Fluorine Hazards with Special Reference to Some Social Consequences of Industrial Processes

by

Margaret Murray
D.Sc. Lond.
Lecturer in Biological Chemistry at Bedford College for Women, University of London

Dagmar C. Wilson
M.D. Glasg., M.R.C.P., F.R.C.O.G., D.P.H.
From the Institute of Social Medicine, Oxford

IN this country the relation of certain industrial developments to human ecology is not as yet sufficiently appreciated. While it is a part of their function to ensure that the laws relating to the health of workers and public amenities are not infringed, it is not a special duty of Government departments to anticipate new industrial hazards or their secondary social effects.

An outbreak of fluorosis in cattle has once more drawn attention to the large amount of fluorine and fluorine compounds being set free by some recently extended industrial processes and has shown the necessity for consideration of the dangers to public health and to agricultural economy existing in the neighbourhood of these undertakings. At least 28 occupations provide the possibility of such dangers (Sappington 1943). In one industry alone, the manufacture of superphosphate fertilisers, more than 4400 tons of fluorine are "wastefully emptied" into the atmosphere of the British Isles annually (Gill 1946), though methods are known for the control, and in some cases for the further utilisation, of the fluorine liberated. Hazards associated with such fluorine evolution concern not only workers inside the factories but also their families living in the neighbourhood and others resident or employed in the area. They may also have economic consequences through damage to crops and animal stock.

Fluorine is derived from certain volcanic rocks and many different geological formations containing phosphates. Commercially, the main English source of fluorine is fluor-spar (calcium fluoride), but for the special purposes of aluminum manufacture cryolite (sodium aluminum fluoride) is imported from Greenland. In human nutrition fluorine is recognised as having a dual role, probably beneficial at one level of intake and definitely harmful at another. As a trace element, the concentration at which fluorine is effective suggests a catalytic effect and/or an inhibitor action on certain enzyme systems. Epidemiological investigation in the United States, combined with standardised grading of dental fluorosis (mottled enamel), showed less dental caries and more teeth of good structure, with a "mild" degree of white mottling (Dean 1944) among people who had used drinking water containing fluorine 0.5-1.0 part per million (p.p.m) for at least the first eight years of life. With higher fluorine levels, staining of the enamel and skeletal changes may develop. In human balance experiments the close correlation between fluorine in the drinking-water and in the urine indicate that elimination of absorbed fluorine is practically complete when the quantity absorbed does not exceed 5 mg. daily (McClure et al. 1945). The provision of the right amount of fluorine in British water-supplies is a matter worthy of further study (Murray and Wilson 1945). Naturally occurring or endemic fluorosis, attributable to water-supplies, and "man-made" fluorosis, due to industrial processes, should be separately considered, though some of their effects may be the same.

In fluorine intoxication the effective poisons are the gaseous fluorine compounds or the fluorine ion; and whenever fluorine tolerance levels are exceeded, systemic illness and bone abnormalities may develop. Fluorine can affect bone at all ages, leading in man to osteosclerosis, whereas tooth structure can only be influenced during development. Gastric derangement is an early diagnostic symptom, and respiratory embarrassment is not uncommon. More precise information on the degree and effects of exposure is obtained by chemical determination of the range of excretion in the urine and, at a later date, by radiological examination of bone. The severity of fluorotic lesions is influenced by the customary diet and bears a definite relation to the economic status of a community (Pandit et al. 1940). Spinal deformity in later life may result from progressive degeneration of malformations laid down in youth; even where fluorine absorption has been excessive, bone symptoms may not be appreciated for some considerable time (Kemp 1946).

EXAMPLES OF FLUOROSIS RECOGNISED IN THIS COUNTRY

Acute Accidental Effects. (1) Consumption of an insect powder containing sodium fluoride by a farmer's wife (Bell 1936).

(2) Gastric upset, among Nottingham workgirls, from fluorine introduced into cake with a baking-powder prepared from rock phosphate (Lancet 1943).

The interdepartmental committee on food standards of the Ministry of Food have now under consideration maximal limits for the fluorine content of calcium acid phosphate sold for use in food (Analyst 1946).

Chronic Absorption. (I) Fluorosis due to drinking-water :

Radiological investigations were carried out on Essex children from Malden, where mottled enamel in Britain was first recognised (Ainsworth 1933). The domestic water has been shown to contain over 3-5 p.p.m. of fluorine, and severe dental fluorosis has been demonstrated and was associated with developmental disturbances of ossification (Kemp et al. 1942).

(2) Fluorosis as an industrial disease, from the known use of fluorine :

(a) From fluor-spar: Wilkie (1940) recognised osteosclerosis radiologically in two Yorkshire workmen occupied in the manufacture of hydrofluoric acid and of aluminium. fluoride. Subsequent analyses showed that their daily urinary output was at least four times that of normal controls.

(b) From cryolite used as a flux in the manufacture of aluminium: the fluorine output of one aluminium factory was studied by the industrial medical research unit under Dr. Donald Hunter (1946). It found that these works handled some 800 tons of cryolite a year, much of which was lost to the atmosphere and settled in particulate form on the surrounding fields, in which grazing sheep and cows developed fluorosis. Inside the factory skeletal fluorosis was demonstrated in 28 out of 264 furnace-men examined, none of whom complained of disability.

(3) " Neighbourhood " fluorosis

(a) From a known source of atmospheric contamination (cryolite): Boddie (1945) recognised fluorosis in sheep on pastures contaminated by the fumes of an aluminium factory 1 1/4 miles distant. Alveolar periostitis not only made it impossible for the sheep to chew their food properly but also led to infection of the sinuses of the skull and to obvious purulent nasal discharge.

In the same part of Inverness-shire we found that the local water-supply had a very low fluorine content (0-2 p.p.m.), but we observed "moderate" dental fluorosis in the milk-teeth of young children whose homes lay within the district contaminated by vapours from the factory chimneys.

Such a condition in the temporary dentition is usually associated with a high maternal intake of fluorine. Children using the same water, whose homes lay outside the affected area, did not show mottled enamel.

(b) From the unsuspected evolution of fluorine from a marine clay used for brickmaking: agriculturists exposed to the fumes of Bedfordshire brick-working (Wilson 1939) complained of respiratory distress.

Bosworth et al. (1941) and Blakemore (1942) studied the onset and prevention of fluorosis among animals in the same neighbourhood. The origin of the fluorine was traced to the local clay used in the brick-factory, which parted with about a third of its fluorine content (550 p.p.m.) at the higher temperatures, above 900 C, of the kiln. Condensed in the flues to an oily mist by association with volatile products from the organic matter in the clay, fluorine drifted down from the chimneys contaminating surrounding pastures to a distance of about a mile on the leeward side. Fluorine values up to 90 p.p.m., were shown by hay and grass.

Farm animals differed in susceptibility, lactating cattle, being the most vulnerable. Cows had such acute osteodystrophy that they sometimes knelt to eat. Values for fluorine in urine often exceeded 20 times the normal figure.

Control observations on cattle in the neighbourhood of south-east Lancashire brick-works using clay deposits of non-marine origin gave negative results.

On a recent visit to the Bedfordshire area we learnt that fluorine hazards to grazing animals had been temporarily met by the "ploughing-up" campaign of the war agricultural emergency committee.

(c) From coals as a possible hazard: Crossley (1941) investigated the amounts of fluorine in British coals of 4 types, anthracite and bituminous. He determined by microanalysis that their fluorine content ranged from 0-175 p,p.m., and concluded that coals containing over 85 p.p.m. Of fluorine were potentially harmful in industry.

In beer manufacture with the direct type of kiln all the fluorine in malting coals passes on to the malt; in their present dilute state British beers contain only 0.4-1.0 p.p.m. Of fluorine, but considerably more fluorine is present in the "culm" (lees) used as a cattle food.

In coal-mines there is intimate association of the fluorine-containing phosphates with the shales of roof and floor, which take part in the formation of dust at the coal-face. It was suggested (International Labour Office 1940) that pulmonary changes took place from the inhalation of dust containing both silica and fluorine.

Fluorine is present in the water from some mines and in the domestic supplies of many mining communities (Kemp and Wilson 1946). Fluorine in coals increased the hazards of fluorosis during the local calcination of ironstone (see below).

(d) From ironstone calcination: Green (1946) identified the cause of lameness and cachexia in some Lincolnshire cattle as an effect of the local burning of ironstone.

The urine of four affected animals contained from 5.1 times the normal amount of fluorine, urinary values of 26-69 p.p.m. being encountered.

Fluorine in the bones was much increased, values from 10,000 p.p.m. in the ash of ribs to 15,000 p.p.m. In the ash femur and vertebrae being shown as compared with 500 p.p.m. In normal bone ash from cattle in other areas.

Water in the cattle drinking-trough did not contain more than 0.5 p.p.m. Of fluorine.

The ironstone contained about 1200 p.p.m. Of fluorine which came down to about 300 p.p.m. on calcining with coal-slack in heaps on the fields.

The coal contained over 100 p.p.m. Of fluorine and was therefore another source of contamination. The smoke drifted on to the surrounding vegetation. Near the calcining mounds grass showed very high values, up to 2200 p.p.m., and more distant stacks, adjacent to the farmhouse, 68-487 p.p.m. Of fluorine. Members of the farmer's household showed raised excretion of fluorine in their urine.

We have studied the ultimate and contributory causes and present manifestations of this particular outbreak of fluorosis, as it affects the public generally.

FARMER X'S HOMESTEAD

Details of Farmer X's family and associated work are surnmarised in the accompanying table.

Environmental Factors. - Ironstone workings in south Lincolnshire lie in an agricultural district of low hills and wide valleys. Mounds formed by the rocky overburden of the mining pits stand out from land, which is both arable and pasture. Some farms are isolated, but many agricultural workers live near small villages. The ironstone industry is of considerable antiquity, but since 1939, owing to war-time requirements, workings have been extended very considerably. About 25-30% of iron is obtained from this rock, which compares favourably with many imported samples. Mining pits are in the form of long trenches 8-40 ft. in depth; land has only been levelled when ore is extracted from near the surface.

Whether the ore is conveyed direct to central blast furnaces or first calcined, so that hygroscopic moisture and other volatile components are driven off, depends on the type of ore and the cost of transport. In this area the ore is mixed, in the field where it is mined, with coal cobbles and slack and "burnt" - i.e., dehydrated - and the resulting cloud of smoke, containing fluorine compounds, drifts over the countryside. The direction of the prevailing wind in this area is shown by deterioration in the growth of field crops in the immediate vicinity of the smoke. Wheat and barley embryos do not mature, and it is customary for farmers to obtain compensation from the mine-owners, based on the difference between the expected and actual grain yield. At the height of calcining the density of fumes may even make driving on neighbouring roads difficult. In one instance a local practitioner, summoned to an accident in daylight, was unable to see where his patient lay.

Farmer X's home, a small brick house with numerous outbuildings, is situated in the midst of his fields, so that "one fence surrounds them all." In this he differs from the owners of the neighbouring fields near the ironstone burning dumps ("cally heaps"), who live elsewhere. A well on his land supplies Farmer X's house; the water, examined twice, has contained 0.4 and 0.6 p.p.m. Of fluorine; the higher figure, obtained in wet -weather, suggests the possibility of surface percolation of fluorine or its compounds.

Domestic and Habitual Factors Increasing the Hazard. - The house is poorly constructed, and the windows do not fit. All the family suffer when fumes drift over the farm. Food in the larder is exposed to these fumes and is covered with red dust when the calcined ore is loaded for dispatch. Farmer X's daughter (case 3) complained that she could not clean the glass on the windows facing the fumes. Subsequent examination by an expert of a piece of window glass from the bedroom of Farmer X's mother (case 8, with a high excretion of fluorine) has confirmed that the changes on the surface of the glass can be explained as due to the action of hydrogen fluoride.

Occupational and Economic Factors. - During the past six years, since ironstone burning has been carried on more continuously and nearer to the farm, 7 horses and 11 cows have died; young cattle and sheep have been under weight; the sheep also have been lame and had nasal discharge; and much poultry has been lost. But for the wartime increase in agricultural prices the farm would have been abandoned. Farmer X (case 1) has also been very worried about his own health and that of his family. A young labourer (case 9), who chose agriculture instead of military duty and was "directed" to this farm, says he would really enjoy his work but for stomach pain.

Nutritional Factors. - Family X has experienced no shortage of milk or pork; pieces of home-cured bacon can be seen hanging up in the kitchen. Their vegetables, grown round the farm, are of poor quality. Surface contamination of food with fluorine compounds may explain the raised fluorine levels in these people's urines.

Educational Factors. - Until the recent investigation of cattle fluorosis, the significance of fluorine in this area had not been appreciated. Farmer X was convinced that both his family and his stock suffered from the ironstone fumes and had sought all possible local diagnostic aid since 1940, but it was only the identification in 1946 of the fluorosis in cattle which provided the clue to the lesser symptoms in the human subjects.

Control Observations. - At a farm adjacent to ironstone pits from which the ore was sent direct to blast furnaces without local calcining there was no sign or history of illness in either the members of the household or in their farm stock. Their domestic water contained 0.35 p.p.m. Of fluorine in wet weather. Fluorine in small quantity is to be expected in the local springs deriving their water from the ironstone beds, and inspection of adolescents in five neighbouring villages showed teeth with a "very mild" degree of mottled enamel.

At the blast furnaces dealing with this ore no history of clinical disability attributable to fluorine was obtained from workmen employed for over fifteen years.

DISCUSSION

The absorption of the products of fluorine combustion by the affected cattle consuming heavily contaminated hay and grass was obviously more intense than by Farmer X's family who presumably consumed only small quantities of contaminated foods. The human clinical symptoms are, however, in line with those recorded in chronic endemic fluorosis among people using waters with a raised fluorine content: Argentine (Roholm 1937); China (Lyth 1946); South India (Shortt et al. 1937); North India (Wilson 1939, Khan and Wig 1945); South Africa (Ockerse 1941); United States (Linsman and McMurray 1943).

Judging from the experience of these countries, it was unlikely that skeletal changes resulting from the absorption of fluorine would be appreciable radiologically within the period, about six years, in which Farmer X's household has been exposed to the effects of the intensive ironstone calcination; there is, however, abundant human evidence from other parts of the world that fluorine intake above tolerance levels over a sufficient period (as shown by raised excretion of fluorine) can lead to cumulative absorption and prove harmful to the human organism.

That fluorine must be regarded as a cumulative poison is well established by chemical and experimental observations. The bones of Danish cryolite factory workers contained about ten times that of average persons, the highest fluorine content being found in the worker with longest exposure; osteoselerosis resulted from the daily retention of about 25 mg. of fluorine (Roholm 1937, Brun et al. 1941). Animals given small amounts of sodium fluoride in the diet showed an increasing fluorine content of their bones (Glock et al. 1941). The accompanying figure shows the increase in fluorine content of the bones of rats fed 7-10 mg. of fluorine a day. A series of estimations of the fluorine content of the fat-free dried rib bones of persons of different ages resident in London for most of their lives is given in the same figure; these also show, on the whole, an increase in fluorine content with age.

Etching of window glass in houses facing industrial fumes should lead to inquiry for possible clinical evidence of fluorine absorption. Recently fluoiosis was recognised in cattle grazing in the neighbourhood of a Shropshire colour and enamel factory. Fluorine values in the urine of the affected cattle ranged from 19-37 p.p.m. Water in the animals' drinking-trough did not contain more than 0.6 p.p.m. Of fluorine, but there was severe contamination of pasture, samples of air-dried material showing 776-115 p.p.m. Of fluorine at distances of 30-600 yards from the factory. During the winter these cattle had been fed on hay cut from another farm, and their exposure to fluorine was mainly at grass in summer; their skeletal lesions were not so pronounced as those of cattle near the brick-works and ironstone dumps (see above); but after three or four years' exposure their molar teeth were worn down to the gums, and the permanent incisors were distorted and misshapen. In the windows of an adjacent farmhouse etching of the glass by the fumes was reported; it was sufficiently severe to necessitate window-glass replacement by the family every two or three years. Human fluorine hazards in this neighbourhood had not yet received attention.

SUMMARY

Fluorine hazards, actual or potential, in this country have been described.

An example has been studied of some important secondary consequences for dwellers in the neighbourhood of certain industrial undertakings.

It is a practical proposition to extract fluorine from fumes before allowing them to pass into the atmosphere. This is already the practice of some firms. In the example studied the substitution of closed kilns in the burning of ironstone would make the amount of fluorine present in the ore and coal immaterial from the public health point of view, but methods for such fluorine control are at present too rarely applied in this country, because fluorine hazards are not sufficiently appreciated.

An investigation to ascertain the nature and location of all industrial processes creating a possible fluorine hazard seems to be desirable.

The need for a better intelligence service and coordinating mechanism to ensure collaboration between Government departments, industries, local authorities, and research workers is also apparent.

We wish to thank Dr. H. H. Green, of the Ministry of Agriculture's veterinary laboratory, Weybridge, for supplying much information and for his help in many different ways; our colleague, Dr. F. H. Kemp, for reporting on the radiological examinations of Farmer X's household, to whom access was very kindly given by their family doctor and the county health authorities concerned; Mr. C. N. Bromehead, of the geological survey, for providing data throughout this inquiry; and Mr. A. C. Pilkington for his examination of glass. We also wish to thank the Medical Research Council for an expenses grant.

REFERENCES

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Analyst (1946) 71, 382 .
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Blakemore, F. (1942) Proc. Nutr. Soc. 1, 211.
Boddie, G. F. (1945) Ibid, 3, 110.
Bosworth, T. J., Green, H. H., Murray, M. M. (1941) Proc. R. Soc. Med. 34, 391.
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- Murray, M. M., Wilson, D.C. (1942) Lancet, ii, 93.
- Wilson, D. C. (1946) Ibid, i, 172.
Khan, Y. M., Wig, K. L. (1945) Indian med. Gaz. 80, 429.
Lancet (1943) i, 440.
Linsman, J. F., McMurray, C. A. (1943) Radiology, 40, 474.
Lyth, 0. (1946) Lancet, i, 233.

(Note: The references contained on page 825 of this article are not included here.)

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