Why Fluoridation Should be Ended in New Zealand

A statement by Professor Paul Connett, PhD,

February 2014.



These are my academic credentials:

1) Cambridge BA (honors) in Natural Sciences 1962.

2) PhD in Chemistry from Dartmouth College, Hanover, NH, USA, 1983

These are the details of my professional experience:

1) I taught chemistry at St. Lawrence University, Canton, NY from 1983 to 2006. My final rank was full professor. My specialty was environmental chemistry and toxicology.

2) From 1985 to 2013 I have been heavily involved in the issue of waste management.  This has involved researching the literature on the dangers posed by incinerators and landfills. This research has led to the publication (with my colleague Tom Webster) of six peer-reviewed papers on dioxin; the organizing of three citizens conferences on dioxin; the evaluation of many health risks assessments performed for incinerators; testimony in court cases and public hearings in many states throughout the U.S.; the production over 50 videotapes on the dangers of incinerators and the details of cost-effective and practical alternatives; over 2000 pro bono presentations to communities and local councils in 49 U.S. states, 7 provinces in Canada and 60 other countries, and the publication of several articles on risk assessment and waste management.

This 28-year involvement on the waste issue culminated with the publication in 2013 of the book, The Zero Waste Solution: Untrashing the Planet One Community at a Time (Chelsea Green, 2013).

3) From 1996 – 2013 I have been researching fluoride’s toxicity and the dangers posed by water fluoridation.  This has involved the writing of many articles, editorials and submissions to regulatory authorities, including an invited 45-minute presentation to the US National Research Council’s panel (in 2003) that was reviewing the toxicology of fluoride in water at the invitation of the US Environmental Protection Agency. This panel published its 500-page landmark review in 2006 (NRC, 2006).

A great deal of my research of the literature on the subject of water fluoridation was published with two co-authors in October 2010, The Case Against Fluoride (Chelsea Green, 2010).

Since 2000 I have served as the executive director of the Fluoride Action Network (www.AmericanHealthStudies.org).

The Case Against Water Fluoridation in New Zealand

I shall discuss this case under several headings:

1) Fluoridation of the public water supply is a bad medical practice

2) The evidence of harm is growing

3) The evidence for any benefit from swallowing fluoride is very weak.

4) The trial that launched fluoridation in NZ was a fraud.

1) Fluoridation of the public water supply is a bad medical practice

This practice should have never begun in NZ or anywhere else. The use of the public water supply anywhere to deliver medical treatment is thwart with problems both practical and ethical. I will list some of these problems below.

1.1 It is impossible to control the dose people get.

Once a chemical is added to the water to treat people (as opposed to treating the water to make it safe or palatable to drink) it is impossible to control the dose people get. People drink very different amounts of water. In short, engineers at the water works can control the concentration added to the water (mg/liter) but no one can control the total dose (mg/day) individuals receive or the dosage (mg/kg/day) that bottle-fed infants receive, a critical consideration because of their very small bodyweight.

1.2 Fluoridation is totally indiscriminate.

Once fluoride is put into the water supply it goes to everyone regardless of age, regardless of health or nutritional status.

Of particular concern – as mentioned above – is that it goes to bottle-fed infants, who are more impacted than adults by the same dose, because of their small bodyweight.

Also of concern are people with poor kidney function who are unable to clear the fluoride from their bodies via the kidneys as effectively as others. It thus accumulates in their bones more rapidly.

It also goes to people with low or borderline iodine intake, which makes them more vulnerable to fluoride’s impact on the thyroid gland (Lin et al., 1991).

In general, according to studies done in India, people with poor diet (low protein, low calcium and low vitamin intake) are more vulnerable to fluoride’s toxic effects.

1.3 It violates the individual’s right to informed consent to medical treatment.

Thus water fluoridation is a violation of a very important medical ethic which is fully described on the website of the American Medical Association (www.AMA.org). It is very surprising that so many medical doctors standby while the community does to everyone what they are not allowed to do to a single patient.

The above arguments would apply to any medicine added to the drinking water and that probably explains why since fluoridation has begun the public water supply has not been used for any other medical treatment. But in addition to the general arguments above, there are other aspects to the fluoride ion, which makes it particularly unsuitable for addition to the drinking water.

1.4 Fluoride is NOT a nutrient.

There is not one single biochemical process in the body that has been shown to require fluoride for normal function (we will see later that fluoride’s predominant action on teeth is topical not systemic). However,

1.5 There are many biochemical processes that are harmed by fluoride (given a sufficient dose).

These include the inhibition of many enzymes. This is the reason that some of the earliest opponents of fluoridation were biochemists like Professor James Sumner from Cornell University, who won the Nobel Prize for his work on enzyme chemistry. More recently fluoride has been shown to activate G-proteins and interfere with the cell’s messaging systems. It can also cause oxidative stress. An excellent summary of fluoride’s biochemistry can be found in the article “Molecular Mechanisms of Fluoride Toxicity” by Barbier et al, 2010.

1.6 The levels of fluoride in mothers’ milk is extremely low.

This level, on average for a woman in a non-fluoridated community, is 0.004 ppm (NRC, 2006, p.40). This means that a bottle-fed baby in a fluoridated community (at 1 ppm) will get about 250 times more fluoride than a breast fed baby in a non-fluoridated community. Bearing in mind the fact that life emerged from the sea where the average level of fluoride is about 1.4 ppm it is remarkable that, other than accumulating in the teeth of sharks, there is little evidence that nature has found any use for this ion in the metabolism of any aquatic or mammalian species, including humans. This is consistent with the low levels in human milk. Nature’s verdict appears to be that the baby a) does not need fluoride and b) that it may be harmed by fluoride. It is more likely that nature knows more about what the baby needs than those who so enthusiastically promote the practice of fluoridation.

1.7 Fluoridation has always been a trade-off between lowered tooth decay and an increase in the prevalence of dental fluorosis (discoloration and mottling of the enamel) but a key question was never satisfactorily answered.

When the fluoridation trials began in 1945 it was known that the trade-off was that approximately 10% of the children would develop dental fluorosis in its mildest form. This was known to be a systemic effect. In other words, it was caused by fluoride interfering with biochemistry during the formation of the enamel during the development of the teeth. The question that was not comprehensively answered before the US Public Health Service endorsed fluoridation in 1950, was: “What other tissues in the body may be interfered with at the same time that fluoride was interfering with the laying down of the tooth enamel?”

One would have reasonably anticipated that diligent efforts would have been pursued to answer the following key questions before fluoridation began:

i) Will the baby’s bone cells also be impacted?

ii) How about the baby’s brain cells?

iii) How about the cells of the glands in the endocrine system?

Sadly, these questions were not pursued in the 1940’s and 1950’s in any depth in the U.S. and very little has been done in fluoridated countries to answer these questions since.

However, proponents do acknowledge that the appearance of dental fluorosis means that a child has been over-exposed to fluoride before the permanent teeth have erupted. The extent to which this is impacting children today in fluoridated countries is disturbing.

In 2000, the review commissioned by the UK government (otherwise referred to as the York Review, estimated that worldwide that the average dental prevalence in communities where the levels of fluoride were about 1 ppm, was 48% with 12.5% at levels of aesthetic concern (McDonagh et al., 2000).

In 2010 the U.S. Centers for Disease Control and Prevention (CDC) reported that 41% of American children aged 12-15 have dental fluorosis, with 8.6% having the mild form (with up to 50% of the enamel impacted) and 3.6% with moderate or severe dental fluorosis (100% of the enamel impacted).  In later arguments in this commentary I will be presenting evidence that fluoride is capable of harming other developing tissues, not just the teeth.

1.8 Worldwide, fluoridation is not a common practice.

Proponents will often imply that fluoridating the drinking water is a common practice. It is not. Most countries do not fluoridate their water. 97% of the European population is not forced to drink fluoridated water. Four European countries have salt fluoridation (Germany, France, Switzerland and Austria), but the majority of European countries have neither fluoridated water nor fluoridated salt, yet according to World Health Organization (WHO) data available online (measured as DMFT in 12-year-olds) tooth decay rates in 12-year-olds have declined as rapidly over the period 1960 to the present in non-fluoridated countries as fluoridated ones and there is little difference in tooth decay rates today (see Cheng et al, 2007). The reasons that European spokespersons have given for not fluoridating their water are usually twofold: a) they do not want to force fluoride on people who don’t want it and b) there are still many unresolved health issues (see a list of statements by country at http://fluoridealert.org/studies/caries01 ).

1.9 Typically fluoridation is promoted via endorsements not via sound science.

When the US Public Health Service (PHS) endorsed fluoridation in 1950, before a single trial had been completed and before any meaningful health studies had been published, it clearly was not the result of solid scientific research. However the PHS endorsement set off a flood of endorsements from other health agencies and professional bodies (see Chapters 9 and 10 in The Case Against Fluoride). Most of these came between 1950 and 1952. These endorsements were not scientific (there was still no solid science that had been established at this point for either effectiveness or safety.  These endorsements simply reflected a subservience to the public policy interests of the U.S. government by professional bodies.  However, promoters of fluoridation for over 60 years have used these endorsements very effectively with the general public as if they were coming from scientific bodies reflecting thorough and comprehensive scientific research. Very seldom is this the case.

2) The evidence of harm is growing

2.1 NZ presents a complicated case

Commenting on the potential adverse health effects of the water fluoridation program in NZ is complicated by the fact that NZ government health agencies have undertaken very few health studies of fluoridated communities. An independent observer of this practice in NZ is thus forced to gauge the risks of this program based upon health studies conducted elsewhere.

2.2 Fluoridated countries worldwide have undertaken very few health studies in fluoridated communities.

NZ is not alone in its failure to undertake health studies in fluoridated communities. Most of the fluoridating countries have paid far more attention to promoting the practice and researching its claimed benefits than investigating any harm it may be causing. Today more effort is going into denying harm than investigating it.

Thus, when assessing harm one is forced to look to studies undertaken in countries, which do not have a fluoridation program to protect. The most important of these are India and China, which have extensive areas with moderate to high levels of fluoride in their drinking water leading to regions, which have made them endemic for both dental and skeletal fluorosis (China News. 2008).

2.3 Studies from countries with endemic fluorosis

In addition to the damage fluoride causes to both the teeth and bone (Li et al., 2001. See also the other bone studies listed in Chapter 17 in The Case Against Fluoride …), it is now becoming clear that fluoride impacts some of the soft tissues (e.g. the brain) before the damage to teeth in children and bones in adults become obvious and visible.

2.4 The weight of evidence that fluoride damages the brain

Since the early 1990s that have been a large number of studies that fluoride can damage the brain and interfere with neurological development in both animals and children. These include:

Over 40 animal studies that show that prolonged exposure to fluoride can damage the brain (e.g. Varner et al., 1998).

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

12 studies (7 human, 5 animal) that link fluoride with neurobehavioral deficits (e.g. Mullenix et al., 1995)

3 human studies that link fluoride exposure with impaired fetal brain development, and

37 out of 43 published studies that show that fluoride lowers IQ, of which 27 were part of a meta-analysis conducted by a team from Harvard (Choi et al. 2012), which included Phillipe Grandjean (www.fluoridealert.org/issues/health/brain)

2.5 A closer look at the IQ studies

After the Harvard University team led by Choi published its meta-analysis of 27 of the IQ studies (most of them conducted in rural China) promoters of fluoridation have claimed that a) there are weaknesses in some of these studies and b) that the concentration of fluoride in the villages where IQ was lowered was too high to be of any significance.

Choi et al., 2012, have acknowledged that there are weaknesses in many of the IQ studies but that nonetheless the results were remarkably consistent with 26 out of 27 studies with the high-fluoride villages showing a lower IQ than the low-fluoride villages. The average overall lowering was about 7 IQ points, which is quite substantial.

As far as the claim of high concentrations is concerned it is true that in two of the 27 studies reviewed the range of concentration in the well water in the high-fluoride village went as high as 11.5 ppm. However, in 9 of the 27 studies the level of fluoride in the high-fluoride village was lower than 3 ppm which is highly relevant to communities drinking water fluoridated water at about 1 ppm, which we will see below.

Even though these studies were of an ecological design (i.e. comparison was made based upon exposure at the population level, based upon  residence in a specific geographical location), several of the studies measured the fluoride in the urine of the children and found an inverse correlation with IQ (e.g. Xiang et al., 2003; Ding et al, 2010). Also Xiang et al., 2011, reported an inverse correlation between the lowering of IQ and the fluoride levels in the plasma of the children. These measures of individual exposure to fluoride strengthen the findings of the ecological studies for this association between exposure to fluoride and lowered IQ.

2.6 Using the IQ studies to assess the risks posed to the NZ population

Before I get into a detailed risk assessment on this matter, I will briefly go through some of the concepts involved in how regulatory bodies determine safe reference doses and safe drinking water standards.

2.6.1 We must take into account the large range of sensitivity to any toxic substance

In any large population we can anticipate a very large range of sensitivity to any toxic substance. Like other human traits such sensitivity follows a normal distribution curve (the famous bell-shaped curve). The average person will have an average response but at the tails of this curve we will have people who are i) very sensitive at one end and ii) very resistant at the other. Typically we assume some people are going to be at least 10 times more sensitive than others. This is then used to generate a safety factor of 10 (sometimes referred to as the intra-species variation safety factor).

Thus if we find harm in a small human study and wish to determine the level that would protect everyone in a large population from that harm this is what we must do. We take the dose, which has been found to cause no harm (the so-called no observable adverse effect level or NOAEL) and divide that dose by 10 to give a safe dose for the most sensitive individual in the population. Frequently we don’t have a NOAEL and so we have to use a LOAEL (the lowest observable adverse effect level) and divide that by 100.

2.6.2 We must estimate doses, not just compare concentrations

Applying these calculations in a real world situation is called a Margin of Safety Analysis and shockingly it is very seldom considered by people who promote fluoridation. They simply use the very crude and highly misleading approach of comparing the concentration used in the study group with the concentration of the fluoride in the water of the fluoridated population.

For example, the American Dental Association denied the relevance of the National Research Council’s groundbreaking review on the toxicology of fluoride in drinking water (NRC, 2006), to water fluoridation because they argued that the NRC panel only found harm in the range of 2 – 4 ppm and in the US we fluoridate in the range of 0.7- 1.2 ppm.

One of several things wrong with this argument is that above-average water drinkers in communities with 0.7 – 1.2 ppm could easily get higher doses than some of the below-average water drinkers in the communities studied at 2 ppm and even 4 ppm. In short, the concentrations maybe different but the doses overlap – and it is the dose that can cause harm.

So I will now attempt a margin of safety analysis based upon the IQ studies

2.7 A Margin of Safety analysis using the IQ studies

I will use the fact that 9 of 27 studies have found an IQ lowering at less than 3 ppm fluoride. Strictly speaking I should use the lowest concentration where a lowering of IQ occurred and that was 0.9 ppm (Lin et al, 1991) but that is complicated by the iodine levels involved. Instead I have used the more conservative approach of using the lowest level found to lower IQ in 5 of the studies listed in Table 1 where the result (lowered IQ) occurred at less than 3 ppm and was statistically significant.

Table 1

2.8 A Margin of Safety analysis –calculations

Step a) As our starting point I will choose the study that found a lowering of IQ at the lowest concentration in these five studies. That was 1.8 ppm (see Table 1).

Step b) Our next task is to estimate the reasonable dose range this represents for the children in the study group – which of course, will depend on how much water they drink and how much they get from other sources. We believe very few of these rural Chinese children use fluoridated toothpaste and thus their daily dose comes largely from the water.

• If they drank 2 liters of water per day at 1.8 mg/liter  (i.e. 1.8 ppm) their daily dose would be (2 L x 1.8 mg/L) = 3.6 mg/day.

• If they drank 1 liter of water per day their daily dose would be 1.8 mg/day

• If they drank 0.5 liters of water per day their daily dose would be approx 0.9 mg/day.

Thus a reasonable estimate of the range of the dose leading to a lowered IQ was approximately 0.9 – 3.6 mg/day.

Step c) Our third task is to determine a safe dose to protect all the infants and children from lowered IQ in a large population.

From this range the LOAEL is 0.9 mg/day. We do not have a NOAEL so we have to divide the LOAEL by 10. So the NOAEL = 0.09mg/day.

Now we need to divide this NOAEL by another factor of 10 to protect for the full range of sensitivity in a large population. Thus the safe dose to protect all children for lowered IQ (the safe reference dose is 0.009 mg/day  

Thus we would not want any child in a large population drinking more than 9 ml of water fluoridated at 1 ppm to protect against lowered IQ. 9 ml is less than two teaspoonfuls of water (10 ml)!

Here is the calculation: 9 ml = 0.009 Liters.  0.009 L x 1 mg/L = 0.009 mg/day

2.9 A Margin of Safety analysis –conclusion

Based upon the five IQ studies that were statistically significant and found a lowering of IQ at less than 3 ppm a responsible regulatory authority would not allow water fluoridation. There simply is not an adequate margin of safety to protect all of NZ’s children from lowered IQ. This result makes fluoridation an unacceptable risk. Little wonder then that fluoridation promoters are doing everything they can to criticize these IQ studies.

Recently (Feb 3, 2014) on TV3 Dr. Broadbent announced the results of an IQ study conducted in Dunedin, NZ (as yet unpublished), which he claims negates the concerns about IQ lowering. Needless to say independent observers will be examining this study to see how sound the methodology and conclusions are. The public has been fooled before by promises of studies by proponents that they claimed would negate key findings of harm (see the osteosarcoma discussion below)

2.10 Fluoride exposure in babies and the risk of lowered IQ. A Comparison between a breast-fed baby and a bottle-fed baby.

When considering harm to babies we have to take into account the extra problem of the baby’s small bodyweight.  To take bodyweight into account we use a different measure of exposure: i.e. dosage instead of dose.

Dose is measured in mg/day, dosage is measured in mg/kilogram bodyweight/day.

If we consider that the safe dose we have determined (0.009 mg/day) was protective of a 20 kg child, then we would obtain the safe dosage  by dividing this safe dose by the 20 kg bodyweight (0.009 mg/day divided by 20 kg = 0.00045 mg/kg/day). Thus a safe dosage, which we can now apply across a range of bodyweights (including a 7 kg baby) is 0.00045 mg/kg/day.

Applying this safe dosage to a 7 kg baby we can calculate the safe dose by multiplying this dosage by 7 kg. Thus the safe dose for a 7 kg baby would be calculated as follows: 7 kg x 0.00045 mg/kg/day = 0.00315 mg/day.

A breast fed baby (with mothers milk at 0.004 ppm) drinking 800 ml a day would get 0.004 mg/L x 0.8 L = 0.0032 mg/day which is just about what we have determined to be safe for the baby (0.00315 mg/day).

So based on these rough calculations, the fluoride that naturally occurs in breast milk does not pose a risk of lowering the IQ in babies.

A bottle-fed baby (with water at 0.7 ppm) drinking 800 ml a day would get 0.7 mg/L x 0.8 Liters = 0.56 mg/day. This is 0.56/0.00315 = approx 180 times higher than the safe level to protect against lower IQ

A bottle-fed baby (with water at 1.2 ppm) drinking 800 ml a day would get 1.2 mg/L x 0.8 Liters = 0.96 mg/day. This is 0.96/0.00315 = approx 300 times higher than the safe level to protect against lower IQ

So whether by accident or by evolutionary “design” mothers’ milk is protective against lowered IQ but formula made up with fluoridated water (0.7-1.2 ppm) is not. The latter delivers a daily dose of fluoride, which is a factor of 180-300 times larger than a safe dose calculated for a 7 kg baby.

2.11 Why is a small downward shift in IQ significant for the whole population

Even a small downward shift in IQ for the whole population maybe highly significant. As Philippe Grandjean (one of the authors of the Harvard meta-analysis by Choi et al, 2012) in his new book (Only Once Chance) explains, a negative shift of 5 IQ points would halve the number of geniuses in our society and double the number of mentally handicapped.

The downward shift caused by fluoride exposure may not be as great as 5 IQ points but nonetheless it is not wise to deliberately add any substance to the water that is known or reasonably anticipated – to cause harm to the neurological development of children.

2.12 The numerous IQ studies underline the recklessness of the fluoridation program

This program was reckless because before it was endorsed by the US Public Health Service there had been no serious attempt to investigate:

a) short-term health effects of exposing babies to 250 times the level of the fluoride that naturally occurs in mothers’ milk at very low levels (1 ppm versus 0.004 ppm, NRC, 2006 p.40)

b) the affect on adults’ bones and other tissues with lifetime exposure, even though it was known that fluoride accumulates in the bone

It is reckless because the NRC (2006) panel reported that certain subsets of the population were exceeding the US EPA’s safe reference dosage of 0.06 mg/kg/day (the so-called IRIS level) drinking water at 1 ppm. These subsets included bottle-fed infants, people with poor kidney function and above average water consumers. Delivery of fluoride to these vulnerable subsets cannot be controlled in any way once fluoride is added to the water.

It is reckless because after 68 years of this practice there are still many unanswered questions about the risks involved. For example the chairman of the NRC (2006) review panel said the following in an interview in Scientific American in January 2008:

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

Fluoridation promoters have since circulated a later statement by Doull expressing his support for water fluoridation. However, his own personal opinion of water fluoridation does not diminish in any way his comments on the poor quality of the research on this matter.

It is reckless because many European countries have demonstrated that there are cost-effective and practical alternatives to fighting tooth decay in children of low-income families (where most of the tooth decay occurs today) which do not involved the unethical practice of forcing fluoride on people that don’t want it.

The most recent success story comes from Scotland.

Instead of water fluoridation, the newly devolved Scottish Government opted, in its 2005 dental action plan (their Childsmile program), to pursue:

a) school-based toothbrushing schemes;

b) the offering of healthy snacks and drinks to children;

c) oral health advice to children and families on healthy weaning, diet, teething and toothbrushing;

d) annual dental check-ups and treatment if required, and

e) fluoride varnish applications  (The Scottish Government, 2005; Macpherson LMD et al., 2010; Turner S et al., 2010; Chestnutt, 2013; Healthier Scotland, Scottish Government, 2013).

Encouraging results have been reported from this national dental programme with the proportion of children in Primary 1 (aged 4–6 years) without obvious dental decay rising from 42.3% in 1996 to 67% in 2012 (Information Services Division  Scotland, 2012).

Similarly, the proportion of children in Primary 7 (aged 10–12 years) without obvious dental decay rose from 52.9% in 2005 to 69.4% in 2011 and 72.8% in 2013 (Information Services Division Scotland, 2013).

The introduction and uptake of nursery school toothbrushing is likely to have contributed to a large extent to the improved oral health in five-year-old Scottish children (Macpherson, 2013).

The BBC reported the success and cost-effectiveness of this program as follows,

“A scheme to encourage nursery children to brush their teeth has saved more than £6m in dental costs, according to a new study.

Childsmile involves staff at all Scottish nurseries offering free supervised toothbrushing every day.

Glasgow researchers found that the scheme had reduced the cost of treating dental disease in five-year-olds by more than half between 2001 and 2010.

The programme was launched in 2001 and costs about £1.8m a year…

An evaluation, funded by the Scottish government and carried out by Glasgow University, found that fewer children needed dental extractions, fillings or general anaesthetics as a result of the programme.

There was also said to be a drop in the number of children needing hospital treatment for dental problems, freeing up operating theatres.

Public Health Minister Michael Matheson said: “This is an amazing achievement and shows just how much can be saved from a very simple health intervention.

“This has seen less tooth decay in children which means less toothache, fewer sleepless nights and less time off school.

“By this simple measure, NHS costs associated with the dental disease of five-year-old children have decreased dramatically.

“More children can just be treated routinely in the dental chair because they need less invasive treatments, so fewer fillings and fewer extractions, and many more children with much better oral health than we have seen in many years.” http://fluoridealert.org/news/nursery-toothbrushing-saves-6m-in-dental-costs/

2.13 Making matters even worse

The fluoridating chemicals used to fluoridate the water supply are not the pharmaceutical grade chemicals as used in dental products. Most of the chemicals used are obtained from the phosphate fertilizer industry’s wet scrubbing systems (see Chapter 3, The Case Against Fluoride). One of the problems with this source is that it is contaminated with a number of other toxic chemicals including arsenic and even trace amounts of radioactive elements.

Arsenic is a known human carcinogen and as such for the US Environmental Protection Agency (EPA) there is no safe level. The EPA’s maximum contaminant level goal (MCLG) for arsenic in drinking water is thus set at zero. This is the ideal goal based on what is safe i.e. to reduce cancer risk.  Fluoridation proponents will argue that after the dilution of these bulk chemicals at the waterworks (by about 200,000 to 1), the level of arsenic is negligible.

They will further argue that this level of arsenic (after dilution) is OK because it is lower than the Maximum Contaminant Level (MCL) set by the US Environmental Protection Agency. The EPA’s MCL for arsenic is 10 ppb. But to use this as a yardstick for what can be ADDED to the water is to confuse the purpose of this standard. As I indicated above the MCLG  (the ideal goal) is set at ZERO for HEALTH reasons. The MCL is set at 10 ppb for ECONOMIC reasons. This is to accommodate communities that have naturally occurring arsenic in their water. For them it would be prohibitively expensive to reach the MCLG – thus the MCL is as compromise between what you ideally want and what you can achieve economically.

It is one thing to set a standard (MCL) to accommodate REMOVAL of arsenic but another thing to use this standard to allow the deliberate ADDITION of arsenic and thus exceed the desired MCLG of zero. This especially applies to an unnecessary practice like fluoridation. As there are other delivery systems (for fluoride) which are cost-effective and do not involve the use of these industrial grade chemicals, increasing the cancer rate even by a small amount is not responsible or acceptable.

In addition to the cancer risks posed by the arsenic present in the fluoridating chemicals used are the cancer risks posed by fluoride itself, especially the risk for osteosarcoma.

2.14 Osteosarcoma: politics versus science.

 Introduction. There was a discovery made in 2001, which, in my view, should have ended fluoridation once and for all. This finding indicated that fluoridation may actually be killing a few – not many –young men each year with a deadly bone cancer called osteosacoma. But that discovery was hidden for four years. Even after the findings were revealed political efforts have continued to downplay or even dismiss these findings. However, there has been no published scientific study that has refuted them. Let me explain.

a) The discovery in 2001 occurred when Elise Bassin, a dentist completing her doctoral thesis at the Harvard Dental School, found in a carefully conducted matched case-control study, that young boys exposed to fluoridated water at 1 ppm in their 6th to 8th years had an associated 5-7 fold increased risk of succumbing to osteosarcoma. Osteosarcoma is a rare but frequently fatal bone cancer.

b) Bassin’s study was first hidden (politics) from the public and scientific community, but was eventually published in 2006. Despite promises from her thesis adviser that his larger study would refute her finding (politics), his study when it was finally published in 2011 failed to do so (Kim et al., 2011).

c) So what we have here is an unrefuted study that indicates that a few young boys may be losing their lives drinking fluoridated water.  I am really amazed that promoters of fluoridation can take this issue so lightly. The small number involved should not justify turning a blind eye to this. As John Colquhoun asked in my videotaped interview with him in 1997 is any saving in tooth decay an adequate exchange for “one death of a teenage boy from osteosarcoma.” (http://fluoridealert.org/fan-tv/colquhoun/ ),

d) I am also disturbed that the Pew Charitable Trusts (a multibillion dollar foundation that is actively campaigning in support of fluoridation) would mischievously claim that the Kim et al (2011) study has put the matter to rest when it clearly has not.

e) The issue of fluoride and osteosarcoma has a long and fascinating history. There is a lot of politics involved, which is not surprising because if this connection was proven it would (or should) end fluoridation immediately. We go into this history in some detail in Chapter 18 of our book, The Case Against Fluoride… Below I have provided a timeline (a more elaborate timeline with full references to all the studies cited can be found at http://fluoridealert.org/studies/cancer05/):

1955.  The bone specialist who studied the bone X-rays of the children in the Newburgh-Kingston trial, pointed out that the age, gender and anatomical distribution of these cortical bone effects were remarkably similar to the occurrence of osteosarcoma (Caffey, 1955).

1963. Harold Hodge referred to Caffey’s observations in 1963, when he stated that, “The higher incidence of cortical defects in the Newburgh children’s long bones, although these changes are considered by the specialist in children’s roentgenology to be ‘normal’ variants (Coffey (sic) 1955) deserves additional study” (Hodge, 1963).

1977. Donald Taves, in a report written for the National Academy of Science, reiterated Hodge’s thoughts but in more detail:

There was an observation in the Kingston-Newburgh (Ast et al., 1956) study that was considered spurious and has never been followed up. There was a 13.5% incidence of cortical defects in bone in the fluoridated community but only 7.5% in the nonfluoridated community. With 474 and 375 children in the respective groups, the t value was 2.85, which is statistically significant (Schlesinger, 1956). Caffey (1955) noted that the age, sex, and anatomical distribution of these bone defects are “strikingly” similar to that of osteogenic sarcoma. While progression of cortical defects to malignancies has not been observed clinically, it would be important to have direct evidence that osteogenic sarcoma rates in males under 30 have not increased with fluoridation [emphasis added]. (NAS, 1977).

1990. The long awaited animal cancer study for fluoride, ordered by the US Congress from the National Toxicology Program (NTP) in 1979, was finally published.  The NTP reported a higher incidence of osteosarcoma in the fluoride treated male rats compared to controls, but none in the female rats or in male or female mice.

1991.  Prompted by findings in the NTP study the National Cancer Institute (NCI) looked at the SEER (Surveillance, Epidemiology, and End Results Program) cancer registries of the US and found an increase in osteosarcoma in young males (but not females) in some of the fluoridated versus non-fluoridated areas (Hoover et al, 1991 a [Appendix E]). The NCI then discounted this finding based upon reanalyses that looked at osteosarcoma rates in relation to duration of fluoridation (Hoover, 1991, b [Appendix F]).  However, these reanalyses suffered from low statistical power because they were based on very small numbers per category, as few as a single osteosarcoma.  Even more serious, in his reanalysis Hoover mistakenly classified many counties as “non-fluoridated” because he did not realize that amongst these Iowa counties, a majority had high enough natural fluoride levels to meet his criteria for “fluoridated”.   This misclassification – calling fluoridated areas non-fluoridated – further explains why his reanalysis failed to confirm his initial findings of a connection between osteosarcoma and fluoridation.

1991. A small study from the Harvard Medical and Dental Schools, co-authored by Chester Douglass (see below) did not find a relationship between fluoridation and oesteosarcoma and even suggested that fluoride might protect against fluoridation. This study was given front-page coverage by the Journal of the American Medical Association(McGuire et al, 1991).

1992. A small study by Perry Cohn (working for the NJ Department of Health) found a higher incidence of osteosarcoma among young males (but not young females) in three fluoridated counties in NJ compared to non-fluoridated areas.

Cohn made an interesting conjecture. He wondered if there was a particular age window that could explain the vulnerability for young boys in this matter. That question lay fallow for a number of years.

1992-2O00. Other studies were published did not find a positive association between fluoridation and increased osteosarcoma.

2001. Bassin successfully defended her doctoral thesis at the Harvard Dental School which identified that “age window of vulnerability” that Cohn had suggested (see details above).

2001-2005. Even though Bassin’s thesis advisor Professor Chester Douglass had signed off on her thesis, in the three years that elapsed after her research was successfully defended he did not warn his peers, the NRC panel or his funders of this dramatic finding (politics). Instead he kept insisting when asked that his “own” study found no relation between osteosarcoma and fluoridation, without indicating that his own graduate student had found the opposite to be the case.

Douglass knew of course if this connection between fluoridation and osteosarcoma was established that it would end fluoridation and stated as much in a paper he had co-authored ten years earlier (McGuire et al., 1991).

2005. Eventually Bassin’s doctoral thesis was found sitting in one of the Harvard libraries in 2005.  The Environmental Working Group charged Douglass with academic misconduct for hiding this finding and asked the NIH (which had funded the study) to investigate.  The investigation was handed over to Harvard. A committee appointed by the Harvard Dental and Medical Schools investigated the matter and in a short 4-paragraph statement exonerated Douglass suggesting the he did not “deliberately” hide these findings. Harvard refused repeated attempts for tem to provide the basis for this decision but they refused.

2006. Bassin’s thesis was subsequently published in the journal Cancer Causes and Control (Bassin et al., 2006). In the same issue of the journal a letter was published from Douglass and another graduate student that stated that his larger study would show that Bassin’s thesis did not hold (Douglass and Joshipura, 2006). Douglass told the NRC panel that this larger study would be available in the Summer, 2006. But it did not appear for five years.

Meanwhile, Douglass’ promise of a study in a letter was used by the NHMRC (2007); Health Canada (2011) and health authorities in the UK as if it was an actually peer-reviewed and published study.

2011. Eventually the Douglass paper was published in 2011, but not in the original cancer journal where his claims were made, nor in a medical journal, but in a dental journal (Kim et al., 2011). It is a very poor study with many flaws but the key fact is that it did not refute Bassin’s findings. Nor could it possibly do so. Because the biometric of exposure was fluoride levels in the bones. There is no way such levels could be used to determine the exposure to fluoride during the critical age window of vulnerability found by Bassin (the 6th to 8th years).

f) Conclusion: a well-researched study found a possible and highly plausible relationship between exposure to fluoridated water – at a specific age range in young boys – and a rare but frequently fatal bone cancer. Despite promises to the contrary, which before publication were used by fluoridation promoters inside and outside of government agencies to downplay these findings, this study has never been refuted.

g) As with the lowering of IQ (discussed above) we are talking serious risks here. When it is clear that tooth decay is being reduced in the vast majority of countries that neither fluoridate their water, nor their salt, nor their milk (see the example from Scotland above), why would anyone today defend putting fluoride into the public drinking water?

3) The evidence for any benefit from swallowing fluoride is very weak.

It comes as a surprise to many that despite claims to the contrary by proponents the evidence that swallowing fluoride reduces tooth decay is very weak. We discuss this weak evidence in chapters 6-8 in our book The Case Against Fluoride…

Remarkably in the 68 years of this practice there has not been a single randomized control trial (RCT) to demonstrate the effectiveness of swallowing fluoride to reduce tooth decay. An RCT is the gold standard as far as demonstrating the effectiveness of any medicine or treatment is concerned.

The result is that promoters have had to rely on far weaker studies – usually ecological studies comparing tooth decay between fluoridated and non-fluoridated communities. This is thwart with difficulties because there are so many confounding factors (income levels, diet, other minerals in the water, level of sunshine affecting Vitamin D3 levels, the possible delayed eruption of the teeth caused by fluoride) effecting tooth decay and if these are not all carefully controlled erroneous results and conclusions can be drawn.

Here I would like to draw attention to just two studies. One because it was very large and the other because it was very precise. These were the studies by Brunelle and Carlos (1990) and Warren et al. (2009).

Both these studies were funded by the US taxpayer and both were conducted by pro-fluoridation researchers. So if there were any bias involved it would not have been in favor of the anti-fluoridation position.

Brunelle and Carlos (1990). This was the largest survey of tooth decay ever undertaken in the U.S. The study was administered by the National Institute for Dental Research (NIDR) now called the National Institute for Dental and Cranial Research (NIDCR). The teeth of 39,000 children from 84 communities were examined. In Table 6 of this report the authors compare the Decayed Missing and Filled Surfaces (DMFS) for children (aged 5-17) who had always lived in a fluoridated community with children who had never lived in a fluoridated community. There were about 8000 children in each group. The average DMFS for children in the fluoridated communities was 2.8 and in the non-fluoridated was 3.4. Thus the average saving was 3.4 – 2.8 = 0.6 tooth surfaces. The extraordinary aspect of this report was the authors, even though this was a government-funded study, did not show that the result was statistically significant.  Even so, the average saving is remarkably small considering what risks are being taken with this practice.

Warren et al., (2009). This study was part of the U.S. government funded “Iowa Study” where children’s tooth decay has been tracked from birth. This enabled the researchers to do something that no other research group has done and that is to examine the relationship between tooth decay and individual exposure to fluoride. All the other epidemiological studies have been population based. The authors in this study were attempting to find the so-called “optimal dose” needed by a child to reduce tooth decay. But they couldn’t find that dose. In fact, they could not find a clear relationship between tooth decay and the amount of fluoride ingested on a daily base (this included from water, from food and from dental products). In their own words the authors concluded that, “These findings suggest that achieving a caries-free status may have relatively little to do with fluoride intake…”

The most likely explanation for this weak evidence is that even prominent promoters of fluoridation have acknowledged that the predominant benefit of fluoride is topical and not systemic (CDC, 1999 and 2001).  Thus the whole rationale for fluoridating water and forcing it on people who don’t want it disappears.  The benefits sought can be better achieved by other means (e.g. fluoride varnishes in children and fluoridated toothpaste for adults). Better still tooth decay in low-income areas can be fought with better diets and education for better dental hygiene. Our kids need more fruit and vegetables, less sugar and more brushing. Such a strategy has the added advantage of fighting childhood obesity and thus would justify every penny spent on the program.

4. The trial that launched fluoridation in NZ was a fraud.

This trial was the Hastings-Napier Fluoridation Trial conducted between 1954 and 1964. The fraud was first discussed by the late Dr. John Colquhoun and his PhD thesis adviser Dr. Robert Mann in an article that appeared in The Ecologist in 1986. Further details were presented in Colquhoun’s thesis in 1987 (which is now available to a wider audience) and further refined by Colquhoun and Wilson in 1999.

4.1 The bare bones of the case.

The Hastings Napier trial was meant to have Hastings as the fluoridated community and Napier as the control. In other words it was going to be cross-sectional study – comparing tooth decay in two cities at the same point in time after one had been fluoridated and the other had not. Shortly into the experiment the control city was dropped, thus the study became a longitudinal one. In this case comparing the tooth decay in one city (Hastings) at the beginning and end of the trial.

For such a comparison to be valid, there must be no change in key parameters during the trial. However, there was a change in one of the key parameters in this trial and it was a major one – the method of diagnosing and treating tooth decay. This was more stringent at the end than it was at the beginning.

At the beginning of the trial school dental nurses were filling indentations (as if they were cavities) but the end they were only filling genuine “holes” in the enamel. Thus the drop in tooth decay attributed to fluoridation was part, or all, the result of making the diagnosis and treatment of tooth decay more stringent.

What makes the final report a fraud was that the authors did not mention the change in diagnosis when claiming the drop in tooth decay was due to fluoridation.

In other words, the whole of the fluoridation program in NZ has been built on the basis of a fraudulent study.

4.2 The “smoking gun” letter.

This letter was obtained by Colquhoun who used the Official Information Act 1982 to obtain all the files pertaining to the Hastings-Napier trial from Department of Health files (1951-1973) now held in National Archives, Wellington. This letter from GH Leslie, the Director of the Division of Dental health of the NZ government, was found in those files and was reprinted in the paper by Colquhoun and Wilson (1999). The letter was written in 1962, some eight years into the ten-year Hastings-Napier trial. Here is the letter:

                                                                                  12, October 1962

Mr. Swann,                                                  


I have delayed acknowledging receipt of Dr. Roche’s letter to you and replying to your minute in the hope that I would by now be able to give a positive reply to your enquiry. I still cannot.


No one is more conscious than I am of the need for proof of the value of fluoridation in terms of reduced treatment. It is something which has been concerning me for a long time. It is only a matter of time before I will be asked questions and I must have an answer with meaning to a layman or I am going to be embarrassed and so is everyone else connected with fluoridation. But it is not easy to get. On the contrary it is proving extremely difficult. Mr. Espia is conferring with Mr. Bock and Mr. Ludwig and I am hopeful that in due course they will be able to make a practical suggestion.

I will certainly not rest easily until a simple method has been devised to prove the equation fluoridation = less fillings


(G.H. Leslie)


Division of Dental Health


According to Colquhoun and Wilson (1998) what was concerning Leslie in 1962 was that the Hastings tooth decay statistics showed little difference between those exposed to fluoridation in Hastings and the rest of unfluoridated New Zealand. In other words, as he makes clear fluoridation wasn’t working and this concerned him greatly as the last sentence indicates, “I will certainly not rest easily until a simple method has been devised to prove the equation fluoridation = less fillings.”

In 1962, the chief dental officer in NZ admits that fluoridation isn’t working – but two years later in 1964 the Fluoridation Trial report “miraculously” shows that it is a great success! But as Colquhoun and Mann showed this “success” was largely based on an artifact – the change of diagnostic for what teeth needed filling.

Conclusion: The Hastings-Napier trial was a fraud. I can find no evidence of a published rebuttal of that conclusion. Certainly Colquhoun’s co-author Professor Robert Mann is not aware of one and I have checked with him.

4.3 Colquhoun one of NZ’s heroes

The late John Colquhoun was a remarkable man who did a remarkable thing.  As chief dental officer of Auckland and as a city councilor Dr. John Colquhoun had once been a very vigorous and successful promoter of fluoridation. However, once he found out from his research (which included a worldwide tour in 1980-81) that he was wrong, he had the courage and the integrity to change his position publicly and spend the rest of his life trying to undo the damage he believed he had caused.  Very few have this kind of integrity.

For those interested I highly recommend that they watch the videotape of my interview with John in 1997. It is titled, “Why I Changed My Mind on Fluoridation.” It can be accessed here, http://fluoridealert.org/fan-tv/colquhoun/

This interview was for me the most inspiring moment in all the 17 years of my involvement in this issue. I saw face to face what scientific integrity was. In my view this sorry practice of fluoridation has gone on for such a long time because of the lack of integrity of those in government agencies who know the truth but are determined to keep this practice going at all costs. Maybe one day we will find out why.

Meanwhile, we need many more citizens of NZ to read the literature on this topic with an open mind. If they do so – and if they are able to insist that their government use the best science available on this topic as well as exercise sound ethical judgment  – this sorry practice must surely be brought to an end.


Please note I have included all the IQ studies listed in the Choi et al (2012) paper as well as some other important references from this paper which I have not discussed individually in this commentary)

An JA, Mei SZ, Liu AP, Fu Y, Wang CF. 1992. Effect of high level of fluoride on children’s intelligence. Chinese J of the Control of Endemic Diseases 7(2):93-94. (in Chinese)

ATSDR (Agency for Toxic Substances and Disease Registry). 2003. Toxicological profile for fluorides, hydrogen fluoride, and fluorine (update). Available online:


Barbier et al. (2010). Molecular Mechanisms of Fluoride Toxicity. Chem Biol Interact. 188(2):319-33 http://www.ncbi.nlm.nih.gov/pubmed/20650267

Bellinger DC. 2007. Interpretation of small effect sizes in occupational and environmental neurotoxicity: Individual versus population risk. Neurotoxicol 28:245-251.

CDC, (2010).  Beltrán-Aguilar, et al “Prevalence and Severity of Dental Fluorosis in the United Stateshttp://www.cdc.gov/nchs/data/databriefs/db53.htm

Chen YX, Han F, Zhou Z, Zhang H, Jiao X, Zhang S, et al. 1991. Research on the intellectual development of children in high fluoride areas. Chinese Journal of Control of Endemic Diseases. 6(supplement):99-100. Available online: http://www.fluoridealert.org/chinese/ (Also available: Fluoride 2008, 41(2):120-124).

Cheng, KK et al. (2007).  “Adding fluoride to water supplies.” BMJ 335:699 http://www.bmj.com/content/335/7622/699?tab=responses

China News. 2008. Twenty-Eight provinces were affected by fluorosis in China. Available online: http://news.qq.com/a/20081216/001707.htm. (in Chinese).

Chioca LR, Raupp IM, Da Cunha C, Losso EM, Andreatini R. 2008. Subchronic fluoride intake induces impairment in habituation and active avoidance tasks in rats. Eur J Pharmocol 579:196-201.

Choi AL, et al. (2012). « Developmental fluoride neurotoxicity: a systematic review and meta-analysis.” Environ Health Perspect 120:1362–1368.

Colquhoun J. and R. Mann (1986). “The Hastings Fluoridation Experiment: Science or Swindle?” The Ecologist 16, no. 6: 243–48.

Colquhoun, J (1987). Education and Fluoridation in New Zealand: An Historical Study,” Ph.D. diss., University of Auckland, New Zealand.

Colquhoun J. and B. Wilson (1999). “The Lost Control and Other Mysteries: Further Revelations on New Zealand’s Fluoridation Trial,” Accountability in Research 6, no. 4:373–94.

Connett, P, Beck, J and Micklem HS. The Case Against Fluoride. Chelsea Green, White River Junction, Vermont, 2010.

Ding Y, Gao Y, Sun H, Han H, Wang W, Ji X, et al. 2011. The relationships between low levels of urine fluoride on children’s intelligence, dental fluorosis in endemic fluorosis area in Hulunbuir, Inner Mongolia, China. J Harzard Mat 186:1942-1946.

Dobbing J. 1968. Vulnerable periods in developing brain. In: Davidson AN, Dobbing J, eds. Applied Neurochemistry. Philadelphia: Davis, pp.287-316.

Fagin, D (2008). “Second Thoughts about Fluoride.” Scientific American, Jan 2, 2008

Fan ZX, Dai HY, Bai AM, Li PO, Li T, LI GD, et al. 2007. Effect of high fluoride exposure in children’s intelligence. J Environ Health 24(10):802-803.

Grandjean P. Occupational fluorosis through 50 years: clinical and epidemiological experiences. Am J Ind Med 1982(3):227-36.

Grandjean P, Landrigan PJ. 2006. Developmental neurotoxicity of industrial compounds. Lancet 368:2167-2178.

Guo XC, Wang R, Cheng C, Wei W, Tang L, Wang Q, et al. 1991. A preliminary exploration of IQ of 7-13 year old pupils in a fluorosis area with contamination from burning coal. Chinese Journal of Endemiology 10:98-100. Available online: http://www.fluoridealert.org/chinese/ (Also available: Fluoride 2008, 41(2):125-128)

Hodge, HC (1963). “Safety Factors in Water Fluoridation Based on the Toxicology of Fluorides,” Proceedings of the Nutrition Society 22: 111–17, http://journals.cambridge.org/action/displayFulltext?type=1&fid=784060&jid=PNS&volumeId=22&issueId=01&aid=784052.

Hong F, Cao Y, Yang D, Wang H. 2001. A study of fluorine effects on children’s intelligence development under different environments. Chinese Primary Health Care 15: 56-57. Available online: http://www.fluoridealert.org/chinese/ (Also available: Fluoride 2008, 41(2):156-160)

Li FH, Chen X, Huang RJ, Xie YP. 2009. Intelligence impact of children with endemic fluorosis caused by fluoride from coal burning. J Environ Health 26(4):338-340. (in Chinese)

Li XH, Hou GQ, Yu B, Yuan CS, Liu Y, Zhang L, et al. 2010. Investigation and analysis of children’s intelligence and dental fluorosis in high fluoride area. J Med Pest Control

26(3):230-231. (in Chinese)

Li XS, Zhi JL, Gao RO. 1995. Effect of fluoride exposure on intelligence in children. Fluoride 28(4):189-192.

Li Y, Jing X, Chen D, Lin L, Wang Z. 2003. The Effects of Endemic Fluoride Poisoning on the Intellectual Development of Children in Baotou. Chinese Journal of Public Health

Management 19(4):337-338. Available online: http://www.fluoridealert.org/chinese/ (Also available: Fluoride 2008, 41(2):161-164)

Li Y, Li X, Wei S. 1994. Effect of excessive fluoride intake on mental work capacity of children and a preliminary study of its mechanism. Journal of West China University of Medical Sciences 25(2):188-91. Available online: http://www.fluoridealert.org/chinese/

Li Y, et al. (2001). “Effect of Long-Term Exposure to Fluoride in Drinking Water on Risks of Bone Fractures,” Journal of Bone and Mineral Research 16 (5): 932–39.

Lin FF, Ai HT, Zhao HX, Lin J, Jhiang JY, Maimaiti, et al. 1991. High fluoride and low iodine environment and subclinical cretinism in Xinjiang. Endemic Dis Bull 6(2):62-67. (in Chinese)

Lu Y, Sun ZR, Wu LN, Wang X, Lu W, Liu SS. et al. 2000. Effect of high-fluoride water on intelligence in children. Fluoride 33(2):74-78. (Also available: The Chinese Journal of

Control of Endemic Disease. 15(4):231-232. (in Chinese) MEDLINE (National Library of Medicine, Bethesda, MD; http://www.ncbi.nlm.nih.gov/pubmed)

McDonagh et al., (2000) “Systematic Review of Water Fluoridation,” British Medical Journal 321, no. 7265: 855–59, www.bmj.com/cgi/content/full/321/7265/855.

Note: The full report that this paper summarizes is commonly known as the York Review and is accessible at http://fluoridealert.org/re/york.review.2000.pdf.

Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. 1995. Neurotoxicity of sodium fluoride in rats. Neurotoxicol Terator 17:169-177.

National Academy of Sciences (1977). Drinking Water and Health. National Academy Press, Washington, DC. pp. 388-389.

NRC (2006). Fluoride in Drinking Water: A Scientific Review of EPA’s Standards. http://www.nap.edu/catalog.php?record_id=11571

Peng YP, Zou J, Yang DF, Li XH, Wu K. 2008. Analysis of water quality from homemade wells in Leshan downtown during 2004-2006. J Occup Health and Damage. 23(4):219-221. (in Chinese).

Poureslami HR, Horri A, Atash R. 2011. High fluoride exposure in drinking water: effect on children’s IQ, one new report. Int J Pediatr Dent 21 (Suppl 1):47.

Ren DL, Li K, Lin D. 1989. An investigation of intelligence development of children aged 8-14 years in high-fluoride and low-iodine areas. Chinese Journal of Control of Endemic Diseases 4:251. Available online: http://www.fluoridealert.org/chinese/. (Also available: Fluoride 2008, 41(4):319-320)

Seraj B, Shahrabi M, Falahzade M, Falahzade FP, Akhondi N. 2006. Effect of High Fluoride Concentration in Drinking Water on Children’s Intelligence. Journal of Dental Medicine 19(2):80-86. (Abstract in English) Available online: http://www.fluoridealert.org/chinese/

Sun MM, Li SK, Wang YF, Li FS. 1991. Measurement of intelligence by drawing test among the children in the endemic area of Al-F combined foxieosis. J Guiyang Medical College.16(3):204-206. (in Chinese)

Sun LY. 2010. Survey of drinking water quality in Jintang County. J Occup Health and Damage. 25(5):277-280. (in Chinese).

Tang QQ, Du J, Ma HH, Jiang SJ, Zhou XJ. 2008. Fluoride and children’s intelligence: a metaanalysis. Bio Trace Elem Res 126:115-120.

TOXNET (National Library of Medicine, Bethesda, MD; http://toxnet.nlm.nih.gov)

Trivedi MH, Verma RJ, Chinoy NJ, Patel RS, Sathawara NG. 2007. Effect of high fluoride water on intelligence of school children in India. Fluoride 40(3):178-183.

Varner JA, Jensen KF, Horvath W, Isaacson RL. 1998. Chronic administration of aluminumfluoride or sodium-fluoride to rats in drinking water: alterations in neuronal andcerebrovascular integrity. Brain Res 784:284-298.

Wang G, Yang D, Jia F, Wang H. 1996. A Study of the IQ Levels of Four- to Seven-year-old Children in High Fluoride Areas. Endemic Diseases Bulletin 11:60-62. Available online: http://www.fluoridealert.org/chinese/ (Also available: Fluoride 2008, 41(4):340-343)

Wang SH, Wang LF, Hu PY, Guo SW, Law SH. 2001. Effects of high iodine and high fluorine on children’s intelligence and thyroid function. Chinese J of Endemiology 20(4):288-290. (in Chinese)

Wang SX, Wang ZH, Cheng XT, Li J, Sang ZP, Zhang XD, et al. Water Arsenic and Fluoride Exposure and Children’s Intelligence Quotient and Growth in Shanyin County, Shanxi, China. Environ Health Perspect 115(4):643-647.

Wang ZH, Wang SX, Zhang XD, Li J, Zheng XT, Hu CM, et al. 2006. Investigation of

children’s growth and development under long-term fluoride exposure. Chinese J Control

Endem Dis 21(4):239-241. (Article in Chinese, Abstract in English)

Water Resources Abstracts (Proquest, Ann Arbor, MI;


Xiang, Q et al. (2003a) “Effect of Fluoride in Drinking Water on Children’s Intelligence,” Fluoride 36, no. 2 (2003): 84–94, http://www.fluorideresearch.org/362/files/FJ2003_v36_n2_p84-94.pdf

Xiang, Q et al.(2003b), “Blood Lead of Children in Wamiao-Xinhuai Intelligence Study” (letter), Fluoride 36, no. 3 (2003):198–99, http://www.fluorideresearch.org/363/files/FJ2003_v36_n3_p198-199.pdf

Xiang, Q et al. (2011). “Children’s serum F and intelligence scores in two villages in China.” Fluoride 44(4):191–194.