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Rodenticides are controversial, due to secondary poisoning and their risks to children, pets and wildlife.
Single feed baits are chemicals sufficiently dangerous that the first dose is sufficient to kill.
Rodents are difficult to kill with poisons because their feeding habits reflect their place as scavengers. They will eat a small bit of something and wait, and if they do not get sick, they continue. An effective rodenticide must be tasteless and odorless in lethal concentrations, and have a delayed effect.
Anticoagulants are defined as chronic (death occurs one to two weeks after ingestion of the lethal dose, rarely sooner), single-dose (second generation) or multiple-dose (first generation) rodenticides, acting by effective blocking of the vitamin K cycle, resulting in inability to produce essential blood-clotting factors — mainly coagulation factors II (prothrombin) and VII (proconvertin).
In addition to this specific metabolic disruption, massive toxic doses of 4-hydroxycoumarin or 4-hydroxythiacoumarin and indandione anticoagulants cause damage to tiny blood vessels (capillaries), increasing their permeability, causing diffuse internal bleedings (haemorrhagias). These effects are gradual, developing over several days. In the final phase of the intoxication, the exhausted rodent collapses in hypovolemic circulatory shock or severe anemia and dies calmly. However, because of the duration of discomfort and pain before death it has been suggested[who?] that the use of rodenticides can be considered as inhumane.
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.
|1,3-indandiones||diphacinone, chlorophacinone, pindone|
These 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.
|Other||Difethialone is considered a second generation anticoagulant rodenticide .|
|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 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 (poison assaults on pets, suicidal attempts) 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.
Metal phosphides have been used as a means of killing rodents and are considered single-dose fast acting rodenticides (death occurs commonly within 1–3 days after single bait ingestion). A bait consisting of food and a phosphide (usually zinc 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 (rest population) can be eradicated by pre-baiting them with nontoxic bait for a week or two (this is important to overcome bait shyness, and to get rodents used to feeding in specific areas by specific food, especially in eradicating rats) and subsequently applying poisoned bait of the same sort as used for pre-baiting until all consumption of the bait ceases (usually within 2–4 days). 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 (i.e., rodents feed on it readily).
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 characteristic for phosphine liberated by hydrolysis. The odor attracts (or, at least, does not repel) rodents, but has 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 (usually aluminium, calcium or magnesium phosphide for fumigation/gassing) may also contain other chemicals which evolve ammonia, which helps to reduce the potential for spontaneous ignition or explosion of the phosphine gas.
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 strychnine-producing plants are grown (Strychnos nux-vomica, in southeast Asia). 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 are:
Calciferols (vitamins D), cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2) 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 (few IUs per kilogram body weight daily, only a fraction of a milligram), and like most fat soluble vitamins, they are toxic in larger doses, causing hypervitaminosis. If the poisoning is severe enough (that is, if the dose of the toxin is high 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 (mainly monohydrogencarbonate calcium cation, partially bound to plasma proteins, [CaHCO3]+), 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 (formation of calcificates, crystals of calcium salts/complexes in the tissues, damaging them), leading further to heart problems (myocardial tissue is sensitive to variations of free calcium levels, affecting both myocardial contractibility and excitation propagation between atrias and ventriculas), bleeding (due to capillary damage) and possibly kidney failure. It is considered to be single-dose, cumulative (depending on concentration used; the common 0.075% bait concentration is lethal to most rodents after a single intake of larger portions of the bait) or sub-chronic (death occurring usually within days to one week after ingestion of the bait). Applied concentrations are 0.075% cholecalciferol and 0.1% ergocalciferol when used alone.
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 (with a different formula than today's Sorexa D), back in 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 renal 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 chemical poisons include:
Non-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 (namely brodifacoum and difethialone), 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.
|The examples and perspective in this article deal primarily with the United States and do not represent a worldwide view of the subject. (January 2014)|
One of the potential problems when using rodenticides is that the dead or weakened rodents are eaten by other wildlife in the area. To minimize this, people deploying rodenticides need to take into account the strength of the poison and the amount of time it takes the poison to take effect.
An increase in strength can cause the rodent to continue feeding before the poison takes effect which can then poison the animal that eats the rodent. A decrease in the amount of time the poison takes can reduce make it harder to rehabilitate other wildlife that has been poisoned (and the current fast-acting poisons don't have antidotes).
For now, this has lead environmental researchers to conclude that low strength, long duration rodenticides (generally first generation anticoagulants) are the best balance between reducing the rat population and decreasing the amount of collateral damage. 
In 2008, "After fully assessing human health and ecological effects, as well as benefits", The EPA announced measures to reduce risks associated with the 10 rodenticides listed below. New restrictions by sale and distribution restrictions, minimum package size requirements, use site restriction, and tamper resistant products would have gone into effect in 2011. These regulations have been delayed pending a legal challenge by one manufacturer, Reckitt-Benkiser.