Abstract
BACKGROUND: Risk factors for osteosarcoma in young people were investigated in a population-based case-control study among residents of New York State, excluding New York City.
METHODS: Cases (n = 130) were diagnosed between 1978 and 1988 at < or = 24 years of age. Controls were randomly selected from birth certificates and were pair matched to cases on year of birth and sex. Exposure information was obtained by telephone interview with a subject and/or parent, and from birth certificates and school and medical records.
RESULTS AND CONCLUSIONS: A significant positive association was observed with height one year before diagnosis (P-value for trend = 0.02). No significant associations were observed between osteosarcoma and weight of body mass index one year before diagnosis, birth length, birthweight, gestational age, having reached puberty, having begun growth spurt, age at puberty, age growth spurt began, medical x-rays, antenatal exposures, family history of cancer, birth defects, or parental occupation.
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Integrative analyses of key genes and regulatory elements in fluoride-affected osteosarcoma.
Osteosarcoma is one of the most malignant tumors in adolescents with severe outcomes while fluoride is one of the most abundant elements in the environment. Epidemiological evidence has elucidated the relationship between fluoride and osteosarcoma, but the molecular mechanisms are extremely complicated. Microarray profiles were downloaded from the Gene Expression
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Drinking water fluoridation and osteosarcoma incidence on the island of Ireland
The incidence of osteosarcoma in Northern Ireland was compared with that in the Republic of Ireland to establish if differences in incidence between the two regions could be related to their different drinking water fluoridation policies. Data from the Northern Ireland Cancer Registry (NICR) and the National Cancer Registry of
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NTP supplemental 2-year study of sodium fluoride in male F344 rats (CASRN 7681-49-4)
In an effort to examine the effect of exposure to sodium fluoride on the incidence of bone tumors induced by ionizing radiation, the femoral-tibial joint of the left hind limb of 100 male F344 rats was irradiated with 3000 R from a 137Cs source and the animals divided into two
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Fluoride exposure and childhood osteosarcoma: a case-control study
OBJECTIVES: This study tests the hypothesis that fluoride exposure in a nonoccupational setting is a risk factor for childhood osteosarcoma. METHODS: A population-based case-control study was conducted among residents of New York State, excluding New York City. Case subjects (n = 130) were diagnosed with osteosarcoma between 1978 and 1988, at
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Low levels of p53 mutations in Indian patients with osteosarcoma and the correlation with fluoride levels in bone
The pathogenesis of osteogenic sarcoma is not known. Recently, chronic fluoride exposure has been incriminated as having a possible etiologic role by causing a nonspecific osteoblast proliferation. We were interested in exploring the possible relationship between fluoride bone content and p53 mutations. We analyzed p53 mutations in various exons in
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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 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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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/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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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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