Skeletal fluorosis in humans: a review of recent progress in the understanding of the disease.
Endemic skeletal fluorosis is a chronic metabolic bone and joint disease caused by ingesting large amounts of fluoride either through water or rarely from foods of endemic areas. Fluoride is a cumulative toxin which can alter accretion and resorption of bone tissue. It also affects the homeostasis of bone mineral metabolism. The total quantity of ingested fluoride is the single most important factor which determines the clinical course of the disease which is characterized by immobilization of joints of the axial skeleton and of the major joints of the extremities. A combination of osteosclerosis, osteomalacia and osteoporosis of varying degrees as well as exostosis formation characterizes the bone lesions. In a proportion of cases secondary hyperparathyroidism is observed with associated characteristic bone changes. Contrary to earlier thinking, severe crippling forms of skeletal fluorosis are seen in paediatric age group too. Increased metabolic turnover of the bone, impaired bone collagen synthesis and increased avidity for calcium are features in fluoride toxicity. Osteosclerotic picture is evident when small doses of fluoride are ingested over a long period of time during which calcium intakes are apparently normal while osteoporotic forms are common in paediatric age group and with higher body load of the element. Alterations in hormones concerned with bone mineral metabolism are seen in fluorosis. Kidney is the primary organ of excretion for fluorides. Age, sex, calcium intake in the diet, dose and duration of fluoride intake and renal efficiency in fluoride handling are the factors which influence the outcome. Serum parameters rarely help in the diagnosis. Elevated urinary fluoride and increased bone fluoride content are indicators of fluoride toxicity. Fluorosis is a preventable crippling disease. No effective therapeutic agent is available which can cure fluorosis. Industrial fluorosis is on the increase on a global basis. Bone density measurement is a tool for early diagnosis.
Related citations in PubMed
- [Changes in mineral metabolism in stage 3, 4, and 5 chronic kidney disease (not on dialysis)].[Nefrologia. 2008]
- Review Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000.[Indian J Pediatr. 1998]
- Skeletal fluorosis: histomorphometric analysis of bone changes and bone fluoride content in 29 patients.[Bone. 1989]
- Skeletal scintigraphic findings in endemic skeletal fluorosis.[Nucl Med Commun. 1993]
- Review Neurology of endemic skeletal fluorosis.
By The Fluoride Action Network (FAN)
Two new North American studies investigated the impact of low-level fluoride consumption on the strength and density of bone.
While these important (yet largely overlooked) studies are not slam-dunks, they provide some of the strongest evidence to date that low-level fluoride exposure alters the quality of bone tissue, and strengthen concerns that fluoride exposure may increase the rate of bone fracture in the population.
Skeletal Fluorosis—A Real Danger of Excessive Fluoride Consumption
The harmful effects of chronic fluoride exposure on bone are well established. Since the 1930s it has been known that fluoride intake causes excessive bone growth, which can result in joint pain, bone pain, and stiffness. These symptoms are difficult to distinguish from arthritis. Other symptoms indicative of early clinical stage skeletal fluorosis include:
Burning, prickling, and tingling in your limbs
Reduced appetite and weight loss
The second clinical stage of skeletal fluorosis is characterized by:
Stiff joints and/or constant pain in your bones; brittle bones; and osteosclerosis
Calcification of tendons, or ligaments of ribs and pelvis
Osteoporosis in the long bones
Bony spurs may also appear on your limb bones, especially around your knee, elbow, and on the surface of tibia and ulna
In advanced skeletal fluorosis (called crippling skeletal fluorosis), your extremities become weak and moving your joints difficult, and your vertebrae partially fuse together, effectively crippling you. You have a heightened risk of developing problems from even mild exposure to fluoride, such as bone fractures, if you:
Are deficient in calcium, magnesium, and/or vitamin C
Have cardiovascular problems
Have kidney problems
How Much Fluoride is Too Much?
What is still not clearly established is whether fluoridated water, consumed over a lifetime, may lead to at least the initial stages of skeletal fluorosis. A threshold intake amount of 10 milligrams (mg) fluoride per day for an adult for a decade or two has been suggested as necessary before skeletal fluorosis is likely to result. Do Americans get this much fluoride? No sufficiently large study has ever been conducted in the US to determine the total intake of fluoride. However, a recent British study looked at a biomarker for fluoride intake, which is the amount of fluoride excreted over 24 hours in urine. It found that several percent of adults were likely already exceeding an intake of 10 mg/day.
The situation may actually be far worse in the US, since in Britain, only 10 percent of the population has fluoridated water, whereas in the US over 65 percent does. Fluoridated water was an important contributor to the high fluoride intake among some individuals in the British study.
Skeletal fluorosis was identified in a 2006 report by the National Research Council (NRC) as an adverse effect that needed to be considered by the EPA in establishing maximum safe levels of fluoride in drinking water. But so far, the EPA has done no serious analysis of the potential for skeletal fluorosis in the US.
How Fluoride Damages Your Bones
The NRC report had even more concern for another effect of fluoride on bone, which is the decrease in bone strength that can result in higher risks of fractures, especially in the elderly. This effect has not been as well studied as skeletal fluorosis, but since fractures of the hip in the elderly are such a serious health problem, often sending patients into a spiral of declining health ending in death, it is crucial to know whether water fluoridation is contributing to decreased bone strength. Some basic information about how fluoride acts in your body is helpful to understanding its health effects.
First, about half of the fluoride you consume is excreted through your kidneys into your urine, while the other half becomes bound in your skeleton. The fluoride that enters your bones is eliminated very slowly. The NRC estimates the biological half-life of fluoride in bone (the time for half of it to be removed) is as long as 20 years.
Unfortunately, most people—especially if you’re drinking fluoridated water on a daily basis—have constant low level exposures to fluoride, they are taking more fluoride into their bones than what is being removed, so the level of fluoride in their bones increase steadily over time.
Young people generally don’t have more than a few hundred parts per million (ppm) of fluoride in their bones, whereas older people living in fluoridated areas can have several thousand ppm, which is the level where skeletal fluorosis begins. Fluoride excretion in urine is reduced in those with decreased kidney function, which is also very common in older people. So, the elderly not only have accumulated higher levels, but they are losing the ability to effectively remove it as well.
An analogy can be made between fluoride accumulating in bone and persistent chemicals such as dioxin or PCBs, which often accumulate, because they also have long biological half-lives in human tissues.
Your bone is constantly being “turned over” in a process called remodeling. The mineral portion of your bone is broken down by one type of cell and then rebuilt by another. Fluoride appears to interfere with this essential process. The result is excessive mineralization and enlargement of your bones, and a disruption of the precise architecture needed to maintain resistance to fracture.
Ironically, while fluoride often does increase your bone mineral density, which is a commonly used measure of bone quality, it simultaneously makes your dense bone more brittle and therefore more subject to fracture. Remember thicker bone does NOT equate to stronger bone…
Can Therapeutic Doses of Fluoride Cause Osteoporosis?
Supporting this are human studies performed, given therapeutic doses of fluoride to try to prevent fractures from osteoporosis, which causes low bone density, often have found increases in fracture rates in the treated patients, even though their bone density increased.
So, the important scientific question is whether water fluoridation can lead to high enough levels of fluoride in your bones to noticeably weaken them. A dozen or so epidemiological studies have investigated this, with mixed results. Some of them show that fairly low levels of fluoride intake can increase the risk of fractures, whereas others have found no effect.
An important recent study tried a different approach.
Instead of looking at the rate of fractures in people exposed to varying amounts of fluoride, it used samples of actual bone from people undergoing hip replacement to see whether the bone fluoride concentration correlated with the mechanical strength of those samples.
This type of study had been done on laboratory animals, but never in humans. The work was completed in 2001 but was not published until 2010. The number of subjects in the study was small, with only 92 people, so the results were not definitive. The authors themselves do not draw any firm conclusions. Yet when the results are examined carefully, there is clear evidence that the people with higher bone fluoride levels had weaker bones, by several different measurements of bone quality.
The most straightforward measurement of bone strength was the amount of compression force the sample could withstand before breaking, which is called the Ultimate Compressive Stress. The people with the highest levels of fluoride in their bone had their sample break under about 50 percent less stress than those with the lowest levels of fluoride. This result was statistically significant.
A serious limitation of the study was that it failed to control for age, even though it found that older people tended to have weaker bones. The problem is that since older people also tend to have higher bone fluoride, to disentangle the effect of fluoride from that of age, they should have controlled for age in some manner. For example, they could have looked at a relatively narrow age range subgroup of their subjects to see if the relationship between fluoride and bone strength could still be detected when age was “held constant”.
Other, more sophisticated methods of controlling for age are also possible.
Government funding for research on fluoride has a history of granting money only to researchers who defend fluoridation, so the decision to leave this study ambiguous may have been to avoid a cut-off in future research dollars.
Other Evidence of Bone Damage Caused by Fluoride Ingestion
Another 2009 study suggests that fluoridated water might also be causing bone changes in young people, long before the bone fluoride concentration reaches the high levels in later life. Several types of bone mineral density measurements (BMD) were made in 11 year olds and related to fluoride intake. Several associations were found. In girls the BMD tended to decrease with higher fluoride intake, while in boys it tended to increase.
The number of children in the study was relatively small and the effects were generally weak.
The study didn’t try to find out whether these changes in bone had an effect on fracture rates, however. It is worth noting that the Chachra study on bones of hip replacement patients also found only weak associations between fluoride and BMD, yet found a clear association between fluoride and bone quality. So the fact that Levy’s study only found weak associations between fluoride and BMD doesn’t preclude the possibility that fluoride in children may be more clearly affecting bone strength.
Simply finding that water fluoridation may be sufficient to cause changes in bone remodeling at this age is worrying. Dental proponents of fluoridation typically ignore all effects of fluoride except on the teeth, or even maintain that there are no such effects.
Clearly, the effect of water fluoridation on bone health cannot be dismissed as non-existent.
When these recent studies are seen in the light of earlier work, the concern is heightened. In one of the best bone fracture studies on adults to date, it was found that hip fracture rates increased steadily starting from the lowest fluoride level examined, which was similar to what many Americans are getting from fluoridated water.
In children, one of the only studies ever conducted looked at fracture rates in relation to dental fluorosis . Dental fluorosis is disrupted enamel development that occurs in children exposed to fluoride. This study found that bone fracture rates rose sharply with increasing severity of dental fluorosis. In the US today, roughly 40 percent of all children have dental fluorosis, and several percent have the more severe stages. This biomarker of childhood fluoride exposure tells us that overexposure and the accompanying risk to bone health starts early.
How to Reduce Your Exposure to Fluoride
Although not discussed in this article, the health effects of fluoride ingestion are numerous. For a list of documented health effects, please see FAN’s Health Effects Database.
The science is quite clear: Fluoride should NOT be ingested. So, first of all, don’t drink fluoridated water. You can remove about 80 percent of the fluoride from your drinking water using a reverse osmosis (RO) filter. It is really hard to remove all of it with virtually any commercial filter. If you are concerned about fluoride the BEST solution is to help the Fluoride Action Network in their campaign to remove it from the water supply entirely.
As discussed above, you are exposed to fluoride from many sources other than the obvious lineup of toothpastes and mouth rinses (which I recommend using fluoride-free versions of as well). Far less obvious sources of fluoride, which I highly recommend avoiding, include:
|Non-organic foods (to avoid pesticide residue)||Food and beverages processed with fluoridated water, including organic processed foods and beverages|
|Mechanically de-boned meat||Pharmaceutical drugs, especially SSRI antidepressants and fluoroquinolone antibiotics like Cipro|
|Soy baby formulas||Instant tea|
|Processed breakfast cereals||Soda and fruit juices|
You’re even exposed to fluoride through air pollution! For more information about airborne fluoride pollution, please review FAN’s Fluoride Pollution page.
One solidly established concept in environmental health is that the effects of toxic agents fall on a continuum of biological change, ranging from undetectable effects at the lowest levels of exposure to severe health damage at very high doses. As exposure to an agent increases, the first detectable effect may be a subtle biochemical change, such as a decrease in the activity of an enzyme. At somewhat higher doses, measurable changes in some physiological functions may occur, but these often are not linked to clear symptoms or adverse effects, and may not be harmful. But as dosage increases, adverse effects begin to appear-at first mild ones, then moderate ones, and finally severe ones.
Most environmental health experts believe that the subtlest detectable effects-those with no outward symptoms, which are not clearly harmful-should be considered “precursors” of more serious effects. By this logic, people who show such subtle changes should be considered at risk for more serious effects if exposure continues.
Skeletal fluorosis, a complicated illness caused by the accumulation of too much fluoride in the bones, has a number of stages. The first two stages are preclinical-that is, the patient feels no symptoms but changes have taken place in the body. In the first preclinical stage, biochemical abnormalities occur in the blood and in bone composition; in the second, histological changes can be observed in the bone in biopsies. Some experts call these changes harmful because they are precursors of more serious conditions. Others say they are harmless.
In the early clinical stage of skeletal fluorosis, symptoms include pains in the bones and joints; sensations of burning, pricking, and tingling in the limbs; muscle weakness; chronic fatigue; and gastrointestinal disorders and reduced appetite. During this phase, changes in the pelvis and spinal column can be detected on x-rays. The bone has both a more prominent and more blurred structure.
In the second clinical stage, pains in the bones become constant and some of the ligaments begin to calcify. Osteoporosis may occur in the long bones, and early symptoms of osteosclerosis (a condition in which the bones become more dense and have abnormal crystalline structure) are present. Bony spurs may also appear on the limb bones, especially around the knee, the elbow, and on the surface of tibia and ulna.
In advanced skeletal fluorosis, called crippling skeletal fluorosis, the extremities become weak and moving the joints is difficult. The vertebrae partially fuse together, crippling the patient.
Most experts in skeletal fluorosis agree that ingestion of 20 mg of fluoride a day for 20 years or more can cause crippling skeletal fluorosis. Doses as low as 2 to 5 mg per day can cause the preclinical and earlier clinical stages.
The situation is complicated because the risk of skeletal fluorosis depends on more than the level of fluoride in the water. It also depends on nutritional status, intake of vitamin D and protein, absolute amount of calcium and ratio of calcium to magnesium in drinking water, and other factors.
In parts of India, China, Africa, Japan, and the Middle Fast, large numbers of people have skeletal fluorosis from drinking naturally fluoridated water. In India about a million people have this disease. Most of the victims live in areas where the water fluoride level is 2 ppm or above, but some cases are found in communities with natural fluoride levels below 1 ppm.
In the U.S., more than a dozen cases of skeletal fluorosis have been reported. Some have occurred at high fluoride levels, others at levels lower than 4 ppm when aggravating conditions were present, such as diabetes or impaired kidney function.
In setting the recommended maximum contaminant level for fluoride in drinking water in 1986, EPA considered only crippling skeletal fluorosis as a health effect and established little or no margin of safety, even for this disease. (A margin of safety is a difference between the maximum contaminant level and the level at which health effects first occur in the most susceptible individuals.) According to a Department of Agriculture survey, about 3% of the U.S. population drinks 4 L or more or water per day. Therefore, about 3 % of the people who live in areas where the water contains the natural fluoride level of 4 ppm allowed by EPA — such as certain communities in Texas or South Carolina — are ingesting at least 16 mg of fluoride a day, not including the fluoride they derive from other sources, such as toothpaste, food, or air.
Also, because a more or less constant percent of intake is accumulated in bone, persons who consume 8 mg a day for 50 years accumulate about the same amount of fluoride in their bones as those who consume 20 mg a day for 20 years. Therefore, for people who drink 2 L or more per day of water with 4 ppm fluoride throughout their lives, there appears to be no margin of safety even for crippling fluorosis. In its regulations for most other drinking water contaminants, EPA has included safety factors of 10 to 100 and has calculated intakes in terms of a lifetime—that is, 70 years instead of 20.
Joseph A. Cotruvo, director of the criteria and standards division of EPA’s Office of Drinking Water, says the fact that so few people in the U.S. have actually developed crippling skeletal fluorosis indicates that fluoride levels found in U.S. water are safe and that there is therefore an observed margin of safety. But critics of EPA’s standard speculate that there probably have been many more cases of fluorosis-even crippling fluorosis-than the few reported in the literature because most doctors in the U.S. have not studied the disease and do not know how to diagnose it.Those who ingest much less than 20 mg of fluoride per day may still be at risk of developing less severe stages of skeletal fluorosis, such as preclinical forms or the subcrippling clinical stages. In its final report, the Surgeon General’s panel said that radiologic changes have been found in bone when fluoride exposure has been about 5 mg per day. Nearly all of those drinking water containing 4 ppm of fluoride and about 3% of the more than 124 million people whose water contains only 1 ppm would have intakes as high as this. It is not known, however, what fraction of those with low-level radiologic changes would suffer joint pains or other clinically obvious adverse health effects. In his landmark study of skeletal fluorosis in cryolite workers in the 1930s, the Danish scientist Kaj Roholm found that some of those with stage I of clinical skeletal fluorosis suffered joint pains and stiffness.
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. Skeletal fluorosis is not even discussed in most medical texts under the effects of fluoride; indeed, a number of texts say the condition is almost nonexistent in the U.S. Even if a doctor is aware of the disease, the early stages are difficult to diagnose.
The possibility that fluoride might cause skeletal abnormalities in children’s bones is of particular concern. In its April 1983 draft report, the Surgeon General’s committee wrote that moderate and severe dental fluorosis in children may be accompanied by skeletal changes. Although this statement was omitted from the final report in September 1983, the committee did urge more research into the skeletal effects of fluoride, particularly in children. It wrote: “The effects of various levels of fluoride intake on rapidly developing bone in young children are not well understood. Also, the modifying effects of total intake, length of exposure, other nutritional factors, and debilitating illness are not well understood.” Since the committee’s report was written, PHS and EPA have undertaken no research in this area.
PHS has conducted several studies that it claims show that fluoride levels found in U.S. water supplies have had no clearly adverse effects on bones. But the majority of these studies either included a study population too small to detect rare effects or excluded people who would be most likely to suffer from skeletal fluorosis, such as those with kidney disease.
EPA’s approach to subtle, preclinical effects of fluoride on the skeleton differs from its usual approach to other environmental agents. For instance, when EPA assessed the health hazards of lead, it made an extraordinary effort to connect the observable effects of low-level exposure (inhibition of certain blood enzymes) with the known adverse effects of slightly higher exposure (decreased synthesis of hemoglobin, anemia, and possible neurotoxic effects). When it set its standard for lead in air, EPA argued that to prevent more serious effects, it needed to limit the more subtle biochemical changes that lead was provoking in millions of children.
By contrast, EPA’s assessment of fluoride in water took an almost opposite tack. By defining the most severe known hazard, crippling skeletal fluorosis, as the only effect it was concerned with preventing, EPA dismissed all degrees of fluoride-induced changes in bones less drastic than crippling fluorosis as not being health concerns.
Because fluoride causes denser bones (osteosclerosis), a number of researchers have compared fluoridated and nonfluoridated areas to see if the incidence and severity of osteoporosis is lower in fluoridated areas. A small number of studies in the past 25 years have reported a lower incidence of hip fractures in areas with fluoridated water, compared with nearby areas with low-fluoride water. For example. a recent report, comparing two towns in Finland, prompted widespread media stories that fluoridation is beneficial to the bones of the elderly, as well as to teeth. But a larger number of well-designed studies have found no evidence of a beneficial effect on osteoporosis. However, some of the profluoridation literature states as a fact that fluoridation will help prevent osteoporosis.
Skeletal fluorosis is a crippling bone disease caused by fluorideMillions of people world-wide are afflicted.
It also affects animals foraging on contaminated feed.
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.
Still under construction — more to come
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:
- Phase 1: sporadic pain; stiffness of joints; osteosclerosis of pelvis and vertebral column (6,000-7,000 ppm F in bone ash).
- Phase 2: chronic joint pain; arthritic symptoms; slight calcification of ligaments; increased osteosclerosis/cancellous bones; with/without osteoporosis of long bones (7,500-9,000 ppm F in bone ash).
- Phase 3: Crippling Skeletal Fluorosis: limitation of joint movement; calcification of ligaments/neck and vertebral column; crippling deformities of spine and major joints; muscle wasting; neurological defects/ compression of spinal cord (more than 8,400 ppm F in bone ash).
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:
- Hodge and Smith 1965 (In Fluorine Chemistry. Academic Press, New York);
- Fluorides and Human Health, WHO 1970;
- Fluoride, and Fluorine and Fluorides. WHO 1984.
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]
- 1 Fluorine Intoxication. A Clinical-Hygienic Study. H K Lewis, London 1937 pp 213-253.
- 2 Review of Fluoride: Benefits and Risks. US Public Health Service, 1991.
- 3 Recommended Dietary Allowances. 10th Edition. Food and Nutrition Board, National Academy of Sciences, 1990.
- 4 Hodge HC. The Safety of Fluoride Tablets or Drops. In: Johansen E, Taves DR, Olsen TO (Eds). Continuing Evaluation of the Use of Fluorides. American Association for the Advancement of Science, Selected Symposium 11. Westview Press, Boulder CO 1979.
- 5 Health Effects of Ingested Fluoride. Committee on Toxicology, National Research Council, National Academy of Sciences Press, Washington DC 1993
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”
|OSTEOSCLEROTIC PHASE||ASH CONCENTRATION
|Normal Bone||500 -1,000|
|Preclinical Phase||3,500 -5,500|
|asymptomatic; slight radiographically-detectable increases in bone mass|
|Clinical Phase I||6,000 – 7,000|
|sporadic pain; stiffness of joints; osteosclerosis of pelvis and vertebral column|
|Clinical Phase II||7,500 – 9,000|
|chronic joint pain; arthritic symptoms; slight calcification of ligaments’ increased osteosclerosis/cancellous bones; with/without osteoporosis of long bones|
|Phase III: Crippling Fluorosis||8,400|
|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