David,
This forum only accepts 20,000 charactors, so I cannot post all the fluoride cancer studies.
Here are some, in response to your claim, "Fluoride is NOT a carcinogen."
David,
This forum only accepts 20,000 charactors, so I cannot post all the fluoride cancer studies.
Here are some, in response to your claim, "Fluoride is NOT a carcinogen."
Known Carcinogen: Pal (2014): Fluoride, a well-established environmental carcinogen, has been found to cause various neurodegenerative diseases in human. Sub-acute exposure to fluoride at a dose of 20mg/kgb.w./day for 30 days caused significant alteration in pro-oxidant/anti-oxidant status of brain tissue as reflected by perturbation of reduced glutathione content, increased lipid peroxidation, protein carbonylation, nitric oxide and free hydroxyl radical production and decreased activities of antioxidant enzymes. Decreased proteolytic and transaminase enzymes' activities, protein and nucleic acid contents and associated DNA damage were observed in the brain of fluoride intoxicated rats. The neurotransmitters dopamine (DA), norepinephrine (NE) and serotonin level was also significantly altered after fluoride exposure. Protective effect of resveratrol on fluoride-induced metabolic and oxidative dysfunctions was evaluated. Resveratrol was found to inhibit changes in metabolic activities restoring antioxidant status, biogenic amine level and structural organization of the brain. Our findings indicated that resveratrol imparted antioxidative role in ameliorating fluoride-induced metabolic and oxidative stress in different regions of the brain.
Known Carcinogen: McCully (2009) “. . . Depletion of thioretinaco ozonide from cellular membranes is suggested to underlie the carcinogenic and atherogenic effects of fluoride and other electrophilic carcinogens.”
Known carcinogen (increase incidence): Marigold (1969) explained that fluoride has a paradoxical action on cancer. Some of the most effective anti-cancer drugs have contained fluoride and yet other inorganic fluoride compounds are powerful carcinogens such as dimethylaminoazobenzene who’s cancer-producing ability is enhanced seven times as much as by substitution of fluoride with other halogens.
Known carcinogen (chronic exposure - shorter life span): Taylor (1954) carried out a total of 12 experiments involving 645 mice. The data indicated that drinking water containing as little as 1ppm of fluoride shortened the life span of cancer-prone mice by an average of 9%, regardless of whether they died of cancer or another disease. In contrast, 1953, Fleming36 transplanted sarcoma 37 into young adult mice and guinea pigs. For a few weeks, one group received 20 ppm NaF in drinking water and another 1,000 ppm intraperitoneally while controls received no fluoride. The fluoride treated animals lived longer, lost less weight and had tumors inhibited by fluoride. One striking difference between Taylor’s and Flemming’s studies is “time and dosage,” Taylor had chronic low dose exposure while Flemming had acute high dose.
Known carcinogenic: Taylor (1965) reported observations from 54 experiments, 991 mice bearing transplanted tumors and 58 experiments with 1817 eggs implanted with mouse cancer tissue. Sodium fluoride accelerated the growth of cancer tissue. Taylor’s work has been repeatedly confirmed. Note: Talyor’s first study was criticized because he did not control the fluoride in animal feed, probably CaF. His subsequent work did control for total fluoride exposure and the results were confirmed.
Known Carcinogen: Suzuki (1991) “We tested the induction of mutagenic effects by in vivo and in vitro bone marrow micronucleus tests. A significant increase in micronucleated polychromatic erythrocytes was observed 24 H after intraperitoneal injection of sodium fluoride at a dose of 30 mg/kg body weight. In the in vitro micronucleus test, the frequency of micronucleated polychromatic erythrocytes was increased significantly at concentrations of 2 and 4 MM. These results indicate that the micronucleus test may be useful in evaluating the cancer risk of sodium fluoride.”39
Known Carcinogen: Pati (1987) “Genotoxicity of Sodium fluoride was evaluated in mice in vivo with the help of different cytogenetic assays.
Known Carcinogen: Tazhibaev (1987) “The test animals were fed with low-grade food during 2-5 months under conditions of acute and chronic action of hydrogen phosphide and hydrogen fluoride induced by inhalation, that resulted in the pronounced impairment of the chromosomal apparatus of the bone marrow cells in the rats. A principal possibility has been established of modification of the hydrogen phosphide and hydrogen fluoride cytogenetic effect by the alimentary action. In particular, it has been found that the effect is significantly higher when the rats are fed with a low-grade ration than under conditions of balanced nutrition.”
NTP mutagenic: According to the National Toxicology Program “the preponderance of evidence” from laboratory “in vitro” studies indicate that fluoride is a mutagenic compound. Many substances which are mutagens, are also carcinogens. As is typical for in vitro studies, the concentrations of fluoride that have generally been tested were usually, but not always, higher (millimolar levels) than the concentrations found in human blood (micromolar levels). In Khalil (1995), the authors found a statistically significant mutagenic effect at a concentration of just 1 micromole (0.019 ppm). This is similar to blood fluoride concentrations among individuals living in fluoridated communities. More recent research has found effects at 24 uM (Zhang 2009) and 34 uM (Tiwari & Rao 2010).
The relevance of the in vitro findings are further amplified by the fact that there are certain “microenvironments” in the body, such as the bones (3,708 ppm Eble DM 1992 JPHD), teeth, kidney (50 fold increase over plasma, NRC 2006), bladder, and pineal gland (21,000 ppm, Luke 1997; 2001), where the cells can be exposed to fluoride levels many times higher than the fluoride levels found in the blood (between none detected and 0.01 ppm).
Bone mineral is regularly broken down by osteoclasts as part of the bone remodeling process, the fluoride sequestered in bones (and other tissues) may be periodically released, exposing bone cells to increased fluoride concentrations. This might help explain why fluoride has been associated, in both human and animal studies, with osteosarcoma (bone cancer). One in vitro study, for example, found that 10 to 19 ppm fluoride caused mutagenic effects in bone cells after 24 to 48 hours of exposure. (Mihashi 1996). According to the authors:
Known Carcinogen: “Significant increases in the frequencies of chromosome aberrations were induced in a dose- and treatment time-dependent fashion when NaF was administered to [rat vertebral bone] cells at 0.5 and 1.0 mM [=9.5 to 19 ppm] for 24 and 48 h. The results indicate that NaF is genotoxic to rat vertebrae, providing a possible mechanism for the vertebrae, as a target organ of NaF carcinogenesis.”
Known Genetic Damage: Humans and apes have been found to be more susceptible to fluoride-induced genetic damage than rodent cells. (Kishi 1993). Chromosome breaks occurred in human and ape cells at fluoride concentrations (19 to 114 ppm) that had no effects on rodent cells. (Note: Fluoride varnish is 22,600 ppm)
Known Mutagenic: 1990 NTP “In summary, sodium fluoride is mutagenic in cultured mammalian cells and produces transformation of Syrian hamster cells in vitro. The reports of in vivo cytogenetic studies are mixed, but the preponderance of the evidence indicates that sodium fluoride can induce chromosome aberrations and sister chromatid exchanges in cultured mammalian cells. These mutagenic and clastogenic effects in cultured cells are supported by positive effects in Drosophila germ cell tests that measure point mutations and chromosome breakage. In vivo tests in rodents for chromosome aberrations provide mixed results that cannot readily be resolved because of differences in protocols and insufficient detail in some study reports to allow a thorough analysis. The mechanism(s) by which these effects result from exposure to sodium fluoride is not known.”
Preponderance of Evidence: 2001 Bassin “The effects of fluoride as a mutagen, carcinogen, and antimutagen are inconsistent, but the preponderance of evidence in cultured mammalian cells indicate that sodium fluoride can induce chromosome aberrations and sister chromatid exchanges.”
Capable: 1993 Environment Canada “Fluoride (as sodium fluoride) should be considered capable of inducing chromosomal aberrations, micronuclei, and sister-chromatid exchanges in vitro in mammalian cells, although the results from such studies have been inconsistent.”
Genotoxic: 1991 HHS “Genotoxicity studies are highly dependent on the methods used… Despite the apparently contradictory reports appearing in the published literature, fluoride has not been shown to be mutagenic in bacteria (Ames test). In some studies fluoride has been reported to induce gene mutations in both cultured rodent and human cells. Fluoride has also been reported to transform rodent cells in vitro. Although there is disagreement in the literature concerning the ability of fluoride to be a clastogen (induce chromosome aberrations) in cultured cells, it has been suggested that fluoride can cause chromosome aberrations in rodent and human cells. Fluoride induced primarily chromatid gaps and chromatid breaks, indicating that the cells are most responsive in the G stage of the cell cycle, i.e., after chromosome duplication in preparation for cell division. Negative results reported in some cytogenetic studies are likely the effect of inadequate test protocols…. Although the mechanism(s) by which these cellular effects result from exposure to fluoride is not known, a number of possible mechanisms have been proposed to explain the genetic activity observed. These mechanisms have been based on the observed reactions of fluoride in solution with divalent cations or necleotides, or the physiological and inhibition protein synthesis, or a result of the direct inhibition of DNA polymerase. Fluoride can react with divalent cations in the cell so as to affect enzyme activities that are necessary for DNA or RNA synthesis, or chromosome metabolism or maintenance; it may react directly with DNA as part of a complex; or it ca disrupt other cellular processes such as cell differentiation or energy metabolism.”
Known Carcinogen: Zhang (2009) “Twenty four agents were used to evaluate this screening assay. We selected the agents, ranging from DNA alkylating agents, oxidative agent, radiation, DNAcrosslinking agent, nongenotoxic carcinogens, precarcinogenic agents, which included . . . sodium fluoride, acrylamide . . . . The results showed that all 20 tested known carcinogenic and genotoxic agents were able to induce gadd153-Luc expression at a sublethal dose.. . . .”
Known Genotoxic, Mutagenic, Teratogenic: Ercivas (2009) “In this study we
concluded that NaF, in 5 and 10 lg/ml NaF concentrations cause genotoxic alterations. So genotoxic, mutagenic and teratogenic effects of NaF need to be carefully screened and evaluated together with other long-term effects using in vitro and in vivo animal test models.”
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