The “heart of the Syrian chemical weapons programme” destroyed?

The Damascus sky lights up with surface-to-air missile fire. Source: Missile Attack on Syria. Photograph: Hassan Ammar/AP

There were no chemical weapons in Damascus. The French, UK and US (FUKUS) surely knew that. So, their missile attack in the weekend had nothing to chemical weapons.

We all know the first casualty of war is the truth. However, it seems that the time truth really gets a flogging is after a highly publicised military operation. All the levels of patriotism, nationalism and bravado are used. No faults can be admitted. And the “enemy” always suffers a horrible defeat.

Then, of course, dissident voices get suppressed or vilified. That is until everyone calms down and the truth starts to sink in.

It has happened before, (remember Iraq). It will happen again. And, although it may be too early to completely burst the bubble of self-declared victory, it happened again in the weekend with the missile attack on Syria by the French, UK and US (the FUKUS team).

The Barezeh Scientific Research Centre, Damascus, before the weekend attack

But the truth is already coming out. The whole attack was based on a lie. The constant reference to proof from classified evidence is complete nonsense. We can see this clearly in the case of the main target – the Barezeh Scientific Research Centre.

This centre was completely destroyed. Most of the missiles launched (76 out of about 105) targeted this centre. But why?

Pentagon Spokesperson U.S. Lieutenant General Kenneth McKenzie declared “We believe that by hitting Barezh, in particular, we’ve attacked the heart of the Syrian chemicals weapon program.”

A Syrian soldier films the damage at the site of the Barzah Scientific Research Center in Damascus on Saturday morning after it was annihilated by 76 missiles. Image source: Daily Mail: Pentagon celebrates airstrikes which ‘crippled’ Syria’s chemical weapons arsenal 

So there you have it. This is maybe the key “fact” that the FUKUS military action centred on. The claim that the  Barezeh Scientific Research Centre was the “heart of the Syrian chemicals weapon program.” That’s where most of the destruction occurred, where most of the missiles were targeted. And US spokespersons claim they have successfully destroyed the Syrian chemical weapons programme.

What does the OPCW say about this centre?

While the FUKUS team has not supplied a single verifiable fact to support their action the Organisation for the Prohibition of Chemical Weapons (OPCW) has supplied plenty of evidence to show the attack was based on a lie. And that evidence was surely known by the intelligence communities in France, UK and USA.

That OPCW evidence is in official reports from their investigators who regularly monitor possible chemical weapons sites in Syria (and other countries). The OPCW regularly monitor the  Barezeh Scientific Research Centre. Here is an extract from one of the latest OPCW reports (23 March 2018) which refers specifically to the Barezeh Scientific Research Centre (see OPCW Document EC-88/DG.1 “PROGRESS IN THE ELIMINATION OF THE SYRIAN CHEMICAL WEAPONS PROGRAMME”).

France, the UK and the USA are, together with Syria, signatories to the Chemical Weapons Convention (CWC). They have access to all these documents. In fact, they have members on the OPCW Executive Council who actively peruse these documents. The permanent representatives are Mr Philippe Lalliot for France, Mr Peter Wilson for the UK and Mr Kenneth D. Ward for the USA. FUKUS must have known that regular inspections did not show the presence of any chemical weapons or relevant chemicals at the Barezh Scientific Research Centre.

OK – they may well argue that these weapons had arrived since the last inspection (last November) or are hidden from the inspectors. If they honestly believed that then they should have used the “‘challenge inspection’ provisions” of the Convention:

“A unique feature of the CWC is its incorporation of the ‘challenge inspection’, whereby any State Party in doubt about another State Party’s compliance can request the Director-General to send an inspection team. Under the CWC’s ‘challenge inspection’ procedure, States Parties have committed themselves to the principle of ‘any time, anywhere’ inspections with no right of refusal.”

Comments from a worker at the centre

The morning after the attack, France 24 interviewed Said Said, an engineer who is head of the centre’s paint and plastics department (see At destroyed Syria lab, workers deny producing toxic weapons):

“The building had three storeys: a basement, ground floor, and second floor. It had labs and departments that were unfortunately completely destroyed, with all their equipment and furniture. Thank God, no one was here. As we work in civilian pharmaceutical and chemical research, we did not expect that we would be hit.”

According to Said Said only non-lethal research and development occurred at the centre. It had been producing antidotes to scorpion and snake venom while running tests on chemical products used in making food, medicine and children’s toys.

“If there were chemical weapons, we would not be able to stand here. I’ve been here since 5:30 am in full health — I’m not coughing.”

The OPCW had visited the site in Barezh in recent years and had declared it free of any toxic weapons.

“The OPCW used to stay in the two upper rooms, and use the labs, and we would cooperate with them completely. The OPCW has proven in two reports that this building and the centre as a whole are empty and do not produce any chemical weapons.”

Update

Here is a video of the interview referred to by France24:

To summarise

The FUKUS group clearly knew there were no chemical weapons at the Barezeh Scientific Research Centre.  They had access to all the OPCW information on that centre. They claim to have relied on classified intelligence to make a different assessment. But that is clearly a lie – not only because “classified’ is the oldest trick in the book to hide the fact there is no evidence. But because any such evidence should have triggered a request by them for a “challenge inspection” – a request which could not have been refused by Syria.

Of course, we are still in the in the propaganda phase of this operation. Patriotism and jingoism are still driving the narrative of officials and politicians. The mainstream media suffers from this too and most real informaiton is coming from alternative media.

But these warmongers have an answer for that. According to Pentagon spokeswoman Dana White:

“The Russian disinformation campaign has already begun. There has been a 2,000% increase in Russian trolls in the last 24 hours therefore we will keep you all abreast of the facts moving forward.”

I expect to be labelled one of “Putin’s useful idiots” (again) or – and this is a new one – one of “Assad’s useful idiots,” any day now for daring to look at the real facts behind this missile attack.

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OPCW on Salisbury poisoning – one step forward, two back?

Organisation for Prohibition of Chemical Weapons headquarters in The Hague. Image credit: Prensa Latina Ready Syria to Cooperate with Organization Against Chemical Weapons

Chemical weapons are a current hot topic. We are bombarded daily with media reports mentioning them. They seem to be driving an increase in international tensions. And all sorts of conspiracy theories are circulating.

In the midst of the fast-moving narratives and claims, sensible people are asking for evidence. That is where the international watchdog, the Organisation for the Prohibition of Chemical Weapons (OPCW) should come in. So I welcome two bits of news which may help in the search for evidence;

1. The completion of the OPCW work requested by the UK to provide independent confirmation of the UK findings on the toxic chemical behind the poisoning of three people (Sergei and Yulia Skripal, a father and daughter, and a local police officer Nicholas Bailey) in Salisbury, UK, and
2. The beginning of the work of an OPCW investigation team, in the Syrian city of Douma where there are claims of a chemical weapons attack.

I will only discuss the OPCW report resulting from the UK request on the Salisbury poisonings – and then only the summary of the report. The UK agreed to declassify the summary but not the full report. We will have to wait until another member state releases the full report – if they ever do. I understand it is “voluminous.”

The summary can be downloaded from the OPCW –  SUMMARY OF THE REPORT ON ACTIVITIES CARRIED OUT IN SUPPORT OF A REQUEST FOR TECHNICAL ASSISTANCE BY THE UNITED KINGDOM OF GREAT BRITAIN AND NORTHERN IRELAND (TECHNICAL ASSISTANCE VISIT TAV/02/18)  These bureaucrats love long titles, don’t they?

It’s only two pages long and really only contains two important paragraphs worth discussing.

Confirmation of UK findings on “identity of the toxic chemical”

This was all the UK requested of the OPCW – that they provide an independent confirmation of the UK findings on the toxic chemical used. Unfortunately the OPCW was not given the mandate to make a full investigation of the incident (as they are now doing in Douma, Syria).

So their findings are (apparently) summarised in paragraph 10:

“The results of analysis by the OPCW designated laboratories of environmental and biomedical samples collected by the OPCW team confirm the findings of the United Kingdom relating to the identity of the toxic chemical that was used in Salisbury and severely injured three people. “

I have two comments on this paragraph.

1: It has been widely misreported. Ideologically driven news media have widely extended the “confirmation” to the UK narrative – the claim that a specific “novichock-type” chemical was used, that it originated in Russia – or even to claim that the OPCW is confirming the whole UK political story. The politicians have, of course, encouraged these misinterpretations. Boris Johnson, UK Foreign Secretary, has claimed a confirmation that the chemical “was a military grade nerve agent – a Novichok,”  (wrong) and that “there remains no alternative explanation about who was responsible – only Russia has the means, motive and record “(see Salisbury incident: Foreign Secretary statement on OPCW report).

Oh well, you know how to detect when politicians are lying, don’t you? Well, we should add “when they give a press release” to “their lips moving.”

An example of media misrepresentation is this from the Wall Stree Journal –  The report puts beyond doubt that it was highly likely Russia carried out the attack on Sergei Skripal and his daughter, using a nerve agent “of high purity”

This is just another example of fake news – especially considering that the UK simply asked for confirmation of their findings on the identity of the chemical used.

2: This paragraph does not actually identify the toxic chemical. It simply confirms the UK findings, without saying what these were. And it goes on to say in paragraph 12:

“The name and structure of the identified toxic chemical are contained in the full classified report of the Secretariat, available to States Parties.”

That is not much use, is it? Apparently they do have specific information about the toxic chemical but they are going to keep it secret. or more specifically the UK is because they could have allowed declassification of the whole report – in the “interests of the transparency” that Boris Johnson claims to support.

Well, let’s look further into this summary to see if we can get an idea of what exactly the OPCW is confirming.

The toxic chemical “identified by the UK”

The most informative section of the summary for this is paragraph 7:

“The team was briefed on the identity of the toxic chemical identified by the United Kingdom and was able to review analytical results and data from chemical analysis of biomedical samples collected by the British authorities from the affected individuals, as well as from environmental samples collected on site.”

Seriously! We are told that the OPCW investigation confirmed the UK expert findings – but we are not told what those findings are – unless we have a security clearance!

I agree – we can vaguely infer what those findings are from the statements of politicians like Theresa May and Boris Johnson. But, as a chemist and not a politician, I would actually like to know what the expert findings of the scientists at Porton Down are.

Findings like these get massaged when they are transferred to politicians and then issued to the media.  Scientists are often put in the position of having their findings misrepresented, exaggerated or downplayed for political interests – and as the misrepresentation is carried out by their political masters they have no comeback. They are effectively silenced.

So, I would love to see the technical findings from the Porton Down scientists, and the technical findings of the OPCW team. Currently, I have no way of reading these unless at some stage another member state (not the UK which classified the report) releases the full document.* I sincerely hope this happens. In this respect, Sergei Lavrov, the Foreign Minister of the Russian Federation, has commented:

“We are currently engaged in a detailed study of this report, there are very interesting moments that arise from reading this document.We will in the very near future try to make them public when experts, both ours and the relevant departments, will deal with this rather voluminous document.”

At the moment all I have is a summary which is strangely very uninformative about the facts. I find its presentation circular – confirmation of the “findings” but the only revelation of the findings is to refer back to the unpublished UK “findings.” Mind you, such circular arguments are commonly used by bureaucrats involved in issues which have political consequences.

So, one step forward. The OPCW has independently confirmed the chemical and structural nature of the toxic chemical used in Salisbury. Good.

But, no specific or scientific information on the very subject the OPCW was asked to confirm – the nature of the toxic chemical used in the Salisbury poisonings.

That, in my view, is two steps back.

*Note: There is already alternative “confidential” information circulating in the media that the Swiss laboratory involved in the “confirmation” of the toxic chemical in the UK samples produced results not mentioned in the OPCW report. These sort of rumours will inevitably continue while the full report remains secret.

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Anti-fluoridationists rejection of IQ studies in fluoridated area.

US anti-fluoride activist Paul Connett claims studies cannot detect an IQ effect from fluoridated water because total fluoride intake is the real problem – but still campaigns against community water fluoridation. Image credit: MSoF “Activist Spouts Nonsense – The Evidence Supports Fluoridation”

This is another article in my critique of the presentation Paul Connett prepared to present to a meeting at Parliament in February.

I deal with his coverage of the studies of IQ effects where community water fluoridation (CWF) is used. There are now actually three such studies (Broadbent et al. 2015, Barberio et al. 2017  and  Aggeborn & Öhman 2016), but Connett pretends there is only one – the Broadbent et al. (2015) New Zealand study.

Maybe because it was the first one to provide evidence challenging his extrapolation of the fluoride/IQ studies (see The 52 IQ studies used by anti-fluoride campaigners) results in areas of endemic fluorosis to areas where CWF is used. It is also the study which seems to have resulted in the most hostility from anti-fluoride campaigners.

So here I will just be sticking with his criticism of the New Zealand study Broadbent et al (2015):

Slide 76 from Paul Connett’s presentation prepared for his February meeting at  parliament buildings

Broadbent’s findings do not “negate all other human studies”

Paul allows emotion to get the better of him as no one is suggesting this at all. The studies Connett refers to are all from areas of endemic fluorosis (see  The 52 IQ studies used by anti-fluoride campaigners), not from areas of CWF.

Broadbent et al (2015) simply concluded that their “findings do not support the assertion that fluoride in the context of CWF programmes is neurotoxic.”  That is a modest statement and Broadbent et al. (2015) simply do not draw any conclusions about the studies Connett relies on. But, of course, Connett is upset because this and similar studies just do not support his attempt to extrapolate results from areas of endemic fluorosis to areas of CWF.

The health problems suffered by people in areas of endemic fluorosis are real and it is right they should be studied and attempts made to alleviate them. But this has absolutely nothing to do with CWF.

“Fatally flawed” charge is itself fatally flawed

Again, Paul has allowed emotions to get the upper hand. It is possible, and necessary, to critique published papers – but critiques should be evidence-based and realistic. Paul’s “fatally flawed” charge (slides 77 & 78) simply displays how much this paper has put his nose out of joint.

But let’s look at the specific “flaws” Paul (and other critics associated with the Fluoride Action Network) claim.

The two villages mindset: Paul alleges that the Broadbent et al (2015) study “essentially compared two groups.” He is stuck in the mindset of most of his 52  studies from areas of endemic fluorosis (see  Fluoride & IQ: The 52 Studies). The mindset of simply comparing the IQ levels of children in a village suffering endemic fluorosis with the IQ levels of children in a village not suffering endemic fluorosis. This simple approach can identify statistically significant differences between the villages but provides little information on causes. For example, most of these studies used drinking water fluoride as a parameter but there could be a whole range of other causes related to health problems of fluorosis.

Professor Richie Poulton, current Director of the Dunedin Multidisciplinary Health and Development Research Unit

In contrast, Broadbent et al. (2015) used “General Linear models to assess the association between CWF and IQ in childhood and adulthood, after adjusting for potential confounders.” The statistical analysis involved includes accounting for a range of possible risk-modifying factors besides CWF., This was possible because the study was part of the Dunedin Multidisciplinary Health and Development Study. This is a highly reputable long-running cohort study of 1037 people born in 1972/1973 with information covering many areas.

The fluoride tablets argument: Connett and other critics always raise this issue – the fact that “In New Zealand during the 1970s, when the study children were young, F supplements were often prescribed to those living in unfluoridated areas.” Often they will go further to claim that all the children in the unfluoridated area of this study were receiving fluoride tablets – something they have no way of knowing.

But the fact remains that fluoride tablets were included in the statistical analysis. No statistically significant effect was seen for them.  Overlap of use of fluoride tablets with residence in fluoridated or unfluoridated areas will have occurred and their influence would be reflected in the results found. Presumably, the effect would be to increase the confidence intervals. As the critics, Menkes et al. (2014), say “comparing groups with overlapping exposure thus compromises the study’s statistical power to determine the single effect of CWF.”  I agree. But this does not negate the findings which are reported with the appropriate confidence intervals (see below).

The point is that the simplistic argument that effects of fluoride tablets were ignored is just not correct. Their effect is reflected in the results obtained.

Potential confounders: Many poor quality studies have ignored possible confounders, or considered only a few. This is a general problem with these sort of studies – and even when attempts are made to include all that the researchers consider important a critic can always claim there may be others – especially if they do not like the results. Claims of failing to consider confounders can often be simply the last resort of armchair critics.

In this case, there is no actual reported association to be confounded (unlike my identification of this problem with the Malin & Till 2015 ADHD study – see Perrott 2017). However, Osmunson et al. (2016) specifically raised possibilities of confounding by lead, manganese, mother’s IQ and rural vs urban residence. Mekes et al. (2014) also raised the rural vs urban issue as well as a possible effect from breastfeeding reducing fluoride intake by children in fluoridated areas.  In their response, Broadbent et al (2015b & 2016) reported that a check showed no significant effect of lead or distance from the city centre and pointed out that manganese levels were too low to have an effect. Broadbent et al (2015b) also reported no significant breastfeeding-fluoride interaction occurred.

Numbers involved: Connett claims the study was fatally flawed because “it had very few controls: 991 lived in the fluoridated area, and only 99 in non-fluoridated” (Slide 77). But the numbers are simply given by the longer term Dunedin study themselves – they weren’t chosen by Broadbent and his co-workers. That is the real world and is hardly a “fatal flaw.”

The 95% confidence intervals

Yes, statisticians always love to work with the large numbers but in the real world, we take what we have. Smaller numbers mean less statistical confidence in the result – but given that Broadbent et al (2015) provides the results, together with confidence intervals, it is silly to describe this as fatally flawed. These were the results given in the paper for the parameter estimate of the factors of interest:

Factor	Parameter estimate	95% Confidence interval	p-value
Area of residence	-0.01	-3.22 to 3.20	.996
Fluoride toothpaste use	0.70	-1.03 to 2.43	.428
Fluoride tablets	1.55	-0.38 to 3.49	.116

Connett did not refer to the confidence intervals reported by Broadbent et al (2015). However, Grandjean and Choi (2015) did describe them as “wide” – probably because they were attempting to excuse the extrapolation of “fluoride as a potential neurotoxic hazard” from areas of endemic fluorosis to CWF.

The argument over confidence intervals can amount to straw clutching – a “yes but” argument which says “the effect is still there but is small and your study was not large enough to find it.” That argument can be never ending but it is worth noting that Aggeborn & Öhman (2016) made a similar comment about wide confidence intervals for all fluoride/IQ studies, including that of Broadbent et al. (2015).  Aggeborn & Öhman (2016) had a very large sample (almost 82,000 were involved in the cognitive ability comparisons) and reported confidence intervals of -0.18 to 1.03 IQ points (compared with -3.22 to 3.20 IQ points reported by Broadbent et al 2015). Based on this they commented, “we are confident to claim that we have estimated a zero-effect on cognitive ability.”

The “yes but” argument about confidence intervals may mean one is simply expressing faith in an effect so small as to be meaningless.

Total fluoride exposure should have been used: Connett says (slide 77) “Broadbent et al did not use the proper measure of fluoride exposure. They should have used total F exposure.  Instead, they used only exposure from fluoridated water.” Osmunson et al. (2016) make a similar point, claiming that the study should not have considered drinking water fluoride concentration but total fluoride intake. They go so far as to claim “the question is not whether CWF reduces IQ, but whether or not total fluoride intake reduces IQ.”

This smacks of goalpost moving – especially as the argument has specifically been about drinking water fluoride and most of the studies they rely on from areas of endemic fluorosis specifically used that parameter.

In their response to this criticism Broadbent et al (2016) calculated estimates for total daily fluoride intake and used them in their analysis which “resulted in no meaningful change of significance, effect size, or direction in our original findings.”

It’s interesting to note that Connett and his co-workers appear to miss completely the point about “wide” confidence intervals made by Grandjean and Choi (2015). Instead, they have elevated their argument to the claim that fluoride intake is almost the same in both fluoridated and unfluoridated areas so that any study will not be able to detect a difference in IQ. Essentially they are claiming that we are all going to suffer IQ deficits whether we live in fluoridated or unfluoridated areas.

This is the central argument of their paper – Hirzy et al (2016). However, the whole argument relies on their own estimates of dietary intakes – a clear example where motivated analysts will make the assumptions that fit and support their own arguments. This argument also fails to explain why the Dunedin study found lower tooth decay in fluoridated areas.

Last time I checked the anti-fluoride campaigners, including Connett, were still focusing on CWF – fluoride in drinking water. One would think if they really believed their criticism that they would have given up that campaign and instead devoted their energies to the total fluoride intake alone.

Conclusions

All studies have limitations and of course, Broadbent et al. (2015) is no exception. However, the specific criticisms made by Connett and his fellow critics do not stand up to scrutiny. Most have been responded to and shown wrong – mind you this does not stop these critics from continuing to repeat them and disregard the responses.

I believe the relatively wide confidence intervals could be a valid criticism – although it does suggest a critic who is arguing for very small effects. A critic who may always find the confidence intervals still exclude their very small effect – no matter how large the study is.

In effect, the narrow confidence intervals reported by Aggeborn & Öhman (2016) should put that argument to rest for any rational person.

References

Aggeborn, L., & Öhman, M. (2016). The Effects of Fluoride In The Drinking Water. 

Barberio, A. M., Quiñonez, C., Hosein, F. S., & McLaren, L. (2017). Fluoride exposure and reported learning disability diagnosis among Canadian children: Implications for community water fluoridation. Can J Public Health, 108(3),

Broadbent, J. M., Thomson, W. M., Ramrakha, S., Moffitt, T. E., Zeng, J., Foster Page, L. A., & Poulton, R. (2015). Community Water Fluoridation and Intelligence: Prospective Study in New Zealand. American Journal of Public Health, 105(1), 72–76.

Broadbent, J. M., Thomson, W. M., Moffitt, T., Poulton, R., & Poulton, R. (2015b). Health effects of water fluoridation: a response to the letter by Menkes et al. NZMJ, 128(1410), 73–74.

Broadbent, J. M., Thomson, W. M., Moffitt, T. E., & Poulton, R. (2016). BROADBENT ET AL. RESPOND. American Journal of Public Health, 106(2), 213–214. https://doi.org/10.2105/AJPH.2015.302918

Grandjean, P., Choi, A. (2015). Letter: Community Water Fluoridation and Intelligence. Am J Pub Health, 105(4).

Hirzy, J. W., Connett, P., Xiang, Q., Spittle, B. J., & Kennedy, D. C. (2016). Developmental neurotoxicity of fluoride: a quantitative risk analysis towards establishing a safe daily dose of fluoride for children. Fluoride, 49(December), 379–400.

Malin, A. J., & Till, C. (2015). Exposure to fluoridated water and attention deficit hyperactivity disorder prevalence among children and adolescents in the United States: an ecological association. Environmental Health, 14.

Menkes, D. B., Thiessen, K., & Williams, J. (2014). Health effects of water fluoridation — how “ effectively settled ” is the science? NZ Med J, 127(1407), 84–86.

Osmunson, B., Limeback, H., & Neurath, C. (2016). Study incapable of detecting IQ loss from fluoride. American Journal of Public Health, 106(2), 212–2013.

Perrott, K. W. (2017). Fluoridation and attention deficit hyperactivity disorder – a critique of Malin and Till ( 2015 ). Br Dent J.

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A conference paper on the maternal neonatal urinary fluoride/child IQ study has problems

Image credit: Do new mothers doing a Ph.D. get enough support?

The anti-fluoride movement has certainly mobilised over the neonatal maternal urinary fluoride study which reported an association with child IQ. They see it as the best thing since sliced bread and believe it should lead to the end of fluoridation worldwide.

They also seem to be putting all their eggs in this one basket and have started a campaign aimed at stopping pregnant women from drinking fluoridated water (See Warning to Pregnant Women: Do Not Drink Fluoridated Water).

So I was not surprised to see a newsletter this morning from the Fluoride Action Network reporting another output from this study – a conference paper (most likely a poster) presented at the  3rd Early Career Researchers Conference on Environmental Epidemiology. The meeting was in Freising, Germany, on 19-20 March 2018.

I had been aware of the poster for the last week so had expected FAN to gleefully jump on it and start promoting it in their campaigns.

Here is a link to the abstract:

Thomas, D., Sanchez, B., Peterson, K., Basu, N., Angeles Martinez-Mier, E., Mercado-Garcia, A., … Tellez-Rojo, M. M. (2018). Prenatal fluoride exposure and neurobehavior among children 1-3 years of age in Mexico. Occupational and Environmental Medicine, 75(Suppl 1), A10–A10.

It’s only an abstract and it may be some time before a formal paper is published, if at all. Posters do not get much in the way of peer review and often not followed by formal papers.  So I can’t say much about the poster at this stage as I never like to make an assessment of studies on the basis of abstracts alone.

But, in this case, I have Deena Thomas’s Ph.D. thesis which was the first place the work was reported. If you are interested you can access it from this link:

Thomas, D. B. (2014). Fluoride exposure during pregnancy and its effects on childhood neurobehavior: a study among mother-child pairs from Mexico City, Mexico. University of Michigan.

I will wait for a formal paper before properly critiquing the poster, but at the moment I find a big discrepancy between the Thesis conclusions and the conclusions presented in the poster abstract.

Thesis conclusions

In her work, Deena Thomas used the Mental Development Index (MDI) which is an appropriate way of determining neurobehavioral effects in young children.

She concluded in her thesis (page 37):

“Neither maternal urinary or plasma fluoride was associated with offspring MDI scores”

And (page 38):

“This analysis suggests that maternal intake of fluoride during pregnancy does not have a strong impact on offspring cognitive development in the first three years of life.”

And further (page 48):

“Maternal intake of fluoride during pregnancy does not have any measurable effects on cognition in early life.”

So – no association found of child MDI score with maternal neonatal urinary F concentrations.

Poster conclusions

But the poster tells a different story.

The abstract concluded:

“Our findings add to our team’s recently published report on prenatal fluoride and cognition at ages 4 and 6–12 years by suggesting that higher in utero exposure to F has an adverse impact on offspring cognitive development that can be detected earlier, in the first three years of life.”

So her conclusions reported in her thesis are exactly the opposite of the conclusions reported in her conference poster!

What the hell is going on?

The data

Obviously, I do not have access to the data and she does not provide it in her thesis. But from her descriptions of the data in her thesis and her poster perhaps we can draw some tentative conclusions.

The table below displays the data description, and a description of the best-fit line determined by statistical analysis, in her thesis and her poster.

Information on data	Thomas Ph.D. Thesis	Conference abstract
Number of mother/child pairs	431	401
Maternal Urinary F range (mg/L)	0.110 – 3.439	0.195 – 3.673
Mean maternal urinary F (mg/L)	0.896	0.835
Model β*	-0.631	-2.40
Model p-value	0.391 – Not significant
95% CI for β		-4.38 to -0.40

*β is the coefficient, or slope, of the best-fit line

Conclusions

Apparently at least 30 data pairs have been removed from her thesis data to produce the dataset used for her poster. Perhaps even some data pairs were added (the maximum urinary F value is higher in the smaller data set used for the poster).

This sort of change in the data selected for the statistical analysis could easily swing the conclusion from no effect to a statistically significant effect. So the reasons for the changes to the dataset are of special interest.

Paul Connett claims this poster “strengthens” the findings reported in the Bashash paper.  He adds:

“This finding adds strength to the rapidly accumulating evidence that a pregnant woman’s intake of fluoride similar to that from artificially fluoridated water can cause a large loss of IQ in the offspring.”

But this comes only by apparently removing the conflicting conclusions presented in Deela Thomas’s Ph.D. thesis. We are still left with the need to explain this conflict and why a significant section of the data was removed.

To be clear – I am not accusing Thomas et al. (2018) of fiddling the data to get the result they did. Just that, given the different conclusions in her thesis and the poster,  there is a responsibility to explain the changes made to the dataset.

From the limited information presented in the poster abstract, I would think the scatter in the data could be like that seen in the Bashash et al. (2017) paper. The coefficient of the best fit line (β) is relatively small and while the 95% CI indicates the fit is statistically significant its closeness to zero suggest that it is a close thing.

However, let’s look forward to getting better information on this particular study either through correspondence or formal publication of a research paper.

Other articles on the Mexican study

Fluoride, pregnancy and the IQ of offspring,
Maternal urinary fluoride/IQ study – an update,
Anti-fluoridation campaigners often use statistical significance to confirm bias,
Paul Connett “updates” NZ MPs about fluoride?
Paul Connett’s misrepresentation of maternal F exposure study debunked,
Mary Byrne’s criticism is misplaced and avoids the real issues

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The 52 IQ studies used by anti-fluoride campaigners

Slide number 30 from Paul Connett presentation prepared for a talk at NZ Parliament buildings in February 2018.

Continuing my critique of the presentation prepared by Paul Connett for his much-publicised meeting at Parliament Building in February. The meeting attracted only three MPs but his presentation is useful as it presents all the arguments anti-fluoride campaigners rely on at the moment.

My previous articles on this presentation are Anti-fluoride activist commits “Death by PowerPoint” and Paul Connett’s misrepresentation of maternal F exposure study debunked.

In this article, I deal with the argument presented in the slide above. it is an argument repeated again and again by activists. Connett has posted a more detailed list of these studies and his description of them in Fluoride & IQ: The 52 Studiesat the Fluoride Action Network website.

Studies in areas of endemic fluorosis

All the 52 studies comment refers to are from regions of endemic fluorosis in countries like India, China, Mexico and Iran where dietary fluoride intake is above the recommended maximum level. People in these areas suffer a range of health problems and studies show cognitive deficits as one of them. However, a quick survey of Google Scholar shows this concern is well down the list (See Endemic fluorosis and its health effects). Only 5% of the Google Scholar hits related to health effects of endemic fluorosis considered IQ effects.

People in high fluoride areas where fluorosis is endemic suffer a range of health problems. Credit: Xiang (2014)

In, most, but not all, cases the major source of fluoride in the diet is drinking water with high fluoride levels (above the WHO recommended 1.5 mg/L). Paul Connett’s logic is simply to extrapolate to low drinking water fluoride concentrations typical of community water fluoridation (CWF). However, we do not see the other health effects like severe dental fluorosis, skeletal fluorosis, etc., where CWF is used.

His logic also ignores the possibility that cognitive deficits may result from other health problems common in areas of endemic fluorosis. Problems such as premature births and low birth weight, skeletal fluorosis or even the psychological effect of unsightly teeth due to severe dental fluorosis.

Comparing “high” fluoride villages with “low” fluoride villages

This approach is simplistic as it simply compares a population suffering fluorosis with another population not. Yes, the underlying problem is the high dietary intake (mainly from drinking water) in the high fluoride villages – but that does not prove fluoride in drinking water is the direct cause of a problem. The examples discussed above, eg., low birth weights or premature births, could be the direct cause.

It is easy to show statistically significant differences of drinking water fluoride and a whole host of fluorosis related diseases between two villages but that, in itself, does not prove that drinking water fluoride is the direct cause. Nor does it justify extrapolating such results to other low concentrations situations typical of CWF.

Paul Connett’s logic ignores the fact that in most of these studies the “low” fluoride villages (which the studies were treating as the control or normal situations where IQ deficits did not occur) had drinking water fluoride concentrations like that used in CWF. It also ignores, or unjustly attempts to dismiss) studies which show no cognitive deficits related to CWF.

A low fluoride concentration study showing an IQ effect

After making a big thing about the large numbers of studies and being challenged by the high fluoride concentrations involved Connett normally goes into a “yes, but” mode and attempts to transfer that credibility of “large numbers” to the very few studies which report effects at low fluoride concentrations.

He usually makes a big thing of the study by Lin et al (1991):

Lin Fa-Fu, Aihaiti, Zhao Hong-Xin, Lin Jin, Jiang Ji-Yong, M. (1991). THE RELATIONSHIP OF A LOW-IODINE AND HIGH- FLUORIDE .ENVIRONMENT TO SUBCLINICAL CRETINISM lN XINJIANG. Iodine Deficiency Disorder Newsletter, 24–25.

Connett claims this study shows a lower IQ when the drinking water F concentration was 0.88 ppm, but the areas suffered from iodine deficiency which is related to cognitive deficits.

The study I reviewed recent by Bashash et al (2017) (see Paul Connett’s misrepresentation of maternal F exposure study debunked) is also on Connett’s list. He doesn’t mention, however, that while an association of child IQ with prenatal maternal urinary fluoride was reported the paper also reported there was no observed association of child IQ with child urinary fluoride concentrations.

Studies not showing an effect

Connett lists 7 studies which showed no effect on IQ. One of these was the well-known Broadbent et al., (2014) study from New Zealand, which he, of course, proceeds to debunk in an irrational and not very truthful manner.

He does not mention the studies from Canada (Barberio et al. 2017 ) and Sweden (Aggeborn & Öhman 2016) which also show no effect of CWF on IQ.

The 6 other studies listed are all Chinese, and not translated. Interesting because Connett’s Fluoride Action Network invested money and time into translating obscure Chinese papers that could support their argument of harm. They obviously did not bother translating those papers which did not confirm their bias.

Conclusion

So, Connett’s 52 studies are rather a waste of time. Based in areas of endemic fluorosis their findings are not transferable to areas where CWF is used. The quality of most papers is low and, usually, the studies are simply a comparison of two villages, one where fluorosis is endemic and the “control” village where it isn’t but drinking water concentrations are like that used in CWF.

Connett simply is not able to properly evaluate, or in some cases even consider, studies which show no effect of fluoride on IQ or were made in areas where CWF exists and no effects are shown.

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Why is it so difficult to get an open discussion on fluoridation?

Yes, I know – everyone’s mind is already made up so participants just talk past each other. People’s positions on this and similar issues have become a matter of identity – people are driven by emotions, not information.

But, the information is there – and while I agree many people are driven by emotions they often attempt to use that information to support their positions. In a sense, the information acts as a proxy for their real driving force – their emotions.

Nevertheless, I have always considered a good-faith scientific exchange on issues like this is possible. I believe the exchange I had with Paul Connett, a US anti-fluoride campaigner, four years ago was a good example of what is possible (see Fluoride Debate or download Connett & Perrott (2014) – the pdf document of the exchange).

So, I always look for the chance to repeat that discussion – and I thought that might happen with my recent articles discussing the Mexican maternal prenatal urinary F/child IQ study. Why, because my recent article Paul Connett’s misrepresentation of maternal F exposure study debunked got a response from Mary Byrne, National Coordinator of Fluoride Free New Zealand. I posted her article as Anti-fluoride group coordinator responds to my article.

I responded to that with Mary Byrne’s criticism is misplaced and avoids the real issues and again I offered her a right of reply.

But no response. In fact, she refuses to answer any of my emails.

OK, I can take a hint – but then I see her claiming on Facebook (see image above) that SciBlogs would not allow this discussion! Would not allow “exposure to both sides!” This is patently untrue and she is completely misrepresenting SciBlogs and me.

Note: SciBlogs is a collection of New Zealand science bloggers. My science-oriented blogs usually appear there by syndication.

The email exchange

So it is worth actually looking at the email exchange where Mary requested publication of her article and we responded. Please note the dates and times and excuse the low magnifications. Here are the emails in sequence:

11 March, 12:51 pm: Mary Byrne requests SciBlogs publish her response to my article.
11 March, 1:06pm: After internal passing on the email, Peter Griffin sends it to me.

Pretty quick service. Remember this was a Sunday.

My response was also pretty quick (considering I usually have my daily power nap at that time). I didn’t have to do much thinking about the issue (please excuse my verbosity).

11 March, 2.11 pm

Mary Byrne did not reply so I went ahead anyway and interpreted the original request to mean that a right of reply post on my blog was acceptable. Her article was posted on Tuesday, March 13 (I already posted on Monday and like to spread posts throughout the week) – Anti-fluoride group coordinator responds to my article. I emailed Mary to let her know her article was posted and I would respond to it.

I posted my promised response to her article on Wednesday, March 14th – Mary Byrne’s criticism is misplaced and avoids the real issues and sent Mary an email to let her know – once again offering her another right of reply.

So, Mary’s claim of SciBlogs not allowing exposure from both sides is completely false.

Incidentally, I have emailed Mary asking her to correct that misrepresentation. She has ignored my email, as she ignored all the other emails I have sent her about this issue. The misrepresentation is still on the Fluoride Free NZ Facebook page.

So, I do not expect Mary to continue this exchange, unfortunately. And I do regret she has chosen to misrepresent the situation in the way she has.

But I guess it is just another case of misrepresentation by an anti-fluoridation activist.

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Mary Byrne’s criticism is misplaced and avoids the real issues

Image credit: BuildGreatMinds.Com

First, thanks to Mary Byrne and FFNZ for this response (see Anti-fluoride group coordinator responds to my article). Hopefully, this will help encourage some good faith scientific discussion of the issues involved in my original article (Paul Connett’s misrepresentation of maternal F exposure study debunked). I am pleased to promote such scientific exchange.

I will deal with the issues Mary raised point by point. But first, let’s correct some misunderstandings. Mary claimed I am a “fluoride promoter” and had “sought to discredit the study via his blog posts and tweets.”

1. I do not “promote fluoride.” My purpose on this issue has always been to expose the misinformation and distortion of the science surrounding community water fluoridation (CWF). I leave promotion of health policies to the health experts and authorities.
2. I have not “sought to discredit the study.” The article Mary responded to was a critique of the misrepresentation of that study by Paul Connett – not an attack on the study itself. This might become clear in my discussion below of the study and how it was misrepresented.

The study

The paper we are discussing is:

Bashash, M., Thomas, D., Hu, H., Martinez-mier, E. A., Sanchez, B. N., Basu, N., … Hernández-avila, M. (2016). Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6 – 12 Years of Age in Mexico.Environmental Health Perspectives, 1, 1–12.

Anti-fluoride activists have leaped on it to promote their cause – Paul Connett, for example, claimed it should lead to the end of community water fluoridation throughout the world! But this is not the way most researchers, including the paper’s authors, see the study. For example, Dr. Angeles Martinez-Mier, co-author and one of the leading researchers,  wrote this:

1. “As an individual, I am happy to go on the record to say that I continue to support water fluoridation”
2. “If I were pregnant today I would consume fluoridated water, and that if I lived in Mexico I would limit my salt intake.”
3.  “I am involved in this research because I am committed to contribute to the science to ensure fluoridation is safe for all.”

Was the reported association statistically significant?

Mary asserts:

“Perrott claims that the results were not statistically significant but his analysis is incorrect.”

That is just not true. I have never claimed their reported association was not statistically significant.

I extracted the data they presented in their Figures 2 and 3A and performed my own regression analysis on the data. This confirmed that the associations were statistically significant (something I never questioned). The figures below illustrating my analysis were presented in a previous article (Maternal urinary fluoride/IQ study – an update). These results were close to those reported by Bashash et al., (2017).

For Fig. 2:

My comment was – “Yes, a “statistically significant” relationship (p = 0.002) but it explains only 3.3% of the variation in GCI (R-squared = 0.033).”

For Fig 3A:

My comment was – “Again, “statistically significant” (p = 0.006) but explaining only 3.6% of the variation in IQ (R-squared = 0.0357).”

So I in no way disagreed with the study’s conclusions quoted by Mary that:

” higher prenatal fluoride exposure, in the general range of exposures reported for other general population samples of pregnant women and nonpregnant adults, was associated with lower scores on tests of cognitive function in the offspring at age 4 and 6–12 y.”

I agree completely with that conclusion as it is expressed. But what Mary, Paul Connett and all other anti-fluoride activists using this study ignore is the real relevance of this reported association. The fact that it explains only about 3% of the IQ variance. I discussed this in the section “The small amount of variance explained“ in my article.

This is a key issue which should have been clear to any reader or objective attendee of Paul Connett’s meeting where the following slide was presented:

Just look at that scatter. It is clear that the best-fit line explains very little of it.  And the 95% confidence interval for that line (the shaded area) does not represent the data as a whole. The comments on the statistical significance and confidence intervals regarding to the best-fit line do not apply to the data as a whole.

Finally, yes I did write (as Mary quotes) in my introductory summary that “the study has a high degree of uncertainty.” Perhaps I should have been more careful – but my article certainly makes clear that I am referring to the data as a whole – not to the best fit line that Connett and Mary concentrate on. The regression analyses indicate the uncertainty in that data by the low amount of IQ variance explained (the R squared values) and the standard error of the estimate (about 12.9 and 9.9 IQ points for Fig 2 and  Fig 3A respectively).

The elephant in the room – unexplained variance

Despite being glaringly obvious in the scatter, this is completely ignored by Mary, Paul Connett and other anti-fluoride activists using this study. Yet it is important for two reasons:

• It brings into question the validity of the reported statistically significant association
• It should not be ignored when attempting to apply these findings to other situations like CWF in New Zealand and the USA.

Paul Connett actually acknowledged (in a comment on his slides) I was correct about the association explaining such small amount of the variance but argued:

• Other factors will be “essentially random with respect to F exposure,” and
• The observed relationship will not be changed by the inclusion of these other factors.

I explained in my article Paul Connett’s misrepresentation of maternal F exposure study debunked how both these assumptions were wrong. In particular, using as one example the ADHD-fluoridation study I have discussed elsewhere (see Perrott, 2017). I hope Mary will refer to my article and discussion in her response to this post.

While ignoring the elephant in the room – the high degree of scattering, Mary and others have limited their consideration to the statistical significance and confidence intervals of the reported association – the association which, despite being statistically significant, explains only 3% of the variation (obvious from the slide above.

For example, Mary quotes from the abstract of the Bashash et al., (2017) paper:

“In multivariate models we found that an increase in maternal urine fluoride of 0.5mg/L (approximately the IQR) predicted 3.15 (95% CI: −5.42, −0.87) and 2.50 (95% CI −4.12, −0.59) lower offspring GCI and IQ scores, respectively.”

I certainly agree with this statement – but please note it refers only to the model they derived, not the data as a whole. Specifically, it applies to the best-fit lines shown in Fig 2 and Fig 3A as illustrated above. The figures in this quote relate to the coefficient, or slope, of the best fit line.

Recalculating from 0.5 mg/L to 1 mg/L this simply says the 95% of the coefficient values, or slopes, of the best fit lines resulting from different resampling should be in the range  -10.84 to -1.74 CGI (Fig 2) and -8.24 to 1.18 IQ (Fig 3A).

[Note – these are close to the CIs produced in my regression analyses described above – an exact correspondence was not expected because digital extraction of data from an image is never perfect and a simple univariate model was used]

The cited CI figures relate only to the coefficient – not the data as a whole. And, yes, the low p-value indicates the chance of the coefficient, or slope, of the best-fit line being zero is extremely remote. The best fit line is highly significant, statistically. But it is wrong to say the same thing about its representation of the data as a whole.

This best-fit line explains only 3% of the variance in IQ – and a simple glance at the figures shows the cited confidence intervals for that line simply do not apply to the data as a whole.

The misrepresentation

That brings us back to the problem of misrepresentation. We should draw any conclusions about the relevance of the data in the Bashash et al., (2017) study from the data as a whole – not just from the small fraction with an IQ variance explained by the fitted line.

Paul Connett claimed:

“The effect size is very large (decrease by 5-6 IQ points per 1 mg/L increase in urine F) and is highly statistically significant.”

But this would only be true if the model used (the best-fit line) truly represented all the data. A simple glance at Fig 2 in the slide above shows that any prediction from that data with such a large scatter is not going to be “highly statistically significant.” Instead of relying on the CIs for the coefficient or slope of the line, Connett should have paid attention to the standard error for estimates from the data as a whole given in the Regression statistics of the Summary output. – For Fig. 2, this is 12.9 IQ points. This would have produced an estimate of “5-6 ± 36 IQ points which is not statistically significantly different to zero IQ points,”  as I described in my article

Confusion over confidence intervals

Statistical analyses can be very confusing, even (or especially) to the partially initiated. We should be aware of the specific data referred to when we cite confidence intervals (CIs).

For example, Mary refers to the CI values for the coefficients, or slopes, of the best fit lines.

Figs 2 and 3A in the Bashash et al., (2017) paper include confidence intervals (shaded areas) for the best fit lines (these take into account the CIs of the constants as well as the CIs of the coefficients). That confidence interval describes the region of 95% probability for where the best-fit line will be.

Neither of those confidence intervals applies to the data as a whole as a simple glance at Figs 2 and 3A will show. In contrast, the “prediction interval” I referred to in my article, does. This is based on the standard error of the estimate listed in the Regression statistics. Dr. Gerard Verschuuren demonstrated this in this figure from his video presentation.

Mary is perfectly correct to claim “it is the average effect on the population that is of interest” – but that is only half the story as we are also interested in the likely accuracy of that prediction. The degree of scatter in the data is also relevant because it indicates how useful this average is to any prediction we make.

Given the model described by Bashash et al., (2017) explained only 3% of the IQ variance, while the standard error of the estimate was relatively large, it is misleading to suggest any “effect size” predicted by that model would be “highly significant” as this ignores the true variability in the reported data. When this is considered the effect size (and 95% CIs) is actually “5-6 ± 36 IQ points which is not statistically significantly different to zero IQ points,”

Remaining issues

I will leave these for now as they belong more to a critique of the paper itself (all published papers can be critiqued) rather than the misrepresentation of the paper by Mary Byrne and Paul Connett. Mary can always raise them again if she wishes.

So, to conclude, Mary Byrne is correct to say that the model derived by Bashash et al., (2017) predicts that an increase of “fluoride level in urine of 1 mg/L could result in a loss of 5-6 IQ points” – on average. But she is wrong to say this prediction is relevant to New Zealand, or anywhere else, because when we consider the data as a whole that loss is “5-6 ± 36 IQ points.”

I look forward to Mary’s response.

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Anti-fluoride group coordinator responds to my article

Image credit: Debate. The science of communication.

My recent article Paul Connett’s misrepresentation of maternal F exposure study debunked got some online feedback and criticism from anti-fluoride activists. Mary Byrne, National coordinator Fluoride Free New Zealand, wrote a response and requested it is published on SciBlogs “in the interests of putting the record straight and providing balance.”

I welcome her response and have posted it here. Hopefully, this will satisfy her right of reply and help to develop some respectful, good faith, scientific exchange on the issue.

I will respond to Mary’s article within a few days.

---

Perrott wrong. New US Government study does find large, statistically significant, lowering of IQ in children prenatally exposed to fluoride

By Mary Byrne, National coordinator Fluoride Free New Zealand.

While the New Zealand Ministry of Health remains silent on a landmark, multi-million-dollar, US Government funded study (Bashash et al), and the Minister of Health continues to claim safety based on out-dated advice, fluoride promoter Ken Perrott has sought to discredit the study via his blog posts and tweets.

Perrott claims that the results were not statistically significant but his analysis is incorrect.

The conclusion by the authors of this study, which was published in the top environmental health journal, Environmental Health Perspectives, was:

“In this study, higher prenatal fluoride exposure, in the general range of exposures reported for other general population samples of pregnant women and nonpregnant adults, was associated with lower scores on tests of cognitive function in the offspring at age 4 and 6–12 y.”

Perrott states the study has “a high degree of uncertainty”. But this contrasts with the

statistical analysis and conclusion of the team of distinguished neurotoxicity researchers from Harvard, the University of Toronto, Michigan and McGill. These researchers have written over 50 papers on similar studies of other environmental toxics like lead and mercury.

RESULTS: In multivariate models we found that an increase in maternal urine fluoride of 0.5 mg/L (approximately the IQR) predicted 3.15 (95% CI: −5.42, −0.87) and 2.50 (95% CI −4.12, −0.59) lower offspring GCI and IQ scores, respectively.

The 95% CI is the 95% Confidence Interval which is a way of judging how likely the results of the study sample reflect the true value for the population. In this study, the 95% CIs show the results are highly statistically significant. They give a p-value of 0.01 which means if the study were repeated 100 times with different samples of women only once could such a large effect be due to chance.

Perrott comes to his wrong conclusion because he has confused Confidence Intervals with Prediction Intervals and improperly used Prediction Intervals to judge the confidence in the results. A Prediction Interval is used to judge the confidence one has in predicting an effect on a single person, while a Confidence Interval is the proper measure to judge an effect on a population. In epidemiological studies, it is the average effect on the population that is of interest, not how accurately you can predict what will happen to a single person.

Despite the authors controlling for numerous confounders, Perrott claimed they did not do a very good job and had inadequately investigated gestational age and birth weight.

Once again Perrott makes a fundamental mistake when he says that the “gestational period < 39 weeks or > 39 weeks was inadequate” and “The cutoff point for birth weight (3.5 kg) was also too high.”

Perrott apparently did not understand the Bashash paper and mistook what was reported in Table 2 with how these covariates were actually treated in the regression models. The text of the paper plainly states:

“All models were adjusted for gestational age at birth (in weeks), birthweight (kilograms)”

Thus, each of these two variables were treated as continuous variables, not dichotomized into just two levels. Perrott’s criticism is baseless and reveals his misunderstanding of the Bashash paper.

Perrott states that the results are not relevant to countries with artificial fluoridation because it was done in Mexico where there is endemic fluorosis. But Perrott is wrong. The study was in Mexico City where there is no endemic fluorosis. Furthermore, the women’s fluoride exposures during pregnancy were in the same range as found in countries with artificial fluoridation such as New Zealand.

The study reports that for every 0.5 mg/L increase of fluoride in the urine of the mothers there was a statistically significant decrease in average IQ of the children of about 3 IQ points. It is therefore correct to say that a fluoride level in urine of 1 mg/L could result in a loss of 5 – 6 IQ points. This is particularly relevant to the New Zealand situation where fluoridation is carried out at 0.7 mg/L to 1 mg/L and fluoride urine levels have been found to be in this range².

There is no excuse for Health Minister, David Clark, to continue to bury his head in the sand. This level of science demands that the precautionary principle be invoked and fluoridation suspended immediately.

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Paul Connett’s misrepresentation of maternal F exposure study debunked

Title slide for Paul Connett’s presentation to parliament

Anti-fluoride campaigners are misrepresenting a recent Mexican study claiming its findings should cause governments around the world to abandon community water fluoridation (CWF). Their claims are unwarranted because the study has a high degree of uncertainty. Activists are misrepresenting the accuracy of the studies findings. Because Mexico has areas of endemic fluorosis the study itself is not relevant to CWF.

Misrepresentation of the Mexican study was a central argument used by US anti-fluoride activist Paul Connett in his recent New Zealand speaking tour. This is shown in the Powerpoint presentation he prepared for his meeting at parliament buildings last month (see Anti-fluoride activist commits “Death by PowerPoint”).

It may have not been used in the end as only 3 MPs turned up. But, given his status in the anti-fluoride movement, this presentation will present the current strongest arguments against CWF. It is therefore worth critiquing his presentation whether it was given or not.

In this article, I will concentrate on Paul’s presentation of the Mexican study and may deal with other arguments used in the presentation in later articles. The paper reporting the study is:

Bashash, M., Thomas, D., Hu, H., Martinez-mier, E. A., Sanchez, B. N., Basu, N., … Hernández-avila, M. (2016). Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6 – 12 Years of Age in Mexico.Environmental Health Perspectives, 1, 1–12.

In Connett’s mind, the study’s results are so overwhelming we should immediately stop fluoridation throughout the world! This was the first and main argument he presented. His title slide and slide no. 10 introducing the study demonstrates the importance to him.

Slide No. 10 introducing Connett’s presentation of the Bashash et al (2017) study.

I have critiqued this study in previous articles – readers can find them at:

Fluoride, pregnancy and the IQ of offspring,
Maternal urinary fluoride/IQ study – an update,
Anti-fluoridation campaigners often use statistical significance to confirm bias and
Paul Connett “updates” NZ MPs about fluoride?

Paul is clearly aware of these articles because he included a note in his presentation about them. I am honoured (it is the only comment in the presentation) and pleased he has made an effort to engage with my critique.

This is what he says:

“Ken Perrott and those who follow him will claim that the wide degree of scatter in the data means the findings of this study are unreliable.  That is an incorrect interpretation of this graph and the study.  The effect size is very large (decrease by 5-6 IQ points per 1 mg/L increase in urine F) and is highly statistically significant.  The fact that urine F can only explain a small amount of the variation of IQ does not invalidate the finding.  Rather, it is a reflection that there are many other factors that affect IQ, most of which are essentially random with respect to F exposure.  For example, individual genetics plays a huge role in IQ (it explains 80% or more of variation in IQ), therefore it would not be possible for F to explain more than the small remaining portion of variation in IQ.  Most studies of other developmental neurotoxins like Pb and Hg find very similar low correlation coefficients, yet there is no debate that their findings are valid.”

This comment provides me with a basis for a more detailed discussion of his use of the study.

The small amount of variance explained

Connett acknowledges my point that the observed relationship with urinary fluoride can explain only a very small amount of the variation in IQ – only 3%. A bit hard to deny considering the high degree of scatter in the data which is obvious even in the slides Connett uses:

Slide 20 where Connett reproduces Fig 2 from the Bashash et al. paper.

But he claims that this:

“does not invalidate the finding. Rather, it is a reflection that there are many other factors that affect IQ, most of which are essentially random with respect to F exposure.”

Here he is, of course, referring to his own “finding” or conclusion – not the authors.

Notice his assumptions:

• Other factors will be “essentially random with respect to F exposure,” and
• The observed relationship will not be changed by the inclusion of these other factors.

Those are huge assumptions. And they are wrong.

Here is a relevant example illustrating the danger of such assumptions – the association between ADHD prevalence and extent of fluoridation observed by Malin & Till (2015). Their association was able to explain between 22% and 31% of the variance in ADHD, depending on the specific data used. Far more than the 3% for the Bashash et al., (2017) study.

Yet, when other risk-modifying factors were included, in this case, mainly altitude, the significant association with fluoridation disappeared. A model including altitude, but not fluoridation, explained 46% of the variability in ADHD (see Perrott 2017 and a number of articles in this blog).

In this case, the incidence of fluoridation was correlated with altitude – fluoridation was simply acting as a proxy for altitude in the Malin & Till (2015) association. So much for Connett’s assurance that other factors “are essentially random with respect to F exposure.”

Other studies have found an association between symptoms of fluorosis and cognitive deficiencies. Choi et al., (2015), for example, reported an association of child cognitive deficits with severe dental fluorosis, but not with water F concentration. But there is a relationship between fluoride exposure and fluorosis prevalence – ie. fluorosis is not random with respect to F exposure. If the health effects resulting from fluorosis are the prime cause of the cognitive deficiency, the inclusion of fluorosis incidence in the multiple regression could produce a model where there is a statistically significant association with fluorosis but not with fluoride expose. That is, the urinary fluoride values could be simply acting as a proxy of fluorosis incidence.

A similar non-random association of premature births and low birth weight could occur because these problems do occur in areas of endemic fluorosis. These could be two of the health issues related to fluorosis but fluoride intake may not be the prime cause (see Premature births a factor in cognitive deficits observed in areas of endemic fluorosis?).

Connett is completely wrong to assume that other risk-modifying factors not considered in the Bashash study would necessarily be random with respect to fluoride exposure. And he is wrong to assume that inclusion of these factors would not change the association of child IQ with mothers’ urinary fluoride reported in the paper.

Notably, the Bashash et al (2017)study did not include any measure of fluorosis as a risk-modifying factor – despite the fact that Mexico has areas of endemic fluorosis. I believe its consideration of gestation period <39 weeks or >39 weeks was inadequate (the normal average period is 40 weeks). The cutoff point for birth weight (3.5 kg) was also high.

The size of the IQ effect

We only have the data in the Bashash et al., (2017) study to go with here and the associations they report are valid for that data. But what about the calculations Connett makes from the reported association.

For example, Connett declares:

” The effect size is very large (decrease by 5-6 IQ points per 1 mg/L increase in urine F) and is highly statistically significant.”

Let’s test this claim – using the association represented in Fig 2 from Bashash, which is the figure Connett and other anti-fluoride activists are using (his slide 20 above).

Firstly, we need to calculate prediction intervals from the data (see Confidence and prediction intervals for forecasted values). The shaded region in the figure used by Connett (Fig 2 in Bashash et al., 2017) represents the confidence interval – the region where there is a 95% probability that a best-fit line for the data lies. The region for the prediction intervals is much larger and Connett may be confused because he has interpreted the confidence interval wrongly. Yet, the prediction intervals are the important measure when considering the effect size.

Here are my graphs for the confidence interval and the prediction interval using data I digitally extracted from the paper (see Maternal urinary fluoride/IQ study – an update).

Let’s consider the predicted values of “child IQ” for urinary F concentrations of 0.5 and 1.5 mg/L.

Urine F (mg/L)	Predicted value	Lower	Higher
0.5	99.8	74.4	125.2
1.5	93.0	67.5	118.4

The prediction intervals are very large. This means the real value for “child IQ” at a urine F value of 0.5 mg/L has a 95% probability of being in the range 74.4 – 125.2. The corresponding range for a urine F concentration of 1.5 mg/L is 67.5 – 118.4. When Connett claims that an increase of 1 mg/mL in mother’s urinary F produces a drop of 5 – 6 IQ points he actually means a drop of 5 – 6 ± 26 IQ points which is not statistically significantly different to zero.

The best-fit line for the data may be statistically significant – but Connett is wrong to say this about his predicted effect of urinary F on child IQ. In fact, over the whole range of urinary F measured there is a 95% probability that IQ remains at 100.

Connett’s claim of a “highly statistically significant” effect size is completely false. If he had simply and objectively looked at the scatter in the data points he would not have made that mistake.

Comparing maternal urinary F levels to other countries

Connett makes an issue of the similarity of maternal urinary F levels found in this Mexcian study to levels found elsewhere. One is tempted to say – so what? After all, I showed above that his claim of a “highly statistically significant” drop in child IQ with increases in maternal urinary F is completely wrong.

He does compare the urine F levels reported by Bashash et al., (2017) with some New Zealand data (Brough et al., 2015) and finds them to be very similar. Interestingly, Brough et al., (2015) reported their urinary F values as indicating fluoride intakes were inadequate for the women concerned. They certainly did not indicate toxicity.

The comparison does highlight for me one of the inadequacies in the Bashash (2017) paper – the inadequate measurements of urinary F. Whereas Borough et al., (2015) used the recommended 24-hr urine collection technique, the data used by Bashash et al (2017) relied on spot rather than 24 hr measurements. These spot measurements were only made once or twice during the pregnancy of these women.

Yes, these were the only F exposure measurements Bashash et al., (2017) had to work with but they are far from adequate.

Conclusions

Paul Connett, as a leader of the anti-fluoridation movement, is completely wrong about the Bashash et al., (2017) study. It will not lead to the end of community water fluoridation throughout the world – nor should it.

He has attempted to ignore, or downplay, the high scatter in the data and the low explanatory power of the relationship between children’s IQ and maternal F exposure found in the study (only 3%). His denial that this relationship may disappear when other more important risk-modifying factors are included is also wrong – as other examples clearly show.

Connett’s presentation of a size effect (5-6 IQ points with a 1 mg/L increase in F exposure) as “highly statistically significant” is also completely wrong. In fact, this size effect is more like 5 – 6 ± 26 IQ points which is not significantly different to zero.

The misrepresentation of this study by Paul Connett and other anti-fluoridation activists demonstrates, once again, that their claims should never be accepted uncritically. This is just one more example of the way their ideological and commercial interests drive them to misrepresent scientific finding.

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Anti-fluoride activist commits “Death by PowerPoint”

We have all sat through boring, and counterproductive, PowerPoint presentations. Boring because the presenter breaks all the rule relevant to the preparation of visual displays. And counterproductive because, in the end, the audience does not remember any of the information the presenter attempts to convey.

David JP Phillips gives some relevant advice on PowerPoint preparation in the video above and similar advice is available online.  All this advice is very helpful for anyone preparing a presentation – although constant reminders of the points and frequent practice or experience are needed to take it on board. The PowerPoint programme seems to tempt even the best presenter to make fundamental mistakes which can reduce the effectiveness of their visual material.

Learning from bad examples

Examples of bad PowerPoint presentations are ubiquitous – but I urge readers to critically consider this recent example. The PowerPoint presentation the anti-fluoride campaigner, Paul Connett, prepared for his recent presentation to a meeting in the NZ Parliament buildings. Fluoride Free NZ (FFNZ) has provided a link to Connett’s presentation – Prof Paul Connett Power Point Presentation to Parliament 22nd Feb 2018.

It has 155 slides for presentation with another 24 extra slides to be held in reserve if he had time. Just the sheer number of slides, let alone the extreme detail on individual slides, violates a basic presentation rule to start with.

Well, I say “prepared” but the recent Fluoride Free NZ newsletter describes it as “The Power Point presentation that Prof Connett showed” to the MPs meeting. I find that hard to believe as only three MPs turned up to the meeting. In such situations, a reasonable person gives up on a detailed presentation and resorts to having a chat with the people who did turn up.

An example of what not to do in a PowerPoint presentation – source  Prof Paul Connett Power Point Presentation to Parliament 22nd Feb 2018

I urge interested readers to download it and have a look. Critique it from the point of view of the advice given by David JP Phillips above. It really is a bad presentation and I don’t believe any objective person could have taken anything meaningful from it. Treat this as a learning exercise.

Mind you, these presentations are usually simply “singing to the choir” – presented to true believers. All indications are that the three MPs who attended that meeting can be described that way. Other MPs were probably well aware that Connett’s presentations given on his recent speaking tour had no relevance to their work – and probably most were aware of his bias and unreliability as a source of scientific information, anyway.

Second reading of fluoridation bill

Parliament will shortly undertake the second reading of the Health (Fluoridation of Drinking Water) Amendment Bill. It is currently 15th on the order paper.  This bill does not deal with the science of fluoridation – parliament wisely leaves that to the experts who can advise them when necessary. The bill simply concerns the procedure for decision-making – specifically suggesting transferring the decision from councils to District Health Boards. The Parliamentary Health Committee has already consulted widely on this – and FFNZ and Paul Connett have had every opportunity to present their views. In fact, Paul Connett and other opponents of fluoridation gerrymandered the system to get much longer presentation times than other submitters. I guess they have plenty of experience of making submissions and know all the tricks.

Note:

Here I am simply treating Paul Connett’s PowerPoint presentation as an example of how not to use PowerPoint. Later I will probably return to his presentation and deal with specific areas where he misrepresents the science.

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