"NEIGHBORHOOD" FLUOROSIS

by G. L. Waldbott and V. A. Cecilioni
Detroit Michigan and Hamilton, Ontario

Fluoride fumes, mainly HF and SiF4, and particulate fluoride compounds, especially NaF, escape from chimneys, storage bins and effluent ponds of factories which employ fluoride compounds as a flux or where fluoride constitutes a by-product of refining and smelting processes. The principal industries involved are those concerned with the production of aluminum, steel, enamel, zirconium, uranium, magnesium, triple phosphate fertilizer, glass, tile and bricks. Fluoride is also liberated into the air wherever wood and coal are burned. Gaseous HF and SiF4 hydrolyze with the moisture of the air and settle on the ground, on plants, fruit, vegetables and on forage for cattle.

In humans, fluoride-contaminated food and water constitute the bulk of fluoride intake in polluted areas. In the vicinity of an Ontario fertilizer plant, dust contained between 9, 000 and 11, 000 ppm of fluoride, near a Michigan iron foundry up to 2, 000 PPM The dust from the fertilizer plant covered practically everything in the area and settled on topsoil. Fluoride fumes etched windows and damaged the finish of automobiles.

The data presented here concern 32 patients. Twenty-eight of them resided near the above-mentioned fertilizer factory, 3 near Iowa fertilizer factories, 1 near a Michigan iron foundry. Four of the 32 were hospitalized for diagnostic studies. Fifteen were examined. In the remaining 13, data were obtained from the medical history given to us by the patients. In all cases, characteristic fluoride damage in plants, livestock and materials was established.

The two conspicuous and readily recognizable manifestations of chronic fluoride poisoning, dental and skeletal fluorosis, are not obligatory features of the disease. Dental fluorosis (or mottling of teeth) occurs only in individuals who have consumed, or have been exposed to, fluoride during childhood. The skeletal changes of the disease develop only after many years of persistent fluoride intake. The latter condition need not be considered here, since the air polluting factories have been in operation less than seven years.

History

Table 1 presents the ages and sexes of the 32 cases, the distance of their residence from the factory, and the symptoms which they presented. Ten of the 32 patients manifested the skin lesions described by Steinegger (2) and by Colombini et al. (3) among residents near fluoride-emitting aluminum plants in the vicinity of Chizzola and of Bolzano, Italy. They are bluish-brown, macular areas, round or oval in shape, about the size of a dime (Fig. 1, 2). They are painless, fleeting in character with a duration of 5 to 10 days. They simulate purpuric lesions or traumatic suffusions but do not exhibit histological evidence of capillary permeability. Microscopically, they show lymphocytic perivascular infiltration and edema in the corium with occasional melanin deposits in the epidermis.

Gradually increasing general malaise and exhaustion leading to complete disability characterizes the disease. All individuals except two boys (sic), ages 12 and 13, reported pain and stiffness in the lumbar and cervical spine with restriction of spinal movements and arthritis in other joints as well. They complained of myalgia and paresthesias in arms, legs and shoulders with impaired muscular power of hands and legs. Consequently, they were no longer able to grip objects securely and their legs tended to collapse when walking. Eight patients had muscular fibrillation, 3 intermittent muscle spasms especially in the big toes suggestive of hypocalcemic episodes, a common feature in acute fluoride intoxication (Table 2).

Bilateral migraine-like headaches were encountered in 20 of the 32 cases. Ten patients complained of visual disturbances (scotomata, blurred vision) which were not corrected by glasses. Two had evidence of incipient retinitis, a condition encountered also in hydrofluorosis (1).

Eighteen of the 32 individuals had gastrointestinal disturbances, the second group of symptoms described in fluorosis. They had frequent nausea, occasional vomiting, pains in the epigastrium and in the intestinal tract, bloating and distention of the abdomen. Sixteen of the 32 had spastic constipation, alternating with diarrhea. Nine had repeated acute abdominal episodes simulating, and diagnosed by their physicians as, volvulus, acute gallbladder disease, "intestinal flu" and the like. Several patients identified these episodes with temporary intake of excessive amounts of fluoride-contaminated food grown near the factory (cabbage, lettuce, beans) (Table 3).

In the third group of symptoms concerning the respiratory tract, nasal and conjunctival irritation was common, especially on windy days; but chronic bronchitis and emphysema was noted in only 4 of the 32 individuals.

More significant, however, is the history of frequent epistaxis in six patients which they related to sudden excessive exposure to dust.

Examination Findings

Examination and laboratory data were unremarkable as is usually the case in the early stage of chronic fluorosis (4). Two patients manifested exaggerated tendon reflexes, especially in the lower extremities. In others, pain was elicited on palpation of the abdomen. Abdominal distention, joint swelling and restriction of joint movements, especially in the lower spine, were noted. In the hospitalized cases, the spinal X-rays showed changes indicative of osteoarthritis. Hypercalcemia, hyperuricemia, slight impairment of liver function were noted but were not sufficiently consistent to be attributed to chronic fluoride intoxication.

Diagnosis

The diagnosis of chronic fluoride intoxication was based on the following criteria:

1. Excessive exposure to fluoride in food, air and water was established by visible damage to crops, livestock and materials. The vegetation showed the typical fluoride damage of margins and tips of leaves and high fluoride levels. The cattle exhibited the characteristic features of fluorosis i.e. exostoses, joint swellings. Fluoride assays of food consumed by cases 20 to 22 and by case 25 yielded values up to 20 times those grown in non-polluted areas (Table 3)

2. The clinical picture is identical in the 32 individuals, and agrees with the non-skeletal phase of fluorosis in industry (5), of hydrofluorosis (6), of "neighborhood" fluorosis described by Murray and Wilson (7) and by Capps and Hunter (8) and with the recently described symptomatology of chronic poisoning due to fluoride intake for therapeutic purposes (9). Fig. 3 presents the incidence of the symptomatology encountered near the Ontario factory compared with that in 28 consecutive cases seen in an allergy practice (G. L.W.) and 28 in general practice (V.A. C.). The difference in the incidence of arthritis in the 3 groups of cases is particularly noteworthy.

3. In four cases, 24 hour urinary fluoride values were obtained; in three cases, biopsy tissue. Table 4 shows a high fluoride content of bone and soft tissue and an unusually high urinary fluoride excretion, namely 7.04 to 12.63 mg. Since in most instances only a fraction of ingested fluoride is excreted in the urine, the daily fluoride intake must have been considerable.

Bibliography

1. Waldbott, G. L.: Incipient Chronic Fluoride Intoxication from Drinking Water 1. Report on 52 cases. Acta Medica Scand. 156:157-168, 1956. Read before the Fourth International Congress of Internal Medicine in Madrid, Spain, Sept. 24, 1956.
2. Steinegger, S.: Endemic Skin Lesions Near an Aluminum Factory, Fluoride, 2:37, January 1969.
3. Colombini, M., Mauri, C., Olivo, R. and Vivoli, G.: Observations on Fluorine Pollution due to Emissions from an Aluminum Plant in Trentino. Fluoride, 2:40, January 1969. http://www.fluoridealert.org/trentino.htm
4. Waldbott, G. L.: Fluoride in Clinical Medicine.. Suppl. 1 ad Vol. 20, Internat. Arch. Allergy Appl. Immunol., 1962.
5. Roholm, Kaj: Fluorine Intoxication: A Clinical Hygienic Study, Arnold Busck, Copenhagen, 1937.
6. Frada, G. , Mentesana, G. and Nalbone, G.: Richerche Sull 'ldrofluorosi, Minerva Medica 54:45-59, 1963.
7. Murray, M. M. and Wilson, D. C.: Fluorine Hazards with Special Reference to Some Social Consequences of Industry Processes. The Lancet 2:821-4, 1946. Paper available online at http://www.fluoridealert.org/Lancet-1946.htm
8. Reynolds Metals Co. vs the Paul Martin family, Transcript of Record Nos. 14990-14991-14992 in the U.S. Court of Appeals for the Ninth District.
9. Rich, C.: J.A.M.A. 196:149, June 27, 1966.

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