The Preskeletal Phase of Chronic Fluoride Intoxication


by Waldbott George L, MD+, , 1998, Fluoride, 31:1, 13-20

Chronic poisoning from most toxic agents is rarely diagnosed by physicians in its initial stage. Most systemic poisons induce vague, subtle symptoms before the appearance of features characteristic of a particular kind of poisoning. For instance, the radial nerve paralysis or the lead line on the gums which are typical of lead poisoning are preceded by numerous vague symptoms such as lack of appetite, general fatigue, gastric pains, and bowel disorders. Similarly, the bone changes characteristic of chronic cadmium poisoning become apparent only after a prolonged, slowly progressive illness with changes in kidney function.1

Roholm, the most astute observer on the health effects of fluoride, was first to outline a wide variety of vague manifestations in conjunction with skeletal fluorosis in cryolite workers (Table 1).2 He also stated that these symptoms are transitory and tend to disappear: "The rule is that for a period of some few days to some few weeks after starting at the factory the worker suffers from these acute gastric attacks, whereafter they disappear, especially the nausea and vomiting. Thereafter some of the workers tolerate the dust without observing the symptoms; others will still have transitory symptoms after holidays, or if the dust quantity temporarily becomes especially high. Cardialgia is less distinctly connected with working in the dust. Sometimes the aforesaid gastric symptoms are accompanied by a slight, passing pressure or pain in cardia..."2


Table 1. Frequency of complaints in cryolite workers with skeletal fluorosis
Symptoms  Men  Women  Total  % of all workers
examined (68)
Gastric (loss of appetite, gastric pain; nausea, vomiting) 42 13 55 80.9
Intestinal (chronic diarrhoea, constipation) 15 8 23 33.8
Circulatory and respiratory (dyspnea, cough, expectoration, palpitation) 23 12 35 51.5
Neuromuscular (joint pains, stiffness, indefinite or localized rheumatic pains) 18 6 24 35.3
Neurological (tiredness, headache, asomnia, vertigo) 12 3 15 22.1
Dermatological {rash) 8 0 8 11.8


Murray and Wilson 3 also refer to vague gastrointestinal and arthritic symptoms in conjunction with exposure to fluoride in their account of nine members of the household of a farm family residing close to a fluoride-emitting factory. Frada and Mentesana recorded disturbances in the bowels in conjunction with skeletal fluorosis in residents of northern Sicily where the water contained between 3 and 6 ppm of fluoride naturally.4 Srikantia and Siddiqui emphasized polydipsia and polyuria in endemic skeletal fluorosis in India.5

I have presented a more detailed description of the above-named clinical syndrome.6-8 Because of the increasing significance of fluoride as an industrial pollutant of air and water and because of the difficulty encountered in the recognition of the early stage of chronic fluoride poisoning a review of the available data is indicated.

In I953, Mrs S S aged 40, a resident of Bay City, Michigan, was referred to me by her physician for allergic studies in order to determine the cause of a gastrointestinal disorder accompanied by migraine-like headaches. My tests revealed that her illness was not due to allergy. She wondered why her condition always tended to clear up when she was away from Bay City but became aggravated upon her return. She questioned whether the Bay City water might be involved, At that time neither she nor I were aware that Bay City's water had been fluoridated since 1951, when her illness began.

In September, 1954, Mrs M E J, age 35, a patient from Highland Park, Michigan, consulted me because of a serious, progressive illness.9 The description of its initial stage resembled that of Mrs S S, of Bay City. Studies at Harper Hospital, (Detroit, Michigan), laboratory tests, and consultations with nine specialists ruled out illnesses with which these specialists were acquainted. The only positive findings were mottled teeth which led to the information that as a child she had resided in an area in China where water naturally contained fluoride in appreciable concentrations. Following her discharge from the hospital she eliminated fluoridated water for drinking and cooking at her home in Highland Park (then fluoridated for 2 years). She recovered completely without medication. Controlled studies with minute doses of fluoride in water proved that she was unusually susceptible to ill effect from fluoride, A few weeks after fluoridation had been discontinued in Saginaw, Michigan, in November 1954, I had an opportunity to examine thirty patients, nine of whom appeared to be afflicted with the same condition.6 Their attention was drawn to fluoride in drinking water because during the weeks since fluoridation had been abandoned they had, for reasons unknown to them, markedly improved or completely recovered from an otherwise progressive chronic illness.

In November 1955, I encountered additional cases during a visit to Charlottesville, Virginia, shortly after fluoridation had been discontinued there, Most im-pressive was the case of Mr J A H, age 67, whose illness had baffled leading clinicians at two medical centers. He had not obtained a diagnosis of his illness nor had he received benefit from treatment. Like the others, he was not aware that fluoride was being added to his drinking water until he unexpectedly recovered his health following discontinuance of fluoridation in that city. In contrast to the Saginaw cases in which the illness was recognized after cessation of fluoridation in Windsor, Ontario, it was detected after fluoride was introduced into the water supply. The local health department, fearing adverse publicity by citizens, did not announce in advance the date when fluoridation would begin. This afforded an excellent opportunity - better than any double blind test - to determine incontrovertibly whether illness from fluoridated water is genuine or imaginary. Two weeks after its inception, when the press announced the event to the public, eight individuals were able to diagnose their own illness. Upon eliminating fluoridated water for drinking and cooking their food, they recovered their health.

During the past two decades I have had experience with more than 400 similar cases.6-16 At least twenty were hospitalized for detailed studies. In others laboratory and double blind tests have been utilized in my clinic. The salient symptoms have been sharp pains in the stomach area associated with nausea, spasticity of the bowels (ileitis, colitis), polydipsia and polyuria, arthritic pains, especially in the lower spine, migraine-like headaches and painful paresthesia in arms and legs with loss of muscular power. Some patients have had ulcers in the mouth, some have had frequent episodes of lower urinary tract disease. Most patients have shown a distinct mental deterioration, mainly loss of memory and of ability to concentrate. Most striking and consistent has been extreme exhaustion, which eventually caused many of them to be bedridden.

One of the most impressive cases in my series is that of N K T, age 45, who consulted me in early April 1975 because of a variety of complaints which his physicians had not been able to diagnose. He had been in perfect health until 1954 when he moved to Milwaukee (fluoridated August 1953) where he developed headaches and low back pain which gradually became so severe that in 1956 he had to seek lighter work as a salesman. The condition became aggravated by nausea and pain in the abdomen, and in fall 1957 he had two episodes of convulsions for which his physicians could find no explanation. Shortly thereafter he moved to Okauchee, Wisconsin (nonfluoridated) * where, unexpectedly, all his symptoms cleared completely. Upon resuming residence in Milwaukee in late 1959 his illness promptly recurred. In 1961 he took another job in Antioch, Illinois, where he remained in good health. Here he consumed the water of a shallow private well about 10 meters deep the composition of which could not be ascertained because it was abandoned after he returned to Milwaukee**where he accepted employment as a salesman in 1968. Almost immediately he began to be aware of persistent backaches, headaches, extreme tiredness, and excessive thirst. His mental faculties gradually deteriorated and he became forgetful and unable to comprehend. He experienced general muscular weakness, tinnitus in both ears, pain, and edema in hands and ankles, and bleeding of the gums After five months he was obliged to stop working. He received a variety of treatments including traction of the spine, muscle relaxing

drugs, and analgesics. Diagnostic studies by his physician revealed, according to the copy of the physician's record, only a minor hearing loss in his left ear. Another attempt at working on a job operating heavy equipment had to be relinquished because of his gradually worsening backaches.

In October I969 he moved to Woodruff, Wisconsin (nonfluoridated)* where his illness again cleared up dramatically without medication. Three years later, on December 1, 1972, he once more took up residence in Milwaukee. Within days the backaches returned, associated with pains and swelling in most other joints, paresthesia in the fingers and muscular fibrillation. Because of the muscular weakness, it became difficult for him to open doors; he had to sleep for at least 12 out of 24 hours. There was a slight, temporary rise in blood pressure (160/90). His condition improved somewhat by taking large amounts of vitamin C (1500 mg daily) and bone meal tablets, but during October 1973 the arthritis gradually became much more pronounced, especially in his knees, and failed to yield to salicylates prescribed by his physician. He also had slight hayfever and considerable nasal discharge. Because of several episodes of acute abdominal pains, he had a cholecystectomy and appendectomy, but abdominal symptoms (pains, bloating, diarrhea) persisted. According to the records obtained from his physician, however, the physical and laboratory findings were unremarkable.

In late 1974, while his health continued to deteriorate, his attention was directed to fluoridated water: a general skin rash on his infant son cleared up promptly and completely as soon as distilled water was substituted for Milwaukee's water in the baby's formula, a measure recommended by a friend. Although skeptical about this apparent cure, the father, urged by his friend, decided to substitute distilled water likewise for himself. The bowel distur-bances, especially the abdominal pains, were promptly alleviated. Within 10 days all other symptoms had disappeared. Since using distilled fluoride-free water he has remained in perfect health operating heavy construction equipment and performing difficult physical work without any of the previous adverse reactions. In June, 1970, his symptoms recurred temporarily. Subsequently on July 20 he learned that, due to failure of the deionization equipment, the water contained 0. 54 ppm fluoride.

In order to confirm the relation of the illness to fluoridated water, I reproduced the disease by a controlled procedure advocated by the editor of the Journal of the American Medical Association in a letter to me dated April 2, 1958: "... Place the patient on a fluoride free water supply until the symptoms have sub-sided and then, unbeknown to the patient, add 2.2 parts per million of sodium fluoride to the water." This concentration is equivalent to 1 ppm fluoride in water, the optimal concentration recommended for fluoridation of drinking water.

I was able to confirm my initial observations by studying the same disease among residents in the environs of fluoride-emitting aluminum and fertilizer factories in Ontario 15 and British Columbia, Canada; Bolzano, Italy; and Southern Ohio, USA. Most of these individuals identified the gastrointestinal symptoms with the ingestion of food grown in their own garden which had been contami- nated by airborne fluoride (Table 1). In some, respiratory symptoms prevailed, presumably precipitated by airborne fluoride and perhaps by other contaminants. Data on the 112 cases from the four areas are presented in Table 2.


Table 2. Symptomatology in 112 cases of neighborhood fluorosis
  Ontario Ohio Italy British
Columbia
 TOTAL 
(%)
28 cases 36 24 24 112
Musculo-skeletal
Arthritis -esp. cervical & lumbar spine
Myalgia, Myasthenia, parasthesias
Spasticity in extremities

26
25
5

7
13


13

9
6
1

42 (38)
58 (52)
6  ( 5)
Gastro-Intestinal
Epigastric pain, nausea, vomiting
Distention, diarrhea, spastic constipation
Acute abdominal episodes
Stomatitis
16
14
7
3
17
10
1
6
16
18

10
8
10
2
2
57 (51)
52 (46)
10 (  9)
21 (19)
Neurological
Migraine-like headaches
Scotomata, blurred vision
Convulsions
Muscular fibrillation
17
8

6
9
3
1

17
13
1

13
3
2
10
56 (50)
27 (24)
4 (  4)
16 (14)
Respiratory
Nasal & conjunctival
Emphysema; asthma
Epistaxis
24
2
5
11
4
4
14
1
2
3
3
1
52 (46)
10 (  9)
12 (11)
Skin
Dermatitis
Chizzola maculae*
1
7
3
16
  1
18
5 (  4)
41 (37)
*Lesions resembling traumatic suffusions described by Waldbott and Steinegger16


I have also studied other cases of chronic fluoride intoxication which were dominated by one major symptom such as convulsions,11 urticaria,12 and, in infants, gastrointestinal hemorrhages 14. In 1973, Petraborg, a Minnesota physician, interviewed and examined 28 individuals in Milwaukee. The medical history of their illness, the uniformity of their complaints, and his personal examinations convinced him that fluoridated water had indeed caused a serious progressive illness.17,18 Another group of 12 physicians in Haarlem, Holland, studied 60 patients, 30 of whom underwent carefully controlled double blind tests.19

Other physicians have diagnosed the disease on their own, among them Dr William P Murphy, a 1934 Nobel Prize winner in medicine, but have hesitated to report these cases in medical journals for reasons discussed below. On at least three occasions to my knowledge, physicians have treated illnesses by advising patients to abandon fluoridated water but have expressly requested the patient not to disclose the diagnosis.


DISCUSSION
The following questions arise in conjunction with the description of this disease: 1. Why must fluoride and no other toxic agent be considered the cause of this disease? 2. What accounts for the wide spectrum of vague

symptoms? 3. What, if any, specific laboratory criteria are available to permit the establish-ment of the diagnosis? 4. Why is the illness not diagnosed more frequently in view of the wide-spread consumption of fluoridated water?

1. Other Possible Causal Sources: The prompt disappearance of the symptoms upon eliminating fluoridated water for drinking and cooking and their return on its resumption could conceivably be attributed to a psychosomatic background of the clinical picture described above. However, in most instances - certainly in the Saginaw and Windsor group - no one was aware that their water had been fluoridated when the disease terminated or began, respectively. In others, the disease was reproduced by blind and double-blind procedures. Furthermore, most individuals had undergone extensive diagnostic tests by competent diag-nosticians and had been treated unsuccessfully with numerous therapeutic measures to which the disease failed to respond. Why would the disease respond to avoidance of fluoridated water but not improve following the many other therapeutic measures which had been previously instituted? For most patients under my own care, unbiased specialists were consulted who ruled out other known diseases. Moreover, the clinical events beginning usually with minor gastrointestinal complaints, excessive thirst, paresthesias muscle pains and fibrillation, headaches, and other inconspicuous neurological manifestations and the progressive nature of the illness, resulting eventually in complete disability, represent a clear-cut syndrome which undoubtedly constitutes an attenuated form of acute fluoride intoxication.8 The latter is also dominated by gastro-intestinal hemorrhages and neuromuscular manifestations, particularly convulsions.11 Some of the symptoms observed in my cases such as the skin lesions, the early changes in the retina or gastric hemorrhages and the skin lesions could not possibly be induced by psychosomatic features.

2. Wide Spectrum of Symptoms: In order to explain the wide spectrum of the symptomatology of this illness, we must recall that the fluorine ion is extremely minute in size and has a high charge density which enables it to penetrate into every cell of the body and become attached to other ions, especially polyvalent ones.20 Usually soft tissue organs do not accumulate the halogen which has a strong affinity for calcified tissue, i.e. bones and teeth. Nevertheless, the presence of sizeable amounts of fluoride has been reported in soft tissue organs,20 particularly in nephritic patients whose kidneys retain more fluoride than kidneys of normal persons. The fact that fluoride permeates readily into every organ of the body where it interferes with many enzyme systems might conceivably account for its effect on the function of so many organs. When fluoride is ingested or imbibed with water the first major target reached is the stomach, the acidity of which produces the highly irritating hydrofluoric acid and thus accounts for the gastric symptoms. The production of ulcers in the mouth can be explained in a similar manner when acid foods are in contact with fluoride excreted in the saliva. The lower urinary tract is involved in reabsorption of fluoride, especially when the urine is acid and hydrofluoric acid is likely to be formed.21 In individuals residing close to fluoride-emitting factories, respiratory symptoms are more prevalent than in hydrofluorosis cases because the respira-tory tract is the first target for inhaled fluorides.20

3. Laboratory Features: In most of my cases of preskeletal fluorosis, fluoride levels in the urine were not excessive, which indicates that the so-called optimal concentration (1 ppm) of fluoride in drinking water is sufficient to induce poisoning in persons intolerant to fluoride. High urinary fluoride excretion does not necessarily correlate with the degree of poisoning 22 nor can poisoning be ruled out when urinary fluoride levels are low. Whereas I was unable to obtain data on fluoride plasma and bone levels, it is doubtful that these parameters are related to the incipient stage of fluorosis.

Occasionally in beginning fluorosis two laboratory findings merit special attention, namely, an increase in alkaline phosphatase and changes in the calcium and phosphorus levels of the blood,23 but due to the inconsistency of these parameters they cannot be considered pathognomonic for fluorosis. In squirrel monkeys maintained on 1 and 5 ppm fluoride in their drinking water for 18 months, Manocha et al24 found that the kidneys "showed significant cytochemical changes, especially in the animals on 5 ppm fluoride in their drinking water." Moreover, in the last 10 months of the study, water consump-tion by animals drinking the fluoridated water was higher than that of the controls on fluoride-free water. Kidney tests for changes in renal enzyme activity might therefore offer a means to detect the early stage of fluoride poisoning.

4. Lack of Recognition of the Disease: Many reasons account for the fact that reports of this disease which have appeared in the medical literature are rare. The absence of conclusive laboratory data, the slow and insidious onset of the disease, the wide spectrum of vague symptoms, the unawareness of physicians of possible side effects from fluoridated water and airborne fluoride all render the diagnosis difficult. Furthermore, physicians are constantly being assured that fluoridation is safe.25 For the same reasons the untoward effects of many other environmental pollutants have escaped our recognition for many decades.

In view of the widespread industrial application of fluoride and its great significance as an environmental pollutant and because of the likelihood that the illness already described affects a sizeable segment of the population, careful review of all available data on this subject is indicated.

REFERENCES
  • 1 Waldbott GL. Health Effects of Environmental Pollutants. Mosby, St Louis, 1973 (2nd Edition 1978).
  • 2 Roholm K. Fluorine Intoxication: A Clinical-Hygienic Study. HK Lewis, London I937 p l38.
  • 3 Murray MM, Wilson DC. Fluorine hazards with special reference to some social consequences of industrial processes. Lancet 2 821-824 1946.
  • 4 Fradą G, Mantesana G, Nalbone G. Recerche sull'idrofluorosi. Minerva Medica 54 451-59 1963.
  • 5 Srikantia SG, Siddiqui AH. Metabolic studies in skeletal fluorosis. Clinical Science 28 477-485 1965.
  • 6 Waldbott GL. Incipient fluorine intoxication from drinking water. Acta Medica Scandinavica 156 157-168 I956.
  • 7 WaIdbott GL. Fluoride in Clinical Medicine. International. Archives of Allergy and Applied Immunology 20 Suppl 1 1962.
  • 8 Waldbott GL. Acute fluoride intoxication. Acta Medica Scandinavica 174 Suppl 400 1963.
  • 9 Waldbott GL. Chronic fluorine intoxication from drinking water. International Archives of Allergy and Applied Immunology 7 70-74 1955.
  • 10 Waldbott GL. Incipient chronic fluoride intoxication from drinking water. II. Distinction between allergic reactions and drug intolerance. International Archives of Allergy and Applied Immunology 9:241-249 1956.
  • 11 Waldbott GL. Tetaniform convulsions precipitated by fluoridated drinking water. Confinia Neurologica 17 339-347 1957.
  • 12 Waldbott GL. Urticaria due to fluoride. Acta Allergologica 13 456-468 1959.
  • 13 Waldbott GL. Allergic reactions to fluoride. Journal of Asthma Research 2 51-64 September I964.
  • 14 Shea JJ, Gillespie SM, Waldbott GL. Allergy to fluoride. Annals of Allergy 25 388-391 July 1967.
  • 15 Waldbott GL, Cecilioni VA. "Neighborhood" fluorosis. Clinical Toxicology 2 387-396 December 1969.
  • 16 Waldbott GL, Steinegger S. New observations in "Chizzola" Maculae. In: Proceedings of the Third International Clean Air Congress of the International Union of Air Pollution Prevention Association. October 8-12, I973, Dusseldorf, Federal Republic of Germany. Verein Deutscher Ingenieure, Dusseldorf 1975 pp A63-A67.
  • 17 Petraborg HT. Chronic fluoride intoxication from drinking water (Preliminary Report). Fluoride 7 47-52 1974.
  • 18 Petraborg HT. Hydrofluorosis in the fluoridated Milwaukee area. Fluoride 10 165-169 1977.
  • 19 Grimbergen GW. A double blind test for determination of intolerance to fluoridated water (Preliminary Report). Fluoride 7 146-152 1974.
  • 20 Waldbott GL. Symposium on the non-skeletal phase of chronic fluorosis. Fluoride 9 5-8 1976.
  • 21 Whitford GM, Pashley DH, Stringer GI. Fluoride renal clearance: a pH-dependent event. American Journal of Physiology 230 527-532 1976.
  • 22 Dinman BD, Bovard WJ, Bonney TB et al. Prevention of bony fluorosis in aluminum smelter workers. Parts 1-4 Journal of Occupational Medicine 18 7-23 1976. Abstract in Fluoride 9 215-216 1976
  • 23 Waldbott GL. Urinary fluoride and calcium excretion in persons suspected of fluoride intolerance. Henry Ford Hospital Medical Bulletin 5 259-268 December 1957.
  • 24 Manocha SL, Warner H, Olkowski Z. Cytochemical response of kidney, liver and nervous system to fluoride ions in drinking water. Histochemical Journal 7 343-355 1975.
  • 25 Smith EH Jr. Fluoridation of water supply. Journal of the American Medical Association 230 1569 1974.


[PAGE 15 footnote]
*  Okauchee water contained 0.15 ppm fluoride, 37 ppm calcium, 17 ppm magnesium and 164 ppm hardness.
**  Milwaukee water contained 0.95 ppm fluoride, 16.1 ppm calcium, 0.6 ppm magnesium, and 80 ppm hardness.
[PAGE 16 footnote]
*  Woodruff water contained 0.10 ppm. fluoride, 42 ppm calcium, 17 ppm magnesium, and 176 ppm hardness.

+ Dr. George Waldbott: (Deceased: July 17, 1982)

Published by the International Society for Fluoride Research



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