Abstract

Data indicating a more rapid increase in cancer death rate in fluoridated than in nonfluoridated cities were analyzed to determine to what extent the net increase observed in fluoridated cities could be attributed to age, race or sex. Between 1952-1969, no significant fluoridation-linked increase in cancer death rate could be observed in populations 0-24 and 25-44 yr of age. In populations 45-64 yr of age, a fluoridation-linked increase in cancer death rate of 15/100,000 population was observed (P < .02); in populations 65+ yr of age, an increase of 35/100,000 was observed (P < .05). The fluoridation-linked increase in cancer death rate could not be ascribed to changes in the racial or sex compositions of the fluoridated and nonfluoridated populations.

• Related Studies :

  • Chromosome aberrations in cultured rat bone marrow cells treated with inorganic fluorides

    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.

  • Serum fluoride and sialic acid levels in osteosarcoma

    Osteosarcoma is a rare malignant bone tumor most commonly occurring in children and young adults presenting with painful swelling. Various etiological factors for osteosarcoma are ionizing radiation, family history of bone disorders and cancer, chemicals (fluoride, beryllium, and vinyl chloride), and viruses. Status of fluoride levels in serum of osteosarcoma

  • The fluorine content in favorite foods of Japanese

    Summary The fluorine content of Japanese foods was determined and the daily intake of fluorine by the individual from the rural diet in the central Japan was estimated with different crop years. In 1958 the fluorine intake of a person was 4.38 mg daily in winter, and in 1965 was 11.13

  • Clastogenic activity of sodium fluoride in great ape cells

    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

  • Analysis of chromosomal abnormalities at anaphase-telophase induced by sodium fluoride in vitro

    Don Chinese-hamster cells were treated with 25, 50, or 75 micrograms/milliliter (microg/ml) of sodium-fluoride (7681494) to determine the chromosomal effects of fluoride exposure on these cells. Cultures were assayed at 12, 24, and 36 hours after initiation of treatment. Chromosomal aberrations were recorded for all the concentrations used. Maximum effect

• Related FAN Content :

  • Fluoride & Liver Cancers in NTP Bioassay

    On October 28, 1988, Battelle Columbus Laboratories submitted its Final Report to the NTP concerning the results of the Mouse study. The principal finding of Battelle's report was that a dose-dependent increase of a rare liver cancer (hepatocholangiocarcinoma) had occurred in the fluoride-treated male and female mice.

  • Fluoride & Osteosarcoma: A Timeline

    Several human epidemiological studies have found an association between fluoride in drinking water and the occurrence of osteosarcoma (bone cancer) in young males. These studies are consistent with the National Toxicology Program's (NTP) cancer bioassay which found that fluoride-treated male rats had an dose-dependent increase in osteosarcoma. Although a number of studies 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 based on recent results, is the critical question with respect to fluoride and osteosarcoma.

  • 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).

  • Micronucleus and Sister Chromatid Exchange Frequency in Endemic Fluorosis

    The rise of sister chromatid exchange (SCE) and micronucleus (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.

  • 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.