ISSN 2398-2993      

Paraquat poisoning


Nicola Bates

Alan Murphy


  • Cause: exposure to paraquat.
  • Signs: gastrointestinal signs and dyspnea; coma and convulsions prior to death.
  • Diagnosis: detection of paraquat in suspect material, rumen contents, urine, blood or other tissues.
  • Treatment: supportive.
  • Prognosis: poor in animals with pronounced signs. Recovery in survivors may take weeks or months.



  • Paraquat is a bipyridilium herbicide. It is a non-selective, foliage-applied contact herbicide and was widely used in agriculture:
    • Domestic products generally contain <5% w/w paraquat ion.
    • Agricultural products are typically 20% paraquat.
    • Some products also contain other herbicides, such as diquat.
  • Poisoning can occur after ingestion of paraquat but is generally not expected after grazing on pasture treated at the correct rate.
  • Poisoning from contaminated feed has been reported in cattle.
  • The oral LD50 of paraquat in cattle is 35-75 mg/kg.


  • Paraquat is rapidly but poorly absorbed from the gastrointestinal tract and concentrates in the lung.
  • Paraquat is poorly absorbed through intact skin but can be absorbed through damaged skin. Prolonged contact to concentrated solutions can damage skin and lead to absorption.
  • Paraquat is poorly absorbed from the lungs but is irritant to lung tissue.
  • Metabolism is minimal and it is primarily excreted unchanged in the urine. Paraquat may be detected in urine for several days after ingestion.
  • Paraquat undergoes a NADPH-dependent reduction to form the free radical which reacts with molecular oxygen to reform the cation and produce a superoxide free radical and will do so continually in the presence of NADPH and oxygen. The superoxide free radicals disrupt cell function and structure, causing lipid peroxidation and cause cell death.
  • The lung is the main target for paraquat toxicity due to active, energy-dependent uptake by alveolar type I and II cells and continuous exposure to atmospheric oxygen. Paraquat seems to produce an acute damaging phase in the lung followed by a reparative phase in which extensive fibrosis occurs, although the fibrosis may be absent or less pronounced in ruminants.
  • Paraquat is non-volatile and strongly and rapidly adsorbed to soils and is biological unavailable in that form.


  • Signs are variable in onset and can be within a few hours to a few days, depending on the dose involved.
  • Death can occur within 24-120 h of ingestion in severe cases.
  • Recovery in animals that survive may be prolonged and take several months.


  • Poisoning can occur wherever paraquat is used but it is restricted or banned in many countries.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Tamuli S M, Pegu S R, Tamuli M K & Baruah G K (2009) Pathology of acute paraquat toxicity in ruminants. Indian J Vet Pathol 33, 156-159 VetMedResource.
  • Pegu S R, Tamuli S M & Baruah G K (2002) Experimental paraquat toxicity in goats with special reference to the respiratory system. Indian J Vet Pathol 26, 73-74 VetMedResource.
  • Suntres Z E (2002) Role of antioxidants in paraquat toxicity. Toxicology 180 (1), 65-77 PubMed.
  • Philbey A W & Morton A G (2001) Paraquat poisoning in sheep from contaminated water. Aust Vet J 79 (12), 842-843 PubMed.
  • Kitazawa K, Kobayashi T, Shibamoto T & Hirai K (1988) Effects of methylprednisolone on acute lung paraquat toxicity in sheep. Am Rev Resp Dis 137 (1), 173-80 PubMed.
  • Webb D B (1983) Nephrotoxicity of paraquat in the sheep and the associated reduction in paraquat secretion. Toxicol Appl Pharmacol 68 (2), 282-289 PubMed.
  • Kiorpes A L, Winter R B, Hodgson D S, Galitzer S J & Savides M C (1982) Pathophysiological effects of paraquat intoxication in domestic ruminants: low dose studies. Vet Human Toxicol 24 (2), 81-5 PubMed.
  • Webb D B (1982) The pathophysiology of paraquat nephrotoxicity in the sheep. J Toxicol Clin Toxicol 19 (9), 911-29 PubMed.
  • Edds G T & Dudley W R Jr (1976) Paraquat toxicity in cattle. Florida Vet J (4), 26-27 VetMedResource.
  • Verma S P & Bahga H A (1976) Acute toxicity studies on paraquat (1,1’diemthyl-4,4’-bipyridinium dichloride). Indian J Anim Sci 46, 408-413.
  • Piskac A & Jordan V (1970) Poisoning of cattle by the herbicide Gramoxone. Veterinářství 20, 471-473.
  • Palmer J S (1969) Toxicity of 45 organic herbicides to cattle, sheep and chickens. US Department of Agriculture Production Research Report 106, 26-27.
  • Calderbank A, McKenna R H, Stevens M A & Walley J K (1968) Grazing trials on paraquat-treated pasture. J Sci Food Agriculture 19, 246-250 VetMedResource.
  • Stevens M A & Walley J K (1966) Tissue and milk residues arising from the ingestion of single doses of diquat and paraquat by cattle. J Science Agriculture 17, 472-475 VetMedResource.

Other sources of information

  • Fitzgerald W, Moriatry J, McElroy M, Malone E, Sheehan M & Casey M (2016) An Unusual Case of Paraquat Poisoning in Two Calves. In: Proc 29th World Buiatrics Congress, Dublin. pp 646.
  • Syngenta (2016) Paraquat Poisoning: a Practical Guide to Diagnosis, First Aid and Medical Management. Revision 8. Website: (pdf download).
  • Eisler R (1990) Paraquat Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. Report 22; Biological Report 85 (1.22) Contaminant Hazard Reviews Report 22. US Department of the Interior, Fish and Wildlife Service, USA.
  • Edwards M J, Hemingway R J, Kinch D A & Slade P (1974) Paraquat: Residue and Toxicology Trial with Cows Fed on Treated Grass. Unpublished report No. AR 2465A from ICI Plant Protection Division (3 December 1974). Submitted to WHO by Syngenta. Pre-GLP. Cited in: Marrs T C & Adeji A (2003) Paraquat. JMPR. World Health Organization, Geneva. pp 203–266. Website:
  • Howe D J T & Wright N (1965) The Toxicity of Paraquat and Diquat. In: Proc 18th NZ Weed & Pest Control Conference. pp 1015-1114.
  • Walley J K (1964) Paraquat Toxicity in Sheep and Cattle. Unpublished report IHR/166 (April 1964) submitted from ICI through Chevron Chemical Co. to FDA. Cited in: World Health Organization (1971) Evaluations of Some Pesticide Residues in Food. Food and Agriculture Organization of the United Nations/World Health Organization. Website:


  • ASPCA Animal Poison Control Center. Website: Tel: +1 (888) 426-4435.
  • Veterinary Poisons Information Service (VPIS). Website: Tel: + 44 (0)2073 055 055.

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