FLUORIDATION AND GASTRIC CANCER

FLUORIDATION AND GASTRIC CANCER

768 better designs of footwear to allow children’s feet to function properly but to insist that shoes merely by external pressure produce deformities ...

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768 better designs of footwear to allow children’s feet to function properly but to insist that shoes merely by external pressure produce deformities is not a sound on

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G. WYNNE GRIFFITH

Anglesey.

argument.

FLUORIDATION

DAVID F. THOMAS.

Lincoln.

SiR,ņThough was glad to see your survey of the fluoridation position I was sorry to find that it restricted itself to one minor aspect of this much vexed questiondental caries in children. It is evident that the point of my letter in The Sunday Times5 was misunderstood. My intention was to refer, not to an optimum fluoride level of 1-2 p.p.m. for caries control ", but to levels of 2 p.p.m. at which the graphs both of Dean and Forrestshow the caries experience at a minimum. The minimum for Forrest’s graph is shown actually at 3-5 p.p.m. at which level objectionable fluorosis would certainly occur. It follows that the levels of 1 or 1-2 p.p.m. commonly referred to as optimal for caries control are in fact " maximal " for the avoidance of a toxic symptom, and even so, it is not possible completely to separate any useful degree of caries control by fluoride in the drinking water from some degree of mottling, however mild at the lower levels. I

SIR,-Many of my friends, both male and female, wear and are proud of shoes that bear no resemblance whatever in shape to the feet inside them. Do these shoes not effect upon the feet that wear them ? experience of nursing in a mental hospital would lead me to believe that much of the old patients’ foot troubles are due to a long term of cobbling on " shoe strings ", with footwear that fits where it touches. KAY MOTTRAM. London, W.5.

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FLUORIDATION AND GASTRIC CANCER

figures are given it is not possible to say whether the disparity noted by Dr. Burrowes (March 26) between the mortality for gastric cancer in two small Lincolnshire towns might have arisen as the result of a chance fluctuation affecting populations of this size. Assuming, however, that this difference is a real " one, available evidence would not support the suggestion that SIR,-As

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the difference could be related to the difference in the fluoride content of the water-supplies concerned. The highest mortality-rates from gastric cancer in this country are to be found in North and West Wales where, so far as I know, no water-supply has ever been reported as containing more than a trace of fluoride. West Hartlepools and South Shields have both had in the past appreciable amounts of fluoride in their supplies (approximately 2’5 and 1-4 p.p.m. respectively). Both are county boroughs. The data on which the following table is based can be extracted from the area mortality report of the 1951 census.1 Two neighbouring county boroughs on the North-East coast (Sunderland and Tynemouth) with fluoride-free water-supplies have been chosen for comparison. The standardised mortality-rate (s.M.R.) is the ratio (expressed as a percentage) of the number of deaths observed in the area to the number that would be expected to occur if the age-specific mortality-rates for England and Wales had applied to the local population. The standard error of the s.M.R. may be taken as the s.M.R. divided by the square root of the number of deaths involved. The period covered is the four years 1950-53.

All four county boroughs have higher than average mortalities when compared with England and Wales, but there is nothing in these figures to suggest that the area mortalities differ significantly among themselves with respect to the fluoride content of their water-supplies.

Curious local differences in the mortality from gastric similar to that noted by Dr. Burrowes have been observed elsewhere in this country and in Holland.2 Stocks and Davies3 have recently been investigating an almost comparable situation affecting two neighbouring towns in Devon. It seems likely that such differences may turn out to be related to differences in either the cancer

Registrar General’s Decennial Supplement, England and Wales, 1951: area mortality. H.M. Stationery Office. 2. Diehl, J. C., Tromp, S. W. Geographical Distribution of Carcinoma in the Netherlands; vol. 2. Oegstoeest, 1955. 3. Stocks, P., Davies, R. I. (in the press). 1.

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not in connection with teeth, but to which is being given to the public by medical officers and others, that fluorides, though admittedly poisonous in big doses, change their nature at the low levels contemplated for fluoridation, and become " beneficial " substances, sometimes even stated to be essential nutrients for the living cell. This is quite unjustifiable. The only proven effect which may be called " beneficial " is that upon a non-living material, the dental enamel. When this is obtained by topical application I understand that no mottling occurs even with a 2% solution. When it is obtained by drinking the water it is accompanied by some degree of dental fluorosis, which has hitherto been accepted as the most sensitive sign of chronic low-grade poisoning (e.g., see Hodge and Smith 8). This provides no basis at all for risking the health of large numbers of people on a mere speculation that there is a critical level below which the fluoride ion loses its toxic character and becomes physiologically beneficial. When, further, we learn from such a high authority as Prof. Hugo Theorell9 that, far from losing its activity as an enzyme-inhibitor at low levels, the fluoride ion can inhibit lipase at 1 part in 5 million, it becomes most extraordinary that the fluoridation discussion should always centre on the dental caries aspect rather than on the desirability of increasing permanently the general intake of a substance having these biochemical properties. Fluorides are common, toxic pollutants of air, water, and vegetation. The eighth symposium of the Institute of Biology, recently published deals with the effects of pollution on living material, and confirms the view that the effects of toxic pollution become recognisable only at high levels, when such crude phenomena as wholesale destruction of fish, crippling fluorosis in cattle, radiation sickness, or the deaths of thousands of Londoners during the 1952 smog, draw attention to the dangers. At lower levels there can be no direct evidence unless experimentation is carried out on an impossibly massive scale. In the absence of such experimentation there must remain a strong presumption in favour of reducing, and above all against deliberately raising, the level of pollution with any toxic substance, especially in an essential of life such as the drinking water of large populations. In the case of fluoride 4. Stocks, P. British Empire Cancer Campaign Annual Report, 1957, suppl. 2, part 2. 5. Sunday Times, Feb. 7, 1960. 6. Dean, H. T., Arnold, F. A., Jr., Elvove, E. Publ. Hlth Rep., Wash. 1942,

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57, 1115. Forrest, Jean R. Brit. dent. J. 1956, 100, 199. Hodge, H. C., Smith, F. A. in Fluoridation as a Public Health Measure; p. 80. Washington, 1954. 9. Communication to the Royal Swedish Medical Board, Stockholm, March 1, 1958. 10. Symposia of the Institute of Biology, no. 8. Edited by W. B. Yapp. London, 1959. 7. 8.