Fluoride Action Network

Kidney Patients Are at Increased Risk of Fluoride Poisoning

Fluoride Action Network | April 2012 | By Michael Connett
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  • It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients accumulate up to four times more fluoride in their bones than healthy individuals, and have similar increases in their blood as well.

    The risk faced by kidney patients has been known since as far back as the 1940s when a team of American doctors suggested that any one with “signs of renal impairment should have radiographic examinations of the skeletal system to rule out the existence of fluoride osteosclerosis.” (Linmans & McMurray 1943). In 1952, at the first congressional hearing on fluoridation, congressional committee members expressed serious concern about the potential for fluoridated water to harm kidney patients. When Dr. Heyroth, a proponent of fluoridation was asked by committee member: “Would you give fluoridated water to one with kidney trouble,” he responded: “No, the advice would be that he drink fluoride-free spring water.”

    The evidence that low-level fluoride exposure kidney patients has continued to mount. Yet, despite repeated calls for government health agencies to conduct systematic studies to verify the safety of fluoride exposures for people with kidney disease, no such research has ever been done.

    Kidney Patients at Increased Risk of Fluoride Poisoning:

    “[A] fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.”
    SOURCE: Schiffl H. (2008). Fluoridation of drinking water and chronic kidney disease: absence of evidence is not evidence of absence. Nephrology Dialysis Transplantation 23:411. [See paper]

    “[C]hildren who present with renal insufficiency before the age of 8 years are at risk for tooth defects. These effects will be more severe in the presence of F, and ingestion of F by young children with renal failure (i.e. F supplements or swallowing F-containing toothpaste) is contraindicated.”
    SOURCE: Lyaruu DM, et al. (2008). The effect of fluoride on enamel and dentin formation in the uremic rat incisor. Pediatric Nephology  23:1973-79.

    “Individuals with kidney disease have decreased ability to excrete fluoride in urine and are at risk of developing fluorosis even at normal recommended limit of 0.7 to 1.2 mg/l.”
    SOURCE: Bansal R, Tiwari SC. (2006). Back pain in chronic renal failure. Nephrology Dialysis Transplantation 21:2331-2332.

    “Persons with renal failure can have a four fold increase in skeletal fluoride content, are at more risk of spontaneous bone fractures, and akin to skeletal fluorosis even at 1.0 ppm fluoride in drinking water.”
    SOURCE: Ayoob S, Gupta AK. (2006). Fluoride in Drinking Water: A Review on the Status and Stress Effects. Critical Reviews in Environmental Science and Technology 36:433–487

    “In patients with reduced renal function, the potential for fluoride accumulation in the skeleton is increased. It has been known for many years that people with renal insufficiency have elevated plasma fluoride concentrations compared with normal healthy persons and are at a higher risk of developing skeletal fluorosis.”
    SOURCE: National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA’s Standards. National Academies Press, Washington D.C. p140 .

    “Skeletal fluorosis seems possible, especially in hot climates or with renal compromise, from drinking excessive quantities of instant or bottled teas. Our observations support the need for better understanding of the amounts and systemic effects of fluoride in teas.”
    SOURCE: Whyte M. (2006). Fluoride levels in bottled teas. American Journal of Medicine 119:189-190.

    “We hypothesize that elevated serum F levels might contribute to the disturbances in mineral ion homeostasis that are observed in patients with CRI [Chronic Renal Insufficiency]. This is of particular concern since the incidence of dental fluorosis has increased due to increased F– uptake from multiple fluoridated sources. The ubiquitous presence of F in food and beverage products regardless of the degree of water fluoridation suggests that the overall F exposure in individuals with CRI may need to be more closely monitored.”
    SOURCE: Mathias RS, et al. (2000). Increased fluoride content in the femur growth plate and cortical bone of uremic rats. Pediatric Nephrology 14:935–939

    “It is important to control the intake of [fluoride] and the prolonged use of fluoridated dental products in subjects with chronic renal insufficiency, to avoid a risk of fluorosis.”
    SOURCE: Torra M, et al. (1998). Serum and urine fluoride concentration: relationships to age, sex and renal function in a non-fluoridated population. Science of the Total Environment 220: 81-5.

    “It would not be surprising if there were some undetected cases of skeletal fluorosis in the Australian population in individuals with pathological thirst disorders and/or impaired renal function. However, the matter has not been systematically examined. This matter should be the subject of careful and systematic review.”
    SOURCE: National Health and Medical Research Council. (1991). The effectiveness of water fluoridation. Canberra, Australia: Australian Government Publishing Service.

    “Though fluorosis is prevalent in certain geographic parts of the world, it is likely to occur in other parts… in people with latent kidney disease even when they consume relatively lower amounts of fluoride than in endemic regions.”
    SOURCE: Reddy DR, et al. (1993). Neuro-radiology of skeletal fluorosis. Annals of the Academy of Medicine, Singapore 22(3 Suppl):493-500.

    “Impairment of renal function can prolong the plasma half-life and contribute to clinical toxicity at lower concentrations of fluoride intake.”
    SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700.

    “Persons with chronic renal failures constitute a possible group at-risk with respect to the occurrence of skeletal fluorosis, because of an increased fluoride retention after oral intake. Based on the results of one study, in which the difference in retention between nephritic patients and healthy persons was quantified (average retention: 65% and 20%, respectively), a total daily intake of about 1.5 mg appears to be the maximum acceptable intake for nephritic patients. In view of the limitations of this comparative study and of the individual differences in retention and sensitivity, this figure must only be regarded as an indication.”
    SOURCE: National Institute for Public Health and Environmental Protection. (1989). Integrated criteria document fluorides. Report No 758474010. The Netherlands.

    “The skeletal complication of fluoride is more common in renal disease. Because of the impairment in renal excretion of fluoride, high circulating concentrations of fluoride may be achieved in renal disease.”
    SOURCE: Pak CY. (1989). Fluoride and osteoporosis. Proceedings of the Society for Experimental Biology and Medicine 191: 278-86.

    “[A] fairly substantial body of research indicates that people with kidney dysfunction are at increased risk of developing some degree of skeletal fluorosis. … However, there has been no systematic survey of people with impaired kidney function to determine how many actually suffer a degree of skeletal fluorosis that is clearly detrimental to their health.”
    SOURCE: Hileman B. (1988). Fluoridation of water.Questions about health risks and benefits remain after more than 40 years. Chemical and Engineering News August 1, 1988, 26-42.

    “Fluoridation of drinking water up to 1.2 ppm apparently does not pose a potential risk to bone provided the renal function is normal... We should, however, recognize that it is difficult to give a strict value for a safe fluoride concentration in drinking water, because individual susceptibility to fluoride varies.”
    SOURCE: Arnala I, et al. (1985). Effects of fluoride on bone in Finland. Histomorphometry of cadaver bone from low and high fluoride areas. Acta Orthopaedica Scandinavica 56(2):161-6.

    “[T]he prolonged administration of Vichy Saint-Yorre water containing 8.5 mg of fluoride ion per liter, provokes a skeletal fluorosis. This intoxication appeared very quickly if the patient suffered from an even mild renal failure. Once again, it is shown that a disturbed renal function predisposes to an excessive retention of fluoride.”
    SOURCE: Boivin G, et al. (1985). [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.

    “Because the kidney is the main pathway of fluoride excretion, patients with chronic renal failure are especially vulnerable to osseous accumulation of ingested fluoride and to potentially deleterious effects.”
    SOURCE: Fisher JR, et al. (1981). Skeletal fluorosis from eating soil. Arizona Medicine 38: 833-5.

    “The finding of adverse effects in (kidney) patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause.”
    SOURCE: Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293.

    “In the human body, the kidneys are probably the most crucial organ during the course of low-dose long-term exposure to fluoride. Healthy kidneys excrete 50 to 60% of the ingested dose. Kidney malfunction can impede this excretion, thereby causing an increased deposition of fluoride into bone. Marier (1977) has reviewed data showing that, in persons with advanced bilateral pyelonephritis, the skeletal fluoride content can be 4-fold that of similarly-exposed persons with normal kidneys. Similarly, Mernagh et al. (1977) have reported a 4-fold higher skeletal fluoride content in persons with the renal failure of osteodystrophy. It has also been shown (Seidenberg et al. 1976; Hanhijarvi 1975) that plasma F- levels can be 3 1/2 to 5 times higher than normal in persons with renal insufficiency. It is thus apparent that persons afflicted with some types of kidney malfunction constitute another group that is more “at risk” than is the general population.”
    SOURCE: Marier J, Rose D. (1977). Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.

    “It seems probable that some people with severe or long-term renal disease, which might not be advanced enough to require hemodialysis, can still experience reduced fluoride excretion to an extent that can lead to fluorosis, or aggravate skeletal complications associated with kidney disease… It has been estimated that one in every 25 Americans may have some form of kidney disease; it would seem imperative that the magnitude of risk to such a large sub-segment of the population be determined through extensive and careful study. To date, however, no studies of this sort have been carried out, and none is planned.”
    SOURCE: Groth, E. (1973). Two Issues of Science and Public Policy: Air Pollution Control in the San Francisco Bay Area, and Fluoridation of Community Water Supplies. Ph.D. Dissertation, Department of Biological Sciences, Stanford University, May 1973.

    “It is generally agreed that water fluoridation is safe for persons with normal kidneys. Systemic fluorosis in patients with diminished renal function, however, seems a reasonable possibility. In such patients, fluoride may be retained with resulting higher tissue fluoride levels than in persons with normal renal function.”
    SOURCE: Juncos LI, Donadio JV. (1972). Renal failure and fluorosis. Journal of the American Medical Association 222:783-5.

    “When we correlated bone fluoride levels with the patient’s disease, it soon became evident that most of the higher levels were found in patients with an advanced chronic renal disease.”
    SOURCE: Call RA, et al. (1965). Histological and chemical studies in man on effects of fluoride. Public Health Reports 80:529-38.

    “The question of the effect of water containing 1 p.p.m. upon patients with severe impairment of kidney function requires special consideration in view of the fact that radiologic evidence of chronic fluorosis has been found in two persons with severe kidney disease who died at the early ages of 22 and 23 years, respectively…”
    SOURCE: Heyroth F. (1952). Hearings Before the House Select Committee to Investigate the Use of Chemicals in Foods and Cosmetics, House of Representatives, 82nd Congress, Part 3, Washington D.C., Government Printing Office, p. 28.

    “All patients with dental fluorosis and anemia and/or signs of renal impairment should have radiographic examinations of the skeletal system to rule out the existence of fluoride osteosclerosis… It is likely that the reason our patient retained fluorine in his bones was that he had renal damage of long standing; without this the osteosclerosis might not have developed.”
    SOURCE: Linsman JF, McMurray CA. (1943). Fluoride osteosclerosis from drinking water. Radiology 40: 474-484.