Abstract
The frequencies of chromosomal aberrations (CA) and micronuclei (MN) in peripheral blood lymphocytes of 40 workers at a phosphate fertilizer factory in North China, were studied. HF and SiF4 are the main air pollutants and small amounts of dust containing fluoride, NH3 and SO2 were also present in the factory. It was shown that the chemicals caused an increase in both CA and MN. The mean frequencies per 100 metaphase of major CA type (chromosome rings, translocations, and dicentrics) of the workers and the non-exposed controls were 0.91 and 0.24 (p < 0.01), respectively. The average percentages of lymphocytes with MN of the workers and the controls were 1.55 +/- 0.71 and 0.62 +/- 0.54 (p < 0.01), respectively. Both CA frequency and MN frequency of the workers increased with length of the chemical exposure period up to 10 years.
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Cytotoxicity, chromosome aberrations and unscheduled DNA synthesis in cultured human diploid fibroblasts induced by sodium fluoride
The effects of exposure of cultured human diploid fibroblasts (JHU-1 cells) to sodium fluoride have been studied with respect to cytotoxicity and induction of chromosome aberrations and unscheduled DNA synthesis (UDS) Cytotoxicity of NaF on JHU-1 cells, as determined by a decrease in colony-forming ability, linearly increased with increasing dose
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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
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The influence of atmospheric hydrogen fluoride on the frequency of sex-linked recessive lethals and sterility in Drosophila Melanogaster
The influence of hydrogen fluoride as an atmospheric contaminant was investigated in the Oregon-r strain of Drosophila melanogaster. Two principal parameters of mutagenicity were used: sex-linked recessive lethals and sterility. The flies were subjected to various levels of HF in fumigation chambers. Sex-linked recessive lethal mutation frequency increasd at each level
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Genotoxic effect and rat hepatocyte death occurred after oxidative stress induction and antioxidant gene downregulation caused by long term fluoride exposure
Studies focusing on possible genotoxic effects of excess fluoride are contradictory and inconclusive. Currently, studies have reported a probable link to oxidative stress, DNA damage and apoptosis induced by fluoride in rat hepatocytes. We developed an in vivostudy administering three doses of fluoride by gavage given to rats for 60 day.
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The mutagenicity of sodium fluoride to L5178Y [wild-type and TK+/- (3.7.2c)] mouse lymphoma cells
L5178Y wild-type and TK+/- (3.7.2c) cells were treated with sodium fluoride over a range of concentrations (10-500 micrograms ml-1) and treatment times (4, 16 and 48 h) covering less than 10-100% survival. The mutant frequency at five genetic loci (resistance to ouabain, 6-thioguanine, excess thymidine, methotrexate and 1-beta-D-arabinofuranosyl cytosine) was
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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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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.
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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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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'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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