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.
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
This should only be used
when there is resistance to other preparations such as Bromodiolone,
Chemical Name: 3-[3-(4′-bromobiphenyl-4-yl)-1,2,3,4-tetrahydro-1-naphthyl]-4-hydroxycoumarin
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.
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).
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.
therapy is vitamin K1 or phytomenadione, which should usually
be administered over a long period of time.
to main Rodenticide Page
to main PiedPiper Page