Herbicides are used routinely for weed control. Most herbicides are quite selective for specific plants and are not as poisonous for animals. Less selective compounds, such as arsenicals, chlorates, and dinitrophenols, are more toxic to animals. Most toxicity problems in animals result from exposure to excessive quantities of herbicides because of improper or careless use or disposal of containers. When herbicides are used properly, problems are rare.
Vegetation treated with herbicides at proper rates normally is not hazardous to animals, including people, and even less so after the herbicides have dried on the vegetation. Specific information on a particular herbicide is available on the label and from the manufacturer, cooperative extension services, or poison control centers.
Herbicide poisoning in animals is rare. With few exceptions, it is only when animals gain direct access to the product that severe poisoning occurs. The history is critical. Sickness after feeding, spraying of pastures or crops near pastures, a change in housing, or direct exposure may lead to a tentative diagnosis of herbicide poisoning. Severe gastrointestinal signs are frequent. Often the nature of exposure is hard to identify because of storage of herbicides in mislabeled or unlabeled containers. Other problems that can lead to exposure include unidentified spillage of liquid from containers or powder from broken bags near a feed source, or visual confusion with a dietary ingredient or supplement. Once a chemical source has been identified, an animal poison control center should be contacted for information on treatments, laboratory tests, and likely outcome.
Longterm disease caused by herbicides is even more difficult to diagnose. It may include a history of herbicide use close to the animal or the animal's feed or water source, or a gradual change in the animal's performance or behavior over several weeks, months, or even years. Occasionally, it involves manufacture or storage of herbicides nearby. Samples of possible sources (such as contaminated feed and water) for residue analysis, as well as tissues collected at necropsy, are essential. Months or even years may be required to successfully identify a problem of longterm exposure.
If poisoning is suspected, the first step in management is to stop further exposure. Any possible source should be removed from the animal's environment. Treatment includes stabilizing the animal and specific antidotal treatments when available. As with any potential poisoning, your veterinarian needs full disclosure of the circumstances (for example, unapproved use or improper storage of a chemical) to best make a diagnosis and begin treatment.
The inorganic herbicides are older compounds that are less expensive and more toxic than newer compounds. They are no longer used much in developed countries.
The use of inorganic arsenicals (sodium arsenite and arsenic trioxide) as herbicides has been reduced greatly because of livestock losses, the long-lasting effects on the environment, and their association with causing cancer. Sodium arsenate and chromic copper arsenate are not currently registered with the Environmental Protection Agency. Arsenic derivatives continue to be available in other parts of the world in wood preservatives and insecticides. These compounds can be hazardous to animals when used as recommended.
The highly soluble organic arsenicals (methane arsonate, methyl arsonic acid) can concentrate in pools in toxic quantities after a rain has washed them from recently treated plants (see Poisoning: Arsenic Poisoning).
Ammonium sulfamate is not currently registered with the Environmental Protection Agency. It is used to kill brush and poison ivy.
Borax has been used as an herbicide and an insecticide. It is toxic to animals if consumed in moderate to large doses. Poisoning has not been reported when borax was used properly but has occurred when borax powder was scattered in the open for cockroach control. Signs of severe poisoning are diarrhea, rapid onset of weakness and an unwillingness to stand, and perhaps convulsions. An effective antidote is not known. Treatment consists of supportive care. Detergents containing borax should be stored away from where pets can get access to them.
Sodium chlorate is seldom used as an herbicide but remains registered. Treated plants and contaminated clothing are highly combustible and constitute fire hazards. Ingestion of treated plants and consumption of feed to which it is mistakenly added as salt can cause chlorate poisoning. Treatment with methylene blue must be repeated frequently. Blood transfusions, fluids, and mineral oil containing 1% sodium thiosulfate may be beneficial in treatment.
Many organic herbicides can cause problems in pets.
Anilide or amide compounds (propanil, cypromid, clomiprop) are plant growth regulators, and some members of this group are more toxic than others. Exposure to these compounds can affect red blood cells and the immune system.
Thebipyridyl compounds or quaternary ammonium herbicides include diquat and paraquat. These herbicides are used at low rates (2 ounces per acre [150 milliliters per hectare]), act quickly, are inactivated on soil contact, and quickly decompose in light. They produce toxic effects in the tissues of exposed animals. Skin irritation and clouding of the cornea can be seen after external exposure, and breathing in these chemicals is dangerous. Animals, including people, have died as a result of drinking from contaminated containers.
Diquat exerts most of its harmful effects in the gastrointestinal tract. Signs of kidney damage, central nervous system excitement, and convulsions occur in severely affected animals. Paraquat has 2 phases to its toxic action after ingestion. Immediate signs include excitement, convulsions, lack of coordination, inflammation of the gastrointestinal tract, loss of appetite, and possibly kidney involvement and breathing difficulty. Eye, nose, and skin irritation can be caused by direct contact, followed within days to 2 weeks by breathing problems.
Treatment includes administration of activated charcoal or other adsorbants in large quantities, medications that cause emptying of the bowels and that increase urine output, and supportive treatment.
Carbamate and thiocarbamate compounds (terbucarb, asulam, carboxazole, EPTC, pebulate, triallate, vernolate, butylate, thiobencarb) are moderately toxic. However, they are used at low concentrations, and normal use should not result in poisoning. Massive overdosage in accidental exposure causes lack of appetite, depression, breathing difficulty, diarrhea, weakness, and seizures.
Aromatic/benzoic acid compounds (chloramben, dicamba) have not caused poisoning after normal use. In overdosage, signs and tissue changes are similar to those described for poisoning by the phenoxyacetic compounds.
Phenoxyacetic and phenoxybutyric compounds (2,4-D [2-4-dichlorophenoxyacetic acid], 2,4,5-T [2,4,5-trichlorophenoxyacetic acid], 2,4-DB, MCPA) are commonly used for weed control. As a group, they are essentially nontoxic to animals when forage has been properly treated. When large doses are consumed, depression, loss of appetite, weight loss, tenseness, and muscular weakness (particularly of the hindquarters) are seen. In dogs, the muscles may remain contracted for longer than normal and have difficulty relaxing. Dogs also become uncoordinated and weak, and may have vomiting and diarrhea.
The use of 2,4,5-T was limited and its registration cancelled because extremely toxic contaminants, collectively called dioxins (TCDD and HCDD), were found.
Dinitrophenolic compounds include dinoseb, binapacryl, and DNOC. The old 2-4 dinitrophenol and dinitrocresol compounds were highly toxic to all animals. 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 or lungs. Signs include fever, difficulty breathing, metabolic abnormalities, a rapid heartbeat, and convulsions, followed by coma and death. Cataracts can develop in animals with longterm dinitrophenol poisoning. Exposure to dinitro compounds may cause yellow staining of the skin, conjunctiva (of the eye), or hair. An effective antidote is not known. Affected animals should be cooled and sedated to help control fever. Atropine sulfate, aspirin, and fever reducers should not be used. Carbohydrate solutions given intravenously and vitamin A injections may be useful.
Organophospate compounds (for example glyphosate, bensulide) are widely used herbicides that have low toxicity. Exposure to toxic amounts is unlikely with recommended application and handling of containers.
Dogs and cats have shown eye, skin, and upper respiratory signs when exposed during or after an application to weeds or grass. Vomiting, staggering, and hindleg weakness have been seen in dogs and cats that were exposed to fresh chemicals on treated foliage. The signs usually disappear when exposure stops, and minimal symptomatic treatment is needed. Washing the chemical off the skin, emptying the stomach, and tranquilizing the animal are usually sufficient (see Poisoning: Organophosphates).
Other organic herbicides include phenyl or substituted urea compounds (diuron, fenuron, linuron, monolinuron), polycyclic alkanoic acids or aryloxyphenoxypropionic compounds (diclofop, fenoxaprop, fenthiaprop, fluazifop, haloxyfop), triazinylsulfonylurea or sulfonylurea compounds (chlorsulfuron, sulfometuron, ethametsulfuron, chloremuron), and triazine, methylthiotriazine, and triazinone compounds (atrazine, cyanazine, prometryn, metribuzin, simazine).
Last full review/revision July 2011 by Barry R. Blakley, DVM, PhD; Cheryl L. Waldner, DVM, PhD; Rob Bildfell, DVM, MSc, DACVP; William D. Black, MSc, DVM, PhD; Herman J. Boermans, DVM, MSc, PhD; Cecil F. Brownie, DVM, PhD, DABVT, DABT, DABFE, DABFM, FACFEI; Raymond Cahill-Morasco, MS, DVM; Keith A. Clark, DVM, PhD; Gregory F. Grauer, DVM, MS, DACVIM; Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT; Larry G. Hansen, PhD; Safdar A. Khan, DVM, MS, PhD, DABVT; Garrick C. M. Latch, MASc, PhD; Gavin L. Meerdink, DVM, DABVT; Lisa A. Murphy, VMD; Frederick W. Oehme, DVM, PhD; Gary D. Osweiler, DVM, MS, PhD; Mary M. Schell, DVM; David G. Schmitz, DVM, MS, DACVIM (LA); Norman R. Schneider, DVM, MSc, DABVT