Fluoride Action Network

Contamination of forest ecosystems by sodium fluoroacetate (Compound 1080)

Source: Proceedings of the Vertebrate Pest Conference, 7(7) | July 7th, 1976 | By JA Peters.
Location: New Zealand
Industry type: Pesticides


Predictive and conceptual models are used to examine the contamination, toxicology, and residues of sodium fluoroacetate (Compound 1080) in relation to its application in vertebrate pest control programmes on forest and pastoral lands. As a pesticide, the toxin appears to be neither mobile nor persistent. Exceedingly slender opportunities exist therefore for significant contamination of susceptible components of the environment.


2. Biomagnification and biological detoxication

Irrespective of whether SFA remains intact at the site of application or is trans located, its ultimate fate lies in the soil. The question can be posed whether by progressive applications, lethal accumulations of the toxin can occur in the soil.

In common with a majority of pesticides (Guyer, 1970) there is abundant evidence that SFA can be degraded into non-toxic components. The carbon-fluorine (C-F) bond of the SFA molecule can be ruptured by enzyme systems present in Pseudomonas and Nocardia species of soil micro-organisms (Goldman, 1965; Goldman and Milne, 1966; Horiuchi, 1962 ; Tonomura, Futai, Tanabe, and Yamaoka, 1965; Davis and Evans, 1962; Kelly, 1965). Microbiological surveys of several Westland, South Island, regions have isolated many bacterial and several fungal species that actively degrade the C-F bond in SFA on carrot substrates (Peters and Mulcock, unpubl. data).

The uptake of SFA by root systems of plants has been examined in the context of its
phytotoxicity and its natural occurrence in several plant genera, e.g., Acacia, Gastrolobium and Oxylobium (references see Peters , 1972; Preuss and Weinstein, 1969; Hall, 1974). Stock losses have been reported in Australia where animals have access to these endemic poisonous plants (Aplin, 1969). No detailed knowledge of this phenomenon exists in the New Zealand situation, although Oxylobium callistachys has been declared a noxious weed by many South Island and several North Island Counties (Fitzharris, 1973) .

SFA is not particularly toxic to plants, but inorganic fluorides are considerably more
toxic. Thus, sufficient circumstantial evidence exists that the predicted values enumerated in Model I II underestimate actual values.

3. Mammalian metabolic responses

SFA acts predominantly on the tricarboxylic acid cycle; a fundamental source of energy conversion from foodstuffs at cell, tissue, and organ levels in living systems (Peters, 1963; Pattison, 1959; Pattison and Peters, 1966 ; Peters, 1972; Peters, 1973). Unlike those pesticides that possess specific affinities for accumulation in vertebrate and invertebrate tissues, SFA (and its toxic cellular metabolite fluorocitrate) has no cumulative effects in viable organs and tissues. Also, sub-lethal doses of SFA have been given to rats in their drinking water for several months without harm (Peters , 1972; Howard, Marsh and Palmateer, 1973).

Thus, the metabolic fate of the toxin must also be considered in the interpretation of the predicted values of Model II I.


Model IV has taken intoxicated venison as the type example, and the species are
regarded as flesh-eating scavengers. The secondary poisoning hazards require cautious interpretation because consideration must be given to the following factors:

1. On weight/weight basis, the toxin is confined predominantly to internal organs and viscera. Also, tissue levels are determined by the amount of toxin and the duration of its distribution within the viable organs , which in turn is related to species susceptibility. Gal, Drewes and Taylor (1961) injected radioactive c14-SFA intraperitoneally into rats and examined the distribution of radioactivity at death. The level of radioactive isotope (c14-sFA/gram wet tissue) decreased in the order of brain, liver, heart, kidney, intestines and stomach, lungs, spleen, testes, carcass muscle , expired CO2, urine. It can be expected that the oral consumption of toxic bait materials would make the stomach of the poisoned carcass the most likely cause of secondary poisoning .

2. As with earlier investigations of toxic carcass meat (Mcintosh and Staples, 1959),
we have not found compositions equal to, or in excess of those predicted in the Model. If however, despite the above, an equal distribution of toxin throughout the carcass is assumed the following types of computations can be derived from the Model .

(1) Liver and kidneys comprise about 2% of the dressed deer carcass (Coop and
Lamming, 1974). Assuming that 15% of the toxic load is contained in liver and kidneys, these organs (1.3 kg) will contain 16 mg toxin (12 mg/kg tissue). This amount would provide about five lethal doses for a dog . For a man to receive one lethal dose it would be necessary that he eat these organs from about eleven deer.

(2) If about 60% of the toxic load is contained in the dressed carcass, this venison
(41 kg) will contain 62 mg toxin (1.5 mg/kg meat).

3. Unlike scavengers in the wild, man prefers to cook his meat. The quantities of
toxic meat in Model IV imply that the meat is consumed in its raw state.

The structural integrity of the SFA molecule becomes unstable at temperatures about 130°C, and decomposition takes place at 200°C (Sunshine, 1969) . We have been unable to detect organofluorine residues in oven-baked meat inoculated with physiological amounts of SFA prior to baking . Similarly, boiled inoculated meat contained no organofluorine residues, but the water contained detectable traces. Grilling could conceivably allow toxic residues to be retained in the interior of the meat. Nonetheless, according to Model IV, gargantuan appetites are required…

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