Another argument against fluoridation is the risk in transporting a dangerous substance.

http://www.azcentral.com/news/articles/0205downtownhaz05.html

Acid spill downtown sends 16 to hospitals

Judi Villa and Jacqueline Shoyeb
The Arizona Republic
Feb. 5, 2005 12:00 AM

A truck traveling through Phoenix leaked more than 110 gallons of hydrofluorosilic acid on Friday, closing a significant part of downtown and keeping residents inside.

Sixteen people - the truck's driver, 11 police officers and four civilians - were taken to hospitals for evaluation because they may have stepped into the liquid. Three firefighters also were evaluated for possible exposure.

Dr. Paul Connett responds to MF.

MF: At last, a voice of reason in the fluoridation debate. Thank you Colin Rix and Diana Donohue.

MF: Can those opposed to fluoridation please explain why more than 100 of the world's leading health and scientific authorities endorse water fluoridation?

PC RESPONSE: Can MF explain why it is with such illustrious support, the vast majority of countries worldwide have not succumbed to this practice? Only a handful of countries – largely English speaking –have more than 50% of their population drinking artificially fluoridated water (i.e. Australia, Columbia, Hong Kong, Ireland, Israel, Malaysia, New Zealand and the United States).

MF: These authorities are the most respected agencies in the world, both government and non-government.

PC RESPONSE: As a scientist I was trained to examine the evidence and not simply rely blindly on "authority" no matter how impressive that authority might appear to be. Respect has to be earned and earned every day by the quality of one’s work and the integrity with which it is applied. Whatever the track record of these agencies has been in other areas, I am sad to say that neither the quality of their work on fluoridation nor the integrity with which they have pursued the issue is very impressive.

PC: Very few of these bodies have done their own independent work or scientific review of this issue. Unfortunately, once the US Public Health Service endorsed fluoridation in 1950 (before one single trial on fluoridation was more than half complete, and before any long term health effects had been studied) most of these agencies –at least the American ones – fell into line. Simply put, they are either part of the US Public Health Service, or they receive a bulk of their research funds from one or more of their agencies. The old adage applies: you don’t bite the hand that feeds you.

PC: Professional organizations like the American Dental Association (ADA) have ways of keeping their members in line on this issue. Here for example is a quote from an 1979 ADA white paper:

"Individual dentists must be convinced that they need not be familiar with scientific reports of laboratory and filed investigations on fluoridation to be effective participants in the promotion program and that nonparticipation is overt neglect of professional responsibility."

PC: Here is another from Dr. Michael Easley, a sometime spokesperson for the American Dental Association and the American Council on Science and Health:

"Like parasites, opponents steal underserved credibility just by sharing the stage with respected scientists who are there to defend fluopridation. Unfortunately, a most flagrant abuse of the public trust occasionally occurs when a physican or a dentist, for whatever persoanl reasons, uses their professional standing in the community to argue against fluoriadtion, a clear violation of professional ethics, the principles of science and community standards of practice." (Easley, 1999)

PC: If they were pursuing a sound policy the dental establishment would not need to intimidate their own rank and file; ridicule opponents and refuse open public debate.

MF: Is it a vast, world-wide conspiracy to poison people, or is it just possible that fluoridation is both safe and effective?

PC RESPONSE: Hardly worldwide, since so few countries actually fluoridate their water. But conspiracy is a loaded word. Let’s simply say that huge economic interests have benefited greatly from the distraction that fluoridation provides:

a) It draws attention away from the harmful effects fluoride has had on workers’ health and the local environment of many industries which either use fluoride in their manufacturing processes (like the aluminum, steel and other metal industries and the nuclear industry) or produce it as a byproduct (like the phosphate, ceramic and brick industries). Their involvement in the propagation of this practice is fully and meticulously documented in The Fluoride Deception by Chris Bryson which was published last year.

b) It drew attention away from one of the causes of tooth decay: over-consumption of sugary foods. The US sugar lobby - the year before the US PHS endorsement of fluoridation - was on record as saying that they wanted to find a way to reduce tooth decay without reducing sugar consumption, and subsequently they have put a considerable amount of money into fluoride research.

c) It draws attention away from the failure of the US to provide decent dental care for poor children. Over 80% of American dentists refuse to treat children on Medicaid.

PC: As far as the quality of fluoridation research is concerned, it is extraordinary to me that the most fundamental of studies has not been performed. For example, even though we have known for years that about 50% of fluoride ingested each day accumulates in our bones and steadily increases over a lifetime, no government promoting fluoridation has yet to undertake a comprehensive analysis of bone levels in their population, (or for that matter plasma levels or urine levels). We are flying blind, even while we are seeing a massive rise in arthritis, osteoporosis, and hip fractures in the elderly. Another example is that even though it has been known for over 60 years that there is a very strong correlation between the severity of dental fluorosis and level of exposure to fluoride before a child’s second teeth have erupted, this obvious biomarker has seldom been used in epidemiological studies to investigate possible connections between fluoride exposure and health concerns in children. Despite the millions of dollars spent by the Australian government on promoting fluoridation they have not sponsored one primary study on health effects on any organ but the teeth.

PC: When the York Review panel examined 3200 papers on the safety and effectiveness of fluoridation not one study was given a high quality rating (i.e. minimal risk of bias). Only 252 met their inclusion criteria (B and C quality –i.e. moderate and high risk of bias). Considering the enormous promotion that fluoridation has received from governments in the US, Australia, Britain, Ireland and New Zealand for over 40 years, it is astonishing to find how low a quality the studies have been which they have largely funded.

PC: As far as the integrity of their work is concerned, let us look at one of the most prestigious agencies on MF’s list of 100: the US Centers for Disease Control and Prevention (CDC). This agency has been quoted worldwide as saying that fluoridation is "one of the top 10 public health achievements of the Twentieth Century" (CDC, 1999). However, as I explained in my earlier comments above, the report on which this statement was based was six years out of date on the health studies it cited to support its claim that the practice was "safe". As far as their demonstration that fluoridation was "effective", the evidence produced was laughable. In the only figure produced in the paper they showed a graph covering the period from the 1960s to 1990s and on this graph they had two lines. One line represented the tooth decay in 12 year olds as measured by decayed missing and filled permanent teeth (DMFT). This line was coming down. A second line showed the percentage of the US population drinking fluoridated water. This line was going up. Voila. Cause and effect. Tooth decay in the US was coming down because the percentage of the US population drinking fluoridate water was going up! One would have thought that such a "prestigious and highly respected agency" before printing this simplistic nonsense would have first checked out to see what was happening to dental decay in 12 year olds in other countries – both fluoridated and non-fluoridated. It turns out that this data is available online from the WHO. It shows just as dramatic declines in tooth decay over the same time period in 16 non-fluoridated countries as in 4 fluoridated ones. Readers can compare the CDC graph with the WHO data (displayed graphically) at http://www.fluorideaction.org/who-dmft.htm. I will leave it to readers to decide whether this CDC figure was an example of gross incompetence or a deliberate attempt to deceive.

MF: Why is it that most of the "scientific studies" quoted by Dr Connett and fellow anti-fluoridationists are irrelevant to optimal water fluoridation,

PC RESPONSE: I consider myself an independent scientist who has patiently and independently examined the literature on this issue for over 8 years (i.e. twice the length of time that I spent on my PhD). It is undignified of MF to attempt to trivialize my efforts by putting scientific studies in quotation marks, and to label me as a "fellow anti-fluoridationist" as if I had joined some cult. None of the scientific studies I cite are irrelevant to optimal fluoridation.

MF: …misquote legitimate health and scientific authorities,

PC RESPONSE: MF gives no example of where I have misquoted any one. Will he please retract this statement or give an example?

MF: …or are taken from junk journals such as Fluoride?

PC RESPONSE: I do not believe that Fluoride is a junk journal. Far from it. It has been one of the few journals to bring the important research on fluoride toxicity being carried out in India and China to the attention of the English speaking world.

MF: As an example, consider the very first "study" quoted by Dr Connett in this forum; Alarcon-Herrera MT et al. (2001). Well water fluoride, dental fluorosis, bone fractures in the Guadiana Valley of Mexico. Fluoride;34:139-149.
Almost all the areas surveyed in the study had naturally occurring fluoride levels many times higher than those found in artificially fluoridated areas.

MF: The authors subjectively selected only bone fractures "that had ever occurred without apparent cause, where a bone fracture would not normally be expected to occur". They admit that validation was a difficult task "because we depended on the subjectivity of both the interviewer and the interviewed". The authors also found that "the incidence of fractures was found to decrease at higher fluoride concentrations", but could not explain why this could be the case. And "studies" of this calibre are used to argue against optimal water fluoridation. Puh-lease...

PC RESPONSE: Here MF completely misses the crucial point. The correlation was not between bone fractures in children and the level of fluoride in the water (i.e. it was not an ecological study) but between bone fractures in children and the severity of their dental fluorosis (a biomarker for fluoride exposure). This correlation was almost linear, with the highest incidence of bone fracture associated with the most severe level of dental fluorosis. This part of the study was blind to the level of fluoride in the water and how much the children may have drunk.

PC: While there may be limitations to this study it is very important since it suggests that dental fluorosis is more than just a "cosmetic effect" as claimed by those promoting fluoridation, and could well signal damage to the bones as well as the dental enamel. Rather than dismissing this study out of hand as MF and most pro-fluoridation governments have, it needs careful repeating. This is especially so since this is not the only evidence that fluoride damages bones in children. In one of the early trials of fluoridation in the US (Schlesinger et al. 1956 see also NAS, 1977). Children in fluoridated Newburgh, NY had significantly more (13.5 versus 6.5%) cortical bone defects than children in non-fluoridated Kingston, NY (the control city). The importance of this is that it is the cortical bone (the outside layer of the bone) which provides the key resistance to bone fracture (particularly in the arms and legs). Any defects in the cortical bone could thus lead to increased fracture rates as observed by Alarcon-Herrera et al (2001).

MF: Why, of the 37 studies quoted by Dr Connett, do only about a third actually relate to optimal water fluoridation?

PC RESPONSE: MF’s arithmatic is rather suspect here. I count 25 studies which directly examine the impacts of "optimal" water fluoridation. It is true that a few of the papers examine effects at higher concentrations (Bachinskii, Li and Xiang) but that is important because while the concentration of fluoride added to water can be controlled, the dose to recipients cannot. It is critically important to find out what effects can occur at higher concentrations as a way of estimating what might happen to those recipients who drink large quantities of water and receive doses from other sources. No regulatory toxicologist would refuse high dose data to tease out effects which might occur in vulnerable individuals within an heterogeneous population. In the studies I cited the authors report serious impacts at only slightly higher concentrations of fluoride in the water (1.5 –4.3 ppm) than the so-called optimal concentration of 1 ppm.

MF: At least a dozen of his quoted authors actually support the caries preventive effect of fluoride and water fluoridation. And yet Dr Connett quotes them to support his case! Does he expect no-one to actually read the articles?

PC RESPONSE: I only make it 6 authors ( Brunelle, Carlos, Spencer, Slade, Davies and Armfield) but do please read the articles MF, because the findings from these pro-fluoridation researchers, strengthens the opponents’ case not weakens it, as you imply. When one reads their papers one finds a huge discrepancy between what they actually found and how they use their findings to support water fluoridation.

PC: For example, in table 6 in the Brunelle and Carlos paper (1990) they indicate an average DMFS for children (5-17) who have all their lives in a non-fluoridated communities of 3.36 and for the fluoridated ones of 2.76. If we subtract 2.76 from 3.36, we get a saving of 0.6 tooth surfaces. This represents a saving of less than 0.5% of the 128 tooth surfaces in a child’s mouth. However, that is not how they report it, they report it as an 18% saving in tooth decay (exploiting the vagaries of comparing two small numbers). Even so this is much smaller than the 40-60% frequently claimed by fluoridation promoters.

PC: More to the point, here is how they describe this miniscule saving of 0.6 of one tooth surface (which was not even shown to be statistically significant) in their abstract, which sadly is often all that busy decision makers get a chance to read:

"Children who had always been exposed to community water fluoridation had mean DMFS scores about 18% lower than those who had never lived in fluoridated communities. When some of the "background" effect of topical fluoride was controlled, this difference increased to 25%. The results suggest that water fluoridation has played a dominant role in the decline in caries and must continue to be a major prevention methodology."

PC: In the abstract of the Spencer et al. (1996) paper the authors write:

"In the press and scientific literature there has been questioning of fluoridation, although the most recent Australian review reasserted its safety and effectiveness. Results from Australian oral epidemiological studies consistently support the accumulated evidence on the effectiveness of water fluoridation. This includes recent evidence that lifetime exposure to fluoridation is associated with average reductions of 2.0 dmfs and between 0.12 and 0.3 DMFS per child compared with non-exposed children."

PC: When we translate the technical terms we find that Spencer et al. are offering a saving of between 0.12 and 0.3 permanent tooth surfaces (out of 128 tooth surfaces in a child’s mouth) as "evidence of the effectiveness of water fluoridation". This is even smaller than the miniscule saving reported by Brunelle and Carlos!

PC: In the abstract of the Armfield and Spencer (2004) paper the authors write:

"The consumption of nonpublic water (i.e. tank and bottle water, PC) on permanent caries experience was not significant."

PC: But that didn’t stop Dr. Spencer in an interview in the Sydney Morning Herald (November, 2004), recommending that bottled water be fluoridated!

PC: I think it is fairly clear that dental researchers worldwide know that in order to keep the money flowing into their research coffers they need to keep supporting the party line, even while revealing to those who take the trouble to actually read their papers, that they are not finding the evidence that water fluoridation is very effective, especially in protecting the permanent teeth.

PC: But possible motivation aside, it is important to stress that it is the promoters’ own literature which wins our argument: today there is no need to fluoridate the community’s water since those communities that don’t fluoridate their water have just as good (permanent) teeth as those that do. There may be several reasons for this, one of them being that there is far greater correspondence between tooth decay and poverty and poor diet than with lack of fluoride. Thus tooth decay in industrialized countries has come down in both fluoridated and non-fluoridated communities (and countries) as standard of living has gone up.

MF: The reason that the practice of water fluoridation continues to grow throughout the world is simple. It strengthens teeth against tooth decay and it's safe. End of story.

PC RESPONSE: You wish!

MF (12/02/2005) has described Fluoride: quarterly journal of the International Society for Fluoride Research as an example of "junk journals". I would be grateful if the reasons for this view could be given. I commenced an association with this journal as an
Associate Editor in 1994 and have been Managing Editor since 1999. The journal indicates in its guidelines to authors that, as far as possible, the "Uniform requirements for manuscripts submitted to biomedical journals" prepared by the International Committee of Medical Journal Editors should be followed (updated last October 2004, and available at www.ICMJE.org). The editorial staff endeavour to follow these requirements. Readers may judge the degree to which they have succeeded at the journal's web page at http://homepages.ihug.co.nz/~spittle/fluoride journal.htm

Response to Rix and Donohoe by Dr Mark Diesendorf follows:

The commentary by Rix and Donohue on my article, “Sustainable development and toxic chemicals: the case of fluoride”, is disappointing, since it is full of the usual pro-fluoridation generalities, sweeping statements, spin substituting for science (e.g. “fluoride occurs naturally”), and appeals to pro-fluoridation authorities. It evades or misrepresents most of my specific points of concern, for example:

1. Many studies have reported skeletal fluorosis in several different countries (including the USA) where fluoride concentrations in drinking water are less than or approximately equal to 2.5 ppm and in one village as low as 0.7 ppm (1), which is even acknowledged in the profluoridation NH&MRC (1991) report. So why do Rix and Donohue persist, in the face of all the evidence, in fostering the false impression that that skeletal fluorosis is only seen above 8 ppm?

2. Toxicology generally requires that average exposure levels to chemicals be a factor of 100 below levels known to cause chronic health damage. This point evaded, as was my specific concern for babies who are fed on milk formula reconstituted with fluoridated water and ingest adult doses of fluoride daily (2) that are 100-200 times the doses received by breast-fed babies.

3. The majority of epidemiological studies published in refereed journals find an increased rate of bone fractures (especially hip fractures) in fluoridated communities. This point was misrepresented with claims that studies that found a positive association had inadequate samples etc. Actually, the reverse is true: most studies that failed to find an association had inadequate samples.

4. There is a substantial body of blind clinical studies, plus one double-blind epidemiological study, demonstrating that some people suffer hypersensitivity reactions to fluoride in drinking water or tablets or toothpaste. Rix and Donohue avoid the point by talking about allergies, which my paper does not mention. There is a difference -- allergies, as defined medically, involve the immune system, while hypersensitivity reactions may or may not involve the immune system.

5. Everyone agrees that large reductions in dental caries have occurred from the 1960s onwards, especially in developed countries. But Rix and Donohue evade my point, that has been published in my 1986 paper in Nature (3), that such reductions occurred in both unfluoridated and fluoridated communities, including prefluoridation Sydney and unfluoridated Brisbane.

6. They misrepresent the results of recent studies on cessation of fluoridation published in international journals, which all find that dental caries either remained the same or decreased following cessation (4).

7. They ignore the recent major study by pro-fluoridationists, Armfield and Spencer (5), which could find no statistically significant benefit of fluoride in permanent teeth of South Australian children. They also ignore the two major studies on 84 US cities using National Institute of Dental Research data, which could find no benefit when DMFT was used as an indicator and only a tiny benefit when DMFS was used (6).

8. Their ‘response’ to my point that fluoridation is mass medication, is to compare fluoridation with vitamin D and folic acid. This implies incorrectly that fluoride is an essential nutrient like a vitamin. But there are case studies of communities with excellent teeth who have very low fluoride intakes and communities with rotten teeth who have high fluoride intakes. Therefore, fluoride at the doses of several mg/day delivered by fluoridated water is neither necessary nor sufficient for sound teeth. It is no more a nutrient than a dental fissure sealant. Therefore, since fluoride is not a nutrient and is used to treat people, it is a medication. That it is used preventively does not change the situation, since there are many preventive medications. That it is a natural substance does not stop it from being a medication, since many medications are, or were originally, natural substances: e.g. penicillin, aspirin and digitalis. Therefore, the ethical arguments about the use of medication – the need to deliver a controlled dose, informed consent, and randomised controlled trials to determine safety and effectiveness – should be applied to fluoridation. The fact that they are avoided demonstrates that fluoride is indeed the protected pollutant.

9. Rix and Donohue attempt to address seriously, if inconclusively, only one of my points. Unlike the Australian Dental Association they concede that the mechanism of action of fluoride on teeth is predominantly topical (i.e. a surface effect), but they claim that there are still benefits from ingested fluoride, because it returns to the mouth in saliva. They omit to inform readers that the resulting fluoride concentration in saliva resulting from the ingestion of 1 ppm fluoride drops rapidly to a a few percent of 1 ppm. The claim that such low concentrations have significant dental benefit is still an unproven hypothesis. Counter-evidence is that animal experiments can find no dental benefit from even high concentrations of fluoride that are introduced directly into the bloodstream, initially bypassing the mouth (7).

In general Rix and Donohue rely on ‘reviews’ and endorsements by pro-fluoridation bodies such as the NH&MRC, Australian Dental Association and Australian Medical Association, which originally endorsed fluoridation in the 1950s and have been defending their position ever since.

In particular, to claim that the 1991 NH&MRC review addressed my concerns, is a sick joke. Although the review was indeed nominally set up in response to a letter from Dr John Colquhoun, Dr Philip RN Sutton and me, its bias was demonstrated by its gross misrepresentations of our case and its failure to cite any of the many refereed publications that we had published on fluoridation in the scholarly literature and submitted to the review (8). I see the NH&MRC review as a public relations document designed to give the superficial appearance of scientific scrutiny without its substance. The PR aspect was demonstrated by the way the executive summary misrepresented the little bits of evidence unfavourable to fluoridation that somehow slipped into the main body of the report – e.g. the fact that skeletal fluorosis is seen in India when fluoride concentration is as low as 0.7 ppm appeared in Section 6.4 but, through slick wording, the executive summary created the false impression that no adverse effects are seen at or below 1 ppm. It appears that Rix and Donohoe did not read beyond the executive summary.

Finally , Rix and Donohue’s choice of compulsory mass chest x-ray campaigns as a precedent and justification of fluoridation, is unfortunate for their case. The campaigns were discontinued because they were creating more cancers through irradiation than lives were saved through the early detection of tuberculosis. They were more dangerous to Australians than fallout from the French nuclear tests that were being carried out at that time. As it happened, it was my colleagues and I in the then Society for Social Responsibility in Science in Canberra who identified the problem and campaigned in the public interest for several years until compulsory chest x-rays were discontinued (9).

Dr Mark Diesendorf
Email: mark@sustainabilitycentre.com.au

References
1. e.g. Singh A, Jolly SS & Bansal BC, 1961, Skeletal fluorosis and its neurological complications, Lancet 1:197-2000; Jolly SS, Prasad S, Sharma R & Chander R, 1973, Endemic fluorosis in Punjab. I. skeletal aspect, Fluoride 6:4-18; Siddiqui AH, 1970, Neurological complications of skeletal fluorosis with special reference to lesions in the cervical region, Fluoride 3:91-96; Misra UK et al. 1988, Endemic fluorosis presenting as cervical cord compression, Arch Environ Health 43:18-21; Pinet A & Pinet F. Endemic fluorosis in the Sahara. Fluoride 1(2):86-93; Juncos LI & Donadio JV 1972, Renal failure and fluorosis, JAMA 222:783-5.

2. Diesendorf M & Diesendorf A 1997, Suppression by medical journals of a warning about overdosing formula-fed infants with fluoride, Accountability in Research 5:225-237.

3. Diesendorf M 1986, ‘The mystery of declining tooth decay’, Nature 322: 125-129.

4. Seppa L, Karkkainen S, Hausen H. 2000, Caries Trends 1992-1998 in Two Low-Fluoride Finnish Towns Formerly with and without Fluoridation. Caries Research 34: 462-468; Kunzel W, Fischer T, Lorenz R, Bruhmann S. 2000, Decline of caries prevalence after the cessation of water fluoridation in the former East Germany. Community Dentistry and Oral Epidemiology 28: 382-9; Kunzel W, Fischer T. 2000, Caries prevalence after cessation of water fluoridation in La Salud, Cuba. Caries Research 34: 20-5; Maupome G, Clark DC, Levy SM, Berkowitz J. 2001, Patterns of dental caries following the cessation of water fluoridation. Community Dentistry and Oral Epidemiology 29: 37-47.

5. Armfield J & Spencer J 2004, Consumption of non-public water: implications for children’s caries experience. Community Dent Oral Epidemiol 32:283-96.

6. Yiamouyiannis J 1990, Water fluoridation and tooth decay: results from the 1986-1987 national survey of U.S. schoolchildren, Fluoride 23:55-67; Brunelle, JA & Carlos JP, 1990, Recent trends in dental caries in U.S. children and the effect of water fluoridation, Journal of Dental Research 69 (special edition): 723-727.

7. e.g. Mirth DB et al. 1985, Comparison of the cariostatic effect of topically and systemically administered controlled-release fluoride in the rat, Caries Research 19: 466-74.

8. Colquhoun J 1991, letter, Aust J Pub Health 15:308-9; Diesendorf M 1991, letter, Aust J Pub Health 15:309-10.

9. Diesendorf M 1975, Low level ionising radiation and man, Search 6 (8): 328-334.

The Rix and Donahue posting on the supposed "safety" of "fluoridation" ignores the evidence on differences between sodium fluoride (tested for safety and well known from toothpaste) and hydrofluosilicic acid (H2SiF6) or sodium silicofluoride (Na2SiF6) -- silicofluorides which were NEVER tested before their use began in the 1940s and was approved by the U.S. Public Health Service in 1950. Working with Myron J. Coplan (a chemical engineer), I've published widely on harmful effects of water treated with silicofluorides that do not occur when sodium fluoride is used. These include increased blood lead levels in children exposed to comparable environmental exposures to lead (e.g., from lead paint in old housing) and higher rates of behaviors associated with lead and other toxins (such as learning disabilities, substance abuse, and violent crime). The issues discussed in the exchanges on "fluoridation" have ignored these effects on BEHAVIOR as established using conventional epidemiological methods and the enormous costs to taxpayers they entail. For instances, because in the U.S. it costs approx. $25,000 (or more) to incarcerate a violent criminal for one year. the added costs of criminal incarceration associated with the use of silicofluorides are in the millions of dollars.

R & D do not seem to be aware that while U.S. government agencies and dental associations have long ignored the difference between sodium fluoride and the silicofluoride, since our publications the National Toxicology Program has nominated the silicofluorides for study. Mr. Coplan and I have therefore proposed a moratorium on the use of silicofluorides until independent testing proves they are safe and explains our contrary findings. The text of such a proposal is below.

roger masters (NOTE: those wishing to know my credentials should consult the U.S. WHO'S WHO for 2005).

---

MOTION FOR A MORATORIUM ON ADDING SILICOFLUORIDES TO PUBLIC WATER UNTIL ADEQUATE BIOLOGICAL TESTING PROVES ABSENCE OF HARMFUL EFFECTS TO CHILDREN'S HEALTH AND BEHAVIOR

Draft Legislation:

“Effective _______, until the addition of either hydrofluosilicic acid (H2SiF6) or sodium silicofluoride (Na2SiF6) to a water supply shall have been found by health effects studies approved by the EPA to be without harmful effects to children’s health and behavior, no public water system within the state of New Hampshire shall use these chemical compounds for the purpose of “fluoridation” (i.e., adjusting the level of fluoride to a target level).


RATIONALE:

Recognizing that 91 percent of U.S. fluoridated water, in systems serving over 116 million people, collectively, has been treated with 200,000 tons per year of commercial grade silicofluorides (H2SiF6 and Na2SiF6), henceforth referred to as “SiFs”; and

Further recognizing that these SiFs have been used for water fluoridation since 1947; and

Noting the Environmental Protection Agency's acknowledgement to Congress, and to others, that it is unaware of any human health safety testing of these silicofluoride compounds; and

Also noting that in 1952, a Select Congressional Committee (82nd Cong., 2d Session) requested studies “to determine the long-range effects upon the aged and chronically ill of the ingestion of water containing inorganic fluorides” yet there is no evidence that any Federal Health agency ever developed a research program to address the issue of health safety of the silicofluorides; and

Noting, too, that health effects studies of fluoridated water performed in animals, including those conducted by the National Institute of Health's National Toxicology Program, have employed sodium fluoride (NaF), the agent first used in water fluoridation in 1945, and not SiFs, the principal agents currently added to water; , , , , , , , , and

Noting evidence that water treated with SiFs is dissimilar from water treated with NaF,
notwithstanding claims to the contrary. In particular, SiFs are unlikely to dissociate completely under water plant conditions, producing only free fluoride and silicic acid without side reactions, , given that the silicofluoride moiety [SiF6]2- can react with Al(OH)3 to produce a number of derivative compounds; and given that the dissociation of [SiF6] 2- is reversible depending on pH and concentration. The latter suggests that SiF residues ingested with fluoridated water will re-associate, both within the stomach (at intra-gastric pH levels of around 2.0) , and during various food preparation steps, producing SiF-related species including silicon tetrafluoride, (SiF4), a known toxin; , , , , , and

Finally, recognizing that commercial SiFs added to water supplies also are likely to be contaminated with fluosiloxanes, with arsenic and other heavy metals, as well as with alpha-emitting radionuclides, since these commercial SiFs are in fact by-products of phosphate rock processes antecedent to those by which uranium is extracted from the phosphoric acid so produced; , , , , and

Acknowledging with concern the fact that in 1950 the U.S. Public Health Service endorsed water fluoridation with silicofluorides in place of sodium fluoride, based largely on cost factors, and using the biological rationale that fluoride uptake by teeth from water treated with Na2SiF6 would be equal to that from NaF;

And recognizing that the US PHS 1950 Health Report declared water treated with NaF or Na2SiF6 biologically equivalent although animal studies conducted in 1930s had shown that even when the amount of fluoride ingested was equal and the total amount of fluoride excreted was also equal, nevertheless animals exposed to fluoride from NaF eliminated more fluoride in feces, while animals exposed to the SiF compounds eliminated three-fold more fluoride in urine;35 and

Reasoning that animals exposed to fluoride in SiFs therefore would be expected to have up to three-fold higher blood levels of fluoride as well, since three-fold higher urine excretion implies at least momentary peaking of blood fluoride --- if not continuously higher circulating blood fluoride levels; and

Further noting that in 1983 when the Surgeon General appointed an expert panel to review “non-dental health effects” of ingested fluoride, the panel was instructed to ignore dental fluorosis because an earlier panel had concluded that fluorosis was merely “cosmetic” so it limited the scope of its review to “death (poisoning), gastrointestinal hemorrhage, gastrointestinal irritation, arthralgias, and crippling fluorosis,” given the essential absence of information about other possible effects in children; 36

Noting also a 1974 German study which found that acetylcholinesterase inhibition, the intended action of the high-risk organophosphate and carbamate pesticides widely used in agriculture and around residences, is exaggerated in the presence of SiF as compared to NaF which is itself an acetylcholinesterase inhibitor;37 and

Recognizing that the prevalence of dental fluorosis, (pre-eruption tooth enamel malformation due to ingested F), expected in 1945 to be 10-12 percent in “optimally fluoridated” areas,38 is now over 25 percent and in some fluoridated communities exceeds 80 percent including a substantial amount of moderate to severe fluorosis;39 and

Noting conclusions from three studies, analyzing data collected from 400,000 children in New York, Massachusetts and elsewhere where NHANES III was carried out, which found evidence that exposure to water fluoridated with SiFs somehow increases blood lead levels, even when these analyses controlled for race, housing age, poverty, congestion, and parental education (p<0.001);40, 41and

Recognizing that elevated blood levels have been found responsible for adverse health effects inflicted in utero such as impaired immune capacity,42 brain damage and developmental problems,43, 44, 45 as well as in early childhood,46, 47, 48, 49, 50, 51and into puberty and adolescence as cognitive impairment and loss of impulse control,52, 53and into adulthood as nephropathy and hypertension,54, 55and into geriatric life;56 and

Recognizing that elevated blood lead has also been found to impair tooth enamel integrity,57 thereby off-setting the intended benefits from exposure to fluoride; and

Finally, acknowledging that in contrast to potential risks from exposure to SiFs added to water supplies, the prevalence of dental caries in “optimally fluoridated” communities today is barely distinguishable from the prevalence of dental caries in non-fluoridated communities;58, 59, 60, 61, 62, 63, 64and the Journal of the American Dental Association recently published a comprehensive study showing that fluoride does not benefit teeth by ingestion, but only via by topical contact;65 and

Citing the American Public Health Association’s explicit endorsement of the precautionary principle as a cornerstone of preventive public health policy, especially in “order to protect the health and well-being of all developing children;” and

Citing Executive Order #13045 which calls upon all federal agencies to ensure that all federal environmental health policies and regulations consider the special sensitivities and vulnerabilities of children; therefore the legislature of the state of New Hampshire:

1. Calls for the immediate cessation of water fluoridation using silicofluorides on the basis that they have never been tested for health safety in humans and may be particularly hazardous to children, the aged and the chronically ill;
2. Calls for the National Institute of Environmental Health Science to undertake a full battery of chronic health effects testing of silicofluoride treated water; and
3. Calls for the US. EPA to establish new standards for the safe level of fluoride exposure with particular reference to children and the results of the recommended NIEHS study

Submitted:

Myron J. Coplan, P.E. Roger D. Masters
Intellequity Consulting Nelson A. Rockefeller Professor
Natick, MA of Government and
508-653-6147 Research Professor
Department of Government
Dartmouth College
Hanover, NH 03755
603 646 1029

References

-
United States Department of Health and Human Services; Centers for Disease Control (CDC)
Fluoridation Census, 1992, Sept 1993.
Reeves TG; "Water Fluoridation; A Manual for Water Plant Operators"; US Public Health Service, CDC
Division of Oral Health, April 1994.
Council on Dental Health , American Dental Association; "Fluoridation in the Prevention of Dental
Caries"; Third Edition, 1953.
Letter to the Honorable Ken Calvert, Chairman of the Subcommittee on Energy and the Environment of the House Committee on Science, from EPA Assistant Administrator J. Charles Fox, June 23, 1999.
Personal letter to Dartmouth Professor Roger D. Masters, from Robert C. Thurnau Chief, EPA Treatment
Technology Evaluation Branch, November 16, 2000.
Wollan M; "Controlling The Potential Hazards of Government-Sponsored Technology": The George
Washington Law Review; V 36 No. 5; pages 1105-1119, July 1969.
Bucher JR, et al; "Results and conclusions of the National Toxicology Program's rodent carcinogenicity
studies with sodium fluoride" Int J Cancer; 48(5):733-7, July 9,1991.
Heindel JJ, et al; “Developmental toxicity evaluation of sodium fluoride administered to rats and rabbits in drinking water”; Fundam Appl Toxicol;30(2):162-77, Apr. 1996.
Sprando RL, et al; "Testing the potential of sodium fluoride to affect spermatogenesis: a morphometric
study"; Food Chem Toxicol.; 36(12):1117-24, 1998.
Sprando RL, et al; "Testing the potential of sodium fluoride to affect spermatogenesis in the rat"; Food Chem Toxicol.;35(9):881-90, 1997.
Collins TF, et al; "Developmental toxicity of sodium fluoride in rats"; Food Chem Toxicol. ;33(11):
951-60, 1995.
Dunipace AJ et al: "Chronic fluoride exposure does not cause detrimental, extraskeletal effects in nutritionally deficient rats"; J Nutr;128(8):1392-400, 1998.
Dunipace AJ et al; "Effect of chronic fluoride exposure in uremic rats"; Nephron; 78(1):96-1031, 1998.
Dunipace AJ et al, "Effect of aging on animal response to chronic fluoride exposure"; J. Dent Res;74 (1) 358-368, 1995.
Li YM, et al; "Genotoxic evaluation of chronic fluoride exposure: sister-chromatid exchange study"; J Dent Res;68(11):1525-8, 1989.
Jackson RD et al; "Lack of effect of long-term fluoride ingestion on blood chemistry and frequency of sister chromatid exchange in human lymphocytes"; Environ Mol Mutagen;29(3):265-71, 1997.
Feldman I, Morken D and Hodge HC; "The State of Fluoride in Drinking Water"; J. Dent Res. Vol 36 (2); 192-202; 1957.
Crosby NT; "Equilibria of Fluosilicate Solutions with Special Reference to The Fluoridation of Public Water Supplies"; J Appl Chem; v19; pp 100-102, 1969.
Busey RH et al; "Fluosilicate Equilibria in Sodium Chloride Solutions from 0 to 60 o C"; Inorg. Chem V 19; pp 758-761, 1980.
Ciavatta L, et al; “Fluorosilicate Equilibria in Acid Solution”; Polyhedron Vol 7 (18); 1773-79; 1988.
Gabovich RD; "Fluorine in Stomatology and Hygiene"; translated from the original Russian and published in Kazan (USSR); printed by the US Govt Printing Office on behalf of the Dept of Health Education and Welfare. US Public Health Service, National Institute of Dental Health; DHEW pub no (NIH) 78-785, 1977.
Roholm K; "Fluorine Intoxication; A Clinical-Hygiene Study"; H. K. Lewis & Co. Ltd, London; 1937.
Lewis RJ, jr.; "Hazardous Chemicals Desk Reference": Van Nostrand Reinhold; Fourth Edition.
Matheson Gas Products; 30 Seaview Drive, Secaucus, NJ; "Effects of Exposure to Toxic Gases" and MSDS for CAS # 7783-61-1; created 1/24/89.
Voltaix, Inc.; Material Safety Data Sheet for Silicon Tetrafluoride (SiF4).
Rumyantseva GI et al; "Experimental Investigation of The Toxic Properties of Silicon Tetrafluoride"; Gig Sanit ;(5):31-33, 1991.
Ricks GM et al; "The Possible Formation of Hydrogen Fluoride from the Reaction of Silicon Tetrafluoride with Humid Air": Am. Ind. Hyg. Assoc. J. (54); 272-276, 1993.
Craig JM; "Fluoride Removal from Wet-Process Phosphoric Acid Reactor Gases"; Ph. D. Dissertation; Univ. Fla. at Gainesville, 1970.
Murray RL; “Understanding Radioactive Waste”; Third Ed.(ed Powell JD); 1982.
Becker Pierre; "Phosphates and Phosphoric Acid: Raw materials, technology, and economics of the wet process"; Marcel Dekker: New York (First ed.) 1983, Second ed., 1988.
Slack AV; "Phosphoric Acid"; Part I; Marcel Dekker: New York, 1968.
Greek BF, Allen OW, and Tynan DE; "Uranium Recovery from Wet Process Phosphoric Acid"; Industrial & Engineering Chemistry; vol 49 (4); 628-636, 669-671, 1957.
Rahn FJ, et al; “A Guide to Nuclear Power Technology”; John Wiley & Sons; New York; 1984.
McClure FJ: "Availability of Fluorine in Sodium Fluoride vs, Sodium Fluosilicate"; Public Health Reports vol 65 No 37; 1175-86; 1950.
35 Kick CH et al; "Fluorine in Animal Nutrition"; Bulletin 558, Ohio State Agricultural Experiment Station, Wooster OH, November 1935.
36 Koop CE, Letter to William D. Ruckelshaus, Administrator, EPA, dated Jan 23, 1984 and transcript of Proceedings of Surgeon General's Ad Hoc Committee on "Non-Dental Health Effects of Fluoride"; April 18-18, 1993, Jay R. Shapiro, Chairman.
37 Westendorf J; "Die Kinetik der Acetylcholinesterasehemmung und Die Beeinflussung der Permeabilitat von Erythrozytenmembranen durch Fluorid und Flurocomplex-Jonen"; Doctoral Dissertation, Universitat Hamburg Fachbereich Chemie; Hamburg; 1975.
38 Dean HT; "Endemic Fluorosis and its Relation to Dental Caries"; Public Health Report 53; 1443-52; 1938.
39 National Research Council; "Health Effects of Ingested Fluoride"; Subcommittee on Toxicology, Board on Environmental Studies and Toxicology, Commission on Life Sciences, National Academy Press: Washington, DC, 1993.
40 Masters RD and Coplan MJ; “Water Treatment with Silicofluorides and Lead Toxicity”; Int. J. of Environ. Studies; 56; 435-449, 1999.
41 Masters RD, Coplan MJ, Hone BT, and Dykes; "Association of Silicofluoride Treated Water with Elevated Blood Lead"; NeuroToxicology 21 (6), 2000.
42 Miller TE et al; “Developmental Exposure to Lead Causes Persistent Immunotoxicity in Fischer 344 Rats”; Toxico Sci. 42; 129-135; 1998.
43 Chanez C, et al; “Effect of lead on Na+,K+ATPase activity in the developing brain of intra-uterine growth-retarded rats”; Neurochem Pathol; 5(1):37-49; 1986.
44 Dietrich KM et al; “Low-Level Fetal Lead Exposure Effect on Neurobehavioral Development in Early Infancy”; Pediatrics; Vol 89 no. 5, 1987.
45 Aschengrau A et al; “Quality of Community Drinking Water and The Occurrence of Late Adverse Pregnancy Outcomes”; Arch Environ Health ; vol 48 no. 2; 105-13, Mar-Apr 1993.
46 Needleman HL; “Low-Level Lead Exposure and the IQ of Children”; JAMA ; Vol 263 no. 5;
Feb 2, 1990.
47 McMichael AJ et al; “Port Pirie Cohort Study: Environmental Exposure to Lead and Children’s Abilities at the Age of Four Years”; New Eng J of Med ; vol 319 no. 8; Aug 25, 1988.
48 Kim R, et al; “A longitudinal study of chronic lead exposure and physical growth in Boston children”;
Environ Health Perspect ; 103(10):952-7, 1995.
49 Leviton A, et al; “Pre- and postnatal low-level lead exposure and children's dysfunction in school”;
Environ Res ; 60(1); 30-43, 1993.
50 Schoen EJ; “Neuroendocrine effects of toxic and low blood lead levels in children”; Pediatrics ;
vol 92 (3), 1993.
51 Eppright TD, et al; “Attention deficit hyperactivity disorder, infantile autism, and elevated blood-lead: a possible relationship”; Mo Med ; 93(3); 136-8, 1996.
52 Walker SW III; “The Hyperactivity Hoax”; St. Martin’s Press; New York, Dec 1998.
53 Bellinger DC, et al; “Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study”; Pediatrics ; vol. 90 (6); 885-61,1992.
54 Loghman-Adham M; “Renal effects of environmental and occupational lead exposure”; Environ Health Perspect ; 105(9); 28-39; 1997.
55 Korrick SA, et al; “Lead and hypertension in a sample of middle-aged women”;
Am J Public Health; 89(3); 330-5, 1999.
56 Vig EK, and Hu H; “Lead toxicity in older adults”; J Am Geriatr Soc ;11):1501-6, 2000.
57 Watson GE, et al; “Influence of maternal lead ingestion on caries in rat pups”; Nat Med;3(9):
1024-5, 1997.
58 Brunelle, JA and Carlos JP; "Recent Trends in Dental Caries in US Children and Effect of Water Fluoridation"; J. Dent. Res 69 Spec Iss; 723-27, 1990.
59 Kobayashi S et al; "Caries Experience in subjects 18-22 years of age after 13 years' discontinued water fluoridation in Okinawa"; Community Dent Oral Epidemiol; 20(2):81-3; 1992.
60 Kumar JV et al; "Changes in Dental Fluorosis and Dental Caries in Newburgh and Kingston, New York"; Am. J. Pub. Hlth. Vol 88, No 12; 1866-70, Dec 1998.
61 Kumar JV and Greene EL; "Recommendations of Fluoride Use in Children"; NYSQJ, Feb 1998.
62 Kunzel W and Fischer T; “Caries prevalence after cessation of water fluoridation in La Salud, Cuba”; Caries Res; 34(1):20-5; 2000 Jan-Feb.
63 Burt BA, Keels MA, Heller KE; “The effects of a break in water fluoridation on the development of dental caries and fluorosis”; J Dent Res.;79(2):761-9, 2000.
64 Seppa L, Karkkainen S, Hausen H; “Caries in the primary dentition, after discontinuation of water fluoridation, among children receiving comprehensive dental care”; Community Dent Oral Epidemiol;28(4):281-8, 2000.
65 Featherstone JDB; "The Science and Practice of Caries Prevention"; JADA Vol 131; 887- 1002, 2000

Correction: My apologies for an error in my posting, 13 February, in the webpage address for Fluoride: quarterly journal of the International Society for Fluoride Research. The correct address is: http://homepages.ihug.co.nz/~spittle/fluoride-journal.htm
It can be reached by clicking on the yellow house in the homepage symbol below.