© Stuart M Bennett 2002


Brodifacoum is very similar to Difenacoum in its chemical structure and anticoagulant effect (they are both 4- hydroxycoumarin derivatives). Brodifacoum is a weak acid which does not readily form water-soluble salts. It does not lose activity after 30 days in direct sunlight. Commercial formulations are stable at least for two years if protected from extreme temperatures and sunlight. The container should be kept closed to maintain activity of formulation (as a bait). The modern 2nd generation anticoagulant rodenticides such as Brodifacoum have proven severe secondary poisoning properties and have been held responsible for the deaths of many birds of prey, particularly rare Red Kites and Buzzards that habitually feed off dead bodies. It was first registered in 1979.

It is only licenced for indoor use in the UK

This also begs the question as to whether the rodents will take the bait from indoors to outdoors, as rats are very inclined to do. Thus placing of these types of bait becomes crucial.

This should only be used when there is resistance to other preparations such as Bromodiolone, Warfarin etc.

Chemical Name: 3-[3-(4′-bromobiphenyl-4-yl)-1,2,3,4-tetrahydro-1-naphthyl]-4-hydroxycoumarin

Chemical Formula: C31H23BrO3

Chemical Structure:

 

LD50/LC50: The oral route is the commonest way of entry and the only one described in the published literature. LD50 oral (female rat) 0.37 to 0.68 mg/kg; LD50 oral (beagle dog) 0.25 to 1 mg/kg; LD50 oral (cat) estimated as 25 mg/kg. The acute dermal toxicity (male rabbits) with intact skin was estimated to be 0.25 to 0.625 mg/kg. When the skin is abraded, the dose is 1.25 mg/kg.

Environmental Effects

        Persistence: brodifacoum is persistent in soils with a half-life of 157 days. It is relatively immobile in soil and the potential for groundwater and surface water contamination is low. It is stable to hydrolysis at pH 5, 7, and 9.

        Solubility: nearly insoluble in water.

        Metabolism: brodifacoum is retained in the tissues at high rates, sometimes remaining in organ systems during the entire lifetime of an exposed animal. In a study that measured the retention of radioactive brodifacoum in the livers of single-dosed rats, 34% of the single dose is found in the liver after 13 weeks, and 11% of the dose remained in the liver for 104 weeks, approaching the normal lifespan of a rat (U.S. EPA MRID 42007502).

Ecotoxicity

Very highly toxic to aquatic organisms. Due to its extremely low solubility and usage patterns, it is assumed that not enough brodifacoum would dissolve in water to create a hazard to nontarget animals. Products used in sewers are water-resistant paraffinized blocks and are not expected to dissolve in water.

Very highly toxic to mammals and birds. Most risks posed to wildlife are through secondary exposure by consuming poisoned rodents. The cited general LD50 for birds is 0.26 mg / kg (U.S. EPA 1998 Reregistration Eligibility Document for Rodenticides).

The greatest hazard posed to wildlife by brodifacoum is that of secondary poisoning. It is highly effective at small doses - usually, a fatal dose will be ingested after a single feeding on baits. Brodifacoum is absorbed through the gut and death usually occurs through gastric hemorrhage.  However, rodents do not die immediately. Most die within 4-5 days of consuming a lethal dose. Until the time of death, target pests continue to consume poisoned bait so that the amount of active ingredient present in one rodent is many more times the amount required to kill it. Wildlife may consume rodents that have consumed large doses of brodifacoum. Death is likely to result from the consumption of only one poisoned rodent, or a predator may accumulate enough brodifacoum after consuming several poisoned prey items to induce life-threatening or fatal effects. The clotting factors affected by a single dose of brodifacoum may remain depressed at sub-normal levels for months in some animals, including birds. Stress or slight wounds incurred in the field, for example, small scratches that normally occur when a raptorial bird captures its prey, are oftentimes sufficient to cause a fatal hemorrhage. This is born out by many field studies all over the world...!

Mode of Action:

Brodifacoum acts by inhibiting the vitamin K epoxide reductase in the vitamin K1-epoxide cycle, impeding the cyclic regeneration of vitamin K1, resulting in hypoprothrombinemia. Under physiological conditions, the oxidation of vitamin K in the hepatocyte is coupled to a carboxylation step essential for activation of prothrombin factors from inactive precursors. Brodifacoum produces hypoprothrombinaemia because the coupled carboxylationreaction is inhibited. If therapeutic doses of vitamin K1 are given, additional substrate becomes available to resume the cycle and continue the carboxylation process, reversing the hypoprothrombinaemia.

Ingestion of brodifacoum is initially asymptomatic, and may continue as such even with prolonged alterations in prothrombin time. No gastrointestinaltract or other symptomatology occurs. Coagulation disturbances may become evident a few days after ingestion, and may be detected only by laboratory studies. In severe poisoning, gumleeding, epistaxis, petechiae, ecchymoses, haematomata, blood in urine and faeces, and genital haemorrhage may occur. Internal bleeding and cerebral haemorrhage may complicate the patient's prognosis.

The specific therapy is vitamin K1 or phytomenadione, which should usually be administered over a long period of time.

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