Letter to HHS-EPA 4-22-12

Washington Action for Safe Water
Bill Osmunson DDS, MPH President
1418 – 112th Ave NE #200
Bellevue, Washington 98004

April 22, 2012

Kathleen Sebelius
U.S. Department of Health and Human Services
200 Independence Avenue SW
Room 603-H
Washington DC 20201
Also sent by email to: Kathleen.Sebelius@hhs.gov
 
Lisa P. Jackson, Administrator
Environmental Protection Agency
Ariel Rios Building
1200 Pennsylvania Ave. NW
Washington, DC 20004
Also sent by email to: FluorideScience@epa.gov

THIRD COMMENT ON FLUORIDATION

 Dear Secretary Kathleen Sebelius, Surgeon General Regina Benjamin, HHS/CDC/EPA,

SUMMARY:  Spittle[1] (2011) “Thus there is no threshold for F neurotoxicity in drinking water, and the only assuredly safe level is zero.”  Fluoride at “normal” concentrations increases cAMP and increased cAMP is reported to impair working memory. Provided below is current research finding harm to the brain, neurobiology of thought with decreased working memory, thyroid damage, cancer, and increased CVD, from fluoride at very low levels.

When fluoridation was first promoted, fluoridation was NOT supposed to do ANYTHING except increase the resistance of teeth to dental caries. Fluoridation was NOT supposed to affect bone, and we now know it does.   Fluoridation was NOT supposed to affect the thyroid, pineal gland, immune system, brain, IQ, electrolyte balance, proteins, etc….but it does.

Please also refer to our previous comments provided on April 19, 2011 and October 2011.

Prystupa[2] (2011) “Fluoride is the extreme electron scavenger, the most corrosive of all elements, as well as the most-reactive.  Fluoride appears to attack living tissues, via several mechanisms. Fluoride renders strong evidence that it is a nonbiological chemical, demonstrating no observed beneficial function or role in organic chemistry, beyond use as a pesticide or insecticide. . .

Conclusion: Due to its insatiable appetite for calcium, fluorine and fluorides likely represent a form of chemistry that is incompatible with biological tissues and organ system functions. Based on an analysis of the affects of fluoride demonstrated consistently in the literature, safe levels have not been determined nor standardized. Mounting evidence presents conflicting value to its presence in biological settings and applications.”

FLUORIDE AND THE BRAIN (emphasis supplied):

About a hundred human and animal studies have reported brain and IQ harm from fluoride.  These are a few recent studies.  Keep in mind that in the USA, about half the total fluoride exposure is from water.  In some countries without fluoride toothpaste, fluoride medications, dental products and pesticides the total fluoride exposure is more accurately considered from water unless the community has other high fluoride sources.  A reasonable method of measuring fluoride exposure is fasting fluoride serum concentrations.

  1. Xiang (2011)[3] “However, the mean IQ was significantly higher and there were fewer children with an IQ less than 80 in the two quartiles with a serum fluoride level of less than 0.05 mg F/ L. Analysis of the overall relationship between IQ scores and serum F levels indicates there may be no serum F level below which adverse effects on IQ might not be present.”

 

  1. Shivaprakash (2011) compared children with and without dental fluorosis and reported a decrease of about 10 IQ points (7 IQ points for boys and 14 IQ points for girls).  (CDC reports 2 out of 5 children in the USA have dental fluorosis and another 1 out of 5 may have dental fluorosis.)

 

  1. Poureslami[4] (2011) “the mean IQ scores of the children in low F Baft was 97.80±15.95, and in high F Koohbanan it was significantly lower at 91.37±15.63 (p = 0.028).”

 

  1. Eswar[5] (2011) “The trend was toward lower IQ with high F water, even though these preliminary findings indicated that the F level in the drinking water was not significantly associated with IQ scores of 12–14 year old children in the high and low F villages. . . .

The bore wells in the two villages were at least 12 years old according to the information supplied by the governing body of each village.”

The Eswar study is the first human study to not find statistical significance of lower IQ or brain damage.  This study’s cohort parents, cohorts as fetuses and perhaps some 13-14 year olds may not have had fluoridated water if some or all bore wells were only 12 years old.  Perhaps the most significant effect on the brain is the effect on genetics,[6] sperm and eggs, fetuses and the first years of life.  Spittle (2011) Leite (2011)[7] Sawan (2010)[8] Ersoy (2011)[9] point out magnesium, calcium, sodium, lead, copper (etc.) may play a significant confounding roll.  Basha[10] (2012) reported exercise and temperature reduced the deleterious effects of fluoride.

The Eswar study combined with animal studies such as the following two Basha (2011) studies reporting multigenerational cumulative damage should raise our concern and protection is a critical national emergency for pre conception, pre and post natal adverse effects of fluoride.

  1. 5.                  Basha[11] (2011) “Multigenerational evaluation was made in rats on exposure to high fluoride (100 and 200 ppm) to assess neurotoxic potential of fluoride in discrete areas of the brain . . . .  Results of this study can be taken as an index of neurotoxicity in rats exposed to water fluoridation over several generations.”

 

  1. Basha[12] (2011) Hence, presence of generational or cumulative effects of fluoride on the development of the offspring when it is ingested continuously through multiple generations is evident from the present study.”

 

  1. Inkielewicz-Stepniak (2012) Fluoride intoxication and dexamethasone treatment produce deleterious effects in bone and brain.  . . . . These data indicate that co-exposure to F and Dex amplifies their respective cytotoxicity in H(2)O(2)- and NO-dependent manner. “[13]

 

  1. Flora (2012) “These results thus highlight the role of arsenic- or fluoride-induced oxidative stress, DNA damage and protein interaction as the major determinants of toxicity, along with the differential toxic effects during arsenic-fluoride interaction during co-exposure.”[14]

 

  1. Mansour[15] (2011) “Results: NaF administration induced oxidative stress as evidenced by elevated levels of lipid peroxidation (51.3, 65.9 and 67.6%) measured as malondialdehyde and total nitrate/nitrite (61.0, 59.7 and 68.9%) in red blood cells, heart and brain tissues. . . .  Conclusion: Lycopene administration could minimize the toxic effects of fluoride indicating its free-radical scavenging and powerful anti-oxidant activities.”

 

  1. 10.              Bhatnagar (2011):  “results indicate that excessive F intake caused morphological changes in NADPH-d/NOS (nitric oxide synthase) positive neurons in the brain, thus increasing nitric oxide (NO) synthesis, which is implicated in F-induced neuron cell death. A possible mechanism of F neurotoxicity is thereby suggested.” [16]

 

  1. 11.              Ding[17] (2011) “Mean value of fluoride in drinking water was 1.31 +/-1.05 mg/L (range 0.24-2.84).  Urine fluoride was inversely associated with IQ in the multiple linear regression model when children’s age as a covariate variable was taken into account (P<0.0001). . . . In conclusion, our study suggested that low levels of fluoride exposure in drinking water had negative effects on children’s intelligence and dental health and confirmed a dose-response relationship between urine fluoride and IQ scores as well as dental fluorosis.”

 

  1. Basha[18] (2010) The effect of fluoride exposure during gestation and post gestation periods were studied to check the status of oxidant, antioxidant and macromolecular changes in CNS and ameliorative role of antioxidants.  . . . The findings evidenced fluoride induced dyshomeostasis caused on antioxidants, enzymes, macromolecules and governed the pathophysiological events leading to functional loss in a dose dependent manner.

 

  1. 13.              Madhusudhan[19] (2010) “Fluoride is toxic to neuronal development and its excessive intake during pregnancy cause adverse effects on neonatal development. . . . The results implied the vulnerability of developing CNS to fluoride toxicity.”

 

  1. 14.              Narayanaswamy[20] (2010) “The developing CNS is highly vulnerable to environmental agents, including fluoride. Fluorosis is one such disorder ensued from excessive consumption of fluoride containing water and/or foods that poses a greater threat to the life. . . . On 21st postnatal day (rats), the concentration of fluoride, biometals, and oxidative stress markers were determined in discrete regions of CNS. The levels of fluoride, copper, and iron increased whereas manganese and zinc were decreased considerably.  . . . The results confirm that the fluoride provoked oxidative stress and biometal deformations are synergistic that successively governs the neuronal damage and developing CNS no longer prevents exacerbations of fluoride.”

 

  1. 15.              Niu[21] (2009)Fluoride (F) and lead (Pb) are two common environmental pollutants which are linked to the lowered intelligence, especially for children. . .  . These findings suggested that alteration of hippocampus glutamate by F and/or Pb may in part reduce learning ability in rats.

THE FLUORIDE BRAIN CONNECTION: Ionic regulation of prefrontal microcircuits.

For perspective, keep in mind the CDC’s 0.02 ppm (1 micromolar is 0.019 ppm) “normal serum fluoride.”  The CDC states: “Normal serum fluoride levels are <20 mcg/L but varies substantially on the basis of dietary intake and environmental levels.”[22]   The CDC does not appear to be suggesting 0.02 ppm (1.05 micromolar or 20 mcg/L) is safe, but rather 0.02 ppm is the concentration Americans have in their serum, with substantial variations. (See page 27 of our first submission for more details on current fluoride serum levels.)  Artru (1997) reported presurgical plasma fluoride concentrations on 14 patients ranged from 0 to 2.3 uM.   Hu[23] (1988 graph below) reported similar cerebral spinal fluid and blood fluoride concentrations 0.010-0.38 ppm (5 to 19 uM).

Gutowska[24] (2012) reported a 19% increase in cAMP (cyclic adenosine monophosphate) at 1 uM (less than 0.02 ppm) of fluoride, 71% increase at 3 uM, 174% at 6 uM, and 221% at 10 uM below the CSF concentrations of some controls in Hu’s study, (see graph below), and slightly below the serum fluoride concentration the CDC considers “normal.”

So what? What is wrong with an increase in cAMP?

Arnsten[25],[26]  (2012) “cAMP is considered important for both cancer and higher order thinking.  In most brain circuits (e.g. hippocampus) cAMP strengthens synaptic connections.  However, in the PFC (prefrontal cortex) cAMP weakens persistent firing and impairs working memory. These seemingly opposite effects arise from cAMP actions on ion channels that dynamically alter the strength of PFC network connections . . .  Opening these channels (cAMP and KCNQ) by high levels of cAMP signaling, e.g., during stress exposure or with α2A receptor blockade, weakens PFC network connections and reduces persistent firing, while blockade of HCN channels restores firing. In this way, exposure to a stressor can rapidly take PFC “off-line” to switch control of behavior to more primitive brain circuits that mediate stress reflexes, such as freezing or fight or flight habitual responses. This mechanism has survival value when faced with danger but may be counterproductive when stressors require thoughtful PFC responses, e.g., during public speaking or when needing to make a complex decision.”

In effect, fluoride is a chemical stressor which inhibits prefrontal cognitive function, consistent with research finding lower IQ and increased mental retardation.

Indeed, when the US states are ranked in order of the whole population fluoridated and mental retardation, the following graph presented in our first supplement is provided here again showing triple the prevalence of mental retardation with increased fluoridation.  The graph on the right is from Xiang’s data comparing two villages with 0.04 ppm and 0.8 ppm serum fluoride concentrations.

Other mechanisms for fluoride damage such as genetics and developmental damage are discussed in our first comment to HHS of 4/11.

FLUORIDE AND THYROID GLAND

  1. Chiba (2012)[27]The chronic treatment with F promoted: (1) decrease in pp185 (IRS-1/IRS-2) tyrosine phosphorylation status in the WAT; (2) increase in IRS-1 serine phosphorylation status in the WAT; (3) increase in plasma concentrations of TNF-a and resistin; and (4) decrease in insulin sensitivity.”

Hosur[28] (2012) “Our observations suggest that thyroid hormone levels were not altered in subjects with dental fluorosis.”  Note: dental fluorosis is an historical consideration of fluoride exposure and occurs during enamel formation prior to the eruption of the tooth.   Measuring thyroid hormone serum levels years after excess fluoride exposure is a valid study only in so far as the researcher is evaluating long term effect.  Hosur’s study with 65 subjects and 10 controls is too small to evaluate long term effects due to numerous confounding factors.

  1. Eliud (2009) “Exposure to high levels of F− in drinking water may decrease insulin mRNA and its secretion from _-cells, and might therefore affect the OGTT.”[29]
  1. Menoyo[30] (2005) “Sodium fluoride (CSA 7681-49-4) 5-20 umol/L in the extracellular space inhibited insulin secretion by isolated Langerhans Islets stimulated with glucose. Insulin secretion followed a negative exponential function.  This phenomenon is rapidly reversible.”
  1. Rigalli[31] (1995) The results of these (rat) experiments indicate that glucose homeostasis is affected when plasma diffusible fluoride exceeds 5 micromo/l.”

NOTE:  Fluoride is not absorbed as effectively in rats as humans, resulting in a 7 to 10 fold lower fluoride serum concentration.  For rats, water with 30 ppm results in fluoride serum concentrations of 0.076-0.143 ppm well within the high range of fluoride found in some human controls and subjects.

Infants are most at risk.  “Infants aged 37-410 days exposed to 0.25 mg fluoride supplement [about one glass of fluoridated water], the mean retention ([assumed] bone uptake) of fluoride ranged from 68.1 to 83.4% (Ekstrand et al. 1994a, 1994 b).  In contrast, retention in adults receiving a fluoride supplement was 55.3% (Ekstrand et al. 1979).”[32]

“Human and animal studies have shown that fluoride is readily transferred across the placenta.” [33]

KIDNEYS:   Chandrajith[34] (2011) “Fluoride as shown in this study causes renal tubular damage. However it does not act alone and in certain instances it is even cytoprotective. The fine dividing line between cytotoxicity and cytoprotectivity of fluoride appears to be the effect of Ca2+ and Na+ of the ingested water on the F− metabolism.”

HEART:  Gutowska[35] (2012) “It is well known that fluoride can increase the inflammatory reactions. . . .The results of our study suggest that fluoride may change the activity of phospholipases in macrophage cells. . . . Secretory phospholipases are associated with the development of the atherosclerotic process. . . NaF at a concentration of 3uM increased [Ca2þ]i value by about 10% (p¼0.032), at 6 mM by 29% (p¼0.012) and NaF at 10 mM by about 20% (p¼0.012).  . . . Although the results obtained in this study were not as spectacular as in other reports which used mM concentrations of NaF [33,36,42,50,61], they indicated that even in small con- centrations fluorides may cause changes in the activity of enzymes taking part in the development of atherosclerosis.”

CANCER:

1.    Some studies suggest a deregulation of cAMP pathways and an aberrant activation of cAMP-controlled genes is linked to the growth of some cancers. See Cancer Research by Abramovitch R, A Pivotal Role of Cyclic AMP-Responsive Element Binding Protein Tumor Progression, Cancer Research, 2004. http://cancerres.aacrjournals.org/content/64/4/1338.full

2.    See also for melanomas, http://cancerres.aacrjournals.org/content/66/19/9483.abstract

3.    See also for ovarian cancer, Simpson (1996) “In malignant tumors there was a significant positive correlation btween the percentage of the RI protein and total cyclic AMP-binding proteins. (P = 0.01).  These data indicate that high tumor lvels of cyclic AMP-binding proteins are associated with serous histology, poor differentiation, and poor patient survival.” http://cancerres.aacrjournals.org/content/2/1/201.abstract and full article http://clincancerres.aacrjournals.org/contnt/2/1/201.full.pdf+html

4.         Levy M. (2011) “Conclusion: Our ecological analysis suggests that the water fluoridation status in the continental U.S. has no influence on osteosarcoma incidence rates during childhood and adolescence.” However, Levy cherry picked the data by removing the two least fluoridated states and highly fluoridated Washington DC (not in the data pool.)  Levy’s elimination of Hawaii based on environmental, geological and hereditary factors is without merit and the data should have been included for comparison.  The elimination of Utah because Utah increased fluoridation at the end of the study is again without merit.

LACK OF BENEFIT:

Tellez[36] (2012) “The prevalence of dental fluorosis reached 100% in this sample. . . .  The prevalence of caries experience (DF-S2) was 54%. . . . When initial caries lesions were included (ICDAS-scores 1-3) the mean DF-S1,2 increased to 10 (sd 5.1).  The association between fluorosis and dental caries was not statistically significant (p>0.05).  Children not only detected the presence of something abnormal in their teeth but also reported feeling embarrassed, and worried due to their dental appearance.  Almost 60% of the children avoided smiling because of their teeth’s appearance.”

EXPOSURE:    Saul (2011)[37] “Fluoride in toothpaste and mouth rinses also is medication. It may be intended as topical, but the reality is different. No matter how it may be applied in their mouths, young children are going to swallow it. Indeed, most of the public and the dental profession have already swallowed belief in fluoride: hook, line, and sinker.”

 

American Dental Association Foundation Grant Application: “After 60 years of community water fluoridation we still do not know how much F is required to prevent caries.”[38]

Peckham[39] (2011) “Water fluoridation continues to be a contentious public health policy. . . .  While traditionally the problem of evidence is characterised as one where policy makers either accept or ignore evidence, a central concern of this article is where poor evidence is promoted by professionals and accepted by policy makers.”

The studies are by no means comprehensive of all the research over the last few months and must be taken with other research provided to HHS.

Why have good people in public health made such a huge mistake promoting fluoridation?  In part, because of a concept of “compartmentalization of tasks.”   Several public health agencies have certain tasks to fulfill and the results of the individual tasks are not under one authority.  EPA has one compartment, FDA another compartment, CDC another compartment, dentists another compartment, public health practitioners, toxicologists, pharmacologists, epidemiologists, university professors, HHS human subject research protection, the courts and politicians are just a few other compartments.  As long as each agency can pass the buck to someone else, no one is held accountable, there is no “doctor” or “legal intermediary” and the myth of fluoridation’s safety and efficacy continues.  The public is harmed in part because public health propaganda artists and CDC/ADA cherry picking dentists still claim fluoridation is safe and effective . . . and it is neither.  By cherry picking committee members, the desired outcomes will be confirmed.

A first step by HHS to suggest a lower concentration of fluoride in water is good but inadequate.  Many are still ingesting too much and being harmed.  Informed consent has been violated.  Without FDA CDER approval, fluoridation of public water must be considered research on humans without their consent in violation of HHS’s human subject research protections.

At a minimum, warnings and cautions from HHS to protect high risk individuals, such as infants and those with kidney, thyroid, bone and heart disorders and those who value brains, must be another step.  The CDC Dental Division has made gross biased errors and must be strictly supervised and downgraded. The phasing out of fluoridation as soon as possible is essential for the safety of the public.  Many are still ingesting too much fluoride from several sources.

 

Weaknesses in the studies should be noted and lack of quality studies on safety should also be considered.  There are no randomized controlled trials evaluating fluoridated public water, in other words, there are no quality studies.  The absence of data is not proof of safety.   Randomized controlled trials can and should be done using fluoride urine and serum for measurements of exposure, controlling for known confounding factors and unknown confounding factors with a margin of safety of at least 10.  Data from research funded by HHS must be published on the internet.

 

Sincerely,

 

Bill Osmunson DDS, MPH President

Washington Action for Safe Water



[1] Spittle B, Neurotoxic Effects of Fluoride, Fluoride 2011;44(3)117-124  http://www.fluorideresearch.org/443/files/FJ2011_v44_n3_p117-124_pq.pdf

[2] Prystupa J, Fluorine-A current literature review. An NRC and ATSDR based review of safety standards for exposure to fluorine and fluorides. Toxicology Mechanisms and Methods, 2011;21(2):103-170.

[3] Xiang Q et al, ANALYSIS OF CHILDREN’S SERUM FLUORIDE LEVELS IN RELATION TO INTELLIGENCE SCORES IN A HIGH AND LOW FLUORIDE WATER VILLAGE IN CHINA, October-December 2011, Fluoride 44(4)191–194  http://www.fluorideresearch.org/444/files/FJ2011_v44_n4_p191-194_pq.pdf

[4]  Shivaprakash PK, Ohri K, Noorani H. Dental Fluorosis vs. IQ of Children of Bagalkot District, India, Fluoride 2011;44(4)260-261, http://www.fluorideresearch.org/444/files/FJ2011_v44_n4_p260-261_pq.pdf

[5] Eswar P, Intelligence Quotients of 12-14 Year Old School Children in a High and Low Fluoride Village in India, Fluoride 2011;44:168-172 http://www.fluorideresearch.org/443/files/FJ2011_v44_n3_p168-172_pq.pdf

[6] Fluoride and Genetic damage FAN,  http://www.fluoridealert.org/f-genetic.htm Accessed 4/14/2012

[7] Leite G. et al, Exposure to lead exacerbates dental fluorosis, Arch Oral Bio, 2011 in Press.

[8] Sawan R. et al, Fluoride increases lead concentrations in whole blood and in calcified tissues from lead-exposed rats, Toxicology 271 (2010) 21-26.

[9] Ersoy I, et al, Serum copper, zinc, and magnesium levels in patients with chronic fluorosis, Biol Trace Elem Res. 2011 Nov;143(2) : 619-24.

[10] Basha PM, Sujitha NS. Combined Influence of Intermittent Exercise and Temperature Stress on the Modulation of Fluoride Toxicity.  Biol Trace Elem Res. 2012 Feb 5

[11] Basha PM, Rai P, Begum S. Evaluation of fluoride-induced oxidative stress in rat brain: a multigeneration study. Biol Trace Elem Res. 2011 Sep;142(3):623-37

[12] Basha PM, Rai P, Begum S, Fluoride toxicity and status of serum thyroid hormones, brain histopathology, and learning memory in rats: a multigenerational assessment. Biol Trace Elem Res. 2011 Dec;144(1-3):1083-94

[13] Inkielewicz-Stepniak I, Radomski MW, Wozniak M., Fisetin prevents fluoride- and dexamethasone-induced oxidative damage in osteoblast and hippocampal cells, Food Chem Toxicol. 2012 Mar;50(3-4):583-9.

[14] Flora SJ, Mittal M, Pachauri V, Dwivedi N., A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice, Metallomics. 2012 Jan;4(1):78-90.

[15] Mansour HH, Tawfik SS, Efficacy of lycopene against fluoride toxicity in rats. Pharm Biol. 2011 Dec 1

[16] http://www.fluorideresearch.org/444/files/FJ2011_v44_n4_p195-209_pq.pdf

[17] Ding Y et al, The relationships between low levels of urine fluoride on children’s intelligence, dental fluorosis in endemic areas in Hulunbuir, Inner Mongolia, China, J Hazard Mater, 2011 Feb 28;186(2-3).

[18] Basha PM, Madhusudhan N., Pre and post natal exposure of fluoride induced oxidative macromolecular alterations in developing central nervous system of rat and amelioration by antioxidants.Neurochem Res. 2010 Jul;35(7):1017-28.

[19] Madhusudhan N, Basha PM, Rai P, Ahmed F, Prasad GR. Effect of maternal fluoride exposure on developing CNS of rats: protective role of Aloe vera, Curcuma longa and Ocimum sanctum. Indian J Exp Biol. 2010 Aug;48(8):830-6.

[20] Narayanaswamy M, Piler MB. Effect of maternal exposure of fluoride on biometals and oxidative stress parameters in developing CNS of rat. Biol Trace Elem Res. 2010 Jan;133(1):71-82.

[21] Niu R et al, Decreased learning ability and low hippocampus glutamate in offspring rats exposed to fluoride and lead, Environmental Toxicology and Pharmacology 28 (2009) 254-258.

[22] http://www.bt.cdc.gov/agent/sulfurylfluoride/casedef.asp Accessed 2/9/11

[23] Huan HY, Shung WS, Fluoride cerebrospinal fluid in patients with fluorosis. J Neurology, Neurosurgery, and Psychiatry 1988;51:1591-1593.

[24] Gutowska I. et al, Activation of phospholipase A2 by low levels of fluoride in THP1 macrophages via altered Ca2þ and cAMP concentration, Prostaglandins, Leukotrienes and Essential Fatty Acids 86 (2012) 99-105.

[25] www.sciencedaily.com/releases/2007/04/070420143324.htm

[26] Arnsten AFT, Jin LE, Guanfacine for the Treatment of Cognitive Disorders:  A Century of Discoveries at Yale, Yale J Biol Med v.85(1); Mar 2012.  For this statement, Arnsten references  Vijhayraghavan S, et al, Inverted-U dopamine D1 receptor actions on prefrontal neurons engaged in working memory. Nat Nurosci. 2007; 10:376-384.  and references Wang M et al. Alpha2A-adrenocptor stimulation strengthens working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex. Cll. 2007;129:397-410. and references.  And references Taylor JR, Birnbaum SG, Ubriani R, Arnsten AFT. Activation of cAMP-dependent protein kinase A in prefrontal cortex impairs working memory performance. J Neurosci. 1999;19(18):RC23.   Runyan JD, Dash PK. Distinct prefrontal molecular mechanisms for information storage lasting seconds versus minutes. Learn Mem. 2005;12:232–238.  Arnsten AFT, Ramos B, Birnbaum SB, Taylor JR. Protein kinase A as a therapeutic target for memory disorders: Rationale and challenges. Trends Mol Med. 2005;11:121–128.

[27] Chiba F, et al, NaF treatment increases TNF-a and resistin concentrations and reduces insulin signal in rats.

[28] Hosur MB et al, Study of thyroid hormones free triiodothyronine (FT3), free thyroxine (FT4) and the thyroid stimulating hormone (TSH) in subjects with dental fluorosis, Eur J Dent 2012 Apr;6(2):184-190.

[29] Eliud A. García-Montalvo, Hugo Reyes-Pérez, Luz M. Del Razo,  “Fluoride exposure impairs glucose tolerance via decreased insulin expression and oxidative stress” Toxicology March 2009

[30] Menoyo I. et al, Effect of Fluoride on the Secretion of Insulin in the Rat, Antidiabetics, Artznlm-Forsch./Drug Res. 55.No.8, 455-460 (2005) Aulendorf (Germany).

[31] Rigalli A et al, Comparative Study of the Effect of Sodium Fluoride and Sodium Monofluorophosphate on Glucose Homeostasis in the Rat, Arzneim-Forsch/Drug Res. 45 (I) Nr. 3 (1995)

[32] FLUORIDES, HYDROGEN FLUORIDE, AND FLUORINE, Chapter 3 HEALTH EFFECTS p 143. www. Atsdr.cdc.gov/toxprofiles/tp11-c3.pdf

[33] FLUORIDES, HYDROGEN FLUORIDE, AND FLUORINE, Chapter 3 HEALTH EFFECTS p 143. www. Atsdr.cdc.gov/toxprofiles/tp11-c3.pdf

[34] Chandrajith et al, Dose-dependent Na and Ca in fluoride-rich drinking water – Another major cause of chronic renal failure in tropical arid regions, Science of the Total Environment 409 (2011) 671-675

[35] Gutowska I. et al, Activation of phospholipase A2 by low levels of fluoride in THP1 macrophages via altered Ca2þ and cAMP concentration, Prostaglandins, Leukotrienes and Essential Fatty Acids 86 (2012) 99-105.

[36] Tellez M et al, Dental fluorosis, dental caries, and quality of life factors among schoolchildren in a Columbian fluorotic area, Community Dent Health, 2012 Mar;29(1)95-9

[37] Saul A, Dispensing with Fluoride, Fluoride, Oct-Dec 2011, 44(4)188-190.

[38] Carey, CM., Chow, LC, Eichmiller FC, Schumacher GE, American Dental Association Foundation Paffenbarger Research Center 6/2003 Grant application.  No publication has been found on the data from this grant.

[39] Peckham S, Slaying sacred cows: is it time to pull the plug on water fluoridation? Critical Public Health, 2011; :1-19

  1. Jim
    April 23rd, 2012 at 06:02 | #1

    Great work Dr Osmunson. We must now ask why city commissions turn a blind eye to this evidence of risk and even deny dental fluorosis exists in their cities. Or say because they have drank the water and are still alive 60 years later it is not possible it could be a risk to any citizen in their mind. And we have 3 attorneys as commissioners who are willing to state such foolish tripe to the newspaper. Ormond Beach Florida does have a warning on their website placed their by the then dentist Mayor after the Nov 9 2006 ADA egram to dentists. Sad thing is I gave all a copy of the egram before I spoke a week later and the Mayor told the commission and public I was wrong the ADA had made no such statement. He had missed their and my memo I guess. None of the other commissioners mentioned his error either. The next meeting he meet me at the door and informed me I had been correct. I reminded him I have never had any doubts about that. He wi9thout a vote put the warning in a newsletter, city website but it still reads like an endorsement of fluoridation as the best policy ever. A year later I got a notice on Cable for the whole county on two public channels for weeks. Free and effective. Daytona has refused to make any notice in spite of a 40% poor black population of 32114 zip which is a known health disaster says the public health department. Protect policy and let the people fend for themselves seems the rule in finding out the truth. The ADA had a secret meeting off the record with me as a agenda item and how to silence me. I had been banned from speaking from some city commissions and then a workshop on fluoridation where those against fluoridation were not allowed to speak. They called us misguided individuals. They then voted 5-0 in the closed comments meeting to keep this benefit to all and safe fluoridation process. No specific studies were mentioned just CDC talking points by people who needed a power point to avoid looking like total fools. Even then they made simple errors no antifluoride person would make. And these clowns draw a salary from my taxes. Two commissioner later told me they were starting to believe me until they heard the facts from the experts. In a debate they would be fools like happened in Austin Tx showed so very well. Same outside San Antio with Bill Wells PHD asking questions of the health department experts who could not wait for the end of the meeting as they had no answers to good questions. Yes they can say a few CDC talking points at best. Beyond that it is like a deer in the headlights. But that seems good enough for a city commission far too often.

  1. April 22nd, 2012 at 23:48 | #1
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