* This is the Veterinary Version. *
Overview of Herbicide Poisoning
Herbicides are used routinely to control noxious plants. Most of these chemicals, particularly the more recently developed synthetic organic herbicides, are quite selective for specific plants and have low toxicity for mammals; other, less-selective compounds (eg, sodium arsenite, arsenic trioxide, sodium chlorate, ammonium sulfamate, borax, and many others) were formerly used on a large scale and are more toxic to animals.
Vegetation treated with herbicides at proper rates normally will not be hazardous to animals, including people. Particularly after the herbicides have dried on the vegetation, only small amounts can be dislodged. When herbicide applications have been excessive, damage to lawns, crops, or other foliage is often evident.
The residue potential for most of these agents is low. However, runoff from agricultural applications and entrance into drinking water cannot be excluded. The possibility of residues should be explored if significant exposure of food-producing animals occurs. The time recommended before treated vegetation is grazed or used as animal feed is available for a number of products.
Most health 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, poisoning problems in veterinary practice are rare. With few exceptions, it is only when animals gain direct access to the product that acute poisoning occurs. Acute signs usually will not lead to a diagnosis, although acute GI signs are frequent. All common differential diagnoses should be excluded in animals showing signs of a sudden onset of disease or sudden death. The case history is critical. Sickness after feeding, spraying of pastures or crops adjacent to pastures, a change in housing, or direct exposure may lead to a tentative diagnosis of herbicide poisoning. Generally, the nature of exposure is hard to identify because of storage of herbicides in mis- or unlabeled containers. Unidentified spillage of liquid from containers or powder from torn or damaged bags near a feed source, or visual confusion with a dietary ingredient or supplement, may cause the exposure. Once a putative chemical source has been identified, an animal poison control center should be contacted for information on treatments, laboratory tests, and likely outcome.
Chronic disease caused by herbicides is even more difficult to diagnose. It may include a history of herbicide use in proximity to the animals or animal feed or water source, or a gradual change in the animals’ performance or behavior over a period of weeks, months, or even years. Occasionally, it involves manufacture or storage of herbicides nearby. Samples of possible sources (ie, contaminated feed and water) for residue analysis, as well as tissues from exposed animals taken at necropsy, are essential. Months or even years may be required to successfully identify a problem of chronic exposure.
To recognize whether an animal has been exposed to herbicides or accidental poisoning, standardized analytical procedures for diagnostic investigation of biologic materials have become established and are subsumed under the term “biomonitoring.” Accurate biomonitoring is an important tool to evaluate human or animal exposure to such herbicides by measuring the levels of these chemicals, their metabolites, or altered biologic structures or functions in biologic materials such as urine, blood or blood components, exhaled air, hair or nails, and tissues. The use of urine is advantageous because of ready availability. As such, urine has been used for biomonitoring of several herbicides, including 2,4-D, 2,4,5-T, MCPA (2-methyl-4-chlorophenoxyacetic acid), atrazine, diuron, alachlor, metolachlor, paraquat, diquat, imazapyr, imazapic, imazethapyr, imazamox, imazaquin, and imazamethabenz-methyl herbicides, with the objective to assess exposure and health risk to exposed animals.
If poisoning is suspected, the first step in management is to halt further exposure. Animals should be separated from any possible source before attempting to stabilize and support them. If there are life-threatening signs, efforts to stabilize animals by general mitigation methods should be started. Specific antidotal treatments, when available, may help to confirm the diagnosis. As time permits, a more detailed history and investigation should be completed. The owner should be made aware of the need for full disclosure of facts to successfully determine the source of poisoning, eg, unapproved use or failure to properly store a chemical.
There are >200 active ingredients used as herbicides; however, some of them are believed to be obsolete or no longer in use. Of these, several have been evaluated for their toxic potential and are discussed below. More specific information is available on the label and from the manufacturer, cooperative extension service, or poison control center. Selected information on herbicides, such as the acute oral toxic dose (LD50) in rats, the amount an animal can be exposed to without being affected (no adverse effect level), the likelihood of problems caused by dermal contact in rabbits (dermal LD50, eye and skin irritation), deleterious effects on avian species, and toxicity to fish in water, is included for some commonly used herbicides (see Table: Herbicide Poisoning). Comparative toxic doses (TD) and lethal doses (LD) of selected herbicides in domesticated species, such as monkeys, cattle, sheep, pigs, cats, dogs, and chickens, is also summarized (see Table: Oral Toxic Doses (TD) and Lethal Doses (LD) of Herbicides in Domestic Species). The information is only a guideline, because the toxicity of herbicides may be altered by the presence of other ingredients (eg, impurities, surfactants, stabilizers, emulsifiers) present in the compound. With a few exceptions, most of the newly developed chemicals have a low order of toxicity to mammals. However, some herbicides, such as atrazine, buturon, butiphos, chloridazon, chlorpropham, cynazine, 2,4-D and 2,4,5-T alone or in combination, dichlorprop, dinoseb, dinoterb, linuron, mecoprop, monolinuron, MCPA (2-methyl-4-chlorophenoxyacetic acid), prometryn, propachlor, nitrofen, silvex, TCDD (a common contaminant during manufacturing process of some herbicides such as 2,4-D and 2,4,5-T), and tridiphane, are known to have adverse effects on development of embryos and reproduction abnormalities in experimental animals. A list of such chemicals is summarized in Herbicides with Potential to Cause Developmental Toxicity in Experimental Animals.
Oral Toxic Doses (TD) and Lethal Doses (LD) of Herbicides in Domestic Species
Herbicides with Potential to Cause Developmental Toxicity in Experimental Animals
* This is the Veterinary Version. *