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Non-Anticoagulant Rodenticides Chapter | 47 619
VetBooks.ir Generally, animals exposed to a sublethal dose can recover compound is an extremely toxic substance, which is com-
monly used as a rodenticide. Inhalation of dust or swal-
in less than 48 h.
lowing can also be fatal. The compound can also be
Treatment absorbed through cuts or abrasions in the skin and lead to
poisoning.
Treatment is based on symptomatic and supportive thera- It is important to note that sodium fluoroacetate is also
pies. In case a significant amount of red squill is retained formed naturally in approximately 40 plants that are native
in the stomach, decontamination (gastric lavage with saline to Australia, Brazil, and Africa after fluoride uptake from
cathartic) is rewarding. The patient must be monitored for soil, water, or air. Examples of plants that contain sodium
cardiac arrhythmias and conduction disturbances. Atropine fluoroacetate are Dichapetalum cymosum, Dichapetalum
sulfate given subcutaneously at 6- to 8-h intervals may pre- toxicarum, Chailletia toxicaria, Gastrolobium grandiflorum
vent cardiac arrest. Phenytoin at 35 mg/kg, TID, should be (“poison peas”), Oxylobium parviflorum,and Acacia geor-
given to dogs to suppress arrhythmias. ginae. Consumption of these plants has resulted in many
serious cases of livestock poisoning and high stock losses
(Oelrichs and McEwan, 1962). Poisoning has also been
Conclusions documented in field workers exposed to fluoroacetate (Suh
Red squill is a botanical rodenticide, and exerts toxicity et al., 1970).
due to cardiac effects. Treatment is symptomatic and
supportive. Toxicokinetics
Sodium fluoroacetate (1080) is rapidly absorbed from the
FLUOROACETATE GI tract. Dust formulations are easily absorbed by inhala-
tion, which is not usually the route for poisoning cases.
Introduction
Compound 1080 is not readily absorbed through intact
Sodium fluoroacetate (compound 1080) is an extremely skin, but it can be absorbed in the case of cuts, abrasions,
toxic white powder that has been used as a rodenticide or dermatitis (Brockman et al., 1955). It is reported that
throughout the world. The compound has the chemical sublethal doses of compound 1080 are completely metab-
formula C 2 H 2 FO 2 .Na, with a molecular weight of 100.02. olized and excreted in 4 days.
Its structural formula is shown in Fig. 47.5. It is used to The bioavailability of sodium fluoroacetate appears to
control rats, mice, squirrels, prairie dogs, foxes, wolves, be similar for oral, injected, and inhaled doses. Dermal
coyotes, and rabbits. The compound is also used to con- absorption is lower because a subcutaneous LD 50 is 10- to
trol brush-tail possums, deer, wild pigs, wallabies, and 15-fold higher than the oral dose. Distribution studies sug-
rooks. It is very toxic to birds, domestic animals, and car- gest that the plasma levels of sodium fluoroacetate are
nivores. Secondary poisoning is very common in birds twice those of tissues. Sheep receiving sodium fluoroace-
and carnivores from eating poisoned carcasses. tate (0.1 mg/kg) contained the residue in plasma, kidney,
Sodium fluoroacetate has many other names, and is heart, muscle, spleen, and liver as 0.098, 0.057, 0.052,
sold under trade names such as Nissol, 1080 gel, 1080 0.042, 0.026, and 0.021, respectively (Eason et al., 1993).
paste, 1080 solution, Tenate, and Tenate 1080. The com- The plasma t 1 /2 is 3.6 6.9 h in goats, 6.6 13.3 h in sheep,
mercial products are provided with a black dye called 1.1 h in rabbits, and 1.6 1.7 h in mice (Eason et al., 1993;
nigrosine (0.5%). Gooneratne et al., 1995). Metabolism of fluoroacetate (i.e.,
defluorination) takes place in the liver. Fluoroacetate and
fluorocitrate salts are excreted mainly in the urine.
Background
Sodium fluoroacetate was discovered by German military Mechanism of Action
chemists during World War II. However, it was not until
later that American chemists discovered its use as a In the body, fluoroacetate (1080) is converted to fluoroci-
rodenticide. The name “1080” refers to the catalog num- trate, which is a potent inhibitor of the enzyme aconitase
ber of the poison, which became its brand name. The in the tricarboxylic acid cycle (Krebs cycle) (Elliot and
Kalnitsky, 1996). As a result, the elevated levels of citrate
in the blood become observable 30 min after administra-
tion and maximum levels at 4 h after administration. It
has been shown that citrate levels are directly influenced
by the thyroid hormone (i.e., free T 3 ; Maruo et al., 1992).
FIGURE 47.5 Structural formula of sodium fluoroacetate. Accumulation of citrate causes toxicity due to reduction