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.
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Cytogenetic effects of hydrogen fluoride gas on maize
Maize seedlings of the genotype C I Sh Wx were fumigated with hydrogen fluoride gas (HF) continuously for 4, 6, 8 and 10 days. Miscrospore mitosis of the treated plants indicated the presence of fragments and bridges suggesting the occurrence of the phenomenon of breakage-fusion-bridge cycle of McClintock. This phenomenon
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Genetic toxicity of fluoride
F- is not mutagenic in standard bacterial systems, but produces chromosome aberrations and gene mutations in cultured mammalian cells. Although there is disagreement in the literature concerning the ability of F- to induce chromosome aberrations in cultured human and rodent cells, the weight of the evidence leads to the conclusion
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The effect of fluorine and lead ions on the chromosomes of human leucocytes in vitro
Human leukocytes in the cultures in vitro were exposed to the action of Pb and F ions at the concentrations of 10-3 M and 10-5 M for Pb and 3.15 x 10-3 M, 3.15 x 10-4 M, 3.15 x 10-5 M for F. Both factors caused structural and quantitative aberrations
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Dental fluorosis and oral health in the African Esophageal Cancer Corridor: Findings from the Kenya ESCCAPE case-control study and a pan-African perspective.
There are no studies of oral health and esophageal cancer in Africa, or of this area's endemic dental fluorosis, an irreversible enamel hypo-mineralization due to early-life excessive fluoride. During 2014-18, we conducted a case-control study of squamous cell esophageal cancer in Eldoret, western Kenya. Odds ratios (AORs (95% confidence intervals))
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Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents—A cost–benefit analysis
Water fluoridation programs in the United States and other countries which have them use either sodium fluoride (NaF), hydrofluorosilicic acid (HFSA) or the sodium salt of that acid (NaSF), all technical grade chemicals to adjust the fluoride level in drinking water to about 0.7–1 mg/L. In this paper we estimate the
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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.
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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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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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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.
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