Abstract

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.

Excerpts

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.

TOXIC RESIDUES IN MEAT

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…

*Read the full paper online at http://fluoridealert.org/wp-content/uploads/peters-1976.pdf

Literature Cited

ADAMS, R.S . 1973 . Factors influencing soil adsorption and bioactivity of pesticides, Residue Reviews 47 : 1-53.

ANNISON, E. F.; HILL, K.J . ; LINDSAY , D.B. ; PETERS, R.A. 1960. Fluoroacetate poisoning in sheep. Journal of Comparative Pathology 70 : 145-155 .

APLIN, T.E.H. 1969 . The poison plants of Western Australia . Bulletins 3483, 3535, 3554, 3662, 3672 . Journal of Agriculture of Western Australia vols 8(1967), 9(1968), 10 (1969).

ATZERT, S. P. 1971. A review of sodium monofluoroacetate (Compound 1080). Its properties, toxicology, and use in predator and rodent control. Bureau of Sport Fisheries and Wildlife, Division of Wildlife Services, U.S . Department of the Interior, Washington, D.C.

BELL, J. 1972. The acute toxicity of four common poisons to the opossum, Trichosurus vulpecula . New Zealand Veterinary Journal 20:212-214 .

CLARK, P.J . 1970 . Registration procedures for agricultural chemicals. The Agricultural Chemicals Board, Wellington, New Zealand.

COOP, I.E. ; LAHHING, R. 1974. Observations from the Lincoln deer farm. Paper presented at the Agricultural Science Convention, New Zealand Institute of Agricultural Science, Lincoln.

CORR, P.V . ; MARTIRE, P. 1971. Leaching by rain of sodium fluoroacetate (“1080”) from baits used for rabbit control. Australian Journal of Experimental Agriculture and Animal Husbandry 11 :278-281 .

DAVIES, J . I.; EVANS, W. C. 1962 . The elimination of halide ions from aliphati~ halogen substituted organic acids by an enzyme preparation of Pseudomonas dehalegenans. Biochemical Journal 82:50 p.

DURHAM, W. F. 1967 . The interaction of pesticides with other factors. Residue Reviews 18:21-103 .

FITZHARRIS, J. 1972 . Report of the Committee on Noxious Weeds Administration. p. 64-66. Government Printer , Wellington, New Zealand.

GAL, E.M.; DREWES , P.A. ; TAYLOR, N.F. 1961 . Metabolism of fluroacetic acid-2-c¹⁴ in the intact rat . Archives of Biochemistry and Biophysics 93 : 1-14.

GODFREY , H.E . R. 1973. Carrot bait distribution within a swath and its significance in aerial poisoning. New Zealand Journal of Experimental Agriculture 1:323-328.

GOLDMAN , P. 1965. The enzymatic cleavage of the carbon-fluorine bond in fluoroacetate. Journal of Biological Chemistry 240:3434-3438 .

MILNE, G.W.A. 1966. Carbon-fluorine bond cleavage. Studies on the mechanism of the defluorination of fluoroacetate . Journal of Biological Chemistry
241 :5557-5559.

GUYER, G. E. (ed.) . 1970 . Pesticides in the soil: ecology, degradation and movement. International Symposium on on Pesticides in the Soil. Michigan State University, East Lansing.

HALL, R.J . 1974. The metabolism of ammonium fluoride and sodium monofluoroacetate by experimental Acacia georginae. Environmental Pollution 6. 267-280.

HAYES, W.J. 1963. Clinical Handbook on economic Poisons. U.S. Department of Health, Education and Welfare . Communicable Disease Center, Toxicology Section, Atlanta, Georgia.

HOWARD, W. E.; HARSH, R.E.; PALMATEER, S.D. 1973. Selective breeding of rats for resistance to sodium monofluoroacetate. Journal of Applied Ecology 10: 731-735.

HORIUCHI , N. 1962. C-F bond rupture of monofluoroacetate by soil microbes. Properties of the bacteria and the enzyme. Seikagaku 34 :92-98 .

KALMBACH, E.R. 1943. Birds, rodents and colored lethal baits. Transactions North
American Wildlife Conference 8:408-416.

KELLY, M. 1965 . Isolation of bacteria able to metabolize fluoroacetate or fluoroacetamide. Nature 208:809-810.

KING, J.E.; PENFOUND, W.T . 1946. Effects of new herbicides on fish . Science 103:487 .

MC INTOSH, 1.G . ; STAPLES , E.L.J . 1959. The toxicity of muscle, liver, and heart of deer poisoned with sodium fluoroacetate (1080) . New Zealand Journal of Science 2:371-378.

~~~~-:-:-~-·; BELL, J.; POOLE, W.S.H.; STAPLES, E.L .J. 1966. The toxicity of sodium monofluoroacetate to the North Island weka (Gallirallus australis grey~). New Zealand Journal of Science 9:125-128.

OSER, B.L . 1971. Toxicology of pesticides to establish proof of safety. In: Pesticides
in the Environment Vol. I, part I I, p. 411-456. White-Stevens, R. (Editor) Marcel
Dekker Inc. New York.

PATTISON, F.L.M. 1959. Toxic Aliphatic Fluorine Compounds. Elsevier Publishing
Company, Amsterdam, Netherlands.

~~~~~~~·; PETERS, R.A . 1966. Monofluoro Aliphatic Compounds . In: Handbook of Experimental Pharmacology. Vol. XX Pharmacology of Fluorides p. 387-458. Smith, F.A. (Editor), Springer-Verlag, New York.

PETERS, J.A. 1973. Toxicology of wildlife control; facts and fancies. N.Z. Forest
Research Institute Symposium 14:173-179. 1974 . Chemical control of vertebrate pests–a perspective. New Zealand Journal of Forestry 19:233-245 .

~~~~~. ; BAXTER , K.J . 1974 . Analytical determination of Compound 1080 (sodium fluoroacetate) residues in biological materials. Bulletin of Environmental Contamination and Toxicology 11 :177-183.

PETERS, R.A. 1963. Biochemical Lesions and Lethal Synthesis. Pergamon, Oxford,
England. 1972. Introduction, and some metabolic aspects of fluoroacetate especially
related to fluorocitrate. In : Carbon-Fluorine Compounds . Chemistry, Biochemistry
and Biological Activities. Ciba Foundation Symposium p. 1-7, p. 55-76. Associated
Scientific Publishers, Amsterdam, Netherlands.

PREUSS, P.W.; WEINSTEIN, L.H. 1969. Studies on fluoro-organic compounds in plants. Defluorination of fluoroacetate. Contributions of the Boyce Thompson Institute 24: 151-156.

REDDINGIUS, J. 1971. Models as research tools . Proceedings of the Advanced StudyInstitute 64-76 .

ROBINSON, W.H. 1970. Acute toxicity of sodium monofluoroacetate to cattle. Journal of Wildlife Management 34:647-648.

STAPLES, E.L . J . 1968. The reduction of the sodium monofluoroacetate (1080) content of carrot baits of various thickness by weathering. New Zealand Journal of Agricultural Research 11 :319-329.

~~~~~. ;1969 . Absorption of sodium monofluoroacetate (1080) solution by carrot baits of various thickness by weathering. New Zealand Journal of Agricultural
Research 11 :319-329.

~~~~~. ;1969 . Absorption of sod ium monofluoroacetate (1080) solution by carrot
baits. New Zealand Journal of Agricultural Research 12:783-788.

SUNSHINE, I. 1969 . Handbook of Analytical Toxicology . p. 523. The Chemical Rubber Company, Cleveland, Ohio, U.S.A.

THOMPSON, W.R.; WEIL, C.S. 1952. On the construction of tables for moving-average interpolation. Biometrics 8:51-54.

TONOMURA, K.; FUTAI, F.; TANABE, O.; YAMAOKA, T. 1965. Defluorination of monofluoroacetate by bacteria. Isolation of bacteria and their activity of defluorination. Agricultural and Biological Chemistry (Tokyo) 29:124-128.

TUCKER, R.K.; HAEGELE, M.A. 1971. Comparative acute oral toxicity of pesticides to six species of birds. Toxicology and Applied Pharmacology 20:57-65.

WEIL, C.S . 1952. Tables for convenient calculation of median effective dose and
instructions in their use. Biometrics 8:249-263.

WORDEN, A. N. 1974. Toxicological Methods. Toxicology 2:359-370.

*Read the full paper online at http://fluoridealert.org/wp-content/uploads/peters-1976.pdf