Vertebrate Pesticide Toxicology Manual (Poisons)


Bromadiolone (Rid Rat®, Contrac®, Supersqueak®)

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2.3 Bromadiolone (Rid Rat®, Contrac®, Supersqueak®)

Chemical Name: 3-[3-(4'- bromobiphenyl-4-yl)-3-hydroxy-1- phenylpropyl]-4-hydroxycoumarin.

Synonyms: Bromadiolone is the approved name

Baits containing bromadiolone include Rid Rat®, Contrac®, Supersqueak®, and are targeted at rodents. Bromadiolone has chemical and biological effects that are similar to brodifacoum. However, it is slightly less potent than both brodifacoum and flocoumafen.

2.3.1 Physical and chemical properties

The empirical formula for bromadiolone is C30 H23 BrO4 and the molecular weight is 527.4. Technical grade bromadiolone (97% pure) is a yellowish powder with a melting point of 200–210ºC. Its solubility at 20ºC is 19 mg/L in water, 730 g/L in dimethylformamide, 8.2 g/L in ethanol, and 25 g/L in ethyl acetate. Bromadiolone is stable at temperatures <200ºC.

2.3.2 Historical development and use

Bromadiolone was synthesised and marketed by a French company in the mid-1970s, and has since been widely used to control commensal and field rodents in many countries. The toxicant was introduced into New Zealand for sale about 1980 and is registered as a rodenticide, and has on occasion been used in New Zealand for rabbit or rat control on islands. It is not widely used in the field in New Zealand. It is not registered in New Zealand for possum control, and is marketed principally for commensal rodent control.


In spite of bromadiolone belonging to a group of more potent second-generation anticoagulants, resistance problems have been encountered in rodents after repeated use overseas. It can, however, be effective, in cases where it has not been used before, against rodents that have become resistant to other anticoagulant rodenticides. In some countries, particularly in Europe, bromadiolone has increasingly been used for field control of rodents, which is leading to secondary contamination of non-target species, including mustelids and birds (Shore et al. 1999). This situation parallels the phenomena we have observed in New Zealand with brodifacoum. Advocates for the use of bromadiolone in the field suggest that there is a lower risk of secondary poisoning compared to brodifacoum because it is less potent.

2.3.3 Fate in the environment

Bromadiolone is a second-generation anticoagulant, and as such has many of the properties that are common to the other anticoagulants. It is only slightly insoluble in water, and binds strongly to the soil, and is slowly degraded. In a study carried out in four types of soil, bromadiolone scarcely moved in soil rich in organic matter, but could be shifted through soil with low clay or organic compounds (WHO 1995).


      1. Toxicology and pathology


Onset of signs

As for other anticoagulants.

Mode of action

Bromadiolone, as a second-generation anticoagulant, interferes with the Vitamin K1-dependent clotting factors when a lethal or sub-lethal dose is ingested. In the liver cells the biologically inactive vitamin K1-2,3 epoxide is reduced by a microsomal enzyme into biologically active vitamin K, which is essential for the synthesis of prothrombin and other clotting factors. Bromadiolone antagonism of the enzyme vitamin K1-epoxide reductose in the liver causes a gradual depletion of the vitamin and consequently of vitamin K-dependent clotting factors, which results in an increase in blood-clotting time until the point where no clotting occurs. It is cumulative and will remain in the system in sub-lethal quantities for extended periods.


Pathology and regulatory toxicology

Generalised haemorrhage is frequently evident at post-mortem. As for other anticoagulants, areas commonly affected are the thoracic cavity, subcutaneous tissue, stomach, and intestine. The heart is sometimes rounded and flaccid with subepicardial and subendocardial haemorrhages. Histomorphological analysis of the liver may reveal centrilobular necrosis as a result of anaemia and hypoxia.

In regulatory toxicology studies, bromadiolone has been shown to lack mutagenicity in in vitro (the Chinese hamster ovary cells) and in vivo (mouse micronucleus) test symptoms, and teratogenic effects (WHO 1995).

Fate in animals

(See section 2.1.4). The persistence of bromadiolone is similar to that of brodifacoum (see Table 11). The half-life in the liver of rats is 170 days (Parmar et al. 1987) and residues have been detected in sheep liver after 256 days (Nelson & Hickling 1994).
Species variation in response to bromadiolone

The acute oral LD50 for various species is detailed in Table 16. No information was found for aquatic toxicology.

Table 16. Acute oral toxicity (LD50mg/kg) of bromadiolone (Hone & Mulligan 1982)

Species LD50(mg/kg)

Dog c.10.0

Rat 0.65 (acute)

Mouse 0.99


Rabbit c.1.0

Guinea pig 2.8

Pig c.3.0

Chicken c.5.0

Rat 0.06 to 0.14  5 (chronic)

2.3.5 Diagnosis and treatment of poisoning

As for brodificoum, see Section 2.1.5 (pp. 57–60).



2.3.6 Non-target effects

Bromadiolone is persistent in the livers of sub-lethally poisoned animals, which heightens the potential risk of accumulated secondary poisoning to non-target species.

Livestock must not be allowed access to bromadiolone baits as residues may persist in the liver for up to 9 months or more (WHO 1995).

There are no published LD50 data on the acute toxicity of bromadiolone to bats, reptiles, or amphibians. However, reptiles are known to be susceptible to brodifacoum, a similar anticoagulant toxicant.

In a laboratory study, only one out of six owls died following 10 days treatment with bromadiolone-poisoned rats, compared with five and six deaths in owls eating brodifacoum-poisoned rats (Mendenhall & Pank 1980). Nevertheless, there are increasing concerns overseas regarding non-target mortality and contamination of raptors where there is broad-scale field use of bromadiolone (Shore et al. 1999). The reduced risk of secondary poisoning from bromadiolone compared with brodifacoum that is suggested by Mendenhall & Pank (1980) may not imply limited risk if there is sufficient exposure to allow bromadiolone to accumulate to toxic levels.


2.3.7 Summary

Advantages

Disadvantages

No licence requirement

Very limited field data in New Zealand, marketed principally for commensal rodents

Antidote available

Persistent and likely to lead to secondary poisoning or contamination of non-target species, if widely used in the field

Effective for rodents






  • Bromadiolone is a synthetic pesticide that was first registered for use approximately 20–30 years ago.

  • Bromadiolone is not readily soluble, it binds strongly to soils, where it is slowly degraded. It is most unlikely to contaminate waterways as it is used principally for controlling commensal rodents or in bait stations.

  • It is a potent anticoagulant, which acts by interfering with the synthesis of vitamin K-dependent clotting factors.

  • Bromadiolone is toxic to mammals, birds, and reptiles.

  • Livestock must not be allowed access to baits containing bromadiolone as residues may persist in the survivors for >9 months.
  • Bromadiolone is effective against rodents that have become resistant to other first-generation anticoagulant rodenticides.

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