Fluoride Toxicity Issues
Deaths or poisonings linked to fluoridation or fluoride products

Since the 1950s, fluoridation proponents have steadfastly maintained that the safety factor of water fluoridation (1 ppm) in relation to the acutely lethal dose is 2,250- to 4,500-fold in adults (represents 5 to 10 grams NaF), and about 250- to 500-fold in a child. In other words, the amount of sodium fluoride (NaF) required to result in acute poisoning causing fatality was 5 to 10 grams (NaF is 45% fluoride ion). This range for toxicity was provided by Harold C. Hodge, the same man who was responsible for erroneously reporting that it would take a daily fluoride intake of "20-80 mg" before skeletal fluorosis would occur in the average individual. Based on several occurrences of water fluoridation over-feeds and individual poisoning reports, It is now known that fluoride's "Probably Toxic Dose" which "should trigger therapeutic intervention and hospitilization -- is 5 mg/kg of bodyweight." This means that many dental products found at home contain more than enough fluoride to kill or seriously harm a small child if ingested.

Akiniwa, Kenji, Re-Examination of acute toxicity of fluoride, Fluoride, 1997, 30:2, 89-104

SUMMARY: The acute toxic dose of fluoride has been believed to be 2 to 5 mg or 8 mg/kg of body weight. However, acute fluoride poisonings have occurred at doses of 0.1 to 0.8 mgF/kg of body weight in the USA. In Japan, a school-based anticariogenic program is being carried out with fluoride mouth rinses containing 500 to 2000 ppm sodium fluoride on approximately 158,000 persons, consisting mainly of elementary and junior high school children. Thus the safety problem of this treatment attracts much attention. Fluoride retention is said to be around 15 to 30% in fluoride mouth rinsing. In this paper, on the basis of toxic doses estimated in outbreaks of fluoride poisoning, the potential for acute poisoning by fluoride ingested during mouth rinsing is assessed. Acute fluoride poisoning is shown to be caused by exposure to lower doses of fluoride than commonly suggested. The toxic dose of fluoride should therefore be re-examined.

[editor's note: see entire paper at: http://www.fluoride-journal.com/97-30-2/302-89.htm]

Arnow PM, et al., An Outbreak of Fatal Fluoride Intoxication in a Long-term Hemodialysis Unit, Annals of Internal Medicine, 1994, 121, 339-344

Foulkes RG, Case report: mass fluoride poisoning, Hooper Bay, Alaska, a review of the final report of the Alaska department of health and human services, April 12, 1993, Fluoride 1994, 27:1, 32-36

SUMMARY: The death of a 41-year-old male and the illness of approximately 296 others on May 21-23, 1992, in Hooper Bay Alaska has been shown to be due to acute fluoride intoxication caused by malfunction of the fluoridation equipment of system 1 of the village’s two-system (well) water supply. Fluoride levels were reported to be as high as 150 ppm.

The "Final Report" prepared by the Section of Epidemiology, Alaska Department of Environmental Conservation (DEC) and the US Public Health Service (USPHS) is dated April 12, 1993. This document shows that gastro-intestinal symptoms were predominant. The investigators "suggest" that the minimum lethal dose for fluoride, when consumed by humans over 24-32 hours, is 20 mg/kg. This is higher than the "probably toxic dose" of 5 mg/kg calculated for a single ingestion (Whitford 1989). Serum half life of 3.5 hours of the hospitalized patient was within the range previously reported (Ekstrand et al 1980). However, the recovery time of 19 days for plasma fluoride and systemic toxicity was longer than previously reported (Heifetz and Horowitz 1986). The level of dose causing illness, 0.3 mg/kg, was 27 times lower than the dose previously reported; for example, the "maximum safely tolerated dose" of 8.0 mg/kg (Heifetz and Horowitz 1986).

The final report cites a number of reasons for the system failure. These include human error, mechanical failure, lack of safety features and failure to comply with regulations.

The report recommends re-affirmation of fluoridation by the Alaska Division of Public Health; the determination by USPHS and DEC that operational safety features are in place; and, that DEC should ensure compliance with regulations.

Keywords: Fluoride poisoning; Hooper Bay, Alaska.


Hooper Bay is a Yup’ik Eskimo settlement of approximately 950 people on the Bering Sea coast of Alaska. In Hooper Bay, as in 150 other rural Alaskan communities, fluoride has been added to drinking water for many years for the purpose of preventing dental caries. A press report states that a survey carried out by the Indian Health service examiners in 1990 on the North Slope Borough of Alaska showed that the dental health of these natives was "the worst in the US" (Ketchikan Daily News).

The enthusiasm for fluoridation of native communities in Alaska, as well as in many areas of the "lower 48 states", includes adjusting some school supplies to 5 ppm, a value in excess of the EPA’s Maximum Contaminant Level of 4 ppm (USPHS/CDC 1985).

In Hooper Bay, both system 1 and system 2 (well) water supplies were fluoridated at 1.2 ppm. On May 21-23, 1992, system 1, owing to a malfunction, delivered fluoride at a level of 150 ppm. This resulted in the death of a 41-year-old male and the illness of approximately 296 others, including one adult female who was admitted to hospital in serious condition.


Among 81 people, interviewed during a household survey, who were served by system 1, 51 (63%) had illness meeting the case definition. This suggested that among all 470 residents of system 1 63%, or 296 of them, developed fluoride poisoning.

All were Alaskan Native of whom 50% were female. Their ages ranged from 6 months to 73 years (median 21 years).

Symptoms. were related primarily to the gastro-intestinal system, i.e., nausea, vomiting, diarrhea, and abdominal pain. Other symptoms included headache, itching, weakness, numbness or tingling of an extremity, shortness of breath, and fatigue. The median latency period (38 cases) ranged from less than 1 to 150 minutes (median 7 minutes) and the median duration of illness (53 cases) ranged from 1 to 132 hours (median 24 hours).

The case of the individual who died was characterized by repeated vomiting and drinking multiple glasses of water. A summary in the Final Report stated that post mortem examination revealed aspiration of gastric contents with pulmonary necrosis and inflammation. Serum calcium was 4.9 mg/dL (norm = 8.4-10.2); magnesium 3.4 mg/dL (norm = 1.7-2.2); and alcohol 0.028%. The urine fluoride level, not corrected for creatinine, was 55 mg/dL. The death certificate listed.the final cause of death as "Acute Overdose, Sodium Fluoride".

Investigation of survivors

The persons from whom information was collected during the household surveys were asked to give urine and blood samples. 41 and 26 consented to have urine and blood, specimens collected, respectively. Urine samples were analyzed for fluoride; serum was analyzed for lactic acid dehydrogenases (LDH), creatinine kinase (CK), aspartate serum transferase (AST), calcium, phosphorus, and magnesium. Both plasma and serum were analyzed for fluoride.

On June 5, 5 of the 7 people with highest urine fluoride levels agreed to have repeat specimens collected. On June 9, 9 of 11 ill people with elevated initial urine fluoride levels agreed to have repeat urine specimens collected and 12 of 20 ill people with abnormal serum chemistry or elevated serum fluoride (greater than 0.03 mgF/L) agreed to have repeat blood specimens.


The mean fluoride level of urine collected May 27-28 (6-7 days after ingestion) was 6.5 mgF/L (n = 26) (range 28.7-1.1 mgF/L). In non-cases (n = 15), the mean was 2.0 mgF/L (range 0.4-3.4 mgF/L).

Serum fluoride levels on samples collected May 27-28 from case-patients (n = 23) were a mean of 0.100 mgF/L and a median of 0.071 mgF/L. Non-cases (n = 3) had a mean of 0.036 mgF/L.

Serum chemistry analysis on May 27-28 (n = 15 case-patients) showed that all had elevated LDH and normal calcium and magnesium. Five had elevated phosphorus; 10 had elevated AST; and 1 had elevated CK. The Report states that on retesting on June 9, continued serum chemistry abnormalities were noted compared to normal values: 8 had low magnesium; 4 had high phosphorus; 2 had high LDH; and 1 had a high AST. A detailed table for these results is not provided, as is the case with the May results.

Dosage Estimates

The level of fluoride in system 1 on May 21-23 was, according to the Report, 150 mgF/L. Estimated intakes of water by 62 persons interviewed ranged from 2 to 140 cc/kg with a mean of 36 cc/kg. From these, the investigators estimated that fluoride doses ranged from 0.3 to 21.0 mg/kg. The man who died consumed an estimated 17.9 mg/kg. Among case-patients, doses and percentages were: 16% had less than 1.0 mg/kg; 34%, less than 2.0 mg/kg; and 21% had greater than 8.0 mg/kg.

The authors note that the estimates did not include fluoride consumed in water used to prepare cooked foods such as soup or vegetables. They state that their studies "suggest" that the minimum lethal dose of fluoride for humans, when consumed over 24 to 32 hours is in the range of 20 mg/kg. This is higher than the "probably toxic dose" of 5 mg/kg calculated for a single acute ingestion (Whitford 1989). The initial serum fluoride level of 9.1 mg/L from the most seriously ill survivor (hospitalized) "provides a value that may be close to the lethal serum level".

Other Findings

Fluoride is cleared from serum exponentially. The serum fluoride half-life for the hospitalized survivor was 3.5 hours. This was within the range (2.4-4.3 hours) previously reported (Ekstrand et al 1980).

Serum fluoride levels in all patients who had at least three fluoride determinations did not return to normal levels within 24 hours as previously reported (Heifetz and Horowitz 1986). The mean fluoride level in case-patients approximately 19 days after ingestion was 0.092 mg/L, nearly three times the mean among the three non-cases on May 27-28. In addition, evidence of systemic toxicity, including abnormalities of magnesium, phosphorus, LDH, and AST, also persisted 19 days. The authors are of the opinion that this has not been previously reported.

The minimum estimated dose that caused illness (assuming a fluoride concentration of 150 mg/L) was 0.3 mg/kg or "approximately, 28 mg of total fluoride". This level is lower than other reports referred to by the authors (Augenstein et al 1991, Duxbury et al 1982, Spoerke et al 1980), and 27 times less than the 8.0 mg/kg recommended as a maximum safely tolerated dose in another report (Heifetz and Horowitz 1986). Further, for the case-patients for whom fluoride dose was estimated, 16% consumed less than 1.0 mg/kg and 34% consumed less than 2.0 mg/kg. The authors write that this "implies that both acute gastro-intestinal symptoms and systemic toxicity may result from doses lower than previously believed."


Owing to the adverse publicity surrounding this episode of hyperfluoridation in Hooper Bay and in light of the many problems that led to it, 11 of 36 villages

(36%) in the Yukon-Kuskokwin Delta voted to discontinue fluoridating their water supplies.

Following the outbreak, the Department of Environmental Conservation (DEC) and the US Public Health Service (USPHS) reviewed other village water systems in Alaska. Of 123 with systems that were evaluated, 12 (10%) were "missing at least one safety feature". None had a twist-lock plug for the fluoride pump electrical connection that is, evidently, a requirement.

T'he Workers’ Compensation Board of British Columbia now includes in its publication, Water Fluoridation, A Manual of Standard Practice (1993), a list of problems identified by those investigating the Hooper Bay incident. These are: operator has minimal training; no fluoride testing by operator; slow response to high fluoride values identified by testing; inadequate labelling of pumps and piping; electrical wiring that signals water pump was corroded (water pump did not turn on); high water level indicator in holding tank that signals on/off operation of water pump and fluoride pump was not activated (fluoride pump was in continuous operation); defective ball valve in fluoride pump allowed pump to operate at 7 times the normal rate; no daily or continuous monitoring of treated water; and possible cross-connection between treated water in the holding tank and fluoride solution in tank (siphon action possible upon incorrect use of long supply hose).


The following recommendations were made by the investigators:

"1. The Alaska Division of Public Health strongly reaffirms its commitment to fluoridation of public water supplies. Water fluoridation is one of the most important methods to prevent dental caries in Alaskan children.

"2. USPHS and DEC should determine that communities with fluoridated water systems have operational standard safety features in place....

"3. DEC should ensure that all community water systems have complied with existing regulations regarding installation of standard safety equipment, training of water system operators, and routine, systematic monitoring and follow-up of fluoride levels and inspection of fluoridation units."


The mass poisoning incident in Hooper Bay, euphemistically called "hyperfluoridation", has not shaken the strongly held belief of Public Health personnel in the safety of fluoridation and its effectiveness in the reduction of dental caries. If the results of the dental survey of the North Slope are applicable to the people of the Yukon-Kuskokwin Delta, the effectiveness of fluoridation is obviously questionable.

So strongly held is the belief in the safety of fluoridation that Public Health personnel in British Columbia could not accept the finding that the death in Hooper Bay was due to acute fluoride intoxication until they were presented with the official Report of the incident.

Although conclusions reached by the investigators regarding the dosage required to produce symptoms are based on assumptions and do not include the ingestion of fluoride from food, they should provide a warning that symptoms, especially of the gastro-intestinal system, may be frequent and unrecognized, particularly among children consuming water in schools fluoridated at 5 mgF/L (up to 5.4 mgF/L) in addition to exposure at home. It is interesting to note that the minimum estimated dose causing illness was interpreted from 0.3 mg/kg to be 28 mg fluoride. Usually, for example, in the USPHS publication Review of Fluoride Benefits and Risks (1991), calculations are based on a 50-kg adult and a 20-kg child dose. These figures indicate total fluoride of 15 mg for adults and 6 mg for children. Is this a deliberate understatement or do the Native people studied weigh more than the "standard" used by USPHS?

It is also interesting to speculate on whether "mandatory" fluoridation of Alaskan Natives plays a role in the "climbing death rates from cancer" reported in the Alaskan press as a result of their review of a report by the US Department of Health and Human Services on death rates for 1984-1988 (Anchorage Daily News 1992). The Alaska Native total death rates from cancer are higher at 211/100,000 than the Alaska non-native total, 166.9/100,000, and the US total (all races) of 171.3/100,000.

Overall, the discrepancy found by the investigators when compared to "conventional" assumptions and the revelation of the obvious hazards of fluoridation systems, especially in rural areas, should call for an extensive review by unbiased observers.


  1. Alaska Department of Health and Social Services. Hooper Bay Waterborne Outbreak - Fluoride, Final Report. April 12 1993.
  2. Anchorage Daily News.Cancer Plagues Natives. p 1 May 28 1992.
  3. Augenstein WL. Spoerke DG, Kulig KW et al. Fluoride ingestion in children: A review of 87 cases. Pediatrics 88 907-912 1991.
  4. Duxbury AJ, Leach FN, Duxbury JT. Acute fluoride toxicity. British Dental Journal 153 64-66 1982.
  5. Ekstrand J., Ehrnebo M, Whitford GM, Jarnberg PO. Fluoride pharmacokinetics during acid-base changes in man. European Journal of Clinical Pharmacology 18 189-194 1980.
  6. Heifetz SB, Horowitz HS. Amounts of fluoride in self administered dental products: Safety considerations for children. Pediatrics 77 876-882 1986.
  7. Ketchikan Daily News. North Slope Dental Health Called Worst in US. Dec.17 1990.
  8. Spoerke DG, Bennett DL, Gullekson DJ. Toxicity related to acute low dose sodium fluoride ingestions. Journal of Family Practice 10 139-140 1980.
  9. US Department of Hea1th and Human Services, PHS.·Review of Fluoride Benefits and Risks. Feb 1991
  10. USPHS/CDC. Fluoridation Census 1985. Department of Health and Human Services, Bethesda MD 1985 pp 28-32.
  11. Whitford GM. The Metabolism and Toxicity of Fluoride. Monographs in Oral Science. Karger, Basel 1989.
  12. Workers’ Compensation Board of British Columbia. Water Fluoridation, A Manual of Standard Practice 1993. p 50.

Richard G Foulkes BA MD, PO Box 278, Abbotsford BC, Canada V2S 4N9.

Gessner BD, Beller M, Middaugh JP, Whitford GM, Acute Fluoride Poisoning From A Public Water System, New England Journal of Medicine, 1994, 330:2, 95-99.

Acute fluoride poisoning produces a clinical syndrome characterized by: nausea, vomiting, diarrhea, abdominal pain, and paresthesias. In May 1992, excess fluoride in one of two public water systems serving a village in Alaska caused an outbreak of acute fluoride poisoning. We surveyed residents, measured their urinary fluoride concentrations, and analyzed their serum-chemistry profiles. A case of fluoride poisoning was defined as an illness consisting of nausea, vomiting, diarrhea, abdominal pain, or numbness or tingling of the face or extremities that began between May 21 and 23. Among 47 residents studied who drank water obtained on May 21, 22, or 23 from the implicated well, 43 (91 percent) had an illness that met the case definition, as compared with only 6 of 21 residents (29 percent) who drank water obtained from the implicated well at other times and 2 of 94 residents (2 percent) served by the other water system. We estimated that 296 people were poisoned; 1 person died. Four to five days after the outbreak, 10 of the 25 case patients who were tested, but none of the 15 control subjects, had elevated urinary fluoride concentrations. The case patients had elevated serum fluoride concentrations and other abnormalities consistent with fluoride poisoning, such as elevated serum lactate dehydrogenase and aspartate aminotransferase concentrations. The fluoride concentration of a water sample from the implicated well was 150 mg per liter, and that of a sample from the other system was 1.1 mg per liter. Failure to monitor and respond appropriately to elevated fluoride concentrations, an unreliable control system, and a mechanism that allowed fluoride concentrate to enter the well led to this outbreak. Inspection of public water systems and monitoring of fluoride concentrations are needed to prevent outbreaks of fluoride poisoning.

[editor's note: see also Fluoride 27:1, 1994 January, 32-36.

Penman AD, Brackin BT, Embrey R, Outbreak of acute fluoride poisoning caused by a fluoride overfeed, Mississippi, 1993, Public Health Rep, 1997 September, 12(5).

OBJECTIVE: To determine the extent and confirm the cause of an August 1993 outbreak of acute fluoride poisoning in a small Mississippi community, thought to result from excess fluoride in the public water supply.
METHODS: State health department investigators interviewed patrons of a restaurant where the outbreak first became manifest and obtained blood and urine samples for measurement of fluoride levels. State health department staff conducted a random sample telephone survey of community households. Public health environmentalists obtained water and ice samples from the restaurant and tap water samples from a household close to one of the town's water treatment plant for analysis. Health department investigators and town water department officials inspected the fluoridation system at the town's main water treatment plant.
RESULTS: Thirty-four of 62 restaurant patrons reported acute gastrointestinal illness over a 24-hour period. Twenty of 61 households that used the community water supply reported one or more residents with acute gastrointestinal illness over a four-day period, compared with 3 of 13 households that did not use the community water supply. Restaurant water and ice samples contained more than 40 milligrams of fluoride per liter (mg/L), more than 20 times the recommended limit, and a tap water sample from a house located near the main treatment plant contained 200 mg/l of fluoride. An investigation determined that a faulty feed pump at one of the town's two treatment plants had allowed saturated fluoride solution to siphon from the saturator tank into the ground reservoir and that a large bolus of this overfluoridated water had been pumped accidentally into the town system.
CONCLUSIONS: Correct installation and regular inspection and maintenance of fluoridation systems are needed to prevent such incidents.

Whitford GM, The Physiological and Toxicological Characteristics of Fluoride, J. Dental Research, 1990, 69:Spec Issue, 539-549

The metabolism and toxicity of fluoride are discussed with emphasis on new scientific findings. The gastric absorption, tissue distribution, and renal excretion of the ion are all influenced by the magnitude and direction of the pH gradient between adjacent body fluid compartments. This mechanism explains the asymmetric distribution of fluoride across cell membranes, and the manipulation of transmembrane pH gradients has proven efficacious in acute fluoride toxicity. The comparative metabolism and relative toxicities of ionic fluoride and monofluorophosphate are discussed. It is no longer certain that there is a difference between the acute toxic potentials of sodium fluoride and those of MFP. It is concluded that the "probably toxic dose" or PTD of fluoride--the dose which should trigger therapeutic intervention and hospitalization--is 5 mg/kg of body weight. As currently packaged, many dental products contain sufficient fluoride to exceed the PTD for young children. There is a need for additional research into the sources, effects, and fate of strongly bound or organic fluoride compounds. Attention is drawn to the fact that, while the metabolic characteristics and effects of fluoride in young and middle-aged adults have received considerable research attention, there is a paucity of such information for young children and the elderly. The increasing prevalence of dental fluorosis is addressed. It is concluded that nondietary sources of fluoride, mainly fluoride-containing dental products, are a major source of ingested fluoride. The article concludes with 12 recommendations for future research.

Whitford GM, Fluoride in dental products: safety considerations, J Dent Res 1987 May;66(5):1056-1060

This review summarizes the nature of acute fluoride toxicity, its time-course, and the fluoride doses that are involved. The generally accepted "certainly lethal dose" range for 70 kg adults, i.e., from 5 to 10 g of sodium fluoride or from 32 to 64 mg fluoride/kg, is discussed. Based on recent case reports of fluoride-induced fatalities, it is concluded that this dose range has little utility in cases involving young children. The concept of a "probably toxic dose" (PTD) is advanced. The PTD, 5.0 mg F/kg, is defined as the dose of ingested fluoride that should trigger immediate therapeutic intervention and hospitalization because of the likelihood of serious toxic consequences. The concentrations and quantities of fluoride in selected dental products are discussed in relation to the PTD. It is concluded that, as these products are currently packaged, most of them contain quantities of fluoride sufficient to exceed the PTD for young children. Recommendations are made to reduce the risk of toxicity associated with their use.

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