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Paraquat

Topic: Chemistry

 From HandWiki - Reading time: 16 min
Short description: Chemical compound used as an herbicide
Paraquat
Paraquat-3D-balls.png
Paraquat.svg
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
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
Main hazards Toxic, environmental hazard
Safety data sheet Aldrich MSDS
GHS pictograms GHS06: Toxic GHS08: Health hazard GHS09: Environmental hazard
H301, H311, H315, H319, H330, H335, H372, H410[3]
P260, P273, P280, P284, P301+310, P305+351+338
Lethal dose or concentration (LD, LC):
57 mg/kg (rat, oral)
120 mg/kg (mouse, oral)
25 mg/kg (dog, oral)
22 mg/kg (guinea pig, oral)[4]
3 mg/m3 (mouse, 30 min respirable dust)
3 mg/m3 (guinea pig, 30 min respirable dust)[4]
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]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

Paraquat (trivial name; /ˈpærəkwɒt/), 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.[5] 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 (lethal) 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[6][7] and is banned in 58 countries.[8][9]

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.

Production and redox reactions

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.[10]

Synthesis of paraquat.png

Use of other methylating agents gives the bispyridinium with alternate counterions. For example, Hugo Weidel's original synthesis used methyl iodide to produce the diiodide.[11]

Paraquat, the dication on the left, functions as an electron acceptor, disrupting respiration in plants by forming the monocation at the center.[12]

Herbicide use

Although first synthesized in 1882,[11] paraquat's herbicidal properties were not recognized until 1955 in the Imperial Chemical Industries (ICI) laboratories at Jealott's Hill, Berkshire, England.[13][14] 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.[15][16]

These properties led to paraquat being used in the development of no-till farming.[17][18][19]

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.[20] Thus, paraquat has been banned in the European Union since 2007.[20]

USGS estimate of paraquat use in the US to 2018

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 10,000,000 pounds (4,500,000 kg) annually.[21]

There is an ongoing international campaign for a global ban, but the cheap and popular paraquat continues to be unrestricted in most developing countries.[22] 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.[23] 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.[24]

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− [math]\ce{ <=>> }[/math] [paraquat]•+

The radical cation is also susceptible to further reduction to the neutral [paraquat]0:[25]

[paraquat]•+ + e− [math]\ce{ <=>> }[/math] [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 (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.[26] This induces necrosis, and unlike with some mechanisms of necrosis, does not produce double-stranded breaks.[27]

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.[28]

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.[29][30]

One example is the "double knock" system used in Australia.[31] 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.[32] Nevertheless, herbicide resistance has been seen for both herbicides in a vineyard in Western Australia[33] – 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.[34] 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.

Toxicity

Paraquat is toxic to humans (Category II) by the oral route and moderately toxic (Category III) through the skin.[35] Pure paraquat, when ingested, is highly toxic to mammals, including humans, causing severe inflammation and potentially leading to severe lung damage (e.g., irreversible pulmonary fibrosis, also known as 'paraquat lung'), acute respiratory distress syndrome (ARDS), and death.[36][37] The mortality rate is estimated between 60-90%.[36]

Paraquat is also toxic when inhaled and is in the Toxicity Category I (the highest of four levels) for acute inhalation effects.[35] 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.[35] Paraquat also causes moderate to severe irritation of the eye and skin.[35] Diluted paraquat used for spraying is less toxic; thus, the greatest risk of accidental poisoning is during mixing and loading paraquat for use.[14]

The standard treatment for paraquat poisoning is first to remove as much as possible by pumping the stomach.[38] Fuller's earth or activated charcoal may also improve outcomes depending on the timing. Haemodialysis, haemofiltration, haemoperfusion, or antioxidant therapy may also be suggested.[36] Immunosuppressive therapy to reduce the inflammation is an approach suggested by some, however only low certainty evidence supports using medications such as glucocorticoids with cyclophosphamide in addition to the standard care to reduce mortality.[36] It is also unknown if adding glucocorticoid with cyclophosphamide to the standard care has unwanted side effects such as increasing the risk of infection.[36] Oxygen should not be administered unless SpO2 levels are below 92%, as high concentrations of oxygen intensify the toxic effects.[39][40] 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.[41] 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 induction of apoptosis and lipid peroxidation which may be responsible for the organ damage.[36] it is known that the alveolar epithelial cells of the lung selectively concentrate paraquat.[42] 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 asphyxiation.[43]

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.[44] 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.

"Paraquat pot"

During the late 1970s, a controversial program sponsored by the US government sprayed paraquat on cannabis fields in Mexico.[45] 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.[46]

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".[47] 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."[48]

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."[49]

Use in suicide and murder

A large majority (93 percent) of fatalities from paraquat poisoning are suicides, which occur mostly in developing countries.[50] For instance, in Samoa 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 southern Trinidad, particularly in Penal, 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.[51] 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.[52]

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.[53] American serial killer Steven David Catlin killed two of his wives and his adoptive mother with paraquat between 1976 and 1984.

Parkinson's disease

According to the WHO (2022), some of the measures to prevent Parkinson's disease include "banning of pesticides (e.g., paraquat and chlorpyrifos) 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".[54] A 2011 study showed a link between paraquat use and Parkinson's disease in farm workers.[55] 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.[6] 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.[56] However, a metareview concluded in 2021 that the available evidence does not support a causal conclusion.[57] 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 and MB with its combined effects has tremendous contribution towards neurodegeneration in PD."[58][59]

In the UK, the use of paraquat was banned in 2007, but the manufacture and export of the herbicide is still permitted. In April of 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.[60] As of November 2023, more than 4,000 cases against Syngenta (manufacturer of Gramoxone) and Chevron (the former distributor) are pending in the paraquat multidistrict litigation in the US; the first trial will start in 2024.[61][62] In 2023, a contributor to The Guardian alleged that internal documents from the case "show Syngenta and Chevron management have known about possible risks associated with paraquat for decades ... Syngenta, with one internal memo in 1985 noting that they depended on it [paraquat] as a 'major product' and 'would do whatever possible to defend it'" and "They talk about developing scientific studies that they can use ... They talk about influencing strategies with regulators."[9] On the contrary, Syngenta "claims it is being targeted by what it calls a 'mass tort machine' of plaintiffs' lawyers".[9]

According to the NIEHS, pesticide exposure has consistently been associated with the onset of Parkinson's disease.[63]

  • A 17-year long, NIEHS-funded study of the links between Parkinson's disease, environment, and genes shows that some pesticides, including paraquat, maneb, ziram, benomyl, and several organophosphate pesticides, including diazinon and chlorpyrifos, contribute to Parkinson's disease onset and progression.[63]
  • People with Parkinson's disease who are exposed to a high level of ten different active ingredients in agricultural pesticides may see their motor and non-motor symptoms progress faster  compared with those who are not, a 2022 study found.[63]
  • Other NIEHS research found that people who occupationally used two pesticides, rotenone or paraquat, developed Parkinson's disease 2.5 times more often than non-users.[63]
  • In addition, people exposed to pesticides in the home or garden may face a greater chance of developing Parkinson's disease.[63]
  • Pesticides may directly or indirectly disrupt the biological pathways that normally protect dopaminergic neurons, the brain cells selectively attacked by the disease.[63]
  • Some pesticides, like rotenone, can directly block the function of mitochondria, the structures that create energy to run the cell. NIEHS researchers showed in mice that disrupting mitochondria through exposure to rotenone early in development changed the epigenome—the chemical tags that turn genes on and off—in ways that persisted throughout life.[63]
  • Other pesticides, like paraquat, have been found to increase production of free radicals that can damage cells.[63]

Some people are more vulnerable to the harmful effects of pesticides because of their age or genetic makeup.[63]

  • Many studies identified genetic variations that provide insight into why certain people appear to be at higher risk of developing Parkinson's.[63]
  • Using data from a NIEHS-conducted agricultural health study, researchers found that Parkinson's risk from paraquat use was particularly high in people with a particular variant of a gene known as GSTT1.[63]
  • Similarly, other research has indicated that people with lower levels of the PON1 gene, which is important for the metabolism of organophosphate pesticides, showed faster progression of the disease.[63]

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, and trifluralin.[63]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 NIOSH Pocket Guide to Chemical Hazards. "#0478". National Institute for Occupational Safety and Health (NIOSH). https://www.cdc.gov/niosh/npg/npgd0478.html. 
  2. ↑ 2.0 2.1 "Paraquat dichloride". International Programme on Chemical Safety. October 2001. http://www.inchem.org/documents/icsc/icsc/eics0005.htm. 
  3. ↑ Sigma-Aldrich Co., 1,1′-Dimethyl-4,4′-bipyridinium dichloride hydrate. Retrieved on 2015-03-29.
  4. ↑ 4.0 4.1 4.2 "Paraquat". Immediately Dangerous to Life and Health Concentrations (IDLH). National Institute for Occupational Safety and Health (NIOSH). https://www.cdc.gov/niosh/idlh/1910425.html. 
  5. ↑ In 1932, the German-American chemist Leonor Michaelis (1875–1949) named paraquat "methyl viologen" and used it as an indicator in redox reactions. See:
  6. ↑ 6.0 6.1 "Two pesticides—rotenone and paraquat—linked to Parkinson's disease, study suggests". 2011. https://www.sciencedaily.com/releases/2011/02/110214115442.htm. 
  7. ↑ Kamel, F. (2013). "Paths from Pesticides to Parkinson's". Science 341 (6147): 722–723. doi:10.1126/science.1243619. PMID 23950519. Bibcode: 2013Sci...341..722K. https://zenodo.org/record/1230928. Retrieved 2018-09-13. 
  8. ↑ "This weed killer is banned in 50 countries. U.S. workers say it's giving them Parkinson's" (in en-US). 2023-12-20. https://www.latimes.com/environment/story/2023-12-20/california-workers-say-herbicide-is-giving-them-parkinsons. 
  9. ↑ 9.0 9.1 9.2 "'Burns me to a crisp': Farmers allege link between popular herbicide paraquat and Parkinson's disease - ABC News". 2023-11-28. https://abcnews.go.com/amp/US/burns-crisp-farmers-allege-link-popular-herbicide-parkinsons/story?id=102449723. 
  10. ↑ "Paraquat and Diquat". IPCS INCHEM. http://www.inchem.org/documents/ehc/ehc/ehc39.htm. 
  11. ↑ 11.0 11.1 Weidel, H.; Russo, M. (1882). "Studien über das Pyridin" (in de). Monatshefte für Chemie 3: 850–885. doi:10.1007/BF01516855. https://babel.hathitrust.org/cgi/pt?id=uiug.30112025861714&view=1up&seq=866. Retrieved 2019-08-13.  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.
  12. ↑ 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". The Journal of Organic Chemistry 55 (13): 4127–4135. doi:10.1021/jo00300a033. 
  13. ↑ Calderbank, A. (1978). "Chapter 9: Bipyridylium herbicides". Jealott's Hill: Fifty years of Agricultural Research 1928-1978. Imperial Chemical Industries Ltd.. pp. 67–86. ISBN 0901747017. https://archive.org/details/jealottshillfift0000peac. 
  14. ↑ 14.0 14.1 "Paraquat". Pesticides News 32: 20–21. 1996. 
  15. ↑ Coats, G. E.; Funderburk, H. H. Jr.; 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. 
  16. ↑ Revkin, A. C. (1983). "Paraquat: A potent weed killer is killing people". Science Digest 91 (6): 36–38. 
  17. ↑ 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. doi:10.1038/197748a0. 
  18. ↑ Hood A. E. M. (1965). Ploughless farming using "Gramoxone". Outlook on Agriculture IV, 6, 286–294
  19. ↑ Huggins D R & Reganold J. P. (2008). No-Till: the Quiet Revolution. Scientific American, July 2008, pp 70–77
  20. ↑ 20.0 20.1 Court of first instance of the European Communities, Press Release No° 45/07
  21. ↑ US Geological Survey (2021-10-12). "Estimated Agricultural Use for paraquat, 2018". https://water.usgs.gov/nawqa/pnsp/usage/maps/show_map.php?year=2018&map=PARAQUAT&hilo=L&disp=Paraquat. 
  22. ↑ Wesseling, C., Corriols, M., Bravo, V., (2005), Acute pesticide poisoning and pesticide registration in Central America, Toxicology and Applied Pharmacology, 207, 697-705.
  23. ↑ "Paraquat dichloride formulations". https://www.pic.int/TheConvention/Chemicals/Recommendedforlisting/Paraquatdichloride/tabid/2396/. 
  24. ↑ Hakim, Danny (20 December 2016). "This Pesticide Is Prohibited in Britain. Why Is It Still Being Exported?". New York Times. https://www.nytimes.com/2016/12/20/business/paraquat-weed-killer-pesticide.html. 
  25. ↑ 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. 
  26. ↑ Summers L.A. (1980) The Bipyridinium Herbicides. Academic Press, New York, NY.
  27. ↑ Hu, Zhubing; Cools, Toon; De Veylder, Lieven (2016-04-29). "Mechanisms Used by Plants to Cope with DNA Damage". Annual Review of Plant Biology (Annual Reviews) 67 (1): 439–462. doi:10.1146/annurev-arplant-043015-111902. ISSN 1543-5008. PMID 26653616. 
  28. ↑ Bus et al. (1984). "Paraquat: model for oxidant-initiated toxicity". Environmental Health Perspectives 55: 37–46. doi:10.1289/ehp.845537. PMID 6329674. 
  29. ↑ 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. 
  30. ↑ 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. 
  31. ↑ 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. 
  32. ↑ 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. 
  33. ↑ "in ryegrass". 25 October 2013. http://www.abc.net.au/news/2013-10-25/wach-herbicide-resistance-wa/5046086. 
  34. ↑ 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. 
  35. ↑ 35.0 35.1 35.2 35.3 Paraquat Dichloride , United States Environmental Protection Agency, accessed 16 August 2007.
  36. ↑ 36.0 36.1 36.2 36.3 36.4 36.5 Li, Luying Ryan; Chaudhary, Bhuwan; You, Chao; Dennis, Jane A.; Wakeford, Helen (2021-06-30). "Glucocorticoid with cyclophosphamide for oral paraquat poisoning". The Cochrane Database of Systematic Reviews 2021 (6): CD008084. doi:10.1002/14651858.CD008084.pub5. ISSN 1469-493X. PMID 34190331. 
  37. ↑ "Inhibitory effect of pirfenidone on pulmonary fibrosis in patients with acute paraquat poisoning". Am J Transl Res 13 (11): 13192–13199. 2021. PMID 34956540. 
  38. ↑ Newstead CG (1996). "Cyclophosphamide treatment of paraquat poisoning". Thorax 51 (7): 659–60. doi:10.1136/thx.51.7.659. PMID 8882068. 
  39. ↑ "Clinical Practice Guidelines 2017 (Updated February 2018) - Emergency Medical Technician". February 2018. http://www.phecit.ie/Custom/BSIDocumentSelector/Pages/DocumentViewer.aspx?id=oGsVrspmiT0dOhDFFXZvIz0q5GYO7igwzB6buxHEgeDBS9BbdRZpZNKt9Y89hp%252bGEhGQslpxcypo2CoaTBAvH7MaSvixBeKvGlIUowiGs7nVw%252f3VVR%252bKz6ygEPikDQqUxUXNJxS4zDc5azOwye4DnC8a0qKrAqXKSx31c954z6Yx7jWXuWMuIVlSjUibKI0t. 
  40. ↑ 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. Archives of Toxicology 4: 415–418. doi:10.1007/978-3-642-67729-8_95. ISBN 978-3-540-10191-8. ISSN 0171-9750. PMID 6933951. 
  41. ↑ Centers for Disease Control, Facts about Paraquat , accessed 13 October 2006.
  42. ↑ Kliegman (2011). Nelson's Textbook of Pediatrics (19 ed.). Elsevier. ISBN 978-1-4377-0755-7. 
  43. ↑ 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. 
  44. ↑ "每年5000绝望农民喝百草枯，自杀首选用药今起禁用". http://www.ikexue.org/archives/41530. 
  45. ↑ Panic over Paraquat, Time Magazine, May 1, 1978
  46. ↑ "Drug Survival News". 6. March 1978. 
  47. ↑ 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.
  48. ↑ 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
  49. ↑ "Paraquat". High Times 1 (91). 1983. 
  50. ↑ Dinham, B. (1996). "Active Ingredient fact sheet, Paraquat". Pesticide News 32: 20–21. 
  51. ↑ Paraquat and Suicide , Pestizid Aktions-Netzwerk e.V. (PAN Germany).
  52. ↑ 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. https://www.businessinsider.com/south-korea-suicide-rate-decrease-2018-6. 
  53. ↑ Emsley, John. Molecules of Murder: Criminal Molecules and Classic Cases. Royal Society of Chemistry Publishing, 2008, p. 195
  54. ↑ "Parkinson disease A public health approach, Technical brief". 2022. https://iris.who.int/bitstream/handle/10665/355973/9789240050983-eng.pdf. 
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  56. ↑ 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. 
  57. ↑ Weed, Douglas L. (September 2021). "Does paraquat cause Parkinson's disease? A review of reviews" (in en). NeuroToxicology 86: 180–184. doi:10.1016/j.neuro.2021.08.006. https://linkinghub.elsevier.com/retrieve/pii/S0161813X21000917. 
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  59. ↑ "Paraquat (herbicide) as a cause of Parkinson's Disease". Parkinsonism Relat Disord: 105932. November 2023. doi:10.1016/j.parkreldis.2023.105932. PMID 38008593. https://www.sciencedirect.com/science/article/abs/pii/S1353802023010118. 
  60. ↑ Claire Marshall; Malcolm Prior (1 April 2022). "UK farmers call for weedkiller ban over Parkinson's fears". BBC News. https://www.bbc.co.uk/news/science-environment-60836892. 
  61. ↑ "'Burns me to a crisp': Farmers allege link between popular herbicide and Parkinson's disease". 28 Nov 2023. https://abcnews.go.com/amp/US/burns-crisp-farmers-allege-link-popular-herbicide-parkinsons/story?id=102449723. 
  62. ↑ Kelleher, Shannon (22 Nov 2023). "Syngenta paraquat secrets featured on ABC News". https://www.thenewlede.org/2023/11/syngenta-paraquat-secrets-featured-on-abc-news/. 
  63. ↑ 63.00 63.01 63.02 63.03 63.04 63.05 63.06 63.07 63.08 63.09 63.10 63.11 63.12 "Parkinson's Disease". NIEHS. 2023-11-03. https://www.niehs.nih.gov/health/topics/conditions/parkinson/index.cfm.  This article incorporates text from this source, which is in the public domain.

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