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Section 3.

4) Health Concerns and key studies omitted. A critique of the Forum's Chapter 11.

4.1 Dental fluorosis.

The Forum's analysis of dental fluorosis is given a fuller treatment in section 5 below. What we found disturbing from the health perspectiven is that unlike fluoride's benefits to teeth, there is little discussion of how fluoride causes dental fluorosis and its relationship to other systemic health effects.

They acknowledge that this is a systemic effect but do not comment on the significance of this finding. They are content to focus only on the visible appearance of the phenomenon. It is described as a "cosmetic" problem; an "aesthetic" problem, even as a public perception which may require study.

They do not discuss the possibility that dental fluorosis is the first visible sign of fluoride's toxic effect on the body. Nor do they discuss the mechanism of how fluoride causes dental fluorosis. They do not discuss denBesten's work indicating that fluoride poisons one of the enzymes involved in the developing tooth (denBesten, 1999). Had they done so, it might have prompted them to consider what other enzymes fluoride might also be poisoning. Others have suggested that fluoride causes dental fluorosis by interfering with the thyroid gland and had they addressed this possibility it might have led them to consider the literature which deals with fluoride's ability to lower the activity of the thyroid gland of those suffering from hyperthyroidism, an issue which they do not address in the report (Galletti and Joyet, 1958, Bachinskii,1985).

4.2 The Alarcon-Herrera et al (2001) study.

One of the many papers not acknowledged, or reviewed, by the Fluoridation Forum was a report by Alarcon-Herrera et al (2001) which appeared in the May 2001 issue of Fluoride, together with an editorial on the same issue. In this study Alarcon-Herrera et al found a strong linear correlation between the severity of dental fluorosis and the frequency of bone fractures in children. The study examined children in an area in Mexico which is naturally high in fluoride. Thus, far from "dental fluorosis" being an inconvenient "cosmetic problem" it may be an indicator of early bone damage. This phenomenon is also covered in our discussion of fluoride and bone damage (section 4.10).

4.3 Tolerable Daily Intakes (TDI).

In their "background" introduction to this topic the authors refer only to the use of "human population" studies and animal studies in determining TDIs. They point out the limitation of human studies for this purpose, because of the usual lack of dose information and interference from exposure to other substances. However, in their discussion, they have neglected to include the use of clinical studies, where humans have been exposed to very precise doses of fluoride for known periods of time. These studies involved giving fluoride tablets to patients with osteoporosis in an effort to reduce bone fractures (see our discussion of bone damage in section 4.10). Moreover, in determining TDIs they avoided using the most sensitive end point found to date, namely the impact on rat brain (Varner et al, 1998).

4.4 A TDI without uncertainty factor.

The authors define a tolerable daily intake (TDI) as "what can be ingested (daily) over a lifetime without appreciable health risk".

In their discussion of the standard way of determining TDIs, they rightly refer to the fact that a No Observable Adverse Effect Level (NOAEL) is first determined and then this is divided by an uncertainty factor (UF). However, when they derived their TDI for children up to age 8 years (0.05 mg/kg/day), they did not apply an uncertainty factor -- they simply took the NOAEL for mild fluorosis in permanent teeth. A tolerable upper intake (for children under 8 years have ) is defined as 0.1 mg/kg/day, which is based on the level which causes moderate dental fluorosis, again without an uncertainty factor being used.

4.5 A huge mistake: a TDI which is enough to kill.

When the authors consider a TDI for children over 8 years and for adults, they state the following: "For children over 8 years and for adults (i.e. not at risk of dental fluorosis) a NOAEL of 10 mg F/kg/day is considered appropriate. In order to attain that level of exposure large amounts of water and toothpaste would need to be consumed over long periods."

A TDI of 10 mg/kg/day (this means a dose of 10 mg of fluoride per kilogram bodyweight per day) would mean that a 60 kg adult would be able to ingest 600 mg/day without harm. In reality, such a high dose would undoubtedly cause serious acute effects and possibly death. This point is made abundantly clear in the next section which deals with acute toxicity. Here a "probable toxic dose" (PTD) is defined as "the minimum dose that could cause toxic signs and symptoms including death and that should trigger immediate therapeutic intervention and hospitalization". The authors set this PTD at 5 mg/kg/day. In other words they defined a tolerable daily intake (10 mg/kg/day) as twice a probable toxic (and possibly lethal) dose (a PTD of 5mg/kg/day)! The same mistake is repeated in the Executive Summary, where the TDI and PTD appear on the same page.

Now clearly the authors have made a major mistake. What is disturbing is that for anyone familiar with toxicology this is a very easy mistake to spot. How many people on this panel proofread this report? Did no one know enough about toxicology to spot this sloppy mistake, which occurred not once, but twice!

If they appear to understand so little about TDIs, what other serious oversights did they make in the discussion of the toxicity and toxicology of fluoride? Moreover, since the Fluoridation Forum authors placed so much emphasis on reviewing other agency's reviews on fluoridation, it raises the question of how well they reviewed and understood these documents?

4.6 Margin of safety.

In our view, the authors should have provided a very clear discussion of the margin of safety of fluoride for the various end points of concern. This would have entailed telling us how many milligrams of fluoride per day is necessary to protect teeth (the therapeutic dose); how many milligrams of fluoride can cause a variety of undesirable end points (the toxic dose). Dividing the toxic dose by the therapeutic dose then gives the "margin of safety" for each end point. With these margins of safety in hand, they then should have compared them with estimated daily doses children and adults are getting in Ireland, to see how far they are edging into, or even exceeding, those safety margins.  Such calculations would reveal that for several important endpoints the margin of safety, if indeed any exists at all, is ridiculously small, especially for a medication for which the dose cannot be controlled, and for one destined to a go to a whole population with a probable ten fold range of sensitivity to any toxic substance, including fluoride.

4.7 Fluoride's Bio-availability and the Pineal Gland.

In a short section on Fluoride Bio-availability, the FF authors state that, "the quantity of fluoride that could affect biological processes is very small as most of the fluoride retained in the body is sequestered in the bones and teeth." However, they fail to acknowledge a very important recent finding by Jennifer Luke (1997, 2001) that fluoride also accumulates in the human pineal gland.

The pineal gland is a small gland which is located between the two hemispheres of the brain. It is responsible for manufacturing a very important hormone called melatonin. This hormone acts like a biological clock. Its release and plasma concentrations are thought to control the timing of various biological events and cycles such as sleep patterns, the onset of puberty and aging. There are three things which make this little gland a target for fluoride accumulation: 1) It is not protected by the blood brain barrier 2) It has a very high perfusion rate by blood and 3) most importantly, it is a calcifying tissue, i.e. like the teeth and the bone it lays down the same crystals of calcium hydroxy apatite. Luke theorized that this gland would highly concentrate fluoride and when she examined the pineal glands from 11 corpses this is exactly what she found. The levels of fluoride on the crystals averaged about 9000 parts per million (ppm), which is extremely high. This work was part of her Ph.D. thesis (1997) and was published in the open literature in 2001.

The second part of her thesis involved examining the effect of fluoride on melatonin production in animals. She found that not only was melatonin production lowered, but the animals reached puberty earlier, as would be predicted. This part of her work has yet to be published in the open literature, although copies of her thesis have been made available to regulatory officials in the US.

What is inexcusable about the FF authors' failure to acknowledge this important work is that it was presented to them in October 2000, as part of Dr. Connett's testimony.

Their attention was also drawn to an interesting finding in the context of Luke's work. The second trial of fluoridation in the US occurred in Newburgh (fluoridated) and Kingston (unfluoridated control) and took place from 1945 to 1955. The health of the children was followed and reported in 1956 (Schlessinger et al). The authors found that the young girls were menstruating on average 5 months earlier in fluoridated Newburgh compared to unfluoridated Kingston. This is consistent with fluoride's ability to shorten the time to the onset of puberty.

We have to ask, why it was that the Irish Ministry of Health would go to the trouble of flying Dr. Connett from the US to Cork, Ireland, to give a presentation to this forum, if they subsequently ignored the most important scientific findings he shared with them? If they felt that the work was unimportant, or premature, then surely they were, at least, obliged to acknowledge that the work exists and then give their reasons for ignoring it?

4.8 Second-hand science:  Review of reviews.

Most of the remainder of Chapter 11 consists of reviews of reviews. Such an exercise might prove of some useful purpose if the reviews in question were conducted by independent or impartial panels. Most of them were not. Most of the Reviews have been commissioned, just like the Fluoridation Forum, by governments who practice fluoridation, and thus it is difficult to disentangle analyses designed to protect a policy from those which genuinely seek scientific and objective answers to serious questions about fluoride's toxicity and margin of safety. Such observations might be considered to be overly cynical were it not for the fact, that nearly all of these reviews have been highly selective in which literature they cite, and seem to consistently "overlook" the studies which indicate that there may be serious problems with this practice. It is interesting to compare the Forum's summary of the York Review (pp. 119-120) with the comments of Douglas Carnall, the Associate Editor of the British Medical Journal, and Professor Trevor Sheldon, the chairman of the advisory panel to the York Review (see Appendix 3).

4.9 Key studies and key issues not covered in the Fluoridation Forum report.

Here are some of the key human and animal studies which were not covered by the Forum.

a) Masters and Coplan.

The most serious omission in our view is their failure to discuss the work by Masters and Coplan (1999, 2000) who have found an association between the blood lead levels in children (as well as violent behavior), and the use of hexafluorosilicic acid (and its sodium salt) to fluoridate water (but not the use of sodium fluoride).

This omission is striking because of the considerable time the Forum spent on discussing the use of hexafluorosilicic acid, the fluoridating agent used in Ireland. What Masters and Coplan have also brought out as a result to the responses to their work in the US (Urbansky and Schock, 2000), is that these agents have never been tested systematically for their long-term toxicology in animals (a fact that the US EPA has now acknowledged, see letter appendix 6). All the testing has been done on sodium fluoride.

Moreover, when dealing with one rebuttal of their work by Urbansky and Schock (2000) they were able to refute the claim that when the hexafluorosilicate ion is diluted it breaks down completely to free fluoride ion and silica and hydrogen ions, quoting a study carried out in Germany in the 1970s (Westendorf, 1975). The importance of this has even been acknowledged by Urbansky himself since he heads up the team at the US EPA which is currently calling for research proposals to find out what silcofluoride complexes and other species are present in aqueous solutions of hexafluorosilicic acid.

In other words, neither the US government nor the Irish government knows either the chemical nature or the toxicity of the chemical substance they are giving to a majority of their citizens in their drinking water.

b) Varner et al (1998).

Another key study missed by the Forum is an animal study where Varner and co-workers showed that rats fed fluoride at 1 ppm in their distilled and de-ionized drinking water (as either aluminum fluoride or sodium fluoride) for one year, had morphological changes to their kidneys and brains, a greater uptake of aluminum into their brains and the formation of amyloid plagues associated with Alzheimers disease. The authors hypothesize that fluoride facilitates the uptake of aluminum into the brain.

c) G-proteins.

It is also puzzling that the Forum authors make no acknowledgement of the fact that there are some 800 studies in the biochemical literature which indicate that fluoride in the presence of a trace amount of aluminium switches on G-proteins. G-proteins are the key molecules involved in getting messages that arrive at the outside of our tissues (such as water soluble hormones, growth factors and some neurotransmitters) across the membranes in order to excite secondary messengers on the inside of the tissues. Thus fluoride can short circuit very important signalling mechanisms in the body. This may prove important to unravelling fluoride's effects on the brain (Strunecka & Patocka, 1999).

d) Luke's work on the pineal gland.

Luke's work is discussed in section 4.7.

e) Other studies on the brain and human behavior and development.

The Fluoridation Forum authors dismiss concerns about fluoride's impact on the central nervous system in their review of the 1999 Canadian Review, where these authors state, "Studies from China claiming children exposed to high levels of fluoride had lower IQs than children exposed to low levels were found to be deeply flawed and provided no credible evidence that fluoride obtained from water or industrial pollution affects the intellectual development of children."

This second-hand dismissal of such an important concern is irresponsible.

While recognizing that some of the Chinese studies did not consider all the possible confounding variables, they do raise serious questions. While the study by Li et al (1995) examined the IQs of children exposed to fluoride air pollution from indoor coal burning, both Zhao et al (1996) and Lu et al (2000) examined the lowering of IQ in children drinking water with fluoride levels as low as 4 ppm. The work of Lin Fa-Fu et al (1991) is also of concern because in this study a lowering of IQ thought to be due to the impact of iodide deficiency was actually exacerbated by moderate fluoride exposure (less than 1 ppm). This and other studies (Varner et al 1998, Zhang et al , 1999) raise the possibility that we have to be concerned not just about fluoride's impact operating by itself but in conjunction with other metal ions, or in nutrient deficiency situations. Nor are these studies confined to China. Calderon et al (2000) found an impact of fluoride on "reaction time and visuospatial organization" in children in a study conducted in Mexico.

Once again a weight of evidence approach is needed. These human findings have to be taken in conjunction with animal studies. Mullenix et al (1995) showed that rats exposed to fluoride developed behavioral effects typically produced by neurotoxic agents. Guan et al (1998) demonstrated an impact of fluoride on the membrane lipid levels in rat brain. Varner et al (1998) showed that fluoride, administered as either aluminum fluoride or sodium fluoride in rat's distilled and de-ionized drinking water at 1 ppm fluoride, damaged the brain and led to greater uptake of aluminum and the formation of amyloid plagues (see 4.9 b).

Why have the Forum authors ignored all these red flags? Who, for one moment, would countenance the administering of fluoride to children to achieve an almost imperceptible benefit to their teeth, if there are serious questions about its impact on their developing brains? The above information needs to be taken in conjunction with the fact that the level of fluoride in mothers' milk (0.01 ppm) is 100 times less than the levels put in the water (1 ppm). While the authors have largely confined their discussions of the impact of fluoride on young children to the aesthetics of dental fluorosis, there may be far more serious consequences that they (or the Reviews that they cite) have overlooked.

As long ago as 1978, Dr. Arvid Carlsson (Nobel Prize winner in Medicine, 2000) voiced similar concerns, when he said "One wonders what a 50-fold increase in the exposure to fluoride, such as occurs in infants bottle-fed with water diluted preparations, may mean for the development of the brain and other organs... Problems associated with this can only be solved by precise and comprehensive epidemiological studies in which, for example, breast-fed and bottle-fed babies are compared in localities with varying water fluoride content. No studies have yet been made."

Such arguments, persuaded the Swedish public and the Swedish parliament not to embark on the fluoridation experiment. The least one would expect from a country, like Ireland, is to very carefully collect the data on these kind of possible impacts. Sadly, they have not done so.

f) Freni's study on fertility, Freni (1994).

Another important study that the Forum authors ignored was Freni's (1994) study of lowered fertility rates in US counties with 3 ppm of fluoride or higher in their water. While 3 ppm is higher than the 1 ppm used to fluoridate water in Ireland, the results of this study pertains to issues of "margin of safety" and discussion of the total dose of fluoride where citizens are exposed to fluoridated water as well as other sources.

g) Many bone studies (see section 4.10).

h) Studies on the thyroid gland (Galletti and Joyet, 1958, Bachinskii, 1985).

i) The case studies of individuals who appear to be highly sensitive to fluoride.

The Forum neglected to discuss the numerous case studies reported by Waldbott (Waldbott et al, 1978) and Moolenburgh (Moolenburgh, 1987) in which individuals have reported various symptoms as a result of exposure to fluoridated water, which disappear when they stop drinking the water. While a number of the Reviews the Forum report cites have dismissed these findings, the dismissals have been of a somewhat cavalier nature, and not as a result of thorough scientific study. In this respect the Forum was remiss in failing to address the concerns raised about the possible contribution of fluoride exposure to the high incidence of irritable bowel syndrome in Ireland.

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