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SCIENCE
WATCH Newsletter: Latest Submission
to NRC Panel on Fluoride/Bone
DIRECTORY: FAN > Health > Newsletter > Issue # 4 FAN SCIENCE-WATCH March 15, 2004 Issue #4: Latest Submission to NRC Panel on Fluoride/Bone On Friday, March 12th, and Monday, March 15th, I submitted the following information to the US National Research Council (NRC). As many of you probably know, the NRC has been requested by the US Environmental Protection Agency (EPA) to review the adequacy of EPA’s current safe drinking water standard for fluoride (the Maximum Contaminant Level - MCL). See: http://www.fluoridealert.org/nrc-review.htm In the following submission, I start by summarizing the data on fluoride & bone damage which I’ve previously sent the panel (see: http://www.fluoridealert.org/bone-data.pdf ; http://www.fluoridealert.org/nrc-letter.pdf ; http://www.fluoridealert.org/nrc-letter2.pdf ). I then provide hard copies of, and commentary on, 11 significant studies on fluoride & bone. I have included my comments on these papers below. Based on the following information, it is clear that the current MCL can not be relied on to protect against fluoride-induced bone damage, including: reduced bone strength, reduced bone density, increased mineralization defects, exacerbation of bone disease in people with kidney disease, and skeletal fluorosis of varying severity. Thus, based on the issue of bone damage alone, the MCL needs to be lowered. This fact has important implications for EPA’s recent decision (January 23, 2004) to allow DOW AgroScience the right to spray a new fluoride pesticide - sulfuryl fluoride - on a wide range of foodstuffs prepared in the US. See EPA’s ruling here. EPA’s decision to give DOW the green light was entirely predicated on the adequacy of the current 4 ppm MCL. Hence, if the current NRC panel concludes that the 4 ppm MCL is inadequate than the EPA will have to revise its policy on sulfuryl fluoride. The NRC’s review of EPA’s fluoride MCL is expected sometime next year (2005). In the meantime, the Fluoride Action Network is working on an appeal to the EPA’s sulfuryl fluoride ruling, which we hope to have completed by next weekend. (EPA’s deadline is March 23, 2004). I will send out more information about the content of our appeal shortly. Michael Connett ----------------- Summation of Data on Fluoride & Bone Damage (at Exposure Levels Relevant to Current MCL) by Michael Connett 1) Water fluoride content EPA's current MCL of 4 ppm equals or exceeds: - The concentrations (1.2-1.4 ppm) found to produce skeletal
fluorosis in India and China. (SOURCE: Singh 1961;
Jollly 1970; Siddiqui 1970; Xu 1997; Choubisa 2001; Bo 2003)
2) Daily Fluoride Dose The daily doses (8 mg/day from 2 liters of water consumption; 12 mg/day from 3 liters; 16 mg/day from 4 liters) produced at EPA's current MCL equal, exceed, or lack an adequate margin of safety for: - The doses (2-8 mg) estimated to cause the early stages
of skeletal fluorosis. (SOURCE: Singh & Jolly
1970) 3) Serum fluoride content The serum fluoride levels (up to 14.1 umol/l – SOURCE: Johnson 1979) produced at half (i.e. 2 ppm) the EPA's MCL equal or exceed: - The serum fluoride levels (2-5 umol/L) associated with
altered bone cell activity. (SOURCE: Farley 1983;
Taves 1970; Pak 1989) 4) Bone fluoride content The *average* bone fluoride levels (6,100-6,400 ppm; SOURCE: Zipkin 1958; Gordin & Corbin 1992) found in adults at the EPA's MCL equal or exceed: - The bone fluoride levels (2,500 - 4,500 ppm) associated
with reduced strength of animal bone. (SOURCE: Mosekilde
1987; Turner 1993; Lafage 1995; Sogaard 1995) References for Bone Data: To see the references, click here ------------ Comments on Submitted Papers: Paper # 1 : 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. This study reports a higher rate of bone fracture, and an increased rate of bone loss, in a US community with 4 ppm fluoride in the water versus a community with 1 ppm. The study highlights the problematic nature of EPA’s assumption (when setting the fluoride MCL in 1985) that crippling skeletal fluorosis is the only relevant adverse bone effect which the MCL should protect against. Common sense alone should indicate that if fluoride can cripple the human skeleton, it can probably cause subtler bone damage before it cripples. This study by Sowers suggests that bone fracture and reduced bone density are 2 such bone effects which can occur before the skeleton is crippled (e.g. before the spinal column is fused into one calcified immobile bone, and before extensive joint calcifications occur throughout the rest of the body). Other bone effects which may occur before the skeleton is crippled, include:
Paper # 2: Phipps KR, Burt BA. (1990). Water-borne fluoride and cortical bone mass: A comparison of two communities. Journal of Dental Research 69: 1256-1260. Consistent with Sowers (1991), this study also reports an increased rate of bone loss in a US community with 3.5 ppm fluoride in its water versus a community with 0.7 ppm. As with Sowers (1991), this study highlights the problems with EPA’s focus on crippling skeletal fluorosis as the only adverse bone effect to protect Paper # 3: 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. I believe this study is extremely important. Written by 2 scientists at the Mayo Clinic (William Johnson & Jennifer Jowsey), as well as Donald Taves from the University of Rochester, this study reports on the Mayo Clinic’s experience with fluoride-induced bone damage in people with kidney disease. As with Juncos & Donadio (1972), this study found that people with kidney disease developed what the authors believed to be fluoride-induced bone damage by drinking water with “just” 1.7 to 2 ppm. What makes this study particularly strong, is that, unlike the earlier study from Juncos & Donadio (1972), the authors here took fluoride measurements of the patients’ serum and bones, and found both to be greatly elevated. In addition, the authors found that when they switched the patient with the severest case of bone disease to a fluoride-free water supply, his symptoms (e.g. bone pain) subsided. In light of these and other findings, the authors conclude:
Again, I believe that if the EPA’s MCL is to fulfill its mission to “protect the most vulnerable”, than it can not just focus on crippling skeletal fluorosis as the only adverse bone effect to protect against (as is currently the case). Rather, the MCL should seek to prevent the pre-crippling effects as well, which in this case is a fluoride-induced exacerbation of bone disease in kidney patients. Interestingly, when the EPA established its MCL in 1985, it acknowledged that the current MCL could not be relied on to protect people with kidney disease. To quote:
“Except” is the key word here. It stands in clear contrast to the EPA’s emphasis of protecting the most vulnerable. To quote:
Paper # 4: Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078. This study reports a case study of a US adult who developed crippling skeletal fluorosis, despite being exposed to water with “just” 2.4-3.5 ppm. In setting its MCL in 1985, the EPA dismissed this study because the patient had experienced chronic excessive thirst. Considering that the goal of the MCL, however, is to protect the most vulnerable subsets of the population, EPA’s rationale for dismissing this finding is unacceptable. Paper # 5: 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. This study found that bone mineralization defects begin to increase when the fluoride content of water increases above 1.5 ppm. To quote:
Paper # 6: Ng AHM, et al. (2004). Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy. Bone 34: 216-224. This study is important for at least 2 reasons. It discovered a high accumulation of fluoride (avg = 3,400 ppm in patients with osteomalacia) in the bones of people with kidney disease (in the greater Toronto area). And, as with Arnala (1985), it found a relationship between the accumulated fluoride and bone mineralization defects in the patients. (NOTE: Since dialysis units now filter out the fluoride from the water, the fact that these patients were on dialysis using fluoridated water should not account for the increased accumulation of fluoride in the bone. Indeed, it has been found that dialysis units which filter out the fluoride, actually serve to reduce the fluoride burden in the body.) Paper # 7: Ittel TH, et al. (1992). Effect of fluoride on aluminum-induced bone disease in rats with renal failure. Kidney International 41: 1340-1348. In light of the recent findings from Ng (2004), as well as the long-held suspicion that fluoride can be a significant contributing factor in aluminum-induced bone disease, this animal study is extremely interesting. The authors found that fluoride exacerbates the aluminum-induced damage to rat bone. Interestingly, the levels of fluoride used in the study are low (20 ppm and 40 ppm in water). Based on my previous analysis of the serum fluoride levels produced in rats at varying water fluoride levels (see Table 7 of my January 29th, 2004 submission), the serum fluoride in these rats would be in the ballpark of 4-8 umol/L. This would be well within the range of serum fluoride in kidney patients living in fluoridated areas (Hanhijavi 1975; Waterhouse 1980; Warady 1989; Torra 1998). Paper # 8a: 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. This recent study from China clearly documents that skeletal fluorosis is caused by water supplies exceeding 1 ppm fluoride. The average level of water consumption in the area being studied was estimated to be 3 liters/day, while the average total fluoride exposure was estimated to be 9.4 mg/day. Please note that 9.4 mg/day is a dose that will definitely be exceeded by some people drinking water at EPA’s current MCL for fluoride. Also note that when the EPA established its fluoride MCL in 1985, it mistakenly believed that skeletal fluorosis only occurred in India and China when the water fluoride concentration exceeded 10 ppm fluoride. To quote:
The most striking problem with this statement by the EPA is not that it has been contradicted by studies published after it was written, but rather, that it had already been contradicted, and frequently so, by seminal research conducted in India during the 40 years preceding the statement. For instance, in two of the most frequently cited papers on skeletal fluorosis in India, (Singh 1961, 1963) skeletal fluorosis was observed at 1.2 ppm and between 1 and 2 ppm, while Siddiqui (1970) reported skeletal fluorosis at 1.2-1.4 ppm, and Jolly (1970) reported fluorosis at 1.4 ppm. Many more studies, meanwhile, reported crippling fluorosis above 2 ppm, but far below 10 ppm, including Pandit (1940); Siddiqui (1955); Kumar (1963); and Krishnamachari (1973). Paper # 8b: Cao J, et al. (2003). Brick tea fluoride as a main source of adult fluorosis. Food and Chemical Toxicology 41: 535-42. This study provides a carefully controlled analysis of the doses of fluoride causing crippling (stage III) skeletal fluorosis in Tibet. The average dose among the adults was found to be 12 mg/day. At the EPA’s current MCL of 4 ppm, a portion of the population (people who drink 3+ L/day) will consume more than 12 mg/day from the water-supply alone. Paper # 9: Eble DM, et al. (1992). Fluoride concentrations in human and rat bone. Journal of Public Health Dentistry 52: 288-291. The following study by Eble measured the fluoride content of bones from 24 patients at an orthopaedic hospital in North Carolina. The study is of particular interest considering the glaring scarcity of recent bone fluoride level data from the US. Also, despite the small sampling, the authors found that 4 of the 24 people’s bones had fluoride levels exceeding 3,000 ppm, with 2 of the samples exceeding 3,500 ppm. To put these figures in perspective, Franke (1975) estimated that the early radiological signs of skeletal fluorosis can be detected when human bone exceeds 3,500 ppm F, while the strength of bone has been found to be reduced in animal studies when the fluoride bone content exceeds 2,500 ppm (Lafage 1995); 2,700 ppm (Mosekilde 1987); and 3,300 ppm (Sogaard 1995). Paper # 10: Mihashi M, Tsutsui T. (1996). Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture. Mutation Research 368(1):7-13. This study provides an important follow-up to the NTP’s 1990 fluoride bioassay. Being that the NTP’s bioassay found a statistically significant increase in osteosarcomas in the fluoride exposed male rats, this study sought to determine if fluoride was genotoxic to rat bone. The authors conclude:
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