In this bulletin – the second in a three-part series examining recent health claims on fluoride made by Public Health Officials in the US – we address a statement from Colorado’s State Dental Director, Dr. Diane Brunson. In addition to being Colorado’s Dental Director, Dr. Brunson was also head of the Association of State and Territorial Dental Directors (ATSDD) at the time she made the statement at issue here.
According to an article in the Boulder-based newspaper The Daily Camera (5/29/01), Dr. Brunson stated that skeletal fluorosis is only found when the water supply contains 80 to 100 ppm fluoride. To quote:
“For skeletal fluorosis — fluoride build-up on bones — people would need to ingest about 80 to 100 parts per million, Brunson said.”
When I first read this, I thought the journalist probably got the numbers wrong and that Brunson could not have made such a demonstrably false claim. So after reading the article I telephoned Dr. Brunson and asked her if this was in fact an error. Brunson informed me, however, that it was not an error; that this is what she had stated.
A bit mystified, I asked for the references she was relying on to support the statement. Brunson told me she was relying on the 1990 cancer bioassay from the US National Toxicology Program. This was the only study Brunson was able to cite, on the phone at least. According to Brunson, the group of rats in the NTP study which drank 79 ppm fluoride in their water developed fluorosis of the bone (in 2 years).
Again, I almost couldn’t believe what I was hearing. There are dozens of human studies published in the scientific literature which provide direct data on the water fluoride concentrations which produce skeletal fluorosis in humans, and Dr. Brunson was relying instead on a single animal study – and an animal study which wasn’t even designed to answer the question at hand!
Furthermore, even if one insisted on ignoring all human data and focusing on this lone animal study, it would still be inaccurate to come away with the conclusion that humans will not develop skeletal fluorosis at water concentrations below 80 to 100 ppm. For starters, the levels of fluoride found in the rats’ bone and blood are levels that many humans consuming water with just 4 ppm fluoride will attain over the course of a lifetime.
The absurdity, however, of Brunson’s statement is probably best illuminated by simply contrasting it with the human data readily available in the scientific literature, including in two prominent reviews by the US Government in the 1990s (NRC 1993; IOM 1997).
According to the US National Research Council (1993), crippling skeletal fluorosis is caused by a daily dose of fluoride ranging between 10 and 20 mg.
According to the US Institute of Medicine (1997), the early stage of clinical skeletal fluorosis is caused by daily doses exceeding 10 mg/day.
A portion of the population drinking water with as little as 4 ppm fluoride will receive doses that fall within this range, while almost everyone living in communities with 10 ppm fluoride will receive these doses.
However, people living in an area with Brunson’s purported threshold concentration of 80 to 100 ppm fluoride, would ingest 80 to 100 mg/day if they drank just 1 liter of water, 160 to 200 mg/day if they drank 2 liters, and a whopping 240 to 300 mg/day if they drank 3 liters – up to 30 times higher than the US government’s estimated threshold dose.
As a matter of fact, the only reason why everyone in a 80 to 100 ppm community would not develop crippling skeletal fluorosis is the simple fact that most people could not drink this water for more than a few days without vomiting and experiencing intense gastrointestinal discomfort – as documented in the previous bulletin. Thus, people could simply not live long enough in such a community to contract the disease to which Brunson was referring.
I’m not sure if Dr. Brunson has since realized the magnitude of her mistake. Perhaps she has. But if not, perhaps someone from Colorado should contact her to fill her in, so that she doesn’t repeat the mistake again to other communities throughout the State of Colorado.
More data underscoring the problems with Brunson’s claim is presented below.
Dr. Brunson’s Claim vs. Published Data:
A) Fluoride levels in water associated with skeletal fluorosis:
BRUNSON: According to Brunson, skeletal fluorosis is only produced when the fluoride level in water reaches 80 to 100 ppm. However:
- Recent comprehensive research from both China and India has definitively shown that skeletal fluorosis starts to occur in those countries when the water fluoride levels reaches 1 to 1.5 ppm. (SOURCE: Susheela 1993; Xu 1997, Choubisa 2001; Bo 2003)
- In the United States, Mayo Clinic scientists detected skeletal fluorosis in areas with just 1.7 to 2 ppm among individuals with kidney disease. (SOURCE: Juncos 1972; Johnson 1979). Another case report from the United States found crippling skeletal fluorosis in a man who had consumed water with just 2.2 to 3.5 ppm (SOURCE: Sauerbrunn 1965) while another case report found skeletal fluorosis in a man drinking water with 4 to 7.8 ppm. (SOURCE: Goldman 1971).
- The US Environmental Protection Agency’s Maximum Contaminant Level, set to protect against skeletal fluorosis, is 4 ppm. (The EPA set this level under the assumption that 10 ppmfluoride would present a clear risk for crippling skeletal fluorosis, and that 4 ppm would provide an “adequate” margin of safety except for people with kidney disease.)
- In France, skeletal fluorosis has repeatedly been documented among people drinking mineral water with 8 ppm fluoride. (SOURCE: Arlaud 1984; Noel 1985; Boivin 1986; Lantz 1987)
B) Fluoride doses associated with skeletal fluorosis:
BRUNSON: People living in areas with 80 to 100 ppm fluoride in their water will ingest a dose of 80 to 100 mg/day if drinking 1 liter of water, and 160 to 200 mg/day if drinking 2 liters of water. This is the dose range that Brunson must, by extension, deem necessary to cause skeletal fluorosis. However:
- Research teams from both India and China have found doses of 9 mg/day to be sufficient to cause clinical skeletal fluorosis (SOURCE: Teotia 1998; Bo 2003).
- According to recent reviews from US Government agencies, a dose of 10 to 20 mg/day is sufficient to cause clinical skeletal fluorosis. (SOURCE: NRC 1993; IOM 1997; ATSDR 2003; see also Whitford 1996)
- A recent well-controlled study from Tibet found that an average intake of 12 mg/day causes crippling skeletal fluorosis in that country. (SOURCE: Cao 2003).
C) Fluoride blood levels associated with skeletal fluorosis:
BRUNSON: People living in areas with 80 to 100 ppm fluoride would be expected to have blood fluoride levels of between 1,500 to 1,900 ppb (Taves 1979). Thus, if blood fluoride is seen as a key factor in producing skeletal fluorosis, than Brunson must deem these levels to be roughly the minimum necessary to produce skeletal fluorosis. However:
- The average blood levels reported in people with skeletal fluorosis ranges from 85 to 480 ppb. (SOURCE: Singla 1976; Susheela 1981, 1996; Li 1986, 1990; Mithal 1993; Barot 1998; Savas 2001; Yildiz 2003)
- Mayo Clinic scientists recommended medical intervention with fluoride-free water when the blood level reaches 95 ppb in order to protect against skeletal fluorosis. (SOURCE:Johnson 1979).
Agency for Toxic Substances & Disease Registry [ATSDR]. (2003). Toxicological profile for Fluorides, Hydrogen Fluoride, and Fluorine. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.
Arlaud J, et al. (1984). [Osteomalacia disclosing bone fluorosis caused by regular consumption of Vichy Saint-Yorre mineral water] Presse Med. 13(39):2393-4.
Barot VV. (1998). Occurrence of endemic fluorosis in human population of North Gujarat, India: human health risk. Bulletin of Environmental Contamination and Toxicology 61: 303-10.
Bo Z, et al. (2003). Distribution and risk assessment of fluoride in drinking water in the West Plain region of Jilin Province, China. Environmental Geochemistry and Health 25: 421-431.
Boivin G, et al. (1986). [Histomorphometric profile of bone fluorosis induced by prolonged ingestion of Vichy Saint-Yorre water. Comparison with bone fluorine levels] Pathol Biol (Paris). 34(1):33-9.
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Goldman SM, et al. (1971). Radiculomyelopathy in a southwestern indian due to skeletal fluorosis. Arizona Medicine 28: 675-677.
Institute of Medicine [IOM]. (1997). Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board. National Academy Press.
Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: Johansen E, Taves DR, Olsen TO, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.
Juncos LI, Donadio JV Jr. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222: 783-5.
Lantz O, et al. (1987). Fluoride-induced chronic renal failure. American Journal of Kidney Disorders 10(2):136-9.
Li C, Ke X. (1990). Ionic, Nonionic, and Total Fluoride in Human Serum. Fluoride 23: 164-170.
Li CS, et al. (1986). Relationships Between lonic Fluoride, Total Fluoride, Calcium, Phosphorus, and Magnesium in Serum of Fluorosis Patients. Fluoride 19: 184-187.
Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with calcium intake. Skeletal Radiology 22(4):257-61.
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National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle Park, N.C.
Noel C, et al. (1985). [Risk of bone disease as a result of fluoride intake in chronic renal insufficiency] Nephrologie. 6(4):181-5.
Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078.
Savas S, et al. (2001). Endemic fluorosis in Turkish patients: relationship with knee osteoarthritis. Rheumatology International 21: 30-5.
Singla VP, et al. (1976). Symposium on the non-skeletal phase of chronic fluorosis: The Kidneys. Fluoride 9: 33-35.
Susheela AK, Jethanandani P. (1996). Circulating testosterone levels in skeletal fluorosis patients. Journal of Toxicology: Clinical Toxicology 34: 183-9.
Susheela AK, et al. (1993). Prevalence of endemic fluorosis with gastro-intestinal manifestations in people living in some North-Indian villages. Fluoride 26(2): 97-104.
Susheela AK, et al. (1981). Chemical Profile of Human Serum in Fluoride Toxicity and Fluorosis: 1. Total Protein-Bound Carbohydrates, Seromucoid and Fluoride Levels. Fluoride 14: 150-154.
Taves DR, Guy WS. (1979). Distribution of fluoride among body compartments. In: Johansen E, Taves DR, Olsen TO, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 159-185.
Whitford G. (1996). The Metabolism and Toxicity of Fluoride. 2nd Revised Edition. Karger: Basel. pp. 138.
Whitford GM. (1992). Acute and chronic fluoride toxicity. Journal of Dental Research 71: 1249-54.
Xu RQ, et al. (1997). Relations between environment and endemic fluorosis in Hohot region, Inner Mongolia. Fluoride 30: 26–28.
Yildiz M, et al. (2003). Bone mineral density of the spine and femur in early postmenopausal Turkish women with endemic skeletal fluorosis. Calcified Tissue International 72: 689-93.