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      Cancer risks attributable to low doses of ionizing radiation: Assessing what we really know

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          Abstract

          High doses of ionizing radiation clearly produce deleterious consequences in humans, including, but not exclusively, cancer induction. At very low radiation doses the situation is much less clear, but the risks of low-dose radiation are of societal importance in relation to issues as varied as screening tests for cancer, the future of nuclear power, occupational radiation exposure, frequent-flyer risks, manned space exploration, and radiological terrorism. We review the difficulties involved in quantifying the risks of low-dose radiation and address two specific questions. First, what is the lowest dose of x- or gamma-radiation for which good evidence exists of increased cancer risks in humans? The epidemiological data suggest that it is approximately 10-50 mSv for an acute exposure and approximately 50-100 mSv for a protracted exposure. Second, what is the most appropriate way to extrapolate such cancer risk estimates to still lower doses? Given that it is supported by experimentally grounded, quantifiable, biophysical arguments, a linear extrapolation of cancer risks from intermediate to very low doses currently appears to be the most appropriate methodology. This linearity assumption is not necessarily the most conservative approach, and it is likely that it will result in an underestimate of some radiation-induced cancer risks and an overestimate of others.

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          Thyroid Cancer after Exposure to External Radiation: A Pooled Analysis of Seven Studies

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            Incidence of cancer in 161 families affected by ataxia-telangiectasia.

            Ataxia-telangiectasia is an autosomal recessive syndrome in which cancers develop in affected homozygotes at a rate approximately 100 times higher than in unaffected age-matched subjects. Retrospective studies have shown that persons heterozygous for the ataxia-telangiectasia gene, who make up about 1 percent of the general population, also have an excess risk of cancer, particularly breast cancer in women. Patients with ataxia-telangiectasia and cells derived from homozygotes and heterozygotes are unusually sensitive to ionizing radiation. Cancer incidence and mortality, mortality from ischemic heart disease, and mortality from all causes were compared prospectively for a mean of 6.4 years in 1599 adult blood relatives of patients with ataxia-telangiectasia and 821 of their spouses, who served as controls, in 161 families affected by ataxia-telangiectasia. In a case-control substudy, we compared documented occupational and fluoroscopic diagnostic exposures to radiation in the 19 female blood relatives in whom breast cancer was first diagnosed during the period of prospective observation with the exposures in 57 matched blood relatives who did not have breast cancer. Cancer rates were significantly higher in the group of blood relatives than in their spouses, specifically in the subgroup of 294 blood relatives who were known to be heterozygous for the ataxia-telangiectasia gene. The estimated risk of cancer of all types among heterozygotes as compared with noncarriers was 3.8 in men and 3.5 in women, and that for breast cancer in women was 5.1. Among the blood relatives, women with breast cancer were more likely to have been exposed to selected sources of ionizing radiation than controls without cancer (odds ratio = 5.8, P = 0.005). Male and female blood relatives also had 3-fold and 2.6-fold excess mortality from all causes, respectively, from the ages of 20 through 59 years. The ataxia-telangiectasia gene predisposes heterozygotes to cancer, particularly breast cancer in women. There is also excess mortality from all causes in adults under the age of 60. Diagnostic or occupational exposure to ionizing radiation probably increases the risk of breast cancer in women heterozygous for ataxia-telangiectasia.
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              Radiation carcinogenesis.

              Research on radiation carcinogenesis during the past 2 decades has focused on cellular and molecular mechanisms for the effects of radiation in mammalian cells. This paper will review several of these areas of research, as they may relate specifically to the induction of cancer by ionizing radiation. Knowledge of the critical DNA damage of biologic importance, and how this damage is repaired, will be discussed in relation to its role in the induction of mutations by radiation. The search for the initiating event in radiation carcinogenesis, as well as other genetic events that may be involved, is discussed in terms of the possible role of the activation of oncogenes or tumor suppressor genes and the loss of cell-cycle checkpoints. Finally, evidence will be described indicating that important genetic consequences of radiation may arise in cells that in themselves receive no direct nuclear irradiation. It has been shown that radiation can, by itself, induce a type of genomic instability in cells, which enhances the rate at which mutations and other genetic changes arise in the descendants of the irradiated cell after many generations of replication. Preliminary evidence has been presented that irradiation targeted to the cytoplasm yields a significant increase in the frequency of mutations. Finally, genetic events including the induction of mutations and changes in gene expression may occur in neighboring cells that receive no direct radiation exposure at all. This 'bystander effect' involves gap junction mediated cell-cell communication, and activation of the p53 damage response pathway. The possible role of these phenomena in radiation carcinogenesis is discussed.
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                Author and article information

                Journal
                Proceedings of the National Academy of Sciences
                Proceedings of the National Academy of Sciences
                Proceedings of the National Academy of Sciences
                0027-8424
                1091-6490
                May 01 2011
                November 25 2003
                November 10 2003
                November 25 2003
                : 100
                : 24
                : 13761-13766
                Article
                10.1073/pnas.2235592100
                283495
                14610281
                2ac6a0b2-6c87-4ad6-b31a-f48f368ad0de
                © 2003
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