Russian Fluoridation Research

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Laxmidhar Panda, Dr. B.B. Kar &  Dr. B. B. Patra
Research Scholars, School of Applied Sciences,
KIIT University, Bhbaneswar, Odisha, India

Key words: Fluorosis, Fluoroapatite,
Biomineralisation, Calcification, Osteosclerosis.

…Excess fluoride may lead to an increased demineralization
leading to the precipitation of Calcium phosphate and
Calcium fluoride and it interferes with calcium metabolism

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  The Ten Major Fluorides  

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TGA Updates – July 2019 + Interpretation

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Osaka Japan – Sars – & Covid-19 – cure – [new research]

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Black Tea Source, Production, & Consumption:
Assessment of Health Risks of Fluoride Intake In New Zealand +

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50 Tons of Cures for Coronavirus – China – Vitamin C

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… Higher levels of aluminium and fluoride 
were related to dementia risk in a population of men and
women who consumed relatively low drinking-water levels of both …
Aluminium & Fluoride in Drinking Water in Relation to Later Dementia Risk

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Ameliorative Effects of Quercetin on Sodium Fluoride-Induced
Oxidative Stress in Rat’s Kidney


Avid Science – Richard Sauerheber

Fluorosis, unsightly at best, was found to afflict
5 million U.S. teenagers aged 12-15 as of 2004

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This thesis draws together research outcomes for sites
predominantly throughout Queensland, Australia. 
A great work – We thank you !

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This paper does not mention fluoride but it needs to be considered

with previous research into Underground Water in Queensland.

Fluorides and radioactive materials
are a deadly combination.


Full original text → HERE

See also


  Atomic Tests in Australia  

 If you ever needed evidence that people 
in high places lie, here it is.

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Fluoride Causes Heart Disease, Stroke and Sudden Death 

Full text → HERE

This brief survey shows that hundreds of scientists have studied the toxic impact of Fluoride on the
cardiovascular system for over 70 years and the detailed evidence of harm is overwhelming.

The general public needs to be warned to minimize their total Fluoride intake. Especially
groups such as the unborn, diabetics and those with compromised
kidneys or thyroid 
must be protected. Promotion of Fluoride and
Fluoridation must cease.

Politicians must purge the bureaucracy of Fluoride promoters.
Not a single excess death caused by water fluoridation can be tolerated.

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… Millions of salmon have instinctively know this for thousands
of years, that is why they go to so much trouble
to swim up rivers to lay their eggs
in fluoride free water.

(Sea water contains fluoride.)
Professor Paul Engelking says fish and fluoride don’t mix.

THIS IS A GREAT VIDEO  HERE ⇐ A slow start but stay with it!

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Zürich Statement on Future Actions on Per-
and Polyfluoroalkyl Substances (PFASs)

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Since 2006, epidemiological studies have documented
six additional developmental neurotoxicants—manganese,
fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane,
tetrachloroethylene, and the polybrominated diphenyl ethers.

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Mind-blowing interview with Judy Mikovits, PhD

Taken down!



In 2014, She co-authored,
“Plague: One Scientist’s Intrepid Search for the 
Truth about Human Retroviruses & Chronic Fatigue Syndrome”

9 More Vaccine Ingredients

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Water Fluoridation: Risky Business for Council-Michael Lusk

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Dr. Richard Sauerheber-Formally apologises to the European Union

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Lawsuit Reveals How Paid Expert Helped 3M 
“Command the Science” on Dangerous Chemicals

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Very Old Research – 80+ years ↓

Rat Research – Fluoride 1934 – U.S. Dept. of Agriculture

Work in this laboratory has shown that fluorine interferes
with the normal development of teeth and bones…

$hame On $low $cience

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Lawsuit Reveals How Paid Expert Helped 3M “Command the Science”

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The Third Digital Revolution to Unleash the Power of Anti-Censorship

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Perchlorate Abundant In Desert –

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PubMed logo

The Relationship between fluoride concentration in drinking
water and mortality rate from uterine cancer
in Okinawa prefecture, Japan 

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Prenatal Fluoride Exposure and Cognitive Outcomes in
Children at 4 and 6–12 Years of Age in Mexico

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Fluoride Is The Major CauseOf Cataract Blindness

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How Understanding Epigenetics Can Save Your Life


New perspective on metals and other contaminants in fluoridation chemicals


PubMed logo

Effectiveness Of Fluoride Varnish…

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See also:


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106 Fluoride Vol. 36 No. 2 106-112 2003 Research Report

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My Views on the Fluoridation of Water 

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Fluoridation, 1979 Scientific Criticisms and Dangers

Philip R.N. Sutton Former Senior Lecturer in Dental Science
University of Melbourne Australia

  Fluoridation Philip Sutton  

An Inconvenient Tooth – Fluoride Documentary

↓  ↓   ↓

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A Scientific Review of EPA’s Standards


Committee on Fluoride in Drinking Water
Board on Environmental Studies and Toxicology
Division on Earth and Life Studies


→ →  NRC_2006  ← ←

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Plumb-solvency Exacerbated by Fluoridation-Dr. Geoff Pain

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WATER -Stroke & Heart Attacks – a short read

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Fluorosis in 89% Carnarvon Aborigines +

Vit.c strip

Bone/joint problems-Fluorosis

Vit.c strip

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You may not be able to imagine that borax, this humble insecticide
and laundry detergent, has the potential of singlehandedly
bringing down our entire economic system !  


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Some of the articles or pieces posted on this site contain copyrighted material.
Credit is given to the author and links are provided to the original source. 
We believe that this constitutes a ‘fair use’.

The peoples of the world have a right to true science.
Deceit and fake $cience need to be exposed.

… Untested chemicals should not be presumed to be safe
to brain development, and chemicals in existing use
and all new chemicals must therefore be tested
for developmental neurotoxicity …


THE LANCET Neurology logo


lancet cont.


Lancet Neurol 2014; 13: 330–38
Published Online
February 15, 2014

Department of Environmental Medicine,
University of Southern Denmark,
Odense, Denmark (P Grandjean MD);
Department of Environmental Health,

Harvard School of Public Health, Boston, MA, USA
(P Grandjean); and Icahn School of Medicine at Mount Sinai,

New York, NY, USA
(P J Landrigan MD)
Correspondence to:

Dr Philippe Grandjean,
Environmental and Occupational Medicine and Epidemiology,
Harvard School of Public Health,
401 Park Drive E-110, Boston,
MA 02215, USA
Neurobehavioural effects of developmental toxicity
Philippe Grandjean, Philip J Landrigan

Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency.
Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence.

In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants:
lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene.

Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers.

We postulate that even more neurotoxicants remain undiscovered.
To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.

Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.


Disorders of neurobehavioural development aff ect 10–15% of all births,1 and prevalence rates of autism spectrum
disorder and attention-deficit hyperactivity disorder seem to be increasing worldwide.2 Subclinical decrements in
brain function are even more common than these neurobehavioural developmental disorders.
All these disabilities can have severe consequences3—they diminish quality of life, reduce academic achievement, and disturb
behaviour, with profound consequences for the welfare and productivity of entire societies.4

The root causes of the present global pandemic of neurodevelopmental disorders are only partly
understood. Although genetic factors have a role,5 they cannot explain recent increases in reported prevalence,
and none of the genes discovered so far seem to be responsible for more than a small proportion of cases.5

Overall, genetic factors seem to account for no more than perhaps 30–40% of all cases of neurodevelopment disorders. Thus, non-genetic, environmental exposures are involved in causation, in some cases probably by interacting with genetically inherited predispositions.

Strong evidence exists that industrial chemicals widely disseminated in the environment are important contributors to what we have called the global, silent pandemic of neurodevelopmental toxicity.6,7

The developing human brain is uniquely vulnerable to toxic chemical exposures, and major windows of
developmental vulnerability occur in utero and during infancy and early childhood.8 During these sensitive life stages, chemicals can cause permanent brain injury at low levels of exposure that would have little or no adverse effect in an adult.

In 2006, we did a systematic review of the published clinical and epidemiological studies into the neurotoxicity of industrial chemicals, with a focus on developmental neurotoxicity.6

We identified five industrial chemicals that could be reliably classified as developmental neurotoxicants: lead, methylmercury, arsenic, polychlorinated biphenyls, and toluene.

We also noted 201 chemicals that had been reported to cause injury to the nervous system in adults, mostly in connection with occupational exposures, poisoning incidents, or suicide attempts. Additionally, more than 1000 chemicals have been reported to be neurotoxic in animals in laboratory studies.

We noted that recognition of the risks of industrial chemicals to brain development has historically needed decades of research and scrutiny, as shown in the cases of lead and methylmercury.9,10

In most cases, discovery began with clinical diagnosis of poisoning in workers and episodes of high-dose exposure. More sophisticated epidemiological studies typically began only much later.

Results from such studies documented developmental neurotoxicity at much lower exposure levels than had previously been thought to be safe. Thus, recognition of widespread subclinical toxicity often did not occur until decades after the initial evidence of neurotoxicity.

A recurring theme was that early warnings of subclinical neurotoxicity were often ignored or even dismissed.11

David P Rall, former Director of the US National Institute of Environmental Health Sciences, once noted that “if thalidomide had caused a ten-point loss of intelligence quotient (IQ) instead of obvious birth defects of the limbs, it would probably still be on the market”.12 Many industrial chemicals marketed at present probably cause IQ deficits of far fewer than ten points and have therefore eluded detection so far, but their combined effects could have enormous consequences. In our 2006 review, 6 we expressed concern that additional developmental neurotoxicants might lurk undiscovered among the 201 chemicals then known to be neurotoxic to adult human beings and among the many thousands of pesticides, solvents, and other industrial chemicals in widespread use that had never been tested for neurodevelopmental toxicity. Since our previous review, new data have emerged about the vulnerability of the developing brain and the neurotoxicity of industrial chemicals. Particularly important new evidence derives from prospective epidemiological birth cohort studies.

In this Review, we consider recent information about the developmental neurotoxicity of industrial chemicals

 page 330 Vol 13 March 2014

Review to update our previous report. 6 Additionally, we propose strategies to counter this pandemic and to prevent the spread of neurological disease and disability in children worldwide.

Unique vulnerability of the developing brain

The fetus is not well protected against industrial chemicals. The placenta does not block the passage of many environmental toxicants from the maternal to the fetal circulation,13 and more than 200 foreign chemicals have been detected in umbilical cord blood.14 Additionally, many environmental chemicals are transferred to the infant through human breastmilk.13 During fetal life and early infancy, the blood–brain barrier provides only partial protection against the entry of chemicals into the CNS.15

 Moreover, the developing human brain is exceptionally sensitive to injury caused by toxic chemicals,6 and several developmental processes have been shown to be highly vulnerable to chemical toxicity. For example, in-vitro studies suggest that neural stem cells are very sensitive to neurotoxic substances such as methylmercury.16 Some pesticides inhibit cholinesterase function in the developing brain,17 thereby affecting the crucial regulatory role of acetylcholine before synapse formation.18 Early-life epigenetic changes are also known to affect subsequent gene expression in the brain.19 In summary, industrial chemicals known or suspected to be neurotoxic to adults are also likely to present risks to the developing brain.

Figure 1 shows the unique vulnerability of the brain during early life and indicates how developmental exposures to toxic chemicals are particularly likely to lead to functional deficits and disease later in life.

New findings about known hazards

Recent research on well-documented neurotoxicants has generated important new insights into the neurodevelopment consequences of early exposures to these industrial chemicals.

Joint analyses that gathered data for lead-associated IQ deficits from seven international studies20,21 support the conclusion that no safe level of exposure to lead exists.22

Cognitive deficits in adults who had previously shown lead-associated developmental delays at school age suggest that the effects of lead neurotoxicity are probably permanent.23 Brain imaging of young adults who had raised lead concentrations in their blood during childhood showed exposure-related decreases in brain volume.24 Lead exposure in early childhood is associated with reduced school performance25 and with delinquent behaviour later in life.26,27

 Developmental neurotoxicity due to methyl-mercury occurs at much lower exposures than the concentrations that affect adult brain function.28 Deficits at 7 years of age that were linked to low-level prenatal exposures to methyl-mercury were still detectable at the age of 14 years.29 Some common genetic polymorphisms seem to increase the vulnerability of the developing brain to methyl-mercury toxicity.30 Functional MRI scans of people exposed prenatally to excess amounts of methyl-mercury showed abnormally expanded activation of brain regions in response to sensory stimulation and motor tasks (fi gure 2).31 Because some adverse effects might be counterbalanced by essential fatty acids from seafood, statistical adjustment for maternal diet during pregnancy results in stronger methylmercury eff ects.32,33

Prenatal and early postnatal exposures to inorganic arsenic from drinking water are associated with cognitive deficits that are apparent at school age.34,35 Infants who survived the Morinaga milk arsenic poisoning incident had highly raised risks of neurological disease during adult life.36

The developmental neurotoxicity of polychlorinated biphenyls has been consolidated and strengthened by recent fi ndings.37 Although little new information has been published about the developmental neurotoxicity of toluene, much has been learned about the developmental neurotoxicity of another common solvent, ethanol, through research on fetal alcohol exposure. Maternal consumption of alcohol during pregnancy, even in very small quantities, has been linked to a range of neurobehavioural adverse effects in off spring, including reduced IQ, impaired executive function and social judgment, delinquent behaviour, seizures, other neurological signs, and sensory problems.38

Newly recognised developmental neurotoxicants

Prospective epidemiological birth cohort studies make it possible to measure maternal or fetal exposures in real time during pregnancy as these exposures actually occur, thus generating unbiased information about the degree and timing of prenatal exposures. Children in these prospective studies are followed longitudinally and assessed with age-appropriate tests to show delayed or deranged neurobehavioural development.

These powerful epidemiological methods have enabled the discovery of additional developmental neurotoxicants.

Early-life exposures to neurotoxic chemicals


Functional maturation

Neurological disease and degenerative changes

Figure 1: Effect of neurotoxicants during early brain development Exposures in early life to neurotoxic chemicals can cause a wide range of adverse effects on brain development and maturation that can manifest as functional impairments or disease at any point in the human lifespan, from early infancy to very old age. Vol 13 March 2014



Figure 2: Functional MRI scans show abnormal activation in the brain

Average activation during finger tapping with the left hand in three adolescents with increased prenatal methylmercury exposure (A) and three control adolescents (B). The control participants activate the premotor and motor cortices on the right, whereas participants exposed to methylmercury activate these areas bilaterally.31

 Cross-sectional data from Bangladesh show that exposure to manganese from drinking water is associated with reduced mathematics achievement scores in school children.39 A study in Quebec, Canada, showed a strong correlation between manganese concentrations in hair and hyperactivity.40 School-aged children living near manganese mining and processing facilities have shown associations between airborne manganese concentrations and diminished intellectual function41 and with impaired motor skills and reduced olfactory function.42 These results are supported by experimental findings in mice.43

A meta-analysis of 27 cross-sectional studies of children exposed to fluoride in drinking water, mainly from China, suggests an average IQ decrement of about seven points in children exposed to raised fluoride concentrations.44 ♦ Confounding from other substances seemed unlikely in most of these studies. Further characterisation of the dose–response association would be desirable.

 The occupational health literature45 suggests that solvents can act as neurotoxicants, but the identifi cation of individual responsible compounds is hampered by the complexity of exposures. In a French cohort study of 3000 children, investigators linked maternal occupational solvent exposure during pregnancy to defi cuts in behavioural assessment at 2 years of age.46 The data showed dose-related increased risks for hyperactivity and aggressive behaviour. One in every five mothers in this cohort reported solvent exposures in common jobs, such as nurse or other hospital employee, chemist, cleaner, hairdresser, and beautician. In Massachusetts, USA, follow-up of a well-defined population with prenatal and early childhood exposure to the solvent tetrachloroethylene (also called perchlor ethylene) in drinking water showed a tendency towards deficient neurological function and increased risk of psychiatric diagnoses.47

  Acute pesticide poisoning occurs frequently in children worldwide, and subclinical pesticide toxicity is also widespread. Clinical data suggest that acute pesticide poisoning during childhood might lead to lasting neurobehavioural defi cits.48,49 Highly toxic and bioaccumulative pesticides are now banned in high-income nations, but are still used in many low-income and middle- income countries. In particular, the organochlorine compounds dichlorodiphenyltrichloroethane (DDT), its metabolite dichlorodiphenyldichloroethylene (DDE), and chlordecone (Kepone), tend to be highly persistent and remain widespread in the environment and in people’s bodies in high-use regions. Recent studies have shown inverse correlations between serum concentrations of DDT or DDE (which indicate accumulated exposures), and neurodevelopmental performance.50,51

 Organophosphate pesticides are eliminated from the human body much more rapidly than are organochlorines, and exposure assessment is therefore inherently less precise. Nonetheless, three prospective epidemiological birth cohort studies provide new evidence that prenatal exposure to organophosphate pesticides can cause developmental neurotoxicity. In these studies, prenatal organophosphate exposure was assessed by measurement of maternal urinary excretion of pesticide metabolites during pregnancy. Dose-related correlations were recorded between maternal exposures to chlorpyrifos or other organophosphates and small head circumference at birth—which is an indication of slowed brain growth in utero—and with neurobehavioural deficits that have persisted to at least 7 years of age.52–54 In a subgroup study, MRI of the brain showed that prenatal chlorpyrifos exposure was associated with structural abnormalities that included thinning of the cerebral cortex.55

Herbicides and fungicides might also have neurotoxic potential.56 Propoxur,57 a carbamate pesticide, and permethrine,58 a member of the pyrethroid class of pesticides, have recently been linked to neuro developmental deficits in children.

 The group of compounds known as polybrominated diphenyl ethers (PBDEs) are widely used as flame retardants and are structurally very similar to the polychlorinated biphenyls. Experimental evidence now suggests that the PBDEs might also be neurotoxic.59

Epidemiological studies in Europe and the USA have shown neurodevelopmental deficits in children with increased prenatal exposures to these compounds.60–62

Thus, the PBDEs should be regarded as hazards to human neurobehavioural development, although attribution of relative toxic potentials to individual PBDE congeners is not yet possible.

Other suspected developmental neurotoxicants

A serious difficulty that complicates many epidemiological studies of neurodevelopmental toxicity in children is the problem of mixed exposures. Most populations are exposed to more than one neurotoxicant at a time, and yet

 332 Vol 13 March 2014


most studies have only a finite amount of power and precision in exposure assessment to discern the possible effects of even single neurotoxicants. A further problem in many epi demiological studies of non-persistent toxicants is that imprecise assessment of exposure tends to obscure associations that might actually be present.63

Guidance from experimental neurotoxicity studies is therefore crucial. In the assessment of potential developmental neurotoxicants, we have used a strength of evidence approach similar to that used by the International Agency for Research on Cancer for assessing epidemiological and experimental studies. Phthalates and bisphenol A are added to many different types of plastics, cosmetics, and other consumer products. Since they are eliminated rapidly in urine, exposure assessment is complicated, and such imprecision might lead to underestimation of the true risk of neurotoxicity. The best-documented eff ects of early-life exposure to phthalates are the consequence of disruption of endocrine signalling.64 Thus, prenatal exposures to phthalates have been linked to both neurodevelopmental deficits and to behavioural abnormalities characterised by shortened attention span and impaired social interactions.65 The neurobehavioral toxicity of these compounds seems to affect mainly boys and could therefore relate to endocrine disruption in the developing brain.66 In regard to bisphenol A, a prospective study showed that point estimates of exposure during gestation were linked to abnormalities in behaviour and executive function in children at 3 years of age.67

 Exposure to air pollution can cause neuro developmental delays and disorders of behavioural functions.68,69 Of the individual components of air pollution, carbon monoxide is a well-documented neurotoxicant, and indoor exposure to this substance has now been linked to defycient neurobehavioural performance in children.70 Less clear is the reported contribution of nitrogen oxides to neurodevelopmental defi cits,71 since these compounds often co-occur with carbon monoxide as part of complex emissions. Tobacco smoke is a complex mixture of hundreds of chemical compounds and is now a well- documented cause of developmental neurotoxicity.72

Infants exposed pre natally to polycyclic aromatic hydrocarbons from traffic exhausts at 5 years of age showed greater cognitive impairment and lower IQ than those exposed to lower levels of these compounds.68

Perfluorinated compounds, such as perfluorooctanoic acid and perfluorooctane sulphonate, are highly persistent in the environment and in the human body, and seem to be neurotoxic.73 Emerging epidemiological evidence suggests that these compounds might indeed impede neurobehavioural development.74

Developmental neurotoxicity and clinical neurology Exposures in early life to developmental neurotoxicants are now being linked to specific clinical syndromes in children. For example, an increased risk of attentiondeficit hyperactivity disorder has been linked to prenatal exposures to manganese, organophosphates,75 and phthalates.76 Phthalates have also been linked to behaviours that resemble components of autism spectrum disorder.77 Prenatal exposure to automotive air pollution in California, USA, has been linked to an increased risk for autism spectrum disorder.78

The persistent decrements in intelligence documented in children, adolescents, and young adults exposed in early life to neurotoxicants could presage the development of neurodegenerative disease later in life. Thus, accumulated exposure to lead is associated with cognitive decline in the elderly.79

Manganese exposure may lead to parkinsonism, and experimental studies have reported Parkinson’s disease as a result of developmental exposures to the insecticide rotenone, the herbicides paraquat and maneb, and the solvent trichloroethylene.80 Any environmental exposure that increases the risk of neurodegenerative disorders in later life (figure 1) requires urgent investigation as the world’s population continues to age.81

The expanding complement of neurotoxicants In our 2006 review,6 we expressed concern that additional developmental neurotoxicants might lie undiscovered in the 201 chemicals that were then known to be neurotoxic to human adults, in the roughly 1000 chemicals known to be neurotoxic in animal species, and in the many thousands of industrial chemicals and pesticides that have never been tested for neurotoxicity. Exposure to neurotoxic chemicals is not rare, since almost half of the 201 known human neurotoxicants are regarded as high production volume chemicals. Our updated literature review shows that since 2006 the list of recognised human neurotoxicants has expanded by 12 chemicals, from 202 (including ethanol) to 214 (table 1 and appendix)—that is, by about two substances per year. Many of these chemicals are widely used and disseminated extensively in the global environment. Of the newly identified neuro developmental toxicants, pesticides constitute the largest group, as was already the case

See Online for appendix

Number Number Identified since 2006

known in known in

2006 2013

Metals and inorganic 25 26 Hydrogen phosphide82

compounds Organic solvents 39* 40 Ethyl chloride83

Pesticides 92 101

Acetamiprid,84 amitraz,85 avermectin,86 emamectin,87

fipronil (Termidor), [FLUORIDE] 88 glyphosate,89 hexaconazole,90

imidacloprid,91 tetramethylenedisulfotetramine92

Other organic compounds 46 47 1,3-butadiene93

Total 202* 214 12 new substances

 *Including ethanol.

Table 1: Industrial chemicals known to be toxic to the human nervous system in 2006 and 2013,

according to chemical group Vol 13 March 2014


Known in 2006 Newly identified

Metals and inorganic compounds Arsenic and arsenic compounds, Fluoride and manganese lead, and methylmercury Organic solvents (Ethanol) toluene Tetrachloroethylene

Pesticides None Chlorpyrifos and DDT/DDE

Other organic compounds Polychlorinated biphenyls Brominated diphenyl ethers

Total 6* 6

DDT=dichlorodiphenyltrichloroethane. DDE=dichlorodiphenyldichloroethylene. *Including ethanol.

Table 2: Industrial chemicals known to cause developmental neurotoxicity in human beings in 2006 and

2013, according to chemical group

Number of IQ points lost

Major medical and neurodevelopmental disorders

 Preterm birth 34 031 025

Autism spectrum disorders 7 109 899

Paediatric bipolar disorder 8 164 080

Attention-defi cit hyperactivity disorder 16 799 400

Postnatal traumatic brain injury 5 827 300

Environmental chemical exposures

Lead 22 947 450

Methylmercury 1 590 000*

Organophosphate pesticides 16 899 488

Other neurotoxicants Unknown

IQ=intelligence quotient. Data from from Bellinger.94 *From Grandjean and


Table 3: Total losses of IQ points in US children 0–5 years of age associated with major risk factors, including developmental exposure to industrial chemicals that cause neurotoxicity 2006. In the same 7-year period, the number of known developmental neurotoxicants has doubled from six to 12 (table 2). Although the pace of scientific discovery of new neurodevelopmental hazards is more rapid today than in the past, it is still slower than the identification of adult neurotoxicants.

 The gap that exists between the number of substances known to be toxic to the adult brain and the smaller number known to be toxic to the much more vulnerable developing brain is unlikely to close in the near future.

This discrepancy is attributable to the fact that toxicity to the adult brain is usually discovered as a result of acute poisoning incidents, typically with a clear and immediate association between causative exposure and adverse effects, as occurs for workplace exposures or suicide attempts. By contrast, the recognition of developmental neurotoxicity relies on two sets of evidence collected at two different points in time: exposure data (often obtained from the mother during pregnancy), and data for the child’s postnatal neurobehavioural development (often obtained 5–10 years later). Because brain functions develop sequentially, the full effects of early neurotoxic damage might not become apparent until school age or beyond. The most reliable evidence of developmental neurotoxicity is obtained through prospective studies that include real-time recording of information about exposure in early life followed by serial clinical assessments of the child. Such research is inherently slow and is hampered by the difficulty of reliable assessment of exposures to individual toxicants in complex mixtures.

Consequences of developmental neurotoxicity

Developmental neurotoxicity causes brain damage that is too often untreatable and frequently permanent. The consequence of such brain damage is impaired CNS function that lasts a lifetime and might result in reduced intelligence, as expressed in terms of lost IQ points, or disruption in behaviour. A recent study compared the estimated total IQ losses from major paediatric causes and showed that the magnitude of losses attributable to lead, pesticides, and other neurotoxicants was in the same range as, or even greater than, the losses associated with medical events such as preterm birth, traumatic brain injury, brain tumours, and congenital heart disease (table 3).94

Loss of cognitive skills reduces children’s academic and economic attainments and has substantial long-term economic effects on societies.4 Thus, each loss of one IQ point has been estimated to decrease average lifetime earnings capacity by about €12 000 or US$18 000 in 2008 currencies.96 The most recent estimates from the USA indicate that the annual costs of childhood lead poisoning are about US$50 billion and that the annual costs of methylmercury toxicity are roughly US$5 billion.97 In the European Union, methylmercury exposure is estimated to cause a loss of about 600 000 IQ points every year, corresponding to an annual economic loss of close to €10 billion. In France alone, lead exposure is associated with IQ losses that correspond to annual costs that might exceed €20 billion.98 Since IQ losses represent only one aspect of developmental neurotoxicity, the total costs are surely even higher.

Evidence from worldwide sources indicates that average national IQ scores are associated with gross domestic product (GDP)—a correlation that might be causal in both directions.99 Thus, poverty can cause low IQ, but the opposite is also true. In view of the widespread exposures to lead, pesticides, and other neurotoxicants in developing countries, where chemical controls might be ineffective compared with those in more developed countries,100,101 developmental exposures to industrial chemicals could contribute substantially to the recorded correlation between IQ and GDP. If this theory is true, developing countries could take decades to emerge from poverty. Consequently, pollution abatement might then be delayed, and a vicious circle can result.

The antisocial behaviour, criminal behaviour, violence, and substance abuse that seem to result from early-life exposures to some neurotoxic chemicals result in increased needs for special educational services, institutionalisation, and even incarceration. In the USA, the murder rate fell sharply 20 years after the removal of lead from petrol,102 a finding consistent with the idea that 334 Vol 13 March 2014


exposure to lead in early life is a powerful determinant of behaviour decades later. Although poorly quantified, such behavioural and social consequences of neuro-development toxicity are potentially very costly.76

Prevention of developmental neurotoxicity caused by industrial chemicals is highly cost effective. A study that quantified the gains resulting from the phase-out of lead additives from petrol reported that in the USA alone, the introduction of lead-free petrol has generated an economic benefit of $200 billion in each annual birth cohort since 1980,103 an aggregate benefit in the past 30 years of over $3 trillion. This success has since been repeated in more than 150 countries, resulting in vast additional savings.

Every US$1 spent to reduce lead hazards is estimated to produce a benefit of US$17–220, which represents a cost- benefit ratio that is even better than that for vaccines.4 Furthermore, the costs associated with the late-life consequences of developmental neurotoxicity are enormous, and the benefits from prevention of degenerative brain disorders could be very substantial.

New methods to identify developmental neurotoxicants

New toxicological methods now allow a rational strategy for the identification of developmental neurotoxicants based on a multidisciplinary approach.104 A new guideline has been approved as a standardised approach for the identification of developmental neurotoxicants.105

However, completion of such tests is expensive and requires the use of many laboratory animals, and reliance on mammals for chemicals testing purposes needs to be reduced.106 US governmental agencies have established the National Center for Computational Toxicology and an initiative— the Tox 21 Program—to promote the evolution of toxicology from a mainly observational science to a predominantly predictive science.107

In-vitro methods have now reached a level of predictive validity that means they can be applied to neurotoxicity testing.108 Some of these tests are based on neural stem cells. Although these cell systems do not have a blood– brain barrier and particular metabolising enzymes, these approaches are highly promising. As a further option, data for protein links and protein–protein interactions can now be used to explore potential neurotoxicity in silica, 109 thus showing that existing computational methods might predict potential toxic eff ects.110 In summary, use of the whole range of approaches along with clinical and epidemiological evidence, when available, should enable the integration of information for use in at least a tentative risk assessment. With these methods, we anticipate that the pace of scientifi c discovery in developmental neurotoxicology will accelerate further in the years ahead.

Conclusions and Recommendations

The updated findings presented in this Review confirm and extend our 2006 conclusions.6 During the 7 years since our previous report, the number of industrial chemicals recognised to be developmental neurotoxicants has doubled. Exposures to these industrial chemicals in the environment contribute to the pandemic of developmental neurotoxicity.

Two major obstacles impede efforts to control the global pandemic of developmental neurotoxicity. These barriers, which we noted in our previous review 6 and were recently underlined by the US National Research Council,111 are: large gaps in the testing of chemicals for developmental neurotoxicity, which results in a paucity of systematic data to guide prevention; and the huge amount of proof needed for regulation. Thus, very few chemicals have been regulated as a result of developmental neurotoxicity.

 The presumption that new chemicals and technologies are safe until proven otherwise is a fundamental problem.111 Classic examples of new chemicals that were introduced because they conveyed certain benefits, but were later shown to cause great harm, include several neurotoxicants, asbestos, thalidomide, diethylstilbestrol, and the chlorofluorocarbons.112 A recurring theme in each of these cases was that commercial introduction and wide dissemination of the chemicals preceded any systematic effort to assess potential toxicity. Particularly absent were advance efforts to study possible effects on children’s health or the potential of exposures in early life to disrupt early development. Similar challenges have been confronted in other public health disasters, such as those caused by tobacco smoking, alcohol use, and refined foods. These problems have been recently termed industrial epidemics.113

To control the pandemic of developmental neurotoxicity, we propose a coordinated international strategy (panel).

Mandatory and transparent assessment of evidence for neurotoxicity is the foundation of this strategy.

Assessment of toxicity must be followed by governmental regulation and market intervention. Voluntary controls seem to be of little value.11

Panel: Recommendations for an international clearinghouse on neurotoxicity The main purpose of this agency would be to promote optimum brain health, not just avoidance of neurological disease, by inspiring, facilitating, and coordinating research and public policies that aim to protect brain development during the most sensitive life stages.

The main efforts would aim to:

Screen industrial chemicals present in human exposures for neurotoxic effects so that

hazardous substances can be identified for tighter control.

Stimulate and coordinate new research to understand how toxic chemicals interfere with brain development and how best to prevent long-term dysfunctions and deficits

•Function as a clearinghouse for research data and strategies by gathering and assessing documentation about brain toxicity and stimulating international collaboration on research and prevention

•Promote policy development aimed at protecting vulnerable populations against chemicals that are toxic to the brain without needing unrealistic amounts of scientific proof Vol 13 March 2014


The three pillars of our proposed strategy are:

legally mandated testing of existing industrial chemicals and pesticides already in commerce, with prioritisation of those with the most widespread use, and incorporation of new assessment technologies; legally mandated premarket evaluation of new chemicals before they enter markets, with use of precautionary approaches for chemical testing that recognise the unique vulnerability of the developing brain; and the formation of a new clearinghouse for neurotoxicity as a parallel to the International Agency for Research on Cancer. This new agency will assess industrial chemicals for developmental neurotoxicity with a precautionary approach that emphasises prevention and does not require absolute proof of toxicity. It will facilitate and coordinate epidemiological and toxicological studies and will lead the urgently needed global programmes for prevention.

These new approaches must reverse the dangerous presumption that new chemicals and technologies are safe until proven otherwise. They must also overcome the existing requirement to produce absolute proof of toxicity before action can be started to protect children against neurotoxic substances. Precautionary interpretation of data about developmental neurotoxicity should take into account the very large individual and societal costs that result from failure to act on available documentation to prevent disease in children.114 Academic research has often favoured scepticism and required extensive replication before acceptance of a hypothesis,114 thereby adding to the inertia in toxicology and environmental health research and the consequent disregard of many other potential neurotoxicants.115 Additionally, the strength of evidence that is needed to constitute “proof” should be analysed in a societal perspective, so that the implications of ignoring a developmental neurotoxicant and of failing to act on the basis of available data are also taken into account.

Finally, we emphasise that the total number of neurotoxic substances now recognised almost certainly represents an underestimate of the true number of developmental neurotoxicants that have been released into the global environment. Our very great concern is that children [?]

Search strategy and selection criteria We identified studies published since 2006 on the neurotoxic effects of industrial chemicals in human beings by using the search terms “neurotoxicity syndromes”[MeSH], “neurotoxic”,“neurologic”, or “neuro*”, combined with “exposure” and “poisoning” in PubMed, from 2006 to the end of 2012. For developmental neurotoxicity, the search terms were “prenatal exposure delayed effects”[MeSH], “maternal exposure” or “maternal fetal exchange”, “developmental disabilities/chemically induced” and “neurotoxins”, all of which were searched for with the limiters “All Child: 0–18 years, Human”.

We also used references cited in the publications retrieved. worldwide are being exposed to unrecognised toxic chemicals that are silently eroding intelligence, disrupting behaviours, truncating future achievements, and damaging societies, perhaps most seriously in developing countries. A new framework of action is needed.


Both authors did the literature review, wrote and revised the report, and approved the final version.

Conflicts of interest

PG has provided paid expert testimony about mercury toxicology for the US Department of Justice. PJL has provided paid expert testimony in cases of childhood lead poisoning. We declare that we have no other conflicts of interest.


This work was supported by the National Institutes of Health, National Institute for Environmental Health Sciences (ES09584, ES09797, and ES11687). The funding source had no role in the literature review, interpretation of data, writing of this Review, or in the decision to submit for publication. The contents of this paper are solely the responsibility of the authors and do not represent the official views of the National Institutes of Health. We thank Mary S Wolff (Icahn School of Medicine at Mount Sinai, New York, NY, USA) and Linda S Birnbaum (US National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA) for their critical reading of the report.



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 + ItQ decrement of about seven points for each sucessive generation.


Double Blue bar ss


 As from today, water fluoridation must be prohibited in all Member States of the EC 

Doug Cross

20th January 2014

(For the PDF version of this comment CLICK HERE ) 

The last legal loophole through which the British and Irish governments have been able to wriggle in their continued imposition of fluoridated water supplies finally closed today. The addition of fluorosilicic acid to any food is now completely banned throughout the entire European Community.

June 2013

This is not a recent event but seems to have been missed by the main media.


7  October 2012

Fluoride Accident South Korea

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Hydrogen Fluoride kills 5

↑ Warning, a disturbing short video ↑

An estimated 8 tons of HF was released.
5 people including the 2 workers perished,
18 responders, workers, reporter wound-up in the hospital,
almost 3000 villagers from 2 villages downwind of the facility
were treated for irritation, exposure.

Five workers were killed and 18 others were injured in the blast at chemical maker Hube Global at the Gumi National Industrial Complex in the industrial city, about 200 kilometers southeast of Seoul.

 The gas leak has cost factories in the industrial complex about 17.7 billion won (US$15.9 million) in lost production, officials said. Hundreds of angry villagers in Gumi who suffered after the massive gas leak moved to a safer region with some residents reporting blood in their saliva. About 110 elderly people in Bongsan-ri village evacuated to a facility about 10 kilometers away.

            Double Blue bar ss

We are sorry if this is a bit technical …
Developmental Fluoride Neurotoxicity:
A Systematic Review and Meta-Analysis

Anna L. Choi,1 Guifan Sun,2 Ying Zhang,3 and Philippe Grandjean1,4

Author information ► Article notes ►

Copyright and License information ►



Although fluoride may cause neurotoxicity in animal models and
acute fluoride poisoning causes neurotoxicity in adults,
very little is known of its effects on children’s neurodevelopment.


We performed a systematic review and meta-analysis of published studies to investigatethe effects of increased fluoride exposure and delayed neurobehavioral development.Methods: We searched the MEDLINE, EMBASE, Water Resources Abstracts, and TOXNET databases through 2011 for eligible studies. We also searched the China National Knowledge Infrastructure (CNKI) database, because many studies on fluoride neurotoxicity have been published in Chinese journals only. In total, we identified 27 eligible epidemiological studies with high and reference exposures, end points of IQ scores, or related cognitive function measures with means and variances for the two exposure groups. Using random-effects models, we estimated the standardized mean difference between exposed and reference groups across all studies. We conducted sensitivity analyses restricted to studies using the same outcome assessment and having drinking-water fluoride as the only exposure. We performed the Cochran test for heterogeneity between studies, Begg’s funnel plot, and Egger test to assess publication bias, and conducted meta-regressions to explore sources of variation in mean differences among the studies.


The standardized weighted mean difference in IQ score between exposed and reference populations was –0.45 (95% confidence interval: –0.56, –0.35) using a random-effects model. Thus, children in high-fluoride areas had significantly lower IQ scores than those who lived in low-fluoride areas. Subgroup and sensitivity analyses also indicated inverse associations, although the substantial heterogeneity did not appear to decrease.


The results support the possibility of an adverse effect of high fluoride exposure on children’s neurodevelopment. Future research should include detailed individual-level information on prenatal exposure, neurobehavioral performance, and covariates for adjustment.


fluoride, intelligence, neurotoxicityA recent report from the National Research Council (NRC 2006) concluded that adverse effects of high fluoride concentrations in drinking water may be of concern and that additional research is warranted. Fluoride may cause neurotoxicity in laboratory animals, including effects on learning and memory (Chioca et al. 2008Mullenix et al. 1995).  A recent experimental study where the rat hippocampal neurons were incubated with various concentrations (20 mg/L, 40 mg/L, and 80 mg/L) of sodium fluoride in vitro showed that fluoride neurotoxicity may target hippocampal neurons (Zhang M et al. 2008). Although acute fluoride poisoning may be neurotoxic to adults, most of the epidemiological information available on associations with children’s neurodevelopment is from China, where fluoride generally occurs in drinking water as a natural contaminant, and the concentration depends on local geological conditions. In many rural communities in China, populations with high exposure to fluoride in local drinking-water sources may reside in close proximity to populations without high exposure (NRC 2006). Opportunities for epidemiological studies depend on the existence of comparable population groups exposed to different levels of fluoride from drinking water. Such circumstances are difficult to find in many industrialized countries, because fluoride concentrations in community water are usually no higher than 1 mg/L, even when fluoride is added to water supplies as a public health measure to reduce tooth decay. Multiple epidemiological studies of developmental fluoride neurotoxicity were conducted in China because of the high fluoride concentrations that are substantially above 1 mg/L in well water in many rural communities, although microbiologically safe water has been accessible to many rural households as a result of the recent 5-year plan (2001–2005) by the Chinese government. It is projected that all rural residents will have access to safe public drinking water by 2020 (World Bank 2006). However, results of the published studies have not been widely disseminated. Four studies published in English (Li XS et al. 1995; Lu et al. 2000Xiang et al. 2003Zhao et al. 1996) were cited in a recent report from the NRC (2006), whereas the World Health Organization (2002) has considered only two (Li XS et al. 1995; Zhao et al. 1996) in its most recent monograph on fluoride. Fluoride readily crosses the placenta (Agency for Toxic Substances and Disease Registry 2003). Fluoride exposure to the developing brain, which is much more susceptible to injury caused by toxicants than is the mature brain, may possibly lead to permanent damage (Grandjean and Landrigan 2006). In response to the recommendation of the NRC (2006), the U.S. Department of Health and Human Services (DHHS) and the U.S. EPA recently announced that DHHS is proposing to change the recommended level of fluoride in drinking water to 0.7 mg/L from the currently recommended range of 0.7–1.2 mg/L, and the U.S. EPA is reviewing the maximum amount of fluoride allowed in drinking water, which currently is set at 4.0 mg/L (U.S. EPA 2011). To summarize the available literature, we performed a systematic review and meta-analysis of published studies on increased fluoride exposure in drinking water associated with neurodevelopmental delays. We specifically targeted studies carried out in rural China that have not been widely disseminated, thus complementing the studies that have been included in previous reviews and risk assessment reports. Go to:


Search strategy. We searched MEDLINE (National Library of Medicine, Bethesda, MD, USA;, Embase (Elsevier B.V., Amsterdam, the Netherlands;, Water Resources Abstracts (Proquest, Ann Arbor, MI, USA;, and TOXNET (Toxicology Data Network; National Library of Medicine, Bethesda, MD, USA; databases to identify studies of drinking-water fluoride and neurodevelopmental outcomes in children. In addition, we searched the China National Knowledge Infrastructure (CNKI; Beijing, China; database to identify studies published in Chinese journals only. Key words included combinations of “fluoride” or “drinking water fluoride,” “children,” “neurodevelopment” or “neurologic” or “intelligence” or “IQ.”  We also used references cited in the articles identified. We searched records for 1980–2011. Our literature search identified 39 studies, among which 36 (92.3%) were studies with high and reference exposure groups, and 3 (7.7%) studies were based on individual-level measure of exposures. The latter showed that dose-related deficits were found, but the studies were excluded because our meta-analysis focused on studies with the high- and low-exposure groups only. In addition, two studies were published twice, and the duplicates were excluded.Inclusion criteria and data extraction. The criteria for inclusion of studies included studies with high and reference fluoride exposures, end points of IQ scores or other related cognitive function measures, presentation of a mean outcome measure, and associated measure of variance [95% confidence intervals (CIs) or SEs and numbers of participants]. Interpretations of statistical significance are based on an alpha level of 0.05. Information included for each study also included the first author, location of the study, year of publication, and numbers of participants in high-fluoride and low-fluoride areas. We noted and recorded the information on age and sex of children, and parental education and income if available. Statistical analysis. We used STATA (version 11.0; StataCorp, College Station, TX, USA) and available commands (Stern 2009) for the meta-analyses. A standardized weighted mean difference (SMD) was computed using both fixed-effects and random-effects models. The fixed-effects model uses the Mantel–Haenszel method assuming homogeneity among the studies, whereas the random-effects model uses the DerSimonian and Laird method, incorporating both a within-study and an additive between-studies component of variance when there is between-study heterogeneity (Egger et al. 2001). The estimate of the between-study variation is incorporated into both the SE of the estimate of the common effect and the weight of individual studies, which was calculated as the inverse sum of the within and between study variance. We evaluated heterogeneity among studies using the I2 statistic, which represents the percentage of total variation across all studies due to between-study heterogeneity (Higgins and Thompson 2002). We evaluated the potential for publication bias using Begg and Egger tests and visual inspection of a Begg funnel plot (Begg and Mazumdar 1994Egger et al. 1997). We also conducted independent meta-regressions to estimate the contribution of study characteristics (mean age in years from the age range and year of publication in each study) to heterogeneity among the studies. The scoring standard for the Combined Raven’s Test–The Rural edition in China (CRT-RC) test classifies scores of ≤ 69 and 70–79 as low and marginal intelligence, respectively (Wang D et al. 1989). We also used the random-effects models to estimate risk ratios for the association between fluoride exposure and a low/marginal versus normal Raven’s test score among children in studies that used the CRT-RC test (Wang D et al. 1989). Scores indicating low and marginal intelligence (≤ 69 and 70–79, respectively) were combined as a single outcome due to small numbers of children in each outcome subgroup.


Six of the 34 studies identified were excluded because of missing information on the number of subjects or the mean and variance of the outcome [see Figure 1 for a study selection flow chart and Supplemental Material, Table S1 ( for additional information on studies that were excluded from the analysis]. Another study (Trivedi et al. 2007) was excluded because SDs reported for the outcome parameter were questionably small (1.13 for the high-fluoride group, and 1.23 for the low-fluoride group) and the SMD (–10.8; 95% CI: –11.9, –9.6) was > 10 times lower than the second smallest SMD (–0.95; 95% CI: –1.16, –0.75) and 150 times lower than the largest SMD (0.07; 95% CI: –0.083, 0.22) reported for the other studies, which had relatively consistent SMD estimates. Inclusion of this study in the meta-analysis resulted with a much smaller pooled random-effects SMD estimate and a much larger I2 (–0.63; 95% CI: –0.83, –0.44, I2 94.1%) compared with the estimates that excluded this study (–0.45; 95% CI: –0.56, –0.34, I2 80%) (see Supplemental Material, Figure S1). Characteristics of the 27 studies included are shown in Table 1 (An et al. 1992; Chen et al. 1991Fan et al. 2007Guo et al. 1991Hong et al. 2001; Li FH et al. 2009; Li XH et al. 2010; Li XS 1995; Li Y et al. 1994; Li Y et al. 2003; Lin et al. 1991Lu et al. 2000Poureslami et al. 2011Ren et al. 1989Seraj et al. 2006Sun et al. 1991; Wang G et al. 1996; Wang SH et al. 2001; Wang SX et al. 2007; Wang ZH et al. 2006; Xiang et al. 2003Xu et al. 1994Yang et al. 1994Yao et al. 19961997; Zhang JW et al. 1998; Zhao et al. 1996). Two of the studies included in the analysis were conducted in Iran (Poureslami et al. 2011Seraj et al. 2006); the other study cohorts were populations from China. Two cohorts were exposed to fluoride from coal burning (Guo et al. 1991; Li XH et al. 2010); otherwise populations were exposed to fluoride through drinking water. The CRT-RC was used to measure the children’s intelligence in 16 studies. Other intelligence measures included the Wechsler Intelligence tests (3 studies; An et al. 1992Ren et al. 1989; Wang ZH et al. 1996), Binet IQ test (2 studies; Guo et al. 1991; Xu et al. 1994), Raven’s test (2 studies; Poureslami et al. 2011Seraj et al. 2006), Japan IQ test (2 studies; Sun et al. 1991; Zhang JW et al. 1998), Chinese comparative intelligence test (1 study; Yang et al. 1994), and the mental work capacity index (1 study; Li Y et al. 1994). Because each of the intelligence tests used is designed to measure general intelligence, we used data from all eligible studies to estimate the possible effects of fluoride exposure on general intelligence. Figure 1

Flow diagram of the meta-analysis.

Table 1 Characteristics of epidemiological studies of fluoride exposure and children’s cognitive outcomes.In addition, we conducted a sensitivity analysis restricted to studies that used similar tests to measure the outcome (specifically, the CRT-RC, Wechsler Intelligence test, Binet IQ test, or Raven’s test), and an analysis restricted to studies that used the CRT-RC. We also performed an analysis that excluded studies with co-exposures including iodine and arsenic, or with non-drinking-water fluoride exposure from coal burning. Pooled SMD estimates. Among the 27 studies, all but one study showed random-effect SMD estimates that indicated an inverse association, ranging from –0.95 (95% CI: –1.16, –0.75) to –0.10 (95% CI: –0.25, 0.04) (Figure 2). The study with a positive association reported an SMD estimate of 0.07 (95% CI: –0.8, 0.22). Similar results were found with the fixed-effects SMD estimates. The fixed-effects pooled SMD estimate was –0.40 (95% CI: –0.44, –0.35), with a p-value < 0.001 for the test for homogeneity. The random-effects SMD estimate was –0.45 (95% CI: –0.56, –0.34) with an I2 of 80% and homogeneity test p-value < 0.001 (Figure 2). Because of heterogeneity (excess variability) between study results, we used primarily the random-effects model for subsequent sensitivity analyses, which is generally considered to be the more conservative method [*] (Egger et al. 2001). Among the restricted sets of intelligence tests, the SMD for the model with only CRT-RC tests and drinking-water exposure (and to a lesser extent the model with only CRT-RC tests) was lower than that for all studies combined, although the difference did not appear to be significant. Heterogeneity, however, remained at a similar magnitude when the analyses were restricted (Table 2). Figure 2 Random-effect standardized weighted mean difference (SMD) estimates and 95% CIs of child’s intelligence score associated with high exposure to fluoride. SMs for individual studies are shown as solid diamonds (), and the pooled SMD is Table 2  Sensitivity analyses of pooled random-effects standardized weighted mean difference (SMD) estimates of child’s intelligence score with high exposure of fluoride. Sources of heterogeneity. We performed meta-regression models to assess study characteristics as potential predictors of effect. Information on the child’s sex and parental education were not reported in > 80% of the studies, and only 7% of the studies reported household income. These variables were therefore not included in the models. Among the two covariates, year of publication (0.02; 95% CI: 0.006, 0.03), but not mean age of the study children (–0.02; 95% CI: –0.094, 0.04), was a significant predictor in the model with all 27 studies included. I2 residual 68.7% represented the proportion of residual between-study variation due to heterogeneity. From the adjusted R2, 39.8% of between-study variance was explained by the two covariates. The overall test of the covariates was significant (p = 0.004). When the model was restricted to the 16 studies that used the CRT-RC, the child’s age (but not year of publication) was a significant predictor of the SMD. The R2 of 65.6% of between-study variance was explained by the two covariates, and only 47.3% of the residual variation was attributable to heterogeneity. The overall test of both covariates in the model remained significant (p = 0.0053). On further restriction of the model to exclude the 7 studies with arsenic and iodine as co-exposures and fluoride originating from coal burning (thus including only the 9 with fluoride exposure from drinking water), neither age nor year of publication was a significant predictor, and the overall test of covariates was less important (p = 0.062), in accordance with the similarity of intelligence test outcomes and the source of exposure in the studies included. Although official reports of lead concentrations in the study villages in China were not available, some studies reported high percentage (95–100%) of low lead exposure (less than the standard of 0.01 mg/L) in drinking-water samples in villages from several study provinces (Bi et al. 2010Peng et al. 2008Sun 2010). Publication bias. A Begg’s funnel plot with the SE of SMD from each study plotted against its corresponding SMD did not show clear evidence of asymmetry, although two studies with a large SE also reported relatively large effect estimates, which may be consistent with publication bias or heterogeneity (Figure 3). The plot appears symmetrical for studies with larger SE, but with substantial variation in SMD among the more precise studies, consistent with the heterogeneity observed among the studies included in the analysis. Begg (p = 0.22) and Egger (p = 0.11) tests did not indicate significant (p < 0.05) departures from symmetry. Figure 3 Begg’s funnel plot showing individual studies included in the analysis according to random-effect standardized weighted mean difference (SMD) estimates (x-axis) and the SE (se) of each study-specific SMD (y-axis). The solid vertical line indicates Pooled risk ratios. The relative risk (RR) of a low/marginal score on the CRT-RC test (< 80) among children with high fluoride exposure compared with those with low exposure (16 studies total) was 1.93 (95% CI: 1.46, 2.55; I2 58.5%). When the model was restricted to 9 studies that used the CRT-RC and included only drinking-water fluoride exposure (Chen et al. 1991Fan et al. 2007; Li XH et al. 2010; Li XS et al. 1995; Li Y et al. 2003; Lu et al. 2000; Wang ZH et al. 2006; Yao et al. 1996, 1997), the estimate was similar (RR = 1.75; 95% CI: 1.16, 2.65; I2 70.6%). Although fluoride exposure showed inverse associations with test scores, the available exposure information did not allow a formal dose–response analysis. However, dose-related differences in test scores occurred at a wide range of water-fluoride concentrations. Go to:


Findings from our meta-analyses of 27 studies published over 22 years suggest an inverse association between high fluoride exposure and children’s intelligence. Children who lived in areas with high fluoride exposure had lower IQ scores than those who lived in low-exposure or control areas. Our findings are consistent with an earlier review (Tang et al. 2008), although ours more systematically addressed study selection and exclusion information, and was more comprehensive in a) including 9 additional studies, b) performing meta-regression to estimate the contribution of study characteristics as sources of heterogeneity, and c) estimating pooled risk ratios for the association between fluoride exposure and a low/marginal Raven’s test score. As noted by the NRC committee (NRC 2006), assessments of fluoride safety have relied on incomplete information on potential risks. In regard to developmental neurotoxicity, much information has in fact been published, although mainly as short reports in Chinese that have not been available to most expert committees. We carried out an extensive review that includes epidemiological studies carried out in China. Although most reports were fairly brief and complete information on covariates was not available, the results tended to support the potential for fluoride-mediated developmental neurotoxicity at relatively high levels of exposure in some studies. We did not find conclusive evidence of publication bias, although there was substantial heterogeneity among studies. Drinking water may contain other neurotoxicants, such as arsenic, but exclusion of studies including arsenic and iodine as co-exposures in a sensitivity analysis resulted in a lower estimate, although the difference was not significant. The exposed groups had access to drinking water with fluoride concentrations up to 11.5 mg/L (Wang SX et al. 2007); thus, in many cases concentrations were above the levels recommended (0.7–1.2 mg/L; DHHS) or allowed in public drinking water (4.0 mg/L; U.S. EPA) in the United States (U.S. EPA 2011). A recent cross-sectional study based on individual-level measure of exposures suggested that low levels of water fluoride (range, 0.24–2.84 mg/L) had significant negative associations with children’s intelligence (Ding et al. 2011). This study was not included in our meta-analysis, which focused only on studies with exposed and reference groups, thereby precluding estimation of dose-related effects.The results suggest that fluoride may be a developmental neurotoxicant that affects brain development at exposures much below those that can cause toxicity in adults (Grandjean 1982). For neurotoxicants such as lead and methylmercury, adverse effects are associated with blood concentrations as low as 10 nmol/L. Serum fluoride concentrations associated with high intakes from drinking water may exceed 1 mg/L, or 50 µmol/L—more than 1,000 times the levels of some other neurotoxicants that cause neurodevelopmental damage. Supporting the plausibility of our findings, rats exposed to 1 ppm (50 µmol/L) of water fluoride for 1 year showed morphological alterations in the brain and increased levels of aluminum in brain tissue compared with controls (Varner et al. 1998).

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. However, as research on other neurotoxicants has shown, a shift to the left of IQ distributions in a population will have substantial impacts, especially among those in the high and low ranges of the IQ distribution (Bellinger 2007).
Our review cannot be used to derive an exposure limit, because the actual exposures of the individual children are not known. Misclassification of children in both high- and low-exposure groups may have occurred if the children were drinking water from other sources (e.g., at school or in the field). The published reports clearly represent independent studies and are not the result of duplicate publication of the same studies (we removed two duplicates). Several studies (Hong et al. 2001Lin et al. 1991; Wang SH et al. 2001; Wang SX et al. 2007; Xiang et al. 2003Zhao et al. 1996) report other exposures, such as iodine and arsenic, a neurotoxicant, but our sensitivity analyses showed similar associations between high fluoride exposure and the outcomes even after these studies were excluded. Large tracts of China have superficial fluoride-rich minerals with little, if any, likelihood of contamination by other neurotoxicants that would be associated with fluoride concentrations in drinking water. From the geographic distribution of the studies, it seems unlikely that fluoride-attributed neurotoxicity could be attributable to other water contaminants. Still, each of the articles reviewed had deficiencies, in some cases rather serious ones, that limit the conclusions that can be drawn. However, most deficiencies relate to the reporting of where key information was missing. The fact that some aspects of the study were not reported limits the extent to which the available reports allow a firm conclusion. Some methodological limitations were also noted. Most studies were cross-sectional, but this study design would seem appropriate in a stable population where water supplies and fluoride concentrations have remained unchanged for many years.
The current water fluoride level likely also reflects past developmental exposures. In regard to the outcomes, the inverse association persisted between studies using different intelligence tests, although most studies did not report age adjustment of the cognitive test scores. Fluoride has received much attention in China, where widespread dental fluorosis indicates the prevalence of high exposures. In 2008, the Ministry of Health reported that fluorosis was found in 28 provinces with 92 million residents (China News 2008). Although microbiologically safe, water supplies from small springs or mountain sources created pockets of increased exposures near or within areas of low exposures, thus representing exposure settings close to the ideal, because only the fluoride exposure would differ between nearby neighborhoods. Chinese researchers took advantage of this fact and published their findings, though mainly in Chinese journals and according to the standards of science at the time.

This research dates back to the 1980s, but has not been widely cited

at least in part because of limited access to Chinese journals. [our emphasis]

In its review of fluoride, the NRC (2006) noted that the safety and the risks of fluoride at concentrations of 2–4 mg/L were incompletely documented. Our comprehensive review substantially extends the scope of research available for evaluation and analysis. Although the studies were generally of insufficient quality, the consistency of their findings adds support to existing evidence of fluoride-associated cognitive deficits, and suggests that potential developmental neurotoxicity of fluoride should be a high research priority. Although reports from the World Health Organization and national agencies have generally focused on beneficial effects of fluoride (Centers for Disease Control and Prevention 1999Petersen and Lennon 2004), the NRC report examined the potential adverse effects of fluoride at 2–4 mg/L in drinking water and not the benefits or potential risks that may occur when fluoride is added to public water supplies at lower concentrations (0.7–1.2 mg/L) (NRC 2006).

In conclusion, our results support the possibility of adverse effects of fluoride exposures on children’s neuro-development. Future research should formally evaluate dose–response relations based on individual-level measures of exposure over time, including more precise prenatal exposure assessment and more extensive standardized measures of neurobehavioral performance, in addition to improving assessment and control of potential confounders.

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Supplemental Material

(94 KB) PDF

Click here for additional data file.(106K, pdf)

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We thank V. Malik, Harvard School of Public Health,

for the helpful advice on the meta-analysis methods.

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This study was supported by internal institutional funds.The authors declare they have no actual or potential competing financial interests.

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

  • • Tang QQ, Du J, Ma HH, Jiang SJ, Zhou XJ. Fluoride and children’s intelligence: a meta-analysis. Bio Trace Elem Res. 2008;126:115–120. [PubMed]

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

  • • U.S. EPA. EPA and HHS Announce New Scientific Assessments and Actions on Fluoride: Agencies Working Together to Maintain Benefits of Preventing Tooth Decay while Preventing Excessive Exposure. 2011 Available:!OpenDocument [accessed 7 January 2011]

  • • Varner JA, Jensen KF, Horvath W, Isaacson RL. Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res. 1998;784:284–298. [PubMed]

  • • Wang D, Di M, Qian M. Tianjin, China: Tianjin Medical University; 1989. Chinese Standardized Raven Test, Rural Version.

  • • Wang G, Yang D, Jia F, Wang H. Research on intelligence quotient of 4-7 year-old children in a district with a high level of fluoride. Endem Dis Bull. 1996;11:60–62. Available: [accessed 20 August 2012]

  • • Wang SH, Wang LF, Hu PY, Guo SW, Law SH. Effects of high iodine and high fluorine on children’s intelligence and thyroid function. Chin J Endemiol. 2001;20(4):288–290. [in Chinese]

  • • Wang SX, Wang ZH, Cheng XT, Li J, Sang ZP, Zhang XD, et al. Arsenic and fluoride exposure in drinking water: children’s IQ and growth in Shanyin County, Shanxi Province, China. Environ Health Perspect. 2007;115:643–647. [PMC free article] [PubMed]

  • • Wang ZH, Wang SX, Zhang XD, Li J, Zheng XT, Hu CM, et al. Investigation of children’s growth and development under long-term fluoride exposure. Chin J Control Endem Dis. 2006;21(4):239–241. [in Chinese; abstract in English]

  • • World Bank. Water Quality Management: Policy and Institutional Considerations. 2006 Available: [accessed 13 June 2012]

  • • World Health Organization. Fluorides. Geneva:World Health Organization. 2002 Available: [accessed 5 September 2012]

  • • Wu TM. Shanghai: Commercial Press (in Chinese); 1936. Second revision of Chinese-Binet Intelligence Test.

  • • Wu T. Beijing: Beijing University Press; 1983. The Chinese Comparative Intelligence Test Guidebook. 3rd ed.

  • • Xiang Q, Liang Y, Chen L, Wang C, Chen B, Chen X, et al. Effect of fluoride in drinking water on children’s intelligence. Fluoride. 2003;36(2):84–94.

  • • Xu YL, Lu CS, Zhang XN. Effect of fluoride on children’s intelligence. Endem Dis Bull. 1994;2:83–84. [in Chinese]

  • • Yang Y, Wang X, Guo X, Hu P. Effects of high iodine and high fluorine on children’s intelligence and the metabolism of iodine and fluorine. Chin J Pathol. 1994;15(5):296–298. Available: [accessed 20 August 2012] [PubMed]

  • • Yao LM, Deng Y, Yang SY, Zhou JL, Wang SL, Cui JW. Comparison of children’s health and intelligence between the fluorosis areas with and without altering water sources. Lit Inf Prev Med. 1997;3(1):42–43. [in Chinese]

  • • Yao LM, Zhou JL, Wang SL, Cui KS, Lin FY. Analysis of TSH levels and intelligence of children residing in high fluorosis areas. Lit Inf Prev Med. 1996;2(1):26–27. [in Chinese]

  • • Zhang J, Gung Y, Guo J. Beijing: Captial Institute of Pediatrics Heatlh Research Office; 1985. Children Intelligence Scale Handbook.

  • • Zhang JW, Yao H, Chen Y. Effect of high level of fluoride and arsenic on children’s intelligence. Chin J Public Health. 1998;17(2):57. [in Chinese]

  • • Zhang M, Wang A, Xia T, He P. Effects of fluoride on DNA damage, S-phase cell-cycle arrest and the expression of NF-κB in primary cultured rat hippocampal neurons. Toxicol Lett. 2008;179:1–5. [PubMed]

  • • Zhao LB, Liang GH, Zhang DN, Wu XR. Effect of a high fluoride water supply on children’s intelligence. Fluoride. 1996;29(4):190–192.

 [*] Human variability

Articles from Environmental Health Perspectives are provided here courtesy of

National Institute of Environmental Health Science – Thank you AFS

                 See also:



106 Fluoride Vol. 36 No. 2 106-112 2003 Research Report

My Views on the Fluoridation of Water 

Vit.c strip

Fluoridation, 1979 Scientific Criticisms and Dangers

Philip R.N. Sutton Former Senior Lecturer in Dental Science
University of Melbourne Australia

  Fluoridation Philip Sutton  

An Inconvenient Tooth – Fluoride Documentary

↓     ↓

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A Scientific Review of EPA’s Standards


Committee on Fluoride in Drinking Water
Board on Environmental Studies and Toxicology
Division on Earth and Life Studies


→ →  NRC_2006  ← ←

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Vit.c strip


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Plumb-solvency Exacerbated by Fluoridation-Dr. Geoff Pain

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Fluorosis in 89% Carnarvon Aborigines +

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Bone/joint problems-Fluorosis

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WATER -Stroke & Heart Attacks – a short read

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You may not be able to imagine that borax, this humble insecticide
and laundry detergent, has the potential of singlehandedly
bringing down our entire economic system !  


Some of the articles or pieces posted on this site contain copyrighted material.
Credit is given to the author and links are provided to the original source. 
We believe that this constitutes a ‘fair use’.

The peoples of the world have a right to true science.
Deceit and fake $cience need to be exposed.









These findings suggest that vitamin C significantly reduced 
the severity and incidence of fluoride-induced embryo toxicity in rats.

Guinea pigs, apes, some fruit
bats and humans share another trait:

The tendency to develop coronary heart disease.
The development of heart disease only occurs in animals and
humans that lack adequate intake of ascorbates through dietary sources.

Lab Rat f

Original ⇒ HERE

PubMed logo

Vit C Rats F. Verma

Jai Research Foundation, Vapi, Valvada 396 108, India 

     Oral administration of sodium fluoride (40 mg/kg body weight) from day 6 to 19 of gestation caused, as comparedto control, significant reductions in body weight, feed consumption, absolute uterine weight and number of implantations. Significantly higher incidenceof skeletal (wavy ribs, 14th rib, <6 sternal centre, dumbell-shaped second and fifth sternebrae, incompleteossification of skull and thickening of tibia) and visceral (subcutaneous haemorrhage) abnormalities were also observed in NaF-treated dams than that of control. Oral administration of vitamin C (50 mg/kg bodyweight) and vitamin E (2 mg/0.2 ml olive oil/animal/day) from day 6 to 19 of gestation along with NaF significantly ameliorates NaF-induced reductions in body weight, feed consumption, absolute uterine weight (only with vitamin E treatment) and number of implantations. Ascompared with NaF-treated alone, the total percentage of skeletal and visceral abnormalities were significantly lowered in fluoride plus vitamin C-treated animals. Vitamin E was less effective. These findings suggest that vitamin C significantly reduced the severity and incidence of fluoride-induced embryo toxicity in rats.

Key Words: fluoride • vitamins • embryo toxicity • amelioration

   Human & Experimental Toxicology, Vol. 20, No. 12, 619-623 (2001)


          See also ↓ 


          See also ↓ 





… going by the above evidence, fluorinated drugs seem to pose
a number of risks associated with the fluorine or fluoride
contained in them. It raises even more concern when
fluoride itself is present in many industries and
products, including food and drinks … 

Prof. Abdul Razak

Professor Dzulkifli Abdul Razak

National Poison Centre
University Sains Malaysia – 
2 Sept. 2001


He is the First Vice-President of the International Association of Universities (IAU),
a UNESCO affiliated organisation based in Paris.
He was President of the Association of Southeast Asia Institutions of Higher Learning from 2007-2008.


   Following the recent withdrawal of the cholesterol-lowering drug Lipobay, there is now a new perspective to the issue, the drug being a fluoride-containing compound. The drug, also known by its generic name, cerivastatin, is one of the many such compounds pulled off the shelves in the last few years.

Cerivastatin was taken off because of at least 40 deaths worldwide, 31 in the US alone. According to a recently released commentary by a Canadian group, Parents of  Fluoride Poisoned Children, a series of fluoride containing drugs or so-called fluorinated drugs have been withdrawn from the market in the last 10 years due to their toxic effects on human beings. One notable example is the combination “Fen-Phen” (a generic combination of fenfluramine and phentermine, the former being a fluorinated drug type) which was said to have weight-reducing effects. Others are dexfenfluramine (Redux) and fenfluramine (Pondimin).

There are at least eight other examples of fluorinated drugs withdrawn so far, because serious side effects on the heart, and for suspected adverse influence on thyroid hormone activity.

They include, last year, cisapride (Propulsid) because of its severe side-effects on the heart. In 1999, two drugs were withdrawn.

These were an anti-allergy drug, astemizole (Hismanal); and grepafloxacin (an antibiotic, Raxar) because they too were associated with similar adverse events.

In 1998, patients with congestive heart failure using the drug mibedrafil (Posicor) showed a trend to higher mortality, causing it to be withdrawn.

Alredase (Tolrestat, an anti-diabetic) was withdrawn in 1997 after the appearance of severe liver toxicity and deaths among several patients. In the same year too fenfluramine (part of Fen-Phen) and dexfenfluramine were withdrawn.

In 1993, flosequinan (Manoplax, a heart drug) was withdrawn when it was shown that the beneficial effects on the symptoms of heart failure did not last beyond the first three months of therapy. After that, patients had a higher rate of hospitalization than patients taking a placebo.

Of the many fluorinated drugs that remain in the market some carry warnings of serious cardiac toxicity, for instance halofantrine, a schizonticidal drug. More specifically, other fluorinated drugs, although they have not yet been withdrawn, are known to cause muscle wasting or rhabdomyolysis; like cerivastatin.

For instance, the PFPC commentary noted that the fluorinated antibiotic fluoroquinolone, used to treat infections, is reported to cause tendonitis and rhabdomyolysis. In fact product information for such antibiotics (enoxacin, fleroxacin, norfloxacin, sparfloxacin, and tosufloxacin) was amended in Japan in October 1994, to state that rhabdomyolysis may occur. Reportedly, the tragic story involving fluorinated drugs (the fluorophenyls in particular, initially limited to industrial use involving dyes and pesticides) can be traced way back to the 1930s when they were used to treat hyperthyroidism.

The use followed a discovery by IG Farben (Bayer) and Knoll’s scientists that all fluoride compounds can interfere with thyroid hormone activity.

In the liver especially, organic fluoride compounds undergo extensive transformation, mainly via oxidative demethylation, involving the thyroid hormone (T3) mediated P-450 enzyme system. And the resulting metabolites may have higher activity and/or greater toxicity than the original compound.

The activity of organic fluoride compounds on the P-450 enzyme system is critical as it relates to the elimination of many other drugs. Inhibition of these enzymes can cause other drugs to accumulate to dangerous levels in the body, leading to hazardous drug interactions. In many cases fluorinated drugs are being implicated as documented in hundreds of well-established studies.

Moreover, adds PFPC, the metabolites produced by organic fluoride compounds in the liver can be transferred to the fetus through various pathways, including circulatory via placental passage, gastrointestinal via fetal swallowing, and respiratory secondary to fetal lung absorption. This may lead to congenital abnormalities as in the case of fluconsazole (Diflucan).

In short, going by the above evidence, fluorinated drugs seem to pose a number of risks associated with the fluorine or fluoride contained in them. It raises even more concern when fluoride itself is present in many industries and products, including food and drinks, without any rigorous evaluation or monitoring.

Of  late, we have managed to label all toothpastes containing fluoride in this country. But this is clearly a minuscule effort in the attempt to regulate the use of fluoride as an inherent poison. We need to do more now.

For more information, contact the National Poison Centre at Universiti Sains Malaysia,
tel: 04-657 0099, fax: 04-656 8417,

USM Uni Logo

Vice-Chancellor, Albukhary International University, Malaysia



Professor Dzulkifli Abdul Razes
recent post is Vice Chancellor
Albukhary University

Source: New Sunday Times (Focus) 2 September 2001


More info on fluorinated medications  HERE




The apoptotic effect was partially reduced by the PKA inhibitor H89.
NaF induced a weak but sustained increase in PKC activity,
whereas the PKC activat or TPA induced a transient effect.

Human & Experimental TOXICOLOGY


( A549 CELLS )


Refsnes MSchwarze PEHolme JALåg M.

Division of Environmental Medicine,
Norwegian Institute of Public Health,
Geitmyrsvn. 75,
PO Box 4404 Nydalen,
N-0403 Oslo,


      In the present study, possible mechanisms involved in fluoride-induced apoptosis in a human epithelial lung cell line (A549) were examined. Sodium fluoride (NaF) induced apoptosis in the A549 cells, with a maximum at 5-7.5 mM after 20 hours of exposure. The number of cells with plasma membrane damage (PI-positive cells) increased moderately up to 5 mM, but markedly at 7.5 mM. Deferoxamine (an Al3+ chelator) almost completely prevented these NaF-induced responses, which may suggest a role for G protein activation.

The apoptotic effect was partially reduced by the PKA inhibitor H89. NaF induced a weak but sustained increase in PKC activity, whereas the PKC activat or TPA induced a transient effect. TPA, which enhanced the NaF-induced PKC activity, was not apoptotic when added alone, but facilitated the NaF-induced apoptosis and the increase in PI-positive cells. PKC down regulation induced by TPA pretreatment almost completely prevented the NaF-induced apoptosis and the increase in PI-positive cells. Pretreatment with the PKC inhibitor GF109203X, which abolished the PKC activity after 3 hours, enhanced the NaF-induced apoptosis. KN93 (a CaM kinase II inhibitor) and W7 (a calmodulin inhibitor) seem to reduce the apoptotic effect of NaF, whereas BAPTA-AM (a Ca2+ chelator) was without effect. The tyrosine kinase inhibitor genistein also markedly reduced the NaF-induced apoptosis, whereas the PI-3 kinase inhibitor wortmannin augmented the response. In conclusion, the present results suggest that NaF induces an apoptotic effect and an increase in PI-positive A549 cells via similar mechanisms, involving PKC, PKA, tyrosine kinase and Ca2+-linked enzymes, whereas PI-3 kinase seems to exert a counteracting effect.

PMID: 12723891 [PubMed – indexed for MEDLINE]

Hum Exp Toxicol. 2003 Mar;22(3):111-23.

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 We Have Included This Info On Arsenic Because
 The F. Used In Drinking Water Also Contains Arsenic

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Some 19.6 million Chinese people are at risk of consuming
arsenic-contaminated groundwater beyond the maximum
threshold set by the World Health Organization…

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 Original → Here 


Environmental Health Perspectives

Synopsis by Lindsey Konkel 


Note: Fluoridated drinking water contains arsenic.4-mice-f

Mice exposed in the womb and after birth to high levels of arsenic were more susceptible to influenza than unexposed mice, according to a new study by Australian researchers. These co-exposures could be an important factor in the development of chronic lung problems later in life, according to the researchers.

Mice exposed in the womb and after birth to high levels of arsenic were more susceptible to influenza than unexposed mice, according to a new study by Australian researchers.

More than 200 million people globally are exposed to arsenic in drinking water that exceeds a U.S. and international standard, according to the World Health Organization.

FEMA  (Federal Emergency Management Agency)

 More than 200 million people globally are exposed to arsenic in drinking water that exceeds U.S.  and internation standards.

Arsenic is an element that is naturally found in soil, and it often taints ground water. It also can come from farm runoff and industrial waste.

Mice exposed in the womb or as newborns to arsenic and influenza were less able to fight infection, had an increased inflammatory response in their airways and altered lung mechanics. These co-exposures could be an important factor in the development of chronic lung problems later in life, according to the researchers.

Cancer has been the biggest concern related to arsenic contamination of water supplies. But previous studies in animals or humans also have suggested that prenatal arsenic exposure may increase susceptibility to respiratory infections or impair lung growth and immune system development. The current study examines how arsenic exposure modifies the mouse body’s responses to influenza infection.

The mice in the study drank water contaminated with 100 parts per billion of arsenic, 10 times higher than a standard set by the U.S. Environmental Protection Agency and WHO. However, some regions in the United States have groundwater that routinely exceeds 50 parts per billion, according to the U.S. Geological Survey. And some countries have severe arsenic problems, particularly Bangladesh, where arsenic reaches as high as 3,000 parts per billion.

The researchers compared the exposed pregnant mice to others that drank arsenic-free water. After their offspring were born, exposure continued to either arsenic-clean or contaminated water.

One week after birth, some mouse pups were inoculated with influenza virus. Mice exposed to both arsenic and influenza had a greater inflammatory response and produced more immune cells than mice exposed to either arsenic or influenza. One week after the influenza infection, arsenic-exposed mice showed higher levels of the virus in their blood than unexposed mice.

“Those mice exposed to both arsenic and influenza had the greatest deficits in lung mechanics,” wrote the study authors from the Telethon Institute for Child Health Research, University of Western Australia and University of Queensland.

An increase in airway responsiveness is one hallmark of asthma.

“These data demonstrate how exposure to arsenic in early life can alter the response to influenza infection resulting in both acute and long-term effects on respiratory health,” they wrote.

While the study suggests that the mouse lung is highly sensitive to arsenic exposure early in life, what these data mean for humans remains unclear. Further research is needed to determine if arsenic-exposed populations are at a greater risk of sickness and death from lower respiratory infections, the authors conclude.

23 August Millions face arsenic contamination risk in China, study finds. Nearly 20 million people in China live in areas at high risk of arsenic contamination in their water supplies, according to a study published on Thursday. The Guardian, United Kingdom.

23 August New predictive method pinpoints arsenic hotspots. European and Chinese researchers have built a model to predict the presence of arsenic groundwater contamination in China and elsewhere where millions are at risk, according to work published Thursday. Agence France-Presse.

23 August Statistical tool predicts arsenic risk in Chinese wells. Arsenic is found naturally in rocks and soil, but exposure to it presents a major public health problem, especially in regions where untreated groundwater is the only reliable source of drinking water. Scientists have deployed a new statistical tool that can help predict the greatest risk of contamination. Voice of America.

23 August Lead, arsenic and mercury found in pills sold online. A warning has been issued about unlicensed Chinese medicines available over the internet which have high levels of lead, mercury and arsenic. Dublin Irish Independent, Ireland.

22 August Young mice exposed to arsenic more susceptible to influenza, respiratory infections. Mice exposed in the womb and after birth to high levels of arsenic were more susceptible to influenza than unexposed mice, according to a new study by Australian researchers. Environmental Health News.

21 August Tornillo water high in arsenic, could cause health risks. The El Paso Equal Voice Network and U.S. Rep. Pete Gallego, D-Texas, hosted a community meeting to address complaints of dirty water in Tornillo, after the El Paso County Tornillo Water Improvement District said the drinking water there exceeds the maximum contaminant level for arsenic. El Paso KFOX TV, Texas.

20 August Heavy metals found in Chinese medicines. Health regulators have issued a warning over some Chinese medicines, saying they contain “dangerously high” levels of lead, mercury and arsenic. Britain’s Medicines and Healthcare products Regulatory Agency said the unlicensed traditional Chinese medicines included some meant for children. Press Association.

16 August EPA to inspect Colorado milling site. Mining inspectors have found heavy pollution from mercury and arsenic inside an unpermitted gold mill on the west side of Mancos, Colorado. It’s “one of the uglier cases of using hazardous chemicals and illegal milling” that state mining regulators have seen, said Julie Murphy, a lawyer for the state Division of Reclamation, Mining and Safety. Cortez Journal, Colorado.

16 August Arsenic remains in China from thousands of Japanese arms. Toxic arsenic remaining in thousands of destroyed Japanese chemical weapons sits in storage at a Chinese armed forces compound in the city of Nanjing, located in eastern China, Kyodo News reported on Thursday. National Journal.

15 August Oregon Superfund cleanup nearing pivotal stage. As recently as 1990, the McCormick and Baxter Creosoting Co. dumped toxic chemicals into the river at its plant a mile south of the St. Johns Bridge — everything from the wood-treatment substance creosote to pentachlorophenol, arsenic, copper, chromium, zinc and other contaminants — which subsequently seeped into the soil and riverbed. Portland Tribune, Oregon.

15 August Japan yet to dispose of arsenic from wartime chemical weapons in China. Japan has yet to dispose of arsenic residue from chemical weapons its Imperial army abandoned in China at the end of World War II, a source close to bilateral relations said Wednesday, noting there are calls for the arsenic to be sent to Japan. Kyodo News, Japan.

14 August Water quality centre in city. An international centre for drinking water quality in Calcutta will be tasked with research on drinking water technologies, health impacts of water contaminants — with special focus on arsenic and fluoride — and the chemistry of sediments. Calcutta Telegraph, India.

10 August Court rules county liable for storm water pollution. The U.S. 9th Circuit Court of Appeals has ruled that Los Angeles County is liable for the level of pollution found in its storm water. The decision, released Thursday, is a win for environmental groups who say the county was responsible for needed cleanup of arsenic, cyanide, lead and mercury. Santa Clarita Signal, California.

A recently published study by researchers at the University of Texas at Arlington found elevated levels of arsenic and other heavy metals in groundwater near natural gas fracking sites in Texas’ Barnett Shale. ProPublica.

8 August Water contamination rises in Texas after natural gas drilling. Researchers comparing samples from Barnett water wells with those predrilling data report that wells near natural gas production sites have elevated levels of arsenic, selenium, and strontium. Chemical & Engineering News.

6 August Friendly bacteria to detox arsenic. A new study has identified bacterial strains capable of oxidising toxic arsenic into a less toxic form, offering a feasible and affordable solution to the problem of arsenic in soil and water. Science and Development Network.

6 August UTA study finds contaminants in ground water near gas wells. High levels of contaminants, including arsenic are present, according to a University of Texas at Arlington study, in private water wells near gas operations. The study is one of the first water quality studies completed in North Texas since gas drilling expanded. Dallas KTVT TV, Texas.

4 August Contaminant found in most US rice causes genetic damage. It’s been more than a decade since scientists first raised an alarm about arsenic levels in rice. A study released last week has shown the first direct link between rice consumption and arsenic-induced genetic damage. Discover.

1 August Health testing, legal issues, to be discussed at Black Leaf meeting. Residents of the Park Hill area can learn about proposed testing of lead and arsenic in their bodies at a community meeting tomorrow, organized by Louisville Metro Councilman David James. Louisville Courier-Journal, Kentucky.

31 July Something in the air: How global warming is spreading toxic dust.   Scientists say several towns in the western United States could become a major source of airborne arsenic poisoning due to global warming and breakneck human expansion. ClimateWire.

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                        ♦  Editors note see:  THE SECRET LIFE OF DUST”





The info in the papers below is probably a little distorted by population,
food and water moving beteen counties. Also in the fluoridated areas
some households may have water filtration equipment.
Both of these factors could influence the results,
suggesting that the damage from fluoridation
is probably even more than these
papers would suggest.

Factors Often Overlooked In Fluoridation Research



Full Text → HERE






This paper does not mention fluoride but needs to be considered
with previous research into Underground Water in Queensland.

Ross Kieinschmit may not be aware of the
existence of this government research.



Full original text → HERE 


Environmental Health logo f

Exposure To Fluoridated Water And Attention Deficit Hyperactivity Disorder
Prevalence Among Children And Adolescents In The United States:
An Ecological Association.
Ashley J. Malinand & Christine Till

New – Link to original text  →  HERE


M&F Cretins f



Judith Litteton ff

Paleopathology of Skeletal Fluorosis m

Original  → HERE  

Ann Choi
Research Scientist
Department of Environmental Health
401 Park Drive
Landmark Center East #3-112-15
Boston, MA 02215


John Y

The National Health Federation
P.O. Box 688, Monrovia, California 91017
Washington,  D.C.,  20002

ABSTRACT: Vitamin C plays an important role in the orderly deposition of fluoride into various tissues. In higher fluoride areas, Vitamin C increases fluoride excretion and normalizes soft and hard tissue fluoride levels and thus prevents the development of fluorosis.  At lower fluoride levels, Vitamin C increases the incorporation of fluoride into teeth.  Fluoridation of water systems in not the solution to optimal incorporation of fluoride into teeth; in cases of Vitamin C deficiency, fluoridation may lead to fluorosis.

(21)  Hardwick & Bunting, J. Dent. Res. 50 (Supplement, Pt. 1), 1212 (1971)

– 7 August 1974 –

While fluoridation of public water systems has been advocated and encouraged by the national and state public health services, a number of questions concerning the need to add fluoride to public waters have gone unanswered.

Mother’s milk, containing as little as 0.01 to 0.05 ppm fluoride confers as much caries resistance on the child as other infants consuming 1 to 2 ppm fluoride present in commercially prepared formulas (1, 2).

In unfluoridated areas, containing natural fluoride levels of 0.1 to 0.5 ppm and even less, there exists a certain part of the population that are free of caries.  In fact, in Nigeria, a population has been found where over 98% of the population is caries free and the fluoride level in their water is within the above range (3).

In a study at Great Lakes Naval Base, the previous life-long residence of caries-free recruits, were examined to determine if any trace elements could be correlated with the low incidence of caries.

The level of fluoride in the drinking water was NOT [our emphasis] implicated.

It has also been noticed that primitive areas in which the people of the area eat unrefined food have a relatively low caries rate as compared to later when these areas became “civilized” and their diets begin to consist of more refined foods.

In these cases, caries rates often soar and addition of fluoride to the water supply is unable to restore the previous caries rate (5, 6, 7).

In areas and among people where nutrition is poor, mottling is observed at levels below the 1 ppm level used to fluoridate public water systems (at levels as low as 0.4 ppm fluoride).

This has been noticed in India (8) as well as among American Negroes whose mottling rate, in the 1-ppm range is higher than that of whites in the same area.

In a comprehensive study in Japan, the fluoride levels associated with the lowest incidence of caries ranged from 0.2 to 0.4 ppm  (9).

In the 1930’s it was found that the ingestion of fluoride causes scurvy-like symptoms and that this was associated with a decrease in the Vitamin C levels of various tissues. Similarities in the symptoms of scurvy and mild fluorosis were also observed  (10, 11).

In 1954, in an area containing 0.34 to 0.8 ppm fluoride in the water, 23% of the children 4-7 years old exhibited mottling (dental fluorosis). The Vitamin C contents in blood for normal children (without mottling) averaged 0.78 mg %. In the mottled enamel group, the blood Vitamin C levels of most children were extremely low (0.15 to 0.3 mg % in 29%, and 0.0 to 0.15 mg % in 31%. Treatment of these subjects with Vitamin C brought substantial improvement  (12).

  NOTE → In 1964-65, the death rate of guinea pig population in Australia had reached epidemic proportion. (The Guinea pig is the only non-primate known that cannot synthesize its own Vitamin C). This death rate was eventually attributed to slightly higher levels of fluoride in feed pellets. Symptoms of sub-acute Vitamin C deficiency were observed. Fluorosis was diagnosed as the cause of death (13). In rats and mice (both of which synthesize their own Vitamin C, no such death rate was reported. U.S.P.H.S. experiments are performed with rats – they do not use guinea pigs (14). Both in the U.S. (15) and Russia (16) Vitamin C is recognized as being capable of retarding the development of fluorosis.

In guinea pigs exposed to fluoride, Vitamin C was found to normalize altered blood Ca, P, and sugar levels, as well as fluoride levels and ash contents in teeth and bone, and fat glycogen, and fluoride levels in the liver. Fed to men exposed to elevated fluoride uptakes, 100mg of Vitamin C increased the excretion of fluoride from 3-5.5 mg/day to 6-8.5 mg/day (17).

Most important, however, are the following findings:

1.) in guinea pig, fluoride added to the diet cannot make teeth more insoluble (caries-resistant) than the addition of  Vitamin C to the diet and-

2.)  in low fluoride areas, dietary supplementation with Vitamin C leads to fluoride deposition in teeth equal to the of higher fluoride areas (18, 19).

In conclusion, it appears that Vitamin C is and essential factor in the deposition of fluoride in, as well as the exclusion of fluoride from, various tissues in the body.

While increased fluoride in teeth had been correlated to caries-resistant of teeth, adequate Vitamin C levels in the diet in areas of 0.1 to 0.5 ppm fluoride (and even 0.01 to 0.05 ppm in the nursing infant) leads to adequate uptake by the teeth. Indeed in animals that manufacture there own Vitamin C (e.g. rats), Fluoride is found not to have a caries protective effect until it reaches levels of 10-20 ppm (14); at these levels it acts as a strong antibacterial in the mouth.

The indiscriminate fluoridation of water systems is not the solution to the problems of tooth decay. In the absence of sufficient Vitamin C, fluoridation will lead to Vitamin C depletion, dental fluorosis, and to abnormal levels of metabolites in blood tissues.

Adequate intake of  Vitamin C may explain why people or populations in low fluoride areas can be caries-free.


(1)           Y. Ericsson, U. Ribelius, Caries Research 5, 78 (1971);

(2)           F.J. McClure, Personal communication.

(3)           A. Sheiham, British Dental Journal 123, 144 (1967;

(4)           J.P. Quinn, NDRI-PR-68-03, (June 1968) 11pp. US Nat.Tech. Inf.

   Serv. Reo. No. AD0839 129;

(5)           S.J. Barnaud Journal 2, Med. Trop. 29, 593 (1969);

(6)           J.A. Cran, Australian Dental Journal 2, 277 (1957);

(7)           F. Prader, Schweiz. Mschr. Zahnhk. 71 885 (1961);

(8)           R.S. Nanda, Indian Journal of Dental Research 60, 1470 (1972);

(9)           Y. Imai, Koku Eisei Gakkai Zasshi 22, 144 (1972);

(10)          P.H. Phillips, J. Biol. Chem. 100, (Proc. Am. Soc. Biol. Chem. 

   Lxxix (1933);

(11)          P.H. Phillips, F.J. Stare, C.A. Elvenhem, J. Biol.

   Chem. 106, 41 (1934);

(12)          N.A. Ivanova, Voprosy Okhrany Materinstva I

    Detstva 4, 29 (1959);

(13)          F.F.V. Atkinson, G.C. Hard, Nature 211, 429 (1966);

(14)          N.M. Stiles, National Institute Of Dental Research,

   Personal Communication;

(15)          J.W. Suttie, P.H. Phillips, The Pharmacology and
                 Toxicology of Fluorine,

  J.C. Muhler, M.K. Hine, Ed.  (Bloomington, Indiana

   University Press,  1959) pp 70-7;

(16)          V.S. Andreeva Voprosy Okhrany Materinstva I Detstva 4, 25 (1959);

(17)          R.D. Gabovich, P.N. Maistruck, Voprosy Pitaniya 22, 32 (1963);

(18)          D. J. Thompson, P. H. Phillips, J. Dent. Res. 45, 845 (1966);

(19)          D. Triers, C.G. Elliott, M.D. Smith, J. K. Dent.

  Res. 47, 1171   (1968);

(20)        W. Buttner, Advances in fluorine Research and
                 Dental Caries Prevention,
                 J. L. Hardwick, H.R.Held, K.G. Konig, Ed.
                 (New York Pergamon Press, 1965) pp. 19-30;


Watch also 


by John A. Yiamouyiannis



Department of Zoology, University School of Sciences,

Gujarat University,
Ahmedabad 380 009, India
R J Verma, D M Guna Sherlin
Jai Research Foundation, Vapi,
Valvada 396 108, India

     Oral administration of sodium fluoride (40 mg/kg body weight) from day 6 to 19 of gestation caused, as compared to control, significant reductions in body weight, feed consumption, absolute uterine weight and number of implantations. Significantly higher incidence of skeletal (wavy ribs, 14th rib, <6 sternal centre, dumbell-shaped second and fifth sternebrae, incomplete ossification of skull and thickening of tibia) and visceral (subcutaneous haemorrhage) abnormalities were also observed in NaF-treated dams than that of control. Oral administration of vitamin C (50 mg/kg body weight) and vitamin E (2 mg/0.2 ml olive oil/animal/day) from day 6 to 19 of gestation along with NaF significantly ameliorates NaF-induced reductions in body weight, feed consumption, absolute uterine weight (only with vitamin E treatment) and number of implantations. As compared with NaF-treated alone, the total percentageof skeletal and visceral abnormalities were significantly lowered in fluoride plus vitamin C-treated animals. Vitamin E was less effective.

These findings suggest that vitamin C significantly reduced the severity and incidence of fluoride-induced embryotoxicity in rats.  ♦

Key Words: fluoride • vitamins • embryotoxicity • amelioration
Human & Experimental Toxicology, Vol. 20, No. 12, 619-623 (2001)

Our note: Unlike humanrats produce vitamin C .



The Case Against Fluoride

book pro

The book concludes that, if proposed today, fluoridation of drinking water to prevent tooth decay would stand virtually no chance of being adopted, given the current status of scientific knowledge.

In part one of  The Case Against Fluoride“The Ethical and General Arguments Against Fluoridation”: The requirement for the informed consent of the patient before administration of a medication is a basic human right. Yet with fluoride, which is added to drinking water as a therapeutic intervention, no such permission is sought or given. The process is enforced on every member of the population. The authors explore this fact in the context of medical ethics. Another aspect is the efficacy of fluoridation as a therapy, which, the authors argue, is marginal at best and deleterious at worst. The fluoride used for water fluoridation is not of pharmaceutical grade, but is in fact a chemical waste by-product. The lack of any rigorous studies as to the efficacy of fluoridation programs, the authors contend, means that the whole process is experimental.

There is no control of  “dose”— how much fluoride anyone receives from the water.

In the case of water fluoridation, according to the above authors, the chemicals that go into the drinking water that more than 180 million people drink each day in the United States are not even pharmaceutical grade, but rather a hazardous waste product of the phosphate fertilizer industry. It is illegal to dump this waste into the sea or local surface water, and yet it is allowed in our drinking water. To make matters worse, this program receives no oversight from the Food and Drug Administration, and the Environmental Protection Agency takes no responsibility for the practice. And from an ethical standpoint, say the authors, water fluoridation is a bad medical practice; individuals are being forced to take medication without their informed consent; there is no control over the dose and no monitoring of possible side effects.

Acute high oral exposure to fluoride may lead to nausea, vomiting, abdominal pain, diarrhea, drowsiness, headaches, polyuria and polydipsia, coma, convulsions, cardiac arrest, and death.

Historically, fluoride was quite expensive for the world’s premier chemical companies to dispose of, but in the 50s and 60s, Alcoa and the entire aluminum industry—with a vast overabundance of the toxic waste—somehow sold the FDA and our government on the insane (but highly profitable) idea of buying this poison and then injecting it into our water supply as well as into the nation’s toothpastes and dental rinses. Consider also that when sodium fluoride is injected into our drinking water, its level is approximately one part-per-million (ppm), but since we only drink one-half of one percent of the total water supply, the hazardous chemical literally “goes down the drain” and voila—the chemical industry not only has a free hazardous waste disposal system, but we have also paid them with our health and our pocketbooks for the process.

The aluminum and phosphate fertilizer industries were not alone. The American government’s atomic weapons program was also producing huge amounts of fluoride and was getting sued by famers for the damage done to their cattle.



A Bibliography of Scientific Literature on Fluoride

↑ ↑ ↑ Very Large File ↑ ↑ ↑

by Paul Connett, PhD
Professor Emeritus of Environmental Chemistry,
St. Lawrence University, Canton,

     Currently, I am traveling in Italy giving presentations on waste management. I have been forwarded a copy of your editorial ridiculing any notion that fluoridation could possibly cause any health problem and that practice is extremely effective at reducing tooth decay.

I will leave your councilors to judge the quality of the evidence that I will share with them on March 14. I write now because I am upset with the bullying tone you have adopted with one of your councilors, Amy Valentine. It is well known that if people are unable to answer a disturbing message they begin by attacking the messenger. You have chosen to do so in this case using the authority of local dentists, the American Dental Association and the Centers for Disease Control and Prevention. However, on this particular issue all these sources are highly suspect because of their very aggressive and long-term promotion of this practice.

It is simply not enough to parrot the phrase that fluoridation is “safe and effective” to win the case. It is incumbent on those who support this most unusual practice (what other chemical is added to the public water supply to treat people rather than treat the water?), which has been rejected by most industrial countries, to provide the scientific evidence for their claims.

To offset the 23 studies from India, Iran, Mexico and China which have shown that high doses of fluoride are associated with lowered IQ in children, where are the studies of the IQ of children living in Plattsburgh or any other fluoridated community in the U.S.? I am not aware of any. Why have they not been done?

The key question, of course, is whether there is an adequate margin of safety between the levels which have caused this harm in other countries and the levels experienced by children in this country drinking uncontrolled amounts of fluoridated water. The lowest level estimated at which IQ was lowered in one of these studies was 1.8 ppm (Xiang et al., 2003). Can you find a single toxicologist or pharmacologist who will tell you that offers an adequate margin of safety for all children exposed to fluoridated water at 1 ppm? For that matter, will they also tell you that there is an adequate margin of safety for all the other health effects discussed in the 507-page report by the National Research Council, “Fluoride in Drinking Water” published in March 2006? Three of the authors of that report don’t think so and have stated so in public.

On the issue of effectiveness, where is the peer-reviewed, published, scientific evidence that the teeth of children in Plattsburgh are “sturdier” than children in non-fluoridated communities in the area? You have none — only anecdotal reports. In fact, a study commissioned by the N.Y. Department of Health, which examined tooth decay in third graders, found absolutely no relationship between tooth decay averaged by county and percentage of the county’s population drinking fluoridated water! Meanwhile, the data collected by the World Health Organization shows no difference in tooth decay in 12 year-olds between fluoridated and non-fluoridated countries .

In my view adding fluoride — a known toxic substance — to the public drinking water at 250 times the level naturally present in mother’s milk (0.004 ppm) is both reckless and foolish, especially now that even promoters of fluoridation like the CDC admit that fluoride works topically, not systemically, i.e. it works by acting on the surface of the tooth not from inside the body (CDC, 1999, 2001).

Not only did your editorial writer question my concerns about fluoride’s ability to damage the brain, but he or she also questioned my suggestion that fluoride also damages the teeth. That’s strange because the CDC has reported that 32 percent of American children have dental fluorosis, a mottling and discoloration of the teeth caused by ingesting fluoride before the permanent teeth have erupted.

While the largest proportion of children thus affected have the condition in its very mild form, over 3-4 percent of children have the condition in its moderate or severe forms, in which 100 percent of the enamel is affected. Moreover, while these enamel defects can be covered by expensive veneers (about $1,000 per tooth) the worrying aspect about this is that it is generally agreed that dental fluorosis is the first indication that the child’s developing body has been over-exposed to fluoride.

Thus, the key question then becomes, while the fluoride is damaging the growing tooth by some systemic mechanism, what other tissues might it be damaging without this obvious and visible telltale sign? This underlines the significance of the IQ studies from countries which do not have a fluoridation program to protect.

So let’s examine the science here, please, not just the reiteration of long-held beliefs.

 → Fluoridation Omission And Errors  
Philip R.N. Sutton
Former Senior Lecturer in Dental Science
University of Melbourne


Logo Kobe Uni.


by Staff Writers
Kobe, Japan (SPX) 23 June 2016



  My Views on the Fluoridation of Water  


  2011 Study – Neurodegenerative changes from

fluoride of brain, spinal cord and sciatic nerve 

Indian research rats brains...


↓  25 July 2013 ↓

Impact of fluoride on neurological development in children.

Malta & F.

Full text →  HERE
Go on to: 








… Neuro-degeneration was clearly evident in the hippocampus,
neocortex, cerebellum, spinal cord and sciatic
nerve on fluoride exposure …



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Neurodegenerative changes in different regions of brain, spinal

cord and sciatic nerve of rats treated with sodium fluoride.

P. Yugandhar Reddy1,  K Pratap Reddy1,  K. Praveen Kumar1

1 Department of Zoology, University College of Sciences, 

Osmania University,  Hyderabad 500 007,

Andhra Pradesh,  INDIA

 January 2011


Fluoride is known to cross the blood-brain barrier and alter the structure and function of neural tissue. There are few authoritative reports on neurodegenerative changes in hippocampus, neocortex, cerebellum, spinal cord and sciatic nerve in fluoride intoxication.
We report the alte-rations in the structure of neuronal tissue 
after chronic administration of sodium fluoride (for 60 days) to rats.

Twelve male Wistar rats were divided equally into two groups: one group received 20 ppm of sodium fluoride (NaF) and the other group (which served as a control) received tap water for 60days. The body weights and organic somatic index of brain in the sodium fluoride treated animals were significantly reduced, relative to the control group. Tissue fluoride levels of hippocampus, neocortex, cerebellum, spinal cord and sciatic nerve, all increased significantly in fluoride treated rats. Electron microscopy of the hippocampus, neocortex, cere-bellum, spinal cord and sciatic nerve showed neurodegenerative changes in the NaF treated group compared to controls. Axon deterioration, myelin sheath degeneration and dark cells with scanty cytop-lasm were observed in spinal cord and sciatic nerve in the treated group. Other distinctive morphological alterations observed were: vacuolated swollen mitochondria in neocortex, hippocampus and cerebellum; myelinated fibers with breaks in continuity (axon partly preserved and partly vacuolated) in hippocampus; myelin splitting and vacuolated schwann cell within the cerebellum and sciatic nerve respectively. Thus, neurodegeneration was clearly evident in the hippocampus, neocortex, cerebellum, spinal cord and sciatic nerve on fluoride exposure.

Key words: sciatic nerve,  cerebellum,  sodium fluoride,  hippocampus,

   transmission electron microscope ©

2011 Deccan College of Medical Sciences.

All rights reserved




Rats manufacture Vitamin C, in their livers, which gives them

some protection from fluoride damage. Human livers

do not have this function, therefore on poor diets

over many years, on lower doses of fluoride

humans will suffer more than rats…





In the township Xinyuan, we examined 250 schoolchildren, aged 7-14 years.
The goiter prevalence was 91% and dental fluorosis 20.80%.
The average level of iodine in drinking water was 5.21 mg/l,
and that of fluoride 0.88 mg/l.




Lin Fa-Fu, Aihaiti, Zhao Hong-Xin,

Lin Jin, Jiang Ji-Yong, Maimaiti, and Aiken.


… Xinjiang Institute for Endemic Disease Control and Research; Office of Leading Group for Endemic Disease Control of Hetian Prefectural Committee of the Communist Party of China; and County Health and Epidemic Prevention Station, Yutian, Xinjiang. Cretinism in iodine-deficiency areas is well known, yet the milder forms of somatic and psychomotor maldevelopment and thyroid dysfunction caused by iodine deficiency may be more difficult to detect. DeQuervain, in 1936, called this milder form “semi-cretinism,” while in 1980 Laggasse used the term “cretinoidism.” It was formally named “subclinical endemic cretinism” at a symposium on subclinical cretinism held in Xinzhou, Shanxi province in 1985.

Currently, attention is being focused on these disorders in China and abroad.

The Hetian prefecture in Xinjiang has reportedly been one of the Asian

areas most severely affected by iodine deficiency disorders (IDD).

During the period 1987-1989, we made a systematic survey of

subclinical endemic cretinism in this district under

a UNICEF aid Project.


General conditions and selection of affected areas – The entire region of Xinjiang in central Eurasia is affected by iodine deficiency. The study area, located between the southern border of Tarim basin and the northern slope of Kunlun Mountains, is arid with sandy soil and an annual precipitation less than 50 mm. The cultivated alluvial plain extends from south to north with a steepening gradient. The geographical distributions of endemic goiter and endemic fluorosis are characterized by marked vertical zones. The inhabitants are of lower socioeconomic status, with an annual mean income of about 200 yuan (RMB) per person.

Area with high fluoride and low iodine levels (Area A) – In the township Xinyuan in the lower reaches of Kliya river in the county of Yutian, north of the highway, we examined 250 schoolchildren, aged 7-14 years. The goiter prevalence was 91% and dental fluorosis 20.80%. The average level of iodine in drinking water was 5.21 mg/l, and that of fluoride 0.88 mg/l.

Area with low iodine level (area B) – In the townships of Langan and Jiayi in the alluvial plain before the mountains and to the south of the highway, we examined 256 schoolchildren, aged 7-14 years. The goiter prevalence was 82% and dental fluorosis of 16.00%. The average water iodine level was 0.96 mg/l and that of fluoride 0.34 mg/l. ...

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M&F Cretins f


Image of 3 Cretins copy

More info on iodine → HERE

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  Iodine and IQ f  


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Newsweek 24 Feb.2015

  Water fluoridation in England linked to higher rates of under-active thyroid  

See also 

Iodine Awareness Week –
Antimicrobial Resistance Emergency






 This fluoride accident was under reported!



7  October 2012


Fluoride Accident South Korea

↓ This Video runs for 65 seconds 

  Hydrogen Fluoride kills 5   

↑ Warning, disturbing short video ↑

Vit.c strip

An estimated 8 tons of HF was released.

5 people including the 2 workers perished,

18 responders, workers, reporter wound-up in the hospital,

 almost 3000 villagers from 2 villages downwind of the

facility were treated for irritation, exposure.

damage related to the leak that totaled some $8.5 million

     Five workers were killed and 18 others were injured in the blast at chemical maker Hube Global at the Gumi National Industrial Complex in the industrial city, about 200 kilometers southeast of Seoul.
The gas leak has cost factories in the industrial complex about 17.7 billion won (US$15.9 million) in lost production, officials said. Hundreds of angry villagers in Gumi who suffered after the massive gas leak moved to a safer region with some residents reporting blood in their saliva. About 110 elderly people in Bongsan-ri village evacuated to a facility about 10 kilometers away.

More than six weeks after eight tonnes of hydrofluoric acid was accidentally released at a chemical plant in South Korea, many of the thousands of local residents who fled the area at the time have reportedly not yet returned to their homes despite assurances from authorities that the area is now safe.

The highly toxic hydrofluoric acid was released on 27 September at the Hube Global chemical plant in Gumi, about 200km from Seoul. The leak killed five workers at the plant and severely injured at least 18 others, including workers and emergency personnel. The plant is reportedly still idle after the accident with no date yet set for resuming operations.

Hydrofluoric acid is used to produce chemical precursors for the pharmaceutical industry and has other industrial applications. Highly corrosive and an acute poison, exposure can cause death and serious damage to the skin, lungs, heart, bones and nervous system.

Initial press reports at the time of the accident said more than 3000 people in villages and farms downwind of the accident inhaled fumes and required emergency treatment for health complaints, including nausea, chest pain, rashes and sore eyes. The accident also contaminated crops and sickened livestock. Around 80 other firms in the area were affected, with damages estimated at more than $20 million (£12.5 million).

The initial government response to the accident, including possible mistakes by firefighters, and a sluggish evacuation of nearby residents, was sharply criticized in the Korean media. The government later acknowledged the severity of the incident on 8 October by designating the area around the plant a ‘special disaster zone’. Since then, additional information about the aftermath of the accident has slowed to a trickle.

Afraid to return home

A recent local news report says that government officials have declared that hydrofluoric acid concentrations in the air, water and soil in the affected area have dropped to levels that are no longer harmful. But the report adds that most residents are still afraid to return to their homes.

Vladimir Sakharov, director of the environmental emergencies preparedness programme at Geneva-based Green Cross Internationaltells Chemistry World that it is possible that hydrofluoric acid concentrations are now below dangerous levels. ‘If the spill was treated with neutralizing substances, normally, the situation should be under control after more than a month,’ he says.

Sakharov adds: ‘Depending on the specifics of the response operations and local conditions, soil may become polluted by fluorides, which are strongly retained by soil components. Then, fluorides may accumulate in plants. To what extent soil is polluted by fluorides and whether it is safe to resume agricultural activities, could be determined by chemical and Eco toxicological analyses and tests.’

The commercial area in Gumi where the accident occurred was originally developed with the goal of attracting high-tech firms. But when high-tech demand failed to materialize, zoning regulations were eased to allow other industries in. In 2008, Hube Global, a South Korean-Chinese joint venture headquartered in Seoul, opened the ill-fated plant to supply raw materials to the electronics, chemicals, cosmetics, pharmaceuticals and biotech sectors.

Human error

Police investigating the accident said that the hydrofluoric acid spill may have been caused by human error as two workers were unloading the chemical from a delivery tanker. A closed circuit security video camera recorded the two workers on top of the tanker, both without protective gear. They were connecting an air hose to a valve in the tanker in order to force the chemical out under high pressure. The video shows white vapour erupting at high pressure from the tanker, engulfing the workers.

Police have said the workers were trying to save time and did not follow proper safety procedures. Prosecutors plan to indict three Hube Global executives.

Firefighters who initially responded to the Hube Global accident were not apparently fully briefed on the risks of hydrofluoric acid, according to some reports. The first to arrive on the scene wore typical firefighting garments and masks – inadequate protection against hydrofluoric acid fumes. Firefighters also spread the hydrofluoric acid further by spraying water on it. At the time of the accident, neither the Gumi city government nor the Hube Global plant had supplies of slaked lime, an agent used to neutralize the acid. Slaked lime was not deployed at the accident scene until the day after the leak.

‘I am sure that RoK (Republic of Korea) specialists and scientists know what and how to respond from now on in,’ Sakharov says.

‘I would urge openness and transparency from RoK authorities, so this could benefit the entire international community.

Lessons from this environmental emergency would be extremely valuable for all countries: what exactly happened, what was done, what went well and what did not work, positive and negative results, achievements and shortcomings, how to prevent such accidents and be better prepared in the future?’

South Korea today began evacuating people from a village near Gumi, where eight tons of hydrofluoric acid leaked out of the city’s Hube Global’s chemical factory on September 27, according to Agence France-Press.

More from GlobalPost: North Korea soldier defects to South Korea across DMZ

(Note: this article has been changed to reflect it was hydrofluoric acid that spilled, not hydrocloric as initially reported by AFP.)

Several dozen villagers were taken to a temporary shelter today, and officials said the rest of Bongsan-ri village’s 300 residents will be moved in later stages. 

The move comes a day after the government launched a three-day probe into the leak amid mounting concerns that it has compromised the health of hundreds, issuing a statement saying authorities may designate “the affected region a special disaster zone,” according to Agence-France Press

Health officials said at least 600 people have so far been treated for health complications caused by the leak, said AFP. The spill was triggered by an accidental explosion that killed five people at the plant.

Hydrofluroric acid is capable of penetrating human tissue and is considered extremely dangerous.

But residents of the area say the government has been slow to respond to health concerns. Today’s relocation came hours after villagers held a meeting to demand they be removed from the region. 

Local leader Park Myung-seok told AFP he and other villagers had “decided to relocate by ourselves as the government is doing nothing for us.”

Residents of another nearby village, Imcheon-ri, are also reportedly calling for relocation. 

Gomi’s disaster management office today said 73 companies have reported
property damage related to the leak that totaled some $8.5 million,
said AFP. A large amount of farmland was also affected. 






“Both the very young and the very old are
most likely to be adversely affected
after exposure to fluorides.”


 Original text →    HERE   ← Thank you Robert

My Views on the Fluoridation of Water

Robert L. Isaacson Distinguished Professor of Psychology Binghamton UniversityA note on terminology: Fluorine is an element in the halogen group as are chlorine and iodine. Of all the known elements, fluorine is the most chemically reactive, most powerful oxidizing, and most electronegative element. It is a stronger oxidizing element than ozone. It reacts with many compounds at room temperature. It is never found in its pure form in nature.Fluoride: Any combination of fluorine with another element or chemical group of elements. Thus, the addition of fluorides to the drinking water can indicate the addition of a large number of chemical agents. The most commonly used fluorides for this purpose are sodium fluoride, NaF, and compounds that contain both fluorine and silicon. Such agents are collectively called “Fluorosilicates.” They include fluorosilicic acid, fluorosilicate, hydrofluosilicic acid, and hexafluorosilicic acid.In 2003 when I accepted an invitation to join the National Research Council’s Committee formed to evaluate the EPA standards for the amount of fluoride that should be allowed in our drinking water, I had no fixed opinion on whether or not fluoride should be added to drinking water. Probably I was asked to serve on the committee because I had organized a series of experiments published between 1993 and 1998 using rats to study the effects of chronic administration of aluminum fluoride in their drinking water. My primary interest was in the effects of aluminum on the brain and behavior. Aluminum fluoride was used because fluoride facilitates the passage of aluminum into the brain. At the time, aluminum was considered by a number of scientists to be an important factor in Alzheimer’s disease. Scientists are still actively investigating this possibility. Our studies had to include the investigation of the effects of the fluoride since the aluminum and the fluoride readily become associated after ingestion. In essence we wanted to know the effects of the aluminum, fluoride, and the aluminum- fluoride complex. 1


In my more than three years working on the National Research Council Committee I learned about the many influences fluoride has on the nervous system and the brain. I also learned about the variety of ways in which people become exposed to it and the work that had been done in trying to determine if fluorides were a hazard to human health and well being. The results and recommendations of this Committee were published late in 2006.2 Slowly, I came to the conclusion that there were strong experimental and clinical indications that fluorides present health hazards to people in many ways. The more I learned, the more I became convinced that the addition of fluorides to drinking water was, and is, a mistake. Accordingly, I decided to share some of my conclusions with any who might wish to know them. Fluorine-containing compounds can affect every living animal and person. Exposure to fluorides can come from the air, the water, and the foods we eat. Fluoride compounds were long used as insecticides. They were especially effective for ants and roaches. Their containers were always boldly marked as a poison and there were warnings on the label to keep them well away from children. This is mentioned only to note that for many years fluorides have been considered to be major health hazards. In regard to health the total accumulation of fluorine in the body is important. Only about half of the amount of fluorides taken in by a person is excreted. The rest stays in the body. Toxic effects are determined by the amount of fluoride stored in the body, current exposure level, and age at the time of exposure. In addition each person has his or her own tolerance level for fluorides. Once this level is exceeded however, dysfunctions of body and/or brain will occur. How these dysfunctions will be expressed depends on the genetic makeup and past experiences of the person. Another factor


that helps determine a person’s sensitivity to fluoride is their age. Both the very young and the very old are most likely to be adversely affected after exposure to fluorides. As noted, different people exhibit a wide range of toxic reactions to fluorides. Some people affected by fluorides complain of general weakness and chronic fatigue, others complain of cramp-like pains in the abdomen, or nausea. Still others express toxin-induced effects by diminished vision, headaches, migraine attacks, or pains in muscles and joints. These fluoride effects have been described in books by Leo Spira (1950, 1959)3 and George Waldbott and his associates (1978).4 It is difficult to determine whether or not a given set of symptoms is a consequence of fluoride intake. It is first necessary to rule out the presence of other diseases that could produce the observed symptoms. A correct diagnosis is best shown by repeated observations of an individual when drinking pure water or water contaminated with a fluoride. These exposures must last for periods of a week or two under conditions in which the patient doesn’t know which type of water is being consumed. If the symptoms disappear when the person is drinking pure water and return with the resumption of drinking the fluoride- treated water, this is evidence that the problems arise from the fluoride. Leo Spira and George Waldbott and his associates used this type of experimental approach in their research. Since people vary so much in their sensitivities to fluorides and also in the nature of their symptoms caused by this toxin, determination of a uniform “safe” level of exposure for everyone is impossible. In a way, fluorides are like ozone: there is no really “safe” level that would protect everyone. The Congressional Safe Drinking Water Act instructed that the level of fluoride in drinking water should be set so as to be safe for everyone


regardless of age or overall health. Increasing the problems that can be induced by fluorine in its different forms is its ability to enhance the effects of other toxins to which we are exposed. For example, fluorides in the drinking water accelerate the absorption of lead, aluminum, and silicon into the body and brain. The toxic effects of lead have been known for hundreds of years. In recent years the focus of attention has been on the learning deficits lead produces in children. The mechanisms proposed for the induction of this effect are not known entirely but there is evidence that many of the most important neurotransmitters of the brain are being affected. These include alterations in dopaminergic, cholinergic, and glutaminergic systems as well as in the “supportive” glia cells of the brain. There is also evidence that lead toxicity may go beyond impairments of intelligence. Indeed, lead toxicity may produce behavioral changes that include loss of impulse control and a related increase in the frequency of violent acts.5 The health hazards associated with enhanced incorporation of lead are not induced by all fluorides but primarily, and maybe only, by the addition of a silicofluoride to our drinking water. The fluoride most often added to our drinking water is hexafluorosilicic acid. This fluorosilicate dissociates when it enters the body. One component contains silicon and another fluorides. As a consequence when silicofluorides are added to our drinking water there are really two toxic hazards: one coming from the fluoride and another from the silicon. Silicon can produce its own toxic effects including the formation of solids (silica and silicates) that can lodge anywhere in the body. In addition the silicon portion also can generate destructive hydroxyl ions in many organs including the brain. The brain damage caused by the production of these free radicals has been related to anti-social behavioral


actions and violence.6 Recently data from 327 towns and cities, some having fluoridated water and others not, have been compared in terms of crime rates. All the communities with fluoridated water had substantially higher rates than did those with non-fluoridated water. This indicates that fluorides can act to enhance the damage being done by other toxins. The impairment of intelligence from lead toxicity is now well established. It is possible that fluorides can produce negative effects on measured intelligence also. The country devoting the greatest attention to this possibility is China. As of February 2007, several groups of Chinese investigators had published over 20 scientific papers on this topic. Scientists from many different areas of China participated in these investigations. The children studied in these reports ranged in age from 4 to 14. All were tested by the same or very similar standardized I.Q. tests. Overall the results came from children tested at different places, at different ages, and tested by different investigators. All the results from China have found that communities with high levels of fluoride in their drinking water have fewer children scoring at the “bright” end of the intelligence spectrum than communities with low or no level of fluoride. Since China does not fluoridate their drinking water, the Chinese studies compare the I.Q. scores of children from towns and school areas that differ in the amount of fluoride naturally present in their water supplies. While not all of Chinese studies were perfectly designed, the large number of studies showing the same pattern of results calls for our attention. A negative effect of fluoride on intelligence seems to be a possibility. Other studies in China have indicated that fluoride exposure in the drinking water of mothers during the 6th to 8th months of pregnancy can


produce anatomical changes in the fetal brains. There are also reports of impaired responsiveness to visual and auditory stimuli in babies in the first three days after birth induced by the intake of fluoridated water by young mothers during gestation.7 The ingestion of fluoride tends to increase the uptake of aluminum by the brain. In the studies done in my laboratory the increase in aluminum in the brains of rats was not a function of the amount of aluminum fluoride given the animals in their drinking water. The smallest dose of aluminum fluoride produced about the same amount of aluminum in the brain as a dose 10 or even a 100 times larger. A small amount of fluoride seems capable of opening aluminum pathways to a maximal degree. It is of great interest that the relative risk of having Alzheimer’s disease is increased when individuals had high amounts of aluminum in the brain coupled with low amounts of fluoride.8 Another observation of interest is that aluminum by itself may not exert toxic affects on the nervous system. It may only become a toxin after joined together with a fluoride to become an aluminum fluoride. 9 The chronic administration of fluorides in rats produces changes in the microscopic structure of the brain. There were significant losses of cells in areas of the hippocampus and the neocortex. Many apparently dead or dying cells were found in areas analogous to locations in which similar dying cells are found in the brains of Alzheimer’s patients. A common and, perhaps universal, characteristic of dementia is a reduction of aerobic metabolism in the brain. The blood supply reaching the brain is the primary supplier of oxygen and nutrients. Reductions in this sole source of brain energy can be due to a number of physical or chemical changes. When the brains of animals chronically exposed to aluminum fluoride were examined histologically, deposits of aluminum-based crystals


were found along the walls of both large and small blood vessels in the brain. Similar deposits were also found in the center of many vessels suspended by collagen fibers. These deposits decreased the normal transfer of oxygen from the red blood cells to the brain since they must have created turbulence in its blood flow. It is of historical interest that Alois Alzheimer, the man for whom a type of dementia was named, noted that most patients with this disorder suffered from atherosclerosis in addition to other brain anomalies. This condition is one in which there are deposits formed on the sides and in the center of arteries in the brain. The deposits disrupt the flow of blood to the brain often cause severe brain damage. Brain functions are entirely dependent on the availability of oxygen. The brain itself consumes 20% of all the oxygen used by the entire body. The brain area most affected by the reduction in oxygen availability is the forebrain. The lower centers of the brain, namely the midbrain and hindbrain, are more resistant to oxygen deprivation. This is why the higher functions of the brain are the first to be affected, as well as the most affected, by oxygen deprivation. Basic motor and visceral functions are often spared even in patients with profound interruptions of normal blood supplies to the brain. One of the best-known chemical alterations produced by fluorides is a reduction in cholinesterases, including acetylcholinesterase. Fluorides also directly affect the actions of many of other important neurotransmitters in the brain. Fluorides seem to have a special attraction to acetylcholine. Nerve cells that synthesize this transmitter have numerous projections to many forebrain areas, including the neocortex and deeper areas of the brain that provide information to the neocortex. Not only do fluorides change the amount of the acetylcholine in the


brain, they selectively block certain receptors that respond to this transmitter. Fluoride reduces the number of one type of “nicotinic receptors” for acetylcholine. Some other nicotinic subtypes are not affected.10 Added to all of the other alterations in structure and function of the brain caused by fluorides, the opportunity for mental and behavioral changes are almost limitless. While the cholinergic system of the brain has been most studied in regard to the effects of fluoride, it is not the only neural transmitter affected. It is likely that all neural transmitter systems are affected by fluoride intake, directly or indirectly. Other anomalies related to fluoride intake are found in many other chemical systems of the brain. During the period from 1956 to 1963, the endocrinologist, Ionel Rapaport, presented evidence of a link between fluoride exposure and the numbers of babies born with Down’s syndrome, (Trisomy 21). For a number of years the only follow up to his work was in the form of epidemiological comparisons between the number of births of such children both to mothers living in fluoridated drinking water vs. the number of such born to mothers births in or non-fluoridated drinking water areas. The demographics of the two or more areas being compared were not fully taken into account in most of the studies. Maternal ages were also not taken into consideration. Overall, the “follow up” studies to Rapaport’s report were not decisive but none of them failed to rule out his original findings. Furthermore, a determination of fluoride effects using standard epidemiological procedures cannot provide convincing information. This is because it is impossible to find populations virtually the same in all regards except for the amount of fluoride in their drinking water. Another problem arises from the difficulty in accurately determining the number of Down’s


syndrome children born. Some investigators use the number of birth certificates on which the attending physician notes that the baby had Down’s syndrome. Other investigators use only closed hospital records made sometime later. Still other investigators use both. Neither method is perfect. The use of entries on hospital records would seem to be the most accurate method since physicians seldom enter the nature of possible deformities like Down’s syndrome on birth certificates after delivery. Indeed because of the possibility of making a mistake from delivery, the diagnosis is not often made until a determination can be made by laboratory results. Probably the best collection of relevant data comes from a study of births of children born in two areas of Atlanta, Georgia, as reported by Erickson et al. in 1976. Two different estimates of the number of Down’s children and normal children were presented. One estimate of Down’s syndrome births was made by the examination of copies of birth certificates and the other was based on hospital records. A re-examination of Erickson’s data by Burgstahler11 showed an overall enhancement of Down’s syndrome births to mothers from the fluoridated area. Later, in 1998 Takahashi did a fine grain analysis of data from a number of sources that included the corrected numbers from the 1966 Erickson report.12 In the Takahashi report a clear-cut relationship between fluoride exposure and the number of affected children was found in mothers 30 years of age and younger. Recently, Juan C. Molino13 and I using only data from hospital records found the same age-fluoride-Down’s syndrome birth effect. In his report Takahashi extended the analysis of his data through the use of a regression analysis. He wanted to determine if there could be any dose that would not increase the likelihood of having a Down’s syndrome child. According to his calculations there was no such dose. All doses of


fluoride caused some enhancement of the likelihood of a woman having such a child. There are other data supporting the idea that fluorides can induce genetic alterations. Evidence indicating biochemical interactions of fluoride with the genetic mechanisms of cell division are presented in the NRC report on Fluoride in the Drinking Water. (See Endnote 2) When the possible benefits and possible dangers of fluoride are considered there really is no comparison. Consider the following: There is no known benefit of adding any form of fluoride to our drinking water. Who would want to increase chances of having a less than perfect child? Who would wish to take a chance on a possible reduction of their own mental capacity? Who would want to have their personality altered by fluoride induced alterations in their brain chemistry? Who would want to increase their odds of developing Alzheimer’s disease? Eliminating the addition of fluoride to our drinking water would remove these possibilities. The cost of doing this is zero. In fact it would enrich the communities now adding fluorides to their drinking water.


Endnotes Varner, J. A., Huie, C. W., Horvath, , W. J., Jensen, K. F., and Isaacson, R. L. (1993) Chronic AlF3 administration: II. Selected histological observations. Neurosci. Res. Comm. 13:99-104.Varner, J. A., Jensen, K. F., Horvath, W. J. and Isaacson R. L. (1998) Chronic administration of aluminum fluoride or sodium fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res., 784: 284-298.Varner, J. A., Horvath, W. J., Huie, C. W., Naslund, H. R., and Isaacson, R. L. (1994) Chronic aluminum fluoride administration. Behav. Neural Biol., 61: 233-241.Isaacson, R. L., Varner, J. A., and Jensen, K. F. Toxin-induced blood vessel inclusions caused by the chronic administrations of aluminum and sodium fluoride. Ann. NY Acad. Sci., 825:152- 166. The final report of the committee was published by the National Academies Press in December 2006, entitled “Fluoride in drinking water.” It can by obtained from the National Academies Press and by special order from any bookstore. The electronic link to the NRC/NAS publication sites:


1 – 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Spira, L. The drama of fluorine, archenemy, of mankind. Milwaukee: The Lee Foundation for Nutritional Research, 1950, 1959. Waldbott, G. L. Fluoridation the great dilemma, Lawrence, KA: Coronado Press, 1978. Masters R. D., Coplan, M.J. Association of silicofluoride treated water lead with elevated blood lead. Neurotoxicology, 2000. 21:1091-1100. Masters, R. D., Coplan M. J. A dynamic, multifactoral model of alcohol, drug abuse and crime: Linking neuroscience and behavior to toxicology. Soc. Sci. Information, 1999, 38: 591-624. Seavy, J., (2005) Water fluoridation and crime in America. Fluoride, 38:11-22. Du Li. (1992) The effect of fluorine on developing human brain. Chinese Journal of Pathology, 21:218-20. Li Jing, Yao L., Shao, Q-L, and Wu, C-Y. (2004) Effects of high fluoride level on neonatal neurobehavioral development. Chinese Journal of Endocrinology, 23: No.5. Belovjovic, G., Jakovlevic, B. (1999) Aluminum and Alzheimer’s disease. Spr. ArArh. Celok 126: 283-289. Strunecka, A. (1999) Aluminum plus Fluoride: a new deadly duo. Dement. 1: 2- 3. Long, Y-G, Wang, Y-N, Chen, J., Jiang, S-F, Nordberg, A., and Guan, Z-Z. (2002) Chronic fluoride toxicity decreases the number of acetylcholine receptors in the rat brain. Neurotox. Terat, 23: 751-757. Burgstahler, A. W. (1966) Fluoridated water and Down’s syndrome. Long abstract of a report of the 21st Conference of the International Society for Brain Research, Budapest. Takahashi, K. (1998) Fluoride-linked Down syndrome births and their estimated occurrence due to water fluoridation. Fluoride, 31: 61-73. Juan Carlos Molina is the Director of the Ferryra Research Institute at the University of Cordoba, Argentina, as well as holding his distinguished professor position there. He also is a visiting research professor at Binghamton University.


Disclaimer: The material in this document represents my opinions, unless otherwise noted. The content may be copied in part or in full without permission when used in a not for profit format. When used for other purposes, the permission of the author is required. The document is not intended to provide medical advice but rather for the sharing of knowledge and opinions of the author. Decisions about health advice should be based on a personal one-on-one basis with an appropriate physician.

Robert L. Isaacson
Department of Psychology & Centre for Developmental
and Behavioral Neuroscience
Binghamton University
Binghamton, NY 13902-6000
Phone: 607 777 6764