CSI mind control programming

I’ll tell you who the anti-american traitors are, it’s the actors in this propaganda piece-of-shit TV show.

These hollywood goblins should chug a big glass of fluorosilicic acid if they think it’s so great.  That’s the chemical they’re putting in our water to brain damage and sterilize us.  When you participate in this mind control psyop you’re guilty of giving those little boys osteoscarcoma (bone cancer). skeletal and dental fluorosis, reduced fertility, brain damage, and many other health problems.

This propaganda is disgusting and evil.   CSI actors, if you’re reading this, please just go kill yourselves.  You hurt little kids for money and you do not deserve to live.

And here is more scientific proof than you ever wanted that fluoride is toxic, especially to children.

Sodium fluoride’s effect on the male reproductive system

From fluoridealert.org

Central Nervous System Damage from Fluorides

by Phyllis J. Mullenix, Ph.D. September 14, 1998

It was 1982 when fluoride was first brought to my attention as a substance in need of investigation. At that time, I was in the Departments of Psychiatry at Boston’s Children’s Hospital and Neuropathology at the Harvard Medical School. My studies focused on detection procedures for neurotoxicity, and they typically considered a variety of environmental and therapeutic agents, i.e., radiation, lead, amphetamine, phenytoin, nitrous oxide. Dr. John Hein, then Director of Forsyth’s Dental Infirmary for Children in Boston, was interested in neurotoxicity studies and invited me to continue this research at Forsyth and to apply it to substances used in dentistry. Fluoride was prominent on his list.

Five years lapsed before our investigations of fluoride began. The delay was due to time spent on technological improvements, specifically development of a computer pattern recognition system for the objective quantification of behavior in an animal model. In early June of 1986, the Forsyth Dental Center was noted for this achievement in the Wall Street Journal and the Boston Herald, and applications of our research grew. The new technology enabled us to study the clinically recognized neurotoxicity associated with the treatment for childhood leukemia. Simultaneously, we started investigations of fluoride, the “safe and effective” treatment for dental caries.

Initially, the fluoride study sparked little interest, and in fact we were quite anxious to move on to something academically more exciting. Using an animal model developed for the study of dental fluorosis, we expected rats drinking fluoride-treated water would behave the same as matching controls. They did not. The scientific literature led us to believe that rats would easily tolerate 175 ppm fluoride in their drinking water. They did not. Reports in the literature indicated that fluoride would not cross the blood brain barrier. But it did. Prenatal exposure to fluoride was not supposed to permanently alter behavioral outcome. It did. Like walking into quicksand, our confidence that brain function was impervious to fluoride was sinking.

Our 1995 paper in Neurotoxicology and Teratology was the first laboratory study to demonstrate in vivo that central nervous system (CNS) function was vulnerable to fluoride, that the effects on behavior depended on the age at exposure and that fluoride accumulated in brain tissues. The behavioral changes common to weanling and adult exposures were different from those after prenatal exposure. Whereas prenatal exposure dispersed many behaviors as seen in drug-induced hyperactivity, weanling and adult exposures led to behavior- specific changes more related to cognitive deficits. Brain histology was not examined in this study, but we suggested that the effects on behavior were consistent with interrupted hippocampal development (a brain region generally linked with memory).

Establishing a threshold dose for effects on the CNS, in rats or humans, was not the intent of this initial investigation. Yet, one fact relevant to human exposure emerged quite clear. When rats consumed 75-125 ppm and humans 5-10 ppm fluoride in their respective drinking waters, the result was equivalent ranges of plasma fluoride levels. This range is observed with some treatments for osteoporosis, and it is exceeded ten times over, one hour after children receive topical applications of some dental fluoride gels. Thus, humans are being exposed to levels of fluoride we know alters behavior in rats.

We concluded that the rat study flagged potential for motor dysfunction, IQ deficits and/or learning disabilities in humans. Confident as we were, the data were only one piece of the puzzle, the overall picture was still emerging. Soon thereafter we learned of two epidemiological studies (Fluoride, 1995-1996) from China showing IQ deficits in children over-exposed to fluoride via drinking water or soot from burning coal. A recent review (International Clinical Psychopharmacology, 1994) listed case reports of CNS effects in humans excessively exposed to fluoride, information that spans almost 60 years. A common theme appeared in the reported effects: impaired memory and concentration, lethargy, headache, depression and confusion. The same theme was echoed in once classified reports about workers from the Manhatten Project. In all, our rat data seem to fit a consistent picture.

Information linking fluoride and CNS dysfunction continues in 1998.

1) A recent study in Brain Research demonstrated that chronic exposure to fluoride in drinking water of rats compromised neuronal (hippocampal) and cerebrovascular integrity (blood brain barrier) and increased aluminum concentrations in brain tissues.
2) Masters and Coplan have reported (International Journal of Environmental Studies, in press) that silicofluorides in fluoridated drinking water increased levels of lead in children’s blood, a risk factor that predicts higher crime rates, ADD and learning disabilities.
3) Luke at the International Society for Fluoride Research (ISFR) meeting in August reported that fluoride accumulated in the human pineal gland, as much or more so than in bones and teeth, and the pineal gland’s melatonin biosynthesis pathway is affected by fluoride.
4) Also at the ISFR meeting, I reported that the fluorinated steroid (dexamethasone) disrupts behavior in rats to a greater degree than does the nonfluorinated steroid (prednisolone). This finding matched results just completed in a study of children receiving steroids as a part of their treatment for childhood leukemia. Dexamethasone, compared to prednisolone, further reduced IQ, specifically impairing reading comprehension, arithmetic calculation and short-term working memory.

Exposure to fluoride goes well beyond that in our drinking water, toothpastes and mouth rinses. Fluoridation of water dictates that it is in food and processed beverages. Pesticides such as cryolite also increase fluoride content of foods. The trend toward fluorinating pharmaceuticals increases fluoride exposure via medication. Fluoride, in various compounds, plays a heavy role in occupational exposures and for people living in close proximity to industry, i.e., aluminum, steel, brick, glass, petroleum, etc. With exposure so common, we can no longer afford to ignore potential CNS consequences of fluoride.

Phyllis J. Mullenix, Ph.D.

Fluoride’s effect on the brain

(www.fluoridation.com) Fluoride’s Neurological Effects: studies show there may be grave implications for Alzheimers, Dementia, Attention Deficit Disorder, reduced IQ in children

Neurotoxicity of fluoride, Fluoride, 1996, 29:2, 57-58 (Editorial by AWB and JC)

The August 1995 issue of this journal contained an abstract (pages 151-152) of an interesting paper by Dr Phyllis Mullenix and her collaborators.1 They recorded behavioral changes in rats after ingestion of fluoride, and found that the severity of the effect on behavior increased directly with plasma fluoride levels and fluoride concentration in specific brain regions. A reading of the full paper is well worthwhile. In their Introduction, after referring to the increase in dental fluorosis in humans after decades of water fluoridation, the authors comment:

“One concern that has not been fully investigated is the link between fluoride and effects an the central nervous system (CNS)…. Many years of ubiquitous fluoride exposure have not resulted in obvious CNS problems such as seizures, lethargy, salivation, tremors, paralysis, or sensory deficits. Still unexplored, however, is the possibility that fluoride exposure is linked with subtle brain dysfunction.”

The carefully designed animal experiment which they report revealed subtle but very real changes in behavior patterns following fluoride ingestion: hyperactivity after prenatal exposure, and cognitive deficits after weanling and adult exposure. Fluoride accumulation in important regions of the rat brain, especially the hippocampus, was found to increase as the drinking water fluoride levels increased. These effects, and the sex differences observed, corresponded to those observed in other studies of hippocampal brain damage.

The authors point out that the plasma fluoride levels recorded in the rats were the same as those sometimes recorded in humans – for example, in children one hour after receiving topical fluoride treatment of their teeth. In their conclusion calling for further rat and human studies they state:

“Experience with other developmental neurotoxicants prompt expectations that changes in behavioral function will be comparable across species, especially humans and rats. Of course behaviors per se do not extrapolate, but a generic behavioral pattern disruption as found in this rat study can be indicative of a potential for motor dysfunction, IQ deficits and/or learning disabilities in humans.”

The authors draw attention to reports from Chinese investigators that high levels of fluoride in drinking water (3-11 ppm) affect the central nervous system directly without first causing the physical deformations of skeletal fluorosis.2-4 Readers of Fluoride will recall the recent (November 1995) research report from China indicating adverse neurological effects on the brain from fluoride exposure.5 This work also suggested that children with dental fluorosis are at greater risk of decreased mental acuity. One can only wonder whether the effects of fluoridated water might extend beyond the appearance of the teeth and include neurotoxicity among children afflicted with dental fluorosis.

Some of our readers may recall also pertinent early clinical findings reported by our founding editor, Dr G L Waldbott, of which Dr Mullenix and her co-workers do not appear to have been aware. These involved a wide range of reversible toxic effects of fluoridated drinking water, including diminished mental acuity and impairment of memory.6-8 In a separate report, Dr Waldbott even gave an account, supported by laboratory data, of a case of tetaniform convulsions induced by drinking fluoridated drinking water.9 For decades proponents of water fluoridation have questioned the validity of these reports without, however, offering objective evidence to refute them. But in the light of the human research in China and now the animal research in the United States, these clinical observations by Dr Waldbott on the neurotoxicity of fluoride in drinking water clearly deserve greater attention and credence. [references not scanned]

Jaqueline Calderon, Machado Blenda, Navarro Marielena, Carrizales Leticia, Ortiz Maria Deogracias, Diaz-Barriga F. Influence of Fluoride Exposure on Reaction Time and Visuospatial Organization in Children, Epidemiology July 2000, Volume 11, Number 4 Supplement S153.

Fluoride exposure is an important public health problem in several Mexican states. In the city of San Luis Potosi, Mexico, above 90% of the children have some degree of dental fluorosis. The main source of exposure to fluoride is tap water. The objective of the study was to evaluate the influence of chronic exposure to fluoride on neuropsychological development in children. Sixty-one children aged 6 to 8 years were included. Fluoride concentration in tap water ranged from 1.2 to 3 mg/L. Fluoride exposure was measured in urine samples by electrothermal ion selective method. Blood lead (PbB) was measured as indicator of lead exposure by atomic absorption spectrophotometry. Height for age index (HAI) was calculated as indicator of past nutritional status. Three tests were used to evaluate the neuropsychological development: (1) Wechsler Intelligence Scale for Children Revisited version for Mexico (WISC-RM), (2) Rey Osterrelth-Complex Figure test and (3) Continuos Performance Test (CPT). Mean value of fluoride in urine was 4.3 mgF/g creatinine (1.6-10.8). Mean PhB value was 6.2 ug/dl (2.0-15.6). After controlling by significant confounders, urinary fluoride correlated positively with reaction time and inversely with the scores in visuospatial organization. IQ scores were not influenced by fluoride exposure. An increase in reaction time could affect the attention process, also the low scores in visuospatial organization could be affecting the reading and writing abilities in these children.

University of North Caroline. Email: Jaqueline.Calderon@sph-unc.edu

Guan ZZ, Wang YN, Xiao KQ, Dai DY, Chen YH, Liu JL, Sindelar P, Dallner G, Influence of chronic fluorosis on membrane lipids in rat brain. Neurotoxicol Teratol 1998 Sep-Oct;20(5):537-42

Brain membrane lipid in rats were analyzed after being fed either 30 or 100 ppm fluoride for 3, 5, and 7 months. The protein content of brain with fluorosis decreased, whereas the DNA content remained stable during the entire period of investigation. After 7 months of fluoride treatment, the total brain phospholipid content decreased by 10% and 20% in the 30 and 100 ppm fluoride groups, respectively. The main species of phospholipid influenced by fluorosis were phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine. The fatty acid and aldehyde compositions of individual phospholipid classes were unchanged. No modifications could be detected in the amounts of cholesterol and dolichol. After 3 months of fluoride treatment, ubiquinone contents in brain were lower; however, at 7 months they were obviously increased in both groups of fluoride treatment. The results demonstrate that the contents of phospholipid and ubiquinone are modified in brains affected by chronic fluorosis and these changes of membrane lipids could be involved in the pathogenesis of this disease.

Department of Pathology, Guiyang Medical College, Guizhou, China. jialiul@public.gy.gz.cn

Jope RS, Modulation of phosphoinositide hydrolysis by NaF and aluminum in rat cortical slices. J Neurochem 1988 Dec;51(6):1731-6

NaF stimulated phosphoinositide hydrolysis in rat cortical slices. The production of [3H]inositol monophosphate was rapid for the first 15 min of incubation with NaF, followed by a plateau. The major product detected was [3H]inositol monophosphate, although significant amounts of [3H]inositol bisphosphate and [3H]inositol trisphosphate were also produced. The stimulation of [3H]inositol monophosphate production by NaF was concentration dependent between 2 and 20 mM NaF. Addition of 10 or 100 microM AlCl3 or aluminum maltol did not alter the effect of NaF, whereas at 500 microM, these aluminum preparations resulted in significant inhibition. Increasing the concentration of K+ from 5 to 20 mM potentiated [3H]inositol monophosphate production induced by carbachol but not by NaF. Incubation with 1 microM phorbol 12-myristate 13-acetate, a phorbol ester, inhibited carbachol-induced, but not NaF-induced, [3H]inositol monophosphate production. These results further support the hypothesis that a guanine nucleotide binding protein that can be activated by NaF is involved in phosphoinositide hydrolysis in brain. The use of NaF provides a means to bypass receptors to study intracellular regulatory sites of phosphoinositide metabolism without disrupting cells.

Department of Pharmacology and Neuropsychiatry Research Program, University of Alabama, Birmingham.

Kay AR, Miles R, Wong RK, Intracellular fluoride alters the kinetic properties of calcium currents facilitating the investigation of synaptic events in hippocampal neurons. J Neurosci 1986 Oct;6(10):2915-20

We have attempted to suppress voltage-dependent conductances in hippocampal neurons by introducing various intracellular agents. Voltage-clamp studies were carried out using acutely dissociated hippocampal neurons from adult guinea pigs. Synaptic events were examined using intracellular recordings in the slice preparation. Sodium conductance was suppressed when the quaternary lidocaine derivative QX 314 was introduced intracellularly. Potassium conductances were blocked by intracellular cesium or Tris. We also found that the anion fluoride could affect calcium conductance by an intracellular action. When anions other than fluoride were used for intracellular recordings, the voltage-dependent calcium current inactivated slowly and showed persistent activation at membrane potentials between -40 and -10 mV. In contrast, when fluoride was present intracellularly, the inactivation kinetics of the calcium current were accelerated and the persistent component of the current was largely suppressed. Intracellular recordings in the hippocampal slice showed that when electrodes contained cesium, QX 314, and fluoride, the spiking and nonlinear responses of the neuronal membrane to depolarization were blocked. In these conditions the time course and voltage-dependence of EPSPs could be examined in detail without complications due to voltage-dependent currents of the postsynaptic cell.

Li Y, Li X, Wei S, Effect of excessive fluoride intake on mental work capacity of children and a preliminary study of its mechanism, Hua Hsi I Ko Ta Hsueh Hsueh Pao,1994 Jun, 25 :2, 188-191 (Translated from Chinese)

We made an investigation in 157 children, aged 12-13, born and grew up in a coal burning pattern endemic fluorosis area and an experiment on excessive fluoride intake in rat. The results showed: (1) Excessive fluoride intake since early childhood would reduce mental work capacity (MWC) and hair zinc content: (2) The effect on zinc metabolism was a mechanism of influence on MWC by excessive fluoride intake; (3) Excessive fluoride intake decreased 5-hydroxy indole acetic acid and increased norepinephrine in rat brain; whether this is also a mechanism of the influence on MWC awaits confirmation.

Li XS, Zhi JL, Gao RO, Effect of Fluoride Exposure on Intelligence in Children, Fluoride, 1995 Nov, 28:4, pp 189-192

The intelligence was measured of 907 children aged 8-13 years living in areas which differed in the amount of fluoride present in the environment. The Intelligence Quotient (IQ) of children living in areas with a medium or severe prevalence of fluorosis was lower than that of children living in areas with only a slight fluorosis or no fluorosis. The development of intelligence appeared to be adversely affected by fluoride in the areas with a medium or severe prevalence of fluorosis but to a minor extent only in areas with only a slight prevalence of fluorosis. A high fluoride intake was associated with a lower intelligence. No correlation was found between age and intelligence in the areas with a medium and severe prevalence of fluorosis. The effect of exposure to a high level of fluoride on intelligence may occur at an early stage of development of the embryo and infant when the differentiation of brain nerve cells is occurring and development is most rapid.

Liu WX, Experimental study of behavior and cerebral morphology of rat pups generated by fluorotic female rat, Chung-hua Ping Li Hsueh Tsa Chih, 1989 Dec, 18:4, 290-292 (Article in Chinese)

In order to study the effects of fluoride on the central nervous system, 33-42-day old rat pups generated by three groups of female Wistar rats, which were given distilled water containing 0, 30 and 60 ppm NaF respectively beforehand as drinking water for 85 days, were used for behavior test and cerebral morphological examination. The results of behavior test showed that the latent period of pain reaction and that of conditioned reflex in the 30 ppm F and 60 ppm F groups were longer than that in the control group (P less than 0.05 or P less than 0.01). morphological examination of the pup brains showed that the nerve cell density of the 60 ppm F group was higher than that of the control group (P less than 0.05). Electronmicroscopically, mild degeneration of organelles of the nerve cells was observed in those brains of the 60 ppm F group.

Mattsson JL, Albee RR, Eisenbrandt DL Chang LW, Subchronic neurotoxicity in rats of the structural fumigant, sulfuryl fluoride, Neurotoxicol-Teratol, 1988 Mar-Apr, 10:2, 127-133

Inhalation exposure of male and female Fischer 344 rats to sulfuryl fluoride [Vikane (Dow Chemical Company) gas fumigant] at 300 ppm for 6 hr/day, 5 days week, for 13 weeks caused diminished wight gain, dental fluorosis, a slight decrease in grooming, decreased flicker fusion threshold, slowing of flash, auditory and somatosensory evoked potentials, mild nasal and pulmonary inflammation, mild kidney effects, and mild vacuolation in the brain. Auditory brainstem responses (ABRs) and brain histology were evaluated two months postexposure in 2 male and 2 female rats. Both the ABRs and brain histology were within normal limits at this time, indicating that these treatment effects were, to at least a great extent, reversible. Exposure to 100 ppm resulted in dental fluorosis and very minor slowing of some evoked responses; all other measures, including brain histology, were normal. No treatment effects were noted at 30 ppm.
Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ, Neurotoxicity of sodium fluoride in rats, Neurotoxicology Teratology, 1995 March,17(2):169-177.

Fluoride (F) is known to affect mineralizing tissues, but effects upon the developing brain have not been previously considered. This study in Sprague-Dawley rats compares behavior, body weight, plasma and brain F levels after sodium fluoride (NaF) exposures during late gestation, at weaning or in adults. For prenatal exposures, dams received injections (SC) of 0.13 mg/kg NaF or saline on gestational days 14-18 or 17-19. Weanlings received drinking water containing 0, 75, 100, or 125 ppm F for 6 or 20 weeks, and 3 month-old adults received water containing 100 ppm F for 6 weeks. Behavior was tested in a computer pattern recognition system that classified acts in a novel environment and quantified act initiations, total times and time structures. Fluoride exposures caused sex- and dose-specific behavioral deficits with a common pattern. Males were most sensitive to prenatal day 17-19 exposure, whereas females were more sensitive to weanling and adult exposures. After fluoride ingestion, the severity of the effect on behavior increased directly with plasma F levels and F concentrations in specific brain regions. Such association is important considering that plasma levels in this rat model (0.059 to 0.640 ppm F) are similar to those reported in humans exposed to high levels of fluoride. [emphasis added]

See also brain2.htm by Dr. P.J. Mullenix

Spittle B, Psychopharmacology of fluoride: a review, Int Clin Psychopharmacol, 9:2, 1994 Summer, 79-82

Although the blood-brain barrier is relatively impermeable to fluoride, it does not pose an absolute barrier and fluoride has the ability to enter the brain. The literature was examined to assess the quality of the evidence for cerebral impairment occurring due to exposure to fluoride from therapeutic or environmental sources. Several surveys of persons chronically exposed to industrial fluoride pollution reported symptoms related to impaired central nervous system functioning with impaired cognition and memory. Examination of individual case reports showed the evidence for aetiological relationships between symptoms and fluoride exposure to be of variable quality. The evidence was seen as being suggestive of a relationship rather than being definitive. The difficulties with concentration and memory described in relation to exposure to fluoride did not occur in isolation but were accompanied by other symptoms of which general malaise and fatigue were central. Possible mechanisms whereby fluoride could affect brain function include influencing calcium currents, altering enzyme configuration by forming strong hydrogen bonds with amide groups, inhibiting cortical adenylyl cyclase activity and increasing phosphoinositide hydrolysis.

[editor's note: this review was published before Mullenix et al., completed their ground-breaking study. The blood-brain barrier is penetrated by fluoride]

Strunecká A, Patoèka J, Pharmacological implications of aluminofluoride complexes, a review of the evidence for pathophysiological effects of aluminium and fluoride on living organism

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 Feb 16;784(1-2):284-98

This study describes alterations in the nervous system resulting from chronic administration of the fluoroaluminum complex (AlF3) or equivalent levels of fluoride (F) in the form of sodium-fluoride (NaF). Twenty seven adult male Long-Evans rats were administered one of three treatments for 52 weeks: the control group was administered double distilled deionized drinking water (ddw). The aluminum-treated group received ddw with 0.5 ppm AlF3 and the NaF group received ddw with 2.1 ppm NaF containing the equivalent amount of F as in the AlF3 ddw. Tissue aluminum (Al) levels of brain, liver and kidney were assessed with the Direct Current Plasma (DCP) technique and its distribution assessed with Morin histochemistry. Histological sections of brain were stained with hematoxylin & eosin (H&E), Cresyl violet, Bielschowsky silver stain, or immunohistochemically for beta-amyloid, amyloid A, and IgM. No differences were found between the body weights of rats in the different treatment groups although more rats died in the AlF3 group than in the control group. The Al levels in samples of brain and kidney were higher in both the AlF3 and NaF groups relative to controls. The effects of the two treatments on cerebrovascular and neuronal integrity were qualitatively and quantitatively different. These alterations were greater in animals in the AlF3 group than in the NaF group and greater in the NaF group than in controls. Copyright 1998 Elsevier Science B.V.

Psychology Department, Binghamton University, Binghamton, NY, USA.

Varner JA, Jensen KF, Horvath W, Issacson RL, The Neurotoxicological Evaluation Of The Chronic Administration Of Aluminum-Fluoride and Sodium-Fluoride, Society for Neuroscience Annual Meeting; San Diego, CA, 1995 Nov, abstract.

This study examined the neurotoxic consequences of the chronic ingestion of AlF₃ and the equivalent fluoride concentration given as low doses of NaF in drinking water. Twenty seven male LE rats, 3.5 – 4.5 months of age, were studied. The animals were divided into 3 groups based on the contents of the drinking water: control, NaF, or AlF₃. Water was available ad libium for 52 weeks. Significantly more rats died in the AlF₃ group than the control group during the study. Histological examinations involved the following stains: Cresy Violet, Bielschowsky silver, H&E, Morin Aluminum fluorescence, Beta Amyloid, Amyloid A, and IgM. Overall, neuronal loss was more prominent in the AlF₃ group than the NaF and control groups in the left hemisphere and in the dentate gyrus of both hemispheres. Toxin-induced abnormalities in the AlF₃ group were more apparent in the left hemisphere cortex but changes were found in the right hemisphere hippocampus. Hippocampal argentophillic reactions were common in both treated groups. Beta amyloid reaction product was enhanced in the thalamus in both toxin groups. More IgM antibody reaction product was found in the right hemisphere cortices of rats in both treated groups. Overall brain and kidney Al content was higher in both toxin groups relative to controls. Indications of glomerular disease were found in both treated groups. This reduction and/or abnormal appearance of cells, the presence of beta-amyloid, IgM, and Al indicate that AlF₃ is neurotoxic when chronically administered in the drinking water of rats. The abnormal appearance of cells and the presence of beta-amyloid, IgM, and Al suggest that NaF also induces neurotoxicity, although somewhat different than that found after AlF₃.

Varner JA, Huie C, Horvath W, Jensen KF, Issacson RL, Chronic AlF₃ Administration: II. Selected Histological Observations, Neuroscience Research Communications, 1993, 13:2, 99-104.

[editor's note: this study shows that the bioavailability of Al from drinking water is increased in the presence of fluoride. The Al content in the brain doubled in treated animals. According to an October 28, 1992 Wall Street Journal Article: "Rats fed the highest doses developed irregular mincing steps characteristic of senile animals.... Post mortem examination of the rat brains disclosed 'substantial cell loss in structures associated with dementia -- the neo-cortex and hippocampus'."]

Yang Y, Wang X, Guo X, Effects of high iodine and high fluorine on children’s intelligence and the metabolism of iodine and fluorine, Chung Hua Liu Hsing Ping Hsueh Tsa Chih, 1994 Oct, 15 (5), 296-298 (Translated from Chinese).

An investigation on children’s intelligence and the metabolism of iodine and fluorine in high iodine and fluorine regions was carried out. The results were as follows. In high iodine and high fluorine areas, the thyroid enlargement prevalence rate among inhabitants and that among children were 3.8% and 29.8%, respectively. The dental fluorosis prevalence rate among inhabitants and that among children was 35.48% and 72.9%, respectively. The pupils’ average intelligence quotient (IQ) was 76.67 ± 7.75, slightly lower than the control point, but that of low intelligent pupils was 16.7%. The urinary iodine and urinary fluoride were 816.25 ± 1.80 micrograms/L and 2.08 ± 1.03 mg/L, respectively, markedly higher than the control point. The thyroid iodine-131 (131I) uptake rate was markedly lower than the control point. The values at 3 h and 24 h were 9.36 ± 1.55% and 9.26 ± 4.63%, respectively. The serum TSH was obviously higher than the control point. These results indicate that high iodine and high fluorine exert severe damage to human body.

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

Abstract: In Shanxi Province, China, children living in the endemic fluoride village of Sima (water supply F=4.12 mg/L) located near Xiaoyi City had average IQ (97.69) significantly lower (p <0.02) mg/L; average IQ = 105.21). These differences were not associated with gender, but the IQ scores were directly related to educational level of the parents.
Introduction: It has been reported that fluoride can penetrate the fetal blood-brain barrier and accumulate in cerebral tissue before birth,¹ thereby apparently affecting children’s intelligence.² In the present study, conducted in April 1993, this hypothesis was further investigated by comparing the performance on IQ tests administered to 320 randomly selected children, age 7 to 14, residing in central Shanxi Province, China, in two suburban villages with significantly different fluoride content in drinking water. [...]
Discussion: The results of this study indicated that intake of high-fluoride drinking water from before birth has a significant deleterious influence on children’s IQ in on of two similar villages. No real differences were found for gender. In the high-fluoride village of Sima the number of children with IQ of 69 or below was six times that in the healthier low-fluoride village of Xinghua. There were also fewer children (20) in Sima with superior IQ scores of 120 or higher than the number (27) in Xinghua. Moreover, the fact that the IQ scores increased more slowly with age in Sima than in Xinghua supports the view that exposure to high levels of fluoride in utero exerts a cumulative adverse effect that is not overcome with increasing age in a high-fluoride community.

References
1. He H, Chen ZS, Liu XM, The effects of fluoride on the human embryo, Chinese Journal of Control of Epidemic Diseases, 1989, 4, 136-137.
   
2. Cheng YX, IQ of children in areas of high fluorine content, Chinese Journal of Control of Endemic Diseases, Supplement 1991.

RELATED ARTICLES

• Ding LI, The nervous systemic complications of chronic fluorosis. Chinese Journal of Endemiology, 1983, 2, 97-98.
  
• Hu YH, Direct damage on nervous system by fluorosis. Compilation of First Conference on Neuropsychiatric Diseases in Xinjian, (1982), 86-88.
  
• Shung-Guan CM, et al., The non-skeletal lesions of endemic fluorosis, Chinese Journal of Internal Medicine, 1982, 21, 217-219.
  
• Du L, Wan CW, Cao XM, The influence of chronic fluorosis on the development of the brain of the human embryo, Journal of Fluorosis Research Communications, 1991, 138

Chinese Fluoride of questionable purity being added to US water

Fluorocarbons – Charles Kettering, and “Dental Caries”

With as much toxic exposure as we get in modern society, I will give credit where credit is due.  There are many good scientists working tirelessly to protect people from environmental hazards.  Many toxins (lead in gasoline for example) have been eliminated due to efforts by researchers like those at Kettering Laboratory.  However, there are dark forces at work in water fluoridation policy.

“Pablum, a popular infant food prepared from bone meal [*], formerly contained as much as 18 ppm. When this amount of fluoride was found to be excessive -it produced mottled teeth- manufacturers reduced the fluoride content of Pablum to between 1.33 and 2.12 ppm”

We don’t need poison chemicals in the baby food then, and we still don’t need it.  in ANY amount. Find me one physician who says there is a biological need for fluoride in the body.  I know of none.  It is not an essential nutrient and causes a range of diseases.

Fluoride and mercury are still 2 of the “old standby” toxins used to brain damage children, reduce fertility and population.  The long term effects are well-understood which is why it’s used. You can still walk into the grocery store and buy fluoridated “baby water.”

There is the public story about preventing cavities, and then the real story behind water fluoridation.  And that is the one you probably haven’t heard, but it’s the one you need to know, to protect yourself and your family.

From fluoride-history.de

see also:

http://www.eh.uc.edu/allweb/history/history.htm

http://www.libraries.wright.edu/special/manuscripts/ms262.html

http://www.runet.edu/~wkovarik/papers/kettering.html

Until they became famous for the “Freon” type refrigerants, the names of Charles Kettering and Thomas Midgley were widely known for their leaded gasoline battle. Tetraethyl lead was first prepared in Europe, in 1859, as a pure compound and during the slow development in European Universities there was no hint that once it would become very important commercially (Seyferth D.: “The rise and fall of tetraethyllead”, Organometallics 22 (2003) 2346 and 5154).

“After leaded gasoline entered the market in 1923-24, a fatal refinery accident drew news media attention to the poisonous nature of the full strength additive and the potential public health risk from fuel containing the dilute additive. Public health scientists insisted that alternatives existed, but industry in general and GM in particular vehemently insisted that tetraethyl lead was the only additive that could be used … When five men died in a New Jersey refinery in October, 1924, a storm of protest and scientific dispute surrounded General Motors, Standard Oil of New Jersey, and E. I. Du Pont de Nemours Corp., the three principal developers of leaded gasoline. G.M. and Standard together  had formed the Ethyl Gasoline Corp., and Du Pont participated as one-third owner of G.M. and as the largest tetraethyl lead manufacturer … ” (http://www.runet.edu/~wkovarik/papers/kettering.html)

The same team that so successfully fought the leaded gasoline battle of the 1920´s, Charles Franklin Kettering, director of General Motors research, Thomas Midgley, his assistant, originator of the idea to use tetraethyl lead as an antiknocking agent, and their “toxicologist” Robert Kehoe, created another, not less important issue in the 1930´s: fluorocarbons used as refrigerants, propellants and fire extinguishers.

Again, Kettering presented the technical devices for the project, a refrigerator, a refrigerant dehumidifying apparatus, an (automatically controlled) air conditioner, an air conditioner for an automobile:

Charles F. KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 1,886,339; filed Dec. 31, 1928; patented Nov. 1, 1932

Charles Frank KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 1,955,192; filed Dec. 30, 1931; patented Apr. 17, 1934

Charles F. KETTERING, assignor to Frigidaire Corporation, Dayton, Ohio: “Refrigeration”, US Patent 1,978,463; filed Jan. 28, 1933; patented Oct. 30, 1934

Charles F. KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 2,093,968; filed Dec. 24, 1934; patented Sept. 21, 1937

Charles F. KETTERING, assignor, by mesne assignments, to General Motors Corporation: “Refrigerating apparatus”, US Patent 2,130,092; filed Dec. 30, 1931, renewed April 28, 1937; patented Sept. 13, 1938

Charles F. KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, filed March 28, 1936; patented Sept. 13, 1938

Charles Franklin KETTERING, assignor to General Motors Corporation, Dayton, Ohio: “Refrigerating apparatus”, US Patent 2,294,036; filed Dec. 29, 1938; patented Aug. 25, 1942

Interestingly, when Midgley developed the “Freon”-type fluorocarbons in 1930, related compounds had already been made elsewhere by a very similar procedure. The manufacture of “fluoroform” (trifluoromethane) was patented by the pharmaceutical company Valentiner and Schwarz, of Leipzig- Plagwitz, Germany, in 1899: German Patents DE 105,916 (filed Jan. 5, 1899), DE 106,513 (Feb. 26, 1899), and U.S. Patent 643,835 (filed May 4, 1899). The inventors reacted silver fluoride with iodoform in the presence of chloroform (i.e. by substitution of another halogen by fluoride derived from a heavy metal fluoride). Next came Methyl fluoride to be  used as a “cold producer or refrigerating agent”: Walter LACHMANN, of Hamburg, Germany: “Method of producing low temperatures by means of methyl-fluoride”, British Patent GB 717; filed in the U.K. on Jan. 9, 1912; pat. Oct. 10, 1912.

1930

In 1930, Thomas Midgley, in cooperation with Albert Leon Henne and Robert Reed McNary, developed the Freons, as a substitute for the toxic gaseous refrigerants (ammonia, butane, methyl chloride (or bromide), sulfur dioxide) in use at that time. ”The pioneer work on organic fluorides of F. Swarts has been used as a basis for the manufacture of dichlorodifluoromethane.” Even toxicity tests had been performed, probably to prevent any unwanted discussions: “Robert A. Kehoe made a preliminary investigation of the toxic properties of dichlorodifluoromethane from which it was evident that this compound was remarkably non-toxic” (Midgley & Henne: Ind. Eng. Chem. 22 (May 1930) 542)

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation: “Heat transfer”, US Patent 1,833,847; filed Feb. 8, 1930; patented Nov. 24, 1931; also German Patents (DE) 623,322; filed Feb. 9, 1930, publ. Nov. 28, 1935; and 630,838; filed Feb. 9, 1930; publ. May 14,1936

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation, Dayton, Ohio: “Manufacture of aliphatic fluoro compounds”, US Patent 1,930,129; filed April 5, 1930; patented Oct. 10, 1933; also German Patent (DE) 573,534 on the separation of certain aliphatic fluoro compounds; filed July 2, 1930; publ. March 16, 1933

Francis R. BICHOWSKY, assignor, by mesne assignments, to General Motors Corporation: “Self propelling fire extinguishing charge containing a double halogen hydrocarbon compound”, US Patent 2,021,981; filed June 23, 1930; patented Nov. 26, 1935

Thomas MIDGLEY, assignor to Frigidaire Corporation, Dayton, Ohio: “Process of preventing fire by nontoxic substances”, US Patent 1,926,395; filed July 31, 1930; patented Sept. 12, 1933

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to Frigidaire Corporation, Dayton, Ohio: “Process of preventing fire by nontoxic substances”, US Patent 1,926,396; filed July 31, 1930; patented Sept. 12, 1933

I. G. Farbenindustrie Aktiengesellschaft of Frankfurt, Germany: “Manufacture of methane derivatives containing chlorine and fluorine”, British Patent GB 370,356; priority Dec. 12, 1930 in Germany, filed in GB on Dec. 11, 1931; granted April 7, 1932

1931

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Dehydration of antimony trifluoride and manufacture of fluorinated aliphatic compounds”, US Patent 2,082,161; filed Jan. 30, 1931; renewed Oct. 16, 1935; patented June 1, 1937

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Fluorination of aliphatic compounds”, US Patent 1,973,069; filed Jan. 30, 1931; patented Sept. 11, 1934 (silicon tetrafluoride + antimony chloride as catalysts for partial fluorination of carbon tetrachloride)

Albert L. HENNE, assignor by mesne assignments, to General Motors Corporation: “Fluoriation in the presence of chlorine as a catalyst”, US Patent 1,990,692; filed Jan. 30, 1031; patented Feb. 12, 1935

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Manufacture of fluorated aliphatic compounds”, US Patent 2,007,198; filed Jan. 30, 1931; patented July 9, 1935

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Method of manufacturing halo-fluoro hydrocarbons”, US Patent 1,978,840; filed Jan. 30, 1931; renewed Sept. 9, 1933; patented Oct. 30, 1934

Thomas MIDGLEY, Albert L. HENNE, Robert Reed McNARY, assignors, by mesne assignments, to General Motors Corporation: “Manufacture of halo-fluoro derivative of aliphatic hydrocarbons”, US Patent 2,007,208; filed Feb. 24, 1931; patented July 9, 1935

Thomas MIDGLEY, Albert L. HENNE, assignors to Frigidaire Corporation, Dayton, Ohio:  “Preparation of aliphatic halo-fluoro compounds”, US Patent 2,013,062; filed Feb. 26, 1931; patented Sept. 3, 1935

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments, to General Motors Corporation: “Manufacture of Antimony trifluoride”, US Patent 2,024,008; filed Feb. 26, 1931; patented Dec. 10, 1935

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: ”Manufacture of pentavalent antimony compounds”, US Patent 1,984,480; filed June 5, 1931; renewed Jan. 9, 1934; patented Dec. 18, 1934

Albert L. HENNE, assignor, by mesne assignments, to General Motors Corporation: “Fluoration of aliphatic halides”, US Patent 2,013,050; filed June 26, 1931; renewed May 10, 1934; patented Sept. 3, 1935

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments, to General Motors Corporation: “Heat transfer and refrigeration”, US Patent 1,968,049; original application Feb. 8, 1930, divided and this application filed Nov. 19, 1931; patented July 31, 1934

Thomas MIDGLEY, assignor, by mesne assignments, to General Motors Corporation: “Process of testing for halogens”, US Patent 1,990,706; filed Dec. 21,1931; patented Feb. 12, 1935

Werner URSUM: “Füllungen für Feuerlöscher”, German Patent DE 587,932; filed July 1, 1931; pat. Nov. 10, 1933

1932

In 1932, it was reported that dichlorodifluoromethane decomposes when passing through a flame (e.g. in an outbreak of fire in a kitchen whereby the refrigerant may be released from the refrigerator) and thereby delivers hydrogen fluoride and hydrogen chloride. Midgley and Henne (Ind. Eng. Chem. 24 (June 1932) 641) were quick to claim: “It is demonstrated that even under the worst possible circumstances life is not endangered.” A footnote in their report (page 644) says: “Experiments conducted by R. A. Kehoe at Cincinnati demonstrate that hydrogen fluoride is not more toxic than hydrogen chloride and hence that these two may be considered together” (a claim contradictory to experiments performed earlier by other researchers).

1934

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors, by mesne assignments to General Motors Corporation, Dayton, Ohio: “Heat transfer and refrigeration”, US Patent 1,968,050; original application filed Nov. 19, 1931; divided and this application filed April 30, 1934; patented July 31, 1934

Thomas MIDGLEY, Albert L. HENNE, Robert R. McNARY, assignors to General Motors Corporation, Dayton, Ohio: “Heat transfer and refrigeration”, US Patent 2,104,882; original application Nov. 19, 1931; divided and this application filed May 1, 1934

HF Toxicity experiments in animals, carried out at the Kettering Laboratory in Cincinnati and reported in 1934 and 1935 by Willard Machle, Frederick Thamann, Karl Kitzmiller, Jacob Cholak, and Eugene W. Scott, were supported in part by Kinetic Chemicals Inc., a subsidiary of E. I. Du Pont de Nemours & Company, manufacturer of the Freons (J. Ind. Hyg. Toxicol. 16 (March 1934) 129; 17 (Sept. 1935) 223; 17 (Sept. 1935) 230).

1935

Albert L. HENNE, assignor to General Motors: “Halide detector”, US Patent 2,136,741; filed Feb. 9, 1935; patented Nov. 15, 1938

“Freon is used not only in household and larger mechanical refrigerating units in cold storage for perishable products but also in the air-conditioning field of buildings, mines, railroad passenger cars, etc. Approximately 1,700 tons of acid spar were used in the manufacture of the new refrigerants in the first ten months of 1935, since which time there has been a noteworthy increase. The Kinetic Chemicals Inc., a Du Pont subsidiary, Wilmington, Delaware, controls and manufactures the ´Freons´ and many of the refrigerator manufacturers are offering equipment containing these gases, particularly Freon.” (Paul Hatmaker, Hubert W. Davis: “The fluorspar industry of the United States with special reference to the Illinois-Kentucky District”, State Geological Survey, Bulletin No. 59, Urbana, Il., 1938, p.82).

1936

Willard Machle of the Kettering Institute examined the “Normal urinary fluorine excretion and the problem of mottled enamel” (Dental Cosmos 78 (1936) 612).

1937

Midgley was awarded the Perkin Medal of the Society of Chemical Industry on January 8, 1937, at a joint meeting of the American Section of the Society of Chemical Industry and the New York Section of the American Chemical Society at the Chemists´ Club, New York (Ind Eng. Chem. 29 (1937) 239). In his talk “From the Periodic Table to Production” (p. 241), Midgley remarked: “C. F. Kettering was a primary factor. Without his guiding genius, faith, patience, and financial support it is likely that neither Ethyl gasoline nor the Freon refrigerants would be in existence today.“

Also in 1937 the idea of another public relations stroke originated in certain dental circles: dental researchers would be asked for a summary on their research efforts relative to the causes and control of dental caries; these summaries could be published in a monograph (J.W. Gies to R.W. Bunting, March 28, 1940; in the R. W. Bunting papers, Bentley Historical Library, University of Michigan). Charles F. Kettering became a counselor in an “Advisory Committee on Research in Dental Caries” of the American Dental Association.

1938

Letters, i.e. requests for summaries,  were sent to almost 200 dental researchers in 25 countries from the “Advisory Committee on Research in Dental Caries” of the American Dental Association´s Research Commission, detailing in the letter-head the participation of the famous Charles F. Kettering of General Motors.

Thomas MIDGLEY, Albert L. HENNE, assignors, by mesne assignments, to Kinetic Chemicals, Wilmington, Delaware: “Fluorination process”, US Patent 2,192,143; filed May 7, 1938; patented Feb. 27, 1940

1939

The compilation of the dental research summaries was published by the ”Advisory Committe on Research in Dental Caries of the Research Commission of the American Dental Association” under the title of “Dental Caries“.

Machle, Scott and Treon, of the Kettering Institute, published the “normal urinary fluorine excretion and the fluorine content of food and water” (Am. J. Hygiene 29 (1939) 139)

1940

A review of “Dental Caries”, which Russell W. Bunting called a “World Almanac of Dental Errors” (R.W. Bunting to J.W. Gies, June 22, 1940; in the R.W.Bunting papers, Bentley Historical Library, University of Michigan), stated: ”A noteworthy departure from committees dealing with technical matters was the inclusion of Mr. C. F. Kettering, well known as an engineer and industrial manager. The inclusion of a layman of such ability brings a freshness of viewpoint from one well  trained in scientific method and gifted with exceptional organizing ability” (J. Am. Dent. Assoc. 27 (Jan. 1940) 117).

Machle and E. E. Evans, of the Kettering Institute, examined the “Exposure to fluorine in industry” (J. Ind. Hyg. Toxicol. 22 (June 1940) 213)

1941

After another set of letters was sent world-wide to dental researchers, the second edition of “Dental Caries” was published by the same Committe that compiled the 1939 version.

Lyle D. GOODHUE, William N. SULLIVAN, assignors to Claude A. Wickard, as Secretary of Agriculture of United States of America, and his successors in office: “Method of applying parasiticides”, US Patent 2,321,023; filed July 29, 1941; patented June 8, 1943

1942

Tests with hydrogen chloride published in 1942 led to the conclusion that “hydrogen chloride has nearly the same immediate toxic action as hydrogen fluoride, but produces less serious residual effects than this compound.” The organs of animals “surviving exposure to hydrogen fluoride showed more frequent and more severe pathological changes than those of animals exposed to hydrogen chloride. The concentration level which appeared safe for long exposure was also much lower in the case of hydrogen fluoride” (J. Ind. Hyg. Toxicol. 24 (Oct. 1942) 222).

In the meantime, the aerosol propellants had also gained importance for military purposes:

Excerpt from Chapter 2, “Historical background”, in Paul A. SANDERS, of E. I. Du Pont de Nemours & Company, “Principles of Aerosol Technology“, Van Nostrand Reinhold Company, New York, etc., 1970:

“One of the most important developments in the aerosol field occurred during World War II. During an investigation to find a way of combating the insects which caused disease among overseas troops, Goodhue and Sullivan, of the Department of Agriculture, developed a portable aerosol dispenser which used “Freon” 12 fluorocarbon as the propellant … From July 1942, when the requirement was 10,000 containers per day, until the end of the war, one company alone, Westinghouse Corporation, supplied over 30,000,000 aerosols to the Armed Forces. Other companies engaged in supplying aerosols for the military included Regal Chemical Company, Brooklyn, New York; Airsol Inc., Neodesha, Kansas; and Bridgeport Brass Company, Bridgeport, Connecticut. Immediately after the war, Westinghouse Corporation dropped out of the aerosol field, but the others continued to produce aerosol products.”

Being active in fluoride research, the Kettering Institute was also approached by Mead Johnson and Company, manufacturer of “Pablum” infant food (J. Ind. Hyg. Toxicol. 24 (Sept. 1942) 199; 25 (March 1943) 112):

“Pablum, a popular infant food prepared from bone meal [*], formerly contained as much as 18 ppm. When this amount of fluoride was found to be excessive -it produced mottled teeth- manufacturers reduced the fluoride content of Pablum to between 1.33 and 2.12 ppm” (George Walbott, Albert L. Burgstahler, Lewis McKinney: “Fluoridation the great dilemma”, Lawrence, Kansas, 1978, p. 39). Mead Johnson replaced the veal bone ash by tricalcium phosphate (George Waldbott: Am. J. Clin. Nutr. 13 (Dec. 1963) 393).

* Lambert D. JOHNSON, Nathan F. TRUE, Barry H. ENGEL, assignors to Mead Johnson and Company: “Food product and method”, US Patent 1,990,329; filed May 8, 1933; patented Feb. 5, 1935

1943

J. F. Treon, Instructor in toxicology, Kettering Laboratory of Applied Physiology, Cincinnati, Ohio, became one of the many people (besides Hodge, Voegtlin, Stokinger …) to supervise research programs for the “Manhattan District” (the project for the construction of the first atomic bomb). In this project fluorocarbons played a major role as coolants and lubricants. “The toxicity of these substances was tested by an experimental program similar to that used by the Toxicology Division of the U. S. Public Health Laboratories.” … “These compounds were found to be moderately toxic to animals upon inhalation, but some of the intermediate products formed in the production of these compounds were found to be toxic to animals in concentrations varying from 70 – 500 parts per million parts of air. The animals exposed to toxic concentrations of these intermediate products of the fluorocarbons died apparently as a result of respiratory failure” (from: HREX Archives, “Manhattan District History, Book I – General, Volume 7 “Medical Program”, printed Dec. 31, 1946; reproduced at the National Archives).

Meanwhile, Albert L. Henne was under contract for the National Defense Research Committee (from July 1, 1942 to June 30, 1943) to find new ways for the synthesis of fluorinated hydrocarbons. However, “the procedures proved insufficient and too lengthy, and were abandoned when it was realized that better results were claimed at Purdue (i.e. Purdue Research Foundation, -> McBee), and when direct fluorination was adopted for large scale production” (from: National Defense Research Committee of the Office of Scientific Research and Development, “Final Report on Fluorocarbons and Related Compounds”, Report OSRD No. 1792, Sept. 10, 1943; “cleared” upon F.O.I.A. request on Sept. 18, 2001).

1946

Harold Simmons Booth et al. describe the use of Freon 12 (dichlorodifluoromethane) for the manufacture of dry uranium tetrafluoride of high purity (J. am. chem. Soc. 68 (1946) 169). The publication of this paper “was delayed for war-time security reasons” as the editor notes in a footnote. Other methods for the preparation of this compound (which was essential for the Manhattan Project for the production of uranium hexafluoride) “yield products containing water and hydrogen fluoride from which it is difficult to separate uranium tetrafluoride without some decomposition.” Freon 12 was found to react quantitatively with uranium trioxide to produce pure anhydrous uranium tetrafluoride at elevated temperatures.

1961

A book by Kettering Lab scientist E. J. Largent, “Fluorosis. The health aspects of fluorine compounds”, Ohio State University Press, 1961, was expressly designed, as indicated on its jacket, to ”aid industry in law suits arising from fluoride damage.”

Mass drugging: The sordid history of water fluoridation