Fluoride Action Network

Exposure Pathways Linked to Skeletal Fluorosis

May 28th, 2012

Excessive fluoride exposure from any source — and from all sources combined — can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include:

  • Fluoridated Water for Kidney Patients
  • Excessive Tea Consumption
  • High-Fluoride Well Water
  • Industrial Fluoride Exposure
  • Fluorinated Pharmaceuticals (Voriconazole & Niflumic Acid)

It is important to stress that these exposure pathways are not exclusive. It is possible that other exposure pathways exist but have yet to be identified, particularly for the pre-skeletal phase of fluorosis, but even for the advanced stages. This is because all stages of skeletal fluorosis, from its preskeletal to crippling phase, closely mimic other rheumatic disorders (e.g., osteoarthritis, rheumatoid arthritis, renal osteodystrophy, spondylosis, DISH), and are thus often misdiagnosed.

Fluoridated Water (Kidney Patients)

“[A] fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.”
SOURCE: Schiffl H. (2008). Fluoridation of drinking water and chronic kidney disease: absence of evidence is not evidence of absence. Nephrology Dialysis Transplantation 23:411.

“Individuals with kidney disease have decreased ability to excrete fluoride in urine and are at risk of developing fluorosis even at normal recommended limit of 0.7 to 1.2 mg/l.”
SOURCE: Bansal R, Tiwari SC. (2006). Back pain in chronic renal failure. Nephrology Dialysis Transplantation 21:2331-2332.

“Persons with renal failure can have a four fold increase in skeletal fluoride content, are at more risk of spontaneous bone fractures, and akin to skeletal fluorosis even at 1.0 ppm fluoride in drinking water.”
SOURCE: Ayoob S, Gupta AK. (2006). Fluoride in Drinking Water: A Review on the Status and Stress Effects. Critical Reviews in Environmental Science and Technology 36:433–487

“The finding of adverse effects in (kidney) patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause.”
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.  [See study]

“It seems probable that some people with severe or long-term renal disease, which might not be advanced enough to require hemodialysis, can still experience reduced fluoride excretion to an extent that can lead to fluorosis, or aggravate skeletal complications associated with kidney disease… It would seem imperative that the magnitude of risk to such a large sub-segment of the population be determined through extensive and careful study. To date, however, no studies of this sort have been carried out, and none is planned.”
SOURCE: Groth, E. (1973). Two Issues of Science and Public Policy: Air Pollution Control in the San Francisco Bay Area, and Fluoridation of Community Water Supplies. Ph.D. Dissertation, Department of Biological Sciences, Stanford University, May 1973.

“It is generally agreed that water fluoridation is safe for persons with normal kidneys. Systemic fluorosis in patients with diminished renal function, however, seems a reasonable possibility. In such patients, fluoride may be retained with resulting higher tissue fluoride levels than in persons with normal renal function.”
SOURCE: Juncos LI, Donadio JV. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222:783-5.

Excessive Tea Consumption

“We describe a 48-yr-old American woman who developed SF from brewed tea. . . .Our patient had elevated bone mineral density . . ., severe chronic bone and joint pain, and kyphosis after consuming 1-2 gallons of brewed orange pekoe tea daily for more than three decades. F(-) levels were high in her serum, urine, and clippings of fingernails and toenails, as well as in our reproduction of her beverage. Renal function was normal. . . . CONCLUSION: Our patient shows that [skeletal fluorosis] can result from chronic consumption of large volumes of brewed tea.”
SOURCE: Izuora K, et al. (2011). Skeletal fluorosis from brewed tea. J Clin Endocrinol Metab. 96(8):2318-24.

“A 49-year-old woman from the state of Illinois, U.S.A., was referred for chronic, widespread, musculoskeletal aches and pains accompanying dense bones.  At age 31 years, she underwent hysterectomy without oophorectomy and had not yet experienced symptoms of menopause.  In her mid-30’s, she became “tired and sore”, and was eventually diagnosed with fibromyalgia by a rheumatologist who reported no inflammatory changes and a positive tender point exam in a fibromyalgic distribution.  She was also found to have osteoarthritis that was particularly  severe  in  her knees.   . . . Appreciation of the significant amounts of F in some modern preparations of  tea suggested to us that [skeletal fluorosis] caused our patient’s high bone mass when she recounted her remarkable volume of instant tea consumed over three decades.  In fact, her beverage, made extra strength in tap water with ~ 1.2 ppm F-, contained 5.8 ppm F- on the day we examined her.  In the U.S.A., this F- concentration exceeds the EPA’s primary standard (enforceable) of 4.0 ppm F- for drinking water, the FDA’s limits spanning  1.4 – 2.4 ppm F- for bottled water or beverages, and the PHS’s optimum levels ranging from 0.7 – 1.2 ppm F- for community water fluoridation. . . . [H]abitual consumption of large volumes of extra-strength instant tea calls for better understanding of the threshold and systemic effects of F contained in this modern preparation of  the world’s most popular beverage.”
SOURCE: Whyte MP, et al. (2008). Skeletal fluorosis from instant tea. J Bone Miner Res. 23(5):759-69.

“We describe 4 patients evaluated at our Metabolic Bone Disease Clinic from May 1, 1997, to July 1, 2006, whose bone disorders resulted from chronic fluoride exposure due to excessive tea intake. Three of these patients had toxic serum fluoride levels (> 15 micromol/L). Although the clinical presentation of the patients varied, all 4 had an unexpectedly elevated spine bone mineral density that was proportionately higher than the bone mineral density at the hip. Other clinical features included gastrointestinal symptoms such as nausea, vomiting, and weight loss; lower extremity pain sometimes associated with stress fractures of the lower extremities; renal insufficiency; and elevated alkaline phosphatase levels. Readily available, tea often contains high levels of fluoride. Obsessive-compulsive drinking behaviors and renal insufficiency may predispose to excessive fluoride consumption and accumulation. The current cases show that fluoride-related bone disease is an important clinical consideration in patients with dense bones or gastrointestinal symptoms and a history of excessive tea consumption. Furthermore, fluoride excess should be considered in all patients with a history of excessive tea consumption, especially due to its insidious nature and nonspecific clinical presentation.”
SOURCE: Hallanger Johnson JE, et al. (2007). Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 82(6):719-24.

“Tea drinking remains popular in the United States and increasingly is suggested to promote health. We caution that skeletal fluorosis can result from consumption of excessive amounts of instant tea because of substantial fluoride levels in some commercial preparations. A 52-year-old white woman consulted in 1998 for dense lumbar vertebras discovered after twisting her back. Spinal discomfort and stiffness for 5 years reflected ‘disc disease.’… Skeletal discomfort intensified during the subsequent year, and included new neck and scapular pain and elbow and knee arthralgias. Bone and joint pains, acquired axial osteosclerosis, well water, soap manufacturing, and periodontal disease suggested skeletal fluorosis… Our encounter with this patient calls for better understanding of the amounts and systemic effects of fluoride in various teas.”
SOURCE: Whyte MP, et al. (2005). Skeletal fluorosis and instant tea. American Journal of Medicine 118:78-82.

“It is possible that fluoride intake from tea may be sufficient to cause fluorosis, and I report here a case which gives some evidence for this. . . . A woman of 55 had been crippled by arthritis for about 25 years. . . . X-rays from the local hospital showed spinal disc degeneration but no obvious signs of fluorosis; some discs showed possible signs of osteoarthritis, and there were some exostoses. . . . She was drinking 3-4 pints of tea daily, and fluoride intake, measured with a specific fluoride electrode, reached over 9 mg. daily. . . . Little more than 3 months after stopping tea-drinking she reported that pain had diminished to the point where she was almost able to do without analgesics, and that mobility had increased so that she had been able to take on a job as representative, involving a considerable amount of walking. The improvement continued, and after 6 months she reported that she was virtually free of pain, and considered she could do without drugs. . . . Possibly some cases of pain diagnosed as rheumatism or arthritis may be due to subclinical fluorosis which is not radiologically demonstrable.”
SOURCE: Cook HA. (1971). Fluoride studies in a patient with arthritisThe Lancet 1: 817.

Industrial Fluoride Exposure

“This paper reports the frequency of occurrence of bone changes caused by fluoride in a population of 358 aluminum smelter workers who had been fluoride exposed for more than 5 years and whose diagnosis had not been made prior to 1971. In the examination, particular attention was paid to degenerative changes of the skeleton and the frequency of spondylosis, arthrosis of the hip and elbow joints as well as changes in the form of diffuse idiopathic skeletal hyperostosis (spondylosis hypeostotica Forestier). A population of 81 foundry workers in aluminum smelters under similar working conditions, but not fluoride exposed, served as controls. . . . Our study shows that hyperostosis of the spine and peripheral skeletal parts occurs more frequently among fluoride-exposed aluminum smelter workers. It is similar to diffuse idiopathic skeletal hyperostosis.”
SOURCE: Runge H, Franke J. (1989). Radiological modifications of the skeletal system among aluminum smelter workers: A 15 year retrospective study. Fluoride. 22: 157-164. [See study]

“Analysis of workers’ complaints showed no specific pain or other symptom that we could refer only to fluorosis…The only characteristic feature would be multiple-joint involvement in the case of fluorosis. This would differentitate fluorosis from monoarticular osteoarthritis (OA), but unfortunately not from multiple-joint osteoarthritis or rheumatoid arthritis (RA). . . . We would like to point out that although fluorosis was rare in our material, only 15.7% of those examined could be assessed as free from any changes in the bones or joints. This finding might suggest that fluoride has nonspecific effects worth evaluating.”
SOURCE: Czerwinski E, et al. (1988). Bone and joint pathology in fluoride-exposed workers. Archives of Environmental Health. 43(5): 340-343.

“In 1242 apparently healthy and actively employed workers of a Canadian aluminum facility, the history of musculoskeletal symptoms, of the incidence of fractures, of neck and back surgery, as well as the x-ray findings were reviewed. A highly significant relationship of exposure to fluoride was established with the frequency of back and neck surgery, fractures, symptoms of musculoskeletal disease and past history of diseases of bones and joints in the absence of the typical findings of skeletal fluorosis. Monitoring exposed workers for the early manifestations of “musculoskeletal fluorosis” is recommended prior to the development of destructive and degenerative changes of the skeleton.”
SOURCE: Carnow BW, Conibear SA. (1981). Industrial fluorosis. Fluoride. 14: 172-181.  [See study]

“The case of chronic intoxication from variable frequent exposure to airborne hydrogen fluoride is presented in a middle-aged man who had been working for ten years at a major oil company operating an alkylation unit. The insidious onset of a wide spectrum of subtle symptoms is emphasized. In view of the marked expansion of the use of hydrogen fluoride in industry, physicians should be alerted to the manifestations of chronic systemic intoxication from this gas.”
SOURCE: Waldbott GL, Lee JR. (1978). Toxicity from repeated low-grade exposure to hydrogen fluoride–Case report. Clinical Toxicology 13: 391-402.

“Fluorotic changes in bones and joints were evaluated in 105 aluminum workers and 20 residents of an endemic fluorosis region in India…The skeletal changes in the aluminum workers exhibited the same characteristics as those of endemic fluorosis. In industrial fluorosis the changes were less advanced than in endemic fluorosis. . . . Whereas in endemic fluorosis, the diagnostic value of skeletal changes is incontrovertible, in industrial fluorosis the findings may be modified by other factors. Among the employees of an aluminum factory the basic group studied, these factors include vibrations, mechanical overstrain, marked variations in temperature and humidity, etc.”
SOURCE: Czerwinski E, Lankosz W. (1978). Skeletal changes in industrial and endemic fluorosis. Fluoride. 11(1): 29-32.  [See study]

High-Fluoride Well Water

“A 54-year-old female resident of Wellston, Okla, was found to have osteosclerosis on a routine chest roentgenogram. Subsequent investigation disclosed the cause of her osteosclerosis to be fluorosis secondary to the ingestion of well water containing [8 mg/L] of fluoride (recommended levels, (0.2 to 1.1 mg/L]). Water samples were also obtained from the 12 wells on properties adjacent to the index case. In three other wells, all at similar depths as the well of the index case, the fluoride concentration of the water was greater than [4 mg/L]. Urine samples from members of the four households who obtain their drinking water from these wells contained elevated urinary fluoride levels. Thus, fluorosis may develop in certain areas of the United States as a result of the natural occurrence of fluoride in the groundwater. Consequently, in known endemic areas, it would appear reasonable to measure the fluoride concentration of the well water at the time of drilling.”
SOURCE: Felsenfeld AJ, Roberts MA. (1991). A report of fluorosis in the United States secondary to drinking well water. Journal of the American Medical Association 265:486-8.

Fluorinated Pharmaceuticals (voriconazole & niflumic acid)

“We have identified a group of transplant patients with periostitis, including the growth of painful palpable exostoses, who were receiving long-term voriconazole therapy. Evaluation identified fluoride excess as the likely cause in subjects in whom a more detailed evaluation was obtained. In addition, discontinuation of voriconazole treatment in subjects with periostitis improved pain symptoms and reduced alkaline phosphatase and plasma fluoride levels. Evaluation of transplant patients taking voriconazole for at least 6 months demonstrated that plasma fluoride levels were uniformly elevated and significantly higher than levels in transplant patients who were not taking voriconazole.”
SOURCE: Wermers RA, et al. (2011). Fluoride excess and periostitis in transplant patients receiving long-term voriconazole therapy. Clin Infect Dis. 52(5):604-11.

“In this article, we review the current literature and illustrate the variety of imaging characteristics of diffuse periostitis in lung transplant patients on voriconazole, a fluoride-containing compound. Many features of our cases resemble periostitis deformans of subacute fluoride poisoning.”
SOURCE: Chen L, Mulligan ME. (2011). Medication-induced periostitis in lung transplant patients: periostitis deformans revisited. Skeletal Radiol. 40(2):143-8.

“Two new cases of osteofluorosis are presented. They are attested by the existence of a bone X-ray densification, by histological lesions of hyperosteoidosis and a large increase in the fluorine content. One is a . . . an 86 year-old man who during 20 years took 500 mg of niflumic acid a day, a non-steroidal anti-inflammatory drug containing 3 fluorine atoms per molecule (i.e., 50 mg fluorine per 250 mg gellule).”
SOURCE: Welsch M, et al. (1990). [Iatrogenic fluorosis. 2 cases]. [Article in French]. Therapie. 45(5):419-22.

“A case of skeletal fluorosis induced by prolonged treatment with niflumic acid, a fast-acting non-steroid antiinflammatory agent, is reported in a 35-year-old woman suffering from rheumatoid arthritis and treated, in addition, with corticosteroids. The case report discussed is, to our knowledge, the third of its kind regarding bone fluorosis resulting from use of this nicotinic derivative. This clinically asymptomatic case of skeletal fluorosis was discovered, as in the 2 previously reported cases, by the examination of bone X-ray (performed as part of the routine work-up for rheumatoid arthritis) which showed evident osteosclerosis. Quantitative histologic study of iliac crest biopsy revealed marked increase in trabecular bone volume and osteoid volume, suggestive of fluorosis. Abnormally high urine and bone fluoride confirmed the diagnosis.”
SOURCE: Meunier PJ, et al. (1980). Niflumic acid-induced skeletal fluorosis: iatrogenic disease or therapeutic perspective for osteoporosis? Clin Orthop Relat Res. 148:304-9.

“An osteosclerosis opacifying the axial skeleton and affecting in particular all of the spine, was observed in two women aged 75 and 42 years who had been suffering from a rheumatoid arthritis developing between 15 and 26 years. It was traced to a chronic fluorine intoxication, stemming from the regular taking, for 10 years and 8 1/2 years, of a non cortisone, anti-inflammatory niflumic acid. This fluorine product has 3 atoms of fluor in its molecule (50.0 mg for a tablet of 250 mg). Its administration to control subjects proved the production of ionized fluor by way of the metabolism, and the accumulation of fluor in the organism.”
SOURCE: Prost A, et al. (1978). [Fluorine osteosis caused by a very long-term niflumic acid treatment in 2 cases of rheumatoid arthritis]. [Article in French]Rev Rhum Mal Osteoartic. 45(12):707-16.