Skeletal fluorosis is a crippling bone disease caused by fluoride
Millions of people world-wide are afflicted.
It also affects animals foraging on contaminated feed.


Skeletal Fluorosis Animal and Human

9.3.2 Domestic Animals (CEPA, Unpublished Final Draft, Inorganic Fluorides, p 144-148)

Skeletal fluorosis is characterized by hyperostosis, osteopetrosis, and osteoporosis (Obel, 1971; Shupe, 1980). An extensive review of cattle fluorosis has been given by Obel (1971). Agriculture Canada (1976) found that 25/36 cattle located on several Cornwall Island farms in the Saint Regis Quebec region displayed real or potential symptoms of chronic fluorosis. This diagnosis was based on the presence of lesions in the teeth and skeleton, as well as measurement of inorganic fluoride levels in blood and urine (Agriculture Canada, 1976). A subsequent study of livestock in this region reported stiffness and inflamed leg joints, dental fluorosis, osteosclerosis, osteonecrosis and bone deformations (Krook and Maylin, 1979).

The degree to which inorganic fluoride can induce skeletal changes varies considerably between the various animal species. Franke (1989) cites data which show that cattle are the most sensitive to skeletal fluorosis, followed by sheep, horses, pigs, rabbits, rats, guinea pigs and poultry. The sensitivity of cattle is attributed to their negative calcium balance, which is particularly noticeable in lactating cattle after calving; another contributing factor is the length of time which the bolus remains in the stomach of ruminants. The calcium found in cow's milk is supplied from both dietary and bone-resorption sources in approximately equal proportions (Comar et al., 1961; Maylin and Krook, 1982). Inorganic fluoride uptake occurs in bone tissue primarily through the replacement of hydroxyl groups of calcium hydroxyapatite, the major mineral phase in bone, causing the incorporation of the inorganic fluoride as calcium fluorapatite. A histological study of humerus bones from cattle exposed to atmospheric inorganic fluorides from a group of phosphate fertilizer factories in southern Brazil showed very little formation of primary spongiosa with reduced numbers and sizes of osteoblasts (Riet-Correa at al., 1986). Osteons were irregular in shape, size, and distribution in compact mandibular bone. Enlarged Haversian canals, irregular distribution of osteocytes, variation in calcium content, resorption cavities, and increased and irregular interstitial lamellae accompanied symptoms of fluorosis. As a result of excessive exposure to inorganic fluoride, capillaries invade the cartilage unevenly and with difficulty so that the border becomes dented, resulting in isolated islands of cartilage (Obel, 1971). Bone marrow becomes fibrous and poor in cells, and hyperactivity of the parathyroid may also occur as a result of decreased systemic calcium.

A drop in milk production has been described amongst cattle in the Massena/St. Regis area (Maylin and Krook, 1982). Milk production in a herd located near an aluminum plant was monitored continuously for 20 years. Milk production started to decrease from the fifth year of inorganic fluoride exposure, and although early losses were not statistically significant, by year eight the losses were significant to the 1% level, and by year 10 to the 0.19 level. Maylin and Krook (1982) also described the symptoms in herd of cattle. By 1972 the conception rates were low, retained placentas were very common and the number of abortions increased. The cows were fed from fodder grown on the farm, samples of which averaged 19.5 ug F-/g dry weight), a value considerably lower than the NAS had determined as detrimental. [emphasis added]

Dental fluorosis is generally characterized by the presence of various enamel defects and lesions such as mottling, hypoplasia, hypocalcification and increased wear. Mottled and defective enamel is believed to be solely an indication of inorganic fluoride exposure during the development of the teeth, as effects are not apparent in teeth which have already erupted prior to exposure (Obel, 1971).

Specifically in cattle dental fluorosis results in chalky-white, yellow or brown discolourations, hypoplasia, pitting and loss of enamel and hyperplasia of the cement. This is sometimes accompanied by gingival hyperplasia (Riet-Correa at al., 1986). Ockerse (1941) observed severe tooth lesions in cattle on a farm where the drinking water contained 11.78 mg F-/L, while Neeley and Harbaugh (1954) found dental lesions but no other symptoms in cattle where water contained 4 to 5 mg F-/L (Obel, 1971). Difficulty in eating was observed, however, in a herd of about 200 Brangus cattle whose water supply contained above 3 mg F-/L. Dental examination revealed that the cattle suffered severe dental fluorosis with the teeth having mottled, eroded, and irregular permanent incisors and black molars with irregular surfaces. Serum samples did not support a diagnosis of fluorosis; however bone tissues contained 2400 ug F-/g (rib), 1300 ug F-/g (metacarpal), and 2015 ug F-/g (mandible), while normal bone levels range from 401 to 1221 ug F-/g (Hibbs and Thilsted, 1983). This case indicates that chronic exposure to inorganic fluoride can be missed if only serum levels are used as an indicator of exposure.

Cows which were exposed to inorganic fluoride in drinking water at concentrations of 5, 10 or 12 mg F-/kg produced significantly fewer calves than the controls. This effect preceded the development of clinical symptoms of fluorosis, which therefore suggests that harmful effects on reproduction cannot be considered a secondary effect of fluorosis (Life Systems Inc., 1985).

Stoddard et al. (1963) fed calves from four months of age 10, 28, 55, and 109 ug F-/g in total ration, (dry matter) for 7.5 years. Taking the milk yield as 100% at a level of 10 ug F-/g in the total ration, the treatments 28, 55, and 109 ug F-/g resulted in milk yields of 93%, 82%, and 60% respectively. A linear relationship was established between the milk yield and the inorganic fluoride content of the feed (r = -0 9999). Stoddard at a1.(1963) concluded that the small differences in milk production at treatment levels below 40 ug F-/g were within natural variation, and this level served as the basis for US forage guidelines.

SOURCE: Government of Canada review, done pusuant to the Canadian Environmental Protection Act (CEPA), "Priority Substances List Assessment Report, Inorganic Fluorides, Unpublished Final Draft, January 1994.

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Still under construction -- more to come
Human Skeletal Fluorosis

Table 1 shows the phases of skeletal fluorosis mentioned in the article below. None of them are likely to be recognised by North American doctors because they are not trained to diagnose fluorosis. The preliminary stages can easily be misdiagnosed for rheumatoid arthritis, osteoarthritis or other similar diseases.
It is also noteworthy to mention that this is not the first "error" made by Harold C Hodge (see poison.htm for more info). Was it really two honest mistakes or did it reflect a hidden agenda?


Official "Safe" Fluoride Intakes Based On Arithmetic Error, Fluoride, 1997, 30:4 (Discussion Section)

What is the minimum intake of fluoride (F) which causes skeletal fluorosis, and how long is it before the onset of this disease? Kaj Roholm's 1937 study of industrial fluorosis showed that phases of skeletal fluorosis could occur, with an F intake of 0.2-0.35 mg/kg of body weight/day, after 2 yrs and 5 months for phase one; 4 yrs and 10 months for phase two and 11 yrs and 2 months for phase three (crippling skeletal fluorosis).1

Descriptions of the symptoms and range of F in bone ash for each clinical phase of skeletal fluorosis follow:

Approximately 50% of ingested fluoride is cleared by the kidneys.2

In 1953, Dr Harold C Hodge, the leading F toxicologist, applying Roholm's intake dosage range of 0.2-0.35 mg/kg/day to the range of weights of 100-229 lbs, concluded that 20-80 mg/day of fluoride intake for 10-20 years would be necessary to produce skeletal fluorosis. This result was published in 1953 by the National Academy of Sciences/National Research Council (NAS/NRC). In 1990, in response to queries about fluoride in a NAS/NRC publication,3 NAS/NRC quoted Roholm as supporting evidence for the statement that "fluorosis occurs after years of daily exposure of 20-80 mg/day". Unfortunately, Hodge had made an incredible blunder, because he had not corrected for pounds (lbs). He had calculated 0.2 mg x 100 (lbs) = 20 mg and 0.35 x 229 (lbs) = 80 mg giving a range of 20-80 mg/day.

This error was repeated in numerous subsequent publications purporting to report the range of intakes required to produce skeletal fluorosis. The erroneous statement was in the NAS/NRC book Fluorides of 1971. In 1991 NAS/NRC in a letter quoted additional supporting references:

This letter also stated "The RDA subcommittee did not conduct experiments and come up with this range; rather, we reported this figure based on the work of others and on review papers." However, all the above reviews had accepted Hodge's miscalculation from Roholm's classic study. Thus all the above supporting references, which have been widely cited to support the safety of water fluoridation, contained the same erroneous information.

The corrected intake range for people between 100-229 lbs is 9.1-36.4 mg/day (based on 2.2 lbs/kg). Hodge partially corrected his error in a 1979 paper stating: "Crippling fluorosis as an occupational disease follows exposures estimated at 10 to over 25 mg of fluoride daily during periods of 10-20 years." 4 In a 1993 American Dental Association pamphlet, Fluoridation Facts, the incorrect dosage range was quoted but cited Hodge's paper of 1979. NAS/NRC finally quoted the corrected Hodge's dosage rate for skeletal fluorosis (SF) (10-25 mg/day of fluoride for 10-20 years) in 1993. It was also stated by NAS/NRC that "it is no longer feasible to estimate with reasonable accuracy the level of fluoride exposure simply on the basis of concentration in drinking water supply." 5.

Extrapolating from Roholm's original figures, it follows that for a 100 lb person, at less than 2.5 mg/day fluoride intake, stage 1 of SF can occur within 10 years. At this same dosage rate, stage 2 of SF can occur after 19 years and crippling skeletal fluorosis after 45 years. There is evidence that some people are ingesting at least 5 mg/day, in which case the stages of skeletal fluorosis can occur after 5, 10 and 23 years, respectively.

NAS has this year proposed to publish, for its sister organization the Institute of Medicine (IOM), "Dietary Reference Intakes", accepting Roholm's dosage range but relating these to early skeletal fluorosis. They then quoted: "... Advanced stages of skeletal fluorosis are associated with intakes of fluoride ranging from 20 to 80 mg/day for 10 or more years (Hodge and Smith 1977, WHO 1984)." The quotes may be accurate but the statements are false. NAS/IOM and other public health bodies must decide whether their task is to advance the health of the public or be apologists for the industries, which produce fluoride toxic wastes.

Hodge, NAS/NRC, and all other public health bodies, who quoted the incorrect dosage rates, were grossly negligent and, in some cases, deliberately misleading. They certainly misled by quoting the incorrect dosage rate for skeletal fluorosis, NOT crippling skeletal fluorosis.

Many reputations are at stake here, but the evidence is clear that the risks of fluoride far outweigh any minor benefit to teeth. Pride has to be swallowed and the precautionary principle applied. An increase in more severe skeletal fluorosis is due to erupt as older people enter the risk window. Water fluoridation should cease immediately and steps should be taken to reduce fluoride in food, drink, and dental products. [emphasis added]

References
Articles from Fluoride, Journal of the International Society for Fluoride Research are reproduced with permission.

Czerwinski E, Nowak J, Dabrowska D, Skolarczyk A, Kita B, Bone and Joint Pathology in Fluoride-Exposed Workers, Archives of Environmental Health, 1988, 43:5, 340-343

Clinical and radiological investigations were performed for 2,258 aluminum workers exposed to fluoride for an average of 17.6 yr (standard deviation = 7.6). Changes in bone and joints were presented in detail in three groups: (1) exposed up to 5 yr (135 cases), (2) exposed from 6-32 years (1,463 cases), and (3) retired workers (660 cases). A semi-quantitative assessment of early fluorosis was introduced. A 20.2% incidence of fluorosis was found, but according to Roholm, only 1.05% was in stage I. The disease was mainly in the pre-stages of O and OI [see note below]. A close relationship between the occurence of fluorosis and the time and degree of fluoride exposure was found. The difficulties in diagnosing skeletal fluorosis result from the questionable sensitivity of the x-ray techniques and from the non-specificity of the associated symptoms. A qualitative method to assess osteosclerosis and bone structure alteration is needed.

"Discussion: ... 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."

NOTE: O: "possible fluorosis (multiple joint pains, motion limited in at least two joints or spine, initial ossifications noticeable on the radiographs)"
OI: "initial fluorosis (advanced painful symptoms, advance limitation of motion in at least two joints or spine, marked ossifications noticed on two or more radiographs, initial osteosclerosis, slight periosteal reaction and thickening of the long-bone cortices"


  EPA scientists take action against EPA for failing to protect public health, 1986



Table 1
OSTEOSCLEROTIC PHASE ASH CONCENTRATION
(mgF/kg)
Normal Bone500 -1,000
Preclinical Phase 3,500 -5,500
asymptomatic; slight radiographically-detectable increases in bone mass
Clinical Phase I6,000 - 7,000
sporadic pain; stiffness of joints; osteosclerosis of pelvis and vertebral column
Clinical Phase II7,500 - 9,000
chronic joint pain; arthritic symptoms; slight calcification of ligaments' increased osteosclerosis/cancellous bones; with/without osteoporosis of long bones
Phase III: Crippling Fluorosis8,400
limitation of joint movement; calcification of ligaments/neck, vert. column; crippling deformities/spine & major joints; muscle wasting; neruological defects/compression of spinal cord
SOURCE: U.S.P.H.S. "Review of Fluoride, Benefits and Risks", 1991 - adapted from: Smith & Hodge, 1979; Franke et al., 1975; Schlegal, 1974

See fluoride.htm for data on daily fluoride intakes


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