Rodenticide


Rodenticides, colloquially rat poison, are typically non-specific pest control chemicals made and sold for the purpose of killing rodents.
Some rodenticides are lethal after one exposure while others require more than one. Rodents are disinclined to gorge on an unknown food, 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.

Classes of rodenticides

Anticoagulants

s are defined as chronic, single-dose or multiple-dose rodenticides, acting by effective blocking of the vitamin K cycle, resulting in inability to produce essential blood-clotting factors—mainly coagulation factors II and VII.
In addition to this specific metabolic disruption, massive toxic doses of 4-hydroxycoumarin, 4-thiochromenone and indandione anticoagulants cause damage to tiny blood vessels, 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 calmly. 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.
ClassExamples
Coumarins/4-hydroxycoumarins
1,3-indandionesdiphacinone, chlorophacinone, pindoneThese are harder to group by generation. According to some sources, the indandiones are considered second generation. However, according to the U.S. Environmental Protection Agency, examples of first generation agents include chlorophacinone and diphacinone.
4-thiochromenonesDifethialone is the only member of this class of compounds.
IndirectSometimes, anticoagulant rodenticides are potentiated by an antibiotic or bacteriostatic agent, most commonly sulfaquinoxaline. The aim of this association is that the antibiotic suppresses intestinal symbiotic 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.

Vitamin K1 has been suggested, and successfully used, as antidote for pets 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 can save a person who has been poisoned, an advantage over some older poisons.

Metal phosphides

Metal phosphides have been used as a means of killing rodents and are considered single-dose fast acting rodenticides. A bait consisting of food and a phosphide is left where the rodents can eat it. The acid in the digestive system of the rodent reacts with the phosphide to generate the toxic phosphine gas. This method of vermin control has possible use in places where rodents are resistant to some of the anticoagulants, particularly for control of house and field mice; zinc phosphide baits are also cheaper than most second-generation anticoagulants, so that sometimes, in the case of large infestation by rodents, their population is initially reduced by copious amounts of zinc phosphide bait applied, and the rest of population that survived the initial fast-acting poison is then eradicated by prolonged feeding on anticoagulant bait. Inversely, the individual rodents that survived anticoagulant bait poisoning can be eradicated by pre-baiting them with nontoxic bait for a week or two and subsequently applying poisoned bait of the same sort as used for pre-baiting until all consumption of the bait ceases. These methods of alternating rodenticides with different modes of action gives actual or almost 100% eradications of the rodent population in the area, if the acceptance/palatability of baits are good.
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 rodents, but has an repulsive effect on other mammals. Birds, notably wild turkeys, are not sensitive to the smell, and will feed on the bait, and thus become collateral damage.
The tablets or pellets 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:
and ergocalciferol are used as rodenticides. They are toxic to rodents for the same reason they are important to humans: they affect calcium and phosphate homeostasis in the body. Vitamins D are essential in minute quantities, and like most fat soluble vitamins, they are toxic in larger doses, causing hypervitaminosis. If the poisoning is severe enough, it leads to death. In rodents that consume the rodenticidal bait, it causes hypercalcemia, raising the calcium level, mainly by increasing calcium absorption from food, mobilising bone-matrix-fixed calcium into ionised form, which circulates dissolved in the blood plasma. After ingestion of a lethal dose, the free calcium levels are raised sufficiently that blood vessels, kidneys, the stomach wall and lungs are mineralised/calcificated, leading further to heart problems, bleeding and possibly kidney failure. It is considered to be single-dose, cumulative or sub-chronic. Applied concentrations are 0.075% cholecalciferol and 0.1% ergocalciferol when used alone, which can kill a rodent or a rat.
There is an important feature of calciferols toxicology, that they are synergistic with anticoagulant toxicants, that means, that 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, 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 alone or alongside an anticoagulant are marketed.
The Merck Veterinary Manual states the following:

Although this rodenticide 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 human. Upon single ingestion, solely calciferol-based baits are considered generally safer to birds than second generation anticoagulants or acute toxicants. A specific antidote for calciferol intoxication is calcitonin, a hormone that lowers the blood levels of calcium. The therapy with commercially available calcitonin preparations is, however, expensive.

Other

Other chemical poisons include:
In some countries, fixed three-component rodenticides, i.e., anticoagulant + antibiotic + vitamin D, are used. Associations of a second-generation anticoagulant with an antibiotic and/or vitamin D are considered to be effective even against most resistant strains of rodents, though some second generation anticoagulants, in bait concentrations of 0.0025% to 0.005% are so toxic that resistance is unknown, and even rodents resistant to other rodenticides are reliably exterminated by application of these most toxic anticoagulants.

Low toxicity rodenticides

or corn meal gluten, have been developed as rodenticides and were approved in the EU and patented in the US in 2013. These preparations rely on electrolyte imbalance to cause death.

Non-target issues

Secondary poisoning and risks to wildlife

One of the potential problems when using rodenticides is that dead or weakened rodents may be eaten by other wildlife, either predators or scavengers. Members of the public deploying rodenticides may not be aware of this or may not follow the product's instructions closely enough.
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 are the best balance between maximum effect and minimum risk.

Proposed US legislation change

In 2008, after assessing human health and ecological effects, as well as benefits, the US Environmental Protection Agency announced measures to reduce risks associated with ten rodenticides. New restrictions by sale and distribution restrictions, minimum package size requirements, use site restriction, and tamper resistant products would have taken effect in 2011. The regulations were delayed pending a legal challenge by manufacturer Reckitt-Benkiser.

Notable rat eradications

The entire rat populations of several islands have been eradicated, most notably Campbell Island, New Zealand, Hawadax Island, Alaska and Canna, Scotland. According to the Friends of South Georgia Island all of the rats have been eliminated from South Georgia Island.
Alberta, Canada, through a combination of climate and control, is also believed to be rat-free.