Tag Archives: fluorosilicate

An open letter to Declan Waugh – new mechanism for fluoride toxicity?

Dear Declan,

You describe yourself as a scientist and fluoride researcher so I feel the responsibility to bring to your attention what I think are major flaws in a recent presentation of yours. I am sure you understand that research and the scientific ethos requires and encourages constructive criticism, and in fact the debate over ideas and hypotheses is an essential part of the scientific process. I offer my criticisms with this in mind and therefore assume you will receive them in the same open spirit  and give them your honest consideration.

Declan-title

In this presentation to the  Nutritional Therapists of Ireland, Health Impacts of Water Fluoridation May 2014 you make several arguments which I think violate basic chemical principles. You then go on to claim a mechanism for many health complaints you claim results from community water fluoridation.This is a novel mechanism because it attributes health problems not to fluoride but to silica resulting from the hydrolysis of fluorosilicates used as fluoridation chemicals.

Below I list the steps in your argument together with my comments on these:

Slide 16:

Declan-15

You claim “ultra fine silica particles”  form on hydrolysis of fluorosilicates. You cite Finney et al (2006) for this. However, nowhere in  Finney et al (2006) is there a reference  to”ultra fine silica particles.”

What they describe is the well-known hydrolysis reaction:

SiF62-(aq) + 4H2O(l) ↔ 4H+ + 6F + Si(OH)4(aq)

The silica species produce is the monomeric molecule Si(OH)4. This soluble (“reactive”) silica exists in solution but has a very complex chemistry. Polymerisation occurs and a number of molecular species are possible in solution. The end product of such polymerisation can be solid silica but, on the other hand, solid silica can support a concentration of monomeric silica in solution.

Yes, molecules in solution are extremely small but it is plain  wrong to describe them as if they were just very small, or “ultra fine,” particles of the solid.

Slide 17:

Declan-17

You now go further describing these molecules as “nanoparticles” and cite Napierska et al (2010) to tell viewers that nanoparticles can have negative health effects. They can be toxic. This is a huge leap, on top of the huge leap in the previous slide.

You have gone from a monomolecular species (Si(OH)4), to a finely divided solid,  to “nanoparticles.”

No way is it legitimate to describe a small molecule like Si(OH)4 as a “nanoparticle.” One definition of a nanoparticle describes is as a “microscopic particle with at least one dimension less than 100 nm.” Simple molecules like Si(OH)4 are thousands of times smaller.

Slide 18:

Declan1w

You now put these ideas together to imply that fluoridation can cause a large range of health problems via formation of nanoparticles during hydrolysis of the fluoridation chemical and their toxic reaction in the bloodstream. I believe your arguments here are false, you have not given any evidence to support them, and in fact you have misrepresented the citations you used.

Silica in drinking water

Your wild “theory” introduces a big can of worms which you should have considered but actually ignore. Silica, reactive or monomolecuar silica, exists in all drinking water, fluoridated and unfluoridated. Here are some examples from New Zealand community water supplies. Please note, fluoridation  is irrelevant. In fact the highest levels of reactive silica occur in an unfluoridated supply.

Fluoride (mg/L) Reactive silica (mg/L)
Hamilton Templeview Site 23.08.13 0.16 37
Hamilton Site 12.02.14 0.19 34
Christchurch Christchurch <0.1 16
Wellington Waterloo 0.78 15.5
Wainuiomata 0.83 12.55
Auckland Auckland 0.81 13.23

None of this is surprising as silica will be derived from all sorts of natural, geological, sources the water contacts.

Did you bother comparing natural levels of reactive silica with what could be expected from the hydrolysis of fluorosilicates? My estimates suggest that fluoridation with fluorosilicate at the optimum level (0.7 mg F/L) would produce a reactive silica concentration of 0.37 mg SiO2/L. Surely you can agree this is miniscule compared with he natural levels of reactive silica in all drinking waters?

Your hypothesis of a toxic role of monomolecular silica in drinking water implies  all drinking water is unhealthy and that, in fact, fluoridation could contribute only an insignificant amount to this toxicity.

A serious charge which most scientists would consider better justification and evidence than you have given so far. Personally I think it would be irresponsible of you not to publicly withdraw these unwarranted claims.

I think there are similar faults in the way you have used statistical health information to imply a link of fluoridation to a whole host of health problems but that is a separate issue. At this stage I look forward to a response to my specific chemical criticisms listed above.

If you wish to defend your hypothesis, or to debate this specific issue and the wider claims you are making, I would be happy to offer you space on the Open Parachute blog for an exchange of articles. This proved a very effective method of scientific discussion in my exchange with Paul Connett (see Fluoride Debate). Many anti-fluoridation activists seem to hold you in the same regard as Paul and rely on your for much of their information. You have also contributed submissions to local body councils in New Zealand considering the fluoridation issue. I am sure you would therefore welcome the opportunity to present your scientific claims to a scientifically literate audience that this exchange can offer.

I look forward to your response.

Kind regards

Ken Perrott.

 

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False balance and straw clutching on fluoridation

The alignment of the poster above with a “balanced” duo of opinion pieces on fluoridation in the recent issue of the Journal of primary healthcare is just too good not to comment on.

The articles are:

Looks a bit uneven, doesn’t it? A Professor of  Dental Epidemiology and Public Health “balanced” against a political  activist? Worse, Atkin’s organisation is an astroturf one set up by the Fluoride Action Network of NZ (FANNZ). Rather clumsily, I add, as they use the same office address! (See Anti-fluoridationist astro-turfing and media manipulation).

Still, I want to comment on the chemical arguments used by Atkin. He is effectively clutching at straws, using very naive interpretations of the chemistry of fluorosilicates and fluoride. As a chemist I find such opportunist distortion of chemistry offensive. Problem is, his and similar arguments are often presented by anti-fluoridation activists and lapped up by their supporters.

Fluorosilicic acid and sodium fluorosilicate are common fluoridating chemicals. When diluted in water the fluorosilicate decomposes to form silica and the fluoride anion. Some anti-fluoridation activists, including Mark Atkin, deny this becuase they wish to deny the relevance of studies showing the safety of fluoride at concentrations used in fluoridating drinking water. So they advance the bogey of  an especially toxic fluorosilicate species. Atkins condenses two of their arguments in this succinct statement:

“Silicofluorides do not fully dissociate to form free fluoride ions in aqueous solution and revert to the silicofluoride ion in acid stomach conditions.”

Hydrolysis of fluorosilicate.

There is some straw clutching going on here in the discussion of the chemistry of fluorosilicates and fluoride which distorts the real chemistry.

The Nuclear Magnetic Resonance work of Finney et al (2006)  (“Reexamination of hexafluorosilicate hydrolysis by 19F NMR and pH measurement”) showed complete decomposition of fluorosilicate species at neutral pH values on dilution. They also showed the presence of surviving fluorosilicate species at low pH values (3 and below) – which is of course irrelevant for water treatment. No one is going to produce drinking water at such acidic values.

Anti-fluoride people are using the observation at low pH values to claim that fluorosilicate species remain in solution at neutral pH values. They sometimes also rely on studies where authors have expressed their results with an indication of precision. For example, Atkin’s activist organisation (the NZ Fluoridation Information Service) claims fluorosilicates:

“do not completely break down into Fluoride ions. This was shown by Crosby in 1969.”

But Crosby (1969) (“Equilibria of fluorosilicate solutions with special reference to the fluoridation of public water supplies”) actually reported:

“sodium fluorosilicate, at the concentration normally present in public water supplies, is dissociated to at least 95%.”

Atkins and his organisation are clutching at a very weak straw there.

Let us be clear – the research indicates that within experimental precision the deocmposition of fluorosilicates is complete and, as expressed by Urbansky (2002), (“Fate of fluorosilicate drinking water additives”):

“equilibrium should have been achieved by the time the water reaches the coinsumer’s tap  if not by the time it leaves the waterworks plant.”

Reversion of fluoride to fluorosilicate?

Atkin’s claim of reversion of fluoride to fluorosilicate “in acid stomach conditions” is also incorrect. He is relying on a simplistic misunderstanding of the nature of “dissociation” of fluorosilicate on dilution.

It is important to recognise the “dissociation” of fluorosilicate species into fluoride and silica at neutral pH values is, in effect, a decomposition. Because of the polymerisation of the silica, and the olation and oxolation reactions involved, the equilibrium is driven to completion – in effect the silica is removed from the reaction. (While it may remain in “solution” or “suspension” for a time it is effectively inert – due to olation – as far as the equilibrium is concerned).

What do I mean by olation? While monomolecular Si(OH)4 is formed on dissociation of the fluorisilicate it rapidly undergoes reactions which lead to exclusion of water and the transformation of Si-OH bonds to Si-O-Si bonds.

(HO)3Si-OH + OH-Si(OH)3

↓ Olation

(HO)3Si-OH-Si(OH)3 + OH

 Oxolation

(HO)3Si-O-Si(OH)3 + H2O

Eventually this leads to formation of colloidal and solid silica. But even while in solution olation and oxolation reduces the reactivity of the silica species.

Just as fluorosilicate species do not reform in your tap water, they do not reform in your stomach. Even if the silica is still in suspension it is no longer present as mono-molecular Si(OH)4 and is effectively inert. So despite the low pH there is no simple equilibrium. Remember too, your drinking water will contain silica derived from other sources besides fluorosilicate (which is probably a minor contributor).

Sure, one can prepares solutions in the laboratory at pH values of 3 or less that contain fluorosilicate species – but once decompostion (involving loss of silica reactivity) occurs at neutral pH values the reaction  is not easily reversed. Especially considering the time lapsed between decomposition of the fluorosilicate and drinking water entering one’s stomach.

HF in stomach

But Atkin still has a fallback postion – if the fluorosilicate doesn’t get you the hydrofluoric acid will. He aserts:

“that 40% of ingested fluoride is absorbed through the stomach wall as molecular hydrofluoric acid (a known mutagen). This negates the ‘all fluoride ions are the same’ deception.”

Yes, in the acid conditions of your stomach F anions will exist in equilibrium with the protonated HF species.

H+ + F ↔ HF

This is also true for other weakly acidic anions – even sulphate – that is just simple chemistry. But, the real danger of the solution in your stomach is that it is very acid, it has a low pH – a very high concentration of hydrogen ions. It is the hydrogen ions that are corrosive. (If anything, the presence of weakly acidic anions like fluoride will actually lower the acidity by removing some of the hydrogen ions). One does not put one’s hand, or any other sensitive tissues, into acidic solution like this. However the stomach is built to handle these conditions.

I understand the molecular species involved in the transfer of fluoride across the stomach wall cells into the blood stream is HF. (Once in the blood HF will convert to fluoride because of the higher pH). So clearly the low pH assists in uptake of F by the body. Don’t forget the concentrations of fluoride, and therefore HF, is actually very low. The protonated species in your stomach solution are not equivalent to the HF (or HCl and H2SO4) chemicals we are used to in their concentrated forms in the laboratory.

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