Fluoride & Bone Cancer (Osteosarcoma)

Fluoride & Bone Cancer (Osteosarcoma)

 

1. Fluoridation & Bone Cancer: Quick History

A substantial body of evidence (both animal and human) currently exists suggesting that fluoride may cause osteosarcoma, a rare and deadly cancer of the bone.

The following is a quick summary of the evidence, followed by more in-depth information.

In 1977, US Congress requested that animal studies be conducted to determine if fluoride causes cancer. Roughly a decade later, these studies were completed by the US National Toxicology Program (NTP 1990).

Among other findings, the National Toxicology Program found a statistically-significant, dose-dependent increase in osteosarcoma among the fluoride-treated, male rats. In other words, the bone cancer rate among fluoride-treated, male rats increased as the dose of fluoride increased.

Considering that bones are the primary site of fluoride accumulation, and that bone cancer in humans is found predominantly among young males, the finding of increased bone cancer in male rats is highly significant. According to a review of NTP’s findings by the World Health Organization:

“Such a (dose-dependent) trend associated with the occurrence of a rare tumour in the tissue in which fluoride is known to accumulate cannot be casually dismissed.” (WHO 2002; emphasis added)

Soon after the NTP’s findings became public, the US National Cancer Institute (NCI) conducted a review of its national cancer registry to see if the rate of osteosarcoma was higher in fluoridated vs. non-fluoridated areas. (Hoover 1991) The NCI’s review found that the occurrence of osteosarcoma in young males was, in fact, significantly higher in the fluoridated versus unfluoridated communities. However, despite this remarkable finding, the NCI concluded that the increased incidence of osteosarcoma in fluoridated areas was unrelated to water fluoridation. According to the US Public Health Service:

“Although the increase in rates of osteosarcoma for males during this period was greater in fluoridated than nonfluoridated areas, extensive analyses revealed that these patterns were unrelated to either the introduction or duration of fluoridation.” (USPHS 1991)

As a follow-up to the NCI’s review, the New Jersey Department of Health conducted its own study of fluoridation & osteosarcoma in various New Jersey counties. (Cohn 1992) As with the NCI, New Jersey’s Department of Health found that the rate of osteosarcoma did in fact occur at higher rates in young males from fluoridated versus unfluoridated areas. Between the years 1970 and 1989, the rate of osteosarcoma (among 10-19 year old males) was found to be 3.5 to 6.3 times greater in the fluoridated versus unfluoridated areas!

Adding further evidence and plausibility to a fluoride-osteosarcoma connection is the existence of numerous laboratory studies reporting that fluoride is a mutagen (i.e. it causes damage to genes). Most chemicals that are mutagens are also carcinogens (i.e. they cause cancer). Of particular interest is a 1996 study published in Mutation Research which reported that sodium fluoride was mutagenic to rat bone. (Mihashi & Tsutsui 1996)

It should also be emphasized that the NTP bioassay for fluoride discussed above also found other types of cancer besides osteosarcoma in the fluoride-treated rats. According to the initial reports by the contractor (Battelle Laboratories), the fluoride-treated animals also had elevated rates of oral and liver cancer. An increased incidence of thyroid cancer was also found. However, under highly questionable circumstances, a review committee in the NTP later downgraded ALL of the non-bone tumors reported by the contractor. The Chief Toxicologist at the EPA’s Office of Drinking Water at the time, Dr. William Marcus, strongly objected to these downgradings, but was later fired by the EPA for voicing his concerns in public.

In summation, the main lines of evidence suggesting that fluoride causes osteosarcoma include:

a) A government-conducted animal study (NTP 1990) finding a dose-dependent increase in osteosarcomas among fluoride-treated rats,

b) National cancer registry data from the US National Cancer Institute (Hoover 1991) showing higher rates of osteosarcoma in fluoridated versus unfluoridated areas (among young males),

c) A study from the New Jersey Department of Health (Cohn 1992) showing higher rates of osteosarcoma in fluoridated versus unfluoridated areas (among young males),

d) Laboratory studies showing that fluoride is a mutagenic agent, including a recent study reporting that fluoride is mutagenic to bone. (Mihashi & Tsutsui 1996) Most mutagens are also carcinogens (i.e. they cause cancer).


2) Interview with Dr. William Marcus, US Environmental Protection Agency 

The following is an excerpt from Gary Null’s 1995 interview with Dr. William Marcus, former Chief Toxicologist at EPA’s Office of Drinking Water. In the interview, Marcus discusses the findings of the National Toxicology Program’s cancer bioassay for fluoride.

Marcus: When I got a hold of the contractor report and reviewed it very carefully, not only was it reporting cancers in the animals, [it was reporting] osteosarcomas which bothered me a lot because I’ve been trying to produce osteosarcomas in animals for almost 20 years and the only luck I ever had was with an experiment in dogs and monkeys, and the osteosarcomas took nearly the lifetime of the animals, and we were using radium which specifically produces that in bones. And here we have a compound commonly available – fluoride – that did it in rats in two years or less. That was upsetting to begin with. Secondarily…in that same study, there were cancers of the liver that are very rare according to the board certified veterinary pathologist at the contractor, Battelle. And those really were very upsetting because they were hepatocholangiocarcinoma, a very rare, rare, liver cancer… Something similar to that occurred with vinyl chloride in a far less well conducted study and it was determined that it was carcinogenic, highly carcinogenic. And then there were several other kinds of cancers found in the jaw and other places and I felt at the time that the report was very, very interesting. It showed that the levels of the fluoride that caused the cancers in the animals were actually lower than those levels seen in people who are ingesting lower amounts but for longer periods of time and that was very very worrisome. It meant that the general population could be exposed to fluoride known to cause cancer in animals and have levels near the cancer being produced in the bones.

Gary Null: And what did you do and what happened?

Marcus: Well I went to a meeting that was held in Research Triangle Park in April 1990, the latter part of April, in which the NTP was presenting their review of the study. And I went with several colleagues of mine, one of whom was a board certified veterinary pathologist who had originally reported hepatocholangiocarcinoma as a separate entity in rats and mice. I asked him if he would have an opportunity to look at the slides to see if that  really was a tumor or the pathologist at Battelle had made an error and he told me after looking at the slide that in fact it was correct. And at the meeting every one of the cancers that was reported by the contractor had been down-graded by the NTP.

Now I’ve been in the toxicology business looking at studies of this nature for nearly 25 years and I’ve never seen that; never ever seen where every single endpoint that was a cancer endpoint had been down-graded. I’d seen one or two endpoints argued over, usually on a definition [of] what is a cancer in that particular tissue. But I’ve never seen every one of them down-graded. I found that very suspicious and I went to see an investigator in the Congress at the suggestion of my friend Bob Carton. And this gentleman and his staff investigated very thoroughly and found out that the scientists at the NTP down at Research Triangle Park had been coerced to change their findings.

Gary Null: Coerced by whom?

Marcus: I never really got that. But the only people that can coerce them were their supervisors.

Gary Null: Why would they want to coerce them? What were they trying, who or what were they trying to protect?

Marcus: Well as you well know fluoride is still recommended as a treatment for prevention of dental caries, tooth decay, and has been touted as such by the Public Health Service since 1953-54 and they ha[ve] a reputation to protect. It wouldn’t do for them to have been making this strong recommendation over the years and now to find out that they have been exposing the general public to a material known, now known, to be potentially carcinogenic in humans. And there have been other studies…”

For background info on EPA’s Firing of Marcus, see:


3) Interview with Dr. J. William Hirzy, US Environmental Protection Agency 

The following is an excerpt of Michael Connett’s interview with Dr. J. William Hirzy, the Senior Vice President of EPA’s Headquarters Union in Washington DC. The interview took place on July 3, 2000, a couple of days after Hirzy testified before the US Senate calling for an independent review of the tumor slides from the NTP bioassay. It is Hirzy’s and the Union’s belief that the downgrading of the tumors was politically motivated and not scientifically defensible.

Q: How was the study conducted? What did they do?

Hirzy: Groups of 50 animals, rats and mice, were dosed with fluoride in their drinking water either at zero, eleven, forty-five, or seventy-nine parts per million fluoride over their entire lives. Normally that is essentially a two year period. And then the animals were autopsied… and their health status was tabulated including tumors and so forth.

Q: And the study was done by an independent contractor?

Hirzy: Done by Batelle laboratories.

Q:
What were Batelle’s findings?

Hirzy: There were tumors in the oral cavities of the test animals. There was osteosarcoma (bone cancer) in male rats. There was also an incidence, a relatively high incidence of rare liver tumors in mice, not the normal kind of liver tumor that is seen. This was hepatocholangiocarcinoma which was a relatively rare and newly discovered tumor actually. The pathologist Melvin Reuber who discovered that was actually part of the review group that worked on this bioassay.

The tumor incidence that was originally reported would have supported a finding of clear evidence of carcinogenicity for sodium fluoride, based on all these tumors that I mentioned. There was also some osteosarcomas not of the bone but found in soft tissue which is a rarity. Taking all of those tumors into account, it would have led to a finding of clear evidence of carcinogenicity. However, a commission was appointed by the Department of Health and Human Services that came down to rescue fluoridation from such adverse findings.

Figure 1 (a) & (b): Histograms showing composites of the neoplasms found in the rats, many cancerous. (From “Fluoride: risks and benefits? Disinformation in the service of big industry.” David R. Hill. http://www.fluoridation.com/calgaryh.htm )


H: Hepatocholangiocarcinoma S: Squamous TFCA: Thyroid follicular cell adenoma O: Osteosarcoma

Q: The American Dental Association claimed that the rats were fed levels of sodium fluoride which humans don’t receive in their diet, 79 parts per million, 45 parts per million, and so the results were irrelevant to humans because the doses were so high. How would you respond to that point?

Hirzy:
Well, it’s common practice in cancer bioassays, in order to limit the number of animals that are used, to give doses that are generally always in excess of what humans get. It’s a matter of statistics basically.

The level of regulatory concern at EPA generally is one person in a million, one person in a hundred thousand, one person in ten thousand, one person in a thousand developing cancer from a particular exposure given the kinds of exposures to a chemical that humans might get. Now in order to mimic that exactly in an animal population you’d have to study a million animals, or a hundred thousand animals, or ten thousand animals, or a thousand animals and this begins to get completely unreasonable in terms of use of animals, cost, and the like.

So what we do is rather to limit the number of animals but increase the dose on the assumption that there’s, what we call, a linear dose response curve…

We do preliminary studies to find out how much of the test material the animals can tolerate without showing overt signs of toxicity. We say that that’s the ‘maximum tolerated dose’ that the animals can have and we say that that’s going to be the upper limit of dosing in this study – with the idea of loading up the animal with the chemical so that with 50 animals in a group the likelihood of them developing cancer, if this material is carcinogenic, is going to be measurable within 50 animals.

And then from the ‘maximum tolerated dose’ the doses are scaled down so that we have a range of doses below the tolerated dose down to a zero control, so that one could plot from zero exposure in the control group to the maximum tolerated dose and then plot the response based on these different doses.

One normally gets some sort of a dose response curve if the material is carcinogenic. And that’s what was seen in the case of sodium fluoride. The highest dose level by the way, 79 parts per million, is relatively low compared to the doses that are given to the animals in other corresponding bioassays. It is not at all unusual in a cancer bioassay for animals to get a 1,000 or 10,000 times the dose that humans get. In this bioassay, the level of 79 parts per million of fluoride was only literally 79 times greater than the so-called ‘optimum’ level. It’s only about 20 times higher than the level which the EPA says is ok to have in your drinking water. That’s a remarkably close level to have the highest dose level in an animal study and to have a positive response for cancer in the anticipated target organ, namely the bone, it’s a remarkable finding.

Q: So have other chemicals been defined as carcinogenic based on studies like this?

Hirzy: Oh yes.

Q: Where they actually dosed the rats at higher levels than they dosed with fluoride?

Hirzy: Yes…And the dose levels are much higher compared to what the human exposures are, as opposed to the situation here. Here the animals got overt, frank bone tumors, bone cancer, malignant cancer of the bone, at a level only twenty times higher than the EPA says is safe to drink. That is a remarkable narrow margin of safety.

Table: Comparison of fluoride dose causing bone cancer with doses used to test other suspected carcinogens and their Maximum Contaminant Levels. From “Fluoride: risks and benefits? Disinformation in the service of big industry.” David R. Hill. http://www.fluoridation.com/calgaryh.htm

Substance

Daily Dose
(mg/kg/day)

Maximum Contaminant Level (MCL)
(mg/litre)

Fluoride

7.9

4

Vinyl chloride

1.7

0.002

Carbon tetrachloride

47

0.005

Benzene

50

0.005

Chloroform

160

0.100

Tetrachlorethylene

386

0.005

Red dye #3

4000

none


Q: Now, is it true that it’s very difficult to produce osteosarcomas in rats?

Hirzy: Yes, it’s a relatively rare tumor in rats and again Dr. Marcus has written of this in his memorandum pointing out the very few incidences in a control population of other bioassays in which osteosarcoma was reported. It’s a very, very low incidence tumor.

Q:
And I believe that the only other chemical that Dr. Marcus knew of that could produce osteosarcoma that quickly was radium.

Hirzy: Radium. That’s right.

Q: And is that a known…

Hirzy: That’s a known human carcinogen as well.

Q: And in the Batelle lab they found a certain kind of liver cancer that you had mentioned.

Hirzy:
Yes.

Q: This was a very rare form of cancer I understand.

Hirzy: That’s right. Hepatocholangiocarcinoma is what it was. It’s basically a rare cancer of the bile duct in the liver.

Q:
And in normal cancer studies if a rare cancer is found in the dosed group of animals, does that usually generate increased interest?

Hirzy: Absolutely. Yes indeed, it does. It increases the evidence of carcinogenicity if a rare cancer shows up in the dosed group and not in the controls.

Q:
And has the EPA or any government health organization followed up to find out, to better understand this relationship between fluoride and this rare liver cancer?

Hirzy:
Not that I’m aware of.

…There’s other evidence for carcinogenicity besides this bioassay. There’s a substantial body of mutagenesis studies, that is studies where a chemical’s ability to cause changes in DNA have been proven. Also, fluoride is known to be an enzyme poison in any number of enzyme systems. And repair of damaged DNA by enzymes is an important anti-cancer mechanism that the body has.

If some of these repair enzymes are inhibited by fluoride, it could indicate fluoride’s ability to work as what we call a ‘promoter’ as opposed to a ‘primary’ carcinogen.

Carcinogenesis is a very interesting and complex subject. There are so called ‘complete carcinogens’ – chemicals that in fact damage the DNA and then allow an aberrant cell to reproduce wildly and develop a malignant tumor. There are other substances which are called ‘promoters’ which do things like inhibit repair enzymes and once an incipient cancer forms – if these repair enzymes are not able to go in, sense the aberrant cell or the aberrant strands of DNA, and either repair the DNA or kill the cell – then the tumor is allowed to grow. Those are classified as promoters.

It may well be that fluoride works in both ways as a primary carcinogen and as a promoter.

Q:
And it would be a promoter of cancer by damaging or inhibiting the enzymes that can be protective?

Hirzy:
That’s right.

Q: If these tumors in the rats weren’t downgraded by the National Toxicology Program, what would have been the ramifications for fluoridation?

Hirzy:
It would have been over. If in fact the classification of Probable Human Carcinogen, which would have flowed from the finding of clear evidence here, it would have required that the EPA set a Maximum Contaminant Level Goal of zero. All carcinogens have a Maximum Contaminant Level Goal of zero. That is, you recall, the health based standard, the one EPA sets saying that at this level we anticipate no adverse health effects in the entire population with an adequate margin of safety. For carcinogens, the policy is no level of exposure is safe, so the MCLG is zero. If it’s zero, it means you can’t add any of this stuff to any water supply and that’s the end of fluoridation.


4) National Cancer Institute’s Data on Fluoridation/Osteosarcoma 

The following is a review of the National Cancer Institute’s national cancer registry data (1973-1989) on fluoridation/osteosarcoma. The NCI’s data revealed that the rate of osteosarcoma is higher, and increasing at a greater rate, in fluoridated vs. non-fluoridated communities. Despite this finding, the NCI dismissed the possibility that fluoridation could be related to the the elevated occurrence of osteosarcomas in the fluoridated areas. In the following review, Dr. John Colquhoun discusses NCI’s data as well as NCI’s rationale for concluding that fluoridation is not related to osteosarcoma. The reference for Colquhoun’s review is as follows: Colquhoun J. (1993). Time trends for bone and joint cancers and osteosarcomas in the surveillance, epidemiology and end results (SEER) program, National Cancer Institute. Fluoride 26: 66.

This study presents incidence rates for bone and joint cancers and osteosarcomas for two time periods (1973-1980 and 1981-1987) collected by the National Cancer Institute from its “SEER” program, a network of cancer registries covering 10% of the USA population. The incidence of all bone and joint cancers over all ages increased only slightly between the two periods. But when examined by age, the rates for under 20-year-olds increased 18% for the sexes combined, reflecting a 23% rise in males and a 13% rise in females. The rise in osteosarcomas among males under 20 was 53%. This rise in bone and joint cancers among males under 20 occurred in fluoridated counties (rise of 39%) but not in non-fluoridated counties (decline of 5%).

Osteosarcoma is the rare bone cancer (around one case per 100,000 of population) which originates most often at the growing ends of bones and is most prevalent among males aged 10 to 19 years. In an earlier study confined to two cancer registries these authors reported “When restricted to persons under age 20, the rates for bone and joint cancers in both sexes rose 47% from 1973-80 to 1981-87 in the fluoridated areas of Seattle and Iowa and declined 34% in the non-fluoridated areas. For osteosarcomas in males under 20, the rates increased 79% in the fluoridated areas and decreased 4% in the non-fluoridated areas.”

However, they claimed that “there was no evidence of an increase in the incidence ratios with increasing duration of fluoridation.” That is, the increase in fluoridated areas had occurred whether the young males had lived all or only a part of their lives in a fluoridated area. Applying the same approach to their larger study of all cancer registries, they arrived at the same conclusion that “these increases are unrelated to the timing of fluoridation, and thus are not linked to the fluoridation of water supplies.”

They admit, however, that in the earlier study “the observed numbers on which some of these incidence ratios are based are relatively small.” To compensate for this problem in their expanded analysis of all registries, they added data to the fluoridated areas (from Detroit, Atlanta, San Francisco and Connecticut) and to the non-fluoridated areas (mainly from Utah and New Mexico), commenting: “The resulting comparison of trends between these different areas could be suspect.” Nonetheless they proceeded with their analysis and concluded: “For none of the categories revealing differences in time trends between fluoridated and non-fluoridated areas is there any evidence of an increase in incidence ratios by duration of fluoridation. For osteosarcomas, there is even some evidence of a decline in the ratio with duration of fluoridation.”

It is possible to interpret these data quite differently. Many will question the assumption, in the first place, that “duration of fluoridation” is an appropriate measure of dose relationship, given the small numbers involved in this extended part of the analysis. Nowhere in their report do the authors attempt to explain why there is a consistent large increase in bone and joint cancers, especially osteosarcomas among young men, in fluoridated areas but not in non-fluoridated areas.


5) New Jersey Department of Health study on Fluoridation/Osteosarcoma

The following is the Executive Summary from the New Jersey Department of Health study on fluoridation/osteosarcoma. In the study, the Department of Health found that young males living in fluoridated communities had significantly higher rates of osteosarcoma than young males living in non-fluoridated areas. The reference for the study is as follows: Cohn PD. (1992). A Brief Report On The Association Of Drinking Water Fluoridation And The Incidence of Osteosarcoma Among Young Males. New Jersey Department of Health Environ. Health Service: 1- 17.

It is well known that fluoride provides important public health benefits by effectively preventing dental caries in children. The Public Health Service (1991) endorses artificial fluoridation of drinking water at a concentration of 0.7-1.2 milligrams of fluoride per liter of water (or parts per million) as the optimally beneficial level for preventing dental caries. The U.S. Environmental Protection Agency (USEPA) allows up to 2 parts per million for artificial fluoridation and up to 4 parts per million for naturally occurring fluoride (National Primary Drinking Water Regulations, 40 CFR 141.11 and 143.3). Other potential sources of fluoride ingestion include food, vitamins, and swallowed toothpaste.

Recently, a national study of drinking water fluoridation at the county level found a significant association with osteosarcoma incidence among males under 20 years of age (Hoover et at 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. Furthermore, the simple study design used did not have individual information on the average amount of water ingested daily, use of dental fluoride supplements, long term residence, other potentially confounding (or causal) exposures, or genetic involvement.

As a follow-up to the study by Hoover et at, 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. No interviews were conducted and data on individual residential history, average amount of water ingested, use of dental fluoride supplements, exposure to other carcinogens and familial cancer history were not available. In addition, the total number of cases was small. Therefore, observations should be interpreted cautiously because: 1) exposure misclassification could lead to under- or overestimation of effects, 2) unmeasured confounding by other potential causes of osteosarcomas could introduce bias leading to under- or overestimation of effects of exposure, and 3) an observed association could be due to chance.

Osteosarcoma incidence between 1979 and 1987 was compared by ecologic epidemiology methods to water supply fluoridation in seven counties in central New Jersey. Twelve cases were diagnosed among males under age 20 in fluoridated municipalities vs eight cases in non-fluoridated municipalities. The rate ratio of incidence in fluoridated vs non-fluoridated municipalities was 3.4 with a 95% statistical confidence interval (95%Cl) between 1.8 and 6.0. All twelve cases in fluoridated municipalities resided in a three county area with the greatest prevalence of fluoridation. The rate ratio of incidence in fluoridated vs non-fluoridated municipalities in the three county area was 5.1 (95%CI 2.7-9.0). Among 10-19 year old males in those three counties, the rate ratio was 6.9 (95%Cl 3.3-13). No other age/sex groups exhibited significant association with fluoridation.

Because of the limitations of the study design and the small numbers of cases that occurred, this analysis does not imply a causal connection between fluoridation and osteosarcoma. From the public health perspective, the findings are not sufficient to recommend that fluoridation of water supplies be halted, but do support the importance of investigating the possible link between osteosarcoma and overall ingestion of fluoride, In addition, it is recommended that dentists identify whether children reside in fluoridated communities and appropriately advise on fluoride supplementation.

Reprints: State of New Jersey Department of Health, Trenton NJ 08625 0360, USA.


6) Review of Fluoridation/Osteosarcoma issue by Dr. John Lee

The following article was published in the journal Fluoride. The reference for the article is as follows: Lee JR. (1993). Fluoridation and bone Cancer. Fluoride 26: 79-82.

The NTP (National Toxicology Program) fluoride/cancer study of rats and mice (1) found a statistically significant dose-related increase of osteosarcoma incidence in male rats and, in addition, found fluoride correlations with thyroid follicular cell adenomas, oral and nasal squamous dysplasia, a rare type of liver cancer (hepatocholangiocarcinoma), and, as might have been expected, extensive osteosclerosis. Following this, the Public Health Service, under Dr Hoover et al, reviewed the limited SEER epidemiological data which also showed a significant association of water fluoridation with osteosarcoma incidence among males under 20 years of age (2). However, the meaning of this association was questioned by the PHS because of the apparent absence of a linear trend of a putative association over time of which water supplies were fluoridated. Despite this question, it is clear from the data that osteosarcoma in young men had increased over time and that this increase was greater in fluoridated areas. Also, a New York State study, excluding New York City, attempted to analyze its hospital and population data in regard to bone cancer incidence since the 1950s (3). However, due to a change in diagnostic classification from body site (ie., simply, “bone cancer”) to cell type (osteochondroma, Ewing’s sarcoma, and osteosarcoma) in the Mid-1970s, the true change in incidence of osteosarcoma cannot be calculated. Despite the fact that osteosarcoma is rare (2.9 cases per million people on average annually in New Jersey), it is the most common primary malignant tumor of bone and is one of the principal cancers of childhood. Dr Cohn therefore thought it appropriate to survey its incidence in New Jersey relative to water fluoridation (4).

In his executive summary, Dr Cohn reports his findings of a strong statistical association between water fluoridation and osteosarcoma in young men but points out that the total number of cases is small and that he obtained no data concerning individual residence history, average water ingestion, use of dental fluoride supplements, exposure to other carcinogens, or family cancer history. For these reasons Dr Cohn advises that the results be interpreted cautiously. However, health decisions most often must be made on data which, from the viewpoint of pure science, are in one way or another incomplete. This is inherent in the practice of medicine.

Tables of the study results are reproduced on the following pages.

It should be noted that twelve cases of osteosarcoma were diagnosed among males under 20 in a three county area with the greatest prevalence of fluoridation. Of these, 2 were of age 0-9 and 10 were of age 10-19 years. The rate ratio of incidence in fluoridated vs non-fluoridated municipalities in the three county area was 5.1 (95% CI 2.7-9.0)*. Among 10-19 year old males in those three counties, the ratio rate was 6.9 (95% CI 3.3-13). No other age/sex groups exhibited significant association with fluoride. Thus it can be seen that, for these populations, the chance of osteosarcoma for males age 10-19 years was 6.9 times higher in the fluoridated municipalities.

As noted by Dr Cohn, the etiology of osteosarcoma has not been established. The fact that rapidly growing bone in adolescent males is most susceptible to the development of osteosarcoma suggests that fluoride, which is known to be toxic to bones and a potent enzyme inhibitor, may act as a cancer promoter during this narrow window of susceptibility. Given this, the available SEER epidemiologic data may be more significant than appreciated by the PHS which discounted the observed fluoride/osteosarcoma correlation on the basis of the absence of a linear trend of association with duration of time the water supplies were fluoridated. However, if fluoride acts as a cancer promoter, rather than an initiator, the duration/latency assumption is not warranted.

In the context of the strong correlation of fluoride to osteosarcoma in male rats in the NTP study and the strong epiderniologic evidence of osteosarcoma incidence increase in young males in the US, especially in fluoridated communities, this report from New Jersey adds considerable weight to the probability that fluoride does indeed increase the risk of osteosarcoma among males.

Furthermore, fluoridation/caries studies of the past two decades (5-7), including the latest National Institute of Dental Research study (7), indicate that caries reduction in U.S. schoolchildren is not significantly correlated with fluoridation status. Therefore, given that osteosarcoma is potentially fatal and caries is not, and that other documented studies show fluoride-related increases in hip fractures, dental fluorosis, and other health damaging effects, it would be wise to cease all artificial fluoridation. Anyone who chooses to give their children additional fluoride in spite of all these risks would still be free to do so. I can think of no other agent with this degree of risk which is mandated by the PHS to be added to our food or water. The decision to use the agent should be left to the individual and his/her health advisor.

References

1. Maurer JY, Cheng MC, Boysen BG, Anderson RL. Two-year carcinogenicity study of sodium fluoride in rats. Journal, National Cancer Institute 82 111811261990.
2. Hoover RN, Devesa S, Cantor K, Fraurneni JF Jr. Time trends for bone and joint cancers and osteosarcomas in the Surveillance, Epidemiology and End Results (SEER) Program, 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, 1991 pp F 1 -177.
3. Mahoney MC, Nasca PC, Burnett WS, Mehus JM. Bone cancer incidence rates in New York State: Time trends and fluoridated drinking water. American Journal of Public Health 81475479 1990.
4. Cohn PD. A brief report on the association of drinking water fluoridation and the incidence of osteosarcoma among young males. New Jersey Department of Health, Trenton NJ November 8 1992.
5. Hildebolt CF, Elvin-Lewis H, Molnar S et al. Caries prevalences among geochemical regions of Missouri. American Journal of Physical Anthropology 78 79-92 1989.
6. Yiamouyiannis J A. Water fluoridation and tooth decay results from the 1986- 1987 national survey of US schoolchildren. Fluoride 23 55-67 1990
7. Brunelle JA, Carlos JP. Recent trends in dental caries in US children and the effect of water fluoridation. Journal of Dental research 69 (Special Issue) 7237281990.


7) Links for Further Reading 

a) New study (2001) finds association between osteosarcoma and high fluoride content of bone. See abstract…

b) A 1996 study discovers possible mechanism of action by which fluoride causes cancer in bone. See abstract…

c) Another study finds relationship between fluoridation status and increased osteosarcoma. See abstract…

d) A critique of a study reporting no association between fluoridation and osteosarcoma. See critique…

e) Higher rate of osteosarcoma found in Republic of Ireland vs. unfluoridated North. See article…

f) A review of NTP’s Cancer Bioassay by former EPA scientist, Dr. Robert Carton. See review…

g) A review of NTP’s Cancer Bioassay by MIT’s Dr. Edward Calabrese. See review…

h) A review of NTP’s Cancer Bioassay by World Health Organization. See review…

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