When water fluoridation was endorsed by U.S. health authorities in the 1950s, it was believed that the water fluoride levels which cause skeletal fluorosis were at least 8 times higher (8 ppm) than the level added to water in fluoridation programs (1 ppm). Since that time, however, case reports have shown that just 1.7 ppm fluoride in water can cause debilitating forms of skeletal fluorosis in individuals with kidney disease. (Johnson 1979; Juncos 1972). According to Mayo Clinic doctors, the fact that small-scale studies have detected skeletal fluorosis at just 1.7 ppm “suggests that a few similar cases may be found in [kidney] patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers.” (Johnson 1979). Despite this and other evidence (including voluminous research from India and China) showing skeletal fluorosis can occur at relatively low levels of fluoride exposure, there has yet to be any systematic research to determine the prevalence of skeletal fluorosis in the United States. As a result, the current prevalence in the U.S. and other western countries remain unknown.

The need for systematic research has recently been highlighted by a flurry of studies documenting advanced skeletal fluorosis in the U.S. among people who consume large quantities of tea. According to the authors of these studies, “many” heavy tea drinkers in the U.S. are likely receiving daily fluoride doses that put them in danger of developing skeletal fluorosis. (Whyte 2008). Further, the studies highlight that individuals with skeletal fluorosis — including those with crippling fluorosis — are routinely and repeatedly misdiagnosed as suffering from other bone and joint diseases (e.g., osteoarthritis).

Scientists have warned for decades that diagnosising fluorosis can be very tricky, both because the joint pains can precede detectable bone changes, and the bone changes themselves can closely mimic the appearance of other diseases, including osteoarthritis, renal osteodystrophy, spondylosis, DISH, hyperparathyroidism, and Paget’s disease.  Due to the lack of systematic research on current rates of skeletal fluorosis, the extent to which people with skeletal fluorosis are being incorrectly diagnosed remains poorly understood.

Skeletal Fluorosis in the U.S. — The Misdiagnosis Problem:

“Fluoride toxicity can present in an insidious manner, and clinicians may overlook its signs and symptoms. Unless recognized and the source of excessive fluoride identified and discontinued, fluoride toxicity can be both progressive and crippling.”
SOURCE: Hallanger Johnson JE, et al. (2007). Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 82(6):719-24.

“Our case report illustrates dramatically that fluorosis can lead to severe disability while closely mimicking a wide variety of other disorders… We believe increased awareness of this unusual disease is needed to enable physicians to make the proper diagnosis.”
SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700.

“Although skeletal fluorosis has been studied intensely in other countries for more than 40 years, virtually no research has been done in the U.S. to determine how many people are afflicted with the earlier stages of the disease, particularly the preclinical stages. Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed [as arthritis]… Even if a doctor is aware of the disease, the early stages are difficult to diagnose. ”
SOURCE: Hileman B. (1988). Fluoridation of water.Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News August 1, 1988, 26-42.

“It should also be noted that chronic fluorosis is not easily diagnosed, and that few physicians have ever seen a case. Three of the cases reported in the U.S. literature were not diagnosed until post-mortem examination revealed excessive fluoride content in the bone. It is possible that the disease may be occurring to some extent without having been recognized.”
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 quite possible that many cases of (skeletal fluorosis) have gone misdiagnosed and unreported over the years… The state of knowledge among practicing physicians, even those in high-fluoride areas, concerning the diagnosis of skeletal fluorosis seems to be deficient and should be more carefully assessed.”
SOURCE: Prival MJ. (1972). Fluorides and human health. Center for Science in the Public Interest, Washington D.C.

“Symptoms of fluoride poisoning are actually common in this country. The question is not at all whether they occur, but when and how often they are produced by fluoride… It is true that reports (of skeletal fluorosis in the U.S.) are few. This is both the cause and the effect of the fact that physicians, by and large, are unaware that such a thing exists. It is hardly mentioned in the textbooks or in the medical literature. ”
SOURCE: Exner FB. (1957). Fallacies of the fluoridation thesis. In: J Rorty, ed. (1957). The American Fluoridation Experiment. Delvin-Adair Co, New York. pp. 29-153.

Case Reports of Skeletal Fluorosis in the U.S.:

“Our patient was a 48-yr-old white woman from Georgia, referred for bone and joint pain, kyphosis, and osteosclerosis documented for dual-engergy x-ray absorptiometry (DXA). She reported worsening, throbbing, severe bone and joint discomfort over the previous decade. Painful areas included her elbows, wrists, hips, knees, and ankles. She had increasing difficulty moving around, driving her car, and conducting her activities. . . . Her dietary history disclosed that she imbibed 1-2 gallons of brewed orange-pekoe and pekoe-cut black tea daily since age 12 yr. She purchased the least expensive ‘store brand’ and used seven ‘twin’ bags (3.7 g tea per twin bag) per U.S. gallon of municipal tap water. . . . Her paternal grandmother and several paternal aunts were said to be kyphotic, but she had not been given an explanation. All close paternal relatives drank tea daily. . . . She was 58.5 inches tall with severe kyphosis since approximately age 30 yr. . . . Radiographs of the patient’s skull, hands, thoracic and lumbar spine, pelvis, and knees showed characteristic findings of [skeletal fluorosis], including diffuse osteosclerosis, sparse and coarsened trabeculae, thoracic kyphosis, as well as soft tissue calcification and ossification. . . . . These observations were typical of phase 3 (crippling skeletal fluorosis).”
SOURCE: Izuora K, et al. (2011). Skeletal fluorosis from brewed tea. J Clin Endocrinol Metab. 96(8):2318-24.

“A 45-year-old white male was found to have radiographic findings of a diffusely dense appendicular skeleton, mild trabecular thickening, and multiple thoracic compression fractures indicating structural weakness. Bone mineral density was above the expected range for his age on the lumbar spine and femoral neck. Social history was significant for well-water consumption and daily instant-tea ingestion of 68 oz (1.89 L) for the past 10–15 years. . . . The differential diagnoses included osteopetrosis, Paget disease, hyperparathyroidism, renal osteodystrophy, osteomalacia, and skeletal fluorosis. Given the patient’s history of well-water and instant-tea consumption, radiographic findings, and increased plasma fluoride, the diagnosis of skeletal fluorosis was given. Fluoride sequesters in bone and enhances osteoblast action, thus toxicity leads to dense but brittle bones. The high concentrations of fluoride in instant tea preparations (1) and groundwater contamination with fluoride (2 ) may both have contributed to this patient’s condition.”
SOURCE: Isbel TS, Villareal-Armamento R. (2010). What Is Your Guess? A Case of Thick but Brittle Bones and Instant Tea. Clinical Chemistry 56(6):1041-42.

“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.”
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.

“The fluoride concentration of water from private wells is not routinely measured. In some areas of Arizona, Colorado, Illinois, Iowa, New Mexico, Ohio, Oklahoma, and Texas, high fluoride concentration of the groundwater occurs naturally. Thus, in these areas, as exemplified by the aforementioned patient, it is possible that fluorosis may develop in individuals who obtain their drinking water from private wells.”
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.

“A 68-year-old white male was being followed in a medical clinic for end-stage renal disease. . . . His medical history was significant for hypertension, adult onset diabetes, and end stage renal disease of unknown etiology. His medications contained no fluoride compounds and his physical examination was within normal limits. He had no history of occupational fluoride exposure, although he had worked on a ranch. Routine radiographs revealed diffuse osteosclerosis throughout the spine and pelvis. Calcification of ligaments in the pelvis was also noted. With these radiographic changes and a subsequent iliac crest bone biopsy, a diagnosis of skeletal fluorosis was made. He required no specific treatment for this condition and subsequently died of his renal disease.”
SOURCE: Bruns BR, Tytle T. (1988). Skeletal fluorosis: a report of two cases. Orthopedics 11: 1083-1087.

“A woman with chronic pyelonephritis developed progressive muscular weakness and bone pain. For twenty years she had habitually ingested fluoride-rich soil. Osteosclerosis was found on x-ray examination, and fluorosis was confirmed by bone biopsy. Renal failure augmented skeletal retention of excessive fluoride intake which, in turn, appears to have intensified symptomatic renal osteodystrophy.”
SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

“A 69-year-old man experienced excessive frequent urge to urinate associated with polyuria in 1958. Mild azotemia appeared in 1960, followed by bone pain, arthralgia of the knees and feet, and spontaneous ‘march fractures’ of both feet – a total of 13 by 1963. . . . Skeletal roentgenograms showed healing fractures of the metatarsals and phalangeal bones of both feet, areas of increased bone density with a coarse trabecular pattern involving predominantly the axial skeleton and the calcification of interosseous ligaments, and new subperiosteal bone formation. . . . After treatment with oral calcium supplements and vitamn D, bone pain decreased but the patient experienced additional fractures. Osteosclerosis increased, but serum alkaline phosphatase values decreased to normal. A bone biopsy specimen taken in 1968 showed healing of osteomalacia. Chemical values showed a high concentration of fluoride in serum (14 uM) and bone and in drinking water (2 ppm or 106 uM) relative to the concentration of fluoride in the urine (78 uM). At this point, the patient was advised to stop drinking tap water and to use only fluoride-free spring water or distilled water for both drinking and cooking. Serum fluoride concentrations decreased (to 8 uM), and for a period of approximately 8 years, the patient was relatively free of bone pain and did not experience further fractures. In 1971, renal function temporarily deteriorated further. After peritoneal dialysis, renal function spontaneously improved. In 1974, the patient fell, sustaining a hip fracture that required internal fixation. Osteomalacia has persisted despite vitamin D therapy and reasonable control of systemic acidosis and secondary hyperparathyroidism. These findings were interpreted as representing adult Fanconi’s syndrome wihth osteomalacia and superimposed fluorosis.”
SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. pp. 275-293. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. [See study]

“”It is generally agreed that water fluoridation (1ppm) is safe for persons with normal kidneys. Systemic fluorosis in patients with diminished renal function, however, seems a reasonable possibility… We describe herein two patients in whom evidence of systemic fluorosis was related to three factors: (1) diminished renal function, (2) increased quantities of fluoride in drinking and cooking water (1.7-2.6 ppm), and (3) polydipsia secondary to polyuria.”
SOURCE: Juncos LI, Donadio JV Jr. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222:783-5.

“The findings of a Papago Indian with the second reported case of fluorotic radiculomyopathy in the United States are presented. Neurological deficits occurring in this entity as a manifestation of spinal cord and nerve root bony compression are decribed. This radiculomyopathy is rare but it is of regional importance since fluorosis is endemic in Arizona. The lack of any potential skeletal or neurological hazards from water fluoridation programs for dental caries prevention is stressed.”
SOURCE: Goldman SM, et al. (1971). Radiculomyelopathy in a southwestern indian due to skeletal fluorosis. Arizona Medicine 28: 675-677.

“The development of advanced fluorosis in this patient exposed to drinking water with less than 4 ppm of fluoride was unusual and was probably a consequence of his excessive water intake.”
SOURCE: Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078.

“The diagnosis of fluoride osteosclerosis was proved by the history of a long residence in areas of endemic fluorosis (water F = 1.2 – 5.7 ppm) and by fluorine analysis of the patient’s bones and teeth… Areas in the United States in which dental fluorosis exists and where the fluorine content of the drinking water is over 3 parts per million should be systematically studied by the public health authorities to determine how widespread the condition of osteosclerosis is. All patients with dental fluorosis and anemia and/or signs of renal impairment should have radiographic examinations of the skeletal systems to rule out the existence of fluoride osteosclerosis.”
SOURCE: Linsman JF, McMurray CA. (1943). Fluoride osteosclerosis from drinking water. Radiology 40: 474-484.

See also: Fluoridation, Dialysis, & Osteomalacia

INDIVIDUALS WITH KIDNEY Disease AT ELEVATED RISK OF FLUOROSIS

“[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.

“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.”
SOURCE: Juncos LI, Donadio JV. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222:783-5.

“The finding of [skeletal fluorosis] 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.

“3 ppm wouldn’t protect the individual with renal insufficiency…”
SOURCE: Wallach S. (1983). Surgeon General’s Ad Hoc Committee on ‘Non-Dental Health Effects of Fluoride.” Transcript of Proceedings, National Institutes of Health, Bethesda, Maryland, April 19.

“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.”
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.

No Systematic Studies of Skeletal Fluorosis Rates in U.S. Residents with Kidney Disease:

“As other causes of osteosclerosis, osteopenia, and calcification of ligaments and tendons are common in end-stage kidney disease, fluorosis may be overlooked until it reaches a late stage.”
SOURCE: Applbaum YK. (2010). Imaging of the skeleton and the joints in CKD. p. 208. In: The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease. (Olgaard K, Salusky IB, Silver J, eds.) Oxford University Press.

“A fairly substantial body of research indicates that people with kidney dysfunction are at increased risk of developing some degree of skeletal fluorosis… However, there has been no systematic survey of people with impaired kidney function to determine how many actually suffer a degree of skeletal fluorosis that is clearly detrimental to their health.”
SOURCE: Hileman B. (1988). Fluoridation of water.Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News August 1, 1988, 26-42.

“In the United States, there have been no reported cases of skeletal fluorosis in persons who drink water containing only one part per million (ppm) of fluoride. However, since no systematic studies have been carried out in patients with renal insufficiency, this possibility cannot be excluded with certainty.”
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.

“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 has been estimated that one in every 25 Americans may have some form of 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.