Fluoride

Screen Shot 2019-05-19 at 5.20.08 PM.pngScreen Shot 2019-05-19 at 5.23.11 PM.pngFluoride is routinely added to municipal water supplies across the U.S. and in a few other countries. It is usually in a synthetic form, namely hydrofluorosilisic acid. This molecule is non-compatible with the natural human biochemical pathways, and not only does it not affect tooth density or structure. It is highly toxic to the body in small, chronic doses, and is shown to numb the senses and render an individual docile, perhaps shedding light on the systematic fluoridation of nazi concentration camps.

Fluoride has a negative charge, and being in fact the most electronegative element, it can readily create strong bonds with many molecules. In our teeth we have calcium and phosphorous crystalline deposits around living connective and vascular tissue. Fluoride, when naturally present in fruits and vegetables as iron fluorine is harmless. It is is trace amounts, as it is a trace mineral, and in organic molecular structure. It is in accord with the biochemical mechanism of our bodies.

Also prevalent in toothpastes are sodium lauryl sulfate and sodium laureth sulfate, both of which are harmful to humans. MSG is also present in some toothpastes, and it bears many different names, and can be hidden even in the more ‘natural’ toothpastes. MSG is an excitotoxin, and it can do severe damage to neurons if consumed even on occasion. Triclosan is a very popular ingredient in main-brand toothpastes, and it too can cross the blood-brain-barrier and cause oxidative damage. It has been proven to be toxic to the immune system and a potent agent in the generation of harmful ROS.

Essentially, fluoride is not the sole perpetrator in the sheer toxicity of the most commonly used toothpastes. These are all loaded with carcinogenic compounds like artificial colors, heavy metals, and petroleum-based synthetic acid-forming substances. Coconut oil has the same strength and efficacy as chlorhexidine in eliminating S. mutans (bacteria that causes bad breath) growth. Activated charcoal and diatomaceous earth are incredible at adsorbing harmful acid-forming microbes (positively charged ((H+)) ) and leaving the alkaline-forming microbes that we need for a healthy buccal mucosa alive, as they are generally negatively charged and thrive best in an alkaline medium. Alkalinity is a function of electrolytic charge and balance.

Thus, for a healthy mouth pH and microflora, it is imperative that we apply non-intrusive and non-toxic means of oral hygiene. Additionally, a diet consisting mostly of raw fruits, melons, berries, vegetable juices, and the occasional tuber, alkaline grain, or phytate-low legume (black beans, lentils, etc) and cooked cruciferous veggies! Health begins in the mouth.

1) https://www.sciencedirect.com/science/article/pii/S0003277814000021

  • Pineal gland: A structural and functional enigma.
  • The presence of all enzymes needed for the synthesis of di-methyl-tryptamine (DMT) in pineal gland explains the near death experience (NDE) phenomenon. The various audio-visual hallucinations in NDE phenomenon occur due to massive increase of DMT in pineal gland before death. A very high concentration of di-methyl-tryptamine (DMT), presence of retinal proteins in 5–10% of pinealocytes, its role in thermoregulation and a possible role as magnetoreceptor in blind men and highest deposits of fluoride in the body are not only interesting but significant for the future research.

2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6017004/

  • Pineal Calcification, Melatonin Production, Aging, Associated Health Consequences and Rejuvenation of the Pineal Gland
  • The mesenchymal stem cells and melatonin participate in this process. Finally, we suggest that preservation of pineal health can be achieved by retarding its premature calcification or even rejuvenating the calcified gland.

3) https://www.karger.com/Article/Abstract/47443

  • Fluoride deposition in the Aged Human Pineal Gland.
  • The pineal contained 16,000±11,070 mg Ca/kg wet weight. There was a positive correlation between pineal F and pineal Ca (r = 0.73, p<0.02) but no correlation between pineal F and bone F. By old age, the pineal gland has readily accumulated F and its F/Ca ratio is higher than bone.

4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213386/

  • Fluoride concentrations in the pineal gland, brain and bone of goosander (Mergus merganser) and its prey in Odra River estuary in Poland.
  • Fluoride concentration in the pineal gland was significantly greater than in the bone and the brain of the duck.

5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5909100/

  • Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum
  • A long-term burden of these ubiquitous toxins has several health effects with a striking resemblance to the symptoms of ASD. In addition, their synergistic action in molecules of aluminofluoride complexes can affect cell signaling, neurodevelopment, and CNS functions at several times lower concentrations than either Al3+ or fluoride acting alone.

6) https://www.ncbi.nlm.nih.gov/pubmed/25577494

  • Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure.
  • Aluminium, fluoride and a combination of aluminium-fluoride treatments caused an increase in brain lipid peroxidation products and reactive oxygen species (ROS) formation. Similarly, an increase in glial activation and inflammatory response were seen in these groups versus the control. Oxidative stress induced glial activation (GFAP) and increased the expression of B cells (CD20). This also corresponded to the extent of tissue damage and lipid peroxidation observed. Taken together, the results suggest a close link between oxidative stress neuroinflamation and degeneration in aluminium-fluoride toxicity.

7) https://www.ncbi.nlm.nih.gov/pubmed/21225510

  • Association of mast cells with calcification in the human pineal gland.
  • Our results lead to the conclusion that the tryptase mast cells play a major role in the pineal calcification process as sites where this process starts and as a source of production of numerous biologically active substances including tryptase that participate in calcification.

8) https://www.ncbi.nlm.nih.gov/pubmed/19241804

  • [Pineal gland, biorhythms and aging of an organism].
  • The changes of structure and functional status of the pineal gland and of the hypothalamic suprachyasmatic nucleus during normal aging and at age-associated pathology are presented as well.

9) https://www.ncbi.nlm.nih.gov/pubmed/2265926

  • Possible role of pineal melatonin in the mechanisms of aging.
  • Recent hypotheses of aging have suggested that cumulative neuronal insults associated with free radical production may be associated with the process of aging.
  • Other studies derived mainly from observations on pinealectomized rats also suggest that diminished melatonin secretion may be associated with acceleration of the aging process. Thus, pineal melatonin may be a natural anti-aging hormone.

10) https://www.researchgate.net/publication/225662618_Fluoride-Induced_Oxidative_Stress_in_Rat’s_Brain_and_Its_Amelioration_by_Buffalo_Bubalus_bubalis_Pineal_Proteins_and_Melatonin

  • Fluoride-Induced Oxidative Stress in Rat’s Brain and Its Amelioration by Buffalo (Bubalus bubalis) Pineal Proteins and Melatonin
  • Fluoride administration significantly increased brain MDA compared with control group, while GSH levels were decreased in fluoride-treated groups, accompanied by the markedly reduced SOD, GPx, GR, and SOD activity.

11) https://www.ncbi.nlm.nih.gov/pubmed/19540901

  • Fluoride exposure impairs glucose tolerance via decreased insulin expression and oxidative stress.
  • However, oxidative stress evaluated by the functional activity of superoxide dismutase (SOD) and generation of the superoxide anion (O(2)(-)), showed significantly decreased SOD activity, in a dose-dependent manner. This was accompanied by an increase in the generation of O(2)(-), and decreased mitochondrial membrane potential in F(-) exposed cells. Insulin secretion was lower in beta-cells exposed to F(-), even in the presence of glibenclamide, the ATP-sensitive K(+) (K(ATP)) channel blocker, suggesting down-regulation of the K(ATP) channel in the cell. Exposure to high levels of F(-) in drinking water may decrease insulin mRNA and its secretion from beta-cells, and might therefore affect the OGTT.

12) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017333/

  • Effect of duration of fluoride exposure on the reproductive system in male rabbits
  • The present study demonstrates that fluoride hampers the reproductive functions of male rabbits and is proportional to the duration of fluoride exposure.

13) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6129794/

  • Chronic Exposure to Sodium Fluoride Triggers Oxidative Biochemistry Misbalance in Mice: Effects on Peripheral Blood Circulation
  • The 50 mg/L F group showed an increase in TEAC levels and a decrease in the GSH content when compared to the control group. In this way, oxidative changes in blood from chronic exposure to F, especially at the highest dose, indicate that F may be a toxic agent and, therefore, the long-term exposure to excessive doses should be avoided.

14) https://www.ncbi.nlm.nih.gov/pubmed/19619626

  • The effects of fluoride on cell migration, cell proliferation, and cell metabolism in GH4C1 pituitary tumour cells.
  • With the highest fluoride concentration, 1072 micromol/L, all of the analysed parameters were significantly reduced, suggesting that this dose is highly toxic in GH4C1 cells. Our results show that biologically relevant concentrations of fluoride are capable of increasing cell migration in tumour cells, suggesting that exposure to fluoride could stimulate tumour invasion.

15) https://www.ncbi.nlm.nih.gov/pubmed/21288074

  • Fluorine–a current literature review. An NRC and ATSDR based review of safety standards for exposure to fluorine and fluorides.
  • 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. Evidence examined in this review of the literature, and specifically the recent report by the National Research Council (NRC), offer strong support for an immediate reconsideration concerning risk vs benefit. Consensus recommendations from several sources are presented.

16) https://www.researchgate.net/publication/269739487_The_effect_of_fluoride_on_the_serum_level_of_calcium_in_the_rat_Rattus_norvegicus

  • The effect of fluoride on the serum level of calcium in the rat (Rattus norvegicus)
  • Fluoride caused the reduction of calcium concentration in serum (p<0.05); the reduction was significantly expressed in female rats (p<0.000).

17) https://www.researchgate.net/publication/287407919_Fluoride-_and_electromagnetic_radiation-induced_genotoxicity_and_impaired_melatonin_secretion

  • Fluoride- and electromagnetic radiation-induced genotoxicity and impaired melatonin secretion
  • Some animal and human work also suggests that fluoride (F) can impair the defensive response to genotoxicity by being deposited in high concentrations in the pineal gland and, through an enzyme-inhibiting action, reducing the secretion of melatonin, a powerful antioxidant able to eliminate free radicals and protect DNA. In having the capacity to be both genotoxic and impair melatonin secretion, F is similar to electromagnetic radiation, at power line frequencies and above, and both have very low or zero thresholds for causing toxicity. In view of the seriousness of neoplasia, the effect of fluoride on melatonin secretion warrants further research.

18] https://www.ncbi.nlm.nih.gov/pubmed/30384060

  • Sodium fluoride induced skeletal muscle changes: Degradation of proteins and signaling mechanism.
  • NaF at low concentration (1.5 ppm) caused myoblast proliferation and when subjected to myogenic differentiation it induced hypertrophy of the myotubes by activating the IGF-1/AKT pathway. NaF at higher concentration (5 ppm), significantly inhibited myotube formation, increased skeletal muscle catabolism, generated reactive oxygen species (ROS) and inflammatory cytokines (TNF-α and IL-6) in C2C12 cells. NaF also enhanced the production of muscle atrophy-related genes, myostatin, and atrogin-1.

19] https://www.ncbi.nlm.nih.gov/pubmed/30419706

  • [Effects of endoplasmic reticulum stress-induced apoptosis in thyroid injury caused by fluoride in rat].
  • The protein expression levels of GRP78 and CHOP in medium and high fluoride groups were respectively 29.68±4.04, 29.90±3.74 and 4.05±1.62, 4.44±1.81, which were significantly higher than those in the control group (separately 23.80±6.36, 2.27±0.89) (P<0.05). Conclusion: Excessive-fluoride intake can induce thyroid injury, and endoplasmic reticulum stress-induced apoptosis might be involved in the injury.

20] https://www.ncbi.nlm.nih.gov/pubmed/30463494

  • Induction of pathological changes and impaired expression of cytokines in developing female rat spleen after chronic excess fluoride exposure.
  • With damage to the splenocyte structure and DNA, the protein expression levels of IL-1β, IL-2, IL-6, and TNF-α were significantly downregulated by exposure to fluoride. Excessive fluoride ingestion caused splenic pathological damage and abnormal cytokine expression in female rats.

21] https://www.ncbi.nlm.nih.gov/pubmed/30469026

  • Role of fluoride induced epigenetic alterations in the development of skeletal fluorosis.
  • The results implies that fluoride induced DNA hypermethylation of these genes may hamper extracellular matrix deposition, cartilage formation, angiogenesis, vascular system development and porosity of bone, thus promote skeletal fluorosis.

22] https://www.ncbi.nlm.nih.gov/pubmed/30472891

  • Exploring the role of excess fluoride in chronic kidney disease: A review.
  • This review proposes that there is a direct correlation between CKD and the consumption of excess amounts of fluoride. Studies particularly show immediate adverse effects on the tubular area of human and animal kidneys leading to CKD due to the consumption of excess fluoride

23] https://www.ncbi.nlm.nih.gov/pubmed/30478774

  • Long-term exposure to low level of fluoride induces apoptosis via p53 pathway in lymphocytes of aluminum smelter workers.
  • Fluoride exposure might induce apoptosis, DNA damage and oxidative stress in a dose-dependent manner in lymphocytes (p < 0.05). The expression levels of p53 and Bax were increased with fluoride exposure in lymphocytes (p < 0.05), whereas the Bcl-2 expression was decreased but not significantly. Taken together, these observations indicate that long-term occupational exposure to low level of fluoride may lead to oxidative stress and induce apoptosis through the p53-dependent pathway in peripheral blood lymphocytes.

24] https://www.ncbi.nlm.nih.gov/pubmed/30519783

  • Sodium fluoride induces apoptosis and autophagy via the endoplasmic reticulum stress pathway in MC3T3-E1 osteoblastic cells.
  • Furthermore, apoptosis is promoted following the inhibition of NaF-induced autophagy. In conclusion, under NaF treatment, the ER stress-signaling pathway is activated, leading to apoptosis and autophagy and affecting the proliferation and survival of MC3T3-E1 cells.

25] https://www.ncbi.nlm.nih.gov/pubmed/30530065

  • A dual-responsive fluorescent probe for detection of fluoride ion and hydrazine based on test strips.
  • Hydrazine (N2H4) and fluoride ion (F-) are regarded as environmental pollutants and potential carcinogens

26] https://www.ncbi.nlm.nih.gov/pubmed/30541189

  • [The effects of resveratrol on mitochondrial biogenesis dysfunction induced by fluoride in human neuroblastoma SH-SY5Y cells].
  • Both the protein and mRNA levels of PGC-1α, NRF1 and TFAM were decresed after 60 mg/L NaF treatment in SH-SY5Y cells (P<0.05) . The relative mtDNA contents and mRNA expression of complexes subunit CO1 and ATP8 were also significantly decreased compared with control (P<0.05) . Mitochondrial membrane potential were also significantly decreased after 60 mg/L NaF treatment in SH-SY5Y cells (P<0.05)

27] https://www.ncbi.nlm.nih.gov/pubmed/30544885

  • Potential Role of Fluoride in the Etiopathogenesis of Alzheimer’s Disease.
  • Studies report fluoride-induced apoptosis and inflammation within the central nervous system. This review attempts to elucidate the potential relationship between the effects of fluoride exposure and the pathogenesis of Alzheimer’s disease. We describe the impact of fluoride-induced oxidative stress and inflammation in the pathogenesis of AD and demonstrate a role for apoptosis in disease progression, as well as a mechanism for its initiation by fluoride.

28] https://www.ncbi.nlm.nih.gov/pubmed/30676163

  • Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice.

29]  https://www.epa.gov/sites/production/files/documents/tsca_21_petition_hfsa_2013-04-22.pdf

The Agency would mandate that citizens of the Unites States not be subjected to unnecessarily increased cancer risks – based on the Agency’s own analysis of arsenic’s carcinogenicity, that as a society we reduce the cost of medical care by a substantial amount, and that the public water systems of the United States no longer be used as extremely profitable hazardous waste disposal sites for the phosphate fertilizer manufacturing industry.

30] https://www.ncbi.nlm.nih.gov/pubmed/30827336

  • Environmental and Genetic Factors Influencing Kidney Toxicity.
  • Choices of exemplary environmental agents to review are based on those with selective effects on the kidneys and for which significant amounts of mechanistic and human data are available. These include the heavy metals cadmium and arsenic, fluoride, the organic solvents trichloroethylene and perchloroethylene, drinking water disinfection by-products haloacids, food and herbal drug contaminants aristolochic acid and melamine, and heat stress.

31] https://www.ncbi.nlm.nih.gov/pubmed/30901911

  • Evaluation of Physicochemical Characteristics in Drinking Water Sources Emphasized on Fluoride: A Case Study of Yancheng, China.
  • The fluoride exposure levels of infants were higher than children and adults, and 3.2% of the fluoride exposure levels of infants were higher than the recommended toxicity reference value of 122 μg kg-1 d-1 as referenced by Health Canada, which might cause dental fluorosis issues; (4) the physico-chemical characteristics are classified the into four groups reflecting F– TAlk, Na⁺-K⁺, SO₄2–Cl-, and pH-TDS, respectively, indicating that fluoride solubility in drinking water is TAlk dependent, which is also verified by R-mode cluster analysis and factor analysis.

32] https://www.ncbi.nlm.nih.gov/pubmed/30920066

  • Fluoride and diethylnitrosamine coexposure enhances oxido-inflammatory responses and caspase-3 activation in liver and kidney of adult rats.
  • Furthermore, the increase in levels of nitric oxide, tumor necrosis factor-α and interleukin-1β, myeloperoxidase and caspase-3 activities as well as histological lesions was more pronounced in the liver and kidney of rats coexposed to DEN and fluoride. Conclusively, coexposure to fluoride and DEN exacerbated hepatorenal damage via enhancement of oxido-inflammatory responses and caspase-3 activation in rats.

33]] https://www.ncbi.nlm.nih.gov/pubmed/29187078

  • Maternal fluoride exposure during gestation and lactation decreased learning and memory ability, and glutamate receptor mRNA expressions of mouse pups.
  • However, no significant changes were observed in GluR1 and mGluR5 mRNA expression levels. Collectively, these findings suggested that F can pass through the cord blood and breast milk and may have deleterious impact on learning and memory of the mouse pups, which was mediated by reduced mRNA expression of glutamate receptor subunits.

34] https://www.ncbi.nlm.nih.gov/pubmed/29267217

  • Chronic Monosodium Glutamate Administration Induced Hyperalgesia in Mice.
  • We found that a dose of 300 mg/kg MSG given for 21 days reduces the pain threshold and is associated with a significant increase in brain NO level. The implications of these findings on food additive-drug interaction, and on pain perception in healthy humans, as well as in those suffering from affections involving chronic pain, are still to be investigated.

35] https://www.ncbi.nlm.nih.gov/pubmed/29402603

  • Monosodium glutamate impairs the contraction of uterine visceral smooth muscle ex vivo of rat through augmentation of acetylcholine and nitric oxide signaling pathways.
  • In conclusion, MSG potentiates the force and inhibits the frequency of contraction of UVSM, and the MSG induced effect is probably mediated through the augmentation of acetylcholine and nitric oxide signaling pathways.

36] https://www.ncbi.nlm.nih.gov/pubmed/29649467

  • Monosodium glutamate ingestion during the development period reduces aggression mediated by the vagus nerve in a rat model of attention deficit-hyperactivity disorder.
  • Finally, vagotomy at the sub-diaphragmatic level before MSG ingestion blocked its effect on aggressive behavior in the isolated SHR. The data suggest that MSG ingestion during the developmental period can reduce aggressive behavior in an attention deficit-hyperactivity disorder model rat, mediated by gut-brain interaction.

37] https://www.ncbi.nlm.nih.gov/pubmed/30244120

  • The toxic effects of monosodium glutamate (MSG) – The involvement of nitric oxide, prostanoids and potassium channels in the reactivity of thoracic arteries in MSG-obese rats.
  • In addition, down-regulation of KATP and BKCa channels influenced hyperpolarizing mechanisms. Our findings suggest that increased prostanoid production and hypersensitivity to thromboxane A2 together with down-regulation of potassium channels and low nitric oxide bioavailability may contribute to the increase in blood pressure found in adult MSG-obese male rats.

38] https://www.ncbi.nlm.nih.gov/pubmed/30273089

  • Patho-physiological and Toxicological Aspects of Monosodium Glutamate.
  • The effect of MSG depends upon its dose, route of administration and exposure time. Public awareness may play a major role in controlling the food adulteration by working in collaboration with National testing facilities to scrutinize each commercial food article from time to time. The aim of this review article is to highlight the deleterious impact of MSG on human health.

39] https://www.ncbi.nlm.nih.gov/pubmed/30277163

  • Anaemogenic, Obesogenic and Thermogenic Potentials of Graded Doses of Monosodium Glutamate Sub-acutely Fed to Experimental Wistar Rats.
  • The current data suggest that consumption of high doses/quantity of monosodium glutamate for a long duration of time could lead to anaemia due to a decrease in red blood cell count and packed cell volume and obesity resulting from an increase in body weight gain.

40] https://www.ncbi.nlm.nih.gov/pubmed/30285727

  • Tinospora cordifolia as a potential neuroregenerative candidate against glutamate induced excitotoxicity: an in vitro perspective.
  • These results suggest that B-TCE may have neuroprotective and neuroregenerative potential against catastrophic consequences of glutamate-mediated excitotoxicity and could be a potential therapeutic candidate for neurodegenerative diseases.

41] https://www.ncbi.nlm.nih.gov/pubmed/30913441

  • Distribution, health risk assessment, and anthropogenic sources of fluoride in farmland soils in phosphate industrial area, southwest China.
  • The results showed that the proportion of anthropogenic sources of soil F was dustfalls (69%) > irrigation water (23%) > air (5%) > chemical fertilizers (3%) in the industrial area. The high F concentration of dustfalls was mainly due to the phosphate rock, phosphogypsum, and surface soils with high F contents from the factories. In order to safeguard human health and alleviate hazards of F to surroundings, the control of pollutants emission from factories was a basic and vital step to reduce F in the soils in industrial areas.

42] https://www.ncbi.nlm.nih.gov/pubmed/24747328

  • Assessing the risk of an excess fluoride intake among Swedish children in households with private wells–expanding static single-source methods to a probabilistic multi-exposure-pathway approach.
  • The proportion of children assessed to be at risk after exposure from drinking water now increased to 48%, and when the probabilistic model was adjusted to also include other possible exposure pathways; beverages and food, ingestion of toothpaste, oral soil intake and dust inhalation, the number increased to 77%. Firstly, these results show how the risk characterization is affected by the basis of comparison. In this example, both of the reference values used are widely acknowledged. Secondly, it illustrates how much of the total exposure may be overlooked when only focusing on one exposure pathway, and thirdly, it shows the importance of considering the variability in all relevant pathways.

43] https://www.ncbi.nlm.nih.gov/pubmed/21255877

  • Effects of the fluoride on the central nervous system.
  • The prolonged ingestion of F may cause significant damage to health and particularly to the nervous system. Therefore, it is important to be aware of this serious problem and avoid the use of toothpaste and items that contain F, particularly in children as they are more susceptible to the toxic effects of F.

44] https://www.ncbi.nlm.nih.gov/pubmed/22000841

  • Triclosan, an antibacterial agent, increases intracellular Zn(2+) concentration in rat thymocytes: its relation to oxidative stress.
  • Therefore, the results may suggest that triclosan at sublethal concentrations induces oxidative stress that decreases cellular thiol content, resulting in an increase in intracellular Zn(2+) concentration by Zn(2+) release from intracellular store(s). Since recent studies show many physiological roles of intracellular Zn(2+) in cellular functions, the triclosan-induced disturbance of cellular Zn(2+) homeostasis may induce adverse actions on the cells.

45] https://www.ncbi.nlm.nih.gov/pubmed/22580217

  • In vitro effects of triclosan and methyl-triclosan on the marine gastropod Haliotis tuberculata.
  • Our results reveal a toxic effect of TCS and MTCS on immune (hemocytes) and/or respiratory cells (gill cells) of the abalone, species living in coastal waters areas and exposed to anthropogenic pollution.

46] https://www.ncbi.nlm.nih.gov/pubmed/22726953

  • Cytotoxicity and inhibitory effects of low-concentration triclosan on adipogenic differentiation of human mesenchymal stem cells.
  • Our study demonstrates that TCS inhibits adipocyte differentiation of hMSCs under concentrations that are not cytotoxic and in the range observed in human blood.

47] https://www.ncbi.nlm.nih.gov/pubmed/22729613

  • Effects of DDT and triclosan on tumor-cell binding capacity and cell-surface protein expression of human natural killer cells.
  • These results indicated that only a portion of the loss of NK lytic function seen with exposures to these compounds could be accounted for by loss of binding function. They also showed that loss of binding function is accompanied by a loss of cell-surface proteins important in binding function.

48] https://www.ncbi.nlm.nih.gov/pubmed/24879426

  • The effects of triclosan on pluripotency factors and development of mouse embryonic stem cells and zebrafish.
  • The two models demonstrated that TCS may affect early embryonic development by disturbing the expression of the pluripotency markers.

49] https://www.ncbi.nlm.nih.gov/pubmed/25170948

  • Synthesis, leishmanicidal and cytotoxic activity of triclosan-chalcone, triclosan-chromone and triclosan-coumarin hybrids.
  • The results indicate that compounds containing small alkyl chains show better selectivity indices. Moreover, Michael acceptor moieties may modify both the leishmanicidal activity and cytotoxicity.

50] https://www.ncbi.nlm.nih.gov/pubmed/25193434

  • Differential effects of triclosan on the activation of mouse and human peroxisome proliferator-activated receptor alpha.
  • These data demonstrate that triclosan had similar cytotoxicity in Hepa1c1c7 and HepG2 cells, but differential effects on the activation of PPARα, the expression of ACOX1, and downstream events including DNA synthesis and apoptosis.

51] https://www.ncbi.nlm.nih.gov/pubmed/26204821

  • Antimicrobial agent triclosan is a proton ionophore uncoupler of mitochondria in living rat and human mast cells and in primary human keratinocytes.
  • Thus, the effects of TCS on mast cell function are due to its proton ionophore structure. In addition, 5 µm TCS inhibits thapsigargin-stimulated degranulation of RBL-2H3 cells: further evidence that TCS disrupts mast cell signaling. Our data indicate that TCS is a mitochondrial uncoupler, and TCS may affect numerous cell types and functions via this mechanism.

52] https://www.ncbi.nlm.nih.gov/pubmed/9217239

  • Sodium lauryl sulfate and triclosan: in vitro cytotoxicity studies with gingival cells.
  • Coexposures of triclosan and SLS were additive in their cytotoxicities towards the S-G epithelial cells and GF fibroblasts. Pretreatment with triclosan potentiated the toxicity of a subsequent exposure of SLS to the S-G cells; a similar pretreatment of the GF fibroblasts with triclosan had no effect on a subsequent challenge with SLS.

53] https://www.ncbi.nlm.nih.gov/pubmed/9584909

  • Triclosan: cytotoxicity, mode of action, and induction of apoptosis in human gingival cells in vitro.
  • When exposed to triclosan for 3 d, a lag in the growth kinetics of the S-G cells was first observed at 0.01 mM triclosan. A reduction in attachment of S-G cells to dentin chips, previously exposed to triclosan for 1 h, was noted at 0.25 mM triclosan and greater. Triclosan-induced cell death was apparently by apoptosis, as noted by fluorescence microscopy and DNA agarose gel electrophoresis of extracted oligonucleosomal fragments.

54] https://www.ncbi.nlm.nih.gov/pubmed/15967278

  • Application of methods for assessing the geno- and cytotoxicity of Triclosan to C. ehrenbergii.
  • These results suggest that C. ehrenbergii could represent a useful organism to evaluate the whole toxicity of pharmaceuticals and personal care products (PPCPs), giving valuable information for a risk assessment.

55] https://www.ncbi.nlm.nih.gov/pubmed/20297919

  • Immunosuppressive effects of triclosan, nonylphenol, and DDT on human natural killer cells in vitro.
  • The negative effects of each of these compounds persisted and/or intensified following a brief (1 h) exposure to the compounds, indicating that the impairment of function cannot be eliminated by removal of the compound under in vitro conditions.

56] https://www.ncbi.nlm.nih.gov/pubmed/21847659

  • Immunotoxic effects of triclosan in the clam Ruditapes philippinarum.
  • Overall, these results suggest a relationship between TCS exposure and changes in the measured immune parameters and indicate immunosuppression in TCS-treated clams.

57] https://www.ncbi.nlm.nih.gov/pubmed/21935973

  • Comparison of in vitro cytotoxicity, estrogenicity and anti-estrogenicity of triclosan, perfluorooctane sulfonate and perfluorooctanoic acid.
  • The overall results demonstrated that triclosan, PFOS and PFOA have estrogenic activities and that co-exposure to contaminants and E(2) produced anti-estrogenic effects. Each of these compounds could provide a source of xenoestrogens to humans and wildlife in the environment.

58] https://www.ncbi.nlm.nih.gov/pubmed/27722057

  • Triclosan in water, implications for human and environmental health.
  • Results from epidemiological studies on the effect of TCS on human health have implicated the compound as responsible for certain allergies and reproductive defects. Its presence in chlorinated water also raises toxicity concern for humans as carcinogenic metabolites such as chlorophenols may be generated in the presence of the residual chlorine.

59] https://www.ncbi.nlm.nih.gov/pubmed/29028533

  • Triclosan-caffeic acid hybrids: Synthesis, leishmanicidal, trypanocidal and cytotoxic activities.
  • The activity is dependent on the length of the alkyl linker with compound 19, bearing a four-carbon alkyl chain, the most performing hybrid. In general, hydroxyl groups increase both activity and cytotoxicity and the presence of the double bond in the side chain is not decisive for cytotoxicity and anti-protozoal activity.

60] https://www.ncbi.nlm.nih.gov/pubmed/29501854

  • Evaluation of triclosan in the Hershberger and H295R steroidogenesis assays.
  • In the H295R assay, TCS from 0.01 to 10 μM had no effect on testosterone production but TCS at 3 μM and above did induce a significant increase in estrogen production. At 10 μM, TCS produced significant cytotoxicity which confounded the interpretation of the estrogenic effect at that concentration. Thus, TCS had no effect on androgen synthesis or activity in the models used, but did enhance estrogen production and suppress serum T4.

61] https://www.ncbi.nlm.nih.gov/pubmed/30949737

  • Research Progress on Toxic Effects and Water Quality Criteria of Triclosan.
  • TCS can exhibit acute toxicity to aquatic organisms, affect the normal expression and physiological function of enzymes and genes, and produce cytotoxicity. Many studies have demonstrated that TCS exerts significant endocrine-disrupting effects on organisms, interfering the normal physiological functions of the reproductive, thyroid, and nervous systems via related signaling pathways. Moreover, we reported current research on the water quality criteria of TCS and discuss possible future research directions.

62] https://www.ncbi.nlm.nih.gov/pubmed/4386956

  • [On the effect of a sodium monofluorophosphate and bromchlorophen containing toothpaste in a chronic animal experiment and on caries in children during a 2-year long unsupervised use].

63] https://www.ncbi.nlm.nih.gov/pubmed/983539

  • [The effect of selenium and fluorine with respect to caries and toxicity to Osborne-Mendel-rats (author’s transl)].
  • In respect to the body weight at the end of the experiment one cannot demonstrate a clear effect using the linear contrast of SCHEFFE, and there also is no infleunce of selenium on the total water consumption, which coincides with the results of the first experiment. The two experiments have shown that Na2SeO4 is toxic in the doses applied…

64] https://www.ncbi.nlm.nih.gov/pubmed/1062766

  • [Toxicity of fluorine preparations].

65] https://www.ncbi.nlm.nih.gov/pubmed/6590578

  • The amounts of fluoride in current fluoride therapies: safety considerations for children.
  • Dentists and physicians should know the fluoride concentration of a patient’s water supply before prescribing fluoride supplements.

66] https://www.ncbi.nlm.nih.gov/pubmed/3714382

  • Amounts of fluoride in self-administered dental products: safety considerations for children.
  • Frequent ingestion of low but excessive quantities of fluoride during the period of tooth formation can lead to dental fluorosis. Particular concern is warranted for the ingestion of fluoride-containing toothpastes by young children and the inappropriate use of dietary fluoride supplements in communities with sufficient fluoride already present in drinking water.

67] https://www.ncbi.nlm.nih.gov/pubmed/3283934

  • Is fluoride a mutagen?
  • Since fluoride is increasingly being used as a drug, and contamination of the total environment by fluoride emissions and solid wastes from industry is a growing problem, a review of the evidence regarding the potential mutagenicity of fluoride may be in order.

68] https://www.ncbi.nlm.nih.gov/pubmed/1819322

  • [Comparative studies of toothpastes and toothpaste ingredients in biological systems. 2. Study of toothpaste ingredients and their effects on cell growth].
  • Substantial inhibition of cell growth was caused by tensides. Preparations with Tego-Betain had a significantly less influence on cell growth than Texapon. Other ingredients as medical soap, fluoride and preservative showed a very low effect.

69] https://www.ncbi.nlm.nih.gov/pubmed/17014382

  • Recovery from skeletal fluorosis (an enigmatic, American case).
  • With removal of F exposure, skeletal fluorosis is reversible, but likely impacts for decades. Patients should be monitored for impending nephrolithiasis.

70] https://www.ncbi.nlm.nih.gov/pubmed/20012384

  • Salivary fluoride concentrations and fluoride ingestion following application of preparations containing high concentration of fluoride.
  • Tooth brushing resulted in high salivary retention rates per amount of fluorides used in the procedure. These data provide initial concept about the possible advantages of some methods of topical fluoride application over others.

72] https://www.ncbi.nlm.nih.gov/pubmed/20650267

  • Molecular mechanisms of fluoride toxicity.
  • This review presents an overview of the current research on the molecular aspects of fluoride exposure with emphasis on biological targets and their possible mechanisms of involvement in fluoride cytotoxicity. The goal of this review is to enhance understanding of the mechanisms by which fluoride affects cells, with an emphasis on tissue-specific events in humans.

73] https://www.ncbi.nlm.nih.gov/pubmed/21255877

  • Effects of the fluoride on the central nervous system.
  • The prolonged ingestion of F may cause significant damage to health and particularly to the nervous system. Therefore, it is important to be aware of this serious problem and avoid the use of toothpaste and items that contain F, particularly in children as they are more susceptible to the toxic effects of F.