Declan Waugh’s misinformation on fluorosilicic acid

Declan Waugh argued recently that silica species produced when fluorosilicates are hydrolysed in water cause a whole range of health problems and deaths. A new theory for him – silica is the problem, not fluoride! He is wrong, of course (see An open letter to Declan Waugh – new mechanism for fluoride toxicity?).

Declan had previously argued the exact opposite. That fluorosilicates do not hydrolyse completely in water and it is the remaining fluorosilicate species that are toxic and cause all these effects. He summarised his arguments and evidence for this in his 2012 report Hexafluorosilicic Acid, Raw Materials, Manufacture, Toxicity and Public Health Concerns as an Active Ingredient in Drinking Water.

This report is typical of Waugh’s writings. He distorts or misrepresents the literature and makes unwarranted inferences. He is not the only person doing this – it’s a common feature of the confirmation bias and cherry picking endemic to the anti-fluoridation movement. However, for some reason some people consider he is an authority on the subject (perhaps they have been fooled by his own hubristic claims to be an “environmental scientist and fluoride researcher”) so his reports get used as evidence and are something quote. For example, the Hamilton City Council listed one of his reports first in the “scientific evidence” which convinced them to stop fluoridation last year (see When politicians and bureaucrats decide the science ). Mark Atkin, the science and legal spokesperson for the local anti-fluoridation group is also fond of citing Declan Waugh – maybe because Waugh is the only source he can find to support his own confirmation bias.

A poster prepared by Declan Waugh to advertise the decisive effect of his submission to the Hamilton City Council fluoride tribunal

In this article I consider some of the claims Waugh makes in the above report and show how he uses distortions and misrepresentation of the literature he cites to support them.

Exaggerating toxicity of fluoride

This part of Waugh’s report is confused but he quotes the relative toxicities of CaF₂ and H₂SiF₆ (1 to 25) to apparently argue “that 1 ppm of hexafluorosilicic ingested orally is the equivalent of 25 ppm calcium fluoride.”  He then seems to argue that the regulated  concentration limits for fluoride are really for CaF₂ – implying that since we use fluorosilicic acid for water fluoridation we should introduce a factor of 25. He seems to say that the limits should not be 1.5 ppm F (he says is set for CaF₂) but 1.5/25 = 0.06 ppm! He says:

“The drinking water standards were established for the much less toxic calcium fluoride which is listed as a moderately toxic compound compared to hexafluorosilicic acid, which is categorised as extremely toxic.”

All this ignores that the toxic species in CaF₂ is the fluoride anion. This is the same for fluorosilicic acid in drinking water as the fluoride anion is the end product of its hydrolysis when added to water. In fact the relevant species is the fluoride anion whatever the source – NaF, CaF₂ or fluorosilicic acid. So the relative toxicities Waugh quotes for solid CaF₂ and concentrated fluorosilicic acid are irrelevant.

Calcium fluoride is relatively insoluble (about 15 ppm CaF₂ = 7.3 ppm F) so when the solid is ingested there is less dissolved fluoride anion available to exert a toxic effect. That is why it is less toxic than the readily soluble NaF and fluorosilicic acid. But CaF₂ is soluble enough to easily maintain the optimum concentration of fluoride anion required for the beneficial effect (0.7 ppm F). One could use it to fluoridate water – although the mechanics would be difficult as very little dissolves. Whatever the source, NaF, CaF₂ or fluorosilicic acid, the end product in drinking water is the same so introduction of such relative toxicities is misleading.

Claim hydrolysis is incomplete

Waugh says:

“When added to drinking water Hexafluorosilicic acid dissociates into free fluoride ions, it is now accepted that this reaction is not complete with the possibility of some silicofluoride compounds remaining present in drinking water.⁵
It is further known that the following fluorosilicate species may be present in treated water. However current analytical methodologies are not yet available to accurately measure or quantify the level of residual fluorosilicates or fluorosilicon complexes that may be present.”

Strange. He is claiming that we currently do not have the analytical methods to measure or quantify residual fluorosilicates but nevertheless “it is now accepted” and “further known” silica fluoride compounds are present in drinking water. Trouble is neither the table he presents, or the paper he refers to (from which the table is taken) say this. They say the exact opposite!

The table simply lists the different silicofluorides species that have been chemically proposed, reported or inferred in solids, gases or solutions. While some of these may logically exist in water (eg SiF₆^2- and Si(OH)₄) there is certainly no evidence that they all do. His reference 5 (Urbansky, E. T. (2002). Fate of fluorosilicate drinking water additives. Chem. Rev., 102, 2837–2854) concludes:

“that in drinking water supply with a pH of 5 or higher, fluoridated with sodium silicofluoride [hexafluorosilicate] to the extent of 16 ppm or less, all of the silicofluoride is completley hydrolysed to slicic acid, fluoride ion and hydrogen fluoride. There can be no question of toxicity of SiF₄ or SiF₆^2- under these conditions.”

As for rate of hydrolysis Urbansky (2002) clearly says “all the rate data suggest that equilibrium should have been achieved by the time the water reaches the consumer’s tap if not by the time it leaves the waterworks plant.” This “equilibrium” is essentially the complete hydrolysis of the fluorosilicate as Urbansky and Schock (2000) make clear:

“Based on the above information on both the thermodynamics of the hydrolysis reaction and it’s kinetics, we can safely conclude that there is essentially no (<< 1 part in a trillion) hexafluorosilicate remaining in drinking water at equilibrium and that equilibrium is rapidly reached from the combine uncaltalyzed and metal-catalysed reactions.”

Claim reaction of silica with fluoride in stomach and bladder

Waugh claims:

“According to Urbansky, a senior US EPA chemist and expert upon water fluoridation chemicals” such compounds [H₂SiF₆, NaF, Na₂SiF₆ and AlF₃] may exist in artificially fluoridated drinking water as well as in low acidic environments within the human body (i.e. Stomach and bladder) after consumption of fluoridated water.³“

And

“It is also now hypothesized that incomplete dissociated SiF residues may re-associate both at intra-gastric pH and in the bladder which are low ph environments⁹ (thereby exposing the consumer to toxic harm) and during food preparation (low pH soft drinks) producing SiF species including silicon tetrafluoride, (SiF₄), a known toxin. It is also believed that commercial SiFs are likely to be contaminated with fluosiloxanes.”

His reference 3 is to Urbansky (2002) and 9 is to Ciavatta, L., Iulianno, M., & Porto, R. (1988). Fluorosilicate Equilibria in Acid Solutions. Polyhedron, 7(18), 1773–7779.

The falseness of his claim that Urbansky provided evidence of the existence of fluorosilicates in drinking water was discussed above. Urbansky and Schock (2000) actually put the theoretical proportion of silica present as fluorosilicate in the “most acidic gastric conditions” at less 0.0002%. As for Ciavatta et al (1988) – their work has no relevance to the stomach or bladder. They studied the reaction of silicic acid and fluoride in 3 Molar Lithium perchlorate with an acidity between 0.3 and 3 Molar. An ideal solution for the laboratory investigate of chemical equilibria but more extreme than conditions in our stomach and bladder.

So again, Waugh has misrepresented the literature and distorted its relevance to the situation in drinking water and our body.

Nevertheless, Waugh get cited as evidence for incomplete fluorosilicate hydrolysis and for recombination in the stomach. For example Mark Atkin relied on this report of Waugh’s in defending this erroneous claim before the NZ Advertising Standards Authority (see Anti-fluoridation advertising deceptive).

Finney et al (2006) is also often used by anti-fluoridationists to claim recombination in the stomach because they showed presence of an intermediate SiF species at pH values below 3.5 (SiF₅^–). Again this is a laboratory study with higher F concentrations and no interfering species. In the real world drinking water (and especially the stomach content) has all sorts of chemical species, many of which react with F, Si(OH)₄ or both. These will displace any theoretically derived equilibria. I have not seen any reports of detection of silicofluorides species in the stomach or bladder. Nor have I seen anything to suggest that these would be any more toxic than fluoride itself – or any of the other chemical species present in the stomach.

Conclusion

Readers having read my comments here and those on Waugh’s theory about silica toxicity (An open letter to Declan Waugh – new mechanism for fluoride toxicity?) might see a pattern:

• Citation of scientific literature to given credibility to Waugh’s claims;
• Misrepresentation of the cited literature – often claiming they report the exact opposite of what they in fact do;
• Confirmation and cherry picking which is very clear to any intelligent reader;
• Attempt to establish himself as a “scientific authority” on fluoridation which can be used by anti-fluoridation activists to support their own claims.

I guess you can fool some of the people some of the time. But it does show that  such material should always be approached critically and intelligently.

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PS: I would of course welcome Declan Waugh’s response to this article. After all, I might be completely wrong – but I won’t know that without some sort of exchange with him.

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