Letter to John Moloney TD on Issue of Fluoridation in Ireland

Mr John Moloney TD, Chairman, Oireachtas Joint Committee on Health & Children, Leinster House, Dublin 2. January 20, 2006. Dear Mr. Moloney, If you detect a certain amount of frustration in my comments below then you are correct. I feel that I have been both used and abused by the bureaucrats and dental policy advisers who spearhead the practice of mandatory water fluoridation in your country. By way of explanation, please allow me to remind you of the circumstances of my involvement in Ireland. Just over 5 years ago I received a phone call from the Irish Department of Health. I was asked whether, if they paid my way, I would fly over to Ireland and testify before the Fluoridation Forum. I was assured that this body genuinely wanted to hear both sides on the issue. I agreed, but, by so doing, intensely annoyed citizens opposed to fluoridation who said the Forum was made up largely of government employees and experts who had spent their professional careers promoting water fluoridation. Along with Dr. Hardy Limeback I did eventually testify before the panel in October 2000. I stated at the outset that I had annoyed citizens by testifying who felt that the panel was just a rubber stamp for the government's pro-fluoridation policy, and then said that the way that they could convince me , and I believed the Irish public, that they were going to take a genuine and comprehensive look at this issue, was to give a fully referenced scientific response to the 50 Reasons to Oppose Fluoridation which I presented to them in writing. Everyone who spoke to me that day -- including panel members, the chairman and the Minister of Health -- assured me that they had an open mind and would examine the issue objectively. At first it looked promising. The chairman formed a sub-committee to prepare a written response to my 50 Reasons and the minutes of their meetings over the next 10 months indicated that they started to do this and that this task was important to them. Needless to say producing 50 reasons to oppose fluoridation is a huge overkill. Some people only need one reason, namely that the government has no right to force medication on its citizens. Be that as it may, I felt that the Forum's considered response to the 50 Reasons would help to raise the level of the debate. In the light of this exercise I was anticipating that I might have to abandon some reasons and modify others. In retrospect however, the first danger signal was the time it took the committee to track down the references I supplied with the 50 reasons. If those involved were experts in the field then most of these studies should have been at their fingertips. Then, despite repeated promises, the Forum announced that they didn't have time to respond and published their 295 page report without answers to the 50 Reasons. Despite repeated requests from the media and TDs over the next two and a half years

the Minister of Health still failed to provide answers. Then, in May 2004, the Green Party paid my way to come over to Ireland and testify before the Joint Committee on Health & Children. I was very encouraged by the response to my appearance. If there was anyone on the panel in favor of fluoridation they certainly didn't make their presence known. I received no hostile questions. Far from it, at least two committee members present made it clear that they were strongly opposed to fluoridation. Another panel member explained how difficult it was making up her mind on an issue like this where they had two groups of experts telling them opposite things. To this I replied that there was a very simple way to determine which side had the credibility by inviting both sides to debate the issue in pubic. I gave my assurance if this was to happen I would return to Ireland to defend my position. However, those promoting fluoridation in Ireland, while exuding great confidence in this measure, have not been willing to debate their position with me, despite numerous invitations to do so. After my testimony to the Joint Committee another year went by and still no answers to the 50 reasons were forthcoming. Then out of the blue I heard that what purported to be answers to the 50 reasons had been posted on the Department of Health's web site, on May 5 2005. When I checked into this I found that no one had signed the 24 page "response", which consisted largely of an attack on the author's (they never mentioned me by name) "poor questions" rather than providing cogent answers to any of them. Instead of specific answers they gave reasons why they were not going to address about a third of the 50 reasons and then addressed the other two thirds generically (in the attachment these comments appear as ANON(I)). I was most disappointed that they didn't have the courtesy to send their response to me in person, although I could understand their intense embarrassment that such a long-delayed and pathetic response must have caused them. A short time later I was told that they had added some more specific responses to the web site, but again they made no effort to indicate which explanation or offering was aimed at which "reason" and again no attempt was made to inform me directly of their response (in the attachment these comments appear as ANON(II)). Before I could go ahead and address their responses (see attachment), I had to make a good faith (and time consuming) effort to try and match their responses to my specific arguments. As I did this it became clear to me why they had done this in such a disorganized and arbitrary fashion. They were not seeking clarity. They did not want people to read the 50 reasons and be able to link their responses to each one, for the simple reason that almost all their responses were very weak. Worse still they had failed to address at least 20 of the 50 reasons at all. By making their response so chaotic I believe they intended to make it very awkward for any but the most persistent reader to know what the heck was going on. If they succeed in this obfuscation then many busy people will throw up their hands and defer to "authority" -- however undeserved that "authority" might be. This often works from a PR point of view but, of course, from a scientist's point of view - and more importantly from the point of view of someone who wants to see good science serving public health policy - this is extremely unsatisfactory and hence my frustration.

After close scrutiny of their specific responses it becomes clear time and time again, the anonymous respondents attempt to simply dismiss every study that has found an inkling of a problem. This they seldom do by actually analyzing the papers in question but rather by relying on others to do their analysis for them. Considering that Ireland is the only European country to have mandatory fluoridation, it is amazing that a) they cannot keep track of the primary literature themselves and b) that they cannot commission their own health studies on crucial end points which still remain unresearched or unresolved. Before you read the anonymous responses to my original 50 reasons, followed by my counter responses (see tha attachment), let me present a few basic points. 1) Ireland is the only country in Europe which has more than 10% of its population drinking artificially fluoridated water. Latest estimates indicate that 73% of the Irish population is drinking fluoridated water. 2) Even though fluoridation has been mandatory in Ireland since 1963 not one single study has been commissioned or conducted in Ireland to examine the health effects of this practice on any tissue except the teeth. In short, they have never made a systematic effort to measure the fluoride levels in the urine, plasma or bones of the Irish people. In other words, they are flying blind as far as relating suspected end points such as arthritis, bone fractures in children, bone cancer in young males, hip fractures in the elderly, gastro-intestinal problems, hypothyroidism, lowered IQ and possibly even Alzheimer's disease to increased fluoride exposure. 3) Instead, Irish promoters rely again and again on second hand reviews conducted by other bodies in other pro-fluoridation countries. Relying on reviews by other countries' agencies might be acceptable on some issues but not with this practice, because these reviews are usually conducted by panels appointed by governments, like Ireland, which seem more intent on protecting this longstanding policy, than protecting the health of their people. 4) The Irish promoters unfamiliarity with the primary, peer-reviewed scientific literature on fluoride toxicity was readily apparent in their Fluoridation Forum report of 2002. Out of 295 pages in the report, only two pages were devoted to primary studies from the literature on tissues other than teeth. Such unfamiliarity with the primary literature was also apparent in their half-hearted responses to the 50 Reasons below, where on most health concerns they respond by citing reviews (some of them pre-dating the study or studies under consideration) rather than examining the studies themselves. 5) In neither the Fluoridation Forum report nor in the anonymous responses below does one get the impression that anyone writing these comments is actually keeping track of latest research on health and fluoridation. They are leaving that to someone else. Not only is this irresponsible but it also violates the intention of the 1960 Fluoridation Act (Section 6). 6) While my major concerns pertain to the dangers of fluoridation and to the unethical nature of this practice, I think it is important to add that there has never been a grade A level study demonstrating that fluoridation is effective. No one has ever done a single

clinically controlled, randomized double-blind trial of fluoride. Such a trial is the gold standard by which the Food and Drug Administration (FDA) in the U.S. decides whether a medicine is safe and effective. Why hasn't a rigorous study of effectiveness ever been conducted? Why do the Fluoridation promoters rely on ecological studies, especially those from more than 50 years ago which have been shown to have serious methodological failings? 7) Nor have the safety issues been answered with such a gold-standard study. Ecological and epidemiological studies are never accepted by the FDA as sufficient evidence that a medication is safe. Specific suspected side effects must be examined during any valid study. Virtually all the reported side effects of fluoride exposure would have to be studied in clinically controlled trials. For example, if thyroid problems have been linked to exposure levels to be expected from use of the medicine, then all the subjects would have to be examined for thyroid effects. 8) Furthermore, since fluoride is a medicine administered to an entire population without any regard to other factors (which is of course totally counter to the most basic pharmacological principles and the principle of informed consent), the only way to satisfy safety requirements would be through conducting massive studies of very large numbers of people given the maximum dose that could be expected from all sources of fluoride. These studies have simply not been done. Instead, what we get again and again is a PR exercise in which proponents tell us like a broken gramophone record that fluoridation is "safe and effective." 9) However, not even the most ardent promoter of fluoridation can deny that children in Ireland are being over-exposed to fluoride. Even ANON (II) concedes that 39% of 15 year olds in Ireland NOW have dental fluorosis ( Section B, Reason 9). The early American promoters of fluoridation had estimated that only about 10% of children would have their enamel impacted in this way, and even then only in its very mild form. This is how the father of fluoridation, H. Trendley Dean described this condition some SEVENTY YEARS AGO: "… we are dealing with a low grade chronic fluoride poisoning of children …" (Dean, 1936). What we don't know is just how serious this chronic poisoning is, because those who promote this practice have no intention of finding out. 10) In essence fluoridation has been promoted like a "religious crusade" rather than a public health intervention subjected to close scientific scrutiny and accountability. 11) If one fact stands out more than any other for the scrutiny of the wise decision maker, it is this: The level of fluoride which occurs in mothers' milk is remarkably low (5 to 10 parts per billion - or 100 to 200 times lower than the level added to water). Moreover, in 1981, Ekstrand published a seminal paper in the British Medical Journal, where he showed that the level of fluoride in breast milk remains low even when the nursing mother receives fluoride supplementation. Ekstrand noted at the time that some kind of "barrier" seems to exist to "actively protect" the newborn from fluoride. 12) In their response to the 50 reasons the anonymous commentators argue that water fluoridation favors the disadvantaged. I argue exactly the opposite. Fluoridation is not

equitable for two reasons. It is precisely the poor who will not be able to afford avoidance measures if they so wish (e.g. reverse osmosis equipment or bottled water for drinking and cooking). Thus they are trapped. Moreover, it is also in families of low income where one can anticipate poor nutrition, which is known to exacerbate fluoride's toxic effects. So the poor are trapped by a practice which could make their health worse. In their first response to the 50 reasons the anonymous commentators made much of the selective nature of the evidence presented to demonstrate the dangers of water fluoridation. They miss the point of the exercise. The task of the critic is to point out the "flaws" in this practice. By its very nature that is a selective process. Those who have taken on the responsibility of imposing this medication on a whole population have to be able to convincingly deal with every criticism. They must be on top of all the evidence. I believe that it was Pascal who said that "An ugly fact can destroy a beautiful theory". In some respects fluoridation is a beautiful theory - the notion that tooth decay can be controlled simply by putting a chemical substance into the water supply is very appealing- but as the 50 reasons makes abundantly clear there are just too many ugly facts in the peer reviewed and published literature to be able to sustain any longer the claim that this practice is "safe and effective." Finally, I would request that after you have read and assessed what follows, you would answer this question: Have the Irish authorities, after FIVE years of agreeing to investigate this policy, with many experts at their disposal, satisfactorily answered all, or even the preponderance, of the 50 reasons? If your considered answer is yes then I urge you to unambiguously endorse continuation of this practice and I will wash my hands of the matter as far as Ireland is concerned. If, on the other hand, your answer is no, then I urge you, through your committee to issue with the minimum of delay a recommendation that this practice be halted in Ireland forthwith. Not only will this prevent unnecessary risks to your citizens but the taxpayers' money wasted on fluoridation committees, fluoridation equipment, fluoridation chemicals, fluoridation monitoring and fluoridation studies on teeth, could be better spent on targeting the children most vulnerable to tooth decay with better education, better diet and targeted dental care. Most other European countries have been able to do this without forcing fluoride on their unwary citizens and their teeth are just as good - if not better - than Ireland's. Since over five years have passed since your Committee first started investigating this policy, I hope that the Committee's recommendation will follow without any further delay. I am respectfully yours, Dr. Paul Connett, Professor of Chemistry, St. Lawrence University, Canton, NY 13617. 315-379-9200 [email protected]

50 Reasons: Connett response to Irish comments p. 1

Paul Connett’s responseto the DOH comments on the 50 Reasons

KEY: In an effort to maintain clarity I have sub-divided the discussion of these50 Reasons into two sections. Section A deals with the bulk of the discussion.Section B deals with ten Reasons (3, 4, 7, 9, 11, 13, 37, 41, 42 and 44), where theexchanges get rather lengthy and detailed.

Another aid to clarity is to provide:

• the original Reason in BLACK• the first anonymous response ANON (I) in BLUE and in Italics• the second anonymous response ANON (II) in GREEN with aCourier typeface• and my responses in RED with an Arial typeface.

I have made a good faith effort to match ANON’s unarranged responses to the 50Reasons in the best way I could. If the anonymous responders are not happywith my “matching” then I am sure they will point this out if they could beencouraged to respond in a more organized manner.

50 Reasons to Oppose FluoridationUpdated April 12, 2004

by Paul Connett, PhDProfessor of ChemistrySt. Lawrence University

Canton, NY 13617

1) Fluoride is not an essential nutrient (NRC 1993 and IOM 1997). No disease hasever been linked to a fluoride deficiency. Humans can have perfectly good teethwithout fluoride.

ANON (I): Statements 1, 11, 16, 33, 34, 36, 37, 40, 41, 42, 43, 46, 47, 48, 49, 50have been grouped together because they contain no supporting references topeer reviewed biomedical literature and/or represent opinions expressed by theauthor or the opinions of others with no references to the peer reviewedbiomedical literature and/ or contain references to the administration ororganization of regulatory agencies in the United States and/or refer to thehistory or sociology of the debate over water fluoridation in the United States.As noted in the introduction, no response is provided in this document to anystatement that is not directly related to an assessment of the benefits and risks


of public water fluoridation based on the best available and most reliableevidence from human epidemiological studies.

CONNETT: In contrast to Anon’s assertion, the fact that fluoride is not anestablished essential nutrient has been repeatedly confirmed by the NationalAcademy of Sciences in the US (NAS 1989; NRC 1993). Does Anon notconsider NAS publications to be “peer reviewed”?

As noted by the NAS, there is no convincing scientific evidence that fluoride isneeded for any biological purpose. To show that it is an essential nutrient wouldrequire depriving fluoride from an animal’s diet and demonstrating a deleterioushealth effect as a consequence. No one has ever done this.

Further, now that it is conceded by most dental researchers (Featherstone 2000; Fejerskov 2004) and the CDC (1999, 2001) that the primary action of fluoride istopical, it is highly improbable that fluoride is an essential nutrient. Almost bydefinition nutrients are ingested.

ANON (I) (continued): Given the evidence supporting the role of fluoride incavities prevention, it can be regarded as a beneficial mineral element forhumans (p9).

Declaring that fluoride is a “beneficial mineral element” because of externalinteraction with the enamel, makes it no more a nutrient than sun screen which isapplied to the skin to protect against UV light. Just because sunscreen offersthis kind of protection does not make it a nutrient – and like the toxic substancefluoride - nor does it make it advisable to swallow.

ANON (II): NO RESPONSE.

CONNETT: Another line of evidence which indicates that fluoride is not a nutrientis the very low level that occurs naturally in mothers’ milk. On average this is0.008 ppm (Institute of Medicine, 1997, page 292). It is highly unlikely that iffluoride was nutrient that the millions of years of evolution which went intodetermining baby’s first meal completely messed up and deprived the baby ofsuch a “nutrient”.

The consequence of the misguided fluoridation program is to give a new bornbaby between 100 and 200 times more fluoride than nature intended. Furtherdiscussion on the significance of giving a baby fluoride in large excess overnature’s intention can be found in Reason 11, Section B below.

2) Fluoridation is not necessary. Most Western European countries are notfluoridated and have experienced the same decline in dental decay as the US (Seedata from World Health Organization in Appendix 1, and the time trends


presented graphically at http://www.fluoridealert.org/who-dmft.htm). Thereasons given by countries for not fluoridating are presented in Appendix 2.)

ANON (I): NO RESPONSE.

ANON (II): The data from the WHO Oral Health Country/AreaProfile Programme (WHO) (cited in the ‘50 Reasons’document) should be interpreted cautiously. For manycountries the caries levels quoted are based on localstudies (reports of studies of national random samples notalways being available). Countries being compared did notuse the same research protocol, hence examiners indifferent countries were not governed by the same agreedclinical criteria. In comparing the oral health status ofdifferent populations in different countries, variations inthe diagnostic methods used during the course of oralhealth surveys will obviously affect the results.Confounding factors also have to be considered wheninterpreting studies on dental caries and include age,gender, social class, ethnicity, country, tooth type(primary or permanent), use of fluoride, method ofmeasurement of caries (clinical exam, radiographs, orboth), and training and calibration of examiners (McDonaghet al., 2000).

Such confounders have not been acknowledged in the ‘50Reasons’ document. Furthermore the only ‘explanatory’variable mentioned in the data provided is the fluoridationstatus of each country. Such an analysis is superficial andinadequate as inter-country comparisons of trends in oralhealth cannot be made on the basis of water fluoridationstatus alone, devoid of consideration of other pertinentcontributory factors. The superficial comparisons that havebeen made between countries on the basis of mean DMFT atage 12 are unwarranted as they fail to acknowledge thediverse factors mentioned above which may have influencedtrends in dental caries.

CONNETT: Even if there are limitations in the WHO’s comparisons, it is far betterthan no analysis or comparison at all, which seems to be the Irish promoters’position on this matter.

Moreover, while inter country comparisons may be questionable for some of thereasons outlined, the WHO figures clearly demonstrate that tooth decay hasbeen declining dramatically within each country regardless of their fluoridationstatus – a fact that is acknowledged by many peer-reviewed studies, but ignoredand obfuscated by Anon (Bohannan 1985; Diesendorf 1986; Heifetz 1988;

http://www.fluoridealert.org/who-dmft.htm


Kalsbeek 1990; Leverett 1991; Brathall 1996; Clarkson 1996; Haugejorden 1996;Reich 2001).

In other words there are other strategies to reduce tooth decay which have beenapplied in Europe without resorting to the draconian approach of forcingmedication on people, regardless of their health status, age, or their preferencein the matter.

3) Fluoridation's role in the decline of tooth decay is in serious doubt. The largestsurvey ever conducted in the US (over 39,000 children from 84 communities) bythe National Institute of Dental Research showed little difference in tooth decayamong children in fluoridated and non-fluoridated communities (Hileman 1989).According to NIDR researchers, the study found an average difference of only 0.6DMFS (Decayed Missing and Filled Surfaces) in the permanent teeth of childrenaged 5-17 residing in either fluoridated or unfluoridated areas (Brunelle andCarlos, 1990). This difference is less than one tooth surface! There are 128 toothsurfaces in a child's mouth. This result was not shown to be statisticallysignificant. In a review commissioned by the Ontario government, Dr. DavidLocker concluded:

"The magnitude of [fluoridation's] effect is not large in absolute terms, is oftennot statistically significant and may not be of clinical significance" (Locker 1999).

CONNETT: The response and counter-responses to this argument are inSECTION B below.

4) Where fluoridation has been discontinued in communities from Canada, theformer East Germany, Cuba and Finland, dental decay has not increased but hasactually decreased (Maupome 2001; Kunzel and Fischer,1997,2000; Kunzel 2000and Seppa 2000).


5) There have been numerous recent reports of dental crises in US cities (e.g.Boston, Cincinnati, New York City) which have been fluoridated for over 20years. There appears to be a far greater (inverse) relationship between toothdecay in children and parental income level than with water fluoride levels.

ANON (I): NO RESPONSE.ANON(II): NO RESPONSE.


CONNETT: It is revealing that the anonymous commentators on the 50 reasonsdid not address this reason. The simple fact is that dental researchers haveoffered little or no evidence that fluoridation can prevent the dental crises nowseen in many fluoridated cities in the US, or protect against the ravages of babybottle tooth decay, a major cause of tooth decay in poor children.

6) Modern research (e.g. Diesendorf 1986; Colquhoun 1997, and De Liefde, 1998)shows that decay rates were coming down before fluoridation was introduced andhave continued to decline even after its benefits would have been maximized.Many other factors influence tooth decay. Some recent studies have found thattooth decay actually increases as the fluoride concentration in the water increases(Olsson 1979; Retief 1979; Mann 1987, 1990; Steelink 1992; Teotia 1994; Grobleri2001; Awadia 2002 and Ekanayake 2002).


CONNETT: Again, it is revealing that the anonymous commentators on the 50reasons did not address this reason, since it seems to fly in the face of the wholefluoridation hypothesis.

7) The Centers for Disease Control and Prevention (CDC 1999, 2001) has nowacknowledged the findings of many leading dental researchers, that themechanism of fluoride's benefits are mainly TOPICAL not SYSTEMIC. Thus, youdon't have to swallow fluoride to protect teeth. As the benefits of fluoride (if anyexist) are topical, and the risks are systemic, it makes more sense, for those whowant to take the risks, to deliver the fluoride directly to the tooth in the form oftoothpaste. Since swallowing fluoride is unnecessary, there is no reason to forcepeople (against their will) to drink fluoride in their water supply. This positionwas recently shared by Dr. Douglas Carnall, the associate editor of the BritishMedical Journal. His editorial appears in Appendix 3.


8) Despite being prescribed by doctors for over 50 years, the US Food and DrugAdministration (FDA) has never approved any fluoride product designed foringestion as safe or effective. Fluoride supplements are designed to deliver thesame amount of fluoride as ingested daily from fluoridated water (Kelly 2000).



CONNETT: Apparently, this extraordinary situation in the US is of no interest tothe Irish commentators. However, they appear to pick and choose what theytake from the American experience! When American authorities conclude thatfluoridation is “safe and effective” they cite them; when we get this glaringanomaly from the very agency that is supposed to approve drugs in the US, theyignore it.

9) The US fluoridation program has massively failed to achieve one of its keyobjectives, i.e. to lower dental decay rates while holding down dental fluorosis(mottled and discolored enamel), a condition known to be caused by fluoride.The goal of the early promoters of fluoridation was to limit dental fluorosis (in itsmildest form) to 10% of children (NRC 1993, pp. 6-7). A major US survey hasfound 30% of children in optimally fluoridated areas had dental fluorosis on atleast two teeth (Heller 1997), while smaller studies have found up to 80% ofchildren impacted (Williams 1990; Lalumandier 1995 and Morgan 1998). TheYork Review estimates that up to 48% of children in optimally fluoridated areasworldwide have dental fluorosis in all forms and 12.5% with symptoms ofaesthetic concern (McDonagh, 2000).


10) Dental fluorosis means that a child has been overdosed on fluoride. Whilethe mechanism by which the enamel is damaged is not definitively known, itappears fluorosis may be a result of either inhibited enzymes in the growing teeth(Dan Besten 1999), or through fluoride's interference with G-protein signalingmechanisms (Matsuo 1996). In a study in Mexico, Alarcon-Herrera (2001) hasshown a linear correlation between the severity of dental fluorosis and thefrequency of bone fractures in children.


CONNETT: It is very serious in my view, that the Irish fluoridation commentatorsfailed to respond to this argument. Promoters usually dismiss concerns aboutdental fluorosis as merely a “cosmetic effect.” Their most outward sign ofconcern is to call for studies to investigate the psychological effects that thismight have on children. However, a more health conscious approach would beto consider what dental fluorosis indicates might be happening elsewhere in thethe body. Like the blue line on the gums of children exposed to excess lead,


dental fluorosis means that children have been over-exposed to fluoride. Eventhe American father of fluoridation, H. Trendley Dean himself described thiscondition as "… a low grade chronic fluoride poisoning of children” (Dean,1936). Such considerations should prompt very careful analysis of themechanisms which have been offered to explain this systemic effect on thegrowing tooth enamel.

The teeth are not the only place where fluoride accumulates; it also accumulatesin the bone and the pineal gland.

As far as the bone is concerned, for healthy individuals approximately 50% of allthe fluoride we take in accumulates there, and for individuals with impairedkidney function the accumulate rate is even higher. Thus it is very striking thatAlarcon-Herrera and coworkers in Mexico found that, in an area with high naturallevels of fluoride in water (1.5 to 5.5 ppm), there was a strong linear correlationbetween the severity of dental fluorosis (a marker of fluoride exposure) and theincidence of bone fractures in children. Nor is this the only indication that fluorideexposure at low levels can impact children’s bones. The 1956 report on theNewburgh versus Kingston trial of fluoridation (used extensively in the promotionof fluoridation) found a statistically significant increase in cortical bone defects inthe fluoridated community (13.5% versus 6.5%). This is important because it isthe cortical bone - the outside layer of the bone – which protects against fracturein the arms and legs.

Bone fractures in children and adults is one of the many health effects which maybe caused by fluoridation which has never been investigated in Ireland.

Another tissue which concentrates fluoride – like the teeth and the bone – is thepineal gland (Luke, 1997). Again the Irish government has made no indicationthat it has followed up on this finding –either attempting to repeat it – orinvestigating the other finding by Luke (1997) that fluoride lowers melatoninproduction in animals (Luke, PhD thesis, 1997).

11) The level of fluoride put into water (1 ppm) is up to 200 times higher thannormally found in mothers' milk (0.005 – 0.01 ppm) (Ekstrand 1981; Institute ofMedicine 1997). There are no benefits, only risks, for infants ingesting thisheightened level of fluoride at such an early age (this is an age wheresusceptibility to environmental toxins is particularly high).

CONNETT: The response and counter-responses to this argument are inSECTION B below. Also see discussion in Reason 1 above.


12) Fluoride is a cumulative poison. On average, only 50% of the fluoride weingest each day is excreted through the kidneys. The remainder accumulates inour bones, pineal gland, and other tissues. If the kidney is damaged, fluorideaccumulation will increase, and with it, the likelihood of harm.


CONNETT: No explanation is offered as to why this important reason was notaddressed.

13) Fluoride is very biologically active even at low concentrations. It interfereswith hydrogen bonding (Emsley 1981) and inhibits numerous enzymes (Waldbott1978).


14) When complexed with aluminum, fluoride interferes with G-proteins (Bigay1985, 1987). Such interactions give aluminum-fluoride complexes the potential tointerfere with many hormonal and some neurochemical signals (Strunecka &Patocka 1999, Li 2003).


ANON(II): A number of areas addressed in the paper byStruneka and Patocka (1999) (cited in the ‘50 Reasons’document) are widely accepted as aluminium toxicity e.g.aluminium related bone disease, dialysis encephalopathy andmicrocytic anaemia.

However, these elevated levels of aluminium only occurredin patients on dialysis (either from dialysis fluid orbecause of aluminium containing phosphate binders).

CONNETT: It was cavalier of ANON to use the toxicity of aluminium acting alone,to ignore the many situations where fluoride in conjunction with a trace amount ofaluminium can cause harm.

There have been literally hundreds of papers in the biochemical literaturedocumenting the ability of fluoride in the presence of a trace amount ofaluminium to switch on G-proteins. G-protein mechanisms have been offered toexplain both fluoride’s ability to cause dental fluorosis (Matsuo 1996) and alter


the rate of bone formation (Caverzasio et al., 1998). Since this signalingmechanism operates throughout the body it is of fundamental importance andshould be studied carefully and not casually dismissed.

15) Fluoride has been shown to be mutagenic, cause chromosome damage andinterfere with the enzymes involved with DNA repair in a variety of cell and tissuestudies (Tsutsui 1984; Caspary 1987; Kishi 1993 and Mihashi 1996). Recentstudies have also found a correlation between fluoride exposure and chromosomedamage in humans (Sheth 1994; Wu 1995; Meng 1997 and Joseph 2000).


ANON(II): The DHSS report (1991) on the benefits and risksof fluoride (cited in the ’50 Reasons’ document) includesthe following text in relation to the mutagenicity offluoride: “the most consistent finding is that fluoride hasnot been shown to be mutagenic in standard tests inbacteria (Ames Test)” (DHSS 1991).

• Kaminsky et al., (1990) have also concluded that there isno evidence that fluoride is genotoxic except in some invitro assays at cyotoxic (sic) concentrations.

CONNETT: While Anon is correct that the Ames test has not been able to detectgenotoxic effects from fluoride, this is irrelevant – since the originator of theAmes test, Bruce Ames, acknowledged that it is an inappropriate method fortesting fluoride (NRDC 1986). According to Ames:

“We have not tested fluoride because our test didn’t seem appropriate forit. The agar medium used in our petri plates contains a high concentrationof chloride ions and I would expect that would interfere with the uptake offluoride into the bacteri” (Letter from Bruce Ames to Arthur Upton,Director, National Cancer Institute, October 19, 1977).

It is, therefore, of particular interest and importance that, according to the USNational Toxicology Program, “the preponderance of evidence” from in-vitrostudies, excluding the Ames test, indicate that fluoride is in fact genotoxic (NTP1990).

ANON(II) (continued): The study by Mihashi and Tsutsui(1996) (cited in the ‘50 Reasons’ document) involvedtreating Rat Vertebral Body-Derived cells (RVBd) withsodium fluoride at 0.5-2.0 mM for 24 hours.


CONNETT: It is interesting that ANON focused only on the concentrations usedand ignored the important source of these rat vertebral bone cells. Mihashi andTsutsui note they were taken from the very strain of rats which had shown anincrease in osteosarcoma in the NTP (1990) fluoride-cancer study and they offerthese results in support of this important finding.

ANON(II) (continued): Two studies were conducted byJackson et al., (1997) to assess the potential for adversephysiologic and genotoxic effects of long-term fluorideingestion in adults residing in three communities withvarying water fluoride levels (0.2 ppm, 1.0 ppm, and 4.0ppm). All were long-time (¡_30 years) residents of theirrespective communities. The investigation provided evidencethat the long-term ingestion of water containing 0.2 ppm,1.0 pmm or 4.0 ppm fluoride did not have any clinicallyimportant physiologic or genotoxic effects in healthyadults.

CONNETT: While Anon is correct that Jackson found no clear evidence ofgenotoxicity in fluoride-exposed humans, they ignore the fact that 4 other studieson fluoride-exposed humans have found evidence of genotoxicity – as wasindicated above (Sheth 1994; Wu 1995; Meng 1997 and Joseph 2000).

16) Fluoride forms complexes with a large number of metal ions, which includemetals which are needed in the body (like calcium and magnesium) and metals(like lead and aluminum) which are toxic to the body. This can cause a variety ofproblems. For example, fluoride interferes with enzymes where magnesium is animportant co-factor, and it can help facilitate the uptake of aluminum and leadinto tissues where these metals wouldn't otherwise go (Mahaffey 1976; Allain1996; Varner 1998).

ANON (I): Statements 1, 11, 16, 33, 34, 36, 37, 40, 41, 42, 43, 46, 47, 48, 49, 50have been grouped together because they contain no supporting references topeer reviewed biomedical literature and/or represent opinions expressed by theauthor or the opinions of others with no references to the peer reviewedbiomedical literature and/ or contain references to the administration ororganization of regulatory agencies in the United States and/or refer to thehistory or sociology of the debate over water fluoridation in the United States.As noted in the introduction, no response is provided in this document to anystatement that is not directly related to an assessment of the benefits and risksof public water fluoridation based on the best available and most reliableevidence from human epidemiological studies.

CONNETT: This is a strange response since Allain 1996 and Varner 1998 areboth peer reviewed studies from the biochemical literature.


ANON(II): A report by Jackson et al., (2002) “Chemistry andBioavailability Aspects of Fluoride in drinking Water”discusses the chemistry of water fluoridation, possibleinteractions between fluoride and other elements in waterand any effects on bioavailability. The authors concludethat the effect of major cations (positively charged ions)calcium and magnesium and sodium on the bioavailability offluoride is very small.

• Jackson et al., (2002) also reported that fluoride at aconcentration of 1mg/l has essentially no interaction withother chemical species in water and negligible impact oncorrosivity of water through the distribution system.

CONNETT: This response misses the point we were making. Fluoride has thepotential to complex with metal ions within the body and thereby interfere withtheir normal function. This is especially true of the magnesium ion which isfrequently involved as a co-factor in enzymes involved with nucleic acidchemistry.

This is what the UK Environment Agency has to say on the matter in adiscussion of the toxicity of hydrogen fluoride:

‘ The fluoride ion itself is highly toxic to living organisms. It binds stronglywith calcium and magnesium and prevents these essential nutrientelements from carrying out their biochemical functions. This is the basisfor the toxicity of inorganic fluorides’. (Environmental Agency website)

ANON(II) (continued): Urbansky and Schock (2000)investigated possible complexation of lead by fluoride andhexafluorosilicate and found that the lead fluoridecomplexes accounted for less than 1% of the total dissolvedlead. They concluded that “no credible evidence exists toshow that water fluoridation, at a concentration of 1mg/lfluoride, has any quantitative effects on the solubility,bioavailability, bioaccumulation or reactivity of lead orlead compounds”. The authors also reported that fluorideat a concentration of 1mg/l will have essentially nointeraction with other chemical species in water andnegligible impact on corrosivity of water towards thedistribution system.

CONNETT: Urbansky’s study was entirely based upon theoretical calculationsand not on any study of fluoride interactions in real life waterworks situations ormeasurments made in children’s blood. Their critique of Masters and Coplan’sfindings (1999), failed to offer any counter explanation as to why blood lead levelin children were higher in communities in Massachusetts where the silicofluorides


were used as fluoridating agents. Moreover, Urbansky and Schock’s critiquepreceded Masters and Coplan’s second paper in 2000 which repeated their1999 Massachusetts findings in the state of NY (This issue is further discussed inReason 44, discussed in SECTION B).

ANON(II) (continued): The Medical Research Council (2002)note that aluminium and fluoride are mutually antagonisticin competing for absorption in the gut. Therefore, themore fluoride in the diet, the less aluminium is absorbed.At the same time, ingestion of aluminium counteracts dentalfluorosis, reducing fluoride stores in teeth and bones.This effect has been demonstrated in experimental animalsand humans (Foster, 1993; quoting Navia 1970). The authorsof the report thus concluded that “fluoride will reducerather than increase any toxic potential from aluminium infood or water”.

CONNETT: While the interactions between aluminum and fluoride are complex(a fact that is not necessarily a source for comfort), the anonymouscommentators fail – or refuse - to acknowledge the important study by Varner etal. (1998) who showed that fluoride increased the uptake of aluminum into rat’sbrain and that this was associated with damage to the brain tissue (seediscussion in reason 17 below).

17) Rats fed for one year with 1 ppm fluoride in their water, using either sodiumfluoride or aluminum fluoride, had morphological changes to their kidneys andbrains, an increased uptake of aluminum in the brain, and the formation of betaamyloid deposits which are characteristic of Alzheimers disease (Varner 1998).


ANON(II): Alzheimer’s disease is a degenerative conditionresulting in dementia, occurring mainly in the elderly.Aluminium has been suggested as a possible cause of, orrisk factor for, Alzheimer’s disease due to its presence inthe brain tissue of Alzheimer’s disease patients(specifically beta-amyloid plaques and neurofibrillarytangles). The proposed link between dietary aluminiumintake and Alzheimer’s disease is still the subject ofconsiderable debate. If absorption of aluminium is reducedby ingestion of fluoride, this condition should be lesscommon in communities with fluoridated drinking water(Foster, 1993; Kraus and Forbes, 1992). The MedicalResearch Council (2002) note that “the possible linkbetween aluminium uptake and Alzheimer’s disease is by nomeans established.”


CONNETT: I agree with Anon (II) that “the possible link between aluminiumuptake and Alzheimer’s disease is by no means established” but once again thecommentators’ miss the point. Varner et al. (1998) didn’t just show that therewas a greater uptake of aluminium into the brain, they showed the formation ofbeta-amyloid deposits which are characteristic of Alzheimer’s disease – indeedthese deposits are used to distinguish (at autopsy) Alzheimer’s disease fromother forms of senile dementia.

I would also note that the MRC (2002) panel was dominated by pro-fluoridation“experts” as well as Department of Health officials who are also known to bepushing fluoridation. How else can one explain their extraordinary conclusionthat more research should be put into investigating the psychological response todental fluorosis than into fluoride’s impact on the central nervous system; theendocrine system (including the thyroid and pineal gland); the reproductivesystem and the kidney! Thus I think we have to be very cautious about giving thiscommittee the final word on these matters.

18) Aluminum fluoride was recently nominated by the Environmental ProtectionAgency and National Institute of Environmental Health Sciences for testing bythe National Toxicology Program. According to EPA and NIEHS, aluminumfluoride currently has a "high health research priority" due to its "knownneurotoxicity" (BNA, 2000). If fluoride is added to water which containsaluminum, than aluminum fluoride complexes will form.


CONNETT: The failure of the commentators to respond to this argument speaksvolumes. They pick and choose which agencies they cite depending on whetherthese agencies, like the MRC(2002), are downplaying fluoride’s health impacts orthose like the EPA (Water division), NIEHS and the NRC which feel that thescience needs to be investigated more thoroughly.

19) Animal experiments show that fluoride accumulates in the brain andexposure alters mental behavior in a manner consistent with a neurotoxic agent(Mullenix 1995). Rats dosed prenatally demonstrated hyperactive behavior.Those dosed postnatally demonstrated hypoactivity (i.e. under activity or "couchpotato" syndrome). More recent animal experiments have reported that fluoridecan damage the brain (Wang 1997; Guan 1998; Varner 1998; Zhao 1998; Zhang1999; Lu 2000; Shao 2000; Sun 2000; Bhatnagar 2002; Chen 2002, 2003; Long2002; Shivarajashankara 2002a, b; Shashi 2003 and Zhai 2003) and impact


learning and behavior (Paul 1998; Zhang 1999, 2001; Sun 2000; Ekambaram2001; Bhatnagar 2002).


ANON(II): In the study by Mullinex et al., (1995) (cited inthe ‘50 Reasons’ document) rats were fed fluoride at levelsup to 125 times greater than that found in optimallyfluoridated water. The study attempted to demonstrate thatrats fed extremely high levels of fluoride (75 ppm to 125ppm in drinking water) showed behaviour-specific changesrelated to cognitive deficits. In addition, the experimentalso studied the offspring of rats who were injected two tothree times a day with fluoride during their pregnancies inan effort to show that prenatal exposure resulted inhyperactivity in male offspring. The external validity ofthese findingsare highly questionable due to the doses administered andthe fact that the body weight and gastrointestinal systemsof rats are not directly comparable with those of humans.

CONNETT: First of all, it is not unusual in animal studies to use high doses.Otherwise an inordinate number of animals have to be used.

Second, the doses used by Mullenix et al. are not that high if one knows that ittakes about five times as much fluoride in drinking water for a rat to reach theequivalent level of fluoride in the plasma as a human. It is the plasma levelswhich are more important when comparing animal and human studies.

Third, since Mullenix et al. published their study there have been over 30additional studies also indicating that fluoride impacts rat brain (seehttp://www.fluoridealert.org/health for a full listing) and one of them foundeffects on the brain at 1 ppm (Varner et al., 1998).

Fourth, shortly after Mullenix published this work the first of a series of studiesfrom China indicated that children’s IQ is lowered at a relatively low level offluoride in drinking water. The latest study by Xiang et al. (2003) estimates thatIQ is lowered at 1.8 ppm, which of course offers no margin of safety for childrendrinking water at 1 ppm a) because of other sources of fluoride and b) youcannot control how much water children drink.

ANON(II) (continued): Two reviewers (Ross and Daston 1995)of the study by Mullinex et al., (1995) have suggested thatthe observations made can be readily explained bymechanisms that do not involve neurotoxicity.

http://www.fluoridealert.org/health


CONNETT: Mullenix has responded to these criticisms (Mullenix 1995).However, the key question is whether the other 30+ animal experiments can beexplained away in this manner.

ANON(II) (continued): They found inadequacies inexperimental design that may have led to invalidconclusions. For example, the results of the experimentwere not confirmed by the use of control groups which arean essential feature of test validation and experimentaldesign. In summary the scientists stated, “we do notbelieve the study by Mullenix et al. 1995 can beinterpreted in any way as indicating the potential for NaF(sodium fluoride) to be a neurotoxicant.” Another reviewer(Whitford 1996) has noted that “it seems more likely thatthe unusually high brain fluoride concentrations reportedin Mullenix et al. were the result of some analyticalerror.”

CONNETT: Whitford’s criticism of Mullenix’s work was circulated privately by theCDC. This is unethical. If the criticism was valid Whitford a) should have sent itto the journal where Mullenix published her article and b) sent a copy to Mullenix.He did neither. When Mullenix was eventually shown the criticism by a thirdparty she was easily able to deal with it. However, this discussion is moot sincethere have been over 30 other animal studies which have shown that fluorideimpacts the brain. The most impressive have been published by ZZ Guan who iscurrently working at the Karolinska Institute in Stockholm.

The pro-fluoridation commentators give no indication that they are aware of anyof these studies and instead have relied on a superficial and now-dated analysisby the MRC (2002) panel.

20) Five studies from China show a lowering of IQ in children associated withfluoride exposure (Lin Fa-Fu 1991; Li 1995; Zhao 1996; Lu 2000; and Xiang2003a, b). One of these studies (Lin Fa-Fu 1991) indicates that even justmoderate levels of fluoride exposure (e.g. 0.9 ppm in the water) can exacerbatethe neurological defects of iodine deficiency.


ANON(II): McDonagh et al., (2000) examined possible adverseeffects associated with water fluoridation including IQ.The authors concluded that the quality of these studies waslow (evidence level C). The studies on IQ did not have aprospective follow-up and did not incorporate any form ofblinding.


The authors of the MRC report (2002) considered the twoChinese studies (Lu et al, 2000; Zhao et al., 1996) whichhave found a positive association between high levels offluoride in drinking water and reduced children’sintelligence IQ.

However, the authors of the MRC report (2002) note thatconfounding factors were dismissed and their possibleinfluence on the results of the study were not adequatelyexplained. At lower fluoride concentrations (e.g. 0.91ppm)which would be more comparable to the levels in fluoridatedwater in the UK and Ireland, a reduction in children’s IQwas not observed. The MRC concluded that furtherinvestigation of the impact of fluoride on intelligence(IQ) is considered to be of low priority.

CONNETT: The MRC (2002) did give further research on IQ a low priority – alower priority than further research on dental fluorosis. This does not do themcredit. Only dental researchers appear to put a lower priority on understandingfluoride’s impact on the brain than fluoride’s impact on teeth.

Moreover, the casual approach adopted by the Irish commentators on thesematters is amply demonstrated by the fact that they put their comments on theDepartment of Health’s site in 2005, which is two years after Xiang et al. (2003)published their study and yet they do not cite this study. This despite the factthat Xiang et al. took care of most, if not all, of the criticisms leveled at theprevious Chinese studies. For example, they controlled for the crucial possibleconfounders of lead and iodine. Why didn’t the Irish commentators mention this?Is it because they do not read the primary literature on health effects but insteadwait for other countries to do the reviews for them?

Their lack of knowledge (or interest?) on fluoride’s impact on the brains of bothanimals and humans is not an isolated instance. In the Fluoridation Forum reportless than two pages out of 295 pages were devoted to the primary literature onhealth effects – and these only dealt with one tissue: the bone.

ANON(II) (continued): In 1999, the Ministry of Health inOntario, Canada undertook a review of the literaturepublished between 1994 and 1999 in relation to fluoride andhealth (Locker 1999). The author concluded that the studiesfrom China claiming that children exposed to high levels offluoride had lower IQs than children exposed to low levelswere deeply flawed and provided no credible evidence thatfluoride obtained from water or industrial pollutionaffects the intellectual development of children.


CONNETT: The Locker review goes even further back in time and thereforecould not take into account the Xiang (2003) study. Locker has an excuse (sincethis study was not published at the time of his review), but the Irishcommentators do not. Incidentally, the impacts of fluoride on the brain gives animportant illustration of why you have to consider both animal studies and humanstudies. The animal studies establish biological plausibility. Any weight ofanalysis of both animal and human studies on the brain would raise a serious redflag on this end point, especially if one considers that the benefit being soughtamounts to little more than 0.6 of one tooth surface out of about 100 toothsurfaces in a child’s mouth!

21) Studies by Jennifer Luke (2001) showed that fluoride accumulates in thehuman pineal gland to very high levels. In her Ph.D. thesis Luke has also shownin animal studies that fluoride reduces melatonin production and leads to anearlier onset of puberty (Luke 1997).


ANON(II): Information on fluoride and the pineal gland islimited and further targeted research may be warranted(Luke 2001). The Medical Research Council (2002) hasconcluded that such research “ is presently of low priorityunless and until critical literature reviews are undertakenthat demonstrate specific research needs.”

CONNETT: I think this is a very cavalier attitude by the MRC to a potentiallyserious finding. There is really no need for Irish authorities to duplicate thisattitude. It may well turn out that one of the reasons that nature has kept fluorideaway from the new born baby (see discussion in Reasons 1 and 11 above) wasto avoid accumulation in the pineal gland and the disruption to melatonin levelsthat this might cause. How difficult or expensive would it be for the Irish or Britishauthorities to subject Luke’s work to serious scrutiny and test the result forrepeatability?

22) In the first half of the 20th century, fluoride was prescribed by a number ofEuropean doctors to reduce the activity of the thyroid gland for those sufferingfrom hyperthyroidism (over active thyroid) (Stecher 1960; Waldbott 1978). Withwater fluoridation, we are forcing people to drink a thyroid-depressingmedication which could, in turn, serve to promote higher levels ofhypothyroidism (underactive thyroid) in the population, and all the subsequentproblems related to this disorder. Such problems include depression, fatigue,weight gain, muscle and joint pains, increased cholesterol levels, and heartdisease.


It bears noting that according to the Department of Health and Human Services(1991) fluoride exposure in fluoridated communities is estimated to range from1.6 to 6.6 mg/day, which is a range that actually overlaps the dose (2.3 - 4.5mg/day) shown to decrease the functioning of the human thyroid (Galletti &Joyet 1958). This is a remarkable fact, particularly considering the rampant andincreasing problem of hypothyroidism in the United States (in 1999, the secondmost prescribed drug of the year was Synthroid, which is a hormone replacementdrug used to treat an underactive thyroid). In Russia, Bachinskii (1985) found alowering of thyroid function, among otherwise healthy people, at 2.3 ppmfluoride in water.


ANON(II): Only three thyroid studies met the inclusioncriteria for the “Systematic Review of Public WaterFluoridation” (McDonagh et al., 2000). No clear evidence ofpotential adverse effects was found. The subsequent MedicalResearch Council Report (2002) commissioned as a result ofthe York Systematic Review on Water Fluoridation by the U.KDepartment of Health discussed the two studies listed inthe York Review in which goitre (hypothyroidism) was theoutcome of interest.

CONNETT: Goitre represents one of the more extreme results of hypothyroidism.There are earlier and more subtle symptoms associated with this debilitatingcondition which need to be considered. This issue needs to be investigated byobserving thyroid hormone levels and basal temperatures. Neither the YorkReview nor the MRC considered such studies. For example they did not refer tothe study of Bachinskii et al (1985) which found decreased thyroid function at 2.3ppm of fluoride in water.

At the recent International Society for Fluoride in Frankfurt, Germany (Sept2005), which was not attended by any government official or researcher fromIreland, Ruiz-Payan from the University of Texas at El Paso, presented herresearch from Mexico where she found lowered thyroid function in adolescents ina community with 1 ppm of fluoride in the water compared to a low fluoridecommunity.

ANON(II) (continued): Two of these studies found noassociation with water fluoride level (Gedalia et al.,1963, Jooste et al., 1999). The third (Lin et al., 1991)found a significant positive association between combinedhigh fluoride/low iodine levels and goitre. However,because this study looked at combined fluoride/iodineuptakes, and has not been published in a peer-reviewedjournal, the findings should be “treated cautiously”. The


MRC report concluded that further work on the effect ofwater fluoridation on thyroid function is of low priority.

CONNETT: It is incorrect to cite Jooste (1999) as showing no effect betweenfluoride and goiter. According to Jooste: “These results indicate that either a highfluoride level in the water or another associated goitrogen, other than iodinedeficiency, may have been responsible for these goitres.”

The fact that the MRC (2002) put a low priority on examining a possiblerelationship between fluoridation and lowered thyroid function is not to theircredit. As I have pointed out elsewhere this same committee put a higher priorityon research into children’s psychological response to dental fluorosis than onfluoride’s impact on the endocrine system, the central nervous system, thekidney or on reproduction. Such a continued obsession with the teeth probablyreflects the presence of many people from the dental profession on the panelrather than with a rational consideration of priorities as far as health isconcerned.

23) Some of the early symptoms of skeletal fluorosis, a fluoride-induced bone andjoint disease that impacts millions of people in India, China, and Africa , mimicthe symptoms of arthritis (Singh 1963; Franke 1975; Teotia 1976; Carnow 1981;Czerwinski 1988; DHHS 1991). According to a review on fluoridation by Chemical& Engineering News, "Because some of the clinical symptoms mimic arthritis, thefirst two clinical phases of skeletal fluorosis could be easily misdiagnosed"(Hileman 1988). Few if any studies have been done to determine the extent ofthis misdiagnosis, and whether the high prevalence of arthritis in America (1 in 3Americans have some form of arthritis - CDC, 2002) is related to our growingfluoride exposure, which is highly plausible. The causes of most forms of arthritis(e.g. osteoarthritis) are unknown.


ANON(II): Endemic skeletal fluorosis in temperate climatesis confined to individuals exposed continuously over manyyears to very high levels of fluoride. Not only arefluoride exposures very high in these climates but alsonutrition is inadequate and high temperatures lead togreater consumption of water than in the UK and Ireland.These cases may be associated with industrial exposures orwith unusually high fluoride levels in drinking water.Skeletal deformities may be associated with or accentuatedby malnutrition and possible other conditions found inareas of long-term social and nutritional deprivation (WHO1994).


• Studies in India (Jolly 1976) found an average dailyfluoride intake of more than 9 milligrams in patients therewith endemic fluorosis.

• Dietary fluoride intake by adults in optimallyfluoridated (1 ppm) areas averages 1.4 to 3.4 mg/day, andin non-fluoridated areas averages 0.3 to 1.0 mg/day(Institute of Medicine, Food and Nutrition Board 1998).

CONNETT: Anon’s assertion that the doses causing skeletal fluorosis in Indiaand China are “very high” is contradicted by their statement that endemicfluorosis has been documented at doses of 9 mg/day – a fact which has beenconfirmed by recent studies (Teotia 1998; Bo 2003; Cao 2003). Not only is 9mg/day lower than the dose (20 mg/day) that fluoridation proponents used to citeas the minimum toxic dose, it is not much in excess of the dose (1.6-6.6 mg/day)that some citizens in fluoridated areas will receive (DHHS 1991). Thus there isvery little margin of safety for this serious bone damage, especially whenconsidering that 9 mg/day was associated with the later stages of skeletalfluorosis. It stands to reason, therefore, that doses of fluoride lower than 9mg/day could cause the earlier stages of the disease, in which arthritic pains canoccur before the onset of demonstrable bone changes.

ANON(II) (continued): Crippling skeletal fluorosis hasnever been a clinically important problem in the UnitedStates, UK or Ireland even though for many generationsthere were many communities whose drinking water containedfluoride at levels which could have produced this disorderin the US (Whitford 1996). There was only one non-industrial case ever reported in the UK (Webb-Peploe andBradley, 1966).

CONNETT: Anon’s focus on crippling fluorosis here is extremely misleading, as itobscures the main concern relating to skeletal fluorosis – namely, the earlystages of the disease. As noted in the 50 Reasons, but not addressed by Anon,the early stages of skeletal fluorosis can be very similar, if not identical, tovarious forms of arthritis (e.g. Osteoarthritis and rheumatoid arthritis). Thus, if theearly stages of skeletal fluorosis are occurring in the US (as several lines ofevidence would suggest), it would be extremely probable that US doctors wouldmisdiagnose the disease with a disease (e.g. osteoarthritis) with which they aremore familiar. Making this probability even more likely is the fact that most USdoctors are given little sophisticated training in diagnosing fluorosis (why learnhow to diagnose something if it "doesn't exist.") Hence, not only are the earlystages of skeletal fluorosis difficult to differentiate from other common bonediseases, but the doctors responsible for making this differentiation have notbeen given adequate training to do so. All told, if an individual living in the US orIreland did in fact have the early stages of skeletal fluorosis, it would beextremely unlikely that they would be correctly diagnosed.


ANON(II) (continued): In temperature climates in thedeveloped countries, crippling skeletal fluorosis is notassociated with water fluoridated to a level of 1ppm.Kaminsky et al., (1990) reported no evidence of skeletalfluorosis among the general US population exposed todrinking water fluoride concentrations lower than 4mg/l intheir summary of the benefits and risks of fluorideingestion.

CONNETT: What Anon does not acknowledge here is the fact that Kaminsky(1990) recognized that people with kidney disease have developed skeletalfluorosis by drinking water with less than 4 ppm fluoride in water (Juncos 1972;Johnson 1979). It appears, therefore, that Anon has as much blatant disregardfor sensitive subsets of consumers as fluoridation proponents here in the US.

It is an astonishing fact that, even though according to the CDC (2002), arthritisimpacts one in three adults in the US (68 million), no effort has been made to seeif any of these cases are caused by or exacerbated by excess fluoride exposure.

For that matter, no fluoridating country, including Ireland, has bothered to trackthe levels of fluoride in their citizens’ urine, plasma or bone. They are flying blindon this and very many other health effects. If you don’t look you don’t find!

24) In some studies, when high doses of fluoride (average 26 mg per day) wereused in trials to treat patients with osteoporosis in an effort to harden their bonesand reduce fracture rates, it actually led to a HIGHER number of fractures,particularly hip fractures (Inkovaara 1975; Gerster 1983; Dambacher 1986;O’Duffy 1986; Hedlund 1989; Bayley 1990; Gutteridge 1990. 2002; Orcel 1990;Riggs 1990 and Schnitzler 1990). The cumulative doses used in these trials areexceeded by the lifetime cumulative doses being experienced by many peopleliving in fluoridated communities.


CONNETT: It is extraordinary that ANON avoided this argument because it refersto human experiment, not animal experiments which they tend to disregard.Moreover, their reluctance to consider these findings is in contrast to thepromoters who used earlier trials of this type to support fluoridation when theythought that they showed that fluoride was strengthening the bones of thesepatients. Another double standard.


25) Nineteen studies (three unpublished, including one abstract) since 1990 haveexamined the possible relationship of fluoride in water and hip fracture amongthe elderly. Eleven of these studies found an association, eight did not. One studyfound a dose-related increase in hip fracture as the concentration of fluoride rosefrom 1 ppm to 8 ppm (Li 2001). Hip fracture is a very serious issue for the elderly,as a quarter of those who have a hip fracture die within a year of the operation,while 50 percent never regain an independent existence (All 19 of these studiesare referenced as a group in the reference section).


ANON(II): The question of the possible impact of publicwater fluoridation on the risk of bone fractures has beenaddressed in the “Systematic Review of Public WaterFluoridation” (McDonagh et al., 2000). Using a qualitativemethod of analysis (i.e. visually examining forest plots),McDonagh et al., (2000) found no clear association of hipfracture with water fluoridation. The evidence on otherfractures follows a similar trend. Overall, the findings ofstudies of bone fracture effects showed small variationsaround the ‘no effect’ mark.

AND (on pages 32-33)

• The York Review included 29 studies on the relation offluoride in water to bone health (McDonagh et al 2000). Thevalidity of the studies were generally assessed as low andall but one were classed at the lowest of the three levelsof evidence that had been specified at the start of thereview. A forest plot of all the bone studies was producedshowing the measures of effect and the 95% confidencelimits for all studies that provided sufficient data toallow calculation. The majority of the measures of effectand their confidence intervals were distributed evenlyaround the line of no effect (1.0) suggesting noassociation with water fluoridation. A meta-regression ofbone fracture studies also found no association with waterfluoridation. The York review team concluded that ‘the bestavailable evidence on the association of water fluoridationand bone fractures (27 of 29evidence level c) show no association’ (McDonagh et al.,2000).

CONNETT; What the commentators fail to acknowledge here is that the Yorkreview disregarded the hip fractures observed by Li et al (2001) which wementioned above, even though there appears to be a dose related increase from1 to 8 ppm in this study. In their meta-analysis the York review only concerneditself with three out of six data points: the hip fracture rates in the two villages


below 1 ppm and the village at 1 ppm. With these there was no statisticaldifference and that was what was incorporated in their meta-analysis. Howeverthe other three villages at 1.5, 3.5 and 4.3 – 8 ppm, all showed an increased riskof hip fractures in the elderly. The rates doubled at 1.5 ppm and tripled at 4.3ppm plus. While, the rate at 1.5 ppm did not show a statistically significantdifference, the result at 4.3 ppm plus was and the linear trend is clear – in fact alinear fit to the data provides a far better fit than a fit involving some thresholdafter 1.5 ppm.

It is interesting to note that I actually presented Li’s results in my presentation tothe Fluoridation Forum in 2000 (As a peer reviewer of the York review I had anadvance copy of the study which had been accepted for publication by then).However, even though bone fractures was the only health effect considered bythe Fluoridation Forum other than dental fluorosis and even though theyconsidered only three primary studies in this area, they chose not to look at thisone.

26) The only government-sanctioned animal study to investigate if fluoridecauses cancer, found a dose-dependent increase in cancer in the target organ(bone) of the fluoride-treated (male) rats (NTP 1990). The initial review of thisstudy also reported an increase in liver and oral cancers, however, all non-bonecancers were later downgraded – with a questionable rationale - by agovernment-review panel (Marcus 1990). In light of the importance of this study,EPA Professional Headquarters Union has requested that Congress establish anindependent review to examine the study's results (Hirzy 2000).


CONNETT: Once again we see the commentators ducking a key animal study.

27) A review of national cancer data in the US by the National Cancer Institute(NCI) revealed a significantly higher rate of bone cancer in young men influoridated versus unfluoridated areas (Hoover 1991). While the NCI concludedthat fluoridation was not the cause, no explanation was provided to explain thehigher rates in the fluoridated areas. A smaller study from New Jersey (Cohn1992) found bone cancer rates to be up to 6 times higher in young men living influoridated versus unfluoridated areas. Other epidemiological studies have failedto find this relationship (Mahoney 1991; Freni 1992).



ANON(II): In their systematic review of water fluoridationMcDonagh et al., (2000), included seven studies ofosteosarcoma, presenting twelve analyses. Seven of thesefound the direction of association to be positive (fewercancers), three found a negative direction of association(more cancers) and two found no relationship (McDonagh etal., 2000). The study by Cohn (1992) (cited in the ‘50Reasons’ document), found a statistically significantassociation between fluoridation and increased prevalenceof osteosarcoma in males. However, this study had thelowest validity score, 2.5 out of 8, of those included inthe systematic review process. The review team concludedthat, from the available research evidence, no associationwas detected between water fluoridation and mortality fromany cancer, or from bone or thyroid cancers specifically(McDonagh et al., 2000).

CONNETT: The York Review’s conclusions on fluoride and osteosarcoma havebeen superceded by a 2001 doctoral thesis from Harvard University (Bassin2001). The Harvard thesis – a case control study utilizing an age-specificanalysis - found that young males exposed to fluoridated water at 0.3 to 1 ppmduring their sixth, seventh and eighth years had a significant increased risk ofdeveloping osteosarcoma by the age of 20. The possibility of a “window ofvulnerability” was actually discussed by Cohn in 1992. The sixth, seventh andeighth years coincides with a boy’s mid-childhood growth spurt.

As osteosarcoma is frequently fatal in young boys, it is very unsettling thatBassin’s thesis adviser Professor Chester Douglass did not report this result tohis funding agency (the NIH). But worse than that, when Douglass was given theopportunity to discuss fluoridation and osteosarcoma in a presentation before theBritish Fluoridation Society in 2002, he said that there was no connection and didnot cite his graduate student’s work, which he himself directed and approved!Even when Douglass submitted a written report on this matter to his fundingagency he again said that he had found no connection between fluoridation andosteosarcoma and this time even offered Bassin’s thesis as a supportingfootnote. Because of a complaint from the Environmental Working Group (EWG)Douglass’s highly questionable conduct is being investigated by both HarvardUniversity and the NIH.)

As detailed elsewhere (Connett 2005a,b), when previous results are re-examinedin the light of Bassin's findings, the balance must shift to a conclusion that thepreponderance of evidence indicates a positive relationship betweenosteosarcoma in young men and exposure to fluoride – particularly whenconsidering the acknowledged biologic plausibility of a fluoride-osteosarcoma link(NTP 1990). The critical ages for exposure appear to be their 6th, 7th, and 8thyears, i.e. during a window of vulnerability when young boy's mid-childhood bonegrowth spurt is taking place.


28) Fluoride administered to animals at high doses wreaks havoc on the malereproductive system - it damages sperm and increases the rate of infertility in anumber of different species (Kour 1980; Chinoy 1989; Chinoy 1991; Susheela1991; Chinoy 1994; Kumar 1994; Narayana 1994a, b; Zhao 1995; Elbetieha 2000;Ghosh 2002 and Zakrzewska 2002). Whilestudies conducted at the FDA havefailed to find reproductive effects in rats (Sprando 1996, 1997, 1998), anepidemiological study from the US has found increased rates of infertility amongcouples living in areas with 3 or more ppm fluoride in the water (Freni 1994), and2 studies have found a reduced level of circulating testosterone in males living inhigh fluoride areas (Susheela 1996 and Barot 1998).


ANON(II): In the study by Freni (1994) (cited in the 50Reasons’ document) the water was fluoridated to 3 ppm ormore which is considerably higher than the optimum levelrecommended for water fluoridation. This study alsocompared county birth data with county fluoride levels andattempted to show an association between high fluoridelevels in drinking water and lower birth rates (Freni1994). The study used population means rather than data onindividual women. Whether or not the fluoride effect on thefertility rate found at the county level also applies toindividual women was not investigated. Population data doesnot adjust for confounding factors such as age of thesubjects. The potential influence of confounding factorsmust also be considered. A large variation exists in thisage range, which more than likely had a large influence onthe findings of the study.

CONNETT: I would dispute the notion that 3 ppm is “considerably higher than theoptimum level recommended for water fluoridation.” One has to remember that inboth the US and Ireland children and adults get exposed to more sources offluoride than just water alone and also that some children drink a lot more waterthan others. Thus ANON (II) is clutching at straws to deny Freni’s 1994 findingson this weak argument. What Freni said in his conclusion was:

“The study results and the wealth of animal data do raise the questionwhether public health concerns and toxicological research should not shifttheir focus from the isolated intake from fluoridated water to the potentialtoxicity of the total fluoride intake.”

While Freni was the first to admit that there were inevitable weaknesses in hispreliminary study, what I find appalling is that no government (including Ireland)


promoting or practicing fluoridation has sought to repeat or refine his study. Whynot?

This failure to do follow-up research to Freni’s study becomes particularly glaringin light of additional published research on humans finding subclinical evidenceof reproductive toxicity from fluoride exposure (Susheela 1996; Ortiz-Perez2003). The study from Ortiz-Perez (2003) found evidence of sertoli cell damageamong humans exposed to 3 to 29 mg/day, while Susheela (1996) foundreduced testosterone levels among male patients with skeletal fluorosis. Thesefindings are of particular interest in light of the long line of animal studiesreporting fluoride-induced damage to the male reproductive system.

ANON(II) (continued): In the study conducted by Chinoy etal., (1994) (cited in the ‘50 Reasons’ document) theeffects of 25, 50 and 250 mM sodium fluoride on humanspermatozoa was investigated in vitro at intervals of 5, 10and 20 minutes. It was reported that sodium fluoride didnot affect the extracellular pH of the sperm “except that aslight acidification was caused by the 250mM dose only”.The doses of fluoride administered to the human spermatozoawere much higher than that provided by public waterfluoridation. They were also administered in vitro whichmakes it more difficult to correlate the findings to the invivo situation.

CONNETT: Anon’s criticism of Chinoy’s 1994 paper overlooks the fact that the50 Reasons document listed many other animal studies showing fluoride candamage the reproductive system. It’s not just Chinoy 1994. Their failure toaddress these suggests they have not read these other important studies.

ANON(II) (continued): A Working Group appointed by theMedical Research Council (2002) did not consider that theavailable evidence supported claims that fluoridated wateraffects the reproductive system and consequently they didnot recommend any further research in this area, noting,“the plausibility of fluoride affecting the reproductivecapacity of humans at the intakes experienced fromfluoridated drinking water is low”.

CONNETT: In light of the human study by Ortiz-Perez published in 2003 (seeabove), Anon’s reliance on the MRC’s 2002 review is inappropriate.

29) The fluoridation program has been very poorly monitored. There has neverbeen a comprehensive analysis of the fluoride levels in the bones, blood, or urineof the American people or the citizens of other fluoridated countries. Based onthe sparse data that has become available, however, it is increasingly evident that


some people in the population – particularly people with kidney disease - areaccumulating fluoride levels that have been associated with harm to both animalsand humans, particularly harm to bone (see Connett 2004).


CONNETT: I can understand why the pro-fluoridation commentators don’t wantto admit that the potential health effects of the fluoridation program have beenvery poorly monitored in Ireland. However, that is the truth of the matter. Notonly have no health studies on any tissue other than the teeth been conducted inIreland in the 42 years of this mandatory policy but the health authorities havenever felt it necessary to systematically track the levels of fluoride in the urine,plasma or bones of the Irish people which would be a basic requirement if onewanted to do a serious epidemiological study on one of the end points inquestion.

A recent (independent) urine analysis of 8 city councilors from Kildare Co., foundexcess levels (>3 mg/L) in 6 of the 8 samples. One of the councilors had urinelevels (6 mg/L) consistent with an intake of 6 mg/day (Irish Independent, June 26,2001). While this was of course a small experiment, it highlights the glaringabsence of such systematic data in Ireland. It also begs the question: if 6 of 8councilors were found to have abnormally high fluoride levels in their urine (>3mg/L), how many other Irish people have abnormally high levels as well?

ANON (II): Proponents of water fluoridation recognise theimportance of continuing scientific research. For example,the National Institute of Dental and Craniofacial Research(NIDCR) hosted a research workshop to identify needs forinternational collaborative research on fluoride (Clarksonet al., 2000). The workshop was co-sponsored with 10partners including the Centre for Disease Control andPrevention (CDC) and the International Association forDental Research (IADR) and was attended by approximately 80experts in fluoride research including government, industryand academia. Based on findings presented by the speakersand discussed extensively at the workshop, the participantsagreed an international research agenda on fluorides(reference).

CONNETT: If one reads the report cited in this reference (Clarkson J, HardwickK, Barmes D, Richardson L (2000). International Collaborative Research onFluoride. J Dent Res 79(4):893-904.) one will quickly see that the researchagenda is dominated by dental interests. Again, it underlines the fact thatdentists have controlled this debate for far too long. Clearly the fluoridationcontroversy issue continues to put huge amounts of money into their researchprograms. However, neither they, nor the governments that support theiragenda, appear to have any real interest in pursuing the effect of fluoride on


tissues other than the teeth. Again, neither Ireland nor most other fluoridatingcountries, has undertaken serious and meaningful health studies of theirpopulations on other tissues despite recommendations that they do so (NHMRC,1991 and NRC, 1993). Nor have they even got to square one on monitoringexposure by looking at fluoride levels in urine, plasma and the bone. Most of thehealth studies are emanating from countries which do not have a fluoridationprogram, like India and China, whose governments are extremely concerned asto what natural fluoride is doing to their citizens. It does Irish and UK authoritieslittle credit that they continue to largely ignore the results of their work.

ANON (II) (continued): Fluoride levels in Irish publicwater supplies are very closely monitored on daily, monthlyand quarterly examinations. A sensitive method formonitoring the total amount of fluoride ingested orabsorbed is to monitor the levels of enamel fluorosis. Thelevels of enamel fluorosis in children and adolescents inIreland have been assiduously monitored since the early1980’s (O’Mullane et al 1986, Whelton et al 1998, 2004).Using Dean’s index, these studies have shown a slightincrease in the prevalence of the questionable, very mildand mild grades of fluorosis. The risk factors for enamelfluorosis have been identified and strategies recommendedfor reducing the prevalence of enamel fluorosis in theRepublic of Ireland (Department of Health 2002,www.fluoridationforum.ie).

CONNETT: Monitoring levels of fluoride in the water supply is irrelevant to theconcerns expressed in the 50 Reasons. Indeed, the concern is not about thetechnical capacity of water suppliers to add the desired level of fluoride to water.The concern, instead, is that 1) individuals are ingesting more fluoride today,from sources other than water (e.g. toothpaste, processed foods, etc) than theywere ingesting 50 to 60 years ago, and 2) some individuals (particularly thosewith kidney disease) are unable to excrete fluoride from their body efficiently.Hence, not only can we not control the amount of fluoride being ingested, but wecan’t control the concentration of fluoride being reached in the organs of sensitiveconsumers.

While studies tracking the prevalence of dental fluorosis are important, they areno substitute for tracking the levels of fluoride in the urine, plasma and bones ofthe population at large, and among sensitive subgroups, and using this data toconduct meaningful epidemiological studies on health concerns. For, as noted inthe 50 Reasons, but unaddressed by Anon, published data already indicates thatindividuals with kidney disease may accumulate levels of fluoride in their bloodthat exceed the levels that have been associated with adverse health effects inanimals and humans.


Further, while Irish investigators have studied the prevalence of dental fluorosisamong Irish children, it is revealing that no Irish study yet utilized the presenceand severity of fluorosis as a biomarker for investigating fluoride’s other possiblehealth impacts on children, including: behavioral problems, lowered thyroidfunction; lowering of IQ; early onset of puberty and bone fractures.

30) Once fluoride is put in the water it is impossible to control the dose eachindividual receives. This is because 1) some people (e.g. manual laborers,athletes, diabetics, and people with kidney disease) drink more water than others,and 2) we receive fluoride from sources other than the water supply. Othersources of fluoride include food and beverages processed with fluoridated water(Kiritsy 1996 and Heilman 1999), fluoridated dental products (Bentley 1999 andLevy 1999), mechanically deboned meat (Fein 2001), teas (Levy 1999), andpesticide residues on food (Stannard 1991 and Burgstahler 1997).


CONNETT: Again another argument without a response. Why not? It is a crucialissue. In their response to reason 29 above the commentators comment on howtightly monitored the levels of fluoride are that are added to the water. However,monitoring fluoride concentrations does not control the dose an individual citizenreceives for the simple reason you cannot control how much water people drinkor the fluoride that they get from the other sources identified in reason 30.

31) Fluoridation is unethical because individuals are not being asked for theirinformed consent prior to medication. This is standard practice for allmedication, and one of the key reasons why most of western Europe has ruledagainst fluoridation (see appendix 2).

As one doctor aptly stated, "No physician in his right senses would prescribe for aperson he has never met, whose medical history he does not know, a substancewhich is intended to create bodily change, with the advice: 'Take as much as youlike, but you will take it for the rest of your life because some children suffer fromtooth decay.’ It is a preposterous notion."


ANON(II): The reader is referred to Chapter 13 in the finalreport of the Forum on Fluoridation in Ireland (Departmentof Health and Children 2002) where the ethical and legaldimensions of water fluoridation are discussed in detail.


• To consider the ethics of water fluoridation is toconsider the balance between its benefits and risks. Theissue of proportionality is at the heart of this questionand is clearly dependent on the precise benefits that mustbe weighed against the precise debits which the processinvolves.

CONNETT: This analysis would appear to break down when one recognizes thatthe benefits accrue to some people while the risks impact others.

Moreover, the benefits in question are very slight: in the US they amount to asaving of 0.6 of one permanent tooth surface out of about 100 tooth surfaces in achild’s mouth (Brunelle and Carlos, 1990, see Reason 2). Who in their right mindwould seek this with the possible risks to a child’s bones, brain, endocrinesystems not to mention the lifetime fluoride accumulation in bone and tissue inpeople of all ages?

ANON (II) (continued): Dr. Richard Hull, an expert in thearea of ethics, was consulted by a sub-group in the Forumon Fluoridation (Department of Health and Children 2002)and the following paragraph is drawn from hisdeliberations:

“It is also worth remembering that government, by itsnature, is paternalistic. Health in general is seenas an area where paternalistic State intervention isjustifiable, and in terms of oral health, the poordietary habits of the Irish people could be seen as ajustification for taking a paternalistic approach.The degree of infringement of bodily integrity bywater fluoridation is relatively minor when comparedto education, for example. This intervention could beseen to breach bodily and mental integrity in a muchmore serious manner. The idea of State interventionis with the aim of protecting health and perhaps life(dental decay may itself be responsible for a smallnumber of deaths each year from anaesthesia), is farmore compelling than is the idea of intervention withthe aim of affecting more value-laden life-stylechoices. This points to an alternative approach – toplace a very strong emphasis on the role of education,informing citizens on the importance of oral hygieneand dietary advice. However, it is all very well toemphasise the value of autonomy, but the desire toeffectively safe-guard the health and safety ofchildren (who are not yet autonomous) could be said toconstitute a strong emphasis”.


CONNETT: I suspect that Dr. Hull has probably been convinced by his dentalcolleagues and government spokespersons that there are no significant healthrisks associated with fluoridation. Had he actually read some of the primaryliterature he may not have been so sanguine in his views on the ethics in thismatter. Dr. Hull’s analysis would only hold in my view if the benefit of waterfluoridation could be achieved without any health risks. If for example, fluoridelowers the IQ of the child, could he still maintain that “The degree of infringementof bodily integrity by water fluoridation is relatively minor when compared toeducation”?

32) While referenda are preferential to imposed policies from centralgovernment, it still leaves the problem of individual rights versus majority rule.Put another way -- does a voter have the right to require that their neighboringest a certain medication (even if it's against that neighbor's will)?


CONNETT: I realize that this argument does not apply to Ireland because theIrish people have never been given the chance to vote on this matter. In thisinstance, Ireland clearly prefers bureaucratic mistakes to democratic ones!

33) Some individuals appear to be highly sensitive to fluoride as shown by casestudies and double blind studies (Shea 1967, Waldbott 1978 and Moolenburg1987). In one study, which lasted 13 years, Feltman and Kosel (1961) showed thatabout 1% of patients given 1 mg of fluoride each day developed negative reactions.Can we as a society force these people to ingest fluoride?


• ANON (II) Challacombe (1996) has addressed the questionof the potential effect of fluoridation on immune function.According to Challacombe (1996) there have been no


confirmed cases of allergy to fluoride or of positive skintesting in humans or in animals and that there is noincreased reporting of allergies of any type withincreasing fluoride use.

There are also no reports of reactions of an allergicnature to fluoride in other substances such as tea, tinnedfish, salt water, where concentrations can be much higherthan in water fluoridation programmes.

CONNETT: Anon’s reliance on Challacombe underscores the problems of relyingon reviews, rather than the primary scientific literature. While Challacombe mayhave said that “there have been no confirmed cases of allergy to fluoride or ofpositive skin testing in humans or in animals” this is incorrect. Allergic, orhypersensitive, reactions to fluoride (both topical and systemic) have beenreported in blind and double-blind studies (Waldbott 1958; Shea 1967;Grimbergen 1974; Mellette 1983), and positive skin testing has been reported forboth humans (Shea 1967) and animals (Stone 1967, 1968). While fluoridationproponents have dismissed these findings on theoretical grounds, they have yetto publish a single blind or double-blind study to actually prove their case.

34) According to the Agency for Toxic Substances and Disease Registry (ATSDR1993), and other researchers (Juncos & Donadio 1972; Marier & Rose 1977 andJohnson 1979), certain subsets of the population may be particularly vulnerableto fluoride's toxic effects; these include: the elderly, diabetics and people withpoor kidney function. Again, can we in good conscience force these people toingest fluoride on a daily basis for their entire lives?


CONNETT: This first response is strange because a) the matter is hardlydisputed in research circles and b) the argument was backed up with peer-reviewed articles in the scientific literature (Juncos & Donadio 1972; Marier &Rose 1977 and Johnson 1979). Moreover, the anonymous commentators can


hardly argue that such vulnerable subsets of the population do not exist inIreland.

• ANON (II): Several large community-based epidemiologicalstudies found no increased renal disease associated withlong-term exposure to drinking water with fluorideconcentrations of up to 8mg/l (DHSS 1991, NRC 1993).

CONNETT: This second response misses the point. In this argument we werenot saying that fluoride damages the kidney (it may) but rather that people withpoor kidney function are more susceptible to fluoride’s toxic effects. This occurssimply because they are not able to clear 50% of the fluoride intake each day likepeople with normal kidney function. A mandatory fluoridation program makes noallowance for these and the other susceptible groups which we can expect to bepresent in any population.

35) Also vulnerable are those who suffer from malnutrition (e.g. calcium,magnesium, vitamin C, vitamin D and iodide deficiencies and protein poor diets)(Massler & Schour 1952; Marier & Rose 1977; Lin Fa-Fu 1991; Chen 1997; Teotia1998). Those most likely to suffer from poor nutrition are the poor, who areprecisely the people being targeted by new fluoridation programs. While being atheightened risk, poor families are less able to afford avoidance measures (e.g.bottled water or removal equipment).


CONNETT: It is difficult to understand why the commentators felt that thisargument was not worthy of a response. In their negligence we see anotherdouble standard. When they were dismissing concerns about skeletal fluorosisthey made a big point of how the bone damage caused to millions of Indians bynaturally occurring fluoride could be written off partly because this damage wasexacerbated by poor nutrition. Have they then concluded that there are nopockets of malnutrition in Ireland? Strange also because in another responsethey were bemoaning the fact that the Irish diet was not up to par with theScandinavian countries (see in particular their response Reason 4 (Section Bbelow) to the Seppa paper which showed that when fluoridation was stopped inFinland, tooth decay did not go up as expected).

36) Since dental decay is most concentrated in poor communities, we should bespending our efforts trying to increase the access to dental care for poor families.The real "Oral Health Crisis" that exists today in the United States, is not a lack of


fluoride but poverty and lack of dental insurance. The Surgeon General hasestimated that 80% of dentists in the US do not treat children on Medicaid.


CONNETT: It is difficult to understand ANON (I)’s unresponsiveness to thisargument. Is ANON (I) suggesting that the issue of the relationship between lowincome and tooth decay in the US is not relevant to Ireland?

ANON (II): The Oral Health in America 2000 proposals (citedin the ‘50 Reasons’ document) highlight the social impactof dental disease in children and note that pain andsuffering due to untreated dental disease can lead todisruption of family life, and problems in eating, speakingand enjoyment of social or school activities. (it is notclear to which of the 50 reasons this response wasdirected, PC).

CONNETT: This response does not deal with our argument but maybe it was notintended to.

37) Fluoridation has been found to be ineffective at preventing one of the mostserious oral health problems facing poor children, namely, baby bottle toothdecay, otherwise known as early childhood caries (Barnes 1992 and Shiboski2003).


38) The early studies conducted in 1945 - 1955 in the US, which helped to launchfluoridation, have been heavily criticized for their poor methodology and poorchoice of control communities (De Stefano 1954; Sutton 1959, 1960 and 1996;Ziegelbecker 1970). According to Dr. Hubert Arnold, a statistician from the


University of California at Davis, the early fluoridation trials "are especially richin fallacies, improper design, invalid use of statistical methods, omissions ofcontrary data, and just plain muddleheadedness and hebetude." In 2000, theBritish Government’s “York Review” could give no fluoridation trial a grade Aclassification – despite 50 years of research (McDonagh 2000, see Appendix 3 forcommentary).


CONNETT: The commentators failed to address this argument, probablycontenting themselves that it pertains only to American history. However,American and Irish history are intertwined on this matter. Ireland was subjectedto intense lobbying and possibly financial inducements from the US Public HealthService to start this practice in the 1960’s. Moreover, American governmentofficials testified in the court case fought over its introduction. Thus the fact thatthe evidence they then cited for effectiveness is now seen to be of a very poorcaliber should be a matter of concern for Irish authorities. As far as Americanassurances of safety are concerned we now know that when the US PublicHealth Service endorsed fluoridation in 1950 not one single trial or health studyhad been completed. Christopher Bryson’s 2004 book “The Fluoride Deception”gives a solid referenced analysis of why America rushed into this practice sounscientifically. If Bryson is correct, the policy had less to do with protectingteeth than reducing liabilities for American industries exposing both their workersand the local environment to excessive fluoride exposure. Irish commentatorsshould also be concerned that the York Review, which they cite often in theirresponse to the 50 reasons, could find no grade A studies on fluoridation’seffectiveness.

39) The US Public Health Service first endorsed fluoridation in 1950, before onesingle trial had been completed (McClure 1970)!


ANON(II): McNeil (1957) and McClure (1970) have noted thatthe initial decision made by the US Public Health Serviceto endorse fluoridation (alluded to in the ’50 Reasons’document) was influenced by several factors, including:

a. The epidemiological studies carried out by Dean in the1930s and1940s and, in particular, Dean’s 21 cities study publishedin 1942. Thisstudy examined the relationship between the cariesexperience of 7,257


12- to 14-year old children from 21 cities in four statesin the US andthe naturally occurring fluoride content of the watersupply.

b. Studies on the general health of populations residing innaturallyfluoridated regions carried out by the USPHS

c. The first Grand Rapids report of 1949.

CONNETT: This certainly is the “party line.” However, the analysis of McNeil andMcClure (both pro-fluoridation) should be balanced with the more recent – andthoroughly documented arguments of Christopher Bryson, as mentioned in 38)above.

ANON(II) cites Dean’s 21 Cities published in 1942, but fails to acknowledge thevery selective nature of this report (Colquhoun 1990). Dean had dental decayfigures from at least 600 counties in the US, so why did he select only 21 citiesfor his analysis? When Austrian researcher Rudolf Ziegebecker combinedDean’s data with all the other data he could find from the US and Europe, hefound a robust relationship between water fluoride concentrations and theseverity of dental fluorosis but little correlation between tooth decay and fluorideconcentration (Ziegebecker, 1981).

ANON(II) cites studies on the general health of populations residing in naturallyfluoridated regions carried out by the US PHS, but other than dental fluorosis nostudies on health had been published in 1950.

ANON (II) cites the Grand Rapids Report of 1949, but this study had only begoing on for four years and thus for children born after 1945 (when the studystarted) not one single permanent tooth had even erupted!

40) Since 1950, it has been found that fluorides do little to prevent pit and fissuretooth decay, a fact that even the dental community has acknowledged (Seholle1984; Gray 1987; PHS 1993; and Pinkham 1999). This is significant because pitand fissure tooth decay represents up to 85% of the tooth decay experienced bychildren today (Seholle 1984 and Gray 1987).

ANON (I): Statements 1, 11, 16, 33, 34, 36, 37, 40, 41, 42, 43, 46, 47, 48, 49, 50have been grouped together because they contain no supporting references topeer reviewed biomedical literature and/or represent opinions expressed by theauthor or the opinions of others with no references to the peer reviewedbiomedical literature and/ or contain references to the administration ororganization of regulatory agencies in the United States and/or refer to the


history or sociology of the debate over water fluoridation in the United States.As noted in the introduction, no response is provided in this document to anystatement that is not directly related to an assessment of the benefits and risksof public water fluoridation based on the best available and most reliableevidence from human epidemiological studies.

CONNETT: Again this is an extraordinary comment considering that we havelisted no less than 4 peer-reviewed and published studies and one governmentalreview which support this argument. Does ANON (I) not believe that pit andfissure decay is a problem in Ireland?

ANON(II): NO RESPONSE.

41) Despite the fact that we are exposed to far more fluoride today than we werein 1945 (when fluoridation began), the "optimal" fluoridation level is still 1 partper million, the same level deemed optimal in 1945! (Marier & Rose 1977; Levy1999; Rozier 1999 and Fomon 2000).


42) The chemicals used to fluoridate water in the US are not pharmaceuticalgrade. Instead, they come from the wet scrubbing systems of the superphosphatefertilizer industry. These chemicals (90% of which are sodium fluorosilicate andfluorosilicic acid), are classified hazardous wastes contaminated with variousimpurities. Recent testing by the National Sanitation Foundation suggest that thelevels of arsenic in these chemicals are relatively high (up to 1.6 ppb after dilutioninto public water) and of potential concern (NSF 2000 and Wang 2000).


43) These hazardous wastes have not been tested comprehensively. The chemicalusually tested in animal studies is pharmaceutical grade sodium fluoride, notindustrial grade fluorosilicic acid. The assumption being made is that by the timethis waste product has been diluted, all the fluorosilicic acid will have beenconverted into free fluoride ion, and the other toxics and radioactive isotopes willbe so dilute that they will not cause any harm, even with lifetime exposure. Theseassumptions have not been examined carefully by scientists, independent of thefluoridation program.

ANON (I): Statements 1, 11, 16, 33, 34, 36, 37, 40, 41, 42, 43, 46, 47, 48, 49, 50have been grouped together because they contain no supporting references to


peer reviewed biomedical literature and/or represent opinions expressed by theauthor or the opinions of others with no references to the peer reviewedbiomedical literature and/ or contain references to the administration ororganization of regulatory agencies in the United States and/or refer to thehistory or sociology of the debate over water fluoridation in the United States.As noted in the introduction, no response is provided in this document to anystatement that is not directly related to an assessment of the benefits and risksof public water fluoridation based on the best available and most reliableevidence from human epidemiological studies.

CONNETT: Another strange response since the discussion relates equally toIreland as it does to the US and other fluoridating countries.

The response and counter-response cited in 42) (see SECTION B below) couldalso be used here.

44) Studies by Masters and Coplan (1999, 2000) show an association betweenthe use of fluorosilicic acid (and its sodium salt) to fluoridate water and anincreased uptake of lead into children's blood. Because of lead’s acknowledgedability to damage the child’s developing brain, this is a very serious finding yet itis being largely ignored by fluoridating countries.


45) Sodium fluoride is an extremely toxic substance -- just 200 mg of fluoride ionis enough to kill a young child, and just 3-5 grams (e.g. a teaspoon) is enough tokill an adult. Both children (swallowing tablets/gels) and adults (accidentsinvolving fluoridation equipment and filters on dialysis machines) have died fromexcess exposure.


CONNETT: While this is factually correct, I will be withdrawing this point in futurepublication of the 50 Reasons as it displaces attention from the real issue. Thereis no chance that someone could get a lethal dose from drinking fluoridated water(although people have died as a result of accidents at water plants where excessfluoride has been inadvertently added to the water supply). The real issue is thehealth problems which will result from long term exposure to fluoridated water,especially among vulnerable subsets of the population.


46) Some of the earliest opponents of fluoridation were biochemists and at least14 Nobel Prize winners are among numerous scientists who have expressed theirreservations about the practice of fluoridation (see appendix 4).


CONNETT: The pro-fluoridation commentators use this generic statement todismiss argument 46, as well as arguments 47 – 50. It is disingenuous of thepromoters to dismiss issues merely because they pertain to “the debate overwater fluoridation in the United States” without acknowledging that America gavebirth to this whole practice and it was American officials who persuaded Irishauthorities to endorse it in the 1960’s and still continue to influence itscontinuation.

One of the main thrusts of those who promote fluoridation in the US is to claimthat only the ill-informed oppose fluoridation. They, like their Irish counterparts,rely heavily on endorsements and reviews by so-called “authorities” to persuadethe public that fluoridation is “safe and effective”. They even try to keep peopleaway from the primary literature. For example, the American Dental Association(ADA) goes as far as telling their members that:

“Individual dentists must be convinced that they need not be familiar withscientific reports of laboratory and field investigations to be effectiveparticipants in the promotion program and that non-participation is overtneglect of professional responsibility.” (ADA, White Paper, 1979, pages10-11)

That is why it is important for Irish officials to realize that there is a solid base ofscientific opinion opposed to fluoridation, which includes Nobel laureates like Dr.Arvid Carlsson (see 47 below) and many of the scientists and scientific bodiesthat advise the majority of European nations which do not fluoridate their water Italso includes many professionals working at the US EPA (see 50 below).

The refusal to debate the issue publicly (as well as some of the other tacticswhich have been used to discredit opponents of fluoridation (see 48, 49)) are


very revealing because they indicate the proponents’ inability to win theargument using the primary literature.

It is appalling to witness the measures taken against some of the Governmentscientists who have spoken out on this issue, as well as academic scientists whohave published findings which do not fit the paradigm of fluoridation’s “safety andeffectiveness” (see 49). Again, such measures would be unnecessary ifproponents had a solid case based upon the primary scientific literature. While Ican understand that it is embarrassing for the anonymous pro-fluoridationcommentators to confront these matters, I believe that they were cavalier in theirrefusal to address arguments 46-50.

47) The recent Nobel Laureate in Medicine and Physiology, Dr. Arvid Carlsson(2000), was one of the leading opponents of fluoridation in Sweden, and part ofthe panel that recommended that the Swedish government reject the practice,which they did in 1971. According to Carlsson:

"I am quite convinced that water fluoridation, in a not-too-distant future, will beconsigned to medical history...Water fluoridation goes against leading principlesof pharmacotherapy, which is progressing from a stereotyped medication - of thetype 1 tablet 3 times a day - to a much more individualized therapy as regardsboth dosage and selection of drugs. The addition of drugs to the drinking watermeans exactly the opposite of an individualized therapy" (Carlsson 1978).

CONNETT: See also a recent video interview with Dr. Carlsson athttp://www.fluorideaction.net, where he described fluoridation as an “obsoletepractice” and said that countries who continued to force fluoride on their citizensshould be “ashamed or themselves.”



CONNETT: See discussion in 46) above.

http://www.fluorideaction.net


48) While pro-fluoridation officials continue to promote fluoridation withundiminished fervor, they cannot defend the practice in open public debate –even when challenged to do so by organizations such as the Association forScience in the Public Interest, the American College of Toxicology, or the USEnvironmental Protection Agency (Bryson 2004). According to Dr. MichaelEasley, a prominent lobbyist for fluoridation in the US, "Debates give the illusionthat a scientific controversy exists when no credible people support thefluorophobics' view" (See appendix 5).

In light of proponents’ refusal to debate this issue, Dr. Edward Groth, a SeniorScientist at Consumers Union, observed that "the political profluoridation stancehas evolved into a dogmatic, authoritarian, essentially antiscientific posture, onethat discourages open debate of scientific issues" (Martin 1991).




49) Many scientists, doctors and dentists who have spoken out publicly on thisissue have been subjected to censorship and intimidation (Martin 1991). Mostrecently, Dr. Phyllis Mullenix was fired from her position as Chair of Toxicologyat Forsythe Dental Center for publishing her findings on fluoride and the brain;and Dr. William Marcus was fired from the EPA for questioning the government’shandling of the NTP’s fluoride-cancer study (Bryson 2004). Tactics like thiswould not be necessary if those promoting fluoridation were on secure scientificground.

ANON (I): Statements 1, 11, 16, 33, 34, 36, 37, 40, 41, 42, 43, 46, 47, 48, 49, 50have been grouped together because they contain no supporting references topeer reviewed biomedical literature and/or represent opinions expressed by theauthor or the opinions of others with no references to the peer reviewed


biomedical literature and/ or contain references to the administration ororganization of regulatory agencies in the United States and/or refer to thehistory or sociology of the debate over water fluoridation in the United States.As noted in the introduction, no response is provided in this document to anystatement that is not directly related to an assessment of the benefits and risksof public water fluoridation based on the best available and most reliableevidence from human epidemiological studies.



50) The Union representing the scientists at US EPA headquarters in WashingtonDC is now on record as opposing water fluoridation (Hirzy 1999). According tothe Union’s Senior Vice President, Dr. William Hirzy:

"In summary, we hold that fluoridation is an unreasonable risk. That is, thetoxicity of fluoride is so great and the purported benefits associated with it are sosmall - if there are any at all - that requiring every man, woman and child inAmerica to ingest it borders on criminal behavior on the part of governments."

CONNETT: Recently this 1999 initiative has since been augmented by 10 otherEPA unions who represent over 7000 professionals working for the US EPA. InAugust 2005 they called for an immediate moratorium on fluoridation until therehas been a full Congressional inquiry (which would force experts from both sidesto testify and be cross examined under oath) and called upon the director of theEPA to put effected bodies on notice of the possibility that the EPA may beforced to lower the Maximum Contaminant Level Goal for fluoride to 0 ppm,because of the recent evidence associating an increase in osteosarcoma inyoung males with exposure to fluoridated water. This initiative is winning supportfrom many doctors, dentists, nurses, scientists and other professionals (seehttp://www.powalliance.org/petition). As of January 7 2006, over 9000 people hadsigned this petition, 14.6% of whom are professionals or hold advanced degrees.


http://www.powalliance.org/petition




Conclusion

When it comes to controversies surrounding toxic chemicals, invested intereststraditionally do their very best to discount animal studies and quibble withepidemiological findings. In the past, political pressures have led governmentagencies to drag their feet on regulating asbestos, benzene, DDT, PCBs, tetraethyllead, tobacco and dioxins. With fluoridation we have had a fifty year delay.Unfortunately, because government officials have put so much of their credibilityon the line defending fluoridation, and because of the huge liabilities waiting inthe wings if they admit that fluoridation has caused an increase in hip fracture,arthritis, bone cancer, brain disorders or thyroid problems, it will be very difficultfor them to speak honestly and openly about the issue. But they must, not only toprotect millions of people from unnecessary harm, but to protect the notion that,at its core, public health policy must be based on sound science not politicalexpediency. They have a tool with which to do this: it's called the PrecautionaryPrinciple. Simply put, this says: if in doubt leave it out. This is what mostEuropean countries have done and their children's teeth have not suffered, whiletheir public's trust has been strengthened.

ANON(I): NO RESPONSE.

• ANON (II): There is no universal and widely accepteddefinition of the precautionary principle. Sandin (1999),for example, has reported 19 different definitions of theprinciple. One legal analysis has further identified 14different formulations of the principle in treaties andnon-treaty declarations (Vanderzwagg 1999 cited in Fosteret al., 2000).

• In an attempt to clarify the meaning and applicability ofthe precautionary principle, the European Commission (EC2000) issued a guidance document in February 2000. TheCommission argued that measures based on the precautionaryprinciple should comply with the basic principles for allother legislation and should incorporate the basicprinciples of risk management. Measures taken should be:

1) Proportional to the chosen level of protection. Measuresbased on the precautionary principle must not be


disproportionate to the desired level of protection andmust not aim at zero risk.2) Non-discriminatory in their application3) Consistent with measures already adopted in similarcircumstances or using similar approaches4) Based on the examination of the potential benefits andcosts of action or lack of action5) Subject to review in the light of new scientific data6) Indicate responsibility for producing the scientificevidence necessary for a more comprehensive riskassessment.

• Whilst the Commission has provided some clarification inaffirming that the precautionary principle must be seen aspart of risk management rather than as an overarchingprinciple and that application of the principle requiresconsideration of both the costs and benefits of action orlack of action, a number of problems remain. Some non-governmental and environmental proponents of theprecautionary principle have strongly opposed both of theseaspects of the EC interpretation of the principle, onceagain highlighting the lack of consensus on the meaning ofthe principle (see Lyons et al., 2000). Moreover theCommunication speaks in general terms about ‘factors’ thatshould be considered leaving broad ambiguity on the precisemeaning and requirements of the precautionary principle(Marchant 2001). The Commission further stressed that theirCommunication was not intended to be the ‘final word’ onthe precautionary principle, rather it was intended to openup the debate and provide the basis for discussions in theCouncil and European Parliament.

• In order to be of any use to policy makers theprecautionary principle, and its applications, must beprecise and detailed within a well-defined framework.Unless and until the principle has been clarified, itremains unworkable and fails to provide practical decision-making criteria for policy-makers.

CONNETT: Here we see a lot of legalistic and semantic verbiage to obfuscatethe obvious. If the Precautionary Principle (however it is defined) does not applyto fluoridation it applies to nothing! How many teeth would have to be saved tojustify even one young boy dying from osteosarcoma? While, the proof of thelatter has not risen to the level of “scientific certainty” it is certainly highlysuggestive, consistent with some epidemiological studies and animal studies andis highly plausible from a biological perspective. The same can be said of manyother serious end points. Thus we should not wait for definitive proof beforeacting. By the time governments get around to doing all the necessary research


it may well be too late for many. It was for exactly this kind of reasoning (basedupon previous failures to act in time) that the Precautionary Principle wasintroduced.

We are looking at a practice for which there are proven safe alternatives, whichhas only minor benefits, has potential life debilitating (increased hip fractures inthe elderly, Li, 2001) and possibly life threatening health effects (osteosarcoma inyoung males, Cohn, 1992 and Bassin, 2001) is being forced on people withouttheir “informed consent” and which the major proponents cannot defend in openpublic debate. In most people’s book that would cry out for an application of thePrecautionary Principle.

SECTION B. RESPONSES.3) Fluoridation's role in the decline of tooth decay is in serious doubt. The largestsurvey ever conducted in the US (over 39,000 children from 84 communities) bythe National Institute of Dental Research showed little difference in tooth decayamong children in fluoridated and non-fluoridated communities (Hileman 1989).According to NIDR researchers, the study found an average difference of only 0.6DMFS (Decayed Missing and Filled Surfaces) in the permanent teeth of childrenaged 5-17 residing in either fluoridated or unfluoridated areas (Brunelle andCarlos, 1990). This difference is less than one tooth surface! There are 128 toothsurfaces in a child's mouth. This result was not shown to be statisticallysignificant. In a review commissioned by the Ontario government, Dr. DavidLocker concluded:

"The magnitude of [fluoridation's] effect is not large in absolute terms, is oftennot statistically significant and may not be of clinical significance" (Locker 1999).


ANON (II): Yiamouyiannis (1990) was not involved in thedesign and conduct of the US National Institute of DentalResearch (NIDR) survey quoted in the ’50 Reasons’ document.Following the NIDR study, Yiamouyiannis obtained a printoutof the dental records and a list of the 84 areas used inthis survey through the United States Freedom ofInformation Act. Using this data Yiamouyiannis calculatedthe number of decayed and filled deciduous teeth (dft) andthe number of decayed, missing and filled permanent teeth(DMFT) for each record. However, the “halo effect” of waterfluoridation was ignored.

That is, non-fluoridated communities located adjacent togeographic regions with fluoridated communities are more


likely to receive the diffused benefits from waterfluoridation as the number of fluoridated communitiesincreases.

CONNETT: Whether or not Yiamouyiannis was involved in the design andconduct of the NIDR’s study is irrelevant. What is important is that he obtainedthe raw data from the study and analyzed it based on standard statisticalmethods. Anon offers no critique of Yiamouyiannis’ statistical analysis, otherthan the fact that he did not examine the impact of the “halo effect” – a criticismthat applies equally to the NIDR authors as well (Brunelle & Carlos 1990).

Anon’s claim that the “halo effect” (I prefer the word “seepage” effect, since halogives the practice almost saintly appeal!) can explain why the difference incavities in the permanent teeth (six tenths of one tooth surface) betweenfluoridated and unfluoridated areas of the US is so small, is a nice theory but itdoes not account well for the experience of regions with little water fluoridation.For example, if the “halo or seepage effect” was the key explanatory factor, onewould expect in British Columbia (the least fluoridated province of Canada), thatone would find rather dramatic differences in cavities between fluoridated andunfluoridated areas. But such differences do not exist (Gray 1987).

Furthermore, if the halo/seepage effect is truly the key explanation for the declineof cavities in unfluoridated areas of the US, than how does one explain thedecline of cavities in western Europe where there is virtually no water fluoridationand thus no possibility of a halo/seepage effect from fluoridated to unfluoridatedareas?

ANON (II) (continued): This “halo effect” arises out of theconsumption of products like bread, milk, bottledbeverages, processed foods and others that are manufacturedin a fluoridated area and consumed in other non-fluoridateddistricts and from movement of people in and out offluoridated areas.

Griffin et al (2001) recently analysed data from the NIDRsurvey to estimate the total contribution of waterfluoridation to caries reduction by including the benefitfrom the diffusion of fluoride from fluoridated communitiesto surrounding non-fluoridated communities via the exportof bottled beverages and processed foods (Griffin et al.,2001). They found that U.S children residing in non-fluoridated areas with low diffusion exposure (DE) in 1986-1987 experienced higher levels of dental caries than didchildren living in fluoridated communities or childrenliving in non-fluoridated (NF) areas with high diffusionexposure. They concluded that a failure to account for thediffusion effect may result in an underestimation of the


total benefit of water fluoridation, especially in highdiffusion exposure regions.

CONNETT: Griffin offers an interesting hypothesis and it needs to be studiedfurther. However, there is a problem with Griffin’s attempt to use the “halo orseepage effect” to explain the very little difference in tooth decay between thosechildren who had drunk fluoridated water all their lives and those who drank non-fluoridated water all their lives, because the same convergence does not occurwith “dental fluorosis.” This can be gleaned from the fact that the NIDR in this1986-87 study simultaneously collected data on dental fluorosis and found a verystrong correlation between residence in a fluoridated area and percentage ofchildren with dental fluorosis and with its severity.

Almost 3 times more children had dental fluorosis in communities with fluoridelevels of 0.7 to 1.2 ppm than those with fluoride less than 0.3 ppm. Clearly, thechildren drinking fluoridated water have a much higher exposure to fluoride fromall sources than the children drinking non-fluoridated water. Thus thehalo/seepage effect cannot explain the fact there is very little difference in toothdecay. Based on the dental fluorosis data the exposure to fluoride is different. Inshort, their tooth decay is very similar but their exposure to fluoride is verydifferent.

Furthermore, the halo/seepage effect cannot be used to explain away the factthat non-fluoridated countries in Europe have as good if not better teeth than inIreland, since there is practically no “benefit” derivable from Irish beverages andfood in these countries. In addition, over 90% of newborns in Sweden are breastfed versus only 40% in Ireland.

There is also an interesting contradiction in the commentators’ comments hereand their response to Reason 41. Here they draw attention to the amount offluoride obtained in non-fluoridated communities via foods and beveragesprepared with fluoridated water, but in Reason 41 they argue that there has beenno increased exposure to fluoride via the food supply since fluoridation began!Specifically, in their response to Reason 41 they cite American studies whichthey claimed showed that there was “little or no change in food fluoride content…as a result of the fluoridation of U.S. water supplies.” Which does ANONbelieve? They can’t have it both ways.

ANON (II) (continued): Kumar and Green (1998) (cited in the“50 Reasons” document) discuss the significant role thatfluoride has played in improving the oral health ofAmericans and advise that practitioners should prescribefluoride therapy based on an understanding of patients’total exposure to fluoride given the increased availabilityof fluoride containing products over the counter in theU.S.


A graph in the article by Kumar and Green (1998) shows themean DMFT among 7-14-year-old lifelong residents ofNewburgh (fluoridated) and Kingston (non-fluoridated) overa fifty-year period. Both communities exhibited a declinein DMFT from 1945 with a leveling off in differences inDMFT between the two communities from 1986 onwards.

Kumar and Green discuss the caries decline in both thefluoridated and non-fluoridated communities as beingattributable to the increased availability of fluoride inthe form of fluoride toothpastes and consumption ofbeverages and foods processed in fluoridated areas –the“halo effect” of water fluoridation. Kumar and Green (1998)also note that although the difference in caries levelsbetween fluoridated and non-fluoridated communities islower today than it was in the early 1950’s, fluoridationcontinues to be an ideal programme for fluoride deliveryfor several reasons, including its cost effectiveness.

CONNETT: Both Kumar and Green work for the NY State Department of Healthwhich is an avid promoter of fluoridation. Thus one needs to distinguish betweenan explanation for which scientific evidence is offered and something which is aconvenient rationalization for continuing support the fluoridation program. Thesimple fact remains that after over 50 years with Newburgh remaining fluoridatedand Kingston remaining unfluoridated, the teeth of the children in unfluoridatedKingston are slightly better than the teeth of the children in fluoridated Newburgh,while their rates of dental fluorosis are lower.

ANON (II) (continued): A study conducted in Co. Kerry byCreedon and O’Mullane (2001) investigated the factorsassociated with high caries levels in 5-year-old childrenin the Kerry Community Care Area of the Southern HealthBoard in Ireland. The mean dmfs of the 263 lifetimeresidents of fluoridated communities was 2.4 compared with6.2 recorded for the 231 lifetime residents of non-fluoridated communities. Using multivariate logisticregression analysis the variables most significantlyassociated with the presence of caries were waterfluoridation status, whether or not the child took the babyfeeding bottle to bed, the age at which tooth brushingbegan and the number of sweet snacks and drinks taken in aday. While there was a wide variation in caries levelsbetween nine geographic areas in Co. Kerry the onlysignificant geographic variation found was betweenfluoridated and non-fluoridated areas. Some 61% of childrenin fluoridated areas were caries-free compared to 39% innon-fluoridated areas (see table 1 below). The authorsconcluded that the prevalence of caries amongst 5-year-old


children in Co. Kerry was highest in those residing in non-fluoridated communities, in those who took a baby feedingbottle to bed, in those who did not commence tooth brushinguntil after two years of age and in those who consumedsweet snacks or sweets drinks between meals three or moretimes per day.

TABLE 1Mean dmft, mean dmfs and percentage caries-free of 5-year-old children by fluoridation status (standard deviation inparenthesis)Fluoridation Mean Mean % Caries % dmftStatus n dmft (SD) dmfs (SD) Free >/4Fluoride 263 1.2 (2.2) 2.4 (5.0) 61 14Non-Flu 231 2.9 (3.9) 6.2 (9.9) 39 31

CONNETT: Yiammouyiannis (1990) found a similar effect on 5 year olds whenusing the very large NIDR database discussed above. He found significantlylower dmft in fluoridated areas (Note the lower and upper case are used todistinguish effects on the primary and secondary teeth respectively; thus dmftmeans decayed missing and filled PRIMARY teeth, whereas DMFT meansdecayed missing and filled PERMANENT teeth). However, he put this findinginto context by also calculating the dmft as the children got older. The differencein dmft shrank to zero by age 8. Furthermore, at ages 6 and 7 it had alreadyshrunk to the point where it was statistically no longer significant.

Yiammouyiannis postulated that this may be evidence that fluoride exposuredelays eruption of teeth. Other studies have found this effect, most strongly inthe youngest children (Feltman 1961; Kunzel 1976; Campagna 1995). As notedby Komarek (2005) the risk of any tooth or tooth surface having a cavity is closelyrelated to how long the tooth was exposed in the oral cavity after eruption.Therefore, any delay in eruption caused by a factor such as fluoride would onlydelay the appearance of cavities, not prevent them. In the long run, the numberof cavities in children with delayed tooth eruption would eventually catch up tothe children with normal eruption as the relative difference in time exposedbecame less. That is exactly what the NIDR data shows – as well as a recentlarge-scale study from Australia (Armfield & Spencer 2004). To conduct a studyor to give data only on 5 year olds is, therefore, very deceptive of the true overallpicture. It can lead to false conclusions such as ANON has made here.

4) Where fluoridation has been discontinued in communities from Canada, theformer East Germany, Cuba and Finland, dental decay has not increased but hasactually decreased (Maupome 2001; Kunzel and Fischer,1997,2000; Kunzel 2000and Seppa 2000).



ANON(II): The studies by Seppa et al., (2000a & b) inFinland and Kunzel et al., (2000) in Germany are two of thestudies cited in the ‘50 Reasons’ document as evidence that‘dental decay has not increased but has actually decreased’with the cessation of water fluoridation. However, thedetails of these studies, in particular their externalvalidity, are neither presented nor discussed. As singlestudies are specific to time, sample, and context itfollows that the results of a particular study may not beapplicable to other populations, settings, treatmentvariables and measurement variables.

CONNETT: These studies were published in peer-reviewed mainstream dentaljournals, by authors who are largely pro-fluoridation.

ANON (II) (continued): The study by Seppa et al., (2000a &b), examined caries trends between 1992 - 1998 in two ‘lowfluoride’ Finnish towns (Kupio and Jyvaskyla). Kupio, atown with 83,000 inhabitants, had been fluoridated(1.0mg/l) since 1959. Water fluoridation ceased in Kuopioin 1992. Jyvaskyla had historically been used as areference town for Kupio in dental caries surveys. Theresults of observations made in 1998 coupled with earlierfindings in 1995 suggested that, following thediscontinuation of water fluoridation in Kupio, caries didnot increase amongst 12 year olds. In 12 year olds therewas a decrease in the percentage of subjects with nocarious legions (caries free) but the mean DMFS value didnot differ consistently from those in Jyvaskyla. It couldbe speculated that an increased use of other preventivemeasures in Kupio after 1992 compensated for the cessationof water fluoridation. However, Seppa et al., note that thenumber of fluoride and sealant applications actuallydecreased markedly in Kupio from 1993 to 1998, probably dueto a policy change towards targeted prevention on the basisof individual needs. (Seppa et al., 2000a & b).

For some time local surveys had suggested that the effectof water fluoridation on caries was decreasing in Kupio(Seppa et al., 2000a & b).In 1973, for example, 13-15 year olds living in Kupio had40% lower average DMFS scores than those living inJyvaskyla, but in a similar survey 9 years later, nodifference could be found. The small percentage of theFinnish population (0.02%) covered by the Kuopiofluoridation scheme would also have rendered negligible thediffusion effect of water fluoridation. Seppa et al., 2000


note that in interpreting their results consideration mustbe given to the fact that most of the processed food anddrinks consumed in Kuopio come from low-fluoride areas(Seppa et al., 2000a & b). Given the almost completeconvergence of caries experience between fluoridated Kuopioand other non-fluoridated parts of Finland and the absenceof the diffusion effect of water fluoridation, the findingthat there was no indication of an increasing trend ofcaries following the cessation of water fluoridation wasnot unexpected.

Caution should be exercised in the interpretation of thisstudy and in assessing the degree to which its results canbe generalised to other countries. A number of commentatorshave noted the inappropriateness of extrapolating dataobtained from Nordic countries to other countries (Forss1999, Seppa 2001). Forss (1999), for example, has notedthat to focus on prevention programmes in Nordic countriesis ‘a most restricted vision’. Furthermore she notes that‘it must therefore be emphasised that it would be dangerousto generalize the results of studies on the efficiency offluoride programs. Data valid in one part of the world maynot be applicable or relevant in other parts.’

The favourable socio-economic position of the Nordiccountries should be noted. The UN Human Development Report(2004) uses as its main measure of social progress theHuman Development Index (HDI) in comparing 162 states. (UNHuman Development Report, 2004). Norway is at the top ofthe table with a HDI rank of 1. Sweden is ranked in 2 ndposition, Finland 13 th , Denmark 17 th and Ireland isranked in 10 th position. Despite Ireland’s favourableoverall ranking, the UN Report notes that proportionatelymore people live in poverty in Ireland than in any otherindustrialised nation outside the US. In terms of poverty,the report ranks Ireland 16 th out of 17 Western countrieswith 15.3% of the population living in poverty. Only the USwith 15.8% in poverty is worse than Ireland. By comparisonSweden is at the top of the table with just 6.5% inpoverty, Norway 7.1%, Denmark 9.1%, and Finland has 8.4% ofthe population living in poverty. In addition the reportalso shows that Ireland spends less on health than anyother Western nation.

Expenditure on health in Ireland is 6.5% of GDP, comparedwith Norway (8.1%), Sweden (8.8%), Denmark (8.5%) andFinland (7%).


CONNETT: It is true that Nordic countries have less poverty than Ireland and thatpoverty is a major factor in predicting tooth decay (Colquhoun 1985). However,as mentioned in the 50 Reasons it is not just in rich, Nordic countries whereresearchers have failed to find an increase in cavity rates following the end offluoridation. Indeed, similar findings have been found in other countries, such asCuba, where the socioeconomic status is much different from Finland (Kunzel2000).

In fact, according to Colquhoun (1985), if only those communities with similarsocioeconomic backgrounds are considered, no discernable difference in cavitiescan be found.

ANON (II) (continued): The dietary and oral hygiene habitsof the respective populations also merit attention. Datafrom the National Health and Lifestyles Surveys in Ireland,(Friel et al, 1999, 2003), which give an overview ofdietary practices internationally, are relevant in thiscontext. Of all countries surveyed the percentage ofstudents who reported eating sweets or chocolate every daywere consistently the highest in Northern Ireland (73-81%),Scotland (71-78%) and Ireland (71-80%). The lowest wereconsistently recorded in Denmark (19-31%), Sweden (14-31%)and Norway (13-30%). Of all countries surveyed the lowestpercentages were recorded in Finland (12- 24%). Similartrends were observed with respect to the consumption ofsoft drinks, again with Finland (6-22%) reporting thelowest consumption and Northern Ireland (69-75%), Ireland(51-75%) and Scotland (60-77%) reporting the highestconsumption.

Local studies of particular population groups in the UK andIreland have also shown that sugars account for between 25%and 29% of pre-school children’s daily food energy, withextrinsic sugars accounting for between 12% and 19%.

In school children sugars account for between 19% and 25%of daily food energy, with extrinsic sugars accounting forbetween 14% and 17%. In adults sugars account for between16% and 28% of daily food energy, with extrinsic sugarsaccounting for between about 8% and 10%. The UK Departmentof Health Committee on Medical Aspects of Food (COMA)recommends that sugars should provide no more than 10-11%of food energy. From the above figures it is clear thatchildren are at particular risk (Pan European Task Force onDental Health, 1998).

In Finland, as in the whole of Scandinavia, all childrenand adolescents are entitled to comprehensive, preventively


oriented dental care and nearly all attend. In addition thepopulation is homogenous in terms of social structure andethnic background (Seppa 2001). Seppa et al., also pointout that the inclusion of non-lifetime residents of thecommunity in their analyses may have diluted the effect ofwater fluoridation (Seppa et al., 2000a & b).

It is facile to assume that because the cessation of waterfluoridation in one small region in Finland did not lead toan observed increase in caries that a similar result wouldbe observed in other countries with much higher riskfactors for dental caries. In a more recent publicationSeppa has directly addressed this issue and has observedthat ‘although discontinuation of water fluoridation had noeffect on caries in Kupio, Finland, water fluoridation isstill effective in countries with a lower level of basicprevention and a less homogenous social structure’ (Seppa2001).

CONNETT: Again, as specifically identified in the 50 Reasons, it is not justFinland where this finding has been reported. It has also been reported inGermany and Canada (Kunzel 2000a; Maupome 2001) and in areas with muchless favorable socioeconomic conditions (e.g. Cuba, Kunzel 2000b).

ANON (II) (continued): Similar observations to the above canbe made concerning the external validity of the Kunzel etal.,(2000) study (also cited in the ‘50 Reasons’ document).In this study it was observed that caries levels continuedto decline in 12 year olds in two towns in East Germanyfollowing the cessation of water fluoridation. In EastGermany the caries decline observed by Kunzel et al.,(2000) took place over a 10 year period from 1985 – 1995,an era which included the significant social transformationin East Germany following reunification in 1990. Kunzel etal., (2000) note that during this period there was anincreased use of topical fluoride, fluoridated salt becameavailable after 1992 and there were also changes in thesupply of food and luxury items and changes in many otherenvironmental factors. In addition there was a completerestructuring of the pattern of dental care, with theadoption of a preventive approach by dental practitioners.It is impossible to appraise the impact of the cessation ofwater fluoridation when such changes in the dental caresystem occurred. None of these factors have been mentionedor discussed by the author of the ‘50 Reasons’ document.

The ‘50 Reasons’ document also fails to acknowledge thetotality of research evidence on the effects of the


cessation of water fluoridation. A number of ‘cessationstudies’ were assessed as part of the systematic review ofwater fluoridation carried out by the University of York(McDonagh et al, 2000). Of 22 analyses of stopping waterfluoridation, 14 found the direction of association to benegative (that stopping water fluoridation led to anincrease in caries). Eight analyses found the direction ofassociation to be positive (that stopping waterfluoridation had not led to an increase in caries in thepreviously fluoridated areas). In many of the studies therewas poor adjustment for potential confounding variables andthe overall evidence was of moderate quality and limitedquantity. In addition some of the studies did not provide ameasure of the significance of the association observed andsome did not provide standard error data. Whilst cognisantof these limitations, the review concluded ‘the bestavailable evidence on stopping water fluoridation indicatesthat when fluoridation is discontinued, caries prevalenceappears to increase in the area that had been fluoridatedcompared with the control area. Interpreting from this datathe degree to which water fluoridation works to reducecaries is more difficult’.

Maupome et al., (2001) (cited in the ‘50 Reasons’ document)compared the prevalence and incidence of caries betweenfluoridation-ended and still-fluoridated communities inBritish Columbia, Canada from a baseline survey and afterthree years. Maupome et al., (2001) reported that theavailability of multiple sources of fluoride other thanwater fluoridation made it more difficult to detect changesin the epidemiological profile of a population withgenerally low caries experience, living in an affluentsetting and with widely accessible dental services. Theprevalence of caries assessed in the children reportedlydecreased over time in the fluoridation-ended communitywhile remaining unchanged in the fluoridated community. Thereported decline in caries was postulated to bemultifactorial in the fluoridation-ended community. Withamenable dental services came the intervention of thedental profession and perhaps improved customs of oralhealth care at home. Very low levels of decay were found atbaseline and at final recording of the data.

The examiners were also different for each study site andthe possibility of variations in the interpretations of thedifferent examiners and examiner bias cannot be ruled out.Maupome et al., (2001) concluded overall that the benefitsof water fluoridation should be weighed against other


preventive methods such as fissure sealing and concludedthat the primary preventive measure of water fluoridation“preserves the integrity of dental tissues overall, ischeaper and is more effective than other preventivemeasures”.

CONNETT: What is clear is that other countries have managed to get toothdecay down without Ireland’s draconian and risky policy of forcing fluoridation onits whole population. Moreover, other communities have been able todiscontinue fluoridation without the calamities that proponents’ claim will occur.

Irish legislators should consider the possibility of using the money saved onfluoridation chemicals, fluoridation equipment, fluoridation monitoring, fluoridationcommittees and research money spent on investigating dental fluorosis rates,into providing Irish parents and Irish children a better education on nutrition anddental hygiene. This would not only be a safer way of preventing tooth decay butwould have the added benefit of protecting the population from obesity and otherdiseases caused by excess sugar and poor nutrition.

7) The Centers for Disease Control and Prevention (CDC 1999, 2001) has nowacknowledged the findings of many leading dental researchers, that themechanism of fluoride's benefits are mainly TOPICAL not SYSTEMIC. Thus, youdon't have to swallow fluoride to protect teeth. As the benefits of fluoride (if anyexist) are topical, and the risks are systemic, it makes more sense, for those whowant to take the risks, to deliver the fluoride directly to the tooth in the form oftoothpaste. Since swallowing fluoride is unnecessary, there is no reason to forcepeople (against their will) to drink fluoride in their water supply. This positionwas recently shared by Dr. Douglas Carnall, the associate editor of the BritishMedical Journal. His editorial appears in Appendix 3.


ANON (II) When the relationship between fluoride intake anddecreased caries prevalence was first recognised it wasassumed that the method of action was due to theincorporation of fluoride into the enamel during enamelformation: that in chemical terms it involved substitutionof the hydroxyl ion with the fluoride ion in hydroxyapatiteleading to the formation of fluorapatite (McClure, Likins1951).

CONNETT: Yes and it now appears that most researchers and the CDC admitthat they were wrong.


ANON (II) (continued): Fluorapatite was deemed to be lesssoluble in acid and this reduction in acid solubility ofenamel was attributed to larger apatite crystals, bettercrystallinity and the buffering action of fluoride releasedfrom enamel crystals during the early stages of acidattack. It was believed that in order for fluorapatite tobe formed it was necessary for the fluoride ion to bepresent during amelogenesis and hence systemic fluoride wasessential.

CONNETT: Yes, that was the assumption and it now appears that mostresearchers and the CDC admit that they were wrong.

ANON (II) (continued): However, later work usingsophisticated enamel biopsy and fluoride analysistechniques revealed no simple relationship between enamelfluoride levels and caries experience. Furtherepidemiological evidence supported this view, in thatcaries reductions were found in teeth already erupted atthe start of fluoridation programmes (Collins and O'Mullane1970, Ast et al., 1950). At about this time, understandingof how a carious lesion develops also began to change.Initially it was believed that the carious lesion developedas a slow, persistent ongoing process; that it started as amicroscopic change leading to a white spot lesion, whichinevitably progressed to a cavity. It is now known thatthis is not the case and that white spot lesions and otherearly carious lesions can remineralise (Holmen et al,1987). A white spot lesion therefore, can behave in threedifferent ways; it can progress to cavity, remain static,or reverse (remineralise). The carious process is adelicate balance between demineralisation andremineralisation and in the mouth there is a constant ‘see-saw’ between these two phenomena depending on thecariogenic challenge present. The presence of fluoride hasbeen shown to promote the process of remineralisation andthe ‘healed’ lesion has been found to be more resistant tocaries attack than a similar unchallenged site.

CONNETT: ANON (II) does not give any evidence that this process is more likelyachieved via fluoridation of water at 1 ppm than by using toothpaste at 1000ppm?

ANON (II) (continued): There is also evidence to show thatlow levels of fluoride in plaque affect plaque metabolism(including glycolysis) inhibiting the process in whichcariogenic bacteria metabolise carbohydrates to produceacid. The persistence of fluoride levels in saliva, of the


order of 0.04 – 0.2 ppm, appears to be critical forremineralisation. This origin of this salivary fluoride isfrom ingested fluoride; thus the “topical” effect is inpart mediated through the “systemic” effect of ingestionand subsequent expression of fluoride in saliva.

CONNETT: According to the CDC, the background saliva fluoride levels influoridated areas are only 0.016 ppm, which is less that what Anon says iseffective at remineralizing enamel (0.04 to 0.2 ppm). Thus, if one agrees withAnon’s analysis then it is more likely that fluoridated toothpaste would have thedesired effect on remineralisation than drinking fluoridated water.

ANON (II) (continued): Whilst there is no doubt thatfrequent topical applications of fluoride will bring abouta large reduction in dental caries for those who arewilling to buy and use fluoride toothpaste or willing toregularly attend a dentist or hygienist for application ofgels, compliance with these procedures may be problematic.This may be particularly true in the case of less well-offsections of the population who are most at risk ofdeveloping dental caries.

CONNETT: Fluoridated toothpaste is universally available and less expensivethan non-fluoridated brands. If there are sub-groups in the Irish population whocannot afford toothpaste then this would be a better place for the government tospend the money than is currently being spent on forcing fluoride on everyonevia their water supply.

• The percentage of population in Ireland who attendregularly for dental care is low, again particularlyamongst the less well-off sections of the population, hencefluoride gels and varnishes are not appropriatealternatives to water fluoridation (O’Mullane et al, 1999).

CONNETT: Have Irish researchers considered the program used in Finland forover 30 years where children and adults have been using xylitol toothpaste,mints and chewing gum to diminish the hold of these same bacteria on theplague? As far as getting compliance from poor children is concerned have Irishresearchers considered giving out free xylitol mints or chewing gum in schools.Noting the proclivity of the Irish to sweet foods and candies documented above,would this not be an attractive alternative to forced medication?

9) The US fluoridation program has massively failed to achieve one of its keyobjectives, i.e. to lower dental decay rates while holding down dental fluorosis(mottled and discolored enamel), a condition known to be caused by fluoride.The goal of the early promoters of fluoridation was to limit dental fluorosis (in its


mildest form) to 10% of children (NRC 1993, pp. 6-7). A major US survey hasfound 30% of children in optimally fluoridated areas had dental fluorosis on atleast two teeth (Heller 1997), while smaller studies have found up to 80% ofchildren impacted (Williams 1990; Lalumandier 1995 and Morgan 1998). TheYork Review estimates that up to 48% of children in optimally fluoridated areasworldwide have dental fluorosis in all forms and 12.5% with symptoms ofaesthetic concern (McDonagh, 2000).


ANON (II): Buzalef et al., (2001) note that factors such asmalnutrition (Rugg-Gunn et al., 1997), altitude or renaldysfunction can produce enamel changes that resemble enamelfluorosis even in the absence of significant exposure tofluoride.

Enamel opacities including fluorosis can be caused by localor systemic events. Local causes include dental trauma andlocal infections. A relatively common local cause of amarking or opacity on permanent teeth is trauma to theprimary predecessor. Systemic events include infections(measles and generalised fevers), metabolic errors (such asphenylketonuria), neonatal disturbances (premature birth,hypocalcaemia and haemolytic anaemia), genetic conditions(amelogenesis imperfecta), endocrinopathies (hypothyroidismand diabetes mellitus) antibiotic consumption (classically,though now rarely, with tetracyclines), nutritionaldeficiencies (including all nutrients and general calorificintake) and asthma (Rugg-Gunn et al., 1999). From aclinical point of view, it is not always possible todistinguish between opacities caused by excessive intake offluoride and opacities resulting from other reasons.

CONNETT: Apart from the antibiotics all these factors were in existence whenTrendley Dean did his pioneering studies on dental fluorosis in the US, in whichhe examined dental fluorosis rates in hundred of communities and correlatedtheir severity with fluoride levels. Moreover, recent research from Hong (2005)has found that some antibiotics (e.g. amoxicillin) may work synergistically withfluoride to increase the fluorosis risk.

ANON (II) (continued): The authors of the York Review(McDonagh et al., 2000) reported that the prevalence offluorosis at a water fluoride level of 1ppm was 48% and forenamel fluorosis of aesthetic concern it was 12.5%. TheReview included 88 studies of dental fluorosis. They werelargely cross sectional designs, with only four controlledbefore-after designs. All of the studies were of evidencelevel C (lowest quality), except one level B study. The


authors also report that there was considerableheterogeneity between results of individual studies.Observer bias may be of particular importance in studiesthat assess fluorosis. Because assessment is subjective,unless the observer is blinded to the exposure status of theperson being evaluated, bias can be introduced. Efforts toreduce potential observer bias were rarely undertaken inthe included studies. The prevalence of fluorosis may beoverestimated by the indices used in the included studiesbecause enamel opacities not caused by fluoride may beincluded. The degree to which the estimated 48% prevalenceof fluorosis at a water fluoride concentration of 1 ppmoverestimates the true prevalence is unknown.

CONNETT: I agree that none of the dental studies considered by the YorkReview reached the quality of a level A study. However, this is an extraordinarysituation considering that most of the low quality studies have been funded bygovernments which have promoted fluoridation for decades. Are these pro-fluoridation governments incapable of finding and funding researchers who cando level A studies? Or are they merely content to receive any study that confirmswhat they want to hear: namely, that fluoridation is “safe and effective”?

ANON (II) (continued): Using data from the National Surveyof US Schoolchildren, Heller et al., (1994, sic 1997)reported that children who consumed water with <0.3 ppm Fand 0.7 – 1.2 ppm F have a fluorosis prevalence of 13.5%and 29.9% respectively.

In a study conducted by Williams and Zwemer (1990), ToothSurface Index of Fluorosis (TSIF) scores of 4-7 werepresent in 1.4% of the “county” children examined (waterfluoridated at a level of 0.2-0.9 ppm F) and in 14% of the“city” children (water fluoridated at a level of 0.9-1,2ppm F) in Augusta or adjoining Richmond County.

The results of the National Survey of Children’s DentalHealth 2002 (Whelton et al., 2004) provide a clear analysisof the prevalence of fluorosis in three age groups (8-, 12-and 15-year-olds) in Ireland. In all three age groups 80%or over of the children were in the normal or questionablecategories. In fully fluoridated areas a score of normalwas given to 76% of 8 year-olds, 71% of 12 year-olds and61% of 15 year-olds. The authors reported 4% of 8 year-olds, 5% of 12 year-olds and 5% of 15-year-olds as havingmild fluorosis. These data indicate that there has been aslight increase in the level of questionable, very mild andmild fluorosis in the past 20 years in Ireland. Strategiesand recommendations to halt this trend are presented in


detail in the Final Report in the Forum on WaterFluoridation in Ireland (www.fluoridationforum.ie). Work isin progress to determine the aesthetic impact of the recentincreased levels of fluorosis in Ireland.

Elsewhere: 23% of 8-year-olds and 39% of 15-year-olds haveenamel fluorosis in the RoI. (it is not clear to which Reason thiscomment was directed, PC)

CONNETT: Our argument stands. The percentage of children with dentalfluorosis in fluoridated communities is far in excess of the intentions of those whopioneered water fluoridation in the US. Moreover, the percentage of children withdental fluorosis in non-fluoridated areas also exceeds the intended levels whichindicates that in the US at least, children are getting too much fluoride evenbefore fluoride is added to their water.

It is interesting to read what the “father of fluoridation”, and first Director of theNational Institute of Dental Research, Dr. Trendley Dean had to say - at varioustimes -about the level and acceptability of the dental fluorosis he anticipated withfluoridation programs.

In 1936, in an address to the Seventh Annual Meeting of the American MedicalAssociation, Dean stated:

"from the continuous use of water containing about 1 part per million, it isprobable that the very mildest forms of mottled enamel may develop inabout 10% of the group." (my emphasis) (Dean, 1936)

After describing the percentages and severity of mottled enamel, which would beexpected at higher fluoride concentrations, he wrote:

"In other words, we are dealing with a low grade chronic fluoride poisoningof children …(my emphasis) (Dean, 1936)

In 1941, he wrote:

"It is obvious that whatever effect the waters with relatively high fluoridecontent (over 2.0 ppm of F) have on dental caries is largely of academicinterest; the resultant permanent disfigurement of many of their users faroutweighs any advantage that might accrue from the partial control ofdental caries" (my emphasis) (Dean et al., 1941, p.762)

In 1952, Dean had this to say in testimony before the Delaney Committee of theUS Congress:

"We don't want any 'mild' when we are talking about fluoridation. We don'twant to go that high and we don't have to go that high…I don't want to


recommend any fluoridation where you get any 'mild'" (Cited in Exner,1960)

Now according to the CDC (2005) we have 6.7% of American kids (aged 6-19),on average, with mild dental fluorosis, and 3.4% with moderate or severe dentalfluorosis! As noted above, these are levels of fluorosis which the “father offluoridation” considered unacceptable.

11) The level of fluoride put into water (1 ppm) is up to 200 times higher thannormally found in mothers' milk (0.005 – 0.01 ppm) (Ekstrand 1981; Institute ofMedicine 1997). There are no benefits, only risks, for infants ingesting thisheightened level of fluoride at such an early age (this is an age wheresusceptibility to environmental toxins is particularly high).


CONNETT: It is surprising that ANON should deny the validity of the researchcited here. The levels of fluoride cited for mothers’ milk is not confined to the USpopulation and Ekstrand is a leading researcher in this field.

• ANON (II) Infant feeding practices including formulafeeding and breast-feeding are discussed in Chapter 12 ofthe report of the Forum on Fluoridation(www.fluoridationforum.ie).

• The Forum on Fluoridation recommends that infant formulashould continue to be reconstituted with boiled tap waterin accordance with manufacturers’ instructions oralternatively ready-to-feed formula may be used(www.fluoridationforum.ie).

CONNETT: Boiling the water will not remove fluoride but only make it moreconcentrated!


ANON (II) (continued): The use of bottled water toreconstitute infant formula is not recommended. Many of thebrands of bottled water available in Ireland are notsuitable for such use, due to the presence of salt andother substances, which may be harmful to infants and youngchildren (www.fluoridationforum.ie).

ANON (II) (continued): The Food Safety Authority of Irelandhas investigated the overall contribution to thedevelopment of fluorosis attributable to infant formula.The subset of the infant population likely to receive thehighest fluoride intake from infant formula reconstitutedwith fluoridated tap water is represented by those infantsbelow the age of four months for whom infant formula is thesole food source and consumption is high relative to bodyweight. The Scientific Committee of the Food SafetyAuthority of Ireland (Department of Health and Children,2002 www.fluoridationforum.ie) concluded that the maximumaverage intake of fluoride from infant formulareconstituted with fluoridated tap water over the firstfour months of life was estimated to be in the range0.105mg/kg b.w/day to 0.172mg/kg b.w/day, depending on bodyweight. This intake was calculated for infants residing inareas served by the 95% of water supplies that achieved anaverage yearly water fluoride level of below 1.03mg/l. Thestatutory upper limit in Ireland is 1mg/l. The remaining 5%of supplies exceeded the statutory limit on a consistentbasis, however the highest average fluoride concentrationcalculated in any of these non-compliant supplies was1.35mg/l.

CONNETT: The anonymous fluoridation promoters fail to acknowledge that thefirst written submission made by the Food Safety Authority of Ireland to theFluoridation Forum, recommended that mothers not use fluoridated tap waterwhen reconstituting formula. They also fail to acknowledge that thisrecommendation has been made by many leading dental researchers (seebelow) – including a member of the Fluoridation Forum itself (John Clarkson).According to Clarkson:

“infant formulas should still be prepared using non-fluoridated water”(Clarkson 2000).

Unfortunately, it seems the Fluoridation Forum placed politics over public healthwhen they decided against informing the public of this recommendation. As notedby a Forum member (Joe Mullen) at a July 10, 2003 parliamentary hearing, hadthe Forum report included a recommendation against using fluoridated water ininfant formula, “it probably would have meant the end of water fluoridation and at


the very least a serious re-appraisal of it.” See:http://www.fluoridealert.org/health/news/09.html

Mullen’s comment is quite significant when considering the followingrecommendations from dental researchers:

"A major effort should be made to avoid use of fluoridated water fordilution of formula powders. In addition, when economically feasible,young infants fed formulas prepared from concentrated liquids shouldhave these formulas made up with nonfluoridated water." Ekstrand J.(1996).

"[W]e recommend use of water with relatively low fluoride content (e.g. 0to 0.3 ppm) as a dilutent for infant formulas and recommend that nofluoride supplements be given to infants." Fomon et al. (2000).

"Breastfeeding of infants should be encouraged, both for the manydocumented, general health benefits and the relative protection againstingestion of excessive fluoride from high quantities of intake of fluoridatedwater used to reconstitute concentrated infant formula early in infancy."Levy et al. (1995).

"When infants are formula-fed, parents should be advised to reconstituteor dilute infant formula with deionized water (reverse osmosis, distilled, orlow-fluoride bottledwater) in order to reduce the amount of systemicallyingested fluoride." Brothwell and Limeback (2003).

"When formula concentrations need to be diluted, it is recommendedparents use low fluoride bottled distilled water (labeled as "purified" or"distilled baby water") or tap water with a reverse osmosis home waterfiltration system attached that removes most of the fluoride." Academy ofGeneral Dentistry.

ANON (II) (continued): The Forum on Fluoridation containsthe following conclusions about the possible risks to younginfants from the consumption of infant formulareconstituted with fluoridated tap water at current levelsof fluoride addition in Ireland:

o There is no significant evidence that any adverse effectother thandental fluorosis is relevant to the assessment of the riskof fluorideintake at levels within the range estimated for younginfants under 4months of age.

http://www.fluoridealert.org/health/news/09.html


CONNETT: Such assurances have a hollow ring to them once one realizes thatno one in Ireland , or most other fluoridating countries, have actually looked forsuch adverse effects as lowered thyroid function, lowered melatonin levels,impaired brain development etc . If you don’t look, you can’t find!

ANON (II) (continued): The risk of moderate dentalfluorosis of the primary or permanent dentition is very lowin exclusively formula-fed infants aged 0-4 months residingin areas served by the 95% of supplies in which the levelof fluoride in water does not exceed the statutory limit.For the remaining infants residing in areas served by the5% of supplies that consistently exceed the statutorylimit, the risk is also considered to be very low, but thesafety margin is reduced.

• In a study by Harding et al., (in press) in which 294 5-year-old children were examined for fluorosis in theirprimary teeth, 62.5% of mothers resident in a fluoridatedcommunity stated that they did not breast feed. Theremaining 37.5% claimed to have breast-fed and formulae fedfor various periods over the first year of life. Theprevalence of dental fluorosis was similar in these twogroups.

CONNETT: This is what Ekstrand and others have written on this same issue.

In 1981, Ekstrand published a paper in the British Medical Journal, where heshowed that the level of fluoride in breast milk remains low (5 to 10 parts perbillion - or 100 to 200 times lower than the level added to water), even when thenursing mother receives fluoride supplementation. Ekstrand noted at the timethat some kind of "barrier" seems to exist to "actively protect" the newborn fromfluoride. Indeed, based on Ekstrand's data, it is now known that the breast-fedinfant receives a lower body burden of fluoride than any other age group in thepopulation. By contrast, if an infant is fed formula made with fluoridated water,they receive the highest body burden of fluoride in the population.

According to Ekstrand's 1981 paper:

"These findings show that plasma fluoride is poorly transferred to breastmilk and infants thus receive almost no fluoride during breast feeding...The existence of a physiological plasma-milk barrier against fluoridesuggests that the newborn is actively protected from this halogen. Hencethe recommendation made in several countries to give breast-fed infantsfluoride supplementation should be reconsidered."


Since the publication of this paper, Ekstrand has repeatedly recommended thatinfants not receive fluoride supplementation or fluoridated formula (Ekstrand1989; Ekstrand 1996; Fomon et al, 2000).

13) Fluoride is very biologically active even at low concentrations. It interfereswith hydrogen bonding (Emsley 1981) and inhibits numerous enzymes (Waldbott1978).


•ANON (II) Emsley et al., (1981) (cited in the ‘50 Reasons’document) review amide-fluoride systems. The authorsconclude that the assertion that fluoride causes geneticdamage, birth defects and cancer cannot be established fromthe chemistry of the ion, which they say is stable inaqueous solution.

CONNETT: What Emsley et al. actually say is that:

“We believe that we have found, in its strong hydrogen bonding potentialtowards the NH group of amides and related biomolecules, an explanationof how this reputedly inert ion could disrupt key sites in biologicalsystems…”

ANON (II) (continued): Emsley et al., (1981) also reportthat fluoride is an essential element in low concentrationsfor various chemical reactions including an intermediatestep in reactions involving amides.

CONNETT: The anonymous fluoridation promoters cannot have it both ways: iflow levels of fluoride can facilitate chemical reactions in the body then they haveto acknowledge that low levels of fluoride could also interfere with otherreactions.

ANON (II) (continued): Many nutrients and chemicals areknown to alter enzyme activity. Observations of suchinteractions in test tube studies provide a very low levelof evidence in themselves and cannot be extrapolated to thereal-life interactions in living tissue.

As McDonagh et al., (2000) have commented “exposure in invitro (laboratory studies) is very different to those invivo (real life situations). In cell culture experimentscells are exposed directly to a fluoride solutioncontaining highly reactive unbound ions. This is verydifferent to exposure in the body…”


CONNETT: However, this does not preclude the use of such studies in a weightof analysis approach in accessing the likelihood that a chemical may causehealth problems in a human population. It is standard practice in toxicologicalrisk analysis to use a combination of biochemical, animal and human studies tomake an assessment of a chemical’s potential health risks.

The McDonagh et al. (2000) review deliberately limited itself to human studieswhich could be subjected to meta-analysis. That they chose this approachshould not negate the many regulatory reviews that use a weight of analysisapproach and take advantage of the clues offered by biochemical and animalstudies, as well as high dose human trials. McDonagh et al., (2000) evenexcluded human epidemiological data for effects above 1 ppm but below 5 ppm,which is blatantly absurd when one remembers that once fluoride is added to thewater one cannot control the dose going to the individual. If one was genuinelyinterested in protecting the health of the population a combination of moderatelylow, medium and high dose human data is exactly what one needs in order totease out the effects one might anticipate for high water consumers and otherswho get high doses of fluoride from other sources than water!

ANON (II) (continued): On the question of toxicologystudies McDonagh et al., (2000) note that “the history ofhealth technology development shows that there have beennumerous new interventions that were promising (or harmful)in animal and laboratory studies that turned out to beineffective (or safe) when tested in humans. One examplewould be the drug omeprazole (Losec) which caused gastrictumours in pre-clinical animal studies. However, suchtumours have not been documented in humans, even inpatients with conditions that require continuous treatmentfor many years. In general, when human data are available,animal or laboratory data provide far less reliableestimates of effect and, as such, do not bear significantweight on decisions about interventions.”

CONNETT: This argument might apply to drug interventions where individualpatients are being targeted with controlled doses, but it shouldn’t apply to asituation where a whole population is being subjected to forced medication with asubstance and the dose cannot be controlled. Under these circumstances thewise determinants of public health policy would not exclude any availabletoxicological or biochemical detail which might throw important clues or light onpossible dangers in the matter.

ANON (II) (continued): Lepo et al., (2000) reviewed thefluoride literature to assist the understanding of thepotential environmental and human health impacts offluoridation of water. The authors noted that in in vitro


laboratory experiments the concentration of fluoride atwhich enzyme inhibition occurs is quite often of the orderof 100 to 1,000 times greater than the concentration atwhich inhibition occurs in humans and such experimentalinhibition is not physiologically meaningful. Normalfluoride soft-tissue levels are in the micromolar rangewhereas enzyme inhibition typically requires millimolarconcentrations.

CONNETT: Inevitably in test tube experiments one is dealing with fluoride inaqueous solution. The key issue in the teeth, bones and possibly pineal gland isthe concentrations in the microenvironments at the interface between the solublepart of the tissue and the mineral phase. Locally this could well reach themillimolar range. Moreover, empirically we can say that something is beinginterfered with at the levels that many children reach in their teeth otherwisedental fluorosis (a systemic effect) would not be an issue. The key question iscould similar situations also occur in the bones, the pineal gland and othercalcified tissues?

37) Fluoridation has been found to be ineffective at preventing one of the mostserious oral health problems facing poor children, namely, baby bottle toothdecay, otherwise known as early childhood caries (Barnes 1992 and Shiboski2003).


CONNETT: Another strange response since our point is clearly documented withtwo articles from the peer-reviewed scientific literature (Barnes 1992 andShiboski 2003) and I would also add the paper by Kelly and Bruerd (1987).

It is hard to believe that baby bottle tooth decay is not also a problem in Ireland.

• ANON (II): One of the objectives of the York systematicreview on water fluoridation (McDonagh et al., 2000) was toexamine whether water fluoridation results in a reduction


of caries across social groups and between geographicallocations, bringing equity. No longitudinal studies werefound by the York review to address this issue. It was thusdecided to include cross-sectional studies only from theU.K as it would be difficult to compare measures of socialclass from different countries. The authors reported thatsome evidence exists that water fluoridation reduces theinequalities in dental health across social classes in 5-and 12-year-olds, using the dmft/DMFT outcome measure. Thiseffect was not seen in the proportion of caries-freechildren among 5-year-olds. The small quantity of studies,differences between these studies and their low qualityrating suggests caution in interpreting these results(McDonagh et al., 2000).

• The data contained in the Children’s Oral Health inIreland Report 2002 (Whelton et al., 2004) generallysupports the published literature, which asserts that theoral health of the less well off is worse than that of therest of the population. In this report, possession of amedical card was used as a surrogate for disadvantage inthe Republic Of Ireland. For the vast majority of the agegroups in the study, ownership of a medical card by theparents or guardians is an indication of low income. Themean number of decayed (visual and cavitated), missing andfilled teeth (vdmft, primary teeth 5-year-olds; VDMFT,permanent teeth 8-, 12- and 15- year-olds) among child andadolescent dependents of medical card holders in theRepublic of Ireland as a whole was 1.9 in full-fluoridatedareas. For the less deprived, dependents of non-medicalcard holders the vdmft/VDMFT was 1.1 in full-fluoridatedareas. In non-fluoridated areas, the vdmft/VDMFT for childand adolescent dependents of medical card holders was 2.6and for dependents of non-medical card holders in non-fluoridated areas, it was 2.1. Child and adolescentdependents of medical card holders in full-fluoridatedareas have a vdmft/VDMFT of 1.9 versus 2.6 in non-fluoridated areas.

The preliminary results of the National Survey ofChildren’s Oral Health 2002(Whelton et al 2004) werepublished in 2004. The decay experience (DMFT) among 12-year-olds in the fluoridated Republic of Ireland (RoI) was1.1 compared to 1.3 in non-fluoridated communities in theRepublic and 1.5 in the non-fluoridated communities ofNorthern Ireland (NI). For 15-year-olds, the DMFT was 2.1in the fluoridated communities of RoI, 3.2 in the non-fluoridated communities of the RoI and 3.6 in the non-


fluoridated communities of NI. 23% of 8-year-olds and 39%of 15-year-olds have enamel fluorosis in the RoI. (it is not clearto which Reason this comment was directed, PC)

CONNETT: ANON argues that fluoridation favors the disadvantaged. We argueexactly the opposite. Fluoridation is not equitable for two reasons. It is preciselythe poor who will not be able to afford avoidance measures if they so wish (e.g.reverse osmosis equipment or bottled water for drinking and cooking). Thus theyare trapped. Moreover, it is also in families of low income where one cananticipate poor nutrition, which is known to exacerbate fluoride’s toxic effects. Sothe poor are trapped by a practice which could make their health worse.

41) Despite the fact that we are exposed to far more fluoride today than we werein 1945 (when fluoridation began), the "optimal" fluoridation level is still 1 partper million, the same level deemed optimal in 1945! (Marier & Rose 1977; Levy1999; Rozier 1999 and Fomon 2000).


CONNETT: Once again the first commentary ignores the 4 peer-reviewed andpublished studies we cite to support our argument.

ANON (II): Heath et al., (2001) investigated the amountsof fluoride ion ingested following use of a variety oftopical fluoride materials commercially available.Fluoride mouthrinses appeared to provide the highestsalivary retention rates per dose of all forms of topicalfluoride. Ingestion rates from concentrated gels wereacceptable when effective evacuation methods were applied.None of the concentrated gels used resulted in elevationsin total blood fluoride levels of concern in adults.

Generally, the use of fluoride supplements on a communitybasis has ceased in Ireland. On an individual basis theyare used as follows:


High risk individuals Over 3 years of age Low fluoride areaChewed/ sucked slowly Using an appropriate dosing schedule(it is not clear to which Reason this comment is addressed, PC)

The U.S. Food and Drug Administration has established“market baskets” which reflect the actual 14-dayconsumption of various food items by an average individualin different age groups, from six-month-old children toadults. In a nationwide study of market baskets from areaswith varying levels of fluoride in water supplies, it wasdetermined that little or no change in food fluoridecontent has occurred as a result of the fluoridation ofU.S. water supplies (Pendrys et al.,1990, Olsen 1986).

CONNETT: We find this assertion hard to believe. The DHHS(1991) review,which post-dates both these studies, estimated that the range of exposure toadults in fluoridated communities was 1.6 to 6.6 mg per day. In this estimatethey had a range of 0.4 to 2.7 mg/day from food, and 0.6 to 3.2 mg/day fromwater and beverages. If this was the dose from food and beverages in 1945 it ishard to understand why the program ever got off the ground as the optimal dosedetermined in those days was 1 milligram per day!

This claim would also appear to contradict their earlier assertions that ahalo/seepage effect explains why the largest survey in the US indicates thatthere is little difference in tooth decay between fluoridated and non-fluoridatedcommunities (see discussion on Reason 3 in SECTION B below).

ANON (II) (continued): The statement in the ‘50 Reasons’document that the “optimal fluoridation level is still 1part per million, the same level deemed optimal in 1945” isincorrect.

Hong-Kong reduced its water fluoride levels to 0.5ppm inthe mid 1990s (Burt 1999). In Canada the optimum level offluoride in the water supplies was lowered from 1.0 - 1.2mg/L to 0.8 - 1.0 mg/L (http://www.hc-sc.gc.ca./waterquality).

CONNETT: Actually, Hong Kong has now eliminated fluoridation altogether.However, Hong Kong and Ontario are rare examples of fluoridating countrieswhich has reacted rationally to this issue of over-exposure to fluoride asevidenced by the huge increase in dental fluorosis rates.

ANON (II) (continued): The Forum on Fluoridation inIreland (Department of Health and Children 2002) haveadvised that, in light of changed circumstances in Irelandand the best available scientific evidence, theFluoridation of Water Supplies Regulations in Irelandshould be amended to redefine the optimal level of fluoride

http://www.hc-sc.gc.ca./waterquality


in drinking water from the present level (0.8 to 1ppm) tobetween 0.6 and 0.8 ppm, with a target value of 0.7 ppm.

CONNETT: Is it not interesting that three years after the Forum report waspublished that this recommendation has not been put into effect! I do not see anyletters to the press from any Fluoridation Forum members complaining aboutthis. Was this just another PR exercise to take the heat off the Minister on thismatter?

42) The chemicals used to fluoridate water in the US are not pharmaceuticalgrade. Instead, they come from the wet scrubbing systems of the superphosphatefertilizer industry. These chemicals (90% of which are sodium fluorosilicate andfluorosilicic acid), are classified hazardous wastes contaminated with variousimpurities. Recent testing by the National Sanitation Foundation suggest that thelevels of arsenic in these chemicals are relatively high (up to 1.6 ppb after dilutioninto public water) and of potential concern (NSF 2000 and Wang 2000).


CONNETT: This is another strange response since it is a statement that isdocumented and a fact that really cannot be disputed.

ANON(II): The monitoring of drinking water in Ireland,general legislation concerning fluoride, fluoride and theaquatic environment, the manufacture of hydrofluorosilicicacid (HSFA), quality control of HFSA, heavy metalsconcentrations in HFSA, and the treatment of drinking waterand technical guidelines are dealt with in detail inChapters 9 and 10 and Appendices 9, 10, 11, 12, 13, 14 and15 of the Report of the Forum on Fluoridation (Departmentof Health and Children 2002) (www.fluoridationforum.ie).

The chemical used to fluoridate public water supplies inthe Republic of Ireland is hydrofluorosilicic acid. Thisproduct must meet the specification for chemicals used for


the treatment of water intended for human consumption bythe European Committee for Standardisation, CEN (1998). Theproduct used in Ireland is produced as a primary productspecifically for the fluoridation of water supplies inIreland and in Spain. Hydrofluorosilicic acid ismanufactured from compoundsand minerals containing both fluoride and silica (e.g.fluorite, apatite) and an acid (usually sulphuric acid).The process of producing hydrofluorosilicic acid is a “wetchemical” process involving the reaction of sulphuric acidwith rock compounds. The resulting gases are passed througha water medium until the concentration reaches 25 – 30%,which is then filtered.

CONNETT: Technically this is correct. However, ANON(II) glosses over the factthat this “wet chemical” process is actually a “wet scrubber system” introduced tocapture the pollutants hydrogen fluoride and silicon tetrafluoride and thus preventthem from damaging the environment. Its disingenuous in my view to suggestthat the production of hexafluorosilicic acid is the purpose of this manufacturingprocess i.e. is the “primary product” of this industry as they claim. The heating ofphosphate rock with sulfuric acid is to produce soluble phosphates and/orphosphoric acid. The hexafluorosilicic acid is a captured pollutant and in its rawstate has to be treated as a hazardous waste unless it can be disposed of as a“product.” In this very real sense water fluoridation allows the phosphatefertilizer industry to avoid the disposal costs of disposing of this waste product ashazardous waste.

• ANON (II) (continued): Because of the nature of the rawmaterials it is recognised in the CEN specification thatlimits should apply for impurities and any toxic substancespresent in the final product. For the purpose of thepresent specification, “toxic substances’’ are thosedefined in the EU Directive 80/778/ EEC of 15 th of July1980. They include such substances as Antimony, Arsenic,Cadmium, Chromium, Lead, Mercury, Nickel and Selenium.Furthermore, the recently adopted water Framework Directive2000/60 /EC and the Water Quality (Dangerous Substances)Regulations, 2001 provide for stringent regulation of allthese substances (Department of the Environment and LocalGovernment (2000, 2001). The standards are consistent withthe recommendations of SCTEE, (EU Advisory ScientificCommittee on Toxicity, Ecotoxicity and the Environment).The quality of drinking water in the EU is subject to verystringent regulation and monitoring.

CONNETT: It will be interesting to see if these anonymous commentators will beas interested in citing European Directives when they examine the new EU


Directive which came into affect on October 31, 2005. This would effectivelymake fluoridation illegal since fluoride is not an authorised medication.

ANON (II) (continued): The Forum on Fluoridation in Ireland(www.fluoridationforum.ie 2002) have investigated themetals content of a small number of samples of the rawfluoridation additive, HFSA. Three random samples of HFSAas used in Ireland were analysed for a range of eight heavymetals.

CONNETT: It amazes me that any one would consider that the taking of threerandom samples could possibly account for the variation we can expect in theconstitution of this waste product. If one is going to take such results seriouslywe need the procedure to be extended over time and subjected to a seriousstatistical analysis. After all, the Irish people have been dosed with theseproducts every day since 1963!

ANON (II) (continued): On the completion of the analyses arisk assessment was prepared. This assessment demonstratedthat, at the concentrations of the respective metals whichwould result in drinking water after the additive had beendiluted to the upper limit of 1 parts per million fluoride,the residual metals concentrations would be a tiny fractionof the guideline values recommended by the World HealthOrganisation. For example, the average test result in threesamples of HFSA from Spain (data from Dublin regionalpublic analyst) contained 1.1 mg/kg arsenic.

After a dilution factor of 352,000 used in ensuring 1 ppmfluoride in water by volume, the concentration of arsenicin water due to HFS acid after fluoridation was 0.0000031.The W.H.O drinking water guideline for the metal is 0.01mg/l. This means that an adult would need to consume288,000 litres of water per week to exceed J.E.F.C.A. SafetyLevels (PWT) (A). (J.E.C.F.A. FAO Joint Expert Committee onFood Additives) (Department of Health and Children 2002).This situation is unlikely to arise.

CONNETT: None of the above response negates the points we were making.The chemicals used are not pharmaceutical grade as used in toothpaste andother dental products. They are industrial grade. Moreover, they have not beentoxicologically tested in the same way that pharmaceutical grade sodium fluoridehas been tested.•ANON (II) (continued): The chemicals used for waterfluoridation in Ireland are manufactured to exactingquality standards.


CONNETT: This would only be true if the Spanish industry is specificallymanufacturing this material as opposed to it being a by-product (captured airpollutant) of phosphate fertilizer manufacture as is the case in the US.

ANON (II) (continued): Within the EU, drinking water,whether fluoridated or non-fluoridated, is subject to thesame stringent regulatory framework for water quality. Itmust be emphasised that the Drinking Water Directives (aswith other community legislation) are adopted only on thebasis of meticulous consideration by the EU Commission andCouncil, by the European Parliament and by appropriatetechnical experts from the member states. Furthermore, inframing proposals to be scrutinised thus, the Commission isguided by an expert group – the Scientific Committee onToxicity and Ecotoxicity and the Environment (SCTEE) – andalso takes into account the medical opinions of the WorldHealth Organisation. The SCTEE committee is completelyindependent of water fluoridation programmes(www.fluoridationforum.ie).

• Council Directive 98/83/EC (European Committee forStandardization 1998) is based on the quality of waterintended for human consumption. This new Directive wasdrawn up in order to adapt the previous Directive of 1980to scientific and technological progress(www.fluoridationforum.ie). The main thrust of theCommission Directive includes reviewing parametric values,and where necessary strengthening them in accordance withthe latest available scientific knowledge (WHO guidelines,Scientific Committee on Toxicology and Ecotoxicology)(http://www.lenntech.com/drinking-water-standards.htm). The1980 EU Directive specifies the Community Limit forfluoride in drinking water as 1.5 mg/l. The 1998 EURegulations maintained the same limit and this is notwithout significance. In Ireland the 1988 Regulationsspecified a limit of 1mg/l F, in line with the upper limitin the National Fluoridation Act. The stricter standard of1mg/l F is also specified in the 2000 Drinking WaterRegulations (European Communities Regulations 2000).However, the latter contains the quality comment: ‘theparametric value is 1 mg/l for fluoridated supplies. In thecase of supplies with naturally occurring fluoride theparametric value is 1.5 mg/l F.’ This a practicalrecognition of the fact that in some areas the naturallevels of fluoride must be accepted up to the limit in theDirective. (Department of Health and Children2002,www.fluoridationforum.ie).

http://www.lenntech.com/drinking-water-standards.htm


CONNETT: Again, it will be interesting to see if these anonymous commentatorswill be as interested in citing European Directives when they examine the newEU Directive which came into affect on October 31, 2005. This would effectivelymake fluoridation illegal since fluoride is not an authorised medication.

44) Studies by Masters and Coplan (1999, 2000) show an association betweenthe use of fluorosilicic acid (and its sodium salt) to fluoridate water and anincreased uptake of lead into children's blood. Because of lead’s acknowledgedability to damage the child’s developing brain, this is a very serious finding yet itis being largely ignored by fluoridating countries.

ANON (II): Urbansky and Schock (2000) examined thechemodynamics of hydrofluorosilicic acid in water anddemonstrated that there is complete dissociation ofhydrofluorosilicic acid in drinking water.

CONNETT: This is incorrect. Urbansky and Schock demonstrated no such thing.They used theoretical calculations to show that there would be nohexafluorosilicate ion left after dilution however that is a far cry from showing thatthere are no silicon fluoride complexes left at all. There are many otherfluorosilicates possibly formed on route to free fluoride and silica. In theirresponse to Urbansky and Schock’s critique Masters and Coplan produced (andtranslated) a PhD thesis from Germany (Westerndorf) which found that at neutralpH there were still two fluoride ions attached to the silicon and that the biologicalproperties of this species was different from free fluoride ion, on which all thetoxicological testing has been done in fluoridating countries.

ANON (II) (continued): Whilst it is true that both fluorideions and silicates form complexes with lead, the fluorideions are more likely to complex with the more abundant ions(aluminium, iron, calcium, carbonate, sulphate) while leadwill complex with the chloride, carbonate, bicarbonate andsulphate ions which are present in larger quantities thanfluoride ions. Free lead 2+ ion is a very minor fraction ofthe soluble lead in most drinking water systems becauselead forms complexes with higher concentrations than thoseassociated with fluoridation so, the use of silicofluorideswould have no significant effect on silica levels or leadhydroxide.

The issue of possible increased blood lead levels and theuse of hexafluorosilicic acid to fluoridate water havereceived much attention from several scientists in recentyears. The work of Masters and Coplan forms part of thebody of scientific literature on this subject (1999).


CONNETT: For commentators who profess to be on top of this issue it isremarkable that they fail to acknowledge Masters and Coplan’s second paper onthis matter which was published in 2000. In this they found the same result in NYstate that they had observed in Massachusetts: namely, that when siliconfluorides are used to fluoridate water there appears to be an increase inchildren’s blood lead.

ANON (II) (continued): In order to understand thesignificance or otherwise of the research by Masters andCoplan a full understanding of the wider role of lead inthe environment is required. A short resume of lead anddrinking water summarised from WHO Guidelines on DrinkingWater for Human consumption follows (1996):

• In tap water, lead may be present as a result ofdissolution from natural sources, but it is mainly as aresult of domestic plumbing, from pipes including solder,fittings or service connections to homes, which may allcontain lead. Human exposure can occur through inhalationof lead dust, drinking lead–contaminated water orconsumption of lead–contaminated food. Lead may also beabsorbed through the skin. Cigarette smoke also containslead.

More than 80% of the total daily intake of lead is fromingestion of food, dust and dirt. The average daily intakeof lead from drinking water has been estimated as 3.8ug/day for children and 10 ug/day for adults (WHO 1996). Thisassumes an average concentration of lead in drinking waterto be 5ug/litre.

• In young children a significant proportion of their totallead intake derives from the ingestion of soil, dirt anddust. Adults absorb approximately 10% of lead contained infood, but young children absorb 4 to 5 times as much. Thegastrointestinal absorption of lead from ingested soil anddust has been estimated to be as high as 30% in youngchildren. A provisional tolerable weekly intake of 25ug oflead per kilogram of body weight for infants and childrenhas been established (intake of 3.5ug/kg per day). This isbased on evidence that, in children, a lead intake of 3 –4ug/ kg of body weight per day is cleared from the body,with no increase in blood lead levels or increased bodyburden of lead. For a 5kg infant with an average waterconsumption of 0.75 litres / day, the guidelinevalue is 0.01mg/ litre. As this group is the most sensitiveto the effects of lead, this value is protective for allother groups.


• A series of articles based on studies conducted by theauthors, Masters and Coplan have attempted to show thatcertain approaches to fluoridating drinking water is linkedto increased levels of lead (11) species in the blood. Ithas been suggested that certain adverse health or socialconditions may be arising because of interactions betweenlead (11) species and inorganic fluoro – compounds,specifically, fluorosilicates and fluoride.

Urbansky and Schock of the United States EnvironmentalProtection Agency have investigated these assertions. Theyconcluded that no credible evidence exists to show thatwater fluoridation has any quantifiable effects on thesolubility, bioavailability, bioaccumulation, or reactivityof lead (0) or lead (11) species compounds (Urbansky andSchock 2000). They further state that the governingfactors are the concentrations of a number of other speciessuch as bicarbonate, hydroxide, or chloride whose effectsfar exceed those of fluoride or fluorosilicates underdrinking water conditions.

Urbansky and Schock (2000) were also of the view thatstatistical techniques used by Masters and Coplan wereinappropriate and that many of the chemical assumptionswere scientifically unjustified and contradicted by knownchemistry data and principles.

CONNETT: That is certainly the view of Urbansky and Schock, but theanonymous commentators would do well to see Masters and Coplan’s responseto Urbansky and Shock’s criticism, all of which is based upon theoreticalcalculations as opposed to real life measurements at the water works or inhuman tissues.________________________________________________

New references from Connett’s response

Academy of General Dentistry. "Monitor Infant's Fluoride Intake"http://www.agd.org/consumer/topics/baby/fluoride.asp

Armfield JM, Spencer AJ. (2004) Consumption of nonpublic water:implications for children’s caries experience. Community Dent OralEpidemiol 32:283-296.

http://www.agd.org/consumer/topics/baby/fluoride.asp


Bachinskii PP, et al. (1985) Action of the body fluorine of healthy personsand thyroidopathy patients on the function of hypophyseal-thyroid thesystem. Probl Endokrinol (Mosk) 31(6):25-9.

Bassin EB. (2001). Association Between Fluoride in Drinking Water DuringGrowth and Development and the Incidence of Ostosarcoma for Childrenand Adolescents. Doctoral Thesis, Harvard School of Dental Medicine.

Beltrán-Aguilar ED, Griffin SO, Lockwood SA. Prevalence and trends inenamel fluorosis in the United States from the 1930s and 1980s. J AmDent Assoc 2002;133:157--66.

Bo Z, et al. (2003). Distribution and risk assessment of fluoride in drinkingwater in the west plain region of Jilin province, China. EnvironmentalGeochemistry and Health 25: 421-31.

Bohannan HM, et al. (1985). Effect of secular decline on the evaluation ofpreventive dentistry demonstrations. Journal of Public Health Dentistry45: 83-89.

Bratthall D, Hansel-Petersson G, Sundberg H. (1996). Reasons for thecaries decline: what do the experts believe? European Journal of OralScience 104:416-22.

Brothwell D, Limeback H. (2003). Breastfeeding is protective againstdental fluorosis in a nonfluoridated rural area of Ontario, Canada. Journalof Human Lactation 19: 386-90.

Campagna L, et al. (1995). Fluoridated drinking water and maturation ofpermanent teeth at age 12. Journal of Clinical Pediatric Dentistry19(3):225-8.

Cao J, et al. (2003). Brick tea fluoride as a main source of adult fluorosis.Food and Chemical Toxicology 41:535-42.

Caverzasio J, Palmer G, Bonjour JP. (1998). Fluoride: mode of action.Bone 22:585-9.

Centers for Disease Control and Prevention (CDC, 2005) Surveillance fordental caries, dental sealants, tooth retention, edentulism, and enamel


fluorosis--United States, 1988-1994 and 1999-2002. Morbidity andMortality Weekly Report Surveillance Summaries 54:1-43.

Clarkson BH, Fejerskov O, Ekstrand J, Burt BA. (1996). Rational Use ofFluoride in Caries Control. In: Fejerskov O, Ekstrand J, Burt B, Eds. Fluoridein Dentistry, 2nd Edition. Munksgaard, Denmark. p 354.

Clarkson JJ, McLoughlin J. (2000). Role of fluoride in oral healthpromotion. International Dental Journal 50(3):119-28.

Colquhoun J. (1985). Influence of social class and fluoridation on childdental health. Community Dentistry and Oral Epidemiology 13:37-41.

Colquhoun J. (1990). Flawed foundation: a re-examination of thescientific basis for a dental benefit from fluoridation. Community HealthStudies 14:288-96.

Connett P, Neurath C, Connett M (2005a). Revisiting the fluoride-osteosarcoma connection in the context of Elise Bassin’s findings: Part 1.Submission to the NRC review panel on the Toxicologic Risk of Fluoride inDrinking Water. March 2. http://fluoridealert.org/health/cancer/fan-nrc.part1.pdf

Connett P, Neurath C, Connett M (2005b). Revisiting the fluoride-osteosarcoma connection in the context of Elise Bassin’s findings: Part II.Submission to the NRC review panel on the Toxicologic Risk of Fluoride inDrinking Water. March 21; revised April 8.http://fluoridealert.org/health/cancer/fan-nrc.part2.pdf

Dean HT. (1936). Chronic endemic dental fluorosis (mottled enamel). J.Amer. Med. Assoc.107: 1269-1273.

Dean HT, Jay P, Arnold FA, Elvove E. (1941) Domestic water and dentalcaries. I. A dental caries study, including L.acidophilus estimations, of apopulation severely affected by mottled enamel and which for the past12 years has used a fluoride-free water. Pub. Health Rep. 56, 365-381.

Dean HT, Arnold FA, Elvove E. (1942) Domestic water and dentalcaries.V. Additional studies of relation of fluoride domestic waters to

http://fluoridealert.org/health/cancer/fan-nrc.part1.pdf

http://fluoridealert.org/health/cancer/fan-nrc.part2.pdf


dental caries experience in 4,425 white children, aged 12 to 14 years, of13 cities in 4 states. Pub. Health Rep. 57, 1155-1179.

Dean (1952) cited by Exner FB (1960) In his analytical commentary onthe 1960 Testimony of Dr. H. T. Dean in the Suit to Enjoin Fluoridation ofChicago's Water (Schuringa versus Chicago).

Ekstrand J. (1989). Fluoride intake in early infancy. Journal of Nutrition119(Suppl 12):1856-60.

Ekstrand J. (1996). Fluoride Intake. In: Fejerskov O, Ekstrand J, Burt B,Eds. Fluoride in Dentistry, 2nd Edition. Munksgaard, Denmark. Pages 40-52.

Fomon SJ, Ekstrand J, Ziegler EE. (2000). Fluoride intake and prevalenceof dental fluorosis: trends in fluoride intake with special attention toinfants. Journal of Public Health Dentistry 60: 131-9.

Gray AS. (1987). Fluoridation: Time For A New Base Line? Journal of theCanadian Dental Association. 53(10): 763-5.

Haugejorden O. (1996). Using the DMF gender difference to assess the"major" role of fluoride toothpastes in the caries decline in industrializedcountries: a meta-analysis. Community Dentistry and Oral Epidemiology24: 369-75.

Heller KE, et al (1997). Dental caries and dental fluorosis at varying waterfluoride concentrations. Journal of Public Health Dentistry 57(3) 136-143.

Hong L, et al. (2005). Association of amoxicillin use during earlychildhood with developmental tooth enamel defects. Arch Pediatr AdolescMed. 159(10):943-8.

Kalsbeek H, Verrips GH. (1990). Dental caries prevalence and the use offluorides in different European countries. Journal of Dental Research69(Spec Iss): 728-32.


Kelly M, Bruerd B. (1987). The Prevalence of Baby Bottle Tooth DecayAmong Two Native American Populations. Journal of Public HealthDentistry 47:94-97.

Komarek A, et al. (2005). A Bayesian analysis of multivariate doubly-interval-censored dental data. Biostatistics 6:145-55.

Kunzel VW. (1976). [Cross-sectional comparison of the median eruptiontime for permanent teeth in children from fluoride poor and optimallyfluoridated areas] Stomatol DDR. 5:310-21.

Leverett DH. (1991). Appropriate uses of systemic fluoride:considerations for the '90s. Journal of Public Health Dentistry 51: 42-7.

Levy SM, Kiritsy MC, Warren JJ. (1995). Sources of fluoride intake inchildren. Journal of Public Health Dentistry 55: 39-52.

Mellette JR, et al. (1983). Perioral dermatitis. Journal of the Associationof Military Dermatologists 9: 3-8.

Mullenix PJ, et al. (1995). Reply. Neurotoxicology and Teratology 17:667-668.

Ortiz-Perez D, et al. (2003). Fluoride-induced disruption of reproductivehormones in men. Environmental Research 93:20-30.

Reich E. (2001). Trends in caries and periodontal health epidemiology inEurope. International Dentistry Journal 51(6 Suppl 1):392-8.

Spittle B. (1993). Allergy and hypersensitivity to fluoride. Fluoride26:267-73.

Stone OJ, Willis CJ. (1967). Enhancement of inflammation by fluorides.Texas Reports on Biology and Medicine 25: 601-6.

Stone OJ, Willis CJ. (1968). The effect of stannous fluoride and stannouschloride on inflammation. Toxicology of Applied Pharmacology 13: 332-8.

Susheela AK, Jethanandani P. (1996). Circulating testosterone levels inskeletal fluorosis patients. J Toxicol Clin Toxicol 34(2):183-9.


Teotia M, et al. (1998). Endemic chronic fluoride toxicity and dietarycalcium deficiency interaction syndromes of metabolic bone disease anddeformities in India: year 2000. Indian J Pediatr. 65(3):371-81.

Waldbott GL. (1958). Allergic Reactions from Fluorides. InternationalArchives of Allergy 12: 347-355.

Ziegelbecker, R. (1981) gwf Wasser Abwasser, 122:495-8 and Fluoride,14: 123-7.

The Appendices and References to the original 50 reasons canbe found at http://www.FluorideAction.net/50reasons.htm

http://www.FluorideAction.net/50reasons.htm

Documents

Letter to John Moloney TD on Issue of Fluoridation in Ireland