One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These “safety thresholds” have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. Fluoride advocates have claimed that no one in the population will be harmed by fluoride exposure when the (1) the bone fluoride content is less than 6,000 ppm, (2) the daily dose is less than 10 or 20 mg/day, (3) the water fluoride content is less than 4 or 8 mg/L, (4) the urinary fluoride content is less than 5 ppm, and (5) the blood fluoride content is less than 95 ppb.
The central fallacy with each of these alleged safety thresholds, however, is that they overlook the wide range of individual susceptibility in how people respond to toxic substances, including fluoride. As the research cited below shows, studies have repeatedly found that people exposed to the the same dose, and the same duration, of fluoride can exhibit markedly different effects. (Similar findings have been found with respect to water fluoride level.) Research has also found that people can develop skeletal fluorosis at far lower bone fluoride levels than are supposedly necessary to cause the disease. Consistent with this, research has found that people exposed to the same water fluoride level, the same dose, and the same duration, of fluoride can exhibit markedly different effects. In the same group of fluoride-exposed workers, for example, some can develop fluorosis within just 2.5 years while others don’t show any changes after 25 years. (Roholm 1937). Similarly, some workers can remain symptom-free even in the advanced stages of skeletal fluorosis, while others can suffer significant symptoms during the earliest stages of the disease. (Franke 1975). The notion, therefore, that there is some uniform upper limit of fluoride exposure that will not produce skeletal fluorosis among anyone in the population is simply incompatible with current knowledge about the variability in how individuals of different nutritonal, health, and genetic backgrounds respond to fluoride exposure.
VARIABLE DEGREE OF SKELETAL FLUOROSIS AT SAME BONE FLUORIDE LEVELS:
U.S. health authorities have long contended that skeletal fluorosis does not occur unless the bone fluoride levels reach a certain threshold concentration. Specifically, it is claimed that the earliest “pre-clinical” phase of skeletal fluorosis does not develop until at least 3,500 ppm fluoride is in the bone, that the first clinical phase of the disease does not develop until 6,000 ppm, and the final crippling phase does not develop until the bone has 8,400 ppm. (PHS 1991). Studies, however, have repeatedly found that people with skeletal fluorosis can have levels far below this range. Indeed, individuals with crippling skeletal fluorosis in the United States have been found to have as little as 1,900 ppm in their bone — a concentration that the PHS contends should not even produce the earliest symptoms of the disease. (Bruns & Tyle 1988).
| Bone Fluoride Levels in People with Skeletal Fluorosis vs. the Alleged Threshold Concentration |
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| Study | Degree of Fluorosis | Bone F | % of Alleged Threshold (DHHS 1991) |
| Bruns (1988) | Stage III | 1,900 ppm | 23% (8,400 ppm) |
| Sandberg (1985) | Stage I | 2,640 ppm | 44% (6,000 ppm) |
| Wepp-Peploe (1966) | Stage III | 2,530 ppm | 30% (8,400 ppm) |
| Morris (1965) | Stage I | 2,040 ppm | 34% (6,000 ppm) |
| Singh (1961) | Stage III | 600 ppm | 7% (8,400 ppm) |
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“[A]vailable data suggest that there is wide variability in individual tolerance to toxic effects of skeletal accumulation of fluoride.” “Fluoride concentrations of 200 to 6500 ppm have been reported in bones which were ‘normal’… But bones from patients with severe chronic fluorosis have been found to contain 700-7000 ppm, 905-13,580 ppm, 1120-6050 ppm, and 2040-11,500 ppm. This overlap with the ‘normal’ range is indicative of wide variability in individual sensitivity to harm.”
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.
“Singh et al (1961) described skeletal fluorosis in individuals with F levels in bones in the 700 to 1600 ppm range. This F level in bones is far below that at which many claim fluorosis cannot occur. Data published by Call demonstrated that F content of bones does not parallel the F content in soft tissue organs. Therefore the presence or absence of ill-effect due to fluoride cannot be established on the basis of the F content of bones.”
SOURCE: Waldbott GL. (1968). Hydrofluorosis in the U.S.A. Fluoride 1: 94-102.
“From tabulations of the present study, it is apparent that the degree of bone change does not correlate well with the amount of fluoride present in the bone.”
SOURCE: Morris JW. (1965). Skeletal fluorosis among Indians of the American Southwest. American Journal of Roentgenology, Radium Therapy & Nuclear Medicine 94: 608-615
“The fluoride content of bone does not appear to be the only factor contributing to the onset of fluorosis. Other metabolic factors must be considered. Concentrations of fluoride from 0.50% to 0.75% (dry, fat-free basis) have been found in ribs, sternum, and vertebrae during postmortem studies of persons with endemic fluorosis, whereas McClure et al reported fluoride values as high as 0.51% to 0.65% in various regions of the skeleton with no associated malfunction or microscopically detectable bone changes.”
SOURCE: Marier JR, et al. (1963). Accumulation of skeletal fluoride and its implications. Archives of Environmental Health 6: 664-671.
Variable response to same dose of fluoride:
For over 40 years health authorities stated that in order to develop crippling skeletal fluorosis, one would need to ingest between 20 and 80 mg of fluoride per day for at least 10 or 20 years. Although health authorities have conceded that this estimate was incorrect, they still contend that there is a single threshold dose (10 mg/day for over 10 years) below which skeletal fluorosis will not develop. (NRC 1993). The idea, however, that there is a uniform safe dose is at odds with research showing great variability in how different individuals respond to one and the same dose of fluoride.
“This pilot study has demonstrated a significant problem of DF [dental fluorosis] and SF [skeletal fluorosis] in two villages in northern Tanzania. Why children from the two villages appear to be equally affected by fluorosis despite significantly higher fluoride levels in the water sources in Tindigani is not clear.”
SOURCE: Shorter JP, et al. (2010). Comparison of two village primary schools in northern Tanzania affected by fluorosis. International Health 2:269-74.
“Metabolically active and vascular bones of children accumulate fluoride at faster and greater rate than adults (at the sites of active growth). In calcium deficient children the toxic effects of fluoride manifest even at marginally high (> 2.5 mg/d) exposures to fluoride.”
SOURCE: SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65:371-81.
“It has been a consistent observation in epidemiologic studies that the clinical severity of fluoride-induced toxic effects is highly variable among persons living in the same environment and exposed to the same risk of fluoride ingestion.”
SOURCE: Wang Y, et al. (1994). Endemic fluorosis of the skeleton: radiographic features in 127 patients. American Journal of Roentgenology 162: 93-8.
“In our study… this spectrum (of radiological features in fluorosis) was present in subjects living in the same village and sharing a water source. Obviously factors other than the amount of fluoride ingested are important in determining the type of skeletal change that occurs in fluorosis.”
SOURCE: Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with calcium intake. Skeletal Radiology 22: 257-61.
“Skeletal fluorosis is highly variable in its clinical severity among individuals living in the same environment and exposed to the same risk of fluoride ingestion… A number of factors govern the amount of fluoride deposited in the skeleton. Important factors include: 1) age of exposure; 2) the duration of exposure; 3) the dose of fluoride (as reflected in the blood concentration); 4) nutritional status; 5) renal status; and 6) individual biological variation.”
SOURCE: Department of Health & Human Services. (U.S. DHHS) (1991). Review of Fluoride: Benefits and Risks. Report of the Ad Hoc Committee on Fluoride, Committee to Coordinate Environmental Health and Related Programs. Department of Health and Human Services, USA.
“We suggest that predisposition to fluorosis (chronic toxicity) is biochemically mediated and genetically determined. This would explain the marked variation in fluorosis prevalence in areas with comparable levels of fluoride intake and the selectivity of the disease within the same area. Further studies are necessary to elucidate the complex interaction between calcium, iodine, sex hormones, vitamins and fluoride ions.”
SOURCE: Anand JK, Roberts JT. (1990). Chronic fluorine poisoning in man: a review of literature in English (1946-1989) and indications for research. Biomedicine & Pharmacotherapy 44: 417-420.
“Individual differences in sensitivity to noxious fluoride seems to be important… [I]t is quite possible to be an aluminum smelter worker for 30 years or longer without showing fluoride-caused bone changes, whereas others develop symptoms of fluorosis after only 10 years…”
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.
“[M]any problems remain unclear. For instance, the disease in many people in highly endemic areas may be very severe whereas approximately half of the local population have no obvious fluorotic symptoms or signs. Patients live in the same village and drink the same high fluorine content water but their presentations differ. In some, osteoporosis and osteomalacia are predominant while in others osteosclerosis is predominant.”
SOURCE: Xu JC, et al. (1987). X-ray findings and pathological basis of bone fluorosis. Chinese Medical Journal 100:8-16.
“Because, despite painstaking research, none of the known causes of bone fluorosis could be found in our patient, a new pathomechanism is being offered for discussion, i.e., increased renal or intestinal absorption or an increase of fluoride deposited in the bone; i.e., an inborn or acquired error of fluoride metabolism. We recently observed a similar case with none of the well-known origins. . . . There may be a so far unknown pathomechanism which is related to increased renal or intestinal absorption of fluoride or increased bone deposits.”
SOURCE: Sandberg D, Zichner L. (1985). A case of bone fluorosis of undetermined origin. Arch Orthop Trauma Surg. 104:191-95.
“The considerable individual variability of skeletal response to excessive fluoride ingestion implies that causative factors other than total daily ingestion of fluoride exist.”
SOURCE: Christie DP. (1980). The spectrum of radiographic bone changes in children with fluorosis. Radiology 136:85-90.
“it is an enigma that people from the same area, drinking water from the same source, have considerable variability in the degree of sclerosis, and indeed may have no roentgenographic changes at all…. The individual response to the fluorides must, for some reason, be greatly variable.”
SOURCE: Morris JW. (1965). Skeletal fluorosis among Indians of the American Southwest. American Journal of Roentgenology, Radium Therapy & Nuclear Medicine 94: 608-615.
Variable Response to the Same Duration of Exposure
Fluoride advocates often state that skeletal fluorosis takes at least 10 years to develop. Research, however, shows that skeletal fluorosis can develop in as few as 6 months in highly exposed children (Teotia 1998), in as little as 11 months in highly-exposed adults with kidney disease (Gerster 1983), and as little as 2 years in highly exposed adults with ordinary kidney function. (Roholm 1937; Franke 1975; Gerser 1983). Research also shows that, at the same general exposure levels, there is a dramatic ten-fold range in the amount of time required to produce the disease. As the following table shows, the same exposure to fluoride can cause skeletal fluorosis in some workers in as few as 2.4 years, while not producing any effect in other workers after 24 years.
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Duration of Exposure that Produces Skeletal Fluorosis |
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| Study | Phase of Skeletal Fluorosis |
Shortest |
Average Exposure |
Longest |
| Roholm 1937 | No Changes | 2.8 |
8 |
24 |
| Roholm 1937 | Clinical Phase 1 | 2.4 |
9.3 |
33.8 |
| Roholm 1937 | Clinical Phase 2 | 4.8 |
9.7 |
28.9 |
| Roholm 1937 | Clinical Phase 3 | 11.2 |
21.1 |
31.2 |
| Franke 1975 | Vague Symptoms | 2 |
10.71 |
25 |
| Franke 1975 | Stage 0-1 | 5 |
12.15 |
33 |
| Franke 1975 | Clinical Phase 1 | 8 |
15.7 |
38 |
| Franke 1975 | Clinical Phase 2 | 11 |
17.6 |
21 |
| Franke 1975 | Clinical Phase 3 | 19 |
19.5 |
20 |
| Runge 1989 | No Changes | 5 |
19.9 |
35 |
| Runge 1989 | Vague Symptoms | 10 |
19.2 |
37 |
| Runge 1989 | Stage 0-1 | 10 |
22.6 |
30 |
| Runge 1989 | Clinical Phase 1 | 10 |
21.1 |
43 |
| Runge 1989 | Clinical Phase 1-2 | 10 |
21.1 |
33 |
| Runge 1989 | Clinical Phase 2 | 16 |
17.5 |
19 |
| Runge 1989 | Clinical Phase 2-3 | 15 |
21.3 |
26 |
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“Fluoride toxicity afflicts children more severely and over a shorter period of exposure (about 6 months) as compared to adults. This is because the rapidly growing bones of children are metabolically active and more vascular and thus absorb and accumulate fluoride faster and in greater amounts than older bones, particularly at the sites of bone growth and physiological calcifications.”
SOURCE: Teotia M, Teotia SP, Singh KP. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65:371-81.
“The length of time required for the index case to develop fluorosis appears to be 7 years, since that is the interval of time that she resided in her current home. This is less than the 10 to 20 years noted in most reports; however, shorter intervals have been reported in children and individuals with exceptionally high fluoride exposure.”
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.
“Individual differences in sensitivity to noxious fluoride seems to be important… [I]t is quite possible to be an aluminum smelter worker for 30 years or longer without showing fluoride-caused bone changes, whereas others develop symptoms of fluorosis after only 10 years; the varying effect of fluoride has been demonstrated by therapy tests for osteoporosis.”
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.
“Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride [18 to 27 mg/day fluoride ion] for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case, and quantitative analysis of bone showed osteomalacia and skeletal fluorosis in the other case. These abnormalities were considered to be the consequence of excessive retention of fluoride due to renal insufficiency.”
SOURCE: Gerster JC, et al. (1983). Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis. British Medical Journal 287(6394):723-5.
“Cases of the 1st phase were observed after 2 5/12 years work, of the 2nd phase after 4 10/12 years, of the 3rd phase after 11 2/12 years. On the other hand the changes were slight in a certain number of the workers, even after long employment…One female worker had no bone changes, though she had been employed for 24 years with one interruption.”
SOURCE: Roholm K. (1937). Fluoride intoxication: a clinical-hygienic study with a review of the literature and some experimental investigations. London: H.K. Lewis Ltd.
“As regards the bone changes… they were pronounced in one male worker who had only been in the factory 5 years, and rather severe also in two female workers who had only been there 6 years.”
SOURCE: Moller P, Gudjonsson SV. (1932). Massive fluorosis of bones and ligaments. Acta Radiologica 12: 269-294.
VARIABLE SYMPTOMS AT SAME CLINICAL STAGE OF SKELETAL FLUOROSIS:
“[W]e found patients with slight radiological changes (subtle signs or O-I) who complained of intense pains in the spine and in the large joints. On the other hand, some patients whose fluorosis was radiologically distinct were almost without complaints.”
SOURCE: Franke J, et al. (1975). Industrial fluorosis. Fluoride 8: 61-83.
Variable Response to SAME DOSE of FLUORIDE in experimental clinical trials:
“The bioavailability may be markedly different from one patient to another.”
SOURCE: Boivin G, et al. (1993). Relationship between bone fluoride content and histological evidence of calcification defects in osteoporotic women treated long term with sodium fluoride. Osteoporosis International 3:204-208.
“The osteogenic response (to fluroide) shows marked interpatient variation.”
SOURCE: Dure-Smith BA, et al. (1991). Fluoride therapy for osteoporosis: A review of dose response, duration of treatment, and skeletal sites of action. Calcified Tissue International 49(Suppl): S64-S67.
“It is still not possible to determine what factors determine those patients who ultimately respond (with higher BMD) to fluoride therapy.”
SOURCE: Hodsman AB, Drost DJ. (1989). The response of vertebral bone mineral density during the treatment of osteoporosis with sodium fluoride. Journal of Clinical Endocrinology and Metabolism 69:932-8.
“Recent data strongly suggest that individual skeletal responsiveness to fluoride therapy varies… The cause or causes of the individual variability in response are unknown.”
SOURCE: Riggs BL. (1983). Treatment of osteoporosis with sodium fluoride: An appraisal. Bone and Mineral Research 2: 366-393.
“An increase in the width of osteoid seams was noted in all the present cases of osteoporosis who were treated with NaF. Since this effect was quite variable, however, the question can be raised whether a relationship to the dose and duration of the therapy exists. Of particular interest in this respect are patients 1, 6, and 7: Despite the smallest total dose of NaF (25 to 50 mg/day NaF) for only short periods of time, an extensive effect on the bone was apparent, whereas in case number 3, who received (94.3 mg/day of NaF) within 350 days, an only minute effect was noted. This applies to case number 4, as well.”
SOURCE: Kuhlencordt F, et al. (1970). The histological evaluation of bone in fluoride treated osteoorosis. In: TL Vischer, ed. (1970). Fluoride in Medicine. Hans Huber, Bern. pp. 169-174.
Genetics as One Possible Explanation for Variability in Response
“Fluoride incorporation into bone depends on many factors, including ingestion from sources in addition to water, age, duration of residency, renal function and other disease states, remodeling rate, and genetic susceptibility. About 40% of the population in areas with water supplies naturally fluoridated at very high levels are unaffected by skeletal fluorosis, and about a third of patients who receive fluoride as a therapy for osteoporosis are described as ‘nonresponders,’ indicating that intrinsic susceptibility to fluoride varies with the individual. A genetic basis for these differences is supported by research with different strains of mice. In a large, diverse urban center like Toronto, therefore, one would expect that the population would display a range of genetic susceptibilities to fluoride…”
SOURCE: Chachra D, et al. (2010). The long-term effects of water fluoridation on the human skeleton. Journal of Dental Research 89:1219-1223.
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