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 humans. 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 ruled out. 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 used properly, problems of herbicide poisoning 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 following 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.
In order to recognize whether a subject is exposed to herbicides, or even accidental poisoning, now standardized analytical procedure for diagnostic investigation of biological materials have become established and these are subsumed under the term“biomonitoring”. Accurately biomonitoring is an important tool that can be used to evaluate human or animal exposure to such herbicides by measuring the levels of these chemicals, their metabolites or altered biological structures or functions in biological media such as urine, blood or blood components, exhaled air, hair or nails, and tissues The use of urine has advantage because of ease of availability. As such urine has been used for biomonitoring of several herbicides such as 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 with the objective to assess exposure and health risk to exposed subjects.
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 in order to successfully determine the source of poisoning, eg, unapproved use or failure to properly store a chemical.
Toxicity and Management of Poisoning
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 rat, the amount an animal can be exposed to without being affected (no adverse effect level), the likelihood of problems caused by dermal contact in rabbit (dermal LD50, eye and skin irritation), deleterious effects on avian species and toxicity to fish in water is included for some commonly used herbicides (TABLE 1). Comparative toxic doses (TD) and lethal doses (LD), of selected herbicides in domesticated species such as monkeys, cattle, sheep, pigs, cats, dogs, chickens is also summarized (TABLE 2). 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), tridiphane and tridiphane are known to have adverse effects on development of
Overview of Herbicide Poisoning
By P. K. Gupta, PhD, Post Doc (USA), Hon DSc PGDCA, MSc VM & AH BVSc, FNA VSc, FASc, AW, FST, FAEB, FACVT (USA), Gold Medalist, Editor-in-Chief, Toxicology International
The Merck Veterinary Manual (2016). Chapter “Herbicide Poisoning” by PK GUPTA 11th edition, Merck & Co. Inc Whitehouse Station, NJ, USA pp 2969-99
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