Rodenticide
While commonly referred to as "rat poison", rodenticides are also used to kill mice, woodchucks, chipmunks, porcupines, nutria, beavers,[1] and voles.
Rodents are disinclined to gorge on an unknown food (perhaps reflecting an adaptation to their inability to vomit),[3] preferring to sample, wait and observe whether it makes them or other rats sick.
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.
[6] 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 the final phase of the intoxication, the exhausted rodent collapses due to hemorrhagic shock or severe anemia and dies.
[15] Phylloquinone has been suggested, and successfully used, as antidote for pets or humans accidentally or intentionally exposed to anticoagulant poisons.
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.
[17] 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).
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.
Birds, notably wild turkeys, are not sensitive to the smell, and might feed on the bait, and thus fall victim to the poison.
[citation needed] 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.
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 action potential propagation between the atria and ventricles), bleeding (due to capillary damage) and possibly kidney failure.
Cholecalciferol produces hypercalcemia, which results in systemic calcification of soft tissue, leading to kidney failure, cardiac abnormalities, hypertension, CNS depression and GI upset.
Upon single ingestion, solely calciferol-based baits are considered generally safer to birds than second generation anticoagulants or acute toxicants.
[23] 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.
[24] In 2008, after assessing human health and ecological effects, as well as benefits,[13] the US Environmental Protection Agency (EPA) announced measures to reduce risks associated with ten rodenticides.
