Rodenticides are made and sold for the purpose of killing . While commonly referred to as " rat poison", rodenticides are also used to kill mice, groundhog, chipmunks, , nutria, , and .
Some rodenticides are lethal after one exposure while others require more than one. Rodents are disinclined to gorge on an unknown food (perhaps reflecting an adaptation to their inability to emesis), preferring to sample, wait and observe whether it makes them or other rats sick. This phenomenon of poison shyness is the rationale for poisons that kill only after multiple doses.
Besides being directly toxic to the mammals that ingest them, including dogs, cats, and humans, many rodenticides present a secondary poisoning risk to animals that hunt or scavenge the dead corpses of rats.
In addition to this specific metabolic disruption, massive toxic doses of 4-hydroxycoumarin, 4-thiochromenone and 1,3-indandione anticoagulants cause damage to tiny blood vessels (capillary), increasing their permeability, causing internal bleeding. These effects are gradual, developing over several days. In the final phase of the intoxication, the exhausted rodent collapses due to hemorrhagic shock or severe anemia and dies. The question of whether the use of these rodenticides can be considered humane has been raised.
The main benefit of anticoagulants over other poisons is that the time taken for the poison to induce death means that the rats do not associate the damage with their feeding habits.
/4-hydroxycoumarins |
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1,3-indandiones | diphacinone, chlorophacinone, pindone
These are harder to group by generation. The U.S. Environmental Protection Agency considers chlorophacinone and diphacinone as first generation agents. According to some sources, the indandiones are considered second generation. |
4-thiochromenones | Difethialone is the only member of this class of compounds. The EPA and California consider this to be an SGAR. |
Indirect | Sometimes, anticoagulant rodenticides are potentiated by an antibiotic or bacteriostatic agent, most commonly sulfaquinoxaline. The aim of this association is that the antibiotic suppresses intestinal symbiosis microflora, which are a source of vitamin K. Diminished production of vitamin K by the intestinal microflora contributes to the action of anticoagulants. Added vitamin D also has a synergistic effect with anticoagulants. |
Phylloquinone has been suggested, and successfully used, as antidote for or humans accidentally or intentionally exposed to anticoagulant poisons. Some of these poisons act by inhibiting liver functions and in advanced stages of poisoning, several blood-clotting factors are absent, and the volume of circulating blood is diminished, so that a blood transfusion (optionally with the clotting factors present) can save a person who has been poisoned, an advantage over some older poisons. A unique enzyme produced by the liver enables the body to recycle vitamin K. To produce the blood clotting factors that prevent excessive bleeding, the body needs vitamin K. Anticoagulants hinder this enzyme's ability to function. Internal bleeding could start if the body's reserve of anticoagulant runs out from exposure to enough of it. Because they bind more closely to the enzyme that produces blood clotting agents, single-dose anticoagulants are more hazardous. They may also obstruct several stages of the recycling of vitamin K. Single-dose or second-generation anticoagulants can be stored in the liver because they are not quickly eliminated from the body.
Zinc phosphide is typically added to rodent baits in a concentration of 0.75% to 2.0%. The baits have strong, pungent garlic-like odor due to the phosphine liberated by hydrolysis. The odor attracts (or, at least, does not repel) rodents, but has a repulsive effect on other mammals. Birds, notably , are not sensitive to the smell, and might feed on the bait, and thus fall victim to the poison.
The tablets or pellets (usually aluminium, calcium or magnesium phosphide for fumigation/gassing) may also contain other chemicals which evolve ammonia, which helps reduce the potential for spontaneous combustion or explosion of the phosphine gas.
Metal phosphides do not accumulate in the tissues of poisoned animals, so the risk of secondary poisoning is low.
Before the advent of anticoagulants, phosphides were the favored kind of rat poison. During World War II, they came into use in United States because of shortage of strychnine due to the Japanese occupation of the territories where the strychnine tree is grown. Phosphides are rather fast-acting rat poisons, resulting in the rats dying usually in open areas, instead of in the affected buildings.
Phosphides used as rodenticides include:
There is an important feature of calciferols toxicology, that they are synergistic with anticoagulant toxicant. In other words, mixtures of anticoagulants and calciferols in same bait are more toxic than a sum of toxicities of the anticoagulant and the calciferol in the bait, so that a massive hypercalcemic effect can be achieved by a substantially lower calciferol content in the bait, and vice versa, a more pronounced anticoagulant/hemorrhagic effects are observed if the calciferol is present. This synergism is mostly used in calciferol low concentration baits, because effective concentrations of calciferols are more expensive than effective concentrations of most anticoagulants.
The first application of a calciferol in rodenticidal bait was in the Sorex product Sorexa D (with a different formula than today's Sorexa D), back in the early 1970s, which contained 0.025% warfarin and 0.1% ergocalciferol. Today, Sorexa CD contains a 0.0025% difenacoum and 0.075% cholecalciferol combination. Numerous other brand products containing either 0.075-0.1% calciferols (e.g. Quintox) alone or alongside an anticoagulant are marketed.
The Merck Veterinary Manual states the following:
Although this rodenticide cholecalciferol was introduced with claims that it was less toxic to nontarget species than to rodents, clinical experience has shown that rodenticides containing cholecalciferol are a significant health threat to dogs and cats. Cholecalciferol produces hypercalcemia, which results in systemic calcification of soft tissue, leading to kidney failure, cardiac abnormalities, hypertension, CNS depression and GI upset. Signs generally develop within 18-36 hours of ingestion and can include depression, anorexia, polyuria and polydipsia. As serum calcium concentrations increase, clinical signs become more severe. ... GI smooth muscle excitability decreases and is manifest by anorexia, vomiting and constipation. ... Loss of renal concentrating ability is a direct result of hypercalcemia. As hypercalcemia persists, mineralization of the kidneys results in progressive renal insufficiency."Additional anticoagulant renders the bait more toxic to pets as well as humans. Upon single ingestion, solely calciferol-based baits are considered generally safer to birds than second generation anticoagulants or acute toxicants. Treatment in pets is mostly supportive, with intravenous fluids and pamidronate disodium. The hormone calcitonin is no longer commonly used.
There are a few drawbacks to contraception. Since it doesn't kill the rodent immediately, it takes longer to see results. Both poisons and contraception need continued application to control the population on an ongoing basis, otherwise the rodent population will quickly rebound.
Inert gas killing of burrowing pest animals is another method with no impact on scavenging wildlife. One such method has been commercialized and sold under the brand name Rat Ice.
The faster a rodenticide acts, the more critical this problem may be. For the fast-acting rodenticide bromethalin, for example, there is no diagnostic test or antidote.
This has led environmental researchers to conclude that low strength, long duration rodenticides (generally first generation anticoagulants) are the best balance between maximum effect and minimum risk.
Alberta, Canada, through a combination of climate and control, is also believed to be rat-free.
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