Tag Archives: fluoridation debate

Fluoride debate: Response to Paul’s 5th article

This is Ken Perrott’s response to Paul Connett’s last article Fluoride debate: Arguments against fluoridation thread. Part 5. Paul.

For Paul Connett’s original article see – Fluoride debate Part 1: Connett.


Paul’s last article was another Gish gallop of arguments and questions he demands I answer.  I discussed the use of the Gish gallop as a tactic for avoidance in my last article. In this article Paul demonstrates how the Gish gallop enables the user to also claim their discussion partner is “ducking” issues and “didn’t address,” “didn’t  acknowledge,” “didn’t comment on” or “didn’t respond to” issues he has raised.

Again, I will not walk into that debating trap and mechanically go through his 30 numbered arguments but will attempt to accommodate as much as is reasonable with some general comments and some specific replies.

Activism and science

This year the fluoridation issue raised questions about the problems of activism for a number of New Zealand scientists. The local scientific community was taken by surprise when the Hamilton City Council in June this year voted to end fluoridation. Surprised because most of us were unaware that the council had decided not to go ahead with a referendum (as we had expected) and instead use a “tribunal” process of consultation. This approach suites activist groups very well. They can be continuously in touch with council decisions, have a membership or contact base that can be organised rapidly and they can saturate such a consultation process with their own submissions.

The Fluoride Action Network of NZ (FANNZ) did this very well. They were able to dominate the consultation process with 89% of the total submissions. (This in a city where referenda have shown about 70% support fluoridation). Being part of Paul Connett’s Fluoride Alert Network they did this on an international scale – about 30% of their submissions were from outside Hamilton with many from outside New Zealand. People like Paul Connett and Declan Waugh made video submissions. These people were promoted as “international experts” or “world experts” on the subject even though they have no credible scientific publications on the subject. Of course local councillors did not have the background to see through that ruse. Reports prepared by the council staff showed the number and international origins of these submissions impressed the council and it’s bureaucracy.

It was easy to conclude that what local scientists lacked was a similar organised activist group. If not specifically devoted to defending the science behind fluoridation then at least to defending science in general. After all, anti-fluoridation activity is not the only area where science gets challenged.

Scientists and health professionals did become active in social communication activity, Facebook, letters to the editor, etc., but I noticed a distinct lack of enthusiasm for any organised activism. No one rushed to form an activist group.

Scientists have a problem with activism because the group thinking and selective use of scientific information inevitably involved is in direct conflict with the scientific ethos. That is why activist scientists tend to face disapproval from colleagues, although this has changed a little recently where the vicious personal attacks on individual climate scientists has made some form of scientific activism essential.

Confirmation bias and activism

Contrary to what many people believe humans are not naturally a rational species. Despite their intelligence and ability to reason they are in practice driven primarily by instinct and emotions. In fact, they would have long become extinct if they relied completely and in all cases on the inefficient and slow process of rationally considering every event that required a response.

This means that confirmation bias and cherry picking information come naturally to us. It is normal to seek information which supports the preconceived ideas and theories we are emotionally attached to. Scientists are just as prone to these human failings as others but the scientific processes help reduce this problem. Scientific ideas and hypotheses are tested by experiential evidence – they are compared against the real world. Theories are judged on their evidential support and not their attractiveness. (This does not deny an important role for speculation). Ideas and theories are exposed to harsh critical consideration by colleagues. All this helps to encourage objectively and reliability of scientific information – while not denying that there are still inevitable residual problems from confirmation bias. The dynamic nature of science and the provisional nature of current theories and ideas, means that over time mistakes arising  from these human frailties can be reduced.

Contrast that with the position of activists, even scientific activists. They are inevitably driven by strong ideological or political aims which naturally encourage confirmation bias and cherry picking. But unlike a scientific researcher they exist in an uncritical, or at least biased, social environment. Group thinking encourages a selective approach to scientific knowledge and a resistance to considering anything conflicting with the activist agenda. While heretics can be encouraged in scientific research they get jumped on in activist groups. Ideas and messages do not get tested against reality – far from it. They are tested for political effectiveness, in the political arena – not the natural world.

In effect, the world of activism is stifling for a person used to the creativity of genuine scientific research. I recognise that at times activism is essential and have myself played an activist role in my past. Now I see it as a necessary evil but not something I could do as a job. I do not envy Paul Connett his job as an executive for an activist organisation. The environment of group thinking and the need to abandon intellectual honesty to the ideological aims of the group are bad enough. But what happens to a scientist in such a position who finds they can longer follow the “party line?” That they no longer “have the faith?” It is a bit like the priest who finds, after years in the job ,they are an atheist. Do they go on hypocritically preaching every Sunday or do they take the honest way out and abandon their job with it’s financial and social security to face an uncertian future?

In scientific research it is expected that we can change our beliefs and ideas in the face of new evidence. Not to do so could lead to loss of scientific prestige and employability. It is the reverse to what Paul would face if he lost his anti-fluoridation convictions.

That is the problem for me – the strong pressure to conform to the activist ideological agenda despite the evidence. I think that colours Paul’s approach to many of the issues in his articles here.

Misleading propaganda

Paul raises the misleading image that was in a Queensland Health brochure again. He sweats blood attempting to imply my approval of that tactic. That is not honest. Especially as I made clear that “I do not support its implied message.” And explained that Paul’s Queensland Health example, and a similar anti-fluoridation brochure I raised, are “extreme exaggerations used to promote a message. Reasonable people should condemn that tactic. “

It is interesting Paul devotes so much time on this brochure in his last contribution to what, after all, is meant to be a scientific exchange, not an exercise in laying guilt for someone else’s transgression.  No one is actually defending the Queensland Health brochure – even Queensland Health! At this stage it seems purely to be a plaything of the anti-fluoridation groups. Paul himself was unable to supply a source or citation yet he had ready access to it and promotes it far and wide.

Don’t know what else I can add – except writing personally to Queensland Health with a complaint. Bit difficult without a citation to its use I could quote. Never mind, my public admonishment here should suffice.

I agree with Paul that we should expect better from our public servants but Paul missed my point “This sort of misrepresentation is probably more common among opponents of fluoridation.” I certainly find misrepresentation by public officials on this subject rare –  anti-fluoride activists make this charge far more often than is justified.

I do not buy Paul’s argument that similar but much more common misinformative propaganda by anti-fluoridation activists is somehow more permissible than the rare piece by a public servant. Especially as we have the power to correct a public servant, submit a freedom of information application, get a retraction and an apology. But try that with anti-fluoride activists and organisations like FAN and FANNZ. No such luck. One is more likely to be abused.

Paul’s complaints in this area would be a bit more convincing if he publicly condemned the misleading propaganda from his own activists. He cannot be unaware of the extreme claims made by members of his Fluoride Alert Network throughout the world. Quite apart from their misrepresentation of the science, which he probably encourages anyway, there are the political and personal harassment of people by sections of his activist network which he cannot be blind to, yet refuses to condemn.

I have yet to see him condemn the atrocious propaganda, lies and personal attacks of propagandists like Alex Jones and Vinny Eastwood. It is not enough to say he doesn’t necessarily support all their positions. The fact that he uses their services, and they use his, makes such weak dissociation disingenuous.

Why is he unwilling to publicly condemn such behaviour?

The Hastings trial

Paul weaves a conspiracy theory around the Hastings’ trial using on one-sided sources and their vague claims. I note that Paul also relies on quotes from letters. He does the same in his book. A colleague analysed the reference list and found many are to newspapers, magazines, newsletters, letters and conversations in meetings (a large proportion are duplicates) (see an impressive-sounding number of references, (therefore good?)). Yet he proudly says “You will note that every argument in this book is backed up with references to the scientific literature – 80 pages in all.” 

I don’t think such vague charges should be the subject of our scientific exchange – especially as they divert attention from the scientific issues involved in planning and interpreting such trials and epidemiological studies. Paul should have looked at the disputes around Colqhoun’s analysis of the New Zealand data. Colqhoun was strongly criticised for reliance on questionable data, crude measurements of caries prevalence and failing to establish residence histories and therefore reliable measures of fluoride intake (see, fir example, Newbrun & Horowitz, 2002). He also placed far more reliance on longitudinal studies than is warranted and was selective in choosing studies which have compared fluoridated and unfluoridated communities.

I looked at the current NZ data, which are similar to that analysed by Colqhoun, in my article Cherry picking fluoridation data. This illustrates a number of things. The national data shows clear differences between children from fluoridated and unfluoridated communities and an ethnic effect attributed to social and economic deprivation. This is just normal school clinic data, without technique standardisation for those making the measurements or proper recording of place of residence. The latter effect probably shows up more strongly after 2004 when a “hub and spoke” dental clinics system was introduced further confusing proper records of likely fluoride intake because one clinic could serve a number of areas – both fluoridated and non-fluoridated. This is a likely explanation for the apparent decline of the effectiveness of fluoridation after 2006.

To illustrate how easy it is to extract data for regions and cities which give meaningless results the plot below shows the data for the Waikato. Clearly the variability in this data, (indicated by abrupt changes year to year) is so large it make interpretation meaningless. Yet this does not stop FANNZ, the local version of Paul’s activist organisation, from hypocritically using just the 2011 data for the Waikato (where by chance children from fluoridated areas show more caries than unfluoridated!). One of their representative end used my graph below, showing the problem of cherry picking, as “proof” for claiming fluoridation increases incidence if caries. During the recent referendum campaigns this misrepresentation by anti-fluoridation activists was rife – yet they consistently ignored or covered up the national data.

There is a lesson in this. Careful and critical analysis of epidemiological data is necessary when considering such data. Effects of technique standardisation and changes, places of residence, mobility of families and diffusion of products from fluoridated into non-fluoridated areas must be considered.

Too often anti-fluoride activists simply select the data that fits their story better. They may even be unaware of what they are doing because confirmation bias is a trap we can all fall into and it can be very tempting if one is simply looking for plots to illustrate an effect. To be fair, I have even seen proponents of fluoridation fall into this trap occasionally.

Margin of safety

Paul mentions margin of safety a lot. He claims that I did not comment on the margin of safety analysis he provided based on the Xiang et al. (2003a,b) study.

Has he not been reading my side of the exchange?

I had put a question to him on his use of this study to determine a margin of safety. After commenting on the quality of the study and the journal Fluoride where it was published I wrote:

Yet Paul uses Xiang’s paper to authoritatively claim it had “found a threshold at 1.9 ppm for this effect.” (What effect he refers to is unclear.) How reliable is that figure of 1.9 ppm (actually 1.85 or 2.32 ppm F in the paper) –  considering the huge variation in the data points of the Figure 1? (Unfortunately the paper is not a lot of use in explaining that figure – reviewers should have paid more attention.)”

Paul did not respond so I repeated my question in a subsequent article asking him “about the huge variability in the data and how the hell one can place any confidence on the result drawn from Xiang’s figure.”

Briefly my question related to the figure used by Xiang et al.

Xiang-1

This is just another example Paul’s selective use of the literature and selective interpretation of parts of it to justify a preconceived claim he wishes to make. In practice, safety limits and margins of safety must be based on a far more extensive review of the literature and involve far less hand waving than Paul demonstrates in this case.

Bottle fed babies – misinformation again

Several times Paul has raised the issue of bottle-fed infants without describing the problem. Broadly, he is making the common anti-fluoridation claim that the reliance of bottle-fed infants on formula made up with fluoridated water causes normal limits for maximum F intake to be exceeded. Usually activists using this argument will refer to health authorities which they claim recommend that formula not be made up using fluoridated water.

The science for the New Zealand situation is clearly described by Cressey et al (2009) in their report Estimated Dietary Fluoride Intake For New Zealanders by Peter Cressey, Dr Sally Gaw and Dr John Love. It is a straightforward desktop study of the “dietary fluoride intakes for a range of age and gender sub-populations based on New Zealand data.” This is how they described their findings for formula-fed infants:

“The estimates for a fully formula-fed infant exceeded the UL [upper level of intake] approximately one-third of the time for formula prepared with water at 0.7 mg fluoride/L and greater than 90% of the time for formula prepared with water at 1.0 mg fluoride/L. However, it should be noted that the current fluoride exposure estimates for formula-fed infants are based on scenarios consistent with regulatory guidelines, rather than on actual water fluoride concentrations and observed infant feeding practices..”

They conclude “the very young appear to be the group at greatest risk of exceeding the UL.” However:

“the rarity of moderate dental fluorosis in the Australia or New Zealand populations indicates that current exceedances do not constitute a safety concern, and indicates that the UL may need to be reviewed.”

They are conceding that in some cases, some of the time, recommended upper levels for fluoride intake can be exceeded for fully formula fed infants. However they do not see this as a real safety concern.

These conclusions lie behind the current advice from our Ministry of Health on this subject. This takes account of the need for review of current ULs and considers use of fluoridated water safe for fully formula-fed infants. However, they also recommend that if parents are concerned (such as over the risk of dental fluorosis) they should use non-fluoridated water for part of the feeding – a peace of mind matter.

The situation in the US is similar

American Dental Association advises:

Yes, it is safe to use fluoridated water to mix infant formula. If your baby is primarily fed infant formula, using fluoridated water might increase the chance for mild enamel fluorosis, but enamel fluorosis does not affect the health of your child or the health of your child’s teeth. Parents and caregivers are encouraged to talk to their dentists about what’s best for their child.”

Where parents want to reduce the risk of dental fluorosis they:

can use powdered or liquid concentrate formula mixed with water that either is fluoride-free or has low concentrations of fluoride.

And the CDC advises:

Yes, you can use fluoridated water for preparing infant formula. However, if your child is exclusively consuming infant formula reconstituted with fluoridated water, there may be an increased chance for mild dental fluorosis. To lessen this chance, parents can use low-fluoride bottled water some of the time to mix infant formula; these bottled waters are labeled as de-ionized, purified, demineralized, or distilled.

This sort of information is often distorted by anti-fluoridation activist propaganda. Very often they claim that authorities like the CDC are recommending as an absolute that parents use non-fluoridated water in preparing formula for infants, and not treat the issue as a peace of mind matter.

Dental fluorosis

Anti-fluoridation activists almost unanimously quote figures for total dental fluorosis (or its equivalent) lumping together everything from questionable to severe. This gives them a nice high figure to promote. But, as I have said before, they use a bait and switch tactic to exaggerate the seriousness of the problem by then considering only the more severe category’s when considering the harm. It is worth actually listening to the anecdotal evidence of practicing dentists on this specific issue. How often do they see fluorosis or similar blemishes which need treatment? And how does this figure compare with the frequency with which they see dental decay serious enough to need treatment? I can think of only one dentist who claims fluorosis is a problem which he often sees and treats – he is an active propagandist for FANNZ. I have caught him telling many porkies about fluoridation and I wouldn’t trust his claims.

Paul attempts to put words in my mouth saying I “claimed there was practically no difference in dental fluorosis prevalence between fluoridated and non-fluoridated communities.” I did point out that the most recent NZ Oral Health Survey found no measurable difference. But I also acknowledged that in general an increase in mild categories is normally observed with fluoridation. What I actually wrote was:

“the incidence of fluorosis for children living in fluoridated may often be the same as, or only slightly greater than, the incidence for children living in non-fluoridated areas.”

This is not a denial of an increase in mild forms of fluorosis as a result of fluoridation. Nor is if a denial that the relatively small difference may reflect the diffusion of the benefits of fluoridation into the non-fluoridated areas through family mobility, poor representation of residence history and the movement of products prepared with fluoridated water.

Paul’s misrepresentation is not the sort of behaviour I expect from a discussion partner in a scientific exchange.

All Paul’s manipulation of figures and his claimed access to the minds and “potential psychological problems for young teenagers” does nothing to change the basic situation. This is that water fluoridation can cause an increase in the mildest classification of dental fluorosis but is generally not thought responsible for the more severe classifications. The later are relatively rare and any increases over recent years is unusually attributed to the wider use of fluoridated toothpaste and fluoride dental office treatments (and their accidental ingestion).

The common anti-fluoridation propaganda gives the impression that the total fluoridation occurrence quoted is all severe and not almost all very mild or questionable. For example, in New Zealand activists often use the figure of 44% occurrence of dental fluorosis when only 2.5% is of any concern.

Selective quoting

I have said again and again that one should attempt to understand the scientific literature intelligently and critically. Hard to do as we all suffer from conformation bias and can’t help being selective. Fortunately working within a scientific community there is pressure from peers who will challenge ones interpretation. This helps encourage objectivity and honesty.

But working in an activist group one does not experience such challenges. If anything there is the challenge to conform with the group thought. Confirmation bias and cherry picking gets encouraged and rewarded. Paul’s activism and bias is very clear in the way he selectively quotes the NRC (2006) report. Just a few examples from his last article in his attempt to justify conclusions he wishes to draw from animal studies using high fluoride concentrations.

“Dunipace et al. (1995) concluded that rats require about five times greater water concentrations than humans to reach the same plasma concentration. That factor appears uncertain, in part because the ratio can change with age or length of exposure. In addition, this approach compares water concentrations, not dose. Plasma levels can also vary considerably both between people and in the same person over time (Ekstrand 1978).” (My emphasis of the bits Paul omitted).

Similarly with Paul’s second quote from the NRC report:

Because many assumptions were involved in estimating the values presented in Table D-2, they should be used with caution. But values support a rat-to-human conversion factor for bone fluoride uptake of at least an order of magnitude.” (My emphasis of the bits Paul omitted).”

Natural and artificial fluoride

Many of people relying on Fluoride Alert for their information are confused about the nature of the hydrated fluoride anion in water. At the mystical end of this confusion is the concept that chemical species derived from man-made process are different in their biological action to that from natural sources, even though chemically there is no difference. At the more “realistic” end there is a refusal to accept that the fluorosilicate anion decomposes on dilution. Then there is the hand waving over the role of calcium that Paul indulges in. He repeats his claim:

“Usually when fluoride occurs naturally in the water it is accompanied by large concentrations of ions like calcium. The presence of the calcium can reduce the uptake of fluoride in the stomach and GI tract. No such protection is offered when the fluoridating chemicals are added to soft water.”

I have had to repeatedly battle out this argument with anti-fluoridation activists who obviously don’t understand basic chemistry but I find this statement amazing for a chemist who should understand the concept of solubility products and the nature of ions in solution.

Contrary to Paul’s suggestion the relationship observed between natural Ca and F concentrations in groundwaters is usually inverse – F concentrations increase as Ca concentrations decrease and vice versa (see for example Handa 1975Geochemistry and Genesis of Fluoride-Containing Ground Waters in India).  Just what we expect when a solid phase like fluorite or apatite is determining solution concentrations at equilibrium.

Here is what one of the commenters on Paul’s last article, Jo Lane, has to say about Paul’s denial of the presence of Ca in treated fluoridated water:

“Point 20 ) Classic example of pseudoscience. Let’s assume that Paul is correct in asserting that the presence of Ca2+ ions affects F- uptake in the GI tract.

Municipal water supplies in NZ have a target hardness (combined concentration of Ca2+ and Mg2+ ions) of 200 mg L-1. Most of this is Ca2+ as Lime (CaO) is typically used to increase pH in one of the final stages of water treatment.

If water was fluoridated to 0.8 mg L-1 F- (unreasonably assuming there is 0 mg L-1 F- to start with) using CaF2 as a source, the concentration of Ca2+ would increase by 0.2 % as compared to using HFA or NaF as a source of F-. This 0.2% change in Ca2+ concentration will not have any appreciable effect on F- uptake in the GI tract.

Given Paul has a PhD in chemistry I cannot believe that he is ignorant of such basic chemistry and so I am left with the unfortunate impression that he is being deliberately deceptive in the way that he presents his arguments.”

I agree. Sure, the Ca concentration in community water supplies will generally be lower than the target value (which is a maximum) but the principle remains. Replacement of fluorosilicic acid by fluorite (CaF2) as a fluoridating agent would have a minuscule effect on calcium concentrations because there is plenty of calcium from other sources – even is soft water.

Paul’s claim is the sort of thing that even an educated chemist might say if they are ideologically driven. This is the problem with activist groups with their own ideological demands and group thinking. It is easy for even the trained person to fall in to an opportunist use of their speciality. And if, like Paul, they are working as an executive of an activist group they don’t have anyone around them to challenge such distortions.

Irish data and reliance on inter-country comparisons

I am pleased Paul admits to being “hasty” in his dismissal of the Irish data. But there are two issues.

1: His problem was more than haste – I was objecting to his attempt to belittle the data by suggesting the Irish workers were biased. I expressed surprise that he would reject the data with that suggestion in a scientific exchange.

2: He appears confused – despite my clear explanation of the data I used. These was the same as used by Cheng et al (2007) – for just one country (Ireland) but separated into the fluoridated and unflouridated areas – not just using the average that Cheng et al used). Paul describes the data as “comparing tooth decay in the Republic of Ireland and Northern Ireland.” Clearly it did not.

Perhaps Paul’s fixation with Declan Waugh’s discredited comparisons of the health statistics for the two countries was pro-occupying Paul’s mind – or perhaps he wanted to divert the discussion into that area.

I repeat the comparison I used below.

The dotted line in the RH figure is effectively what Cheng et al (2007) used for Ireland in the LH figure.

At the time I explained the problems in making the inter-country comparisons Paul was insisting on:

“Simple comparison of countries obscures all sorts of effects such as differences in culture, history, social and political policies, etc. Such plots are also influenced by changes and differences in dental treatment and measurement techniques.”

However, as Paul raises the issue again it is worth commenting again on the flippant way he and other anti-fluoridation propagandists use inter-country comparisons like this. This is the hand-waving involved in claiming the data shows no effect of different fluoridation policies. I will use a figure from Paul’s book to illustrate the problem.

Paul claims his figure shows no difference between the countries – but did he do anything to check that? Did he actually measure the slopes for the different countries? Or did he just wave his hands and say there is clearly no difference?

Fortunately with so few countries it is relatively easy to compare the slopes. I have done so using the data from the WHO site and found the average decline was 0.17 DMFT/year for fluoridated countries and 0.13 DMFT/year for the non-fluoridated countries. This suggests the decline of DMFT in the fluoridated countries was about 25% greater than in the non-fluoridated countries.

Local anti-fluoridation activists reacted strongly to my analysis claiming it is obvious that the analysis is useless. I am sure Paul will point out that the figure of 25% will not be statistically significant – and I agree. The scatter in the rates of decline among the different countries is very large. On top of that the original data itself is hardly very good with generally only 2 data points for each country.

But if the variation is great enough to make a 25% difference in slopes non-significant then what value do such figures have for Paul’s argument? Using simple hand waving and eye-balling to claim no difference is deceptive because he hides that variation. We just don’t expect such comparisons to show the differences due to fluoridation policies. Variation and the influence of confounding factors have too great an influence.

Paul continues to ignore systemic role

Although he concedes it wrong to create the impression that the current surface or topical mechanism for the beneficial role of fluoridated water on existing teeth is the only mechanism he still persists in ignoring any role for ingested fluoride. Any systemic effect. He asks “why are we forcing people to swallow fluoridated water at all?” He ask why I am “not merely advocating swishing and spitting out fluoridated water, or fluoridated mouthwash or using fluoridated toothpaste.”

I have answered that question several times but Paul continues to ignore my response. He claims my  description of the normal and natural role of fluoride in bioapatites do not get is anywhere. He ignores my reference to scientific reports of the participation of ingested fluoride in improving oral health, especially through its beneficial role before teeth erupt.

Unfortunately Paul cannot get past his emotive description of a social health policy as “forcing” something on people. His naive assertion that normal consumption of water should be replaced by “swishing and spitting out” or by a mouthwash or toothpaste also shows he just does not understand the nature of a social health policy. I discussed this in more detail in my last article.

Hirzy’s conspiracy theory

Paul’s colleague in FAN, Bill Hirzy, is unhappy about my reference to his use of a conspiracy theory – the claim that fluoridation is used as a way of disposing of industrial waste. I was referring to Bill’s claim in his section of Paul’s article:

“Water fluoridation, especially with FSA in the U.S., is not at all about improving dental health; it is rather about U.S. taxpayers paying phosphate producers billions of dollars for the privilege of having our public drinking water systems used to dispose of an acid that would otherwise have to be managed in a hazardous waste facility, and thereby improving the bottom lines of phosphate producers.”

He defends himself by attempting a diversion into USGS data showing 94% of fluoroslicic acid produced as a byproduct by phosphate manufacturers goes to water fluoridation systems.

I don’t doubt those figures. M. Michael Miller, in his article Fluorspar gives similar data for 2004:

“About 38,700 t of byproduct fluorosilicic acid valued at $5.15 million was sold for water fluoridation, and about 1 2,300 t valued at $2.71 million was sold or used for other uses”

Miller’s 75% of byproduct fluorosilicic acid sold for water fluoridation is lower that the 94% Hirzy quotes but the difference could result from some of the material being converted to other products before sale.

So, if a quarter of byproduct fluorosilicic acid, or its conversion products, find markets other than water fluoridation what is it about this quarter which makes it a valuable, saleable product – while the 75% sold for water fluoridation must be classified as a waste product and need a conspiracy for its disposal?

Extensive possibilities for fluorosilicic acid uses

As mentioned above there is certainly a market for fluorosilicic acid,and it’s conversion products, apart from use as a water fluoridation agent. I believe that market will probably increase further because the decline in fluorite sources will increase the use of phosphate ores as a source of fluorine chemicals. This will mean that fluorosilicic acid will become more commonly used as an intermediate in the preparation of many, if not most, fluoride chemicals produced.

Currently fluorosilicic  acid can be used in the tanning of animal hides and skins, oil well acidifying, electroplating, glass etching, as a commercial laundry sour,  sterilising agent, in cement and wood preservatives, in the manufacture of ceramics, glasses and paints, in lead refining, etc. it can also be used to manufacture hydrofluoric acid, another important industrial chemical and intermediate for many other fluorine compounds. It can also be converted to aluminium fluoride and cryolite which are important  in the   conversion of alumina ores to aluminium metal.

Ultimately the fluorosilicic acid byproduct from the phosphate industry could become the Teflon on your frying pan, the refrigerant compound in your refrigerator or incorporated in the many products you use every day.


Anyone wanting to follow the debate and/or check back over previous articles in the debate can find the list of articles at Fluoride Debate.

See also:

Similar articles on fluoridation
Making sense of fluoride Facebook page

Fluoridation debate: Against Fluoridation Thread. Part 6.

This is Paul Connett’s response to Ken Perrott’s last article Fluoridation debate: Why I support fluoridation – 2nd reply to Connett.

For Ken Perrott’s original article see – Fluoride debate: Why I support fluoridation.


When is Ken going to present his case for fluoridation?

In his thread Ken has had three opportunities to present the Case for Fluoridation, but he seems to be content to nibble around the edges. His stating over and over again that the fluoride ion is a natural constituent of apatites doesn’t get us very far. I was expecting by now that Ken would have tackled three basic questions head on:

1) Is it Ethical?

2) Is it Effective?

3) Is it Safe?

The ethics

I was expecting the ethical case to be tackled with rigor, but Ken quickly dismissed the central question of whether fluoridation was medical treatment as simply a matter of semantics. Clearly, if fluoridation is medical treatment or even simply human treatment, it violates the individual’s right to informed consent for such treatment. So simply declaring this to be a matter of semantics dodges a very important issue – and for many opponents of fluoridation the central issue.

So let me ask Ken if he will accept this two-part definition of a medicinal product from the European Union Directive 2004/27/EC:

Medicinal product:

(a) Any substance or combination of substances presented as having properties for treating or preventing disease in human beings; or

(b) Any substance or combination of substances which may be used in or administered to human beings either with a view to restoring, correcting or modifying physiological functions by exerting a pharmacological, immunological or metabolic action, or to making a medical diagnosis.

No RCTs after 68 years

As for the second and third questions I was expecting Ken to layout the scientific studies that had convinced him that fluoridation was both safe and effective. Ideally, one would have wanted him to give a link to a randomized controlled trial (RCT) establishing the effectiveness and assessing the safety of this practice. This after all is the gold standard for such matters. However, after 68 years of this practice this has not been attempted.

Failing an RCT one would have wanted to see Ken identify the best quality studies that have convinced him that the practice he advocates and defends actually works to a meaningful extent against a background of other sources of fluoride, and does not present any dangers – especially to those he particularly wants to help, children from low-income families.

Moreover, since this is a practice being forced on millions of people – and in thousands of cases against their expressed opposition –one has the right to anticipate that proponents would be able produce the highest quality studies that overwhelmingly demonstrate their case. With a forced measure like this, one would have anticipated little room for any doubt about whether it worked or not, and by which mechanism it worked. Moreover, should harm be demonstrated at some higher dose level, one would have anticipated that proponents would be able show that the margin of safety would be so high that the even the most vulnerable individuals in society would be protected no matter how much water they drank and no matter how much fluoride they got from other sources.

So where is this overwhelming evidence of effectiveness and safety Ken?

 Ken has ducked key discussions and questions

So far Ken has provided little evidence to demonstrate any of the above reasonable expectations for such a practice. He has even ducked key discussions on the difference between concentration (mg/liter), dose (mg/day) and dosage (mg/kg/day). Comparisons based only on concentrations – and not on dose or dosage – such as used by Siegal and Sparrow in their respective diagrams, are seriously limited if not meaningless. Nor has he addressed even the need for a margin of safety analysis when harm has been found at high doses. Ken does not deny that harm (e.g. hip fractures and lowered IQ) has been found only that the concentration (ignoring the issue of dose) was too high to be of significance

This refusal to lay out his case in comprehensive scientific terms was most clearly revealed in his response to two things I asked for in my last posting:

 a) Where is the body of scientific evidence that indicates that fluoride is not a neurotoxicant?

b) Provide a list of primary studies that have most convinced him that fluoridation is safe for the bottle-fed infant and lifelong exposure for the adult.

As far as a) is concerned, I offered a large body of evidence that fluoride was a neurotoxicant:

 Over 40 animal studies show that prolonged exposure to fluoride can damage the brain.

19 animal studies report that mice or rats ingesting fluoride have an impaired capacity to learn and remember.

12 studies (7 human, 5 animal) link fluoride with neurobehavioral deficits

3 human studies link fluoride exposure with impaired fetal brain development

37 out of 43 published studies show that fluoride lowers IQ, of which 27 were part of a meta-analysis conducted by a team from Harvard (Choi et al.) (www.fluoridealert.org/issues/health/brain)

Contrary to arguments by proponents the vast majority of these IQ studies were carried out at concentrations which offered little or no margin of safety to protect all children in a large population drinking uncontrolled amounts of fluoridated water and getting fluoride from several other sources, including sources unlikely to be available to many of the children in these studies (e.g. fluoridated toothpaste and bottle-feeding with formula made up with fluoridated tap water). Up to 10 of the studies in the Choi analysis had levels in the high fluoride village of 3 ppm or less.

So that was the weight of evidence on my side of the pan scale, it is only after seeing what Ken can put in the pan on his side of the scale that independent observers can make a scientific judgment on the true weight of evidence (see more below). Only then can we know if it is wise to ignore the many red flags being waved on this issue.

But Ken ignored this reasonable request preferring instead to rehash his criticisms of just Xiang’s work.

The need for a weight of evidence approach

What we need here – not only on neurological effects but for all the health concerns – is a weight of evidence approach. In this approach the quality, quantity, and relevance of all available evidence should be weighed and balanced (synthesized) to arrive at a conclusion. For the question of fluoridation, some of that evidence comes from animal experiments, some from epidemiological studies, some should come from RCTs on effectiveness (which amazingly -as indicated above – don’t exist for fluoride), some from medical case reports, some from basic biological/chemical/physical knowledge, and some from ethical considerations. This is what the National Research Council did in its 2006 report (except the NRC didn’t examine the ethical issues), and what we tried to do in our book and what I had hoped Ken would have attempted in presenting his Case For Fluoridation.

As far as b) is concerned, this was Ken’s reply:

 Paul wants me “to list the primary studies that you have read which most convinced you that fluoridation is both safe for the bottle-fed baby and for the adult over lifelong exposure.” In thinking about this I have concluded it is a strange request because I don’t think creative scientists think that mechanically.

My concepts and ideas derive from multiple sources – I never put my eggs all in one basket as it were. I can find I am impressed by something in a paper which also has something which doesn’t impress me. Consequently I take what I can from wherever I can and try to critically understand what I read.

It’s a bit like that with people. You have to accept them warts and all and avoid the immaturity of placing anyone on a pedestal – a sure way to later find they have feet of clay.

So unfortunately I cannot satisfy Paul’s request. He will have to deal with the actual arguments I put forward.

I am sorry Ken, I don’t mean to be rude but I find this response a total waffle. If you have the science to support the safety of fluoridation – and can discount many of the health concerns that I and others have raised – then you should be able to present that case using primary health studies, and preferably primary health studies carried out in NZ. You should then be able to buttress that with all the other scientific information available and then apply a weight of evidence analysis as discussed above. After all it is a practice you want to see imposed on others; as such it is your case to win. If you can’t do that then your support of water fluoridation is highly suspect and amounts to little more than posturing. So I would like to tighten up this discussion and ask you some very specific questions.

A few very specific questions pertaining to health concerns

At the outset, before I lay out these questions, I have to acknowledge the fact that in some respects this is not a level playing field for opponents and proponents of fluoridation. It may appear that I am demanding too much from Ken. I admit that the matter is intrinsically unfair. For a critic of fluoridation it is only necessary to produce one ugly fact – one health concern that has not been resolved – to put the practice into question. I can produce several.

On the other hand a proponent of a measure that is being forced on millions of people should be on top of every health concern. A proponent should be able to demonstrate (or at least feel satisfied) that every health concern has been addressed in such a way (i.e. via careful study) so as to leave no residual concerns. It is tough burden but is the nature of the beast when proposing or supporting a health measure that is forced on millions of people.

The shocking fact is that many health questions were unresolved when fluoridation was launched in 1945 and endorsed by the US Public Health Service in 1950 (see chapters 9 and 10 in The Case Against Fluoride…).

There are many health concerns that have not been carefully studied

I am afraid that the sad truth is that there are many serious health concerns with respect to swallowing fluoride and lifelong exposure to fluoridated water and other sources in our daily lives that have simply not been carefully studied in fluoridated countries and thus still unresolved. The York Review (McDonagh et al., 2000) reached this conclusion in 2000, as did the chairman, John Doull, of the NRC (2006) review. In an interview in Scientific American (Jan, 2008), the NRC chairman was quoted as saying:

“What the committee found is that we’ve gone with the status quo regarding fluoride for many years—for too long really—and now we need to take a fresh look . . .In the scientific community people tend to think this is settled. I mean, when the U.S. surgeon general comes out and says this is one of the top 10 greatest achievements of the 20th century, that’s a hard hurdle to get over. But when we looked at the studies that have been done, we found that many of these questions are unsettled and we have much less information than we should, considering how long this [fluoridation] has been going on.” (Fagin, 2008).

Doubtless Ken will point out that Doull has since made a statement supporting water fluoridation, which has been circulated by proponents. However, his own personal opinion of water fluoridation does not diminish in any way his comments on the poor quality of the research on this matter. What is even more distressing is that since the NRC (2006) report was published practically none of the research recommended by the committee has been carried out.

Ken will find out for himself how poorly fluoridated countries – especially New Zealand – have investigated the health concerns pertaining to fluoridation, if he opens his parachute and seeks answers to the very specific questions I have listed below.

My specific questions for Ken pertaining to health concerns

1) Can you find studies that have convinced you that lifelong exposure to fluoridated water and other daily sources of fluoride (i.e. total daily dose of fluoride) is not increasing the risk of arthritis or arthritic-like symptoms, which have been identified as being the first symptoms of fluoride toxicity in research on skeletal fluorosis (see, e.g., Boillat 1980; Czerwinski 1988; Hileman 1988). These symptoms occur long before we reach bone levels that cause crippling skeletal fluorosis, the only end point considered by the US EPA when they determined the safe drinking water standard for fluoride in 1986 (i.e. 4 ppm).

2) Repeating two earlier requests, can you produce the studies that have convinced you that long term exposure to fluoridated water and other common sources of fluoride causes no damage to individuals with impaired kidney function?

3) Can you find studies that have convinced you that exposure to fluoridated water and other daily sources of fluoride (i.e. total daily dose of fluoride) is not increasing the risk of lowered thyroid function, including among those with suboptimal iodine intake (Galleti and Joyet, 1958; Lin 1991). This is an especially relevant question in light of the increase in iodine deficiency seen in the U.S. and other western nations over the past 30 years, as well as the large increases in the incidence of hypothyroidism. Lowered thyroid function would be one explanation for lowered IQ and would also explain the delayed eruption of the teeth for which there is some evidence.

4) Can you find any study that has refuted the key finding by Bassin et al., 2006, that there appears to be an age-specific nature to the risk of boys developing osteosarcoma when exposed to fluoride? In a matched case-control study Bassin found that boys exposed to fluoridated water in their 6th to 8th years had a 5-7 fold increased risk of succumbing to osteosarcoma by the age of 20. Note: The much-anticipated study by Bassin’s thesis advisor Chester Douglass (Kim et al, 2011) failed to address Bassin’s central thesis concerning the age-specific nature of the risk despite prior claims that it would (Joshipura and Douglass, 2006)

5) Can you find any attempt by any health agency in any fluoridated country to investigate in a scientific manner a) the many anecdotal reports, b) case studies by Waldbott, 1955; Shea et al., 1967; Grimbergen, 1974; Petraborg, 1974, 1977; and c) a clinical trial by Feltman, 1956 and Feltman and Kosel, 1961, that suggest that some individuals (may be 1% of the population) are very sensitive to low levels of fluoride exposure (e.g. 1 mg per day)? These individuals report experiencing a variety of symptoms that are reversed when the source of fluoride is removed and reappear when the fluoride is introduced. Please note: The Australian National Health and Medical Research Council recommended such scientific studies be carried out in 1991 (NHMRC, 1991), but not one has been carried out in the 22 years since this recommendation was made. See more discussion on this topic in chapter 13 of our book and in Spittle (2008).

6) Can you find any attempt by any health agency in any fluoridated country to follow up the finding by Schlesinger et al, 1956 in the Newburg-Kingston, NY fluoridation trial, that the young girls in the fluoridated community were menstruating on average 5 months earlier than the young girls in the non-fluoridated community?

7) Repeating an earlier request discussed above, can you provide a list of animal and human studies that nullify the weight of evidence I have listed above that indicate that fluoride is a neurotoxicant with an inadequate margin of safety to protect all children (including those with nutrient deficiencies) drinking uncontrolled amounts of fluoridated water in addition to fluoride ingested from other sources?

8) Can you point to any studies conducted in fluoridated countries that have convinced you that exposing babies to fluoridated water causes no other damage to their developing tissues other than the damage to their growing tooth cells leading to dental fluorosis? Or is this just wishful thinking on the part of proponents? Is it likely that the fluoride ion would confine its biochemical interference only to the growing tooth cells? What about bone cells? Brain cells? Thyroid gland cells?

9) Can you find any study carried out in NZ or any other fluoridated country that has set out to assess total exposure to fluoride by monitoring fluoride levels in bones at either biopsy during operations or at autopsy? Note: this was another suggestion made by the Australian NHMRC in 1991 but was never pursued by any Australian health agency.

10) What studies carried out in NZ have investigated any health concerns in fluoridated communities? I couldn’t find many can you? Would you agree that the absence of study is not the same as absence of harm?

The evidence of fluoridation’s effectiveness is weak

Similarly, we need to tighten up the discussion of fluoridation’s effectiveness. A scientific proponent like Ken should be able to present the primary scientific studies and weight of evidence analysis that has convinced him that drinking fluoridated water leads to a significant reduction in tooth decay. Being able to offer a theoretical mechanism of action (and I discuss some of Ken’s ideas on this below) is only part of the requirement.

In chapters 6-8 of our book we present the case that the evidence that swallowing fluoride or drinking fluoridated water reduces tooth decay by a significant amount – is very weak – especially in the permanent teeth. This is especially apparent in the larger studies like the US National Institute of Dental Research (NIDR) study reported by Brunelle and Carlos in 1990 (this incidentally was the largest survey of tooth decay ever carried out in the US). The authors looked at 39,000 children in 84 communities and reported an average saving in tooth decay for 5 to 17-year-olds of just 0.6 of one permanent tooth surface (see Table 6). This meager saving of 0.6 of one tooth surface out of over 100 permanent tooth surfaces in a child’s mouth was not even shown by the authors to be statistically significant. I think for most people such a benefit – even if it was real – would be of an insufficient magnitude to justify forcing the practice on people or taking the many health risks involved, especially the possibility that we may be lowering the IQ of some of our children.

So where are the comparable studies that Ken has read that offset the Brunelle and Carlos study and the other studies and reviews that we cite in chapters 6-8 (Ziegelbecker, 1981, 1993; Leverett, 1982; Colquhoun, 1984, 1986,1987, 1990, 1992, 1995 and 1997; Diesendorf, 1986; Colquhoun and Mann, 1986; Gray, 1987; Yiamouyiannis, 1990; Steelink, 1992; Teotia and Teotia, 1994; Spencer et al., 1996; de Liefde, 1998; Kumar et al., 1998; Colquhoun and Wilson, 1999; Locker, 1999; McDonagh et al, 2000; Kumar et al., 2005; Komárek et al, 2005; Cheng et al., 2007; Pizzo et al., 2007; Osmunson, 2007 and Warren et al., 2009).

To these studies we must add in a weight of evidence approach two other facts: 1) several modern studies have not found tooth decay to increase when fluoridation has been stopped in various communities in Finland, former East Germany, Cuba and British Columbia, Canada and 2) the many press reports from major cities in the US of a dental crisis in low-income areas even though they have been fluoridated for over 20 years (for citations see Chapter 8 in The Case Against Fluoride…).

Again what we are looking for here is a presentation of the evidence by Ken that would persuade an independent observer that the weight of evidence for effectiveness is very strong and outweighs the evidence of little benefit presented in the studies cited above.

Ken’s topical mechanism via saliva and plaque

 As with other proponents of fluoridation, Ken asserts that fluoridated water works topically, by increasing the level of fluoride in saliva and plaque. There is scarce data, however, to support this claim. Ken cites four papers (only one of which is a primary study), but as I discuss below, these papers do little to answer the key questions: namely: (1) are the saliva and plaque F levels produced by fluoridation high enough and of sufficient duration to prevent caries, and, if so, (2) are the differences in saliva and plaque F levels between children in fluoridated and non-fluoridated communities of sufficient magnitude to produce a meaningful difference in caries?

There is scarce data in the four papers Ken cites (Cury & Tenuta 2008, Martínez-Mier 2012; Featherstone 1999, Bruun & Thylstrup 1984). Of the papers, only Bruun & Thylstrup 1984 is an actual study, and it deals with a high-fluoride community (2.31 ppm), and thus, were it a study on adverse health effects, I suspect Ken might claim it irrelevant to fluoridation.  But, assuming it is relevant, it’s worth noting that – although the authors found a lower caries rate in the high-F community (vs a community with 0.36 ppm) — the authors note that their “analyses relating the individual fluoride concentrations in whole saliva to the clinical caries scores within each of the two areas indicated that no causal relationships seem to exist between these two parameters.” So, while the authors conclude that “frequently increased availability of fluoride in the oral fluids due to [waterborne fluoride] has an important relationship to the reduced caries experience observed in the high F area,” their conclusion can be questioned, particularly as it relates to the 0.7 ppm water F level used in fluoridated communities.

So, what is the evidence that the saliva and plaque levels produced by fluoridated water exerts a significant topical benefit? According to the reviews that Ken cites (and the notably few studies that these reviews reference), the average saliva F level among children in a community with 1.2 ppm fluoride is 16.5 ppb with daily fluctuations that range as high as 144 ppb (Oliveby 1990, cited by Cury). To put these saliva levels in context, Featherstone states that 30 ppb is the lowest level at which fluoride has been observed to have an effect on tooth mineralization, with >80 ppb being the “optimum” (Featherstone 1999). Featherstone supports this statement by citing a single study – Brown (1977). Assuming that Brown’s study can be replicated, it is evident that the average saliva F level in a 1.2 ppm community — let alone a 0.7 ppm community — is not sufficient to affect tooth mineralization. Any topical effect of fluoridated water, therefore, must either come from the transient spikes in saliva F or the residual F in plaque. Judging by the papers Ken cites, the evidence supporting either of these scenarios is meager at best.

I’ll start first with the transient spikes in saliva F. While spikes in saliva F in fluoridated areas can exceed the levels (30 to 80 ppb) that Featherstone claims can affect teeth, this does not tell us a great deal. To be relevant, it must be shown that the transient spikes are not only high enough, but long enough, to have an effect. Neither Featherstone, nor any of the other papers cited by Ken provides data to answer this question. Further, even if the transient spikes are of sufficient duration to have an effect, it must be asked whether this effect is of any practical import in the current era when the vast majority of children in non-fluoridated areas brush their teeth with fluoride toothpaste? The importance of this latter question is obvious in light of Featherstone’s observation that “fluoride can be retained at concentrations in the saliva between 0.03 and 0.1 ppm for 2-6 hours” after the use of fluoridated dental products.

I’ll now turn to the question of plaque fluoride. Only one of the papers cited by Ken appears to provide any data on the difference in plaque F levels between fluoridated and non-fluoridated communities (Cury & Tenuta 2008). The plaque F data that Cury & Tenuta cite is not only unpublished, but is at rather stark odds with previously published data (See Whitford 2005). Cury & Tenuta claim “an almost 20-fold difference” in plaque F levels (3.2 ppm vs. 0.2 ppm). Whitford, however, found far higher F levels in the plaque (~50 to 450 ppm) and a far smaller difference (2-to-5 fold) between the fluoridated and non-fluoridated community. But Whitford’s study was itself quite peculiar as the unfluoridated community was in Brazil, but the fluoridated community was in the U.S. If children in the U.S. community had greater exposure to fluoride from other sources (which is not only possible, but likely), then the difference in plaque F levels is even smaller than Whitford’s study suggests.

In any event, whatever the difference in plaque F levels is, we should have ample data showing that this differential is sufficiently large to produce a significant and practical effect. I am unaware of any such study, so I will be quite curious to see how many Ken can cite. This shouldn’t, of course, be a difficult task: if plaque F is considered the main vehicle by which fluoridated water exerts a topical benefit, there should be no shortage of primary studies that Ken can cite demonstrating that the plaque F seen in fluoridated areas [x plaque F level] is far superior to the plaque F level seen in non-fluoridated areas [y plaque F level]. I look forward, therefore, to seeing the studies that Ken cites — particularly when considering that Buzalaf found that toothpastes containing 500 ppm fluoride are not effective at controlling caries (Buzalaf 2013).  By way of reference 500 ppm is more than twice the background plaque F levels seen in fluoridated areas according to Whitford, 2005.

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Anyone wanting to follow the debate and/or check back over previous articles in the debate can find the list of articles at Fluoride Debate.

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