Fluoride - Demand AARP Take Action

[CarryAnne]

“The evidence that fluoride is more harmful than beneficial is now overwhelming… fluoride may be destroying our bones, our teeth, and our overall health.” - Dr. Hardy Limeback,  former President of Canadian ADA, Head of Preventive Dentistry at Univ of Toronto, 2006 National Research Council Scientist (2007)

The 2006 National Research Council on Fluoride in Drinking Water commented to the EPA that fluoridation at 1 ppm can be anticipated to be harmful for those with reduced renal function and the elderly. The NRC confirmed that fluoride not excreted by kidneys builds up in bones, resulting in arthritic pain and increased brittleness. However, there were no EPA studies on the whole health impacts of fluoridated water on susceptible population such as kidney patients, children, those with prolonged disease or the elderly. There still aren’t. 

However, there is mounting science from other sources that “optimally fluoridated” water, which is known to cause varying degrees of dental fluorosis in 58% of Black American adolescents and 36% of White American adolescents, is causing subtle deficits in ability to remember or focus. That same “optimal level” has also been proved in a 2014 study as being nephrotoxic in rats with chronic kidney disease. Chronic kidney disease (CKD) affects approximately 15% of Americans, although CKD is quadruple the rate in Black Americans, and predictably worse in older Americans. 

Perhaps the most horrifying part of the story of fluoridation is that not only is at least 50% of every drop of fluoride that has passed the lips of a Baby Boomer permanently stored in bones, fluoride isn't the only poison in packages of fluoride that originate as the waste product of aluminum an phosphate industry. 100% of the fluoride sampled in a 2014 study was contaminated with aluminum; arsenic and lead were other common contaminants. In other words, fluoridated water serves as a delivery system for aluminum and lead into our bones and our brains. As we all know, aluminum is associated with Alzheimers in adults, and lead is associated with learning disabilities in children. Approximately 15% of the population who is sensitive to chemicals cite inability to think clearly and overwhelming fatigue as symptoms of exposure to fluoridated water. 

Our generation was part of a great human experiment. It may have had noble intentions based on the faulty hypothesis that  drinking fluoridated water prevented cavities. It is now known that any perceived benefits of fluoride are from tooth brushing.  Our grandchildren are the third generation in this travesty. I suggest we all DEMAND the AARP stand up for us and our grandchildren by issuing a strong position paper calling for the cessation of water fluoridation. 

SCIENCE REFERENCES

1. 2014 in Toxicology. Effect of water fluoridation on the development of medial vascular calcification in uremic rats. (“Optimal levels” worsen kidney function😞 http://www.ncbi.nlm.nih.gov/pubmed/24561004
    
2. 2015  in Neurotoxicology and Teratology. Association of lifetime exposure to fluoride and cognitive functions in Chinese children: A pilot study.  (Children with visible dental fluorosis perform less well on memory tasks, correlating with the degree of severity of their fluorosis. One of a series of human and animal studies with the same consistent findings.😞 
1. http://www.ncbi.nlm.nih.gov/pubmed/25446012  
2. http://braindrain.dk/2014/12/mottled-fluoride-debate/ 
   
   
3. 2014 in Physiology and Behavior. Fluoride exposure during development affects both cognition and emotion in mice. (Measurable behavioral changes😞 http://www.ncbi.nlm.nih.gov/pubmed/24184405
   
   
4. 2014 in International Journal of Occupational and Environmental Health. A new perspective on metals and other contaminants in fluoridation chemicals. (All samples of fluoride are contaminated with aluminum, plus other contaminants like arsenic, lead and barium); 
1. http://www.ncbi.nlm.nih.gov/pubmed/24999851
2. http://momsagainstfluoridation.org/sites/default/files/Mullenix%202014-2-2.pdf
   
   
5. 2014 in Scientific World Journal. Water Fluoridation: A Critical Review of the Physiological Effects of Ingested Fluoride as a Public Health Intervention. (Health risks and cost don't justify minimal and questionable dental benefit.):  http://www.hindawi.com/journals/tswj/2014/293019/

RACIAL INEQUITY (FOIA)

Here are three Oct 2014 news articles on the content of the Freedom of Information Act documents. Rev. Andrew Young, former UN ambassador has pursued them with the CDC, but to little effect. Civil Rights leaders have been calling for an end to community water fluoridation (CWF) since 2011. 

• 1. Black Americans disproportionately harmed: http://www.thenewamerican.com/usnews/health-care/item/19317-feds-blacks-suffer-most-from-fluoride-fl...
• 2. CDC, ADA and Pew inappropriate relationships: http://benswann.com/do-newly-released-emails-reveal-conflict-of-interest-between-the-cdc-and-the-ada...
• 3. Kidneys, Civil Rights & Ralph Nader: http://portland.indymedia.org/en/2014/10/428383.shtml

2015 LEGAL ARGUMENT (GROSS DISPROPORTIONALITY) 

There is a legal initiative in Peel, Ontario (pop 1.3m) to remove fluoride from the water supply based on the principle of gross disproportionality, i.e. marginal benefit does not justify great risk of harm. There is also a political effort afoot in Canadian govt to mandate fluoridation and thereby make the legal argument moot. I suggest this document is well-worth printing.  http://fluoridealert.org/wp-content/uploads/peel.june2014.pdf

• a. The first 19 pages of this document is about the legal strategy. It includes summary of US legal cases that found water fluoridation harmful to the public, but legal under US "police power" mandate.
• b. Starting on page 20 is a devastating affidavit by Dr. Kathleen Thiessen, NAS/NRC scientist and international expert in risk assessment. Very readable summary of science indicating harm to populations in “optimally” fluoridated communities. 

POPULATION WITH LOW CHEMICAL THRESHOLD

1. In excess of 25% of previously healthy Gulf War Veterans have Multiple Chemical Sensitivities, which includes sensitivity to fluoride. See: http://www.va.gov/rac-gwvi/docs/committee_documents/gwiandhealthofgwveterans_rac-gwvireport_2008.pdf 
1. EXCERPT: “It is well established that some people are more vulnerable to adverse effects of certain  chemicals than others, due to variability in biological processes that neutralize those chemicals, and clear them from the body.” - Research Advisory Committee on Gulf War Veterans’ Illnesses 2008 
2. Affidavit of Dr. Hans Moolenburgh: https://fluorideinformationaustralia.files.wordpress.com/2013/01/affidavit-moolenburgh.pdf
1. Except: “As a summary of our research, we are now convinced that fluoridation of the water supplies causes a low grade intoxication of the whole population, with only the approximately 5% most sensitive persons showing acute symptoms.The whole population being subjected to low grade poisoning means that their immune systems are constantly overtaxed. With all the other poisonous influences in our environment, this can hasten health calamities.” 
3. PubMed Listed Studies on immune system response: 
1. a. Fluoride makes allergies worse, rats (1990): http://www.ncbi.nlm.nih.gov/pubmed/1707853 
2. b. Fluoride makes allergies worse, in vitro (1999): http://www.ncbi.nlm.nih.gov/pubmed/9892783
3. c. Immune system of the gut (2010): http://www.hindawi.com/journals/iji/2010/823710/ 
4. d. ASIA Syndrome, adjuvant impact (2011): http://www.ncbi.nlm.nih.gov/pubmed/20708902
5. e. Gene predicts fluoride sensitivity (2015): http://www.ncbi.nlm.nih.gov/pubmed/25556215
6. f.  Brain has an immune system (2015): http://www.ncbi.nlm.nih.gov/pubmed/26030524

AARP - STAND UP on our behalf! 

[CarryAnne · Accepted solution]

 Dr. Joel Bohemier’s presentation to the Commissioners of Collier County, FL  includes quotes for EPA, CDC and others under oath from TSCA trial depositions. This presentation was part of the Commissioners deliberation that resulted in its unanimous vote to end fluoridation last week: https://unite.live/widgets/4142/recording/player#  

It is in the hands of Judge Chen, now, but I've got to say that the closing on Feb. 20th was odd.

Not only did Judge Chen pepper both attorneys with questions, the EPA attorneys seemed to admit that fluoride exposure at doses consistent with water concentration of 1.5 ppm, 2 ppm and 4 ppm had been proven to result in lower IQ per studies of mom-child pairs performed in Canadian and other communities across the world. They admitted this despite the official policy of the U.S. EPA stating there is no harm up to 4 ppm (the actionable threshold for remediation) other than mild cosmetic dental fluorosis (tooth staining) at or above 2 ppm. The Canadian government has an actionable threshold of 1.5 ppm which is consistent with the WHO guidelines. 

When Judge Chen challenged the EPA that per both plaintiff and defense witnesses, shouldn't there be a protective uncertainty or safety factor of at least ten to protect consumers applied to 2 or 4 which would protect teeth from moderate dental fluorosis which a recent Health Canada is concern at 1.56 ppm and from severe dental fluorosis which the 2006 National Research Council (NRC) said was an adverse health risk at 4 ppm which would also protect brains, EPA Defense attorney said that would be an interesting thought experiment, but Plaintiff attorney didn't argue about dental fluorosis (which by the way is positively associated with lower IQ and learning disabilities) so the judge could not legally do so. Frankly, it almost seemed like the EPA attorneys were threatening the Judge. 

Judge Chen pushed back about EPA "Health Protective Assumption" guidelines, but EPA insisted that the Judge must not act based on science or consumer protection, but on strict interpretation of statutory law and the skill of the Plaintiff attorney in proving his case. 

On the other hand, Plaintiff attorney was clear that the Toxic Substances Control Act (TSCA) only requires that any specific use of a chemical (fluoridation programs) not pose an "unreasonable risk" to consumers which include susceptible sub-populations like pregnant women and their offspring and bottle-fed babies. All five plaintiff witnesses were quite clear that optimally fluoridated water per CDC guidelines is subtly and permanently damaging the brains of millions of children. Even EPA witnesses and attorneys admitted that there is "something there" in the scientific evidence showing neurotoxic effects at 0.7 ppm, but argued it is not clearly defined enough to identify a "Point of Departure" for the EPA to perform a risk assessment. 

Really? 

Three Benchmark Dose Analyses which are the gold standard for beginning risk assessments and established uncertainty factors have identified that 0.2 mg/L, which is one tenth of 2 ppm, as harmful. This suggests that no fluoride exposure is safe for baby brains and is a scientifically justifiable Point of Departure in anyone's book.  

BMCL

But let's make it even easier for thick-headed fluoridationists to understand: 

• No amount of fluoride in water or food is safe for pregnant women and their fetuses; bottle-fed infants and young children; the elderly and any in fragile health, such as diabetics or those with thyroid or kidney disease. 

[CarryAnne · Accepted solution]

 “Today’s ruling represents an important acknowledgement of a large and growing body of science indicating serious human health risks associated with fluoridated drinking water. This court looked at the science and acted accordingly. Now the EPA must respond by implementing new regulations that adequately protect all Americans – especially our most vulnerable infants and children – from this known health threat.” - Wenonah Hauter, Director of Food & Water Watch in “Historic Court Decision in Fluoridation Toxicity Case Orders EPA to Act” (Sept. 25, 2024)

Well, it as been a busy few weeks! 

Not only was the final NTP Systematic Review, "Fluoride Exposure: Neurodevelopment and Cognition" published in August (despite political efforts by HHS/PHS and ADA to scuttle it) after five (or was it six) peer reviews, the Final Findings and Conclusion of Law from a lengthy de novo trial was rendered in September with excellent detail, and the 2024 Cochrane Systematic Review, "Water fluoridation for the prevention of dental caries," published in October repeated that dental fluorosis is an adverse effect of fluoridation, a practice which provides no benefit to adults or lower socio-economic groups. The Cochrane authors also wrote that the very small benefit they were able to document to children from "poor quality" studies at high risk of bias "may not be real." 

In other words, community water fluoridation is all risk and no benefit. Fluoridation is dental mythology, a magic potion tooth-fairy tale. The most important thing is that Judge Chen ordered the EPA to take action to eliminate the risk to consumers. 

• UNSAFE: p. 2:  the Court finds that fluoridation of water at 0.7 milligrams per liter (“mg/L”) – the level presently considered “optimal” in the United States – poses an unreasonable risk of reduced IQ in children.

• HAZARD: p 5:   The pooled benchmark dose analysis concluded that a 1-point drop in IQ of a child is to be expected for each 0.28 mg/L of fluoride in a pregnant mother’s urine. This is highly concerning, because maternal urinary fluoride levels for pregnant mothers in the United States range from 0.8 mg/L at the median and 1.89 mg/L depending upon the degree of exposure. Not only is there an insufficient margin between the hazard level and these exposure levels, for many, the exposure levels exceed the hazard level of 0.28 mg/L.
  
  

• CERTAINTY: p. 77: The scientific literature in the record provides a high level of certainty that a hazard is present; fluoride is associated with reduced IQ. There are uncertainties presented by the underlying data regarding the appropriate point of departure and exposure level to utilize in this risk evaluation. But those uncertainties do not undermine the finding of an unreasonable risk; in every scenario utilizing any of the various possible points of departures, exposure levels and metrics, a risk is present in view of the applicable uncertainty factors that apply.
  
  

• VULNERABILITY: p. 76: The size of the affected population is vast. Approximately 200 million Americans have fluoride intentionally added to their drinking water at a concentration of 0.7 mg/L. See Dkt. No. 421 at 206-07 (undisputed). Other Americans are indirectly exposed to fluoridated water through consumption of commercial beverages and food manufactured with fluoridated water
  
  

• SUSCEPTIBILITY: p. 76: Approximately two million pregnant women, and over 300,000 exclusively formula-fed babies are exposed to fluoridated water. The number of pregnant women and formula-fed babies alone who are exposed to water fluoridation each year exceeds entire populations exposed to conditions of use for which EPA has found unreasonable risk; the EPA has found risks unreasonable where the population impacted was less than 500 people. 

[rs5526]

We've already gone over this. Eating and drinking fluoride cannot and does not reduce dental decay (Teotia; Ziegelbecekr; Yamouyiannis;  Sutton) . The levels in saliva bathing teeth (0.016 ppm) are 94,000 times less concentrated than in toothpaste.

What I defend pepole for is bone health. Fluoride accumulates in bone during lifelong eating/drinking where it alters the crystal structure of bone. In only 15-20 or so years in a fluoridated city fluoride is in bone at levels above that added into toothpaste, all in bone where it does not belong. Bone is living tissue that is a repository for blood calcium.

I defend people's rights to healthy bone tissue.

Adding fluoride into water that fluoridationists deem is somehow created deficiently is ineffective, harmful, and in violation of Federal water law.

The FDA has never approved of fluoride ingestion and ruled that added fluoride in water is an uncontrolled use of an unapproved drug. 

Thank you.

[RandyJ913440]

Richard Sauerheber – What “we’ve already gone over” are examples of your extremely biased and often demonstrably false, unproven (and/or misleading and irrelevant) opinions and speculations of what the body of evidence on fluoridation means.

As a perfect example, you just claimed, “Adding fluoride into water that fluoridationists deem is somehow created deficiently is ineffective, harmful, and in violation of Federal water law.  The FDA has never approved of fluoride ingestion and ruled that added fluoride in water is an uncontrolled use of an unapproved drug.”  Provide a citation to the specific “Federal water law” you believe fluoridation violates.  Provide a citation to the FDA ruling that community water fluoridation is “uncontrolled use of an unapproved drug”.  Explain why, if your claims are valid, the FDA regulates bottled water which can contain the same fluoride levels as found in optimally fluoridated water as a “Food.  Also, what exactly do you mean by “water that fluoridationists deem is somehow created deficiently”. and how that statement is that relevant to anything?

Do you reject out-of-hand the references provided that demonstrate a benefit of community water fluoridation (CWF)?

Do you reject out-of-hand the scientific consensus that CWF is a safe and effective public health measure?  You certainly have provided no alternative except a non-scientific outlier consensus.

[BillO538145]

Randy,

Continuing:

Chromosomal anomalies and Primary DNA Damage:  Tiwari (2010) “Our study

has supported the role of As [arsenic] and F [fluoride] as potent genotoxic agents, since in vitro exposure of both caused increased chromosomal anomalies along with primary DNA damage, in human peripheral blood cultures.”[1]         

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.. . . .”[2]

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.”[3]

 Known Genotoxic: Kleinsasser (2001) “For fluoride concentrations of 2 ppm to 35 ppm, non vital cells of less than 10% could be shown. After incubation with 71 ppm and 213 ppm Olaflur, there were 15% and 43% of damaged cells, respectively. Weak genotoxic effects on mucosal cells as well as on lymphocytes could be demonstrated at all concentrations tested. In fluoride concentrations of 213 ppm genotoxicity increased to max.”[4]   

Known DNA Damage: Chen (2000) “To investigate the effects of fluoride on DNA damage

as well as the effects of selenium and zinc against fluoride respectively or jointly in pallium neural cells of rats, single cell gel electrophoresis was used to detect the DNA damage of neural cells prepared in vitro. The results showed that the degree of DNA damage in the fluoride group and the selenium group were significantly greater than that in control group (P < 0.01). The damage in the fluoride group was even more serious. The damage in the fluoride + selenium group and fluoride + zinc group was slighter than that in the fluoride group but with no significant difference. The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group(P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively.”[5]

Known Genotoxic     Rivedal (2000) ”In the present work, 13 compounds [chlordane, Arochlor 1260, di(2-ethylhexyl)phthalate, 1,1,1-trichloro-2, 2-bis(4-chlorophenyl)ethane, limonene, sodium fluoride, ethionine, o-anisidine, benzoyl peroxide, o-vanadate, phenobarbital, 12-O-tetradecanoylphorbol 13-acetate and clofibrate] have been tested for their ability to induce morphological transformation and affect intercellular communication in Syrian hamster embryo (SHE) cells… In vitro morphological transformation of SHE cells is now one of the most frequently used cell transformation systems. Around 500 chemicals have been tested in this system, and a good correlation has been obtained with the ability of compounds from different chemical groups to cause tumours in animals and humans. The SHE cell transformation assay also responds to tumour promoters and carcinogens not detected by tests for genotoxicity… [N]ine of the 13 tested substances (TPA, o-vanadate, DEPH, phenobarbital, Arochlor 1260, clofibrate, o-anisidine, limonene and NaF) are considered positive for induction of morphological transformation.”[6]

Known Genotoxic:    Mihashi (2000)“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 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.”[7]

Known Genotoxic: Khalil (1995)       “The genotoxic effects of inorganic fluorides were investigated by treating cultured rat bone marrow cells with varying concentrations (0.1-100 microM) of potassium fluoride (KF) and sodium fluoride (NaF) for different durations (12, 24 and 36 h) and measuring the incidence of cells with aberrations and number of breaks per cell. Both forms of fluoride were found to be weak mutagens relative to the positive control N-methyl-N-nitro-N-nitrosoguanidine (MNNG). A specificity of fluoride ion in inducing chromosome aberrations (CA) was indicated by the observation that both NaF and KF behaved almost equivalently in this study and at significantly higher variations from the results with potassium chloride (KCl) and sodium chloride (NaCl).”[8]

Known Mutagen:  Gritsan (1993)      “The testing of hydrogen fluoride (HF) for its mutagenic activity by fumigation of barley seedlings showed that the mutation rate was linear with dose. It was found that the cytogenic effects of gaseous fluoride on grain crops was correlated with the fluoride content in plant tissue.”[9]

Chromosome Aberrations - early cell cycle dependent: Hayashi (1993) “A

significant increase in the incidence of chromosome aberrations was observed only in cultures treated with NaF during early and/or middle S phases of cell cycle. These results suggest that cytotoxicity and clastogenicity of NaF to cultured human diploid fibroblasts are cell cycle dependent, and that the cells in early and middle S phases are more sensitive to the effects.”[10]

Species Dependent  Kishi (1993)     “Conflicting evidence has been reported concerning the mutagenicity of sodium fluoride (NaF), especially clastogenicity at concentrations of more than 1 mM. NaF is known to induce chromosome aberrations at these concentrations in human cells, but not in most rodent cells. We considered that such species-specific difference in chromosomal sensitivity would be derived from the phylogenetic distance between rodents and man. To clarify the role of interspecies differences, we investigated the chromosomal sensitivity to NaF in cell lines from various primates, which diverged into many species, including rodent-like prosimians and human-like great apes. The results showed that the clastogenicity of NaF was limited to human and great ape cells. . . . .”[11]

Induction of mutagenic effects:      “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.”[12]

Induce mutations: “Sodium fluoride was found to induce gene-locus mutations at the thymidine kinase (tk) and hypoxanthine guanine phosphoribosyl transferase (hgprt) loci in human lymphoblastoid cells.”[13]

Aberrations dependent on cell cycle:  Suzuki (1989) “Inducibility of chromosome

aberrations of the cells following treatment with sodium fluoride was also dependent upon the phase of cell cycle.”[14]

Promotes Cancer:     Jones (1988) “Sequential treatment of Syrian hamster embryo (SHE) cells with a chemical carcinogen followed by sodium fluoride (NaF) resulted in a higher yield of morphologically transformed cell colonies than treatment of the cells with carcinogen alone… This enhancement/promotion of cell transformation by NaF was only expressed after the cells had been pretreated with either directacting carcinogens or procarcinogens.”[15]

Randy, some more to follow.

[1] Tiwari H, Rao MV. (2010). Curcumin supplementation protects from genotoxic effects of arsenic and fluoride. Food & Chemical Toxicology 48(5):1234-8.

[2] Zhang R, et al. (2009). A stable and sensitive testing system for potential carcinogens based on DNA damage-induced gene expression in human HepG2 cell. Toxicology In Vitro. 23(1):158-65.

[3] Erciyas K, Sarikaya R. (2009). Genotoxic evaluation of sodium fluoride in the Somatic Mutation and Recombination Test (SMART). Food & Chemical Toxicology 47(11):2860-2.

[4] Kleinsasser NH, et al. (2001). [Cytotoxicity and genotoxicity of fluorides in human mucosa and lymphocytes]. Laryngorhinootologie 80(4):187-90.

[5] Chen J, et al. (2000). [Effects of selenium and zinc on the DNA damage caused by fluoride in pallium neural cells of rats]. Wei Sheng Yan Jiu. 29(4):216-7.

[6] Rivedal E, et al. (2000). Morphological transformation and effect on gap junction intercellular communication in Syrian hamste... embryo cells as screening tests for carcinogens devoid of mutagenic activity. Toxicology In Vitro 14(2):185-92.

[7] Mihashi M, Tsutsui T. (1996). Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture. Mutation Research 368:7-13.

[8] Khalil AM. (1995). Chromosome aberrations in cultured rat bone marrow cells treated with inorganic fluorides. Mutation Research 343:67-74.

[9] Gritsan, NP. (1993). Cytogenetic effects of gaseous fluorides on grain crops. Fluoride 26: 23-32.

[10] Hayashi N, Tsutsui T. (1993). Cell cycle dependence of cytotoxicity and clastogenicity induced by treatment of synchronized human diploid fibroblasts with sodium fluoride. Mutation Research 290: 293-302.

[11] Kishi K, Ishida T. (1993). Clastogenic activity of sodium fluoride in great ape cells. Mutation Research 301:183-8.

[12] Suzuki Y, Li J, Shimizu H. (1991). Induction of micronuclei by sodium fluoride. Mutation Research 253:278.

[13] Crespi CL, et al. (1990). Sodium fluoride is a less efficient human cell mutagen at low concentrations. Environmental Molecular Mutagenesis 15:71-7.

[14] Suzuki N, Tsutsui T. (1989). [Dependence of lethality and incidence of chromosome aberrations induced by treatment of synchronized human diploid fibroblasts with sodium fluoride on different periods of the cell cycle]. [Article in Japanese] Shigaku. 77(2): 436-47.

[15] Jones CA, et al. (1988). Sodium fluoride promotes morphological transformation of Syrian hamster embryo cells. Carcinogenesis 9: 2279-84.

[DavidF928895]

BillO,

let's talk about water fluoridation & Cancer.  The American Cancer Society seems to have reached different conclusions than you & fluoridealert regarding interpretations of quality studies.  

https://www.cancer.org/cancer/cancer-causes/water-fluoridation-and-cancer-risk.html

This is the American Cancer Society's discussion in its entirety.  (The ACS doesn't take money from Alternative Health snake-oil salesmen who benefit from any form of paranoia, Fluoridealert does.)

"What have studies found?

More than 50 population-based studies have looked at the potential link between water fluoride levels and cancer. Most of these have not found a strong link to cancer. Just about all of the studies have been retrospective (looking back in time). They have compared, for example, the rates of cancer in a community before and after water fluoridation, or compared cancer rates in communities with lower levels of fluoride in drinking water to those with higher levels (either naturally or due to fluoridation). Some factors are hard to control for in these types of studies (that is, the groups being compared may be different in ways other than just the drinking water), so the conclusions reached by any single study must be looked at with caution.

And there are other issues that make this topic hard to study. For example, if fluoridation is a risk factor, is the type of fluoride used important? Also, is there a specific level of fluoride above which the risk is increased, or a certain amount of time or an age range during which a person would need to be exposed?

Osteosarcoma is a rare cancer. Only about 400 cases are diagnosed in children and teens each year in the United States. This means it can be hard to gather enough cases to do large studies. Smaller studies can usually detect big differences in cancer rates between 2 groups, but they might not be able to detect small differences. If fluoride increased the risk only slightly, it might not be picked up by these types of studies.

Assessments by expert groups

Small studies by themselves might not provide the answers, but taken as a whole they tend to have more weight. Several systematic reviews over the past 25 years have looked at all of the studies published on this subject.

In its review published in 1987, the International Agency for Research on Cancer (IARC), part of the World Health Organization, labeled fluorides as “non-classifiable as to their carcinogenicity [ability to cause cancer] in humans.” While they noted that the studies “have shown no consistent tendency for people living in areas with high concentrations of fluoride in the water to have higher cancer rates than those living in areas with low concentrations,” they also noted that the evidence was inadequate to draw conclusions one way or the other.

In 1991, the US Public Health Service issued a report on the benefits and risks of fluoride. When looking at a possible link with cancer, they first reviewed the results of studies done with lab animals. They concluded that the few studies available “fail[ed] to establish an association between fluoride and cancer.” They also looked at population-based studies, including a large study conducted by the National Cancer Institute. They concluded: “Optimal fluoridation of drinking water does not pose a detectable cancer risk to humans as evidenced by extensive human epidemiological data available to date, including the new studies prepared for this report.”

The National Research Council (NRC), part of the National Academies, issued a report titled “Health Effects of Ingested Fluoride” in 1993. Its conclusion was that “the available laboratory data are insufficient to demonstrate a carcinogenic effect of fluoride in animals.” They also concluded that “the weight of the evidence from the epidemiological [population-based] studies completed to date does not support the hypothesis of an association between fluoride exposure and increased cancer risk in humans.” The report recommended that additional well-designed studies be done to look at the possible link to cancers, especially osteosarcomas.

In the United Kingdom, the National Health Service (NHS) Centre for Reviews and Dissemination, University of York, published a systematic review of water fluoridation in the year 2000. After searching through the medical literature, they included 26 studies in their analysis, all of which were considered to be of “low” to “moderate” quality. They concluded, “Overall, no clear association between water fluoridation and incidence or mortality of bone cancers, thyroid cancer, or all cancers was found.” However, they also noted, “Given the level of interest surrounding the issue of public water fluoridation, it is surprising to find that little high quality research has been undertaken.”

The National Research Council issued an update of its 1993 review in early 2006. While the review included some new data, the results of this report were essentially the same: “On the basis of the committee’s collective consideration of data from humans, genotoxicity assays, and studies of mechanisms of actions in cell systems, the evidence on the potential of fluoride to initiate or promote cancers, particularly of the bone, is tentative and mixed.”

The European Scientific Committee on Health and Environmental Risks (SCHER) reviewed the evidence on water fluoridation in 2010. It concluded that the evidence linking fluoride in water to osteosarcoma was “equivocal,” and that therefore “fluoride cannot be classified as to its carcinogenicity.”

In 2011, the state of California’s Carcinogen Identification Committee (CIC) reviewed the evidence and concluded that “fluoride and its salts has not been clearly shown to cause cancer.”

The general consensus among the reviews done to date is that there is no strong evidence of a link between water fluoridation and cancer. However, several of the reviews noted that further studies are needed to clarify the possible link.

More recent research

Several studies looking at a possible link between water fluoridation and cancer have been published in recent years.

A partial report of a study from the Harvard School of Public Health, published in 2006, found that exposure to higher levels of fluoride in drinking water was linked to a higher risk of osteosarcoma in boys but not in girls. However, researchers linked to the study noted that early results from a second part of the study did not appear to match those of the report. They therefore advised caution in interpreting the results.

The second part of the Harvard study, published in 2011, compared the fluoride levels in bones near tumors in people with osteosarcoma to the levels in people with other types of bone tumors. The researchers found no difference between the fluoride levels in the two groups.

More recent studies have compared the rates of osteosarcoma in areas with higher versus lower levels of fluoridation in Great Britain, Ireland, and the United States. These studies have not found an increased risk of osteosarcoma in areas of water fluoridation."

[DrChuckHaynie]

The final nail on the box dismissing the cancer claims was the 2011 California Carcinogen ID Committee determination by unanimous vote that fluoride does not cause cancer at ANY concentration.  

California has all of the submissions made to the committee for consideration, including those from Fluoride Action Network and other opponents here:

http://www.oehha.ca.gov/prop65/public_meetings/cic092311.html

No systematic review before or since has found fluoridation related to cancer cases. Why would America's Pediatricians, Family Physicians and Internal Medicine specialists advocate for fluoridation if it causes cancer?

[BillO538145]

Hi Chuck,

Sorry it has taken a bit for me to get back to your comment.  I wanted to get some research on fluoride and cancer on the table.  

(Your comment in italics)

Chuck:  "The final nail on the box dismissing the cancer claims was the 2011 California Carcinogen ID Committee determination by unanimous vote that fluoride does not cause cancer at ANY concentration."  

Bill:  Committee was biased.

Nothing in science is nailed shut.  Beware of any suggestion that science is static. No scientist is satisfied with research. 

There are several ways to achieve the desired results with research reviews.  For example, suppose Ford wanted to know which pickup truck is the best pickup truck.  Simply, ask each Ford dealer what make is their favorite pickup truck.  The results are in the sampling.  

How many scientists on the California Carcinogen ID Committee were opposed to fluoridation and how many in favor when the committee was formed?  How was the committee charged and the scope, etc.

  The NRC 2006 committee asked three people who were neutral or opposed to fluoridation to be on the committee and the results were of greater concern and caution, with specific recommendations which the EPA has still not followed.   

Chuck: "California has all of the submissions made to the committee for consideration, including those from Fluoride Action Network and other opponents here:

http://www.oehha.ca.gov/prop65/public_meetings/cic092311.html

No systematic review before or since has found fluoridation related to cancer cases. Why would America's Pediatricians, Family Physicians and Internal Medicine specialists advocate for fluoridation if it causes cancer?"

Bill:  No ethical person would intentionally cause cancer in humans.  And no ethical person without bias, reading the research would be comfortable giving everyone an uncontrolled dosage (not everyone drinks 1 liter of water a day up to 10 mg more fluoride/day) of fluoridated water when they don't know anything about the patient or have the patient's consent or know how much fluoride the patient is getting from other sources. 

A person supporting fluoridation is recommending giving everyone up to 7 -10 mg of fluoride a day.  Would you put your professional license on the line and write a prescription for everyone without them being a patient of record for 7 or 10 mg/day of fluoride?  

Science is not a belief system.   Church has the nails in the cross/coffin.  Science has no nails in any theory.  

[Drjohnnyjohnson]

Hey Bill,

Why didn't you hang around in Potsdam, NY last night after your fluoridation presentation by Skype?  You missed out on the best part of the presentation.  

1. How you have the intestinal fortitude to show mild fluorosis that you've cut down and put veneers over at the cost of $10-15,000 (your numbers) is a sin.  Why don't you ask your buddy Hardy Limeback about what he teaches and promotes as a conservative alternative to mild fluorosis?  He would tell you to use microabrasion to remove these areas if people even asked to have it addressed.  

Hardy has told me that "you Americans" put veneers over these areas as we aren't taught microabrasion.  Well, I guess that you've made him correct.

Have you ever considered bleaching a patient's teeth and/or microabrasion?  

2.  It was very interesting how you, like FAN and other fluoridation opponents, avoid commenting or even acknowledging the National Toxicolog Program's Report which showed absolutely no IQ or neurological deficits, or any effects of any of the 9 areas that they studied?  YOU pushed, praised and hailed this study that would be the one to end fluoridation.  As you know, this prestigious group is not stacked with pro-fluoridation scientists.

The NTP looked at fluoride levels in water that the rats were given at 0ppm, 10ppm, and 20ppm.  As you know, this coorelated to fluoride levels in water for humans of 0.7ppm (community water fluoridation) and at the EPA Maximum Contaminant Level of 4mg/L (ppm).  No neurological issues from fluoride whatsoever.  Why not just comment on it, Bill?  

https://www.ncbi.nlm.nih.gov/pubmed/29404855

Incidentally, Israel voted to restart fluoridation and is going throught the steps to do so.  You again misrepresented this fact last night stating that they voted it out without stating that they voted it back in. 

3.  You should learn the difference between Severe Early Childhood Caries (S-ECC) and Early Childhood Caries (ECC) if you are to continue seeing children as you stated that you do.  Those slides that you showed, which happen to be almost exactly the ones that Paul Connett shows, is Severe Early Childhood Caries.  These are distinctly different.  Making claims about community water fluoridation and S-ECC is incorrect.  You should be speaking about water fluoridation and ECC.  As a matter of information, community water fluoridation reduces hospitalization under general anesthetic for full mouth rehabilitation of children with ECC by 2/3rds to 3/4ths.  If you need the references for these studies conducted in the U.S., U.K., and Israel, I can supply them to you for your next presentation.

Maybe sometime you can actually come to one of these meetings instead of Skyping in like you did last night and in Cortland, NY.  We can then face off in testimony and you'll have to back up your abuse of the credible science,  unlike we, the American Fluoridation Society, uses the credibly conducted science to help decision-makers make educated, informed decisions.  That would be fun.  

Best wishes,

Johnny 

Johnny Johnson, Jr., DMD, MS

Pediatric Dentist

Diplomate American Board of Pediatric Dentistry

Life Fellow American Academy of Pediatric Dentistry

President, American Fluoridation Society (AFS), a non-profit all volunteer group of healthcare professionals that do not accept a penny for what they do.  AFS is funded by Delta Dental of California's Education and Research Fund.

www.AmericanFluoridationSociety.org

[BillO538145]

And to continue:

Clastogenic: Albonese (1987) “Chromosomal aberrations were recorded for all the concentrations used. . . .The authors conclude that sodium-fluoride may be considered to be clastogenic in these cells.”[1]

Genetic Damage:  Caspary (1987) “While the results in this paper demonstrate the ability (of fluoride) to induce genetic damage in cultured mammalian cells, the potential risks to animals or man are not addressed.”[2]

Genotoxic and suggested carcinogenic:   Tsutsui (1984) “Mass cultures of cells treated with NaF (75 or 100 micrograms/ml) for 24 hr, followed by continuous cultivation for 35 to 50 passages, developed the ability to grow in soft agar and to produce anaplastic fibrosarcomas when injected into newborn hamsters. In contrast, no morphological and neoplastic transformation was observed in untreated cells. Furthermore, a significant increase in chromosome aberrations at the chromatid level, sister chromatid exchanges, and unscheduled DNA synthesis was induced by NaF in a dose- and time-dependent manner. These results indicate that NaF is genotoxic and capable of inducing neoplastic transformation of Syrian hamster embryo cells in culture. A potential for carcinogenicity of this chemical, which is widely used by humans, is suggested. However, the carcinogenic risk of this chemical to humans may be reduced by factors regulating in vivo dose levels.”[3]

DNA Damage: Tsutsui (1984)            “A significant increase in the frequency of chromosome aberrations at the chromatid level was observed in treated cells in a dose-dependent manner… These results suggest that NaF causes DNA damage in human diploid fibroblasts in culture.”[4]

DNA Damage:  Tsutsui (1984)           “The effect of treatment of cultured human oral keratinocytes with sodium fluoride (NaF) has been investigated with respect to induction of unscheduled DNA synthesis (UDS)… Significant levels of UDS were induced in a dose-related fashion by NaF treatment. The results suggest that NaF causes DNA damage in cultured human oral keratinocytes.”[5]

Neoplasm:     Greenberg (1982) The results of this investigation indicate that young leukocytes chronically exposed to elevated fluoride levels have the potential for an irreversible shift toward the formation of neoplasm.”[6]

Chromosome damage at artificial fluoridation concentrations:             “Human

leucocytes in the cultures in vitro were exposed to the action of lead and fluorine ions… Both factors caused structural and quantitative aberrations in the chromosome set, which seems to indicate their mutagenic character. It is noteworthy that the smallest of the applied concentrations of fluorine ions (3.15 x 10-5M) is equal to the concentration of these ions in the running water of Szczecin, given for the prevention of caries.”[7]

Mutagenic agent: Mohamad (1977)  “These findings indicate that HF in addition to being a mutagenic agent is also able to reduce crossing over in certain chromosome segments.”[8]

Genetic damage: Gerdes (1971) “Two strains of Drosophila melanogaster were treated with

sub-lethal levels of gaseous hydrogen fluoride for six weeks. Egg samples were collected at various times for hatchability determinations. Adults reared from these samples were evaluated for fecundity and fertility. Treatment with HF caused a marked reduction in hatchability and fecundity in the more sensitive strain. Male fertility was depressed but female fertility remained stable over the test period. The reduction of these parameters in the offspring of populations subjected to low levels of atmospheric HF contamination for prolonged periods suggests that HF causes genetic damage.”[9]

Genetic aberrations: Gerdes (1971) “Results indicate that treatment increased the incidence of genetic aberrations as measured by at least two parameters.”[10]

Known mutagen: Mohamed (1970)  “These findings indicate that HF is a mutagenic agent.”[11]

 DNA damage: Wu (1995)“In recent years, SCE analysis has been considered to be a sensitive method for detecting DNA damage. There is a clear relationship between a substance’s ability to induce DNA damage, mutate chromosomes, and cause cancers. The SCE frequency in the human body in peripheral blood lymphocytes is very steady, and does not vary with age or sex. Any increase of the SCE frequency is primarily due to chromosome damage. Thus using a method to detect SCE for exploring the toxicity and harm caused by fluoride is of great importance. The results in this paper showed an obvious increase in the SCE frequency of the patients with fluorosis, indicating that fluorine had some mutagenic effects, and could give rise to DNA damage.”[12]

The Oral Health Research Institute at the Indiana University School of Dentistry has repeatedly failed to find any evidence of genotoxic effects from fluoride exposure, whether in fluoride-exposed humans or animals. (Jackson 1997; Li 1995; Dunipace 1995; Jackson 1994). 

Chromosome aberrations: Joseph (2000) “Our results indicate that there is a significant increase in the frequencies of chromosome aberrations and SCE in one of the village populations exposed to a fluoride concentration higher than the permissible limit. The lymphocytes of these residents were also more susceptible to a clastogen such as Mitomycin-C than the other populations and displayed a significant increase in chromosome aberrations.”[13]

Chromosome aberrations Meng (1997)“Our study here provides evidence that the air pollutants at the phosphate fertilizer factory, in which HF and SiF4 are the main chemicals, could induce both CA (chromosomal aberrations) and MN (micronuclei) in human blood lymphocytes in vivo. Our earlier observation on sister-chromatid exchanges (SCE) of peripheral blood lymphocytes from this same population showed that the mean SCEs/cell of the workers was significantly higher than that of the controls (p < 0.01). The results of our studies imply that even if the concentration of the chemical pollutants in the air is low (e.g. F 0.50-0.80 mg/m 3), it may cause damage to genetic material at the chromosomal level… it is suggested that chromosomal abnormalities induced by fluoride could be the results from interaction with the enzymes responsible for DNA synthesis or repair, rather than directly with

DNA.”[14]

Mutagenic Agent: Wu (1950 “The results in this paper showed an obvious increase in the SCE frequency of the patients with fluorosis, indicating that fluorine had some mutagenic effects, and could give rise to DNA damage. The fact that the SCE frequency of the healthy people in the endemic regions was also higher than that of the controls in the non-endemic regions suggests that early harm by fluorine can be cytogenetically detected in the sub-clinical patients with fluorosis who could not be given an early diagnosis clinically. Under normal circumstances, the incidence rate of micronucleus is very low, usually 0-2%. The normal value checked in this paper is 0-2%, which agrees with that reported in the literature. The results show that the mean value of the micronucleus rate of the fluorine-toxic patients was 1.94 + 0.86% (range 1-15%) which is 2-3 times more than that of 0.57 + 0.44% in the controls… To sum up, the rise of SCE and MN in the peripheral blood lymphocytes of the fluorine-intoxicated patients indicates that fluorine is a mutagenic agent which can cause DNA and chromosomal damage.”[15]

Meng (1995) “Our study here provided evidence that the air pollutants at the phosphate fertilizer factory, of which HF and SiF4 are the main chemicals, could induce SCEs in human blood lymphocytes in vivo. These results imply that even if the concentration of the chemical pollutants in the air is low (e.g.F: 0.50 – 0.80 mg/m3), it may cause damage to genetic material at the chromosomal level, although the general health of the workers in the phosphate fertilizer factory was found to be satisfactory.”[16]

[1] Albanese R. (1987). Sodium fluoride and chromosome damage (in vitro human lymphocyte and in vivo micronucleus assays). Mutagenesis 2:497-9.

[2] Caspary WJ, et al (1987). Mutagenic activity of fluorides in mouse lymphoma cells. Mutation Research 187:165-80.

[3] Tsutsui T, Suzuki N, Ohmori M. (1984) Sodium fluoride-induced morphological and neoplastic transformation, chromosome aberrations, sister chromatid exchanges, and unscheduled DNA synthesis in cultured syrian hamster em.... Cancer Research 44:938-41.

[4] Tsutsui T, Suzuki N, Ohmori M, Maizumi H. (1984). Cytotoxicity, chromosome aberrations and unscheduled DNA synthesis in cultured human diploid fibroblasts induced by sodium fluoride. Mutation Research 139:193-8.

[5] Tsutsui T, Ide K, Maizumi H. (1984). Induction of unscheduled DNA synthesis in cultured human oral keratinocytes by sodium fluoride. Mutation Research 140(1): 43-8.

[6] Greenberg SR. (1982). Leukocyte response in young mice chronically exposed to fluoride. Fluoride 15: 119-123.

[7] achimczak D, Skotarczak B. (1978). The effect of fluorine and lead ions on the chromosomes of human leucocytes in vitro. Genetica Polonica 19: 353-7.

[8] Mohamed AH. (1977). Cytogenetic effects of hydrogen fluoride gas on maize. Fluoride 10: 157-164.

[9] Gerdes RA, et al. (1971). The effects of atmospheric hydrogen fluoride upon Drosophila melanogaster. II. Fecundity, hatchabili... and fertility. Atmospheric Environment 5:117-122.

[10] Gerdes RA. (1971). The influence of atmospheric hydrogen fluoride on the frequency of sex-linked recessive lethals and ... Drosophila Melanogaster. Fluoride 4: 25-29.

[11] Mohamed AH. (1970). Chromosomal changes in maize induced by hydrogen fluoride gas. Canadian Journal of Genetics and Cytology 12: 614-620.

[12] Wu DQ, Wu Y. (1995). Micronucleus and sister chromatid exchange frequency in endemic fluorosis. Fluoride. 28(3):125-127.

[13] Joseph S, Gadhia PK. (2000). Sister chromatid exchange frequency and chromosome aberrations in residents of fluoride endemic regions of South Gujarat. Fluoride 33(4):154-158.

[14] Meng Z, Zhang B. (1997). Chromosomal aberrations and micronuclei in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research 393: 283-288.

[15] Wu DQ, Wu Y. (1995). Micronucleus and Sister Chromatid Exchange Frequency in Endemic Fluorosis. Fluoride 28(3):125-127.

[16] Meng Z, et al. (1995). Sister-chromatid exchanges in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research 334(2):243-6.

[BillO538145]

And more research on cancer:

Chromosome aberrations: Joseph (2000) “Our results indicate that there is a significant increase in the frequencies of chromosome aberrations and SCE in one of the village populations exposed to a fluoride concentration higher than the permissible limit. The lymphocytes of these residents were also more susceptible to a clastogen such as Mitomycin-C than the other populations and displayed a significant increase in chromosome aberrations.”[1]

Chromosome aberrations Meng (1997)“Our study here provides evidence that the air pollutants at the phosphate fertilizer factory, in which HF and SiF4 are the main chemicals, could induce both CA (chromosomal aberrations) and MN (micronuclei) in human blood lymphocytes in vivo. Our earlier observation on sister-chromatid exchanges (SCE) of peripheral blood lymphocytes from this same population showed that the mean SCEs/cell of the workers was significantly higher than that of the controls (p < 0.01). The results of our studies imply that even if the concentration of the chemical pollutants in the air is low (e.g. F 0.50-0.80 mg/m 3), it may cause damage to genetic material at the chromosomal level… it is suggested that chromosomal abnormalities induced by fluoride could be the results from interaction with the enzymes responsible for DNA synthesis or repair, rather than directly with

DNA.”[2]

Mutagenic Agent: Wu (1950 “The results in this paper showed an obvious increase in the SCE frequency of the patients with fluorosis, indicating that fluorine had some mutagenic effects, and could give rise to DNA damage. The fact that the SCE frequency of the healthy people in the endemic regions was also higher than that of the controls in the non-endemic regions suggests that early harm by fluorine can be cytogenetically detected in the sub-clinical patients with fluorosis who could not be given an early diagnosis clinically. Under normal circumstances, the incidence rate of micronucleus is very low, usually 0-2%. The normal value checked in this paper is 0-2%, which agrees with that reported in the literature. The results show that the mean value of the micronucleus rate of the fluorine-toxic patients was 1.94 + 0.86% (range 1-15%) which is 2-3 times more than that of 0.57 + 0.44% in the controls… To sum up, the rise of SCE and MN in the peripheral blood lymphocytes of the fluorine-intoxicated patients indicates that fluorine is a mutagenic agent which can cause DNA and chromosomal damage.”[3]

Meng (1995) “Our study here provided evidence that the air pollutants at the phosphate fertilizer factory, of which HF and SiF4 are the main chemicals, could induce SCEs in human blood lymphocytes in vivo. These results imply that even if the concentration of the chemical pollutants in the air is low (e.g.F: 0.50 – 0.80 mg/m3), it may cause damage to genetic material at the chromosomal level, although the general health of the workers in the phosphate fertilizer factory was found to be satisfactory.”[4]

Chromosome Aberrations: Sheth (1994)“A number of investigators have utilized the SCE

(Sister Chromatid Exchange) test to study the genotoxicity of fluoride. In the present study, human populations directly exposed to fluoride in drinking water in endemic regions of North Gujarat were investigated to evaluate the possible effect of fluoride on SCE. To the best of our knowledge this is the first report on genotoxic effects following long-term fluoride intake in an endemic area in India… The results of the present investigation suggest that in fluoride-affected persons exposed to 1.95 – 2.2 ppm fluoride in drinking water chromosomal alterations as indicated by SCE frequency and chromosome aberrations were higher than in normal persons exposed to 0.6 – 1.0 ppm drinking water fluoride.”[5]

 DNA Damage and Fluorosis: Li (1991)“With peripheral blood lymphocyte culture, a study of SCE and micronuclei test was done in 24 patients with fluorosis and same number of normal people as control. The results obtained showed that in the patient group the mean value of SCE per cell and the frequency of micronuclei were 10.24±1.67 and 1.42‰ ,respectively, while in the control only 7.62 ± 0.80 and 0.33‰, respectively, were found. And both of the two respective parameters, statistically, were in significant difference. These findings suggested that excess fluorine would cause increases of SCE frequency and micronuclear number in lymphocyte and make DNA damaged.”[6]

SCE Rate Induced: Velazquez-Guadarrama (2005): “The results concerning the SCE rate

induced by sodium fluoride are shown in Table 1. Although no significant increase was observed with the two low doses tested (from 2 to 4 mg/kg), a significant SCE increase was found with the three highest doses. The cumulative frequency of these data reveals about 70% of cells with four SCE in the group treated with the high dose, a value which is twice the level of the negative control.”[7]

Chromosome Damage: Mohamed (1982)“Cytological studies on bone marrow cell chromosomes and spermatocytes showed that 1-200 ppm F (as sodium fluoride) was able to induce chromosomal changes in a dose-dependent manner. The frequency of the induced chromosomal damage was significantly higher in each treatment than in the controls. The observed abnormalities included translocations, dicentrics, ring chromosomes, and bridges plus fragments, or fragments by themselves. There was a significant correlation between the amount of fluoride in the body ash and the frequency of the chromosomal abnormalities.”[8]

Chromosomal aberrations: Gileva (1975)“Cryolite concentrations of 3 mg/m3 as well as a mixture of 0.5 mg/m3 of cryolite and 0.35 mg/m3 of hydrogen fluoride increases 3 1/2 to 4 1/2 times (over controls) the percentage of cells with chromosomal aberrations in the bone marrow of rats. The data indicate the need for further study of the mutagenic features of fluoride compounds in relation to their potential for harmful impact on the mechanism of inheritance in humans.”[9]

Mutagen: Voroshilin (1975) “The mutagenic effect of hydrogen fluoride in concentration 1.0 mg/ m-3 was studied in rats and mice. Prolonged inhalation of this compound increased the frequency of cells with chromosome abnormalities in the bone marrow of albino rats. The mutagenic effect was higher in older animals.”[10]

Acceleration of tumor tissue growth: Taylor (1965) “In 54 tests involving 991 mice bearing transplanted tumors and 58 tests including 1817 tumor-bearing eggs, data were obtained which indicated a statistically significant acceleration of tumor tissue growth in association with comparatively low levels of NaF.”[11]

NTP 1990:   Dose-Dependent increase in Osteosarcoma: NTP (1990)               In

1977, the U.S. Congress requested that animal studies regarding the potential of a fluoride/cancer connection.  NTP and published the study in 1990.

The main finding of NTP’s 1990 study was a dose-dependent increase in osteosarcoma (bone cancer) among the fluoride-treated male rats. However, despite the fact that 1) the cancer occurred in the target organ (bone) for fluoride accumulation, that 2) the increase in bone cancer was statistically-significant, that 3) the doses of fluoride were low for an animal cancer study, and that 4) NTP acknowledged it is “biologically plausible” that fluoride could induce bone cancer, the NTP ruled that the study only provided “equivocal evidence” that fluoride was the cause of the cancer.

          According to a report in Chemical & Engineering News: “A number of government

officials who asked not to be identified also have told C&EN that they have concerns about the conclusions of the NTP study. They, too, believe that fluoride should have been placed in the “some evidence” category, in part because osteosarcoma is a very rare form of cancer in rodents.”

In addition to increased bone cancer, the NTP study also found increases in rare liver cancers, oral...NTP ruled, however, that the cancers were not related to the fluoride treatment despite reaching “statistical significance” in some of NTP’s analyses.

[1] Joseph S, Gadhia PK. (2000). Sister chromatid exchange frequency and chromosome aberrations in residents of fluoride endemic regions of South Gujarat. Fluoride 33(4):154-158.

[2] Meng Z, Zhang B. (1997). Chromosomal aberrations and micronuclei in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research 393: 283-288.

[3] Wu DQ, Wu Y. (1995). Micronucleus and Sister Chromatid Exchange Frequency in Endemic Fluorosis. Fluoride 28(3):125-127.

[4] Meng Z, et al. (1995). Sister-chromatid exchanges in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research 334(2):243-6.

[5] Sheth FJ, et al. (1994). Sister chromatid exchanges: A study in fluorotic individuals of North Gujurat. Fluoride 27: 215-219.

[6] Li J, et al. (1991). The influence of high-fluorine on DNA stability in the human body. Chinese Journal of Endemiology.  [Article in

Chinese]

[7] Velazquez-Guadarrama N, Madrigal-Bujaidar E, Molina D, Chamorro G. (2005). Genotoxic evaluation of sodium fluoride and sodium perborate in mouse bone marrow cells. Bulletin of Environmental Contamination and Toxicology 74(3):566-72.

[8] Mohamed AH, Chandler ME. (1982). Cytological effects of sodium fluoride on mice. Fluoride 15(3):110-18.

[9] Gileva EA, et al. (1975). The mutagenic activity of inorganic fluorine compounds. Fluoride 8(1):47-50. [Originally published in Russian; condensed from Gig. Sanit., 37(1):9-12, Jan. 1972.]

[10] Voroshilin SI, et al. (1975). Mutagenic effect of hydrogen fluoride on animals. Tsitol Genet. 9(1): 42-44.

[11] Taylor A, Taylor NC. (1965). Effect of sodium fluoride on tumor growth. Proceedings of the Society for Experimental Biology and Medicine 119:252-255.

[BillO538145]

Procter and Gamble:

Procter & Gamble, releases the findings of its own rat study of fluoride and cancer they conducted between 1981-1983.  While Procter and Gamble’s study finds several bone tumors in the fluoride-treated animals (versus none in the controls), the results do not achieve statistical significance and Proctor & Gamble’s scientists dismiss them as random. According to the published report:

“All bone neoplasms were considered to be incidental and spontaneous and not related to fluoride treatment, because of their low incidence and random distribution”[10]

In 1991, the FDA publishes a review of Procter & Gamble’s rat study. The FDA identifies two additional osteosarcomas in the fluoride-treated rats which were not identified in Procter & Gamble’s published report. The FDA states:

“The adequacy of the gross examination at necropsy was questioned based upon the rat tumors that were not identified by the contract (Procter & Gamble) laboratory” (FDA 1991).

The FDA notes that the incidence of bone tumors in the Procter & Gamble study still do not achieve statistical significance. The FDA thereby concurs with Procter & Gamble that the bone tumors are incidental.

Contributes to Osteomas: Maurer 1993, the FDA also reviews Procter & Gamble’s mouse study.  Among both sexes of the fluoride-treated mice, there is a significant, dosedependent increase in osteomas, although no osteosarcomas. The occurrence of the osteomas is believed to be related to the presence of a virus in the mice; however, the FDA finds:

“Active virus was found in the osteomas but not in animals that did not have osteomas. It is clear, nonetheless, that if [the virus] had a role it was only in the presence of fluoride.”

Known Osteosarcoma Association: Cohn 1992.  The New Jersey Department of

Health conducts a study of osteosarcoma occurrence in Central New Jersey,  “An Epidemiologic Report on Drinking Water and Fluoridation.” The study finds a statistically significant relationship between fluoridation and osteosarcoma among males less than 20 years old: 

“Recently, a national study of drinking water fluoridation at the country level found a significant association with osteosarcoma incidence among males under 20 years of age (Hoover et al., 1991). However, the meaning of the association was questioned by the authors because of the absence of a linear trend of association with the duration of time for which the water supplies were fluoridated… As a follow-up to the study by Hoover et al., a small study of similar design was initiated by the New Jersey Department of Health to compare drinking water fluoridation at the municipal level with the municipal residence of osteosarcoma cases at the time of diagnosis… The study observed an association between fluoridation of water and osteosarcomas among males under 20 years of age in seven Central New Jersey counties.”

Known Carcinogenic: Lee[1] 1993 Reported 6.9 times higher osteosarcoma incidence for males aged 10-19 years old when comparing fluoridated and non-fluoridated seven counties in the central New Jersey area.

Known Carcinogenic: Yiamouyiannis, 1993, analyzes the National Cancer Institute’s data in addition to two other databases containing fluoride exposure/ osteosarcoma information. Like NCI’s investigators (Hoover 1991), Yiamouyiannis finds osteosarcoma rates to be higher among young males under 20 in fluoridated versus unfluoridated areas. To quote:

“Recent studies showing substantial increases in the incidence of bone cancer and osteosarcoma in males (but not females) exposed to fluoride gave us the unique opportunity of using females as a control group to determine whether there is a link between fluoridation and bone cancer in males. Using three different data bases, we found that 

• the bone cancer incidence rate was as much as 0.95 cases a year per 100,000 population higher in males under age 20 living in fluoridated areas;
• the osteosarcoma incidence rate was 0.85 new cases a year per 100,000 population higher in males under age 20 living in fluoridated areas; and
• for males of all ages, the bone cancer death rate and bone cancer incidence rate was as much as 0.23 and 0.44 cases higher per 100,000 population, respectively, in fluoridated areas. These findings indicate that fluoridation is linked to an increase in bone cancer and deaths from bone cancer in human populations among males under age 20 and that this increase in bone cancer is probably all due to an increase in osteosarcoma caused by fluoride.”

Genotoxic Mihashi 1996 report fluoride is genotoxic to rat bone. The authors note that the fluoride-induced genotoxicity in bone reinforce the biologic plausibility of a fluorideosteosarcoma connection. The authors used the same type of rat (F344/N) used in NTP’s cancer bioassay.

“Because the origin of osteosarcoma is considered to be osteoblastic/osteogenic cells, the ability of sodium fluoride to induce chromosome aberrations in these cells provides a mechanistic basis for the occurrence of osteosarcomas observed in sodium fluoride treated animals in the NTP study. Ingested fluoride is accumulated in bone, suggesting that osteoblastic/osteogenic cells in the bone microenvironment can be exposed to high levels of fluoride during bone formation. Our data and the NTP findings provide evidence that bone can be an organ for NaF carcinogenesis.”[2]

Gandhi (2017)[3] “Oxidative stress is reported to negatively affect osteoblast cells. Present study reports oxidative and inflammatory signatures in fluoride-exposed human osteosarcoma (HOS) cells, and their possible association with the genes involved in osteoblastic differentiation and bone development pathways. HOS cells were challenged with sublethal concentration (8 mg/L) of sodium fluoride for 30 days and analyzed for transcriptomic expression. In total, 2632 transcripts associated with several biological processes were found to be differentially expressed. Specifically, genes involved in oxidative stress, inflammation, osteoblastic differentiation, and bone development pathways were found to be significantly altered. Variation in expression of key genes involved in the abovementioned pathways was validated through qPCR. Expression of serum amyloid A1 protein, a key regulator of stress and inflammatory pathways, was validated through western blot analysis. This study provides evidence that chronic oxidative and inflammatory stress may be associated with the fluoride-induced impediment in osteoblast differentiation and bone development.” 

 Note: Although the 8 mg/L Gandhi used is sublethal, it is much higher than blood concentrations but not out of range for bone fluoride concentrations which can reach higher, over 800 ppm.   Gandhi (2017) appears to dovetail with Wei (2014) below.

Wei (2014)[4] Chronic excessive fluoride intake may cause fluorosis, which chiefly manifests as bone damage (or skeletal fluorosis). However, the molecular mechanism of skeletal fluorosis has not been clarified up to the present. The objective of this study was to analyze the effects of fluoride treatment on two of bone morphogenetic protein family member (BMP-2 and BMP-3) expression and cell viability using human osteosarcoma MG-63 cells as a model. Sodium fluoride (NaF) had pro-proliferation effects at relatively moderate concentration, with 5 × 10(3) μmol/L having the best effects. At 2 × 10(4) μmol/L, NaF inhibits cell proliferation. BMP-2 and BMP-3 expression was significantly induced by 5 × 10(3) μmol/L NaF and, to lesser extent, by 2 × 10(4) μmol/L NaF. Correspondingly, mothers against decapentaplegic homolog 1 (Smad-1) increased at both doses of NaF, which indicated the BMP signaling pathway was activated. Notable increases in secreted alkaline phosphatase (ALP) were observed when cells were treated with 5 × 10(3) μmol/L NaF. A BMP specific inhibitor LDN193189 suppressed cell proliferation induced by 5 × 10(3) μmol/L NaF. Also, 2 × 10(4) μmol/L NaF induced apoptosis but likely through a mechanism unrelated to the BMP pathway. Collectively, data show that NaF had dose-dependent effects on cell proliferation as well as BMP-2 and BMP-3 expression in MG-63 cells and suggested that cell proliferation enhanced by NaF-induced BMP members may be a molecular mechanism underlying skeletal fluorosis.

Note: Wei (2014) reported specific effects at 5 × 10(3) μmol/L NaF, which is 9.5 mg/L (ppm), close to Gandhi’s 8 ppm.  

Sandhu (2011)[5] “The present study was planned to analyze serum fluoride, sialic acid, calcium, phosphorus, and alkaline phosphatase levels in 25 patients of osteosarcoma and age- and sex-matched subjects with bone-forming tumours other than osteosarcoma and musculo-skeletal pain (controls, 25 each). . . Mean serum fluoride concentration was found to be significantly higher in patients with osteosarcoma as compared to the other two groups. The mean value of flouride in patients with other bone-forming tumors was approximately 50% of the group of osteosarcoma; however, it was significantly higher when compared with patients of group I. Serum sialic acid concentration was found to be significantly raised in patients with osteosarcoma as well as in the group with other bone-forming tumors as compared to the group of controls. There was, however, no significant difference in the group of patients of osteosarcoma when compared with group of patients with other bone-forming tumors. These results showing higher level of fluoride with osteosarcoma compared to others suggesting a role of fluoride in the disease.”

Huo (2013)[6] [Saos-2 cells are osteosarcoma cells] “We found that fluoride enhanced the proliferation of Saos-2 cells in a dose-dependent manner and 0.2 mM of fluoride resulted in a higher expression of osteoblast marker genes. In addition, immunofluorescence analysis showed that the promotion effects of 0.2 mM of fluoride on Saos-2 cells differentiation were associated with the activation of the BMP/Smad pathway.”

Huo (2013) Figure 1. “Growth curve of fluoride-treated Saos-2 cells. Saos-2 cells were seeded into 96-well plates and cultured with different concentrations of NaF for 24, 48, and 72 h as indicated in the “Materials and Methods.” The WST assay was performed to quantify the cytotoxicity of fluoride to Saos-2 cells. Asterisk indicate the significant differences.”

Huo (2013) Fig. 3

Content of Smad1 and p-Smad1/5 protein in fluoride-treated Saos-2 cells. Laser scanning confocal microscopy was used to detect expression of Smad1 and p-Smad1/5 proteins after exposure to NaF (200×). a, c Control (0 mM NaF) and b, d 0.2 mM NaF groups; a, b Smad1 and c, d p-Smad1/5. Three wells were assayed for each experimental treatment, and three separate experiments were performed

Note:  For comparison, 0.2 mM x 1,000 μmol/mM = 200 μmol X o.oo19 μmol/L NaF = 0.38 mg/L (ppm) sodium fluoride.

[1] Lee JR Fluoridation and Bone Cancer, Fluoride, Vol.26. No.2 1993   Accessed 4/25/2015 http://www.fluorideresearch.org/262/files/ FJ1993_v26_n2_p079-164.pdf

[2] (Mihashi M, Tsutsui T. (1996). Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture. Mutation Research 368(1):7-13. May.)

[3] Gandhi D, Naoghare PK, Bafana A, Kannan K, Sivanesan S .Biol Trace Elem Res. Fluoride-Induced Oxidative and Inflammatory Stress in Osteosarcoma Cells: Does It Affect Bone Development Pathway?  2017 Jan;175(1):103-111. doi: 10.1007/s12011-016-0756-6. Epub 2016 May 28.

[4] Wei Y1, Wu Y, Zeng B, Zhang H.  Effects of sodium fluoride treatment in vitro on cell proliferation, BMP-2 and BMP-3 expression in human osteosarcoma MG-63 cells. Biol Trace Elem Res. 2014 Dec;162(1-3):18-25. doi: 10.1007/s12011-014-0148-8. Epub 2014 Oct 14.

[5] Sandhu R1, Lal H, Kundu ZS, Kharb S.  Serum fluoride and sialic acid levels in osteosarcoma. Biol Trace Elem Res. 2011 Dec;144(1-3):1-5. doi: 10.1007/s12011-009-8382-1. Epub 2009 Apr 24.

[6] Huo L1, Liu K, Pei J, Yang Y, Ye Y, Liu Y, Sun J, Han H, Xu W, Gao Y. Fluoride promotes viability and differentiation of osteoblast-like Saos-2 cells via BMP/Smads signaling pathway. Biol Trace Elem Res. 2013 Oct;155(1):142-9. doi: 10.1007/s12011-013-9770-0. Epub 2013 Aug 7.

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1. Concerns with NTP Review of Carcinogenicity of Fluoride

Despite criticism, the NTP maintains their assessment of “equivocal evidence.” In 1991, NTP scientists publish a paper which concludes:

“The current findings are weakly supportive of an association between sodium fluoride administration and the occurrence of osteosarcomas in male rats, but are not conclusive… [I]n view of the widespread exposure of the population to fluorides from a variety of sources it would appear prudent to re-examine previous animal and human epidemiologic studies, and perform further studies as needed to evaluate more fully any possible association between exposure to fluorides and the occurrence of osteosarcomas of bone.”[1]       

            NTP review comments on page 10, include:

1. “Dr. Ashby, the second principal reviewer, agreed with the conclusions. However, he considered the definition for equivocal evidence of carcinogenic activity to be insufficiently precise for male rates. . . .” He suggested: “Taken together the current findings are inconclusive, but are weakly supportive of an association between sodium fluoride administration and the occurrence of osteosarcomas in male rats.”
2. Silbergeld, “pointed out that the doses used were not orders of magnitude above human exposure levels. She supported further research on genotoxicity and on mechanisms of sex differences seen.”
3. Gold noted that this was an unusual study in that there was not a zero control group.”
4. “There was discussion by Dr. McKnight with Dr. J. Haseman, NIEHS, as to why data from paired (age-matched) controls were not used in primary data tables.
5. Zeise “reiterated the need expressed by other Panel members for designing another study with higher top doses. Dr. Zeise noted that the fluoride concentrations in high-dose rats were within the range observed in humans and the differences in pharmacokinetics and deposition of fluoride in bone between humans and animals should be studied.”
6. Yiamouyiannis said, “a dose-dependent relationship between fluoride and the number of male rats with oral squamous cell tumors and a dose-dependent relationship between oral squamous cell metaplasia dn tumors in female rats along with the increased incidence of osteosarcomas in male rats supported a finding of clear evidence of carcinogenic activity of fluoride in rats.”
7. Those representing dentists and industry objected to the conclusions.

When fluoride damages DNA, is the damaged DNA make the offspring more

susceptible to cancer?   With the current research, objection to the NTP study should also be made to the lack of a “life-time” exposure from preconception with parents, throughout life of the offspring.   Starting the rats and mice at 5 and 4 weeks of age in the NTP study, did not demonstrate the effects of the fluoride on sperm, egg, fetus, and during a major growth period of their early lives. 

Downgrading by NTP of non-bone tumors (liver, oral, and thyroid) found with increased incidence among the fluoride-treated animals is controversial.  

Concerns with NTP study:  The journal Chemical & Engineering News reports:

“A number of other government officials who asked not to be identified also have told C&EN that they have concerns about the conclusions of the NTP study. They, too, believe that fluoride should have been placed in the “some evidence” category, in part because osteosarcoma is a very rare form of cancer in rodents.”

Cancer diagnosis upheld:    Battelle’s diagnosis of hepatocholangiocarcinoma was upheld by the scientist (Dr. Melvin Reuber) who first identified hepatocholangiocarcinoma as a distinct cancer. As noted by EPA toxicologist Dr. William Marcus:

“Melvin Reuber, M.D., a board certified pathologist and former consultant to EPA and part time EPA employee, reviewed some of [the] pathology slides and the Batelle report. . . . [Reuber] first published the work that identified hepatochangiocarcinoma as a pathologic entity. . . . Dr. Reuber reviewed the pathology slides and stated that these lesions are indeed hepatocholangiocarcinoma.”[2]

Despite Reuber’s concurrence, the NTP ultimately downgraded the hepatocholangiocarcinoma finding. The NTP did so through a two-step process. First, NTP’s “Quality Assurance” pathogist reclassified them as hepatoblastomas (another form of liver cancer). Then, while conducting their statistical analysis, NTP reclassified the hepatoblastomas as hepatocarcinomas – a more common form of tumor. Because there was no significant increase in hepatocarcinomas among the fluoride-treated animals, the NTP concluded that there was no effect.

            The NTP has issued the following statements about this analysis:

“During the pathology review procedures several of the tumors diagnosed originally as hepatocholangiocarcinomas were considered more apppropriately callled hepatoblastomas.”[3]

“The study pathologist (Battelle) diagnosed hepatocholangiocarcinomas in one special control female, one low dose male, one low dose female, one medium dose male, three high dose males, and three high dose females. The QA (Quality Assurance) pathologist confirmed the presence of these tumors but felt that most of them were more appropriately diagnosed as hepatoblastomas.”[4]

“The incidences of liver neoplasms in all groups of dosed and control male and female mice were higher than incidences previously seen in NTP studies, but did not appear related to chemical treatment. Several hepatoblastomas and hepatocholangiocarcinomas were diagnosed in male and female mice. Hepatoblastoma and hepatocholangiocarcinoma of mice are phenotypic variants of hepatocellular carcinoma with characteristic cell types and morphologic patterns. The hepatoblastomas contained a cell population which resembled embryonal liver cells as well as neoplastic cells characteristic of a typical hepatocellular carcinoma, whereas the hepatocholangiocarcinomas exhibited both hepatocyte and biliary differentiation. As phenotypic variants of hepatocellular carcinoma, the incidences of these neoplasms were combined with the other hepatocellular neoplasms for analysis. The appearance of these phenotypic variants in dosed animals is unusual, and the biologic significance, if any, is unknown.”[5]

Summary of NTP study by LANCET:

“The original study was directed from 1985 to 1987 by Dr John D. Toft II, manager of the pathology section at Battelle Memorial Institute in Columbus, Ohio. The Battelle study’s principal finding was the occurrence of an extremely rare liver cancer, hepatocholangiocarcinoma, in male and female mice. In 1989, the NTP asked Experimental Pathology Laboratories, of Sterling, Virginia, to review Battelle’s data. At this point, the liver cancer finding, along with a diagnosis of metaplastic and precancerous cells in the mouths of rats, was downgraded.

The only effect of fluoride that was left after these reclassifications and still another review by a board of pathologists and others was osteosarcoma. Dr Marcus believes the Battelle diagnosis of liver cancers was sound and should have been included in the NTP report. This, he says, would change “the (NTP) equivocal finding… to at least some evidence or clear evidence of carcinogenicity”.

NTP’s failure to emphasize another finding also figured in Dr Marcus’ critique. Three out of four in-vitro tests, he says, proved fluoride to be mutagenic, “supporting the conclusion that fluoride is a probable human carcinogen”. A careful reader can find this information in the text of the report, but the authors make no mention of these data in their conclusions.”[6]

Summary of NTP study by C&E News: 

“The final report for the study was prepared by the NTP staff, but the testing itself was done by Battelle Columbus Laboratories under contract to NTP. A report prepared by Battelle was audited by a quality assurance contractor, and a separate group of pathologists reviewed the studies. In the process, a number of positive findings in the original Battelle report were downgraded. Slides first diagnosed as showing a rare form of liver cancer called hepatochlolangiocarcinoma were later said to indicate hepatoblastoma, another type of rare malignant lesion, and finally to show the far more common cancer hepatocarcinoma. These hepatocarcinomas were combined with the other hepatocarcinomas found in both treated and control animals, Marcus said. In addition, dose-dependent oral lesions noted in the Battelle report were downgraded from dysplasia and metaplasia to degeneration. Some other liver carcinomas were eventually reclassified as nonmalignant lesions. Because of what he calls systematic downgrading of the slides, Marcus has written a memo to the director of the criteria and standards division in the office of drinking water asking that EPA assemble an independent board of pathologists to review the slides again.[7]

Summary of NTP by Yiamouyiannis: 

“In 1977, Congress instructed the U.S. Public Health Service to conduct animal studies to determine whether or not fluoride causes cancer. As a result, the National Toxicology Program retained the Battelle Memorial Institute in Columbus, Ohio to perform two studies, one on mice, and another on rats.

Doctor John T. Toft, II, manager of the Pathology Section at Battelle, was placed in charge of the NTP mouse study. On October 28, 1988, after a year of analyzing these results, Doctor Toft completed the pathology narrative and final report.

The most significant finding was the occurrence of an extremely rare form of liver cancer, hepatocholangiocarcinoma in fluoride-treated male and female rats — mice, excuse me.

Among male mice, no such cancers were observed among 79 in the control group. At 11 parts per million, the lowest dose used, one was observed among 50 male mice; and 45 parts per million, one was observed among 51 male mice and at seventy-nine parts per million three were observed among 80 male mice.

Using historical controls and doing a binomial analysis of this, the odds of these results occurring by chance are less than one in two million. Normally, we consider it significant one in twenty; this is one in two million.

Making these findings even more convincing are the results with female mice. In the control group, no hepatocholangiocarcinomas were observed among eighty. At 11 parts per million, one was observed among 52. At 45 (ppm), none were observed among 50. And at 79 parts per million, three were observed among 80 female mice — female mice.

Based on these findings, and these findings alone, there was clear evidence of the carcinogenic activity of the fluoride in mice receiving 11, 45, or 79 parts per million in drinking water for two years or less.”[8]

PHS confirms risk:    The Public Health Service and NCI in 1991 report that the incidence of osteosarcoma throughout the U.S. has increased at a greater rate among young males in fluoridated areas vs. unfluoridated areas. The NCI, however, dismisses this result because of an inability to demonstrate a linear-dose relationship between the duration of fluoridation and the increased osteosarcoma incidence in fluoridated areas:

“In summary, analysis of incidence data from the SEER program has revealed some age- and sexspecific increases over time for bone and joint cancers, and for osteosarcomas, which are more prominent in fluoridated than in non-fluoridated areas. However, on further analysis these increases are unrelated to the timing of fluoridation, and thus are not linked to the fluoridation of water supplies.” (Hoover 1991)

Calabrese[9] 1993 was requested by the East Bay Municipal Utility District to conduct an independent appraisal of the 1990 NTP report.  He found the NTP’s choice of the word “equivocal” to be confusing, inappropriate and not consistent with what most people would call equivocal, for the following reasons:

1. Its own definition of equivocal is in disagreement with the generally accepted definition of equivocal.
2. The findings with the male rat clearly exceeded marginal increases and are biologically plausible given the capacity for fluoride to both concentrate and be biologically active in bone.
3. The statistical analysis for trend effects is stronger than pair-wise comparisons since it uses all available data not just data from two comparison groups, yet this point is never acknowledged.
4. The basic reality is that humans can be exposed in critical target tissues to as much fluoride as the high dose rats while consuming water at the EPA maximum contaminant level of 4 mg/liter.

[1] Bucher JR, et al. (1991). Results and conclusions of the National Toxicology Program’s rodent carcinogenicity studies with sodium fluoride. International Journal of Cancer 48(5):733-7. July 9.

[2] Marcus W. (1990). Memorandum from Dr. William Marcus,to Alan B. Hais, Acting Director Criteria & Standards Division Of... of Drinking Water, US EPA. May 1, 1990.

[3] Bucher J. (1990). Testimony at Board of Scientific Counselors, National Toxicology Program; Peer Review of Draft Techn... Report of Long-Term Toxicology and Carcinogenesis Studies and Toxicity Study, Sodium Fluoride; Research Triangle Park, North Carolina, Thursday, April 26, 1990.

[4] Hamilton BF. (1989). Carcinogenesis bioassay of sodium fluoride with dosed water in B6C3F1 mice: Quality Assessment Narrative. Experimental Pathology Laboratories, Inc. p. 26-27.

[5] Bucher JR, et al. (1991). Results and conclusions of the National Toxicology Program’s rodent carcinogenicity studies with sodium fluoride. International Journal of Cancer 48: 733-737.

[6] Sibbison JB. (1990). USA: More About Fluoride. The Lancet 336(8717): 737. Sept 22.

[7] Hileman B. (1990). Fluoride bioassay study under scrutiny. Chemical & Engineering News September 17

[8] Yiamouyiannis J. (1990). Testimony before Board of Scientific Counselors, National Toxicology Program; Peer Review of Draft Technical Report of Long-Term Toxicology and Carcinogenesis Studies and Toxicity Study, Sodium Fluor...; Research Triangle Park, North Carolina, Thursday, April 26, 1990.

[9] Calabrese, EJ, Lee, JR, Evaluation of the National Toxicology Program (NTP) Cancer Bioassay on Sodium Fluoride, Fluoride 26

(1) 1993  Accessed 4/25/15 http://www.fluorideresearch.org/261/files/FJ1993_v26_n1_p001-078.pdf

[10] Maurer JK, et al. 1990. Two-year carcinogenicity study of sodium fluoride in rats. Journal of the National Cancer Institute 82(13): 1118-26. July 4.

[BillO538145]

THE DOSE OF FLUORIDE USED BY NTP 2006:

“the level of fluoride the low- and mid-dose animals had in their drinking water was within an order of magnitude of what humans are exposed to when drinking water containing the EPA-established maximum level of 4 ppm fluoride. This is almost unheard of in animal bioassays. Usually, animal exposure is four to six orders of magnitude more than what humans receive.”[1]

“it is important to note that the dose range is not, as is sometimes the case, orders of magnitude higher than that encountered in human population, nor is the body burden expressed as concentrations in bone orders of magnitude higher than that found in human populations also ingesting fluoride.”[2]

“the difference between the animal study and the human exposures is not nearly as great as typical with synthetic chemicals.”[3]

“I think it’s important to realize that even though the water concentrations were higher than what we see, or what humans are exposed to, the bone concentrations were not.”[4]

“a small number of osteosarcomas occurred in mid- and high-dose male rats. These neoplasms occurred with a significant dose response trend, but at a rate wtihin the upper range of incidences previously seen in control male rats in NTP studies. Three of the tumors arose in the vertebra, a site not commonly associated with chemically induced osteosarcomas. Bone is known to accumulate fluoride, and fluoride has been shown to be genotoxic to some mammalian cells in culture. No osteosarcomas were seen in female rats, and several osteosarcomas seen in mice occurred with an incidence that did not suggest a relationship with sodium fluoride exposure.Taken together, the current findings are inconclusive, but are weakly supportive of an association between sodium fluoride administration and the occurrence of osteosarcomas in male rats.”90

20 Large City Comparison:  Burk91 1977, head of cytochemistry section of the USA National Cancer Institute, reported year-by-year average observed cancer death rates of ten large central cities of the United States, which served as the control group and remained un-fluoridated from 1940 through 1968.  These were compared for the years 1940 through 1968 with the year-by-year average observed cancer death rates of ten large central cities of the United States which served as the experimental group and remained unfluoridated from 1940 through 1951, but fluoridated between 1952 and 1956, and remained fluoridated through 1968 and thereafter.92‑    The experiment came to an end in 1968 because fluoridation was introduced in the control cities step-by-step from and after 1969.  The necessary data are available for all years except for 1951 and 1952.  Seven million in ten control cities and eleven million in ten experimental cities over about thirty years.   Cancer rates in the fluoridated cities (CDRo(+F) clearly increased faster compared to the non fluoridated cities at a rate of 31.3 excess cancer deaths per 100,000 persons.

                                1940               1950               1950               1970

     CDRo(+F)                  154.2               181.8             186.3               222.6

     CDRo(- F)                  153.5               181.3              l83.6              188.8   

USPHS responded in defense of their policy that Burk had not adjusted for age, race or sex.  PHS was suspicious the subject cities had all aged faster.  However, Burk had adjusted for demographic variables and he testified to the fact to Congress and to the courts of law.  In response Arthur Upton provided the “Upton Statement” in a 17 page

• National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health ...search Triangle Park, N.C. 71-73.
• . most important versions of the epidemiological data here in question, including reference to related laboratory studies, and conventional adjustments for age, race, and sex, are the following: Dean Burk & John Yiamouyiannis, Fluoridation and Cancer: Age Dependence of Cancer Mortality Related to Artificial Fluoridation, 10 FLUORIDE 123 (1977) [hereinafter Burk & Yiamouyiannis];

Dean Burk and J. R. Graham, Lord Jauncey and Justice Flaherty: Opposing Views of the Fluoridation-Cancer Link, 17 FLUORIDE 63

(1984) [hereinafter Burk & Graham]; Pierre Morin et al., Les fluorures versus le cancer et les maladies congentales: l’image globale,

GOURVERNEMENT DU QUEBEC, MINISTERE DES AFFAIRES SOCIALES (The 1984); Pierre Morin et al., Fluorides, Water Fluoridation,

Cancer, and Genetic Diseases, 12 SCI. & PUB. POL’Y 36 (1985); Rudolf Ziegelbecker, Zur Frage eines Zusammenhanges zwischen

Trinkwasserfluordierung, Krebs, und Leberzirrhose, 218 GWF WASSER/ABWASSER 111 (1987); Dean Burk et al., A Current Restatement and Continuing Reappraisal Concerning Demographic Variables in American Time-Trend Studies on Water Fluoridation and Human Cancer, 61 PROC. PA. ACAD. OF SCI. 138 (1988) [hereinafter Burk, Graham, & Morin].

92

.  See Burk & Yiamouyiannis, supra note 108, at 104; Burk, Graham, & Morin, supra note 108, at 138.

document.[5]  Upton set for an adjustment in weighted averages, suggesting cancer mortality actually grew 1% faster in the unfluoridated cities.  

1950                     1970                  Change

CDRo/CDRe  (+F)             1.23                      1.24                     +.0l

CDRo/CDRe  (-F)              1.15                      1.l7                      +.02

Cities	1940	1950	1960	1970
CDRo (+F)	154.2	181.8	186.3	222.6
CDRe (+F)	128.1	146.9	146.9	174.7
CDRo/CDRe (+F)	1.204	1.238	1.268	1.274
CDRo-CDRe (+F)	26.1	34.9	39.4	47.9

Burk and Yiamouyiannis[6]  demonstrated Upton’s flaw.  Upton had simply used 1950 with 1970 and failed to also consider data reported in-between those two points, and before and after the two points.  

CDRo (-F)	153.5	181.3	183.6	188.8
CDRe (-F)	140.3	155.5	155.5	166.0
CDRo/CDRe (-F)	1.094	1.166	1.181	1.137
CDRo-CDRe (-F)	13.2	25.8	28.1	22.8

The change in CDRo/CDRe = [(1.274-1.137) – (1.268-1.181)] + [(1.204-1.094) – (1.238-1.166)] = +.088.  This coefficient means that, relative to what might be expected in light of the demographic structure of the two populations here in question, adjusted cancer mortality grew about 9% faster in the fluoridated cities.

In terms of CDRo-CDRe, fluoridation is associated with [(47.9-22.8) – (39.4-28.1)] + [(26.1-13.2) – (34.9-25.8)] = 17.6 excess cancer deaths per 100,000 persons exposed after 15-20 years.  

Burk and Yiamouyiannis reported 17.6 additional cancer deaths per 100,000. 

Apparently Black males have a higher cancer rate than White males.  Returning to Burk’s data and correcting for race might show a further increase.  

[1] Hileman B. (1990). Fluoride bioassay study under scrutiny. Chemical & Engineering News September 17.

[2] Silbergeld E. (1990). Peer Review of Draft Technical Report of Long-Term Toxicology and Carcinogenesis Studies and Toxicit... Study, Sodium Fluoride; Research Triangle Park, North Carolina, Thursday, April 26, 1990. p. 62-63.

[3] Gold  IBID p. 71.

[4] Zeise L. IBID . p. 79.

[5] National Cancer Program (Part 2), Hearings Before the Subcomm. of the Comm. on Government Operations, 95th Cong. 471 (1977) [hereinafter National Cancer Program].

[6] Dr. John Yiamouyiannis executed an adjustment of the basic data, using weighted averages and US-1950 as the standard population, exactly as stipulated in the Upton Statement.  He adjusted only for the years after 1950, deriving CDRo values for 1950 and 1970, by linear regression analysis of the CDRo data for 1950 and 1953-1969, and showed an association in terms of CDRo/CDRe = +.042, and in terms of CDRo-CDRe = 12.4 cancer deaths per 100,00 persons exposed within after fifteen to twenty years after the introduction of fluoridation in the experimental cities.  See National Cancer Program, supra note 109, at 64-65.  The main objection to this technique came from Dr. David Newell of the Royal Statistical Society in defense of the Upton Statement.  He claimed that, because populations between census years and thus denominators in intercensal CDRs must be estimated by linear interpolation, they are not reliable data, and therefore not suitable for linear regression analysis.  See Aitkenhead v. Borough of West View, No. GD-4585, Trial Transcript, May 8, 1978, at 72, 72A, 73-76 (Allegheny Court of Common Pleas, Pa).  This criticism was exploded by none other than Dr. Guy Newell, Deputy Director of the NCI, who supervised preparation of the Upton Statement and introduced it before Congress.  Later speaking as a professor of epidemiology at the University of Texas, he stated emphatically that use of linear interpolation to derive denominators in intercensal CDRs is “accepted procedure” in modern applied epidemiology, and, therefore, perfectly reliable.  See Safe Water Found. of Texas v. City of Houston, No. 80-52271, Trial Transcript, Jan. 26, 1982, at 1648-54 (151st Jud. Dist., Tex.).  The correctness of undertaking a linear regression analysis of intercensal CDRs in which the denominators were estimated by linear interpolation was further confirmed by Dr. Hubert Arnold, professor of statistics at the University of California, Davis.  See National Cancer Program, supra note 109, at 580. The propriety and necessity of such use of interpolated data, based on fundamental principles of inductive logic, is discussed in Burk & Graham, supra note 108, at 68-69, and Burk, Graham, & Morin, supra note 108, at 143-44.

[BillO538145]

Review of Levy (2012)

Levy 2012.   As evidence of fluoride’s lack of carcinogenicity, PHS 2015 cites at 77, Levy 2012. 

The Levy 2012 study concludes that water fluoridation in the U.S. is not associated with an increased risk of osteosarcoma. Levy 2012 use a notably crude measurement for determining fluoride exposure, the National Cancer Institute’s SEER data, average fluoridation rate of the child’s STATE of residence at the time of diagnosis rather than exposure a decade earlier. 

By contrast, when the NCI conducted its analysis of the SEER data in 1990 (in which NCI found elevated rates of osteosarcoma among young males in fluoridated areas), the NCI considered the fluoridation status on the COUNTY level — a smaller unit which is less prone to classification error.  A study without significance is not proof of safety.  The Levy study thus sheds little light on fluoride’s possible relationship to osteosarcoma.  

Blakey et al (2014) [1]

“The study objective was to examine whether increased risk of primary bone cancer was associated with living in areas with higher concentrations of fluoride in drinking water.” 

This is an ecological study where cases were obtained from cancer registries and fluoride levels in drinking water from regional companies, Drinking Water Inspectorate, and Scottish Water.  The record does not show total fluoride exposure, supplements, blood, bone, urine or any other fluoride concentration measurement, nor whether the cohorts were actually drinking the water or swallowing toothpaste.  “Other sources of fluoride are not taken into consideration.”  

In contrast with Bassin’s 2006 study, cases with Blakey 2014 were divided into three age groups, 0-14, 15-29 and 30-49 years of age at diagnosis.   Bassin’s study used each year of life and contacted each water source to ensure the address while growing up actually received fluoride in the water (10% reporting error) and the subject lived in that location.  Bassin found ingestion of fluoridated water during 6-8 years of age increased cancer several years later.  By including all ages 0-14 in one group and 15-29 in another group, Blakey would have “watered down the evidence” and not account for the high risk growth spurts reported by Bassin.  Blakey assumes fluoride consumption was consistent throughout the study time-frame.

Blakey 2014 reported, “The monitoring data suggests that levels in some AF areas were much lower than 1 ppm.  Indeed, 33% of AF WSZs were below 0.7 ppm. . . and 61% of AF SAUs had such a level.  This suggest that 35% of populations residing in AF areas were being supplied with AF water dosed below the optimal level.”  

Blakely 2014 states, “Furthermore, although the overall results contradict those from Bassin’s study, the use of total accumulated fluoride dose rather than a specific time in life course prevents any direct comparisons being made.”

Osteosarcoma is a rare cancer (Blakely 2.64/million) and unless a study is carefully controlled, the data can be easily diluted, negating significance.  

Blakely’s Table 1 is produced here for the purpose of understanding the importance of age.  In this study, an increase in osteosarcoma is evident during 15-29 years of age and over 49 years of age.  Studies must include age and measured fluoride serum, urine, and bone concentrations.  Perhaps the rate of bone turnover is reduced during middle age.  Fluoride accumulates with time and seniors have higher bone fluoride concentrations perhaps triggering risk.

Age-group (years)	!                                    Number of osteosarcoma cases	!                                      Number of Ewing sarcoma cases
Males	Females	Total	Males	Females	Total
0-14	406	411	817	356	303	659
15-29	821	494	1315	516	284	800
30-49	266	168	434	116	75	191
0-49	1493	1073	2566	988	662	1650

Gelberg et al (1994)

The PHS 2015 failed to consider Gelberg KH. (1994) reporting, “When fluoride exposure

increases, the following bone responses generally occur: 1) an increase in the number of osteoblasts, 2) an increase in the rate of bone formation, 3) an increase in the serum activity of alkaline phosphatase, and 4) an inhibition of osteoblastic acid phosphatase… The increase in osteoblast proliferation and activity may increase the probability that these cells will undergo malignant transformation.”[2]

The case-control study by Gelberg, published first as a PhD dissertation (Gelberg 1994) and then later in two peer-reviewed journals (Gelberg 1995, 1997), may represent the most substantive study on fluoride/osteosarcoma previous to Bassin’s 2001 analysis.

While Gelberg has errors, such as stating cases were females when they were males, and reversing cases and controls in the “Total Fluoride” and “Toothpaste” categories in Tables 2 and 3,  primary concerns with Gelberg’s work relates to the methods used to analyze her data.

Gelberg uses data from NY Cancer Registry and state rather than county fluoridation rates. Gelberg, like Hoover 1991,[3] never analyzes her data with subjects divided into a simple two-category model: exposed versus unexposed, but rather quartiles.

However, for males the lower “quartile” group shows a borderline statistically significant increased risk OR of 2.8 (95%CI 1.0-8.1). For females the OR is even higher and statistically significant at 10.5 (95%CI 1.2-91). For both males and females in the higher “quartiles” of exposure, the ORs are no longer significant, but the risk for osteosarcoma generally stays above 1.0. If, instead of breaking the data into “quartiles”, it had been broken into just “exposed” and “unexposed”, it is quite possible the exposed group would have a significantly elevated risk for osteosarcoma compared to the unexposed group.

In looking for other possible risk factors for osteosarcoma, Gelberg (1994) found that a history of exposure to dental x-rays was significantly related to the development of osteosarcoma (OR 4.0; 95%CI 1.3-12) . Dental x-rays were, in fact, one of the few variables Gelberg examined that had an effect reaching statistical significance.  

However, increased dental x-rays would indicate possibly more frequent dental visits which indicate  more frequent topical applications of fluoride (22,300 ppm fluoride) in the dental office.  The efficacy of fluoride varnish is mixed, and risks have not been studied. 

Bassin 2006; Cohn 1992; Hoover 1991 are consistent with the National Toxicology Program’s (NTP) cancer bioassay which raised concerns that fluoride-treated male rats had a dose-dependent increase in osteosarcoma. (Bucher 1991). Although a number of studies including PHS 2015 citations have failed to detect an association between fluoride and osteosarcoma, none of these studies have measured the risk of fluoride at specific windows in time, which is the critical question with respect to fluoride and osteosarcoma.

A report by the National Academy of Sciences (NAS), titled “Drinking Water and Health”, expresses concern about a possible connection between water fluoridation and osteosarcoma in young males:

“There was an observation in the Kingston-Newburgh (Ast et al, 1956) study that was considered spurious and has never been followed up. There was a 13.5% incidence of cortical defects in bone in the fluoridated community but only 7.5% in the non-fluoridated community… Caffey (1955) noted that the age, sex, and anatomical distribution of these bone defects are `strikingly’ similar to that of osteogenic sarcoma. While progression of cortical defects to malignancies has not been observed clinically, it would be important to have direct evidence that osteogenic sarcoma rates in males under 30 have not increased with fluoridation.” (NAS 1977)

[1] Blakey, K, Feltbower, R et al, Is fluoride a risk factor for bone cancer?  Small area analysis of osteosarcoma and Ewing sarcoma diagnosed among 0-49-year-olds in Great Britain, 1980-2005. Int J Epidemiol. 2014 Feb; 43(1): 224-234.

[2] Gelberg KH. (1994). Case-control study of osteosarcoma. Doctoral Thesis, Yale University. p. 13.

[3] Hoover R.N., Devesa S.S., Cantor K.P., Lubin J.H., Fraumeni J.F. (1991). Time trends for bone and joint cancers and osteosarcomas in the Surveillance, Epidemiology and End R.... National Cancer Institute. In: Review of Fluoride: Benefits and Risks Report of the Ad Hoc Committee on Fluoride of the Committee to Coordinate Environmental Health and Related Programs US Public Health Service.

[DavidF928895]

BillO, 

We must consider the fact that there have been over 4000 studies on fluoride alone.  Some studies are peer-reviewed, some studies have been debunked.

It is odd isn't it.  When one looks at the discussion presented by the American Cancer Society on water fluoridation, ( https://www.cancer.org/cancer/cancer-causes/water-fluoridation-and-cancer-risk.html ) one would think water fluoridation does not lead to any kind of cancer.  In the studies the ACS presents there is either No Evidence, (For example:  "In 2011, the state of California’s Carcinogen Identification Committee (CIC) reviewed the evidence and concluded that “fluoride and its salts has not been clearly shown to cause cancer.”), or there is No Strong Evidence for any link between the two.  

On the other hand, when one looks at your cherry-picked non-peer reviewed studies, one would think that osteosarcoma and other forms of bone cancer are almost a certainty.

Considering the fact that there are roughly 400 cases of the bone cancer, osteosarcoma, per year in the U.S., and considering the fact that hundreds of millions of people enjoy the health benefits of optimally fluoridated water on a daily basis, you would think, according to your cherry-picked studies, that hospitals would be over-run with these bone-cancer victims.  But they aren't are they.

The American Cancer does not accept funding from unethical alternative health businesses which routinely receive warning letters from the FDA.  Fluoride Alert, & the Fluoride Action Network do.  The sole existence of the American Cancer Society does not depend on the creation of some controversy, where no controversy actually exists.  The existence of Fluoridealert does. 

Perhaps that is why we see such different interpretations between the American Cancer Society & Fluoridealert when it comes to water fluoridation and cancer. 

Dr. Bill, have you ever had any relationship with the Fluroide Action Network? 

[BillO538145]

What did some reviewers say?

Thiessen’s Review of Kim et al. (2011), (Referenced in PHS 2015 as evidence of safety).

“The paper by Kim et al. (2011) is part of the Harvard osteosarcoma study. The paper describes a comparison of bone fluoride levels in cases of osteosarcoma and a set of controls. The authors report no significant difference in bone fluoride levels between cases and controls and no significant association between bone fluoride levels and osteosarcoma risk. 

“To give some context it is important to know that an earlier part of the Harvard osteosarcoma study, namely the work of Bassin et al. (2006; based on a 2001 dissertation by Bassin 2001), reported an association between age-specific fluoride exposure and risk of osteosarcoma, with the highest risks for childhood exposure for young males. Bassin's study involved 103 cases under the age of 20 (median age, 13.7) and 215 matched controls (median age, 14.5; matching based on age, gender, and distance from the hospital) from the orthopedics departments of the same hospitals. Cases were diagnosed between November 1989 and November 1992. Bassin estimated fluoride exposure from drinking water and fluoride supplements or rinses for each participant, for each year of life, based on residential histories. Bassin et al. describe the limitations of their study and point out that additional studies with larger numbers of osteosarcoma patients, with incidence under age 20, that examine age-specific and sex-specific associations are required to confirm or refute the findings of the current study. 

“The NRC report (NRC 2006, pp. 329-330) was published shortly before the Bassin et al. paper appeared, but included an analysis of Bassin's dissertation (2001), which reported essentially the same findings. The NRC also reported a personal communication from C. Douglass of the Harvard School of Dental Medicine, describing a second study involving 189 cases and 289 controls. This study was said to include residence history, detailed interviews about water consumption, and fluoride assays of bone specimens and toenails of all subjects. The NRC committee was told that the preliminary results indicated no statistically significant association with fluoride intakes and that the results were expected to be reported in the summer of 2006. The NRC report describes some concerns about possible bias (in either direction) in the selection of controls and the expectation that the study could have limited statistical power to detect a small increase in osteosarcoma risk due to fluoride exposure. 

“When Bassin's work was published (Bassin et al. 2006), the same issue of the journal contained a letter to the editor by Douglass and Joshipura (2006), both of whom were coauthors on an earlier paper describing Bassin's exposure analysis (Bassin et al. 2004). This letter mentioned that preliminary findings from the second set of cases did not appear to replicate the earlier work (Bassin's study) and indicated that their findings, which were “currently being prepared for publication,” did not suggest an overall association between fluoride and osteosarcoma. It also indicated that both a fluoride intake history and a bone specimen were being obtained for each participant, and that their preliminary analysis indicated that the fluoride content of the bone was not associated with excess risk of osteosarcoma. However, this letter provided no data and therefore constitutes no more than an opinion. 

“The paper by Kim et al. (2011) was submitted to the Journal of Dental Research in January 2011 and published electronically in late July 2011. No mention is made of why it took 5 years from the time Douglass and Joshipura indicated that their findings were “currently being prepared for publication.” Nor is it obvious why the paper was published in a dental journal, when it does not deal directly with anything related to dentistry. Other recent papers that include some of the same coauthors (specifically, C. Douglass and R.N. Hoover) have been published in cancer research journals, (e.g., Savage et al. 2007; Mirabello et al. 2011a,b,c), as was Bassin's work (Bassin et al. 2006). 

“Kim et al. (2011) describe a study involving 137 cases (37 ages 0-14, 72 ages 15-29, 13 ages 30- 44, and 15 ages 45 and older) and 51 controls, with cases diagnosed between 1993 and 2000. 

“Although there is mention of “orthopedic” controls (patients with benign tumors or non- neoplastic conditions), only “tumor” controls were in fact used. The selection of cases and controls was affected in part by the need to obtain bone specimens. The cases had a median age of 17.6 years, the controls, 41.3 years. Kim et al. report no significant difference in the median fluoride concentration in bone between matched osteosarcoma case and tumor control in 32 pairs where age matching was possible. In an unmatched analysis of all cases and controls, the median bone fluoride concentration was significantly higher in controls than in cases. The authors conclude that their study “did not demonstrate an association between fluoride levels in bone and osteosarcoma.” 

“The use of an individual measure of fluoride exposure (bone fluoride concentration) is important to note. However, as the authors themselves point out, “if risk is related to exposures at a specific time in life, rather than total accumulated dose, this metric would not be optimal” (Kim et al. 2011). Bone fluoride concentration is a measure of cumulative fluoride exposure to the time of diagnosis and surgery. Given a “lag time” of at least 5 years between initiation and diagnosis of most cancer types, the bone fluoride concentration at time of diagnosis can be affected by fluoride exposures that occurred after the cancer was initiated. Most importantly, a bone fluoride concentration at time of diagnosis says nothing about fluoride exposure at specific ages, so it does not address the key finding of Bassin et al. (2006). 

“The osteosarcoma cases analyzed by Kim et al. (2011) included 28 individuals aged 30 or older. The actual number of patients under 20 years old is not given, but was said to be too few to provide sufficient statistical power. Thus the cases analyzed by Kim et al. are not fully comparable to the cases analyzed by Bassin et al. While osteosarcoma obviously occurs in adults, the majority of cases occur in children and young adults (Sergi and Zwerschke 2008; Mirabello et al. 2011a,b,c; Savage et al. 2007); Kim et al. (2011) themselves indicate that osteosarcoma is more prevalent in individuals less than 20 years old. Kim et al. have not explained their justification for including older individuals, other than to have large enough numbers to do their statistical analyses. The possibility that different mechanisms are involved in pediatric and geriatric osteosarcoma has not been addressed. 

“As mentioned, the controls were all patients with malignant bone tumors other than osteosarcoma, apparently because bone samples were more readily available for tumor controls than for other controls (Kim et al. 2011). Kim et al. point out that if “fluoride levels were related to bone cancer in general, the current study design would be unable to detect this. There is no published evidence of such an association.” There also is no published evidence clearly demonstrating a lack of such an association. The one small finding that has been published (as part of an appendix to a Public Health Service report) was an excess of Ewing's sarcoma in fluoridated counties as opposed to nonfluoridated counties (Hoover 1991). This was explained as an artifact of the analysis. However, given the distinct lack of adequate analyses of fluoride exposure and other types of bone cancer, the use by Kim et al. (2011) of tumor controls alone obviously has to be regarded with caution. 

“Bassin et al. (2006) limited their analysis to 103 cases diagnosed before the age of 20 (median age 13.7) and used 215 orthopedic controls (median age 14.5). Kim et al. (2011) used a much broader range of ages among cases, together with a relatively small set of controls very different in age from the cases and who were themselves bone cancer patients. While there were apparently limitations in selecting controls who could provide bone samples, nevertheless, the result is that the analysis by Bassin et al. had a much better set of controls than did the analysis of Kim et al. 

“Kim et al. (2011) report a higher median fluoride concentration of controls compared with cases, which they attribute to the older ages of the controls than the cases. Comparison of the distributions of bone fluoride concentrations between cases and controls (Figure, part D) indicates that the ranges are not greatly different. Given that the median age of the controls is more than twice the median age of the cases (41.3 vs. 17.6), the obvious conclusion is not a lack of association between fluoride exposure and osteosarcoma, but considerably higher average exposure (by a factor of 2) in cases and controls, in order to reach similar bone fluoride concentrations. Kim's 2007 dissertation, on which the 2011 paper is based, reports estimates of “median cumulative lifetime water fluoride” of 14.4 ppm year for the cases and 16.5 ppm year for the controls. These cumulative exposures together with the median ages of the two groups again indicate higher average fluoride exposure among cases than controls, by a factor of 2. Rather than refuting the work of Bassin et al., these findings by Kim et al. support an association between fluoride exposure and osteosarcoma. 

“In order to obtain the estimates of median cumulative lifetime water fluoride, Kim had to develop the exposure histories for the individual cases and controls. In addition, her dissertation indicates that the exposure histories were available for the orthopedic (noncancer) controls. Douglass and Joshipura (2006) indicated that exposure histories were being obtained. Any meaningful comparison of Kim's findings with those of Bassin et al. (2011) will require use of the individual exposure histories to look at exposures at various ages, as opposed to just the comparison of bone fluoride concentrations. 

“As an incidental note, the bone fluoride concentrations reported by Kim et al. (2011, Figure) for both osteosarcoma cases and tumor controls, extend into the range reported for skeletal fluorosis (NRC 2006).

Also of note is that Kim et al. (2011) found that a history of broken bones was a significant predictor of osteosarcoma risk. An increased risk of bone fracture has been associated with fluoride exposure in a variety of studies (e.g., NRC 2006; Alarcón-Herrera et al. 2001; Danielson et al. 1992).”[1]

A National Cancer Institute (NCI) report[2] on Kim (2011), failed to appreciate using a different cancer for controls is not “normal” bone fluoride concentration.  

The NCI states “they [Kim] measured fluoride concentration in samples of normal bone adjacent to a person’s tumor. . . The analysis showed no difference in bone fluoride levels between people with osteosarcoma and people in a control group who had other malignant bone tumors.” 

Thiessen’s Review of Comber et al. (2011) (Comber et al was cited by the PHS 2015 recommendation as evidence fluoride is not carcinogenic and safe.)

“Comber et al. (2011) compare osteosarcoma rates in nonfluoridated Northern Ireland and in partially fluoridated Republic of Ireland, with the latter data divided between fluoridated and nonfluoridated areas. They report no significant differences in either age-specific or age- standardized incidence rates of osteosarcoma between fluoridated and nonfluoridated areas. 

“Comber et al. also describe several limitations of their study, including uncertainty about fluoridation status of particular areas (the possibility of misclassification), the possibility that the place of residence at the time of diagnosis may not be an accurate proxy for lifetime exposure to fluoridated water, and the lack of an accurate measure of total fluoride exposure. Perhaps the most important limitation pointed out by Comber et al. is the relative rarity of the cancer and the correspondingly wide confidence intervals of the relative risk estimates. They estimate that the risk for a fluoridated population would need to be at least 1.7 times that of the nonfluoridated population (a 70% increase) for a statistically significant effect to be detected. In other words, fluoride could cause a 50-60% increase in risk of osteosarcoma, and this study would not be able to detect it. 

“With respect to using the place of residence at the time of diagnosis as a proxy for lifetime exposure to fluoridated water, Comber et al. point out that if fluoride exposure at a specific age is critical to osteosarcoma development (citing Bassin et al. 2006), use of the fluoride estimation at the time of diagnosis is less valuable. In other words, their analysis cannot evaluate the importance of age-specific exposure. 

“With respect to the lack of an accurate measure of total fluoride exposure, the authors mention that at least one-third of fluoride intake is estimated to come from sources other than drinking water, citing tea, fish, and toothpaste as examples. The authors do not discuss the possibility that variability in total fluoride intake within the Irish populations could overwhelm differences between populations in fluoride intakes from drinking water alone. 

“In summary, the paper by Comber et al. does not demonstrate an absence of a relationship between fluoride exposure and osteosarcoma, simply that any effect of fluoridated water (as opposed to total fluoride intake) is not large enough to detect by the methods employed.”[3]

[1] Thiessen IBID  Pages 12-14.

[2] Kim FM, Hayes C, Williams PL, et al. An assessment of bone fluoride and osteosarcoma. Journal of Dental Research 2011; 90(10):1171–1176.  https://www.cancer.gov/about-cancer/causes-prevention/risk/myths/fluoridated-water-fact-sheet#q4  Accessed 2/14/2017

[3] Thiessen IBID p. 12.

[BillO538145]

Nothing in science is "settled."  We have theories which must constantly be retested and tested again in light of the new research and understanding.  Nothing in science is written in stone.  There are no absolutes, no "never" and "always."  We scientists must live in a state of discovery.  

I have provided some research on the basics and will now go into some of the specific cancers.

1. BONE CANCER:

PHS 2015 notes about 100 unique comments regarding fluoride as a carcinogen.  Of the many references provided to PHS 2015, they include nine references and dismiss carcinogenicity.  Osteosarcoma is the singular cancer listed. PHS 2015 references: 

1. PHS 2015 lists Bassin 2006[1] as reporting an association between fluoride and osteosarcoma; although PHS 2015 does not go into specifics.   

CHESTER DOUGLASS HISTORY: 

DOUGLASS REPORTS NO ASSOCIATION:  A team of Harvard scientists, led by

Dr. Chester Douglass, publish the preliminary findings of a large case-control analysis of fluoride and osteosarcoma (McGuire et al 1995). In the preliminary analysis the authors report no association between fluoride and osteosarcoma. 

DOUGLASS REPORTS ELEVATED RISK:  To the NIH, Chester Douglass

reports “all” of his analyses which assumed bottled water contains no fluoride found that fluoridated drinking water (>0.7 ppm) is associated with elevated, but not statistically significant, rates of osteosarcoma.  Douglass later expresses concern about the ramifications to water fluoridation from reporting that fluoridation is associated with an elevated, even if not statistically significant, rate of bone cancer:

“Because of the importance of the question at hand, we think the policy implications of reporting that the relative risk maybe higher than 1.5 would have consequences for fluoridation health policies.”

 DOUGLASS REPORTS NO RISK:              In 1995, 1998 & 2002 Douglass states that

the study shows fluoridation has either no effect, or a slightly protective effect, on osteosarcoma rates. 

DOUGLASS KNOWS THERE IS RISK: However, Douglass’s signature is on Bassin’s

2001 thesis using Douglass’s data which found a statistically significant increase in osteosarcomas. 

DOUGLASS REPORTS NO RISK:                In 2004, the National Research Council

(NRC) begins a review of the safety of currently allowable levels of fluoride in drinking water.  Douglass submits a summary of his fluoride/osteosarcoma study to the NRC, claiming no significant association between fluoridation and osteosarcoma.  Douglass even cites Bassin’s study as one of 2 supporting references for this summary of no fluoride osteosarcoma association.  Douglass fails to report that Bassin found a statistically significant, 5-to-7-fold risk of osteosarcoma among boys drinking fluoridated water a decade prior to their diagnosis of cancer.

Bassin et al published some of her thesis data in 2006.  She reports that boys drinking fluoridated water during the ages of 6 to 8 have a five-fold increased risk of developing osteosarcoma during their teenage years:

“We observed that for males diagnosed before the age of 20 years, fluoride level in drinking water during growth was associated with an increased risk of osteosarcoma, demonstrating a peak in the odds ratios from 6 to 8 years of age. All of our models were remarkably robust in showing this effect, which coincides with the mid-childhood growth spurt. For females, no clear association between fluoride in drinking water during growth and osteosarcoma emerged.”[2]

The Bassin study is consistent with other studies.  The fluoride carcinoma risk appears age and cell cycle dependent.   

DOUGLASS ADMITS SOME ASSOCIATION:  Douglass publishes a letter in the

same issue in which he publicly discloses for the first time that he had found some associations between fluoride exposure and osteosarcoma in the (retrospective) dataset that Bassin analyzed. 

DOUGLASS CAUTIONS AND PROMISE: Douglass states that he was unable to

replicate these findings in a new (prospective) dataset, and thus cautions readers from making any conclusions based on Bassin’s findings. Douglass notes, however, that he has yet to conduct an age-specific analysis on the prospective data. He notes though that he is planning on doing so. To quote:

 “A parallel analysis of age-specific exposure to fluoride, especially during growth periods, is also being pursued by our study team in the second set of cases of our study. Accordingly, readers are cautioned not to generalize and over-interpret the results of the Bassin et al. paper and to await the publications from the full study, before making conclusions, and especially before influencing any related policy decisions.”[3]

Note: As of April, 2015 Douglas, to our knowledge, has not published the agespecific analysis on the prospective data.

COMPLAINT AGAINST DOUGLASS:         The Environmental Working Group filed a complaint of scientific misconduct with the National Institute of Health which launched an investigation run by Harvard University; however, EWG is reported to have not been contacted.  

NO INTENT TO MISREPRESENT:  Harvard issued a short, one page press release announcing that Douglass did not “intentionally misrepresent” the research.

To be continued:

[1] Bassin EB et al, Age-specific fluoride exposure in drinking water and osteosarcoma (United States).  Cancer Causes Control 2006;17:421-8

[2] Bassin EB, et al. 2006. Age-specific fluoride exposure in drinking water and osteosarcoma (United States). Cancer Causes & Control 17(4):421-8. May.)

[3] Douglass CW, and Joshipura K. 2006. Caution needed in fluoride and osteosarcoma study. Cancer Causes & Control 17(4):481-82. May.

[BillO538145]

Randy,

Lets look at some studies.

Fluoride exposure is systemic, potentially affecting all tissues.   Evidence is mounting that age and “timing” along with dosage, host health, race, and synergistic chemicals are all significant.  

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.[1]

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.”[2]

Known carcinogen (increase incidence): Marigold[3] (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[4] (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, Fleming[5]36 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)[6] 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)[7] “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)[8] “Genotoxicity of Sodium fluoride was evaluated in mice in vivo with the help of different cytogenetic assays.

Known Carcinogen:  Tazhibaev (1987)[9] “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.”[10] 

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.”[11]

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.”[12]

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.”[13]

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.”[14]

Airborne Fluoride:  “Fluoride has displayed mutagenic activity in studies of vegetation, insects, and mammalian oocytes. There is a high correlation between carcinogenicity and mutagenicity of pollutants, and fluoride has been one of the major pollutants in several situations where a high incidence of respiratory cancer has been observed. For these reasons, the relation between airborne fluoride and incidence of lung cancer needs to be investigated.”[15]

More to follow:

[1] Pal S, Sarkar C, Protective effect of resveratrol on fluoride induced alteration in protein and nucleic acid metabolism, DNA damage and biogenic amines in rat brain Environ Toxicol Pharmacol. 2014 Sep;38(2):684-99. doi: 10.1016/j.etap.2014.07.009. Epub 2014 Jul 23.

[2] McCully KS, Chemical pathology of homocysteine. IV. Excitotoxicity, oxidative stress, endothelial dysfunction, and inflammation., Ann Clin Lab Sci. 2009 Summer;39(3):219-32

[3] Marhold, J. and Matrka, M.: Ca=inogenicity and Oxidation of Fluoro- Derivatives of Dimethylaminoazobenzene. Fluoride 2:85, Apri11969.

[4] Taylor, A.: Sodium fluoride in Drinking Water of Mice. Dental Digest, 60:170, 1954.

[5] Fleming, H,S.: Effect of fluorides on the Tumors 37 After Trans- plantation to Selected Locations in Mice and Guinea Pigs. Journ. of Dent. Res. 32:646, October 1953

[6] Taylor, A.: Effect of Sodium fluoride on Tumor Growth. Proceedings of the Society for Experimental Biology and Med. 119:252-5, 1965.

[7] Suzuki Y, Li J, Shimizu H. (1991). Induction of micronuclei by sodium fluoride. Mutation Research 253(3):278.

[8] Pati PC, Bhunya SP. (1987). Genotoxic effect of an environmental pollutant, sodium fluoride, in mammalian in vivo test system.  Caryologia 40:79-87.

[9] Tazhibaev ShS, et al. (1987). [Modifying effect of nutrition on the mutagenic activity of phosphorus and fluorine compounds.] Vopr Pitan. Jul-Aug;(4):63-6.

[10] Mihashi M, Tsutsui T. (1996). Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture. Mutation Research 368(1):7-13.

[11] National Toxicology Program [NTP] (1990). biochemical responses of cells treated with fluoride. Sodium fluoride inhibits both protein and DNA synthesis in cultured mammalian cells. The inhibition of DNA synthesis may be a seco...Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle Park, N.C.

[12] Bassin EB. (2001). Association Between Fluoride in Drinking Water During Growth and Development and the Incidence of Ostosarcoma for Children and Adolescents. Doctoral Thesis, Harvard School of Dental Medicine. p. 15.

[13] Environment Canada. (1993). Inorganic Fluorides: Priority Substances List Assessment Report. Government of Canada, Ottawa.

[14] Department of Health and Human Services. (1991). Review of fluoride: benefits and risks. Report of the Ad Hoc Subcommittee on Fluoride. Washington, DC. p. 70. (There is also an abbreviated report)

[15] Marier J, Rose D. (1977). Environmental Fluoride. National Research Council of Canada. Associate Committe on Scientific Criteria for Environmental Quality. NRCC No. 16081.

[BillO538145]

Randy,

Lets talk science rather concensus.  Remember, the masses can be wrong.  Marketing can change public opinion.

The next few posts will be just a touch on one aspect of fluoride, carcinogenicity.

The “biological plausibility” of a fluoride-osteosarcoma link (and other cancers) is widely acknowledged in the scientific literature. When the connection between a chemical and a cancer is biologically plausible, studies that detect an association between the two are taken more seriously.

              Three lines of plausibility in a fluoride/cancer connection:

1                    Ames[1] 1976, reported about 90% of organic compounds that were found to be mutagenic are also carcinogenic.  

2                    Tissues such as bone, bladder, kidney, brain, are principal sites for fluoride accumulation in the body, and the rate of accumulation is increased during periods tissue turn over, such as for bone the development and osteoclastic osteoblastic activity.

3                    Fluoride is a mitogen. For example, osteosarcoma is a cancer caused by an abnormal proliferation of the osteoblasts.

All tissues which come in contact with higher concentrations of fluoride should be considered for a fluoride cancer connection. 

In short, fluoride’s ability to induce mutagenic damage in fluoride-rich environments coupled with its ability to stimulate proliferation of osteoblasts provides a compelling biological basis by which fluoride could cause, or contribute to cancer.  The only relatively “static” tissue high in fluoride appears to be dentin.  Cancer of the dentin or enamel is not reported.   

[1] Ames, BN et al, Mutagens and carcinogens.  Science, 194:132-133, 1976.

Next, lets look at a snipet of studies.

[RandyJ913440]

Thank you Dr. Haynie for your succinct response to Dr. Osmunson’s CWF causes cancer claims 09-04-2018 03:14 PM.  He is still avoiding my request that he explain his earlier comments 08-27-2018 01:40 AM, redefining the Scientific Consensus as an “Endorsement Consensus”, claiming 08-19-2018 02:18 AM that “Endorsements are not science”, claiming 07-09-2018 09:09 PM that “Most endorsements are not backed by a good scientific review of all sides of the literature” and making accusations of the CDC, ADA and AAP that, “None reviewed the science. All the so called "scientific" organizations were all puppets of each other with fluoridation.”

Dr. Osmunson – Let’s look at your statement 09-04-2018 02:04 PM, “Lets talk science rather consensus.  Remember, the masses can be wrong.  Marketing can change public opinion” just before you dumped over 16,000 words into the discussion in an apparent attempt to support your claim that drinking optimally fluoridated water is a significant risk factor for causing cancer.  That was one of the most remarkable examples of Gish Gallop I have ever seen… 

If you believe your interpretation of the “evidence” actually supports the conclusion that optimally fluoridated water is obviously and dangerously carcinogenic, why on earth are you presenting this devastating news and “evidence” on a public forum instead of demanding a meeting with members of the American Cancer Society, the Canadian Cancer Society (and other relevant expert organizations) to instruct them on your “correct way” to evaluate the evidence.

Following protocols that are even remotely scientific would first and foremost require presenting legitimate scientific evidence to the relevant experts and convincing them that your interpretations are legitimate.  But that’s the whole issue with these anti-F opinions, isn’t it?  Relevant experts have evaluated the evidence you just presented and have not accepted your anti-F conclusions. 

In fact, the ACS states, “In 1993, the Subcommittee on Health Effects of Ingested Fluoride of the National Research Council, part of the National Academy of Sciences. … The Subcommittee concluded that none of the data demonstrated an association between fluoridated drinking water and cancer” and “A 1999 report by the CDC supported these findings. The CDC report concluded that studies to date have produced “no credible evidence” of an association between fluoridated drinking water and an increased risk for cancer” and “In 2011, researchers examined the possible relationship between fluoride exposure and osteosarcoma in a new way. … The analysis showed no difference in bone fluoride levels between people with osteosarcoma and people in a control group who had other malignant bone tumors.” and “More recent population-based studies using cancer registry data found no evidence of an association between fluoride in drinking water and the risk of osteosarcoma or Ewing sarcoma.”

 https://www.cancer.gov/about-cancer/causes-prevention/risk/myths/fluoridated-water-fact-sheet#r6

The CCS publically states, “Based on current evidence, CCS believes it is unlikely that adding fluoride to water raises the risk of cancer, including osteosarcoma, in humans. At the same time, we know that there are many benefits to water fluoridation, especially for people who have less access to dental care. We will continue to watch this area of research and update our information as we learn more.”

http://www.cancer.ca/en/prevention-and-screening/reduce-cancer-risk/make-informed-decisions/know-you...

Does the fact that neither of these organizations supports your outlier interpretation of the cancer-related evidence mean that you extend your 07-09-2018 09:09 PM accusations of the CDC, ADA and AAP to the ACS and CCS? 

That libelous claim reads in part, the “CDC references the ADA and AAP,  and the ADA and AAP reference each other and the CDC.  Circular referencing.”, and “the credibility of those so called 'scientific' organizations has been seriously tarnished.  They do not protect the public.  They are lemmings, followers, part of a herd, not scientists.  Scientists question and do not assume and base their science on trust”, and “Yes, they are the best in their field and experts, but not in fluoridation“.

So, do you believe members of the ACS and CCS are "the best in their fields", but they can’t get it right when evaluating the carcinogenic risks of community water fluoridation (CWF) - Really?

You still have not addressed my questions about the necessity of the scientific consensus to protect the public from rampant fear-mongering by anti-science activists (ASAs).

Actually, challenging the current Scientific Consensus (or Expert Consensus) with new, legitimate evidence is a critical element of the scientific method.

Naomi Oreskes: Why we should trust scientists:

https://www.youtube.com/watch?v=RxyQNEVOElU
https://vialogue.wordpress.com/2014/06/26/ted-naomi-oreskes-why-we-should-trust-scientists/

Nor have you provided a rational explanation (besides claiming everyone who disagrees with you is a lemming) to explain why only a small group of outlier, alternative health organizations support the anti-F opinions – in contrast to all major science and health organizations (and their members) that either publically recognize the benefits of CWF or have not made public statements that CWF is a harmful public health measure.

Nor have you provided a logical alternative to replace accepting the scientific consensus when the public is evaluating complex, scientific conclusions.  Unfortunately two of your claims are true, “Marketing can change public opinion”

Nor have you provided a logical alternative to replace accepting the scientific consensus when the public is evaluating complex, scientific conclusions.  Unfortunately two of your claims are true, “Marketing can change public opinion”  – ASAs simply throw out masses of fear-laced misinformation and misdirection and try to scare the public into trusting their conclusions, and because of that mistaken trust, “the masses can be wrong“, which reminds me of Kaa's attempt to hypnotize Mowgli into trusting him. 

https://www.youtube.com/watch?v=vDs57R6MYsY

Randy Johnson

[DavidF928895]

RandyJ asks BillO, "If you believe your interpretation of the “evidence” actually supports the conclusion that optimally fluoridated water is obviously and dangerously carcinogenic, why on earth are you presenting this devastating news and “evidence” on a public forum instead of demanding a meeting with members of the American Cancer Society, the Canadian Cancer Society (and other relevant expert organizations) to instruct them on your “correct way” to evaluate the evidence."

Response:  Probably because it is easier to convince lay persons and a few conspiracy theorists who have graduated from the University of Google that controversy exists where there is no controversy,  than it would be to convince knowledgeable  people with legitimate scientific training.

[CarryAnne]

“The controversy about fluoridation was inevitable because fluoridation was, in a real sense, conceived in sin. Fluoride is a major waste product of industry and one of the most devastating pollutants of the aluminum industry. The government not only dismissed the danger and left industry free to pollute, but it has promoted the intentional addition of fluoride - most of which is recycled industrial waste - to the nation’s drinking water.” - Prof. Albert Schatz  (1995)

DavidF last comment, per usual, is not only not factual but also uses a mix of logical fallacies in order to achieve his goal of burrying useful information under a mountain of rhetoric. 

The purpose of this forum thread started in February 2015 that had 60 supportive comments from about 20 seniors prior to the troll invasion is to share personal testimony and advocate for a ban on fluoridation. The fluoride 'rapid response' team that overhelmed the thread in June 2018 has disrupted the conversation with flights into every possible distraction, one of which was arguing over environmental harm (another about  Einstein's theories). RossF responded to the environmental issue first with an appropriate abstract documenting that yes, U.S. National Marine Fisheries Services knew in 1980s that salmon are harmed at fluoride concentrations of 0.5 ppm. 

DavidF's reply that attacked RossF misrepresented a reply that provided 23 affadavits on harm from 1993 (not the 1960s) which included one from a lawyer who said he did NOT accept the client's word of fluoride poisoning, but was subsequently provided with the medical report from his client's physician that indeed, it was well documented that some people including the client, Mr. Riggins, are harmed by fluoridation. The lawyer reported that those client medical records struck a chord in him regarding his own health issues. In addition to the 1993 affadavits from doctors, scientists and lawyers that attested to human harm from fluoridation, this forum includes personal testimony of harm which David ignores, including mine. 

But as to environmental harm from fluoridation which at least is relevant if a little off topic, since I can't find my earlier comment with a list of a dozen environmental citations on harm cause plants & animals due to fluoridation waste water, here they are again (I have more): 

1. Mullenix PJ. A new perspective on metals and other contaminants in fluoridation chemicals. International Journal of Occupational and Environmental Health. 2014 Apr-Jun;20(2):157-66.  http://www.ncbi.nlm.nih.gov/pubmed/24999851 
   
   
2. Camargo, J.A. 2003. Fluoride toxicity to aquatic organisms: a review. Chemosphere, 50:251-264. https://www.ncbi.nlm.nih.gov/pubmed/12656244  
   
   
3. Pacific Northwest Pest Management Handbook (2018) “Fluorine Toxicity in Plants” by J.W. Pscheidt, Extension Plant Pathology Specialist, OSU. https://pnwhandbooks.org/plantdisease/pathogen-articles/nonpathogenic-phenomena/fluorine-toxicity-pl...
   
   
4. Karina Caballero-Gallardo, Jesus Olivero-Verbel and Jennifer L. Freeman. (2016) Toxicogenomics to Evaluate Endocrine Disrupting Effects of Environmental Chemicals Using the Zebrafish Model. Current Genomics. 17:6. 515-527.
   http://benthamscience.com/journals/current-genomics/volume/17/issue/6/page/515/ 
   
   
5. Jianjie C Wenjuan X, Jinling C, Jie S, Ruhui J, Meiyan L. Fluoride caused thyroid endocrine disruption in male zebrafish (Danio rerio). Aquat Toxicology. 2016 Feb;171:48-58.
   https://www.ncbi.nlm.nih.gov/pubmed/26748264 
   
   
6. Huan Zuo. Liang Chen. Ming Kong. et al. Toxic effects of fluoride on organisms. Life Sciences. Volume 198, 1 April 2018, Pages 18-24.
   https://www.sciencedirect.com/science/article/pii/S0024320518300456 
   
   
7. AW Burgstahler, RF Freeman, PN Jacobs. Toxic effects of silicofluoridated water in chinchillas, caimans, alligators, and rats held in captivity. Research report. Fluoride 41(1)83–88 January-March 2008. http://www.fluorideresearch.org/411/files/FJ2008_v41_n1_p083-088.pdf 
   
   
8. Maas RP, Patch SC, Christian AM, Coplan MJ. Effects of fluoridation and disinfection agent combinations on lead leaching from leaded-brass parts. Neurotoxicology. 2007 Sep;28(5):1023-31. http://www.ncbi.nlm.nih.gov/pubmed/17697714
   
   
9. Richard G Foulkes & Anne C Anderson. Research Review: Impact of Artificial Fluoridation on Salmon Species in the Northwest USA and British Columbia, Canada. Fluoride Vol.27 No.4 220-226 1994. Included: http://fluoridation.com/enviro.htm  
   
   
10. Kausik M and Sumit N. Fluoride Contamination on Aquatic organisms and human body at Purulia and Bankura District of West Bengal, India. Bull. Env. Pharmacology. Life Sci., Vol 4 [7] June 2015: 112-114. http://bepls.com/june2015bepls/18.pdf  
    
    
11. Sauerheber R. Physiologic Conditions Affect Toxicity of Ingested Industrial Fluoride. Journal of Environmental and Public Health. 2013:439490.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3690253/ 
    
    
12. Sauerheber R. Disabled Horses: Racehorse Breakdown and Artificially Fluoridated Water in Los Angeles. Fluoride 46(4)170–179 October-December 2013. http://www.academia.edu/6508850

[DavidF928895]

Carry Anne, your quote:  “The purpose of this forum thread started in February 2015 that had 60 supportive comments from about 20 seniors”

Response:   I didn’t get the memo.  Please show me where the rules for this thread are written so I can review them.  All I see is a title indicating that you are “Demanding” the AARP do something for you.  Should I be demanding something also?  Is that what this is about?

Ok, Carry Anne, since you want to talk about this again, There is not one documented case of any human being who has ever suffered harm because they drank optimally fluoridated water . . even for as much as a lifetime.

Your quote:  “DavidF's reply that attacked RossF misrepresented a reply that provided 23 affadavits on harm from 1993 (not the 1960s) which included one from a lawyer who said he did NOT accept the client's word of fluoride poisoning, but was subsequently provided with the medical report from his client's physician that indeed, it was well documented that some people including the client, Mr. Riggins, are harmed by fluoridation. The lawyer reported that those client medical records struck a chord in him regarding his own health issues.”

When I click on “a reply,” it takes me to kf’s comment which says:  “The sworn testimony of George W. Kell, Esq. (pg58) includes both his personal medical history and documents having received medical records from the doctor of his client, Mr. Riggins.”

And here is the link that KF provided:  https://firewaterfilm.files.wordpress.com/2013/04/affidavits-safe-water-assn_plaintiff-vs-fond-du-la... 

Let’s look at Page 58 and see if it says what you say it says.  Again, this is what you said that it says:  “a lawyer who said he did NOT accept the client's word of fluoride poisoning, but was subsequently provided with the medical report from his client's physician that indeed a lawyer who said he did NOT accept the client's word of fluoride poisoning, but was subsequently provided with the medical report from his client's physician that indeed, it was well documented that some people including the client, Mr. Riggins, are harmed by fluoridation.”

Really?  Here’s what the Affidavit actually says:  “he brought in a report from a doctor which stated that persons who had previously experienced nephritis or hepatitis were known to be more susceptible to chronic fluoride poisoning.”  That’s all it says.  There are no personal medical records which are ever mentioned.  And this report was from 1968!!  That was the science of the time.

There is no mention of “documented medical records.”  I didn’t misrepresent anything.  You, in your attempt to demand that the AARP does what you want them to do, are lying about what the Affidavit says. 

Moreover your quote:  "23 affadavits on harm from 1993 (not the 1960s)"

Response:  The incident we are discussing happened in 1968.  From the Affidavit:  "8.)  In the early part of 1968 a Mr. Riggins, alleging total disability, consulted me, "

Moreover, George Kell, the guy who is giving the testimony didn’t suffer any harm from drinking optimally fluoridated water.  He himself says that the water he drank had several times the amount of fluoride in it than optimally fluoridated water.  Moreover, he provided no documentation attributing any of his problems to fluoride, water, fluoridated water, or anything for that matter.  He diagnosed himself!!

You also say that I ignore personal stories of harm, including yours.  That’s because you provide no documentation of anything either.  You could be a simple hypochondriac, you could be suffering from chlorine sickness, you could be suffering from any number of things.  Who knows.  The bottom line is that you diagnosed yourself, and you are not a doctor, and there is no documentation of anything you say. 

Question:  How many doctors have you seen, given them your “fluoridated water” hypothesis, had them tell you that you were wrong, before you just decided to go with your own non-professional diagnosis? 

You say that fluoridated water inflames your rashes when you bathe.  Really?  Have you ever walked in the ocean on the beach, since the ocean has twice the level of fluoride as optimally fluoridated water.  Were your rashes inflamed by that water?

By the way, none of the links to studies that you provided shows that salmon are harmed by cities who fluoridate their water and discharge treated effluent into rivers.  All irrelevant to the discussion, unless you are trying that age-old tactic of gish galloping.

[RandyJ913440]

CarryAnne – You still have not answered the questions I asked you on 08-26-2018 &  08-30-2018 or adequately addressed my three observations on 08-21-2018 of how you continually and disingenuously manipulate and misrepresent information.   You are certainly better at not answering questions than you are answering them.

These are shortened questions – my original questions were posted on 08-26-2018 05:47 PM, and again on 08-30-2018 04:12 PM after your failure to address them.

I find it remarkable that you seem to believe a public. anti-science thread with the sole stated purposes, “to share personal testimony [anecdotal observations] and advocate for a ban on fluoridation”, by disseminating flawed interpretations of the scientific evidence would not be challenged by individuals who actually care about accurate evaluations and presentations of scientific evidence.

It is my obligation as a scientist to challenge false, dangerous, anti-science propaganda.

Back to the questions you are avoiding, starting with your inability to understand various logical fallacies, yet you have apparently mastered employing them:

Explain how my asking you a series of questions designed to examine your publically posted statements and positions and my requests for clarifications can, in any way, be defined as “A straw man fallacy” where “statements and positions are misrepresented by opponents” (08-30-2018 07:46 AM)?  I actually requested that you explain more clearly your statements and positions so I don’t misrepresent them.  Specifically:

Q1)  Do you accept the fact that the support of CWF by virtually all nationally and internationally recognized science and health organizations constitutes the scientific consensus that fluoridation is safe and effective – YES or NO – and the related sub-questions posted previously.

Q2) Do you accept as true Dr. Osmunson’s 07-09-2018 09:09 PM claim about the CDC, ADA and AAP, “Johnny, the credibility of those so called "scientific" organizations has been seriously tarnished.  They do not protect the public.  They are lemmings, followers, part of a herd, not scientists.  Scientists question and do not assume and base their science on trust”?  And do you believe that it applies it to the other 100+ organizations that do not publically denounce fluoridation and their hundreds of thousands of representatives?

Q3) Since you have gone out of your way to bring vaccination into the fluoridation conversation, do you also believe vaccination policies (to use your 08-24-2018 10:07 AM language) are also “an immoral medical mandate that forces contaminated product into bodies of convenient consumers regardless of impact on individuals in vulnerable populations who include senior citizens”?  Or do you accept the scientific consensus that the benefits of vaccination far outweigh any risks?

Q4A) You still have not addressed my 08-21-2018 01:00 PM correction to your blatant misrepresentation of the precautionary principle.

Q4B) You also did not provide an answer to my question, “If your claim ‘The evidence of harm caused by fluoridation is substantial and definitive’ is even remotely valid, how can you possibly explain the fact, which has been brought up and ignored by FOs  numerous times, that all of the major science and health organizations continue to publically recognize the scientific consensus that community water fluoridation is safe and effective and that there are no such organizations that support the anti-F agenda.”  Oh, that’s right – you have listed six alternative health organizations…

Q5) Did you actually describe in your comments (08-22-2018 06:59 AM), (08-19-2018 01:05 PM), (07-25-2018 11:30 PM) & (07-25-2018 11:30 PM) the ADA, EPA and ATA and their members as (corrected version) -- “[affected by] financial benefit, ignorant, willful blindness, morally corrupt, cowards &/or sociopaths"  Note: I corrected my original use of the term greedy.  If I am still misrepresenting your statements, please explain what you actually meant by those comments.

Update:  It is interesting to observe that in your “correction” comment 08-30-2018 11:03 AM, you don’t reference or highlight your 08-22-2018 06:59 comment “Willful blindness and financial benefit affect both organizations [ADA & EPA] and individuals and are eminently rational rationales for refusal to change, although also morally corrupt.”

Instead you reference your 08-19-2018 01:05 PM post in which you only accuse some dentists who “intentionally support fluoridation for this purpose [financial benefit]” and continue with “Most are either ignorant or willfully blind. Others are either cowed into silence per my previous comments or are indeed sociopaths motivated by power, prestige and paychecks.”

Q6) Do you also extend your description of fluoridation supporters in Q5 to all the hundreds of thousands of professionals who are members of all the other science and health care organizations that continue to recognize the benefits of CWF and have not publically denounced CWF?  Or do you have another explanation for why those professional health care providers choose to remain silent – or publically support the practice?

Q7) Another of my questions (08-21-2018 09:36 PM) I don’t remember you answering: ”By your ‘logic’ those who demand that drinking water chlorination be halted because chlorine has been used as an immoral chemical weapon (and creates a toxic brew of disinfection byproducts which have not been proven by randomized controlled trials to be completely safe) have a legitimate argument.  Do you believe that even if disinfection does help prevent diseases, disinfection policy is immoral mass poisoning because toxic chemicals are used and there may be health risks from overexposure to disinfection byproducts?”

You are still dodging my questions and providing additional false &/or irrelevant comments, opinions and conclusions.

You still have not provided a rational explanation of why, if fluoridation opponents (FOs) actually have legitimate scientific evidence to support their claims of harm, the scientific consensus that fluoridation is a safe and effective public health measure has not changed in over 70 years.  Or, if you believe the scientific consensus on fluoridation is irrelevant, you have not explained what your alternative would be.  It appears your alternative is to do whatever it takes to convince the public to blindly trust and accept fear-based, minority, outlier opinions.

Also, you have not provided a rational explanation of why you would trust or accept any claims made by any health professionals who supported or did not denounce CWF:

1. If, as Dr. Osmunson’s apparently believes, those professionals who accept the scientific consensus that fluoridation is safe and effective “are lemmings, followers, part of a herd, not scientists.“
2. And, as you apparently believe, they are “[affected by] financial benefit, ignorant, willful blindness, morally corrupt, cowards &/or sociopaths"

Q8 - New) Are all these science and health professionals selectively lemmings, willfully blind, greedy (sorry, [affected by] financial benefit), corrupt, etc., only when it comes to their understanding of the science related to fluoridation?  
~> If so, how would Dr. Osmunson’s 07-09-2018 09:09 PM claim “Yes, they are the best in their field and experts, but not in fluoridation” be even remotely justifiable?

As noted elsewhere, the IAOMT Position Paper Against Fluoride Use with “over 500 citations”, your lists of studies and articles FOs have interpreted as supporting their cause, dozens of opinions from other FOs, and what you accept as “inconsistencies between policy & scientific data” are completely irrelevant to any scientific discussion of the scientific consensus that fluoridation is safe and effective. 

All the tactics of anti-science activists (ASAs) are nothing more than marketing strategies designed and implemented to try and scare the public (most of who are not trained and experienced in science or medicine) into believing the anti-F arguments and interpretations of the evidence have some legitimate credibility.  If the interpretation of “evidence” by anti-F, ASAs was even remotely legitimate and credible, FOs would have been able to change the scientific consensus in discussions with relevant experts and there would be no need to try and scam the public.

Randy Johnson

[rs5526]

The Christian thing to do is to defend the rights of the needy, not to find fault and judge them. 

So my opposition to fluoridating people is an attempt to defend kids, elderly, and in particular the poor who can't afford to buy clean bottled water that has no artificially added fluoride materials.

It is pretty clear to me. 

[RandyJ913440]

Richard Sauerheber – One of your claims is actually partly correct (09-02-2018 04:16 PM), "The Christian [or any honorable] thing to do is to defend the rights of the needy, not to find fault and judge them."  So my support for community water fluoridation is an attempt to defend kids, elderly, and in particular the poor based on the scientific consensus that fluoridation is safe and effective.

It is pretty clear to me. 

For the record, fluoridation opponents, utilize reckless, anti-science, paranoid tactics to demand that a safe, effective public health measure which reduces dental decay in communities be abandoned.  They appear to believe there are no negative consequences to their actions.  Scientific studies from over 70 years, however, clearly show that dental decay rates in low-fluoride areas are higher than in communities with optimal levels of fluoride ions – particularly among those with lower, socioeconomic backgrounds.

References: 

Associations of Community Water Fluoridation with Caries Prevalence and Oral Health Inequality in Children: (2017, Kim, et al.) “These results suggest that CWF programmes are effective in the prevention of caries on permanent teeth and can reduce oral health inequalities among children. The implementation of CWF programmes should be sustained to overcome oral health inequalities due to socio-economic factors and improve children's overall oral health.”

Hospitalizations for dental infections: optimally versus nonoptimally fluoridated areas in Israel. (Klivitsky, et al., 2015) “These results clearly indicate that there is an association between adequacy of water fluoridation and hospitalization due to dental infections among children and adolescents. This effect is more prominent in populations of lower socioeconomic status.”

Comparative effectiveness of water and salt community-based fluoridation methods in preventing dental caries among schoolchildren:  (2016, Fabruccini A, et al.) “CONCLUSION: Fluoridated water appears to provide a better protective effect against dental caries than fluoridated household salt among schoolchildren from developing countries.”

The benefits of water fluoridation across areas of differing socio‐economic status: (2008, Australian Research Centre for Population Oral Health) “The results confirm that there is strong evidence of the effectiveness of water fluoridation across SES groups, even when using an area‐based measure of SES split into 10 categories of disadvantage. Both area‐based SES and the concentration of fluoride in the tap water where children live were related to child oral health outcomes.”

Fluoridation and dental caries severity in young children treated under general anaesthesia: an analysis of treatment records in a 10-year case series: (2013, Kamel, et al.) “Children with severe dental caries had statistically significantly lower numbers of lesions if they lived in a fluoridated area. The lower treatment need in such high-risk children has important implications for publicly-funded dental care.”

The costs and benefits of water fluoridation in NZ: (Moore, et al.) “Community water fluoridation remains highly cost-effective for all but very small communities. The health benefits-while (on average) small per person-add up to a substantial reduction in the national disease burden across all ethnic and socioeconomic groups.”

Water Fluoridation: Health Monitoring Report for England, 2018: "Children from all areas benefited from fluoridation, but children from relatively deprived areas benefited the most. PHE results do not provide convincing evidence of higher rates of hip fracture, Down’s syndrome, kidney stones, bladder cancer, or osteosarcoma due to fluoridation."

Effectiveness of water fluoridation in the prevention of dental caries across adult age groups: (2017, Do, et al.) “Access to FW was associated with caries experience in Australian adults. The magnitude of associations varied between age groups, dependent on the natural history of caries and its measurement by DMFS.”

The differences in healthcare utilization for dental caries based on the implementation of water fluoridation in South Korea: (2016, Cho MS, et al.) “The implementation of water fluoridation programs and these periods are associated with reducing the utilization of dental health care. Considering these positive impacts, healthcare professionals must consider preventive strategies for activating water fluoridation programs...”

A 4-year assessment of a new water-fluoridation scheme in New South Wales, Australia: (2015, Blinkhorn AS, et al.) “Fluoridation of public water supplies in Gosford and Wyong offers young children better dental health than those children who do not have access to this public health measure.”

Community water fluoridation and health outcomes in England: (2015, Young, et al.) “This study uses the comprehensive data sets available in England to provide reassurance that fluoridation is a safe and highly effective public health measure to reduce dental decay. Although lower rates of certain nondental outcomes were found in fluoridated areas, the ecological, observational design prohibits any conclusions being drawn regarding a protective role of fluoridation.”

Summary of: An alternative marker for the effectiveness of water fluoridation: hospital extraction rates for dental decay, a two-region study: (2014, Chestnutt, G.) “After ranking by IMD, DSRs of hospital admissions for the extraction of decayed or pulpally/periapically involved teeth is lower in areas with a fluoridated water supply.”

Water fluoridation in the Blue Mountains reduces risk of tooth decay: (2009. Evans, et al.) “Tooth decay reduction observed in the Blue Mountains corresponds to high rates reported elsewhere and demonstrates the substantial benefits of water fluoridation.”

Community water fluoridation and health outcomes in England: a cross-sectional study: (Young, Et al., 2015) “This study uses the comprehensive data sets available in England to provide reassurance that fluoridation is a safe and highly effective public health measure to reduce dental decay.”

[RossF715288]

On fluoride and salmon, the abstract of a paper in the North American Journal of Fisheries Management, 9:154-162, 1989, ‘Evidence for Fluoride Effects on Salmon Passage at John Day Dam, Columbia River, 1982—1986’ by David Damkaer and Dougas Dey of the National Marine Fisheries Service, Northwest Fisheries Center reads:

Abstract.—There is evidence that fluoride from an aluminium plant near John Day Dam had a significant negative effect on passage time and survival of adult Pacific salmon Oncorhynchus spp. at the dam. In 1982, fluoride concentrations of 0.3-0.5 mg/L were recorded at the dam. These concentrations were probably representative of fluoride levels at the dam in earlier years as well, based on the aluminium plant's fluoride discharge records since 1971. From 1980 to 1982, the time (>150 h) required for upstream migrants to pass John Day Dam and the mortality (>50%) of migrants between Bonneville and McNary dams (below and above John Day Dam) were unacceptably high. Bioassay experiments on the behaviour of upstream migrating adult salmon suggested that fluoride concentrations of about 0.5 mg/L would adversely affect migration. Subsequent experiments suggested that 0.2 mg F/L was at or below the threshold for fluoride sensitivity of chinook salmon O. tshawytscha and below the threshold for fluoride sensitivity of coho salmon O. kisutch. Beginning in 1983 and continuing through 1986, fluoride discharges from the aluminium plant were greatly reduced and there was a corresponding drop in fluoride concentrations in the river. Concurrently, fish passage delays and inter-dam losses of adult salmon decreased to acceptable levels (28 h and <5%, respectively).       

[DavidF928895]

RossF, from the Abstract you presented:

"There is evidence that fluoride from an aluminium plant near John Day Dam had a significant negative effect on passage time and survival of adult Pacific salmon Oncorhynchus spp. at the dam."

These higher concentrations of discharged fluoride are irrelevant to community water fluoridation.  It's kind of like saying that because pressurized, concentrated levels of oxygen can cause oxygen toxicity, therefore breathing air with the optimal level of oxygen is dangerous and somehow relevant to "anti-oxygen" arguments.  

Limnologist Joe Carroll has provided calculations of the effect of community water fluoridation into the Columbia River in Oregon.  This would be relevant to water fluoridation.  You may review his calculations here:  https://ilikemyteeth.org/wp-content/uploads/2013/05/Water-Expert-Letter-Fish-Impact-2005.pdf

But I thank you for your irrelevant comment.

[RossF715288]

DavidF references an April 2005 letter from Joe Carroll and highlights “…we have numerous supported and documented examples that demonstrate the excellent health value in community drinking water fluoridation . . . “.

A year from that Carroll letter the major National Research Council report ‘Fluoride in Drinking Water: A Scientific Review of EPA's Standards’ (2006) provided evidence that endocrine systems and thyroid functions are impaired at exposure levels to fluoride below the consumption levels expected from drinking what is described as optimally fluoridated water.

NRC (2006) also says that kidney patients and diabetics are susceptible subpopulations that are particularly vulnerable to harm from ingested fluorides as low as 1ppm concentration.

The U.S. National Kidney Foundation says that kidney patients should be notified of the potential risk of fluoride exposures.

NRC (2006) also states that fluorides accumulate over time in the pineal gland but at the time of the report, whether fluoride exposure causes decreased nocturnal melatonin production or altered circadian rhythm of melatonin production in humans had not been investigated.

As a calcifying tissue that is exposed to a high volume of blood flow, the pineal gland is a major target for fluoride accumulation in humans with the calcified parts of the pineal gland containing the highest fluoride concentrations in the human body - higher than either bone or teeth.

The 2006 report did, however, state that fluoride is likely to cause decreased melatonin production and to have other effects on normal pineal function, which in turn could contribute to a variety of effects in humans.

Grandjean and Landrigan in their paper ‘Neurobehavioural effects of developmental toxicity’ in the March 2014 issue of the The Lancet stated that epidemiological studies since 2006 had identified fluoride as a developmental neurotoxicant i.e. a chemical that can injure the developing brain. They warned that untested chemicals should not be presumed to be safe to brain development and that chemicals in existing use, like fluoride, and all new chemicals must therefore be tested for developmental neurotoxicity.

Choi et al. in their Environmental Health Perspectives paper ‘Developmental Fluoride Neurotoxicity: A Systematic Review and Meta-Analysis’ showed results that supported the possibility of an adverse effect of fluoride exposure on children’s neurodevelopment and that future research should include detailed individual-level information on prenatal exposure adn neurobehavioral performance. 

A recent study, Bashash et al. ‘Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6–12 Years of Age in Mexico’ published last September in the peer-reviewed journal, Environmental Health Perspectives, by a team of investigators at the University of Toronto, McGill, the Harvard School of Public Health, and other institutions found an association between prenatal exposure to fluoride and cognitive development disorders in children. 

In this study, higher prenatal fluoride exposure, in the general range of exposures reported for other general population samples of pregnant women and non-pregnant adults, was associated with lower scores on tests of cognitive function in the offspring at age 4 and 6–12 years. 

The study’s findings, combined with evidence from existing animal and human studies, reinforce the need for additional research on potential adverse effects of fluoride, particularly in pregnant women and children, and to ensure that the benefits of population-level fluoride supplementation outweigh any potential risks. 

The precautionary principle states that if an action or policy has a suspected risk of causing harm to the public domain (affecting general health or the environment globally), the action should not be taken in the absence of scientific near-certainty about its safety. The burden of proof about absence of harm falls on those proposing an action, not those opposing it.

The precautionary principle is intended to deal with uncertainty and risk in cases where the absence of firm evidence and the incompleteness of scientific knowledge carries potentially serious implications for society.

AARP members will be interested to know that the independent Cochrane Collaboration, which provides high-quality information informing decisions on health issues, found that searching for ‘before and after’ studies did not find any on the benefits of fluoridated water for adults.

Fluoridation of community water fluoridation is well outdated. There are safer, more effective and cheaper ways of implementing sound community oral health programmes.  

[DavidF928895]

Thanks Ross.  This is a great example of what they call “Gish Galloping.”  You had originally brought up an incident about an aluminum plant which had harmed the environment with discharge into a river.  You saw the word “Fluoride” and therefore, in your mind, it must be a valid argument against Community Water Fluoridation, and you presented it as such.

After I pointed out that this factual incident was completely irrelevant to optimally fluoridated water, rather than attempt to defend your comment, you simply move on to a bunch of other arguments which also have the word “Fluoride” in them.

Ok, the 2006 NRC.  There is nothing in that report which says drinking optimally fluoridated water is harmful to anyone.  If there is, I’d like to see it.  (It’s nice to say stuff, but it’s better when you can actually prove it.)

To the contrary.  Dr. John Doull was the Chair of that committee.  This is his quote:  “"I do not believe there is any valid scientific reason for fearing adverse health conditions from the consumption of water fluoridated at the optimal level."  https://ilikemyteeth.org/wp-content/uploads/2013/03/Doull-Email-on-CWF-March-2013.pdf

He was asked about it, and that’s what he said.  So, again, please show me where, in the 2006 NRC, that committee agreed with anything you just said.  Just because it may have appeared in some junk literature doesn’t mean the NRC agreed with it. 

You bring up Grandjean & Choi and “A Systematic Review and Meta-Analysis.”  Question:  Do you even know what that was, or are you just parroting anti-CWF propaganda that you read somewhere?

What we are talking about here is a Review of 27 non-peer-reviewed papers that came from Central Asia & China, Mongolia, Iran, etc.  In China, atmospheric fluoride levels are as much as 100 times higher than they are in the U.S.  In other places in Asia, fluoride levels in water are higher than 33 times the optimal level.  In other words, we are talking about what might happen from high levels of environmental fluoride exposure. 

But you saw the word “Fluoride,” therefore, somehow this is relevant to Community Water Fluoridation. 

Anna Choi herself said, “These results do not allow us to make any judgment regarding possible levels of risk at levels of exposure typical for water fluoridation in the U.S.,” the researchers said in an e-mail response to questions from The Eagle.  https://www.kansas.com/news/article1098857.html

And you brought up a study from Mexico, where, again, Community Water Fluoridation is not practiced. 

And you bring up the “Precautionary Principle” (which you have parroted perfectly.  You say, “The precautionary principle states that if an action or policy has a suspected risk of causing harm to the public domain (affecting general health or the environment globally), the action should not be taken in the absence of scientific near-certainty about its safety.”

Ok, in that case all transportation should end immediately, since millions more people are harmed and killed from automobiles & air travel than have ever been harmed by drinking optimally fluoridated water. . there is harm to the global environment from mass transportation.  Or are you going to be hypocritical about this & say, ‘No, I need my car.’

You also say, “The precautionary principle is intended to deal with uncertainty and risk in cases where the absence of firm evidence and the incompleteness of scientific knowledge carries potentially serious implications for society.”

I don’t know what kind of “firm evidence” you are asking for.  Since hundreds of millions of people drink this stuff every day, they have been for over 70 years now, and there has never been one documented case of any human being who was ever harmed in any way from drinking optimally fluoridated water . . even for as much as a lifetime.

There has never been one other study which has looked at so many people over so great a time span.  So, just what kind of "firm evidence" are you looking for?  

I asked another writer on this AARP webpage for even one documented example of harm, and the best she could come up with was a sworn affidavit from 1968 in which a lawyer diagnosed himself because one of his clients, who also diagnosed himself, wanted to sue the EPA.

But again, I thank you for all of your irrelevant comments and I look forward to the next batch of gish galloping from you.

[rs5526]

I did not say I hated lawsuits. I said my folks didn't believe that is the way to  settle things but many people do and that is their right. 

James Deal is not t a criminal. So answering his questions is not wrong. 

Sorry to burst your bubble but I find James to be intelligent and very good at organic gardening and he believes we need to stop putting wastewater into our rivers and other things I also believe in.

Again this has nothing to do with the holocaust. 

My credentials from UCSD I cannot change so I don't see the problem. The chemistry department told me I can publish what I want under the  UCSD banner which acknowledges  where I was taught, both undergrad and grad degrees and the school of medicine. 

I've published math articles and physics articles (and on fluoride toxicology while collaborating with Dr. Benson there)  

. I am classified staff at Palomar College and am a private group teacher. Unpublished letters I write list UCSD as where my degrees are from. So?