Rodenticide

thumb|150x150px|Typical rat poison bait station (Germany, 2010)

Rodenticides are chemicals made and sold for the purpose of killing rodents. While commonly referred to as "rat poison", rodenticides are also used to kill mice, woodchucks, chipmunks, porcupines, nutria, beavers, and voles.

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 vomit), 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

thumb|Poison baits infused with peanuts to attract rodents

Anticoagulants

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, 4-thiochromenone and 1,3-indandione anticoagulants cause damage to tiny blood vessels (capillaries), 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.

First-generation rodenticidal anticoagulants generally have shorter elimination half-lives, require higher concentrations (usually between 0.005% and 0.1%) and consecutive intake over days in order to accumulate the lethal dose, and are less toxic than second-generation agents.
Second-generation anticoagulant rodenticides (or SGARs) are far more toxic than those of the first generation. They are generally applied in lower concentrations in baits—usually on the order of 0.001% to 0.005%—are lethal after a single ingestion of bait and are also effective against strains of rodents that became resistant to first-generation anticoagulants; thus, the second-generation anticoagulants are sometimes referred to as "superwarfarins".

{| class="wikitable"

! Class

! Examples

| Coumarins/4-hydroxycoumarins

First generation: warfarin, coumatetralyl
Second generation: difenacoum, brodifacoum, flocoumafen and bromadiolone.

| 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.

| 4-thiochromenones

| Difethialone is the only member of this class of compounds. The EPA and California consider this to be an SGAR.

Metal phosphides

thumb|Rat poison vendor's stall at a market in [[Linxia City, China]]

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 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 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 wild turkeys, 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.

thumb|A rat poison at the shopping mall in Tuen Mun, Hong Kong

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:

aluminium phosphide (fumigant and bait)
calcium phosphide (fumigant only)
magnesium phosphide (fumigant only)
zinc phosphide (bait only)

Hypercalcemia (vitamin D overdose)

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 D. 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 action potential propagation between the atria and ventricles), 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 (30,000 IU/g) and 0.1% ergocalciferol (40,000 IU/g) 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 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.</blockquote>

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.

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 (a dry ice formulation).

Non-target issues

alt=A tree squirrel sits atop a rodent bait station in a garden, holding and eating a blue bromadiolone tablet.|thumb|A tree squirrel eating rodenticide from a bait station intended for rats

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. There is evidence of secondary poisoning being caused by exposure to prey.

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.

Proposed US legislation change

thumb|Secondary poisoning is caused by eating poisoned prey, showing how predators are effected not being the target within the environment. 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. Alaska's [[Hawadax Island (formerly known as Rat Island), Macquarie Island and Canna, Scotland (declared rat-free in 2008). According to the Friends of South Georgia Island, all of the rats have been eliminated from South Georgia.

Alberta, Canada, through a combination of climate and control, is also believed to be rat-free.

References

External links

National Pesticide Information Center
Fact Sheet on EPA's Proposed Risk Mitigation Decision for Nine Rodenticides
EPA Rodenticide Cluster Reregistration Eligibility Decision Fact Sheet