Health for all: Overview of
Herbicide Poisoning: prevention is better than cure
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.
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
·
Overview of Herbicide Poisoning
Toxicity and
Management of Poisoning
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