Fluoridation: A Clinician's Experience

GEORGE L. WALDBOTf, MD, Warren, Mich

ABSTRACfz In 1954 I described a case of chronic fluoride poisoning from artificially fluoridated water, In which the patient exhibited a multisymptomatic clinical picture without noticeable skeletal changes. Subsequently, others and I have confirmed this "nonskeletal phase" of the disease from fluoride in 'water and in air (in workers in fluoride-emitting factories and in people residing near such factories) and from fluoride-containing drugs. Further details on this disease arc presented. In view of the constantly expanding use of fluoride in industry as well as its Increase In food, water, and other hidden sources and because of the reactivity of the fluoride ion, the implications of these findings with respect to the etiology of several heretofore unexplained

illnesses are discussed. ( s eo c f'''~ ~ 7- Ob)

MOST PATIENTS with chronic intoxication from a p'oisonous substance exhibit a variety of subtle symptoms before features typical of the respective poisoning become manifest. In chronic lead poisoning, children complain usually of general malaise, headaches, gastrointestinal upsets, and similar vague manifestations for years before the appearance of more tangible evidence, such as the lead line of the gums and the radial palsy.' Similarly, in long-term exposure to carbon monoxide, intermittent episodes of vertigo, chest pain, and headache are com mon long before evidence of damage to the brain and heart develop.' Since these subtle manifestations are common to many other diseases, early diagnosis of any low-grade poisoning is usually most difficult.

It is therefore not surprising that the effects of long-term intake of fluoride other than its characteristic features in bones (osteosclerosis) and teeth (mottling) have not been brought to the attention of the medical profession, despite prolonged and extensive lise of fluoride both for prophylaxis against tooth decay and in the treatment of osteoporosis. Indeed, a wide spectrum of subtle, slowly developing symptoms were described in the classic monograph by Roholrn! 40 years ago in conjunction with skeletal changes in cryolite workers exposed to large amounts of airborne and ingested fluoride. It has since been elaborated upon by other investigators in fluoride-exposed industrial workers,34 in persons residing near fluorideemitting factories,8.n in areas where water naturally contains high levels of fluoride,'! in persons drinking artificially fluoridated water .. •·21 and recently in a case of subacute intoxicarion caused by habitual inhalation of an organofluoride anesthetlc."

On Feb 8-10,1978, the Ad Hoc Committee, Strategy Workshop for Osteoporosis Research, studying short-

Reprint requests '0 Dr. Waldbou. 11670 Marlin Rd. Warren. Mich 48093.

term the use of fluoride ion in doses ten to 100 times those considered effective for prevention of dental

'. caries, advised against the use of this method of treatment because the "potential for long-term toxic effects has not been evaluated." They explained that "unanticipated late manifestations of toxicity" may become evident after many years. Others23 have pointed to the development of gastrointestinal hemorrhage in infants and young children after the use of minute, presumably safe doses (0.5 mg) of sodium fluoride for prevention of tooth decay.

An editorial published in June 1978 by the American Dental Association" also suggested the possibility of adverse effects from the formerly accepted practice of supplementing fluoride in infants and young children and recommended "lowered extra dietary fluoride doses." The administration of sodium fluoride tablets in milligram doses to.pregnant women is no longer legal according to the Food and Drug Administration."

I became aware of adverse effects of fluoridated water'in 1954 and have since encountered several hundred cases oflow-grade nonskeletal toxicity due to the minute amounts present in artificially fluoridated water (1 mg/l,OOO ml). The following case material presents some of the data obtained concerning this disease, with particular reference to its diagnosis.

CASE REPORTS

Case 1. In 1954, a 40-year-old female resident of Bay City, Michlgan, was referred to me by .her family physician for allergic studies because of painful spastic bowels, frequent nausea and vomiting, bloating of the abdomen, polydipsia and polyuria. and persistent migralne-like headaches of about three years' du ration. A diagnostic survey, however, failed to show that allergy was involved. Whenever she was away from the city, her mouth and throat no longer fell dry and she was no longer thirsty, nor did she experience the cramps in

the abdomen and the headaches. Neither she nor I realized at lhal . / time that Bay City'S water had been Iluoridated since 1951. ~

Case 2. In the fall of 1954 the case of a 35.year-old woman of Highland Park, ~ichigan, provided more tangible evidence of

March 1960 • SOUTHERN MEDICAL JOURNAL • Vd. 73. No.3

301

Waldbott • FLUORIDATION

poisoning from fluoridated water." Very noticeable white and brownish stains on her teeth had been diagnosed by her dentist as dental fluorosis. She was constantly nauseated. vomited frequently. had periodic. sharp epigastric pain and diarrhea. and complained of pain in the lower back. Her general health had gradually deteriorated until she was bedridden. Although her physician had suggested that the current illness might be related to drinking water. Highland Park's water. fluoridated since 1952. could not have been responsible for the dental condition because mottling occurs only during the tooth-forming years. up to age 12.

She reported progressive weight loss. had repeated hematuria. uterine hemorrhages. and constant pain throughout her head. Her eyesight had gradually deteriorated. She had noticed scotomas in both eyes and lesions on the arms and legs. resembling somewhat subcutaneous traumatic suffusions. Weakness in the hands and arms prevented grasping certain objects. Furthermore. due to loss of control of her legs and lack of coordination of her thoughts she eventually became incoherent. drowsy. and forgetful and was obliged to give up her housework.

I n her childhood she had lived in a natural fluoride area in China where dental fluorosis was common. Roentgenograms of arms. legs. and pelvis. however. showed no evidence of skeletal fluorosis. which is characterized by thickening of bone substance. calcification of ligaments and tendons. and arthritis of the spine.

The patient was hospitalized for diagnostic studies. Consultations by a neurologist. an orthopedist. an ophthalmologist. a hematologist, a cardiologist. an endocrinologist. and a gynecologist were unrevealing. They considered the illness serious but were at a loss to establish an overall diagnosis. One consultant suggested the disease might possibly be of psychosomatic origin. The examination was essentially negative. except for tenderness in the lumbar spine. exaggerated patellar reflexes. and decreased muscle power in both hands. The only remarkable laboratory finding was a blood calcium level of 11.6 mg/dl. The 24-hour urine specimen contained 1.38 mg of fluoride and another. 1.37 mg.*

Until completion of the preliminary tests in the hospital. the patient had used fluoridated Highland Park water that she had brought with her to the hospital in plastic bottles. After the tests were completed. she began drinking u nfluoridated (0.1 ppm) Detroit water. Within two days the gastrointestinal symptoms and headaches subsided without medication. and she was soon well enough to be discharged.

At home she strictly avoided fluoridated water for drinking as well as for cooking her food and avoided both tea and seafood because of their high fluoride content. The headaches. eye disturbances. and muscular weakness disappeared in a most dramatic manner. After about two weeks her mind began to clear. and she had a complete change in personality. For the first time in two years she was able to undertake her household duties without having to stop and rest. Within a four-week period she had gained five pounds. During the following two years. numerous studies were done with the patient's consent.

On On II. 1955. she was given an intradermal injection of sodium fluoride 0.1 ml of a I: 1.000 solution or 0.1 mg. which produced an erythema about 3 cm in diameter. Within 30 minutes of the injection a red streak developed along the arm from the site of the injection leading toward the axillary lymph glands. The patient had paresthesias in the hands and fingers and a frontal headache which reached its climax after about four hours and lasted for 48 hours. This was accompanied bv general malaise; there were no other symptoms. A few days later she was given a similar test with saline solution with no effect whatsoever.

To determine urinary fluoride excretion. on Aug 15. 1956 she was given 15 mg of sodium fluoride in 300 ml of water on an empty stomach. She was not aware that the water contained fluoride. Within ten minutes her fac~ became flushed and she developed an excruciating headache associated with marked nausea. sensation of flashing lights in both eyes. and severe pain in the arms and legs. This was followed shortly by diarrhea and cramping pain in the lower abdomen. Throughout the day the patient was semicomatose and for three more days felt "dazed." She noticed multiple

·The urine was collected in a glass jar. These values, therefore. were 'probably 100 low since fluoride tends to combine with silicates in glass.

suffusion-like lesions on her body and a swelling of salivary and parotid glands. features which had been present two years previ. ously during her illness.

The episode was so severe that all further testing had to be aban doned. The patient recovered completely without treatment other than avoiding Highland Park's fluoridated water. The ease with which this disease could be reproduced repeatedly by administering 1/ minute amounts of fluoride was striking. /?

Comment, In November 1954, at the request of Dr.

W. P. Martzowka in Saginaw, Michigan, I reviewed the case histories of30 people with an unusual disease. He had become suspicious of fluoridated water because their illness gradually cleared completely after termination of fluoridation in Saginaw, Nine of the 30 people described a disease identical to that of the Highland Park case. Some had had relief when they were away from Saginaw for even short periods, Most of them had not been aware they had been drinking fluoridated water until they were confronted with voting on fluoridation. Some of the 21 individuals whose illness I had not related to fluoride at that time suffered exclusively from bladder and bowel symptoms which, as I later learned, are also a part of the clinical picture of chronic fluoride poisoning. Another patient, a I2-year-old boy, had epileptiform convulsions, probably caused by calcium deprivation, a major feature of acute fluoride iruoxication.!"

Case 3. One of the Saginaw patients, a 42-year-old salesman. was about to give up hisjob because of progressive pain and numbness in his hands which prevented grasping the steering wheel of his car. This condition became so severe that he often had to stop on the highway. Finally he became suspicious of Saginaw's water because the disease invariably improved when he was on extended sales trip, away from Saginaw. When fluoridation was abandoned there. he quickly recovered.

Comment. In contrast to the Saginaw cases, in which the illness was recognized after cessation of fluoridation, in Windsor, Ontario, ill effects were detected after fluoride was introduced into the water supply on Sept II, 1962. The local health department did not announce in advance when fluoridation would begin. This afforded an excellent opportunity, more reliable than a double-blind test, to determine whether fluoridated water was the culprit. Two weeks after its initiation, when the press announced the event to the public, eight individuals had diagnosed their own dis-

ease. It

Cases 4,5, Two of the eight. a 57-year-old nurse and a 38-year-old woman. who had been in the habit of drinking one or two glasses of water before breakfast. suddenly had abdominal cramps and vomiting immediately after their customary morning drink. During t lie course of the day, they developed headaches. pain in rhe lower spine. and numbness and pains in the arms and legs. Never before had they had any such discomfort. They were not then aware thai Windsor's water was being fluoridated. The nurse's physician first provisionally considered a stomach ailment. but his medication was of no avail. After several days of careful observation. he suspected the water might somehow be involved and advised her to disconrin ue drinking il but asked her not 10 disclose his diagnosis 10 anyone lest it jeopardize his position in the eyes of some of his colleagues. The other patient resorted to the use of distilled water on her own. Bolh recovered promptly upon eliminating fluoridated water.

Case 6. A I :~-year-old schoolgirl had increasingly sever ..

302 March 1980 • SOUTHERN MEDICAL JOURNAL • Vol 73, No.3

Ilti!:rainc-likc headaches starting in mid-September 1962. Simultaneollsly. pain and numbness in the arms and legs and a distinct deterioration in her mental alertness interfered with her attendance 31 school. A consulting neurologist ruled out a brain tumor. and inlradermal skin tests to determine whether the headaches were of 311ergic origin were negative. On the advice of an individual who had been similarly affected. the child stopped drinking Windsor water. (-ler illness began to subside and after ten days her health was completely restored. On Mondays and Thursdays. however. the headaches recurred when. inadvertently. after gym classes, she quenched her thirst with Windsor tap water. These recurrences ceased upon confining her drinking at school to her own distilled •• IICr. Subsequently, a double-blind test under the guidance of the Windsor physician confirmed the relationship of the disease to nuoridated water.

Comment. The Windsor and Saginaw cases also recurrence on its resumption, and recurrences after

proved beyond doubt that no chemical other than fluoride intake from sources other than water (all

fluoride caused the disease, because the illness oc- without the patients' knowledge that they-were being

curred after the addition and subsided promptly after exposed to or consuming the halogen) and their fail-

rhe removal of fluoride from the drinking water, with- ure to respond to other therapeutic measures clearly

out the patients' knowledge. Numerous similar cases established the diagnosis.

have since come to my attention from many fluori- In many instances, additional double-blind studies

dated areas of the United States. In Milwaukee, in were done. After strict elimination of fluoridated wa-

April 1969, I interviewed several patients who devel- :/ ter, the patients received three identical bottl~s of oped the disease shortly after moving into the city.26 V' w.at~r labeled No.1.' 2, or 3. !wo bottl.es contained

Case 7.The climax of my experience wasthe case ofa 45-year-old distilled water, while the third contained 1 ppm

male Milwaukee resident, examined on April2, 1976, who moved to fluoride as sodium fluoride. The patients consumed

three different localities. during a three-year period." His .illness the water of bottle No.1 for one week bottle No.2 the

promptly cleared each time he moved away from the fluoridated . '. .

water supply of Milwaukee and recurred upon his return. He had second, and bottle No.3 the third. Neither the patient

had m~ kno~ledge of f1~orida~ion nor o~ the .fac~ that in the three nor the physician was aware which bottle contained

towns m which he regained his health his drinking water was not fluoride. Other tests consisted of injections of NaF at

fluoridated (0.1 - 0.15 ppm).

Comment. Other physicians have brought similar cases to my attention. The following account of a patient studied by Dr. C. D. Marsh of Memphis. Tennes- .I see, is a typical example. II'

Case 8. A 62-year-old woman residing in Memphis (not fluoridated at that time), invariably developed the above-described symptoms on trips to Washington, DC, and Richmond, Virginia, during 1952 to 1956, and always improved promptly within a few days after her return home. 1M This experience drew her attention to drinking water as a possible source of her trouble, though she had no kllOlvledge of fluoride or Fluoridatlon. When she learned that both 1I'"shington and Richmond added fluoride to the water supply, she averted recurrences on future trips to the two cities by taking several bottles of Memphis water with her and avoiding fluid foods.

She subsequently had sudden new episodes of this illness, this time 10 her surprise while she was at home. Dr. Marsh was able to trace these recurrences to a tranquilizer (trifluoperazine) prescribed by him and. on another occasion, to a new toothpaste. Neither she nor her physician had been aware that both the drug and the toothpaste contained fluoride.

After the patient had regained her health, 1 gave her. with her consent. an intradermal injection of 1 mg of fluoride. She was not ;II,'are of the nature of the test. Within half an hour she developed excruciating pain in the abdomen, headache, backache, and profuse nasal discharge, followed by diarrhea and lethargy-the same group of symptoms from which she had suffered on previous occasions from fluoridated water, toothpaste, and the fluoride-containing Iranquilizer. Subsequently, a double-blind test carried out by' Dr. Marsh further confirmed fluoride as the cause of the disease.

DISCUSSION Diagnosis

The events in these cases leave no doubt that the illness was caused by fluoridated water. The prompt recovery when no longer consuming the water, the

TABLE 1. Number of Cases of Nelgt-borhood Auorosls Stude<!

Dunnville. Ontario (1968) Wabash. Indiana (1969)

No.o/Cam 28

6

Fertilizer factory Secondary aluminum smeller

Sourrt

Kitirnat, BC (1971) Bolzano, Italy (1971)

22

Aluminum smelter

24

Aluminum and magnesium smelter

Clarington. Ohio (1972) Buckeystown. Md (1976) Urbana. Ohio (1978)

36

Aluminum smelter

58

Aluminum smelter Enamel smelter

TOIaI

various concentrations.

The manifestations encountered in the above cases are identical to those observed in individuals working in or residing near fluoride-emitting factories, except for the additional respiratory involvement in intoxication from airborne fluoride. I have studied nearly 200 cases here and abroad (Table 1), some of which have been described elsewhere." In 1978 Waldbott and Lee!

reported a detailed account of a patient who was exposed intermittently for ten years to HF fumes in an oil refinery and who exhibited the identical clinical picture. The first detailed report in the US literature was that of a 27-year-old nurse, habitually sniffing a fluoride-containing anesthetic, who manifested the same symptoms before the development of skeletal changes."

Laboratory Criteria

In an attempt to establish laboratory criteria for this disease, I have studied urinary fluoride excretion in more than 300 patients and carried out other biochemical determinations. In my experience, urinary fluoride measurement is not reliable in determining exposure to or ingestion of fluoride unless the values are markedly elevated, which is unlikely when fluoridated water is consumed at 1 ppm (about 1.0 to 1.5 mg of fluoride a day). Urinary fluoride certainly provides no clue concerning an ill effect from the halogen, since some patients with severe symptoms eliminated in their urine less than 1.5 mg of fluoride, whereas others

Waldbott • FLUORIDATION 303

Mf. R.R. 43 'If. Arthritis

Ca++ In urine mQj24 hr.

800

F-In urine mQ/24 hr.

5

600

6.8 mg. F- orally

~ Low Co ++ diet

~\ 1

4

lC XXX

3

High Co" diet

~

400

2

200

-- on F- water DISTILLED WATER __

0.8 p.p.m.

X ARTHRALGIA

I

Urinary F- and Ca" excretion in 43-year-old man with chronic artlvitis (0.8 ppm in drinking water) on low and high calcium diets. Notice positive correlation of urinary ftuoride with calcium levels. High urinary fluoride excretion at outset of study was caused by excessive consumption of tea.

with higher values showed no ill effect. We must also consider that young children have a greater tendency toward fluoride retention than adults. Their low urinary fluoride values, therefore, can be misleading with regard to evaluating fluoride intake and its effects on health. Moreover, after cessation of excessive fluoride intake, larger amounts than are being taken into the system are being excreted in the urine due to sequestration of stored fluoride."

Some correlation of urinary fluoride and calcium excretion was noted occasionally, as in a 43-year-old man who was a heavy tea drinker* (Figure), but this finding was by no means consistent. Similarly, increased levels of alkaline phosphatase, lactic dehydrogenase, and serum uric acid were noted but were not sufficiently consistent to be significant. In September 1978 I observed a 29-year-old woman with low serum copper values (87 JLg/dl) (normal, 90 to 150) and high urinary copper values (75 mg/24 hr) (normal, 0 to 38) which became normal as the patient's symptoms of poisoning (mainly paresthesias, myopathy, headaches, arthralgia, and episodes of gastroenteritis) subsided after switching to distilled water. A disturbance in copper metabolism has been reported by Allcroft and Burns!" in fluorosis of cattle. I have also noted minor electroencephalographic and retinographic changes coincidentally with the neurologic features, which likewise cleared as soon as the patients recovered. Critique

During the 1950s and early 1960s, numerous authors took issue with the diagnosis of nonskeletal fluorosis in some of the cases described herein. It has

\ ·Tea leaves contain lip to 200 ppm Illioride.

been stated that no other physicians have reponed nonskeletal and nondental changes in fluorosis.w Ac-

----

tually many of my patients were referred to me lQ

confirm another physician's diagnosis of fluor!i_e poisoning." Objections have been raised concerning the technic of the double-blind tests because in some 01 my studies the concentration-not the dose-of fluoride was higher than 1 pprn.i" Throughout the years I have made numerous modifications of this test, always with the same results. Some have said the diagnosis has not been "documented,"31.32 referring possibly to the absence of fluoride determinations in the blood. Serum fluoride assays are desirable, especially in acute intoxication, but because the halogen is promptly removed from the bloodstream, they do not represent an obligatory criterion of fluoride exposure, and certainly not of adverse effects due to fluoride.

Fluoride determinations of the iliac crest, performed at my request on several individuals, were in the range of 450 to 550 ppm, values which some COilsider "normal" and others consider slightly elevated."

Wide Spectrum of Symptoms

The multiplicity of symptoms, their vagueness in the initial stage of the disease, and the fact that they are common to many other diseases have been another reason for questioning the diagnosis." Fluoride is one of the most active of the electrolytes and it readily penetrates the membranes of every cell in the body. It is present at high levels in soft tissue,26 not exclusiveh in teeth and bones as formerly believed.3s We mllst therefore anticipate that in chronic fluoride intoxication numerous organs are involved in view of its known action on many enzymes and its strong affinity

for calcium. Ii'

It has recently been reported that in an acid body fluid (gastric juice, urine) fluoride tends to form the irritating hydrofluoric acid;" which provides a reasonable explanation for the development of gastritis in hyperacidic patients and for urinary tract disease. In

60 retired workers of a fluoride-emitting aluminum smelter, Czerwinski and Lankosz" encountered an incidence of gastritis in 50% and of gastric duodenal ulcers in 12%.** In a 9-year-old boy, who was twice subjected to gastric surgery, doses of fluoride equivalent to those consumed in water fluoridated at 1 ppm induced gastric hemorrhage before physicians recognized that the damage was caused by fluoride tablets.26 Some infants have had gastrointestinal bleeding caused by daily ingestion of vitamins containing 0.5 mg offluoride.P In a recent survey in an Ohio town, colitis occurred in 21.7% and acute abdominal episodes suggestive of bowel obstruction in 17.8% of 109 cases / exposed to fumes from an enamel srnelte r.P It-

J oint involvement, one of the most common features

··Castric ulcer was also encountered ill skeletal Iluorosis due 10 hOlbilllal inhalation ofa Iluuride-containing 'lneslilelic2<!

304 March 1980 • SOUTHERN MEDICAL JOURNAL • Vol 73, No.3

of skeletal fluorosis, is frequently encountered in the ~;:;;keletal stage already described. Pinet and Piner" h-;e shown that the radiologic findings of endemic skeletal fluorosis ( Itl8 cases) in the Sahara are identical to those attributed elsewhere in elderly persons to "aging." With advancing age, fluoride levels in the body increase, as does also the incidence of arthritis ..

Damage to arteries is suggested by the finding of high fluoride levels (up to 8,400 ppm) in two individu;115 less than 20 years old from Grand Rapids (fluoridated since 1945) and 2,340 ppm in another individual in a non fluoridated city.3s In the aorta fluoride deposilion does not correlate with that of calcium," and thus irs effects are not likely to be neutralized by combining with calcium. In one premature infant with calcification of arteries throughout his body, the aorta contained 59 ppm fluoride." Pericapillary toxic inIlammation was found on histologic examination of Chizzoia maculae,II.43.44 a feature (described later) occurring early in the disease, which might conceivably .. represent the initial stage of a calcifying process. .

Kaul and Susheela'" elaborated on the explanation of the neuromuscular involvement. Polydipsia and. polyuria have been documented repeatedly in fluorosis," as well as experlmenrally.v-? The evidence f have presented furnishes a reasonable explanation lor the multiplicity of the manifestations.

In reviewing the wide spectrum of symptoms, it ,ltould be noted that often only a few symptoms are present, rather than the complete clinical picture described, For instance, a 17-year-old white boy had excruciating chest pain (fibromyositis?) for three years associated with polydipsia and polyuria (up to 3,530 nil/day, containing 3.2 mg of fluoride) and frequent headaches. After other possible explanations for the disease were ruled out he eliminated fluoridated wa-· ter. whereupon the pain subsided completely. On one occasion when the patient inadvertently neglected to follow strictly his distilled water regimen the pain rerurred for two days. Arthritis dominated the clinical picture in the patient in the Figure, lower urinary tract disease or colitis was predominant in others.

I n several publications,II.43.44 attention has been drawn to the suffusion-like, round or oval, pinkishhrown lesions on the extremities and trunk, mainly. in women and children, .designated Chizzola maculae, which must be considered an early and important diagnostic sign of the disease. These lesions clear after li\'e to seven days without changing color, in contrast 10 traumatic suffusions. They are usually asymptomatic but do occur in conjunction with mottled teeth in children, especially during the summer rnonths.

Implications of Findings

. The omnipresence of fluoride in the environment, lis slrong reactivity, and its presence in numerous or-

TABLE 2. Examples 01 Hidden Sources 01 Auorlde .....

Air near welding operations

in fertilizer factories

Asbestos

Bottled water

Coal

Detergents

Dust near aluminum smelter

fiberglass factory

Fertilizer

Pollen

Tobacco

Wood dust

ppm 0.6· 157· 0.6· 10.2··

70 ·579 0.8· 12.2 14·1440 0.4·65.4 5420·6200 40.4

0.003·41.1 2.4·5.62 17·26.8

1.1 • 12.6

·0.5· 112 rriglcu m. ··0.5 • 8.5 mglcu m.

gans ofthe body are likely to have far reaching implications. They might furnish a clue to the etiology of certain illnesses of unknown causes. Fluoride enters our body from food, water, and air, and from many other hidden sources in our environment (Table 2).

During recent decades the great expansion of the use of fluoride, especially in the smelting, glass, enamel, oil, and 'numerous other industries, has paralleled its increase in our daily diet, in our water supplies, and in the air we breathe. Would it not be desirable, therefore, to explore to what extent this highly reactive ion present in everybody's bloodstream contributes in a given population to the etiology of certain kinds of arthritis, gastritis. colitis. lower urinary tract disease, chronic headache. and other neurologic symptoms which in the past have defied a satisfactory explanation?

References

I. Waldbott GL: Httdlh Effects of Environmml41 Pollulanls. St. Louis. C. V.

Mosby Co .• 2nd Ed. 19'78. pp 141·150; 105

2. Roholm K: Fluorine I~: A Clinittd Hygienic Study. Copenhagen.

Arnold Busck, 1957

3. Franke J. Rath F. Runge H. et al: Industrial fluorosis. FluorUU 8:61·85. 1975

4. Czerwinski E. Lankosz W: Fluoride-induced changes in 60 retired alurninum workers. Fluoritk 10:125·156. 1977

5. Waldbott GL. Lee JR: Toxicity from repeated low-grade exposure to hydrogen fluoride-cease report. Clin Toxicol 15:591-'102. 1978

6. Murray MM. Wilson DC: Fluorine hazards with special reference to some social consequences of industrial processes. Lance; 2:821·824. 1946

7. Schmidt CW: Auftreten von Nachbarschaftsl1uorose unter der Bevolkerung einer sachsischen Kleinsradt. Disch Gtsundl,~lsw 3 I: 1271·1274. 1976

8. Zhavoronkov AA: Non-skeletal forms of fluorosis. ArM Patol 59:83·91. 1977

9. Waldbott GL. Cecilioni VA: "Neighborhood" fluorosis. elin Taxieol 2:587·596. 1969

10. Waldbou GL: chronic fluoride intoxication due to air pollution. Proceedings of the Second International Clean Air Congress of the International Union of Air Pollution Association. Dec 6-11. 197~. Washington. DC. Englund·:HM. l3eery WT (eds). New York. Academic Press. f971

II. Waldbott GL. Steineg~erS: New observations on "Chizzola" maculae.

Proceedings of the Third International Clean Air Congress. Dusseldorf. Federal Republic or Germany. Oct 8·12. 1973. Dusseldorf. Verlag des Vereins Deutscher Ingenieure, 1975. p A65

12. Waldbott GL: Pre-skeletal fluorosis near an Ohio enamel factory: a preliminary report. Vet Hum ToxicoI21:4.8. 1979

15. Frada G. Mentesana G. Nalbone G: Richerche sull fdrofluorosi, Minnva Mtd 54:451·459. 1965

14. Waldbott GL: Chronic fluorine intoxication from drinking water at the one part per million concentration: a case report. Inl Arch Alkrgy Appl Immunol 7:70·74. 1955

Waldbott • FLUORIDATION 305

15. Waldbon Gl: Incipient chronic fluoride intoxication from drinking water, I. Report on 52 cases. Acta Med Scond 156:157-168. 1956

16. Wa1dbon Gl: Tetaniform convulsions precipitated by fluoridated drink-

ing water. Corifin Neural 17:339-347. 1957 .

17. Waldbon Gl:Urticaria due to fluoride. Acta Allergol 13:456468. 1959

18. Waldbon (;l: Fluoride in clinical medicine (monograph).lnt Arch Allergy Appll",munol 20 (suppl 1): 1962. pp 1-60

19. waldbon Gl: Hydrofluorosis in the USA. Fluonk 1:94-102. 1968

20. Perraborg HT: Hydrofluorosis in the fluoridated Milwaukee area.

Fluoride 10: 165-169. 1977

21. Giimbergen GW: A double-blind test for determination of intolerance to fluoridated water (preliminary report). Fluoride 7: 146-152. 1974

22. Klemmer PI; Hadler NM: Subacute fluorosis. a consequence of abuse of all organoffuoride anesthetic (pan 1). Ann Inurn Med 89:607-611. 1978

23. Shea II. Gillespie SM. Waldbon Gl: Allergy to fluoride. Ann Allergy 25:38lr.391. 1967

24. Concern about dietary fluoride supplementation (editorial). J Am Den; Assoc 96: 1158. 1978

25. Oral prenatal drugs containing fluorides for human use. Fed Reg !l1:23248 (May 28). 1975

26. Waldbon Gl. Burgstahler AW. McKinney Hl: Fluonllation: The Grea; [)ikmmo. lawrence. Kansas. Coronado Press. 1978. pp 110. 111.249-251; 253: 148-168; 162

27. Likins RC. McOure FJ. Steere AC: Urinary excretion of fluoride following defluoridation of a water supply. Public Heallh Rep 71 :217-220. 1956 28, Allcrofl R. Burns KN: Alleviation of industrial fluorosis in a herd. Fluoride 2:55-59. 1969

29. Fluoride. Tuth and Health. Report of the Royal College of Physicians of london. Pitman Medical. 1976. p 63

30. Jenkins GN: Fluoride. World Rev Nutr Diet 7: 138-203. 1967

!II. 32.

33. 34.

Menezer IF: Fluoridation and the allergist.J AJlhma Res !I:121-131. I",.,. Waldbon ci, Dr. Waldoon's reply re fluoride allergy (lener).J Asthma H 3:249-251. 1965 ..

Waldbon Gl: The physiologic and hygienic aspects of the absorp'It", .. inorganic fluorides. Arch Environ Health 2:155·167. 1961 .

Schlesinger .ER: Statements on adverse systemic effects Irom fluorida, ewater. Fluondes and Human Health. WHO Monograph Senes No. 59, 19:.·

p 309 .

Smith FA. Gardner DE. leone NC. et alr The effects of the absorption ... fluoride. Atch Environ Health 21 :330. 1960

Whitford GM. Pashley DH. Stringer GI: Fluoride renal clearance. pH-dependent event. Am J PhYJiol 230:527-532. 1976

Pi net A, Piner F: Endemic fluorosis in the Sahara. Fluoride I :86-93. I ~"i. Ceever EF, McCann HG. McClure Fl. et al: Fluoridated water, skeltl' structure, and chemistry. HSMHA f(eaith Rep 86:820-828. 1971 .

Waldbon Gl: Fluoride and calcium levels in the aorta. E.'pm"", 22:835-841.1966

Kaul RD,.Sushec:la AK: Ev.idence of muscle liberdegeneration in rabbIt. treated With sodium fluoride. Fluonde 7:177-181. 1974'

Whitford GM. Taves DR: Fluoride-induced diuresis: .J>lasma concenu, tions in the rat. Proe Soc Exp Bioi Med 137:458460. 1971

Whitford GM. Taves DR: Fluoride-induced diuresis; renal-tissue suh",· concentrations. functional, hemodynamic. and histologic correlates in Ih, rat. Anesthesiology 39:416427, 1973

Cristofolini M. largaiolli 0: Le Macchie di Chizzola. Riv Mtd Trentia ·1 fasc 'I, 1966

Waldbon Gl, Cecilioni VA: "Chizzola" maculae. Culis 6:331-334. :1:1: 1970

35.

36. 37. ss.

39.

40,

41.

42.

43.

44.

45. Waldbon GL, Oelschlager W: Fluoride in environment. Fluoride 7:~~". 222, 1974

Continuedfrom page 287

13. Mount HTR: Hydrocortisone in .the rreatment of intervertebral disc protrusion. Can Med Assoc J 105: 1279-1280. 1971

14. Winnie AP, HanmanJT; Meyers HlJr, et al: Pain clinic 11. Intradural and extradural corticosteroids for sciatica. Antsth Analg 51 :990-1003, 1972

15. Dilke TFW, Burry HC. Grahame R: Extradural corticosteroid injection ill management of lumbar nerve root compression. Br Med J 2:635·6:1;. 1973

16. Brown FW; Management of diskogenic pain using epidural and in. tradural steroids. Clin Orlhol' 129:72-78, 1977

306 March 1980 • SOUTHERN MEDICAL JOURNAL • Vol 73, No.3

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