Abstract
BACKGROUND: Recent animal studies of the potential carcinogenicity of fluoride prompted an examination of bone cancer incidence rates. METHODS: Trends in the incidence of primary bone cancers, including the incidence of osteosarcomas were examined among residents of New York State, exclusive of New York City. Average annual osteosarcoma incidence rates in fluoridated and non-fluoridated areas were also compared. RESULTS: Among persons less than 30 years of age at diagnosis, bone cancer incidence among males demonstrated a significant increase since 1955, while incidence among females has remained unchanged. A significant decrease in bone cancer incidence rates since 1955 was observed among both males and females age 30 years and over at time of diagnosis. Osteosarcoma incidence rates have remained essentially unchanged since 1970, among both younger and older males and females. The average annual age adjusted incidence of osteosarcomas (1976-1987) in areas served by fluoridated water supplies was not found to differ from osteosarcoma incidence rates in non-fluoridated areas. CONCLUSIONS: These data do not support an association between fluoride in drinking water and the occurrence of cancer of the bone.
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Aluminum stimulates the proliferation and differentiation of osteoblasts in vitro by a mechanism that is different from fluoride.
Micromolar concentrations of aluminum sulfate consistently stimulated [3H]thymidine incorporation into DNA and increased cellular alkaline phosphatase activity (an osteoblastic differentiation marker) in osteoblast-line cells of chicken and human. The stimulations were highly reproducible, and were biphasic and dose-dependent with the maximal stimulatory dose varied from experiment to experiment. The mitogenic
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Fluoridation and cancer: The biology and epidemiology of bone and oral cancer related to fluoridation
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
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Fluoride exposure in public drinking water and childhood and adolescent osteosarcoma in Texas.
PURPOSE: The purpose of this study was to examine the association between fluoride levels in public drinking water and childhood and adolescent osteosarcoma in Texas; to date, studies examining this relationship have been equivocal. Using areas with high and low naturally occurring fluoride, as well as areas with optimal fluoridation,
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Revisiting the fluoride-osteosarcoma connection in the context of Elise Bassin's findings: part I
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An assessment of bone fluoride and osteosarcoma
The association between fluoride and risk for osteosarcoma is controversial. The purpose of this study was to determine if bone fluoride levels are higher in individuals with osteosarcoma. Incident cases of osteosarcoma (N = 137) and tumor controls (N = 51) were identified by orthopedic physicians, and segments of tumor-adjacent
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NTP Bioassay on Fluoride/Cancer (1990)
In 1977, the U.S. Congress requested that animal studies be conducted to determine if fluoride can cause cancer. The result of the Congressional request was an extensive animal study conducted in the 1980s by the National Toxicology Program (NTP) and published in 1990. The main finding of NTP's study was a dose-dependent increase in osteosarcoma (bone cancer) among the fluoride-treated male rats.
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Fluoride's Mutagenicity: In vitro Studies
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 (i.e. they can cause cancer). As is typical for in vitro studies, the concentrations of fluoride that have generally been tested
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Fluoride/Osteosarcoma Link Is Biologically Plausible
The "biological plausiblility" of a fluoride-osteosarcoma link is widely acknowledged in the scientific literature. The biological plausibility centers around three facts: 1) Bone is the principal site of fluoride accumulation, particularly during the growth spurts of childhood; 2) Fluoride is a mutagen when present at sufficient concentrations, and 3) Fluoride can stimulate the proliferation of osteoblasts (bone-forming cells).
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A Critique of Gelberg's Study on Fluoride/Osteosarcoma in New York
The case-control study by Gelberg, published first as a PhD dissertation and then later in two peer-reviewed journals, may represent the most substantive study on fluoride/osteosarcoma previous to Bassin’s 2001 analysis. In assessing Gelberg’s data, we were at first struck by the existence of several notable errors in both the thesis and papers. While these errors do raise questions about the study, our primary concern with Gelberg’s work relates to the methods she used to analyze her data.
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Fluoride's Mutagenicity: In vivo Studies
Consistent with dozens of in vitro studies, a number of in vivo studies, in both humans and animals, have found evidence of fluoride-induced genetic damage. In particular, research on humans exposed to high levels of fluoride have found increased levels of "sister chromatid exchange" (SCE). As noted in one study: "In
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