] For instance, inSamoa from 1979 to 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 southernTrinidad, particularly inPenal–Debe from 1996 to 1997, 76 percent of suicides were by paraquat, 96 percent of which involved the over-consumption of alcohol such as rum.[66] British fashion celebrityIsabella Blow died by suicide using paraquat in 2007. Paraquat is widely used as a suicide agent in developing 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.[67]
The indiscriminateparaquat 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.[68] American serial killerSteven 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.[69]
According to theWHO (2022), some of the measures to preventParkinson's disease include "banning of pesticides (e.g., paraquat andchlorpyrifos) and chemicals (e.g.,trichloroethylene) which have been linked to PD and develop safer alternatives as per WHO guidance" and "accelerate action to reduce levels of and exposure to air pollution, an important risk factor for PD".[70] A 2011 study showed a link between paraquat use and Parkinson's disease in farm workers.[71] 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.[72] A 2013 meta-analysis published inNeurology found that "exposure to paraquat ... was associated with about a 2-fold increase in risk" of Parkinson's disease.[73] A review in 2021 concluded that the available evidence does not support a causal conclusion.[74] In 2022 and 2023, two reviews from India "decisively demonstrated that paraquat is a substantial stimulant of oxidative stress … and is associated with Parkinson's disease (PD)"; and stated that "From the studies we can consider that PQ andMB with its combined effects has tremendous contribution towards neurodegeneration in PD."[75][76]
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, aclass action lawsuit againstSyngenta is ongoing; the company rejects the claims but has paid £187.5 million into a settlement fund.[77] As of August 2024, more than 5,700 cases against Syngenta (manufacturer of Gramoxone) andChevron (the former distributor) are pending in the paraquat multidistrict litigation in the US; the first of 10 bellwether trials will start in 2024.[78][79][80] On April 15, 2025, attorneys representing plaintiffs in themultidistrict litigation entered into a settlement agreement.[81][82] The settlement came as the first bellwether trial was six months away.[81]
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.[83]
According to theNIEHS, pesticide exposure has consistently been associated with the onset of Parkinson's disease.[84]
Some people are more vulnerable to the harmful effects of pesticides because of their age or genetic makeup.[84]
Further research into links between preventable exposures and Parkinson's disease, as well as preventative therapies, could help reduce the incidence of the disease. For example, using protective gloves and other hygiene practices reduced the risk of Parkinson's disease among farmers using paraquat,permethrin, andtrifluralin.[84]
Notes
This article incorporates text from this source, which is in thepublic domain.Further reading
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