Organic Herbicides Toxic to Animals

Anilide, acetamides, or amide herbicides (eg, propanil, cypromid, clomiprop, bensulide, dimethenamid) are plant growth regulators, and some members of this group are more toxic than others.

Aromatic and benzoic acid herbicides (eg, chloramben, dicamba, and naptalam) have a low order of toxicity to domestic animals, and poisoning after normal use has not been reported. Environmental persistence and toxicity to wildlife are also low. In 2018, dicamba was blamed for polluting approximately 4% of US soybean fields because this herbicide is volatile, meaning it spreads to nearby areas. It is estimated that approximately 70% of plants die after dicamba exposure, and honey production is down 40–50% in areas where the chemical is used (1).

There is no suitable antidote. Supportive treatment is recommended.

The bipyridyl compounds (diquat, paraquat) produce toxic effects in the tissues of exposed animals by development of free radicals. Tissues can become irritated after contact. For example, mouth lesions have been observed after contact with recently sprayed pastures. Skin irritation and corneal opacity occur on external exposure to these chemicals, and inhalation is dangerous. Animals, including humans, have died as a result of drinking from contaminated containers.

Paraquat and diquat have different mechanisms of action. Diquat exerts most of its harmful effects in the GI tract. Clinical signs after consuming diquat include anorexia, gastritis, GI distention, and severe loss of water into the lumen of the GI tract. Renal impairment, CNS excitement, and seizures occur in severely affected individuals. Unlike with paraquat, lung lesions are uncommon. Although lung lesions are uncommon, respiratory distress may be observed.

Paraquat has a biphasic toxic action after ingestion. Immediate effects include excitement, seizures, or depression and incoordination. Clinical signs similar to those of diquat, including dyspnea, may be observed. Irritation of the mucosal membranes and skin may result from direct contact within days to weeks after exposure. Pulmonary lesions as a result of lipid-membrane peroxidation and destruction of type I alveolar pneumocytes are reflected in progressive respiratory distress. Lesions evident on necropsy include pulmonary edema, hyaline membrane deposition, and alveolar fibrosis.

There is no specific treatment. Because these chemicals are absorbed slowly, intensive oral administration of adsorbents in large quantities and cathartics is advised. Bentonite or fuller's earth is preferred; however, activated charcoal will suffice. Toxicity of paraquat is enhanced by deficiency of vitamin E or selenium, oxygen, and low tissue activity of glutathione peroxidase. Therefore, vitamin E and selenium with supportive therapy may be useful in early stages of intoxication. Excretion may be accelerated by forced diuresis induced by mannitol and furosemide. Oxygen therapy and fluid therapy are contraindicated.

Carbamate and thiocarbamate herbicides (eg, terbucarb, asulam, carboxazole, EPTC, pebulate, triallate, vernolate, butylate, thiobencarb) are moderately toxic; however, they are used at low concentrations, and poisoning problems would not be expected from normal use. Massive overdosage, as occurs with accidental exposure, produces clinical signs similar to those induced by the insecticide carbamates. Thiobencarb appears to increase permeability of the blood-brain barrier (2). There is no suitable antidote. Supportive treatment is recommended.

Several substituted dinitrophenols alone or as salts, such as dinitrophenol, dinitrocresol, dinoseb, and binapacryl, are highly toxic to all classes of animals (LD₅₀ 20–100 mg/kg body weight) (3). Poisoning can occur if animals are sprayed accidentally or have immediate access to forage that has been sprayed, because these compounds are readily absorbed through skin and lungs. Dinitrophenolic herbicides markedly increase oxygen consumption and deplete glycogen reserves.

No effective antidote for dinitrophenolic compounds is known. Affected animals should be cooled and sedated to help control hyperthermia. Physical cooling measures (eg, cool baths or sponging and keeping the animal in a shaded area) are recommended. Atropine sulfate, aspirin, and antipyretics should not be used.

Dextrose-saline infusions, in combination with diuretics and tranquilizers such as diazepam (not barbiturates), are very useful. Phenothiazine tranquilizers are contraindicated. IV administration of large doses of sodium bicarbonate (in carnivores), parenteral vitamin A, and oxygen therapy may be useful. If the toxin was ingested and the animal is alert, emetics should be administered; if the animal is depressed, gastric lavage should be performed and treatment with activated charcoal administered.

In ruminants with methemoglobinemia, methylene blue solution (2–4%, 10 mg/kg, IV, every 8 hours during the first 24–48 hours), and ascorbic acid (5–10 mg/kg, IV, every 8 hours during the first 24–48 hours) are useful (3, 4).

Imidazolinone herbicides include imazapyr, imazamethabenz-methyl, imazapic, imazethapyr, imazamox, and imazaquin. These are selective broad-spectrum herbicides. There is no suitable antidote. Supportive treatment is recommended.

Organophosphate compounds such as glyphosate, glufosinate, and bensulide are broad-spectrum, nonselective systemic herbicides. Glyphosate and glufosinate exist as free acids; however, because of their slow solubility they are marketed as the isopropyl amine or trimethylsulfonium salts of glyphosate and the ammonium salt of glufosinate. They are toxic to fish.

Following consumption of sprayed forage, immediate toxicity of glyphosate is likely very low at most environmental concentrations.Since approximately 2015, evidence started to accumulate in the scientific literature that glyphosate might have other genotoxic, carcinogenic, and neurotoxic effects (5). However, glyphosate does not cause inhibition of cholinesterase.

Dogs and cats show eye and skin irritation, dyspnea, nausea, and ataxia when exposed during or subsequent to an application of organophosphate herbicide to weeds or grass. Clinical signs usually disappear when exposure ceases, and minimal treatment is needed. The surfactant polyoxyethyleneamine, however, may result in hemolysis and GI, cardiovascular, and CNS effects. Treatment should include washing the chemical off the skin, evacuating the stomach, and tranquilizing the affected animal. Massive exposure with acute clinical signs due to accidental poisoning should be handled as an organophosphate poisoning.

Bensulide, listed as a plant growth regulator, has an oral LD₅₀ in rats of 271–770 mg/kg (6); in dogs, the lethal dose is > 200 mg/kg (7). The most prominent clinical sign is anorexia, but other clinical signs are similar to those caused by 2,4-D poisoning.

Phenoxy acids and their salts and esters (2,4-D [2-4-dichlorophenoxyacetic acid], dalapon, dichlorprop [2,4-DP], 2,4,5-T [2,4,5-trichlorophenoxyacetic acid], 2,4-DB, MCPA, MCPB, mecoprop, and silvex) are commonly used to control undesirable plants. As a group, they are essentially nontoxic to animals, except silvex, which is unusually very toxic compared to others within this class. Complications are more likely to be observed when large doses are consumed. The oral LD₅₀ for 2,4-D and 2,4,5-T in dogs is 100–800 mg/kg (8). Even large doses, up to 2 g/kg, have not been shown to leave residues in the fat of animals. These compounds are plant growth regulators, and treatment may result in increased palatability of some poisonous plants as well as increased nitrate and cyanide content.

The use of 2,4,5-T was curtailed because extremely toxic contaminants, collectively called dioxins (TCDD and HCDD), were found in technical-grade material. TCDD is considered carcinogenic, mutagenic, teratogenic, and fetotoxic and is able to cause reproductive damage and other toxic effects. Although improved manufacturing methods have decreased the level of the contaminants, use of this herbicide is very limited worldwide.

Treatment is usually supportive. IV fluids should be given to promote diuresis. Adsorbents and drugs that aid in restoration of liver function are recommended.

Polycyclic alkanoic acids or aryloxyphenoxypropionic compounds (diclofop, fenoxaprop, fenthiaprop, fluazifop, haloxyfop) have moderately low toxicity (acute oral LD₅₀ in rats is variable and can range from 400 mg/kg to > 4,000 mg/kg) (8). These compounds are more toxic if exposure is dermal. The dermal LD₅₀ of diclofop in rabbits is only 180 mg/kg (9). There is no suitable antidote. Supportive treatment is recommended.

Protoporphyrinogen oxidase (protox) inhibitors may be diphenyl ether (DPE) or non–diphenyl ether (non-DPE) such as nitrofen and oxadiazon. Numerous other non-oxygen-bridged compounds (non-DPE protox inhibitors) with the same site of action (carfentrazone, JV 485, and oxadiargyl) have been marketed. Protox inhibitors have little acute toxicity and are unlikely to pose an acute hazard in normal use. These compounds increase porphyrin levels in animals when administered orally; the porphyrin levels return to normal within a few days. There is no suitable antidote. Supportive treatment is recommended.

The most commonly used substituted aniline herbicides are alachlor, acetochlor, butachlor, metolachlor, and propachlor. Low doses in rats and dogs do not produce any adverse effects; however, long-term exposure in dogs causes liver toxicity and affects the spleen.

Compared with other substituted anilines, propachlor is severely irritating to the eye and slightly irritating to the skin. Propachlor produces skin sensitization in guinea pigs. High doses of propachlor produce erosion, ulceration, and hyperplasia of the mucosa and herniated mucosal glands in the pyloric region of the stomach and hypertrophy and necrosis of the liver in rats. In dogs, there is poor diet palatability, which results in poor feed consumption and weight loss. There is no suitable antidote. Supportive treatment is recommended.

Triazines and triazoles have been used extensively as selective herbicides. These herbicides are inhibitors of photosynthesis and include both asymmetric and symmetric triazines. Examples of symmetric triazines are chlorostriazines (simazine, atrazine, propazine, and cyanazine), thiomethyl-s-triazines (ametryn, prometryn, terbutryn), and methoxy-s-triazine (prometon). Metribuzin is a commonly used asymmetric triazine.

These herbicides have low oral toxicity and are unlikely to pose acute hazards in normal use, except ametryn and metribuzin, which may be slightly to moderately hazardous. They do not irritate the skin or eyes and are not skin sensitizers. The exceptions are atrazine, which is a skin sensitizer, and cyanazine, which is toxic by the oral route. Susceptibility of sheep and cattle to these herbicides is appreciably high.

Atrazine poisoning in cattle can result in increased salivation, agitation, tremors, and death. Although not specific, pulmonary congestion may be observed (10). There is no suitable antidote. Supportive treatment is recommended.

Toxicity of triazinylsulfonylurea or sulfonylurea herbicides (chlorsulfuron, sulfometuron, ethametsulfuron, chloremuron) appears to be quite low. The oral acute LD₅₀ in rats is in the range of 4,000–5,000 mg/kg (11). The dermal acute LD₅₀ in rabbits is approximately 2,000 mg/kg (6). There is no suitable antidote. Supportive treatment is recommended.

Triazolopyrimidine herbicides include cloransulam-methyl, diclosulam, florasulam-methyl, flumetsulam, and metosulam. The acute oral toxicity is very low. There is no suitable antidote. Supportive treatment is recommended.

Ureas and thioureas (polyureas) are available under different names such as diuron, fluometuron, isoproturon, linuron, buturon, chlorbromuron, chlortoluron, chloroxuron, difenoxuron, fenuron, methiuron, metobromuron, metoxuron, monuron, neburon, parafluron, siduron, tebuthiuron, tetrafluron, and thidiazuron. Of these, diuron and fluometuron are the most commonly used in the US, whereas isoproturon is mostly used in other countries. In general, these compounds have low acute toxicity and are unlikely to present any hazard in normal use, except tebuthiuron, which may be slightly hazardous. Cattle are more susceptible than sheep, cats, and dogs to polyurea herbicides.

Clinical signs and lesions are similar to those described for the phenoxyacetic herbicides. The substituted urea herbicides induce hepatic microsomal enzymes and may alter metabolism of other xenobiotic agents.

Recovery from diuron intoxication is quick (within 72 hours), and no skin irritation or dermal sensitization has been reported in guinea pigs. After repeated administration, hemoglobin levels and RBC counts are substantially decreased, while methemoglobin concentration and WBC counts are increased. Increased pigmentation (hemosiderin) in the spleen is observed histologically. Linuron in sheep causes erythrocytosis and leukocytosis with hypohemoglobinemia and hypoproteinemia, and hematuria. On histological evaluation, severe congestion of the red pulp with corresponding atrophy of the white pulp of the spleen and depletion of the lymphocyte elements have been reported. Degeneration of the liver and muscular dystrophy may also be observed. The acute LD₅₀ of isoproturon in rats is similar to that of diuron.

Polyurea herbicides have been suspected to have some mutagenic effects but do not have carcinogenic potential. In general, these compounds do not cause developmental and reproductive toxicity, except for monolinuron, linuron, and buturon, which are known to cause some teratogenic abnormalities in experimental animals. There is no suitable antidote. Supportive treatment is recommended.

Bromacil and terbacil are commonly used methyluracil compounds. Toxic doses of bromacil can be hazardous, especially for sheep; however, no field case of toxicity has been reported. The nitrile herbicides, ioxynil and bromoxynil, may uncouple and/or inhibit oxidative phosphorylation. Ioxynil, presumably because of its iodine content, causes enlargement of the thyroid gland in rats.

A number of substances are used as defoliants in agriculture. For example, sulfuric acid is used to destroy potato haulms, and two closely related trialkylphosphorothioates (DEF and merphos) are used to defoliate cotton. A notable feature of the latter treatment is that it produces organophosphate-induced delayed neuropathy in hens. Chlomequat is used as a growth regulator on fruit trees. The clinical signs of toxicity in experimental animals indicate that it is a partial cholinergic agonist.

• Gupta RC, Gupta PK. Toxicity of herbicides. In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. 4th ed. Elsevier; 2025:565-579.

• PubChem. National Library of Medicine.

• Also see pet owner content regarding herbicide poisoning.

1. Freese B. Center for Food Safety comments on the Arkansas State Plant Board’s proposal to restrict dicamba use. Center for Food Safety. 2017.

2. Pentyala SN, Chetty CS, Korlinara G, Pentyala S. Permeability changes in the blood-brain barrier of neonate and adult rats after thiobencarb exposure. Vet Hum Toxicol. 1993;35(6):509-511.

3. Lorgue G, Lechenet J, Riviere A, eds; Chapman MJ, Eng ed; Whitehead A, trans. Clin Vet Toxicol. Blackwell Science; 1996.

4. Burrows GE, Horn GW, McNew RW, Croy LI, Keeton RD, Kyle J. The prophylactic effect of corn supplementation on experimental nitrate intoxication in cattle. J Anim Sci. 1987;64(6):1682-1689. doi:10.2527/jas1987.6461682x

5. Martins-Gomes C, Silva TL, Andreani T, Silva AM. Glyphosate vs. glyphosate-based herbicides exposure: a review on their toxicity. J Xenobiot. 2022;12(1):21-40. doi:10.3390/jox12010003

6. Fisher N, Vlahovski F, Weil E, Rigo W Jr. Farm Chemicals Handbook. Meister Publishing. 1991.

7. Yeary RA. Oral intubation of dogs with combinations of fertilizer, herbicide, and insecticide chemicals commonly used on lawns. Am J Vet Res. 1984;45(2):288-290. doi:10.2460/ajvr.1984.45.02.288

8. PubChem. Accessed December 23, 2025.

9. Worthing CR, Hance RJ. The Pesticide Manual. Vol 9. British Crop Protection Service; 1991:262.

10. Props A J, Richards HJ, Hooser SB, Burcham GN, Wilson-Frank CR. Atrazine intoxication in cattle, confirmed by gas chromatography–mass spectrometry. J Vet Diagn Invest. 2021;33(6):1163-1167. doi:10.1177/10406387211036765

11. Levitt G, Ploeg HL, Weigel RC Jr, Fitzgerald DJ. 2-chloro-N-[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)aminocarbonyl]benzenesulfonamide, a new herbicide. J Agric Food Chem. 1981;29(3):416.