Rodenticide

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Typical rat poison bait station (Germany, 2010

Rodenticides, colloquially rat poison, are pest control chemicals intended to kill rodents.

Rodenticides can be single or multiple dose. Because rodents are unable to vomit they are naturally cautious about what they eat and will wait to ensure they do not become ill before eating a large amount of bait,[1][2] known as bait shyness or poison shyness.

Rodenticides may present risks to children, pets and wildlife due to secondary poisoning.

Chemical preparations[edit]

Anticoagulants[edit]

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. The question of whether the use of these rodenticides can be considered humane has been raised.[3]

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,[4] 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 agents are far more toxic than 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".[5]
Class Examples
Coumarins/4-hydroxycoumarins
1,3-indandiones diphacinone, chlorophacinone,[7] pindone

These are harder to group by generation. According to some sources, the indandiones are considered second generation.[8] However, according to the U.S. Environmental Protection Agency, examples of first generation agents include chlorophacinone and diphacinone.[6]

Other Difethialone is considered a second generation anticoagulant rodenticide .[9]
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[edit]

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 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:

Hypercalcemia[edit]

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, wihich can kill a roten 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 (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 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."[10]

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[edit]

Civilian Public Service worker distributes rat poison for typhus control in Gulfport, Mississippi, ca. 1945.

Other chemical poisons include:

Combinations[edit]

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.

Alternatives[edit]

More environmentally-safe preparations, using natural ingredients such as powdered corn cob, have been developed and were approved in the EU and patented in the US in 2013. These preparations rely on lethal dehydration to cause death.[11][12]

Non-target issues[edit]

Secondary poisoning and risks to wildlife[edit]

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.[13]

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.[14]

Proposed US legislation change[edit]

In 2008, after assessing human health and ecological effects, as well as benefits,[6] the US Environmental Protection Agency (EPA) 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.[13]

Notable rat eradications[edit]

The entire rat populations of several islands have been eradicated, most notably Campbell Island, New Zealand (11,300 ha),[15] Hawadax Island, Alaska (formerly known as Rat Island, 2,670 ha)[16] and Canna, Scotland (1,030 ha, declared rat-free in 2008).[17]

Alberta, Canada, through a combination of climate and control, is believed to be rat-free.[18]

See also[edit]

References[edit]

  1. ^ "Smithsonian: Why rodents can't throw up". Retrieved 4 April 2015. 
  2. ^ "How do rats choose what to eat?". 
  3. ^ Meerburg BG, Brom FWA, Kijlstra A (2008). "The ethics of rodent control". Pest Manag Sci 64 (12): 1205–11. doi:10.1002/ps.1623. PMID 18642329. (subscription required (help)). 
  4. ^ Vandenbroucke V, Bousquet-Melou A, De Backer P, Croubels S (October 2008). "Pharmacokinetics of eight anticoagulant rodenticides in mice after single oral administration". J. Vet. Pharmacol. Ther. 31 (5): 437–45. doi:10.1111/j.1365-2885.2008.00979.x. PMID 19000263. 
  5. ^ Kotsaftis P, Girtovitis F, Boutou A, Ntaios G, Makris PE (September 2007). "Haemarthrosis after superwarfarin poisoning". Eur. J. Haematol. 79 (3): 255–7. doi:10.1111/j.1600-0609.2007.00904.x. PMID 17655702. 
  6. ^ a b c "Final Risk Mitigation Decision for Ten Rodenticides | Pesticides | US EPA". Retrieved 2008-12-24. 
  7. ^ "LONG ACTING ANTICOAGULANT RODENTICIDES". Retrieved 2008-12-24. 
  8. ^ "Anticoagulant Rodenticide Toxicosis in the Dog and Cat". Retrieved 2008-12-24. 
  9. ^ Saravanan K, Kanakasabai R, Thiyagesan K (June 2003). "Field evaluation of difethialone, a new second generation anticoagulant rodenticide in the rice fields". Indian J. Exp. Biol. 41 (6): 655–8. PMID 15266918. 
  10. ^ "Merck Veterinary Manual - Rodenticide Poisoning: Introduction". 
  11. ^ "EU approves powdered corn cob as biocidal active". Chemical Watch: Global Risk & Regulation News. 15 August 2013. Retrieved 22 August 2013. 
  12. ^ "IFI Claims Patent Services (Google)". Retrieved 4 April 2015. 
  13. ^ a b "Rodenticide manufacturer defies EPA, requests hearing on anticoagulant use". Retrieved 4 April 2015. 
  14. ^ "Poisons used to kill rodents have safer alternatives". Retrieved 4 April 2015. 
  15. ^ "NZ Government: Campbell Island conservation sanctuary rat free". Retrieved 4 April 2015. 
  16. ^ Borrell, Brendan (18 January 2011). "Where eagles die". Nature. doi:10.1038/news.2011.24. 
  17. ^ "Island which spent £600,000 getting rid of rats over-run with rabbits". Daily Telegraph. 27 April 2010. Retrieved 4 April 2015. 
  18. ^ "The history of rat control in Alberta". Retrieved 4 April 2015. 

Further reading[edit]

  • Plunkett, Signe J. (2001). Emergency Procedures for the Small Animal Veterinarian. Harcourt Publishers. pp. 289–292. ISBN 0-7020-2487-2. 
  • Gfeller, Roger W.; Shawn P. Messonnier (2004). Small Animal Toxicology and Poisonings. Mosby. pp. 321–326. ISBN 0-323-01246-9. 

External links[edit]