Fluoride Action Network

Full Text:

MANY different factors leading to relative or absolute deficiency of iodine may cause changes in the thyroid gland. May (1935) found that the administration of fluorine to rats produced hypoplasia of the thyroid epithelium with altered staining reaction of the colloid. Having experimented with over 800 patients, he advocated internal fluorine therapy in the treatment of toxic goitre. The evidence of alteration in thyroid structure in the experimental production of chronic fluorosis in animals is conflicting (Roholm 1937).


In making a clinical investigation of the occurrence of human dental fluorosis (Wilson 1939) I obtained a history of the existence of endemic goitre associated with cretinism in many areas where the presence of fluorine was recognised geologically. In North India a focus of endemic goitre has long been known in the Punjab plains (McCarrison 1913). The report of the Punjab government hospitals and dispensaries (1939) showed how numerous were the cases of goitre seeking treatment from this area. Macnamara (1880) studied the distribution of goitre in the Punjab plains before the introduction of the present extensive system of canal irrigation, at a time when the majority of the townspeople were dependent on local wells. In certain towns he found nearly all the inhabitants with goitre, and saw numerous cretins and dwarfs. Dogs and goats also had goitre. He observed that poverty and bad food led to increase in the size of the goitre, but noted that a colony of river fishermen did not show any thyroid enlargement. In this goitrous area of the Pubjab I observed a high degree of human dental fluorosis, as evidenced by mottled enamel among villagers still using well-water in the neighbourhood of Hundewali, where Heron (1913) found that the older Aravalli rocks emerge through the alluvium. Samples of these rocks were found to have a wide range of values for fluorine content, varying from 30 to 3200 parts per million. Geodetic investigations suggest that these older rocks extend between the Chenab and Ravi rivers, in an area coinciding with the downward extension of goitre in the Punjab plains.

In England the decrease of endemic goitre in recent times has been attributed to the improvement of village water-supplies and the closing of wells (Ash 1926). Cretinism was formerly associated with areas where the incidence of goitre was high (Norris 1848), but Joll, in 1932, found no focus of endemic cretinism remaining. Stocks (1928), reviewing the results of the Board of Education survey of goitre amongst English school-children, concluded that there was a belt where goitre was comparativelv prevalent, extending, chiefly in rural areas, from Cornwall north-eastwards through Somerset, into Oxfordshire between the Cotswold and Chiltern hills, on into Northamptonshire, thence northwards to Derbyshire and up the Pennine chain. Orr (1931) named places in Cornwall, Somerset, Gloucester, Buckingham, Cumberland and Durham which were conspicuous in this respect.


The geological outcrop of rocks containing fluorine has been described in England in Cornwall, Derbyshire, Cumberland and Durham (Carruthers and Pocock 1922), Somerset (Kingsbury 1939) and Buckingham (Bromehead 1940). The known distribution of fluorine in the soil of England, therefore, corresponds closely with the present or former distribution of endemic goitre, and I was interested to know whether the distribution in England of mottled enamel, as further evidence of the local occurrence of fluorine in the water, had any association with the distribution of endemic goitre. Inquiries were therefore made, and cases of dental fluorosis detected among rural school-children using well-water in the neighbourhood of all known fluorine deposits. Mottled teeth were also found in villagers using well-water associated with the Oxford clay and to a less extent with the lias clay in Northampton, Oxford and Gloucester. In all those areas where dental fluorosis was present it was ascertained from the inhabitants that goitre still occurs.

I made a more detailed investigation of the state of the teeth of Somerset village children in a part of the rural district of Langport, in the neighbourhood of the villages of Charlton Mandeville and Long Sutton, two of the areas of high goitre incidence described by Stocks and by Young (1936), where the water-supply has remained unchanged from the time of their observations. In this area all the 378 children attending the seven local schools were examined. An adjoining area, the village of Somerton, not included by Stocks or Young in the area of endemic goitre, was selected as control, and all the 103 children in the two schools examined. The degree of dental fluorosis as manifested by mottling and staining of the enamel was recorded and graded according to the scale of Dean (1939).

In the control area the breadth of the thyroid gland of the school-children was measured as suggested by Stocks (1928), but in the goitrous areas treatment with iodides had been given, so that measurements of the thyroid were worthless as evidence. The breadth of the gland in the control area never exceeded 42 mm.; the normal breadth of the gland for children of comparable age always lies below this measurement. Thus there were no signs of endemic goitre among the control children.

Of the 378 children examined in the area previously mapped as goitrous, 55 showed some degree of dental fluorosis, while of the 103 children examined in the control area, none was affected (see table). Taking the occurrence of dental fluorosis among the children as evidence, it can be concluded that fluorine is present in the drinking-water in two of the places in Somerset found by Stocks and by Young to be areas of high goitre incidence. The evidence identifying the presence of fluorine in drinking-water as one factor in the causation of endemic goitre is thus strengthened. I do not suggest, naturally, that this is the only factor, and fully realise that the intervention of other factors operating against the production of goitre may completely overcome the action of fluorine in promoting it. For instance, Young and others (1936) noticed that a weekly call by a fish-monger’s van at an isolated village might completely counteract the effects of a local deficiency of iodine an observation of interest in connection with the low incidence of goitre found in the coastal areas of Essex where a high degree of human dental fluorosis has been described (Ainsworth 1933, Donaldson 1936).

Number showing dental fluorosis Control Area. No thyroid enlargement
Children Examined F2 F3 F4 F5 Total Children examined Showing dental fluorosis
378 25 21 7 2 55 103 0
Fluorosis is graded according to Dean (1938). F1 = normal; F2 = doubtful; F3 =,very light; P4 = light; P5 = moderate (mottled); F6 – moderate (stained brown); F7 – somewhat serious; F8 = serious.



The distribution of endemic goitre in the Punjab and in England is related to the geological distribution of fluorine and to the distribution of human dental fluorosis (mottled enamel).

Inquiry showed the presence of dental fluorosis among school-children in two areas of Somerset where two previous observers had recorded a high incidence of goitre, and the absence of dental fluorosis in an adjoining area selected as control where endemic goitre was absent.

Observations in India were made during the course of nutritional investigations towards which financial assistance was received from the Royal Society. I am indebted to Mr. C. E. N. Bromehead, of the geological survey, and to Mr. Evans, geological department, Burmah Oil Co., for assistance on questions of geology; Dr. H. H. Green kindly analysed Kirana rock samples for fluorine; and Sir William Savage provided information about Somerset water-supplies.

This is the first of a series of studies of fluorosis.


Ainsworth, N. J. (1933) Bri. dent. J. 55, 233.
Ash, W. M. (1926) J. State Med. 34, 627.
Bromehead , C. E. N. (1940) Personal communication.
Carruthers, R. G., and Pocock, R. W. (1922) Mem. geol. Sur. Special reports on the mineral resources of Great Britain Vol. IV.
Committee on Iodine Deficiency and Thyroid Disease (1936). Spec. Rep. Ser. med. Res. Coun., Lond. No. 217.
Dean, H. T. (1938) Bull. Off. int. Hyg. publ. 30, 1280.
Donaldson, S. K. (1936) Annual report of the school dental officer for Essex.
Heron, A. M. (1913) Rec. geol. Sur. India, 43, part III.
Joll, C. A. (1932) Diseases of the Thyroid Gland, London.
Kingsbury, A. W. G. (1939) Nature, Lond. 144, 1013.
McCarrison, R. (1913) Etiology of Endemic Goitre, London.
Macnamara, F. N. (1880) Climate and Medical Topography in their relation to the Disease Distribution of the Himalayan and Sub-Himalayan Districts of British India, London.
May, W. (1935) Klin, Wschr. 14, 790.
Norris, H. (1848) Med. Times Gaz. 17, 257.
Orr, J. B. (1931) Spec. Rep. Ser. med. Res. Coun., Lond., No. 154
Roholm, K. (I J37) Fluorine Intoxication, London.
Stocks, P. UP28) Quart, J. Med. 21, 223.
Wilson D. C. (1939) Nature, Lond. 144, 155.