The focus of FAN’s Science Watch Bulletin is normally limited to new studies published in the open scientific literature. However, in the next 3 issues (see 2nd & 3rd issues), I will be making an exception to this rule by focusing on statements made recently by public health officials in the United States. All three statements relate to the issue of fluoride toxicity.
I’m writing the following series to draw attention to a disturbing phenomena: the ignorance on fluoride toxicity repeatedly demonstrated by officials who implore communities to add this substance to their water.
In the first part of this series, I will examine a statement made recently by Dr. William Kassler, the Medical Director of New Hampshire’s Department of Health & Human Services. On September 9, 2004, Dr. Kassler wrote a commentary, published in New Hampshire’s Union Leader newspaper, touting the benefits of water fluoridation.
In his article, Kassler stated that humans who drink water containing 100 parts per million fluoride (100 times the level added to water) do not suffer any adverse health effects, with the exception of dental fluorosis. Here are Kassler’s own words:
“For generations, millions of people have lived in areas where the natural level of fluoride in drinking water is higher than that recommended for community fluoridation; sometimes at 10 to 100 times the recommended level. The only risk associated with this high level of fluoride is dental fluorosis.”
For reasons documented below, this is truly a remarkable statement. Before detailing why, however, let me note that the problem here is not simply that Kassler made a mistake. Everyone makes mistakes. The problem is that to make a mistake of this magnitude requires a breathtaking degree of ignorance, and by extension incompetence, on the subject. In other words, we’re not talking about an error of detail, but of basic orientation.
Consider the following:
100 ppm fluoride in water, which Dr. Kassler says is safe, is so severely hazardous to human health that within the first day of exposure many humans will begin suffering the effects of acute fluoride poisoning (Ref: Hoffman 1980; Peterson 1986; Sidhu 2002). The immediate effects of the poisoning will include vomiting, nausea, abdominal pain, diarrhea, profuse sweating, and fever. At particular risk will be infants consuming formula reconstituted with water, as such infants would receive doses sufficient to kill (Ref: Whitford 1992).
In the impossible event that humans could actually survive for more than a couple of years in such a community, the skeleton would become so poisoned with fluoride that any movement of the joints would be a cumbersome, painful task. For many, paraplegia would eventually result when the fluoride-deformed spine encroached into, and damaged, the spinal cord (Ref: Singh 1961; Fisher 1989; Wang 2004). And that’s just the skeletal aspect of the disease.
Nonetheless, the concentration (100 ppm) that would produce these effects is the same concentration that Dr. William Kassler told voters – who would soon be voting on a fluoridation referendum in Manchester, NH – to be perfectly safe. In an ideal world, one would think that voters (who pay Dr. Kassler’s salary) deserve better than that.
However, if there is no one with political clout watching, such statements will continue to be made by other officials in similar positions of authority. In the next two bulletins, we will look at two similarly fallacious statements made by two similarly placed health officials who, like Dr. Kassler, are paid by the public to protect their health.
Below, I have provided a compilation of published information documenting the harm that would occur in a community drinking 100 ppm fluoride in water. I have separated this data into acute effects versus chronic effects. Acute effects are those that occur right away, while chronic effects are those that occur over a period of months/years.
One can only wonder how many people in Manchester, NH, voted yes to fluoridation this September based on the “expertise” of Dr. Kassler, who wrote his commentary three days before the vote.
Acute fluoride toxicity at 100 ppm:
1) Water with a concentration of 100 ppm F is:
1a) Higher than the concentrations (51 ppm, 92 ppm, and 93.5 ppm) documented in the scientific literature to produce immediate signs of acute toxicity, including: “abdominal cramping, nausea, headache, diarrhea, vomiting, diaphoresis (profuse sweating), and fever.” (SOURCE: Hoffman 1980; Peterson 1986; Sidhu 2002).
2) An infant drinking the typical amount of formula consumed in one feeding (14.75 ml per pound of bodyweight) would ingest a dose of fluoride (3.25 mg/kg):
2a) Three to ten times higher than the dose (0.3 to <1 mg/kg) reported to produce immediate signs of acute toxicity (SOURCE: Augenstein 1991; Gessner 1994), and within the range (3.1 to 4.5 mg/kg) reported sufficient to kill (SOURCE: Whitford 1992).
3) A 30 kg child drinking 350 ml (e.g. the amount of liquid in a can of soda) would ingest a dose of fluoride (1.17 mg/kg):
3a) Higher than the doses (0.3 to <1mg/kg) reported to produce immediate signs of acute toxicity, e.g. nausea, vomiting, and abdominal pain. (SOURCE: Augenstein 1991; Gessner 1994)
Chronic fluoride toxicity at 100 ppm:
4) Water with a concentration of 100 ppm F is:
4a) Seventy to hundred times higher than the concentration (1 to 1.4 ppm) found to cause skeletal fluorosis in India and China. (SOURCE: Susheela 1993; Xu 1997, Choubisa 2001; Bo 2003)
4b) Fifty to sixty times higher than the concentration (1.7 – 2 ppm) found by Mayo Clinic scientists to cause skeletal fluorosis in the United States among individuals with kidney disease (SOURCE: Juncos 1972; Johnson 1979).
4c) Twenty-five times higher than the US Environmental Protection Agency’s Maximum Contaminant Level (4 ppm).
4d) Thirteen to twenty-five times higher than the concentrations (4 to 8 ppm) associated with a two-fold to three-fold increase in hip fractures. (SOURCE: Sowers 1991; Li 2001)
4e) Thirteen times higher than the concentration (8 ppm) repeatedly found to cause clinical skeletal fluorosis in France. (SOURCE: Arlaud 1984; Noel 1985; Boivin 1986; Lantz 1987)
5) An adult drinking an average of 1 liter per day with 100 ppm fluoride, would ingest a daily dose of fluoride (100 mg/day) which is:
5a) Five to ten times higher than the daily dose (10-20 mg/day) estimated by the US Government to cause crippling skeletal fluorosis within twenty years. (SOURCE: NRC 1993; Whitford 1996; ATSDR 2003)
5b) Eight to ten times higher than the daily dose found to produce crippling skeletal fluorosis in Tibet. (SOURCE: Cao 2003)
5c) Three to five times higher than the dose (20 to 34 mg/day) found in clinical trials to increase the rate of hip fracture within one to four years. (SOURCE: Inkovaara 1975; Gerster 1983; Dambacher 1986; Gutteridge 1990, 2002; Hedlund 1989; Bayley 1990; Orcel 1990; Riggs 1990; Schnitzler 1990)
5d) Three to five times higher than the dose (20-34 mg/day) found in clinical trials to cause disabling arthritic and gastrointestinal pains. (SOURCE: Inkovaara 1975, 1991; Riggs 1980, 1990; Dambacher 1986; Das 1994; see also Spak 1989)
5e) Five times higher than the dose (22 mg/day) found in clinical research to immediately exacerbate the symptoms of pre-existing rheumatoid arthritis. (SOURCE: Duell 1991)
6) The average blood level of fluoride (1.9 ppm – SOURCE: Taves 1979) to be expected in a community with 100 ppm fluoride in water, is:
6a) Two to three times as high as the blood levels (0.68 – 0.95 ppm) found to be toxic to the human kidney within hours of exposure. (SOURCE: Cousins 1973; Mazze 1977)
6b) Seven times higher than the blood level (0.278 ppm) found to cause “rheumatic complications” in human clinical trials (SOURCE: Pak 1989).
6c) Four to twenty-four times higher than the blood levels (0.085 to 0.48 ppm) reported in humans suffering from clinical skeletal fluorosis. (SOURCE: Singla 1976; Susheela 1981, 1996; Li 1986, 1990; Mithal 1993; Barot 1998; Savas 2001; Yildiz 2003).
6d) Twenty times higher than the cut-off point (0.095 ppm) at which Mayo Clinic scientists recommend medical intervention with fluoride-free water. (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.
Augenstein WL, et al. (1991). Fluoride ingestion in children: a review of 87 cases. Pediatrics 88: 907-12.
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.
Bayley TA, et al. (1990). Fluoride-induced fractures: relation to osteogenic effect. Journal of Bone and Mineral Research 5(Suppl 1):S217-22.
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.
Cao J, et al. (2003). Brick tea fluoride as a main source of adult fluorosis. Food and Chemical Toxicology 41: 535-42.
Choubisa SL. (2001). Endemic fluorosis in Southern Rajasthan, India. Fluoride 34: 61-70.
Cousins MJ, Mazze RL. (1973). Methoxyflurane nephrotoxicity: A study of dose-response in man. Journal of the American Medical Association 225:1611-1616.
Dambacher MA, et al. (1986). Long-term fluoride therapy of postmenopausal osteoporosis. Bone 7: 199-205.
Das TK, et al. (1994). Toxic effects of chronic fluoride ingestion on the upper gastrointestinal tract. Journal of Clinical Gastroenterology 18(3):194-9.
Duell PB, Chesnut CH. (1991). Exacerbation of rheumatoid arthritis by sodium fluoride treatment of osteoporosis. Archives of Internal Medicine 151: 783-4.
Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700.
Gerster JC, et al. (1983). Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis. British Medical Journal (Clin Res Ed) 287(6394):723-5.
Gessner BD, et al. (1994). Acute fluoride poisoning from a public water system. New England Journal of Medicine 330:95-9.
Gutteridge DH, et al. (2002). A randomized trial of sodium fluoride (60 mg) +/- estrogen in postmenopausal osteoporotic vertebral fractures: increased vertebral fractures and peripheral bone loss with sodium fluoride; concurrent estrogen prevents peripheral loss, but not vertebral fractures. Osteoporosis International 13(2):158-70.
Gutteridge DH, et al. (1990). Spontaneous hip fractures in fluoride-treated patients: potential causative factors. Journal of Bone and Mineral Research 5(Suppl)1:S205-15.
Hedlund LR, Gallagher JC. (1989). Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride. Journal of Bone and Mineral Research 4:223-5.
Hoffman R, et al. (1980). Acute fluoride poisoning in a New Mexico elementary school. Pediatrics 65: 897-900.
Inkovaara JA. (1991). Is fluoride treatment justified today? Calcified Tissue International 49 Suppl:S68-9.
Inkovaara J, et al. (1975). Prophylactic fluoride treatment and aged bones. British Medical Journal 3(5975):73-4.
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 Y, et al. (2001). Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. Journal of Bone and Mineral Research 16(5):932-9.
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.
Mazze RI, et al. (1977). Inorganic fluoride nephrotoxicity: prolonged enflurane and halothane anesthesia in volunteers. Anesthesiology 46(4):265-71.
Mithal A, et al. (1993). Radiological spectrum of endemic fluorosis: relationship with calcium intake. Skeletal Radiology 22(4):257-61.
National Research Council [NRC]. (1993). Health effects of ingested fluoride. Report of the Subcommittee on Health Effects of Ingested Fluoride. National Academy Press, Washington, DC.
Noel C, et al. (1985). [Risk of bone disease as a result of fluoride intake in chronic renal insufficiency] Nephrologie. 6(4):181-5.
Orcel P, et al. (1990). Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. Journal of Bone and Mineral Research 5(Suppl 1): S191-4.
Pak CY. (1989). Fluoride and osteoporosis. Proceedings of the Society for Experimental Biology and Medicine 191: 278-86.
Petersen LR, et al. (1988). Community health effects of a municipal water supply hyperfluoridation accident. American Journal of Public Health 78: 711-3.
Riggs BL, et al. (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. New England Journal of Medicine 322:802-809.
Riggs BL, et al. (1980). Treatment of primary osteoporosis with fluoride and calcium. Clinical tolerance and fracture occurrence. Journal of the American Medical Association 243:446-9.
Savas S, et al. (2001). Endemic fluorosis in Turkish patients: relationship with knee osteoarthritis. Rheumatology International 21: 30-5.
Schnitzler CM, et al. (1990). Bone fragility of the peripheral skeleton during fluoride therapy for osteoporosis. Clinical Orthopaedics (261):268-75.
Sidhu KS, Kimmer RO. (2002). Fluoride overfeed at a well site near an elementary school in Michigan. Journal of Environmental Health 65: 16-21.
Singh A, et al. (1961). Skeletal fluorosis and its neurological complications. Lancet 1: 197-200.
Singla VP, et al. (1976). Symposium on the non-skeletal phase of chronic fluorosis: The Kidneys. Fluoride 9: 33-35.
Sowers M, et al. (1991). A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. American Journal of Epidemiology 133: 649-660.
Spak CJ, et al. (1989). Tissue response of gastric mucosa after ingestion of fluoride. British Medical Journal 298:1686-7.
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.
Wang W, et al. (2004). Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature. Spine 29 :E75-8.
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.