2015-01-06

This is the third and last article in a series critiquing contributions to the Fluoride Free NZ report “Scientific and Critical Analysis of the 2014 New Zealand Fluoridation Report“ which is aimed at discrediting the recent review Health Effects of Water Fluoridation: a Review of the Scientific Evidence produced by the Royal Society of NZ together with the Office of the Prime Minister’s Chief Science Advisor (hereafter refered to as the Royal Society Review).

My first article, Peer review of an anti-fluoride “peer review”,  discussed Kathleen Theissen’s contribution. (It also discussed a draft contribution by Chris Neurath which does not appear in the final version). The second article, Cherry-picking and misinformation in Stan Litras’s anti-fluoride article, critiques Stan Litras’s contribution. This one discusses H. S. Micklem’s contribution.

See The farce of a “sciency” anti-fluoride report for an analysis of the close relationships between the authors and peer reviewers of the Fluoride Free NZ report and anti-fluoride activist groups.

There are a few smaller articles by Paul Connett and Mark Atkins. They do not deal with the contents of the Royal Society Review so I will not comment on them here.

This article below completes my critique of the Fluoride free NZ report.

H. S. Micklen, who wrote the second article in the Fluoride Free NZ report, is one of the coauthors, together with Paul Connett, of the book  The Case against Fluoride which anti-fluoride activists treat as gospel. His article was “peer-reviewed” by James Beck, the other co-author of the book.

In my comments I use the section headings used by H. S. Micklem.

Dental fluorosis

I think Micklen’s comments on dental fluorsis are quite muddled. He confuses the relevance of the different grades of dental fluorosis and unfairly attributes the more severe forms to community water fluoridation (CWF). Consequently he calculates a cost of dental treatment which is wrong.

Recently I put dental fluorosis, its different grades and its contribution to oral health satisfaction into context with the image below (see Water fluoridation and dental fluorosis – debunking some myths):



Dental fluorosis of grades none, questionable, very mild and mild are common in countries suitable for CWF – in both fluoridated and unfluoridated areas. Fluoridation may cause a small increase in mild grades. But these first 4 grades (none – mild) are judged purely “cosmetic. In fact children and parents often judge the grades “questionable – mild” more highly than “none.” Research finds these milder forms of dental fluorosis often improve dental health related quality of life (Do and Spencer, 2007; Chankanka et al., 2010; Peres et al., 2009; Biazevic et al., 2008; Büchel et al., 2011; Michel-Crosato et al., 2005).

Micklem is straw-clutching to take one reference used by the Royal Society Review out of context to imply that these studies are wrong because “subjects liked the appearance of a complete set of artificially white teeth.” He says “they did not like the whiteness associated with fluorosis.”  But the authors actually say:

“The ranking of images of teeth with a fluorosis score of TF 1 may lead to the inference this sample of 11 to 13 year olds do not consider milder presentations of fluorosis to be aesthetically objectionable. The very white teeth represented an unnatural presentation that could only be achieved by cosmetic procedures. . . . This is consistent with previous work related to dental aesthetics [18,19] whereby teeth with mild forms of fluorosis (TF 1, TF2) were rated similarly.”

Micklem raises the bogey of the cost of veneers (up to $1750 per tooth) but this is just scaremongering as veneers would not be used for teeth with these mild grades of fluorosis.

Moderate and severe grades of dental fluorosis are common in areas where fluorosis is endemic, but relatively rare where CWF is used. Occurences in the later case, despite the low concentrations of fluoride in treated drinking water, will have other causes – high natural levels in well water, industrial pollution, excessive consumption of toothpaste, etc.

Treatment of moderate and severe cases of dental fluorosis using veneers may well be appropriate for a very few young people in countries like New Zealand and the US but it is misleading to attribute this to CWF. Interestingly, Micklem’s misattribution mirrors that of Ko and Thiessen (2014). They also assumed all moderate and  severe dental fluorosis was caused by CWF thereby enabling them to declare no cost benefit to CWF because of the required dental treatments.

Micklem has simply continued the anti-fluoride propagandist tradition of confusing data for the relative amounts of different grades of dental fluorosis and attributing problems with the rare moderate and severe forms to the more common questionable and mild forms.

Neurotoxicity and IQ

In this section Micklem attempts to contrast the Choi et al (2012) metareview with the Broadbent et al (2014) study. He erroneously refers to both as being relevant to CWF and “the case that water fluoridation poses a development risk to human intelligence.”

Let’s make this clear. The Choi et al (2012) review did not include studies of CWF. The authors made clear that their results should not be seen as relevant to CWF. Most of the brief reports they reviewed studied areas of endemic fluorosis and Xiang (2014) (one of the authors of an included study) gives some idea of how this is manifested in a title slide to a recent talk.



The only study Micklem comments on that involved CWF was that of Broadbent at al (2014).  Micklem describes this as “inconclusive” but does not say why. Do I detect some bias there?

Given the available studies I think the Royal Society review was justified in concluding “that on the available evidence there is no appreciable effect on cognition arising from CWF.”

Passing on to the question of the Choi et al (2012) metareview, which is not relevant to CWF. Micklen concedes that included studies were individually  “not strong” but argues “the existence of so many studies almost all saying the same (important) thing” should be treated with attention and respect. I agree – but lets not allow that attention and respect to be blind. Let’s be aware of the limitations and attempt to understand what the results might mean.

The authors of that metareview have extended their work to making their own measurements in a pilot study (Choi et al., 2014). In this new paper they did not find a significant relationship between cognitive deficit measurements and drinking water fluoride. We need to accommodate this finding in our assessment of the metareview.

Choi et al (2014) did find a significant association of cognitive deficits with severe dental fluorosis.  Perhaps we need to respect that finding and give it some attention. Rather than the assuming the mechanism of such cognitive deficits is the speculated but unproven neurotoxic activity of fluoride we should be open to other possible mechanisms (Perrott 2015)..

I have done so with my article Severe dental fluorosis the real cause of IQ deficits? and would welcome any feedback Micklem could give on this. I feel that the effects of a physical deformity like severe dental fluorosis on learning is a more realistic mechanism (for which there is a lot of published evidence) than some sort of vague chemical toxicity which has never been noted at these low concentrations.

Incidentally, Micklem attempts to discredit the Royal Society’s understanding of the Choi et al (2012) saying it suggested that the measured IQ reduction was “arguably negligible.” The Royal Society review actually said:

“Setting aside the methodological failings of these studies, Choi et al. determined that the standardised weighted mean difference in IQ scores between “exposed” and reference populations was only -0.45. The authors themselves note that this

difference is so small that it “may be within the measurement error of IQ testing”.[172]”

Choi et al., (2012) said:

“The estimated decrease in average IQ associated with fluoride exposure based on our analysis may seem small and may be within the measurement error of IQ testing.”

And their abstract reported the “standardized weighted mean difference in IQ score between exposed and reference populations was –0.45 (95% confidence interval: –0.56, –0.35).”

There has been some confusion because Choi et al., (2012) used a standardised weighted mean difference to accommodate the different IQ scales used in the studies they reviewed. But their warning about the small size of the calculated difference and its relationship to measurement errors in IQ testing is relevant.

The Royal Society Review did indeed make a mistake in the executive summary where it referred to a claimed IQ shift of “less than one IQ point” when it should have said “less than one standard deviation.” I discussed this in Did the Royal Society get it wrong about fluoridation? and noted that even Harvard University made the same mistake in its inital press release of the Choi et al (2012) work.

I think the Authors of the Royal Society Review should correct that mistake, as Harvard University did – but it does not change the fact there is no mistake in the review’s evaluation of the Choi et al (2012) paper.

Lead

In this section Micklem attempts to cast doubt on the Royal Society Review’s comments on the form of fluoride in drinking water and a possible role of fluoride in releasing lead from pipe fittings.

The hydrolysis of fluorosilicic acid when diluted during water treatment may not be completely understood (nothing ever is) but recent high quality research (Urbansky & Schock 2000; Urbansky 2002; Finney et al., 2006) has confirmed the review’s statement it is “effectively 100% dissociated to form fluoride ion under water treatment conditions.” Despite acknowledging the need for more and better research Urbansky (2002) concluded “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 debate only exists among anti-fluoride propagandists because of selective and motivated reliance on old and poor quality research, together with confirmation bias. For example, the report by Crosby (1969) that “evidence from specific-ion electrode and conductivity measurements at 25° confirms that sodium fluorosilicate, at the concentration normally present in public water supplies, is dissociated to at least 95%” is interpreted by Coplan et al., (2007) as “proof” the fluorosilicate is 5% unhydrolysed!

Micklem relies on then papers of Master et al., (2000), Copelan et al 2007 and Mass et al., (2007) to argue that fluoride treatment chemical enhances lead release from pipes. However, I think an objective assessment of these paper would conclude the authors argue determinedly for a preconceived hypothesis and that many of their arguments are irrelevant and faulty. This is not to dismiss their finding on lead levels in drinking water – but as Masters et al., (2000) themselves point out – “statistical association should not be confused with causation.”

Similarly, I suggest that Micklen’s reliance on Sawan et al., (2010) to support Copelan’s hypothesis amounts to special pleading as those workers used drinking water concentration of 100 mg/L of fluoride and 30 mg/L of lead.

Osteosarcoma

Micklem uses the old anti-fluoride activist trick of fixating on a cherry-picked paper which fits his agenda and downplaying or attempting to discredit papers which don’t. He concentrates on Bassin et al (2006), despite its description by its authors as “an explanatory study” requiring “further research” to “confirm or refute” its conclusions. That paper fits Micklem’s agenda because it found a statistically increased risk of osteosarcomas in male boys exposed to water fluoridated at 1.2 mg/L F.

In such a complex area, for a cancer with such a low incidence, a balanced overall consideration of research reports is necessary. All papers have their advantages and drawbacks so conclusions should be derived from proper consideration of the total research findings – as the Royal Society review appears to have done.

The Bassin (2006) findings have not been confirmed by any later work – despite a range of such studies (Kim et al., 2011; Comber et al., 2011; Levy and Leclerc 2012; Blakey et al., 2014). The Royal Society Review pointed out previous reviews had all concluded that “based on the best available evidence, fluoride could not be classified as carcinogenic in humans.” And that “more recent studies have not changed this conclusion.”

Micklem hasproduced nothing to counter that conclusion.

Cardiovascular and renal effects

Micklen attempts to use the paper, Martín-Pardillos et al., (2014), cited by the Royal Society Review, against the reviews conclusions. The review presents the paper this way:

“A number of studies indicate that fluoride may reduce aortic calcification in experimental animals and humans.[199] This preventive effect was recently confirmed by in vitro experiments, but in vivo findings from the same studies showed the opposite result – that phosphate-induced aortic calcification was accelerated following exposure of uremic rats to fluoride in water at around 1.5 mg/L.[200] The authors suggested that chronic kidney disease could be aggravated by relatively low concentrations of fluoride, which (in turn) accelerates vascular calcification. However, further studies are required to test this hypothesis.”

Martín-Pardillos et al., (2014) proceeded from the hypothesis that fluoride did not initiate calcification but because it is attracted to calcified deposits it may influence subsequent crystallisation of the calcified material.

Their in vitro results indicated a protective effect against calcification. While the opposite was observed with the 5/6 nephrectomised rats with induced calcification they still concluded:

“The direct inhibition of ectopic calcification could still occur in vivo when the renal function is correct, such as during aging or even the initial stages of diabetes, and this possibility deserves further research.”

This is relevant to healthy humans without chronic kidney disease (CKD).

The acceleration of induced vascular calcification with the 5/6 nephrectomised rats does raise the need for further studies, and monitoring the situation with humans suffering CKD. But let’s not forget the rat model was extreme. Rats had all of one kidney and 2/3 of the other kidney removed. They were also fed a phosphate enriched diet and the induced CKD was clearly indicated by urea and creatine blood concentration.

Of course these findings are relevant when considering ongoing research and monitory the situation of CKD human patients. As the authors say “the effects of fluoride on renal function and vascular health are more complicated than expected.”

However, the current advice of the National Kidney Foundation is that:

“Dietary advice for patients with Chronic Kidney Disease (CKD) should primarily focus on established recommendations for sodium, calcium, phosphorus, energy/calorie, protein, fat, and carbohydrate intake. Fluoride intake is a secondary concern.”

Given that such patients are already monitory their diet and more advanced cases also probably regularly monitory blood indicators  any possible effect of fluoride for individuals should be detected. It is likely that by the time any problem with fluoride in drinking water is indicated other problems will also have occurred and patients will be taking steps such as water filtering and careful dietary management to handle their situation.

In fact individually directed management of food and drinking water appears to be a sensible way of handling problems if they do occur with a few people.

Micklem’s “call for CKD sufferers to be warned to avoid tap water” is too extreme and alarmist. Already the advice is that persons with CKD should be notified of the potential risk of fluoride exposure and be kept up to date with new research. Any patients who are particularly worried can then take steps like using filtered water for their own peace of mind. This seems more appropriate than denying the rest of the population access to a simple, effective and safe (for them at least) social policy like CWF.

Conclusions

This completes my critique of the Fluoride Free NZ report.

The original Royal Society review, Health Effects of Water Fluoridation: a Review of the Scientific Evidence, was prepared in response to a request from councils for a summary of the current science on CWF. This is because over the last few years activists political groups, like Fluoride Free NZ (and its international associate Fluoride Action Network) have bombarded New Zealand councils with misinformation and distortion of the science in campaigns to prevent CWF or get it removed

Councils do not have the expertise to critical consider claims made by such activist groups and have adopted a policy of requesting central government take over their responsibilities on the issue. Until that happens, however, councils will continue to have such decisions forced upon them.

The Royal Society review provides a timely and authoritative source of information for councils. Understandably Fluoride Free NZ feels somewhat trumpted by the review. So it is understandable this activist groups, and the international associate will use their media influence to try to discredit it.

This report is an attempt to fool councils by pretending to be objective and international. Yet, as my articles in this series show, it is simply a put-up job. It is not objective – all the authors and “peer reviewers” are working for or associated with the Fluoride Action Network or its associates. The articles follow the typical cherry-picking and confirmation bias of such activist organisations.



See The farce of a “sciency” anti-fluoride report for an analysis of the close relationships between the authors and peer reviewers of the Fluoride Free NZ report and anti-fluoride activist groups.

The Fluoride Free report is simply disingenuous – a sham aimed at fooling councils.

References

Bassin, E. B., Wypij, D., Davis, R. B., & Mittleman, M. a. (2006). Age-specific fluoride exposure in drinking water and osteosarcoma (United States). Cancer Causes & Control : CCC, 17(4), 421–8.

Biazevic, M. G. H., Rissotto, R. R., Michel-Crosato, E., Mendes, L. A., & Mendes, M. O. A. (2008). Relationship between oral health and its impact on quality of life among adolescents. Brazilian Oral Research, 22(1), 36–42.

Blakey, K., Feltbower, R. G., Parslow, R. C., James, P. W., Gómez Pozo, B., Stiller, C., … McNally, R. J. (2014). Is fluoride a risk factor for bone cancer? Small area analysis of osteosarcoma and Ewing sarcoma diagnosed among 0-49-year-olds in Great Britain, 1980-2005. International Journal of Epidemiology, 43(1), 224–34.

Broadbent, J. M., Thomson, W. M., Ramrakha, S., Moffitt, T. E., Zeng, J., Foster Page, L. A., & Poulton, R. (2014). Community Water Fluoridation and Intelligence: Prospective Study in New Zealand. American Journal of Public Health, 105(1), 72–76.

Büchel, K., Gerwig, P., Weber, C., Minnig, P., Wiehl, P., Schild, S., & Meyer, J. (2011). Prevalence of Enamel Fluorosis in 12-year-Olds in two Swiss Cantons. Schwiz Monatsschr Zahnmed, 121(7/8), 652–656.

Chankanka, O., Levy, S. M., Warren, J. J., & Chalmers, J. M. (2010). A literature review of aesthetic perceptions of dental fluorosis and relationships with psychosocial aspects/oral health-related quality of life. Community Dentistry and Oral Epidemiology, 38(2), 97–109. x

Choi, A. L., Sun, G., Zhang, Y., & Grandjean, P. (2012). Developmental fluoride neurotoxicity: A systematic review and meta-analysis. Environmental Health Perspectives, 120(10), 1362–1368.

Choi, A. L., Grandjean, P., Sun, G., & Zhang, Y. (2013). Developmental fluoride neurotoxicity: Choi et al. Respond. Environmental Health Perspectives, 121(3), A70.

Choi, A. L., Zhang, Y., Sun, G., Bellinger, D., Wang, K., Yang, X. J., … Grandjean, P. (2014). Association of lifetime exposure to fluoride and cognitive functions in Chinese children: A pilot study. Neurotoxicology and Teratology, 47, 96–101.

Comber, H., Deady, S., Montgomery, E., & Gavin, A. (2011). Drinking water fluoridation and osteosarcoma incidence on the island of Ireland. Cancer Causes & Control : CCC, 22(6), 919–24.

Coplan, M. J., Patch, S. C., Masters, R. D., & Bachman, M. S. (2007). Confirmation of and explanations for elevated blood lead and other disorders in children exposed to water disinfection and fluoridation chemicals. Neurotoxicology, 28(5), 1032–42.

Crosby, N. T. (1969). Equilibria of fluorosilicate solutions with special reference to the fluoridation of public water supplies. Journal of Applied Chemistry, 19(4), 100–102.

Do, L. G., & Spencer, A. (2007). Oral Health-Related Quality of Life of Children by Dental Caries and Fluorosis Experience. Journal of Public Health Dentistry, 67(3), 132–139.

Eason, C., & Elwood, JM. Seymour, Thomson, WM. Wilson, N. Prendergast, K. (2014). Health effects of water fluoridation : A review of the scientific evidence. Royal Society of New Zealand and Office of the Prime Minister’s Chief Science Advisor, Wellington.(p. 74).

Finney, W. F., Wilson, E., Callender, A., Morris, M. D., & Beck, L. W. (2006). Reexamination of hexafluorosilicate hydrolysis by 19F NMR and pH measurement. Environmental Science & Technology, 40(8), 2572–7.

Kim, F. M., Hayes, C., Williams, P. L., Whitford, G. M., Joshipura, K. J., Hoover, R. N., & Douglass, C. W. (2011). An assessment of bone fluoride and osteosarcoma. Journal of Dental Research, 90(10), 1171–6.

Ko, L., & Thiessen, K. M. (2014). A critique of recent economic evaluations of community water fluoridation. International Journal of Occupational and Environmental Health

Levy, M., & Leclerc, B.-S. (2012). Fluoride in drinking water and osteosarcoma incidence rates in the continental United States among children and adolescents. Cancer Epidemiology, 36(2), e83–e88.

Maas, R. P., Patch, S. C., Christian, A.-M., & Coplan, M. J. (2007). Effects of fluoridation and disinfection agent combinations on lead leaching from leaded-brass parts. Neurotoxicology, 28(5), 1023–31.

Martín-Pardillos, A., Sosa, C., Millán, A., & Sorribas, V. (2014). Effect of water fluoridation on the development of medial vascular calcification in uremic rats. Toxicology, 318C, 40–50.

Masters, RD; Coplan, MJ; Hone, BT; Dykes, J. (2000). Association of silicofluoride treated water witrh elevated blood lead. NeuroToxicology, 21(6), 1091–1100.

Michel-Crosato, E., Biazevic, M. G. H., & Crosato, E. (2005). Relationship between dental fluorosis and quality of life: a population based study. Brazilian Oral Research, 19(2), 150–155.

Peres, K. G., Peres, M. a, Araujo, C. L. P., Menezes, A. M. B., & Hallal, P. C. (2009). Social and dental status along the life course and oral health impacts in adolescents: a population-based birth cohort. Health and Quality of Life Outcomes, 7, 95.

Perrott, K. W. (2015). Severe dental fluorosis and cognitive deficits. Neurotoxicology and Teratology. In press.

Sawan, R. M. M., Leite, G. A. S., Saraiva, M. C. P., Barbosa, F., Tanus-Santos, J. E., & Gerlach, R. F. (2010). Fluoride increases lead concentrations in whole blood and in calcified tissues from lead-exposed rats. Toxicology, 271(1-2), 21–6.

Urbansky, E. T. (2002). Fate of fluorosilicate drinking water additives. Chem. Rev., 102, 2837–2854.

Urbansky, E. T., & Schock, M. R. (2000). Can Fluoridation Affect Water Lead Levels and Lead Neurotoxicity ? In American Water Works Association Annual Conference (pp. 1–31).

Xiang, Q. (2014) Keynote Address on IQ studies published in China. Fluoride Action network.

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