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 don't 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 after 1 - 2 weeks post ingestion of the lethal dose, rarely sooner), single-dose (second generation) or multiple dose (first generation) cumulative rodenticides. Fatal internal bleeding is caused by lethal dose of anticoagulants such as brodifacoum, coumatetralyl or warfarin. These substances, in effective doses are antivitamins K, blocking the enzymes K1-2,3-epoxide-reductase (this enzyme is preferentially blocked by 4-hydroxycoumarin/4-hydroxythiacoumarin derivatives) and K1-quinone-reductase (this enzyme is preferentially blocked by indandione derivatives), depriving the organism of its source of active vitamin K1. This leads to disruption of the vitamin K cycle, resulting in inability of production of essential blood-clotting factors (mainly coagulation factors II (prothrombin), VII (proconvertin), IX (Christmas factor) and X (Stuart factor)).
In addition to this specific metabolic disruption, toxic doses of 4-hydroxycoumarin/4-hydroxythiacoumarin and indandione anticoagulants cause damage to tiny blood vessels (capillaries), increasing their permeability, causing diffuse internal bleedings (haemorrhagias). These effects are gradual, they develop in course of days and are not accompanied by any nociceptive perceptions, such as pain or agony. In final phase of the intoxication, the exhausted rodent collapses in hypovolemic circulatory shock or severe anemia and dies calmly. Rodenticidal anticoagulants are either first generation agents (4-hydroxycoumarin type: warfarin, coumatetralyl; indandione type: pindone, diphacinone, chlorophacinone), generally requiring higher concentrations (usually between 0.005 and 0.1%), consecutive intake over days in order to accumulate the lethal dose, poor active or inactive after single feeding and less toxic than second generation agents, which are derivatives of 4-hydroxycoumarin (difenacoum, brodifacoum, bromadiolone and flocoumafen) or 4-hydroxy-1-benzothiin-2-one (4-hydroxy-1-thiacoumarin, sometimes incorrectly referred to as 4-hydroxy-1-thiocoumarin, for reason see heterocyclic compounds), namely difethialone.
Second generation agents are far more toxic than first generation, they are generally applied in lower concentrations in baits (usually in order 0.001 - 0.005%), are lethal after single ingestion of bait and are effective also against strains of rodents that became resistant against first generation anticoagulants; thus, the second generation anticoagulants are sometimes referred to as "superwarfarins".
Sometimes, anticoagulant rodenticides are potentiated by an antibiotic, most common the sulfaquinoxaline. The aim of this association (e.g. warfarin 0.05% + sulfaquinoxaline 0.02%, or difenacoum 0.005% + sulfaquinoxaline 0.02% etc.) is, that the antibiotic/bacteriostatic agent suppresses intestinal/gut symbiotic microflora, that represents a source of vitamin K. Thus, the symbiotic bacterias are killed, or their metabolism is impaired and the production of vitamin K by them is diminuted, an effect, which logically contributes to the action of anticoagulants. Antibiotic agents other than sulfaquinoxaline may be used, f.e. co-trimoxazole, tetracycline, neomycin or metronidazole. Further synergism used in rodenticidal baits is that of an association of an anticoagulant with a compound with vitamin D-activity, i.e. cholecalciferol or ergocalciferol, see below. Typical formulas used are f.e. warfarin 0.025 - 0.05% + cholecalciferol 0.01%.
In some lands, there are even fixed three-component rodenticides, i.e. anticoagulant + antibiotic + vitamin D, f.e. difenacoum 0.005% + sulfaquinoxaline 0.02% + cholecalciferol 0.01%. 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 - 0.005% are so toxic, that no known resistant strains of rodents exists, and even rodents resistant against other derivatives are reliably exterminated by application of these most toxic 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. In addition, since some of these poisons act by inhibiting liver functions and in progressed stage of poisoning, several blood-clotting factors as well as the whole volume of circulating blood lacks, a blood transfusion (optionally with the clotting factors present) can save a person who inadvertently takes them, an advantage over some older poisons.
The main benefit of anticoagulants is the time taken for the poison to induce death means that the rats do not associate death with eating the poison. In fact the rat will often die from being bitten by a fellow rat, which can lead to the offending rodent to be outcast from the group.
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 alterning 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 amount of around 0.75-2%. The baits have strong, pungent garlic-like odor characteristic for phosphine liberated by hydrolysis. The odor attracts (or, at least, does not repulse) 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 phopsphide 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, therefore the risk of secondary poisoning is low.
Before the advent of anticoagulants, phosphides were the favored kind of rat poison. During the World War II, they came in 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 south-east 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:
- aluminium phosphide (fumigant only)
- calcium phosphide (fumigant only)
- magnesium phosphide (fumigant only)
- zinc phosphide (in baits)
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 beneficial to mammals: 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 miligram), 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 (myocard 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, or 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), 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 concetration baits, because effective concentrations of calciferols are more expensive, than effective concentrations of the most anticoagulants. The historically very first application of a calciferol in rodenticidal bait was in fact the Sorex product Sorexa® D (with a different formula than today's Sorexa® D) back in early 1970s, containing warfarin 0.025% + ergocalciferol 0.1%. Today, Sorexa® CD contains a 0.0025% difenacoum + 0.075% cholecalciferol combination. Numerous other brand products containing either calciferols 0.075 - 0.1% (f.e. Quintox®, containing 0.075% cholecalciferol) alone, or a combination of calciferol 0.01 - 0.075% with an anticoagulant are marketed.
In family pets, accidental ingestion is generally considered safe for cats but dangerous for dogs. 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 (zinc phosphide, bromethalin, f.e.). 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:
- ANTU (α-naphtylthiourea; specific against Norway rat, Rattus norvegicus)
- Barium (a toxic metal) compound
- Bromethalin (which affects the nervous system, no antidote)
- Chloralose (narcotic acting condensation product of chloral and glucose)
- Crimidine (2-chloro-N, N,6-trimethylpyrimidin-4-amine; a synthetic convulsant poison, antivitamin B6)
- 1,3-Difluoro-2-propanol ("Gliftor" in the former USSR)
- Endrin (organochlorine cyclodiene insecticide, used in the past for extermination of voles in fields during winter by aircraft spraying)
- Fluoroacetamide ("1081")
- Phosacetim (a delayed-action organophosphorous rodenticide)
- White phosphorus
- Pyrinuron (an urea derivative)
- Sodium fluoroacetate ("1080")
- Tetramethylenedisulfotetramine ("tetramine")
- Thallium (a toxic heavy metal) compounds
- Zyklon B (hydrogen cyanide absorbed in an inert carrier)
Mechanical rat traps are one possible alternative to poisons; another alternative is to have a dog. Both of these methods have a disadvantage of being comparatively messy, a particular problem when the building with a rat problem is to be uninhabited for some months. Anticoagulants have the advantage that their first effect is dehydration from blood loss, causing the unfortunate rodent to leave the building in search of water. Another alternative is the use of biological, non-toxic, yet lethal baits, consisting of anhydrous powdered maize/corn cobs, containing high fractions (over 40%) of α-cellulose, which is incorporated into a solid, gastric-resistant matrix, that is dissolved in the gut. The α-cellulose anhydrous powder released in the gut of the rodent disrupts water and electrolyte balance and so kills the rodent. This material is commonly formulated with taste and flavour additives to increase its palatability, and is compressed into granulate of appropriate size (granules of bigger size for rats, smaller granules for mice). This material is completely non-toxic, leaves no harmful residues, is environmentally friendly and accidental ingestion of it by pets or children is simply treated by giving laxatives, plenty of water and electrolytes. Dead rodents killed by this mean pose no risk of secondary poisoning.
Newer rodenticides have been developed to work with by reducing the sperm count in males to deprive them of the ability to procreate rather than to kill rodents outright. They are usually administered in the breeding seasons of most rodents.
- "RODENTICIDES, source: Journal of Vertrinary Medicine, archives, vol. 27, May, 1998". IPM Of Alaska, Solving Pest Problems Sensibly. Retrieved 2006-07-07.
- National Pesticide Information Center
- Fact Sheet on EPA's Proposed Risk Mitigation Decision for Nine Rodenticides
- EPA Rodenticide Cluster Reregistration Eligibility Decision Fact Sheet