Skeletal Fluorosis
“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.” – Chemical & Engineering News
Prolonged, excessive exposure to fluoride can cause a debilitating bone disease known as skeletal fluorosis. The disease develops insidiously and can be difficult to distinguish from a number of other bone and joint diseases. Research shows that individual susceptibility to fluorosis varies greatly across the population, both with respect to the doses and duration of exposure that can cause the disease, and the skeletal manifestations and symptoms that result. Although skeletal fluorosis used to be considered a non-issue in the United States and other western countries, recent research suggests that many people — particularly heavy tea drinkers and those with kidney impairment — may unknowingly be suffering from some form of the disease.
Skeletal Fluorosis: A “Diagnostic Riddle”
One of the reasons doctors fail to detect skeletal fluorosis is because the symptoms and appearance of fluorosis can closely resemble other, more commonly known, bone and joint diseases. This is true for both the early and late stages of the disease.
In the initial stages, known as “pre-skeletal” fluorosis, a patient may suffer a variety of symptoms in the absence of any detectable bone changes, including joint pains, joint stiffness, and gastric distress. (Czerwinski 1988; Cook 1971). The absence of bone changes makes this pre-skeletal phase difficult to diagnose, because the symptoms are indistinguishable from common forms of arthritis, such as osteoarthritis and rheumatoid arthritis.
Even when bone changes do develop, correct diagnosis can remain elusive. This is because the bone changes in skeletal fluorosis mimic the bone changes in other diseases, including osteoarthritis, renal osteodystrophy, spondylosis, DISH, Paget’s Disease, and osteopetrosis. In 2011, for example, a team of U.S. scientists reported that a Georgia woman with crippling skeletal fluorosis, as evident by her severe hunchback (“kyphosis”), had to wait up to 18 years before doctors were able to diagnosis her condition as being caused by fluoride. (Whyte 2011). Other U.S. studies have reported similar results. Since doctors have difficulty diagnosing even the crippling stages of fluorosis, it is likely that earlier, subtler forms of the disease will often elude detection.
Outdated Science
For over 40 years, U.S. health authorities insisted that skeletal fluorosis cannot develop unless a person ingests 20 milligrams of fluoride per day for over 10 years. U.S. health authorities now concede, however, that skeletal fluorosis can occur at doses as low as 10 mg/day. (NRC 1993; Whitford 1996; IOM 1997; ATSDR 2003). This revised estimate, however, is itself outdated, as recent research has found that doses as low as 6 mg/day can cause early stages of the disease.
Another error underlying U.S. safety standards is the notion that skeletal fluorosis does not occur at water fluoride levels below 8 ppm. (IOM 1997; EPA 1985). Studies in India and China have repeatedly documented skeletal fluorosis at levels as low as 0.7 to 1.5 ppm fluoride. Even studies in the United States — despite being very small in scope — have reported advanced skeletal fluorosis in kidney patients at 1.7 ppm, (Johnson 1979) and crippling skeletal fluorosis at just 2.2 to 3.5 ppm. (Sauerbrunn 1965).
Individual Susceptibility to Fluorosis Varies Greatly Across the Population
The claim that skeletal fluorosis cannot occur if an individual consumes less than 10 mg/day of fluoride obscures the individual variability, and complexity, of fluorosis. As with any other toxic substance, individual susceptibility to fluoride varies considerably across the population. Research has documented, for example, that:
- Some individuals can develop skeletal fluorosis despite having “safe” levels of fluoride in their bones and without any known excessive exposure to fluoride; (Sandberg 1985)
- Individuals receiving the same dose of fluoride can exhibit dramatically different bone responses; (Chachra 2010)
- Individuals with pre-skeletal fluorosis can suffer excruciating pain, while individuals with advanced fluorosis can remain symptom-free; (Franke 1975)
- Although U.S. health authorities claim that fluorosis only develops after 10 or more years of exposure, children can develop the disease in as little as 6 months, (Teotia 1998), and some adults have developed it in as little as 2 to 7 years (Gerser 1983; Fratzl 1995; Felsenfeld 1991).
Skeletal Fluorosis can Present Differently in Different Individuals
Skeletal fluorosis is a far more complex disease than is generally perceived. This fact is highlighted by the very different forms the disease can take based on an individual’s nutritional status, health status, age, genetics, and exposure to aluminum. Whereas the dominant feature of skeletal fluorosis is generally considered to be hyper-dense bone in the spine (axial osteosclerosis), research has documented that:
- Some fluorosis victims can suffer primarily from osteoarthritis without noticeable osteosclerosis in the spine,
- Other fluorosis victims can suffer primarily from osteomalacia, osteoporosis, and/or secondary hyperparathyroidism without prominent osteosclerosis.
- To the extent that doctors rely on osteosclerosis in the spine as the telltale marker of fluorosis, victims will continue to fall through the cracks.
Common Causes of Fluorosis
Excessive fluoride exposure from any source — and from all sources combined — can cause skeletal fluorosis. Certain exposure pathways, however, present a uniquely high risk. These pathways include:
- Fluoridated Water for Kidney Patients
- Excessive Tea Consumption
- High-Fluoride Well Water (more likely to be a factor among deep wells)
- Industrial Fluoride Exposure
- Fluorinated Pharmaceuticals (Voriconazole & Niflumic Acid)
- Indoor coal burning (a common practice in China)
Bone Fracture
“One cannot help but be alarmed by the negative effects of fluoride on bone strength consistently demonstrated in animal models.” – Dr. Charles Turner, Indiana University.
No one disputes that high doses of fluoride wreak havoc on bone tissue. Millions of people throughout the world, for example, currently suffer a debilitating bone disease called skeletal fluorosis, which is caused by overexposure to fluoride. For many years, however, fluoride advocates believed that fluoride could also benefit bone due to its ability, under certain circumstances, to increase bone mass. Attempts to use fluoride as an experimental treatment for osteoporosis, however, resulted in more fractures, not less.
More recently, studies of human populations have reported increased fracture rates in communities with 4 mg/L fluoride in the water, and animal studies have consistently found reductions in bone strength from fluoride exposures. Although an increased fracture risk has not been consistently demonstrated at the fluoride levels (0.7-1.2 mg/L) added to water in fluoridation programs, the current weight of clinical, animal, and epidemiological evidence suggests that some individuals in fluoridated communities — particularly those with kidney disease — will suffer fragile bones as a result of their overall fluoride intake, including from fluoridated drinking water.
Clinical Trials: High-Dose Fluoride Increases Fracture Rates
For many years, however, fluoride advocates believed that fluoride, under controlled conditions, could benefit bone due to its ability to increase bone mass. In the 1960s, scientists began using fluoride as an experimental drug for the treatment of osteoporosis. Instead of reducing the number of fractures, however, numerous clinical trials reported that the fluoride treatment increased the rate of fractures (particularly hip fractures) and caused a number of several other side effects, including gastric distress and joint pain. Based on these results, the FDA rejected the use of fluoride as a medical treatment for treating osteoporosis.
Animal & In Vitro Studies: Fluoride Exposure Weakens Bone
Consistent with the clinical trials, numerous animal and in vitro studies have reported that bone strength declines with increased fluoride exposure. As noted in the Journal of Bone and Mineral Research,
“[O]ne cannot help but be alarmed by the negative effects of fluoride on bone strength consistently demonstrated in animal models.” (Turner 1995).
Epidemiological Studies:
Fluoride at 4 mg/L Increases Fracture Risk
Following the disastrous results of the experimental trials, researchers began investigating whether current fluoride exposures in the population could pose a similar risk. Although the clinical trials had used high doses of fluoride (20 to 34 mg per day), the trials only lasted for short periods of time (6 months to 4 years). It stands to reason, therefore, that people exposed to lower levels of fluoride for much longer periods of time could be at risk as well.
To determine this, investigators began comparing the bone density and bone fracture rates of communities with varying levels of fluoride in the water. Two consistent findings from these studies emerged: fluoride levels in drinking water (4 mg/L) that are still considered “safe” by the EPA reduce the density of cortical bone and increase the bone fracture rate in a population. Based in part on this research, the U.S. National Research Council (NRC) called on EPA to reduce the allowable levels of fluoride in water. EPA has yet to do so.
Fluoride at 1 mg/l: Mixed Evidence of Fracture Risk
A number of studies have sought to determine whether fluoridated drinking water (1 mg/L) also increases the risk of bone fracture. The results of these studies have been mixed, with some studies finding increases in bone fracture, other studies finding no effect, and others finding reductions in fracture risk. As noted by scientists on both sides of the fluoride debate, however, the usefulness of these studies is limited. Most of the studies, for example, only examined older populations that had no exposure to fluoridated water during their childhood (the period of life with the highest rate of fluoride accumulation in bone). Most of the studies, in fact, involved adult populations with less than 20 years of exposure to fluoridated water. The available epidemiological studies on fluoridation and bone fracture provide few definitive answers about the impact of lifetime exposures to artificially fluoridated water.