The problem of fluorosis in farm animals in Britain
is not due to the high fluorine content of rock phosphate
deposits, volcanic soils, or water supplies, but arises from the
emission of fluorine containing gases and dusts from industrial plants.

by
RUTH ALLCROFT, Senior Research Officer,
Veterinary Laboratory, Ministry of Agriculture,
Fisheries and Food, Weybridge, Surrey, England.

[ We have taken the liberty of editing out parts
of this talk that do not relate to fluoride.]

 Please find full text below ↓

www.grassland.org.nz/publications/nzgrassland_publication_1874.pdf

We wish to remind readers that vitamin C is important in reducing the damage caused by fluorides and that unlike cattle and sheep humans do not make vitamin C in their livers or kidneys, and on poor diets humans therefore suffer more than animals especially as we live longer and therefor will accumulate more fluoride. 

“Although the production of good pasture is a starting point, one end point is a prime, healthy animal. At Weybridge, we have many animal health problems associated wrth the grazing of apparently good pastures, and it is some of these problems that I propose to discuss this afternoon:

… Fluorine

The problem of fluorosis in farm animals in Britain is not due to the high fluorine content of rock phosphate deposits, volcanic soils, or water supplies, but arises from the emission of fluorine containing gases and dusts from industrial plants. If the density of our industrial areas is considered in relation to the relatively small area of the whole country, it can be readily understood that a great deal of agricultural land must be adjacent to industrial works.

The chief sources of fluorine contamination of grassland and crops are:

(1) steel and metal works when the method of production involves the use of large amounts of fluorspar as a flux ;

(2) brickworks, where the source is usually the local clay, although coal is sometimes a contributory factor;

(3) production of aluminium by the electrolytic reduction of alumina;

(4) glass, enamel, and colour works where fluorine compounds are often added to facilitate melting and to give the finished products certain properties ;

(5) the calcining of iron-stone where the sourtie is mainly the fluorine-rich ore itself;

(6) potteries and other ceramic industries where the materials used in manufacture are high in fluorine;

(7) collieries, power stations and other industries which consume large quantities of pulverised low-grade coal with a high fluorine content.

It is generally accepted that the fluorine content of most plants, with the exception of the roots, is not readily affected by the amount of fluorine in the soil. There seem to be a few exceptions to this, notably the tea plant and the camellia, which appear to be fluorine collectors, but common fluorine values for

[ page ] 61

The chief chemical sign of fluorosis in severely affected cattle is lameness, which is frequently associated with marked skeletal abnormalities such as an increase in diameter of bones and well defined exostoses. Enlargement and gross exostoses in bovine limb bones (left) compared with normal bones (right).

Uncontaminated animal foodstuffs lie between 1 and 10 p.p.m. on a dry matter basis. Excessively high values’ up to 2000 p.p.m. have been reported (Green 1946) on herbage near sources of emission of fluorine compounds. Herbage and soil samples provide useful corroboration, but are not suitable alone for assessing

[ page] 62

degree and extent of contamination, since results will depend on climatic conditions around the time of sampling, on the direction of the prevailing winds, and on the topography of the surrounding terrain. It is difficult to suggest a minimum fluorine value for con- taminated pastures at which clinical cases of fluorosis will occur, because of the variable factors first men- tioned, and because the all-important factor is the length of time over which the foodstuff is consumed at any particular level of contamination. And since development of clinical symptoms is slow, a pasture analysis only demonstrates that contamination is present; it cannot give a direct correlation of the degree of fluorosis in the animal.

Present evidence suggests that the order of susceptibility of farm animals to fluorosis is calves, dairy cows, other bovines, sheep, pigs, horses, and poultry, but this order may be revised when comparative tests on a known and comparable body weight intake have been carried out, The chief clinical ,symptom in severely affected cattle is lameness, and it is this which usually suggests the possibility of fluorosis and leads to a closer investigation of the herd. The lameness is frequently associated with marked skeletal abnormalities such as an increase in diameter of limb bones and well-defined exostoses. Dental lesions in the permanent teeth of cattle reared on affected farms are one of the best indications of the presence and degree of fluorosis. They include loss of lustre, pitting, staining in parts of the defective enamel, and excessive and irregular wear. Clinical diagnosis can be confirmed by determination of the fluorine content of urine and bone samples.

Although the total economic loss due to fluorosis is not great when considered in relation to that caused by the major transmissible diseases, it is a matter of serious concern in affected areas and methods of control are being studied both by industry and agriculture. Reduction of emission can be achieved to some extent in some industries by trapping and washing the dusts and gases, but in others the practical difficulties and the costs would be so great that it is unlikely that efficient devices could be installed. Some degree of agricultural control can be achieved by farming with the fluorine hazard in view, e.g., improvement of pasture management, limitation of grazing periods; keeping pigs and poultry instead of cattle and sheep, or using the land for production of crops only. The possibility of alleviating the effects of fluorosis in cattle

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by feeding certain mineral supplements is also being investigated by the Ministry on an experimental farm on which fluorosis occurs.

References

Allcroft, R. Proc. XV Int. Vet. Congr., Stockholm, Vol. I, Pt. 1, pp. 573. 1953.

Allcroft R. Vet. Rec., Vol. 66, pp. 517. 1954.
Allcroft, R., and Lewis, G. Proc. 7th Int. Grassland Congr., N.Z.

(in press). 1956.
Allcroft, R., Scarnell, J., and Hignett, S. L. Vet. Rec., Vol. 66,

pp. 367. 1954.
Allcroft, W. M. Vet. J.. Vol. 103, pp. 75. 1947.
Bartlett, S., Brown, B. ‘B., Foot, A. S:, Rowland, S. J., Allcroft

R., and Parr, W. H. Br. Vet. J., Vol. 110, pp. 3. 1954. Blaxter, K. L.; and McGill, R. F: Vet. Revs. and Annot., Vol. 2,

 pp. 35. 1956.
Blaxter, K. L., and Sharman, G. A. M. ,Vet. Rec., Vol. 67;‘ pp.

108. 1955.
Breirem, K., Ender, F., Halse, K., and Slagsvold, L. Acta Agr.

Suecana, Vol. 3, pp. 89. 1949.
Cunningham, I. J. N.Z. J. Sci. Tech, Vol. 17, pp. 775. 1936. Cunningham, I. J. N.Z. J. Agric;, Vol. 90, pp. 196. 1.955. Dick, A. T. Aust. Vet. J., Vol. 29, pp. 233. 1953.
Dick, A. T. Aust. Vet. J., Vol. 30, pp. 197. 1954.
Ferguson, W. S., Lewis, A. H., and Watson, S. J. J. .Agr. Sci.,

 Vol. 33, pp. 44. 1943.
Green,-H. H. Proc. Roy. Soc…Med., Vol. 39, pp. 795. ..1946. Green, H. H. N.V.M.A. Publ. NO. 17, pp. .60. 1948.
Jam?;;;, S., and Harbour, H. E. Vet. Rec., Vol. 59, pp. 102.

 G4

 McElroy, W. D.; and Glass, B., eds. Symposium on Copper Metabolism, pp. 246-270. Johns Hopkins Press, Baltimore, 1950.

Osb&& A. D., Featherstone, J., and Herdan, G. Vet. Rec., Vol.. 66, pp. .409, 1954.

 Parr, W. H., and Allcroft, R. Unpublished data. 1956. Patterson, J. B. E. Nature, Vol. 157, pp. 555. 1946. Shand, A. B.V.A. Publ. No. 23, pp. 58. 1952.
Stewart, J. Guernsey Breeders’ J., Vol. 7, pp. 43. 1953. Stewart, J. Scot. Agric., Vol. 34, pp. 68. 1954.

Stewart, J., Mitchell, R.L., and Stewart, A. B. Emp. J. Exp.

Agr., Vol. 14, pp. 145. 1946.
Stewart, J., and Reith, J. W. S. J; Comp. Path., Vol. 66,

_ PP. 1.

 1956.
Swan, J. B., and Jamieson, N. D. N.Z. J. Sci. Tech. *(in II Iress).195?.

DISCUSSION

Col. Stafford, Springston: You have just listened to the most lucid speech on the deficiencies. of a number’ of elements which are essential to animal life. Now it has been stated that the nH of a good nasture soil.runs between 6.5 and 7. I can oniy give you a-little .of my own experience; once you get the pH over 7, as you do where lime has been put on the land in excess, then you get disastrous results in ,bone formation, especially in young stock. I must congratulate the speaker on a wonderful paper.

Q. Does Dr Allcroft know .of any cases where farmers whose stock have been affected by fluorosis obtained compensation against the particular industrial enterprise which has been the cause of it?

A. Do you mean as a result of a legal claim or do you mean as a result of private negotiations between farmer and industry?

Q. I am concerned with’ the common Iaw right.

A. 1 do know of cases. Some industries do, by private arrange- ment, pay compensation to farmers whose land is -adjacent and is severely contaminated.

Q. What is the reason for the incidence of increased grass staggers on pastures fertilised with nitrogen in the early ipring ?

A. We have no explanation. The increased incidence is not only confined to pastures treated with nitrogen. We have found that by topdressing those. pastures with magnesite it increases the magnesium uptake. of the pasture. The incidence of staggers has been reduced but the incidence cannot be correlated with magnesium content alone, although it was beneficial in the cases we tried.

Q. if crops are grown where there is fluorine contamination do they take up the fluorine and pass the trouble on to somebody else ?

A. No, it is not a case of passing it on to somebody else. It has been shown that most plants do not take up fluorine from the soil. There are two exceptions: the tea plant and the camellia which appear to be fluorine collectors. Most grasses and root crops do not take it up from soils. It is mostly a question of contamination of the surface therefore humans get off lightly because we do not eat grass. The inner parts of cabbages and similar crops are not high in fluorine, only the outer coverings which are removed. Cereal grains are also quite safe.

Is fluorine cumulative ? Can small quantities be safely absorbed over long periods or will they produce clinical symptoms ? It is sometimes the practice to add fluorine to drinking water.

Yes, it is cumulative, but if the intake is small animals cattle do seem to be able to stand considerable amounts without any adverse clinical symptoms at all. If they are continually exposed to it there will be a gradual build-up to three or four thousand parts per million. A concentration of five to six hundred parts per million is normal. It usually takes several years before you get clinical symptoms, then they first show as dental lesions.

. . ….•…. . .

H. van Rensburg: Would water containing more than 30 parts per million of fluorine have detrimental effects on cattle, and how soon ? The problem occurs in Tanganyika where we have very high percentages of fluorine in the water and would like to hold young cattle -on the areas for 6-18 months. How long could we safely keep them there?

Dr Allcroft : With 30 parts per million in the drinking water you would get clinical effects if you keep them there for 18 months. You could expect to get severe dental

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lesions in the permanent teeth when they came through. If they were then removed and spent the rest of their lives away from it, they might not be so bad, but still there would be harmful effects. Do you have to keep them there that length of time?

H. van Rensburg: We have not kept them in this specific area for any length of time,. but in other areas. where~there is a high fluorine content in the water it is very noticeable amongst stock -and humans that their teeth are severely affected. Conditions I am referring to would only apply to cattle afterwards drafted to market for slaughter.