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      Occurrence of 210Po and Biological Effects of Low-Level Exposure: The Need for Research

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          Abstract

          Background: Polonium-210 ( 210Po) concentrations that exceed 1 Bq/L in drinking-water supplies have been reported from four widely separated U.S. states where exposure to it went unnoticed for decades. The radionuclide grandparents of 210Po are common in sediments, and segments of the public may be chronically exposed to low levels of 210Po in drinking water or in food products from animals raised in contaminated areas.

          Objectives: We summarized information on the environmental behavior, biokinetics, and toxicology of 210Po and identified the need for future research.

          Methods: Potential linkages between environmental exposure to 210Po and human health effects were identified in a literature review.

          Discussion: 210Po accumulates in the ovaries where it kills primary oocytes at low doses. Because of its radiosensitivity and tendency to concentrate 210Po, the ovary may be the critical organ in determining the lowest injurious dose for 210Po. 210Po also accumulates in the yolk sac of the embryo and in the fetal and placental tissues. Low-level exposure to 210Po may have subtle, long-term biological effects because of its tropism towards reproductive and embryonic and fetal tissues where exposure to a single alpha particle may kill or damage critical cells. 210Po is present in cigarettes and maternal smoking has several effects that appear consistent with the toxicology of 210Po.

          Conclusions: Much of the important biological and toxicological research on 210Po is more than four decades old. New research is needed to evaluate environmental exposure to 210Po and the biological effects of low-dose exposure to it so that public health officials can develop appropriate mitigation measures where necessary.

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          Most cited references112

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          Cell death by mitotic catastrophe: a molecular definition.

          The current literature is devoid of a clearcut definition of mitotic catastrophe, a type of cell death that occurs during mitosis. Here, we propose that mitotic catastrophe results from a combination of deficient cell-cycle checkpoints (in particular the DNA structure checkpoints and the spindle assembly checkpoint) and cellular damage. Failure to arrest the cell cycle before or at mitosis triggers an attempt of aberrant chromosome segregation, which culminates in the activation of the apoptotic default pathway and cellular demise. Cell death occurring during the metaphase/anaphase transition is characterized by the activation of caspase-2 (which can be activated in response to DNA damage) and/or mitochondrial membrane permeabilization with the release of cell death effectors such as apoptosis-inducing factor and the caspase-9 and-3 activator cytochrome c. Although the morphological aspect of apoptosis may be incomplete, these alterations constitute the biochemical hallmarks of apoptosis. Cells that fail to execute an apoptotic program in response to mitotic failure are likely to divide asymmetrically in the next round of cell division, with the consequent generation of aneuploid cells. This implies that disabling of the apoptotic program may actually favor chromosomal instability, through the suppression of mitotic catastrophe. Mitotic catastrophe thus may be conceived as a molecular device that prevents aneuploidization, which may participate in oncogenesis. Mitotic catastrophe is controlled by numerous molecular players, in particular, cell-cycle-specific kinases (such as the cyclin B1-dependent kinase Cdk1, polo-like kinases and Aurora kinases), cell-cycle checkpoint proteins, survivin, p53, caspases and members of the Bcl-2 family.
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            Induction of sister chromatid exchanges by extremely low doses of alpha-particles.

            The induction of sister chromatid exchanges (SCE) was examined in Chinese hamster ovary cells irradiated in the G1 phase of the cell cycle with alpha-particles from a plutonium-238 source. A significant increase in the frequency of SCE occurred with doses as low as 0.31 mGy (31 millirads). Although 30% of the cells showed an increased frequency of SCE at this dose, less than 1% of cell nuclei were actually traversed by an alpha-particle. A dose of approximately 2.0 Gy was necessary to produce a similar increase in SCE by X-rays. These results indicate that genetic damage may be induced by low doses of alpha-radiation in cell nuclei not actually traversed by an alpha-particle. This phenomenon may have important implications in the estimation of risks of such exposures.
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              Smoking and female infertility: a systematic review and meta-analysis.

              The high prevalence of smoking among women in their reproductive years continues to be a matter of concern. The negative effects of smoking on general health are well known, but smoking may also affect fertility. The objective of the present study was to perform a systematic review of the literature to determine whether there is an association between smoking and risk of infertility in women of reproductive age, and to assess the size of this effect. In the 12 studies used for this meta-analysis, the overall value of the odds ratio (OR) for risk of infertility in women smokers versus non-smokers was 1.60 [95% confidence interval (CI) 1.34-1.91]. Studies of subfertile women undergoing in-vitro fertilization (IVF) treatment also show a reduction in fecundity among women smokers. A meta-analysis of nine studies found an OR of 0.66 (95% CI 0.49-0.88) for pregnancies per number of IVF-treated cycles in smokers versus non-smokers. Despite the potential limitations of meta-analyses of observational studies, the evidence presented in this review is compelling because of the consistency of effect across different study designs, sample size and types of outcome. However, continued reassurance is needed that the calculated overall effect is not in fact due to confounding variables.
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                Author and article information

                Journal
                Environ Health Perspect
                Environ. Health Perspect
                EHP
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                26 April 2012
                September 2012
                : 120
                : 9
                : 1230-1237
                Affiliations
                [1 ]Environmental Sciences Graduate Program, University of Nevada–Reno, Reno, Nevada, USA
                [2 ]Laboratory for Molecular Epidemiology, University of California at San Francisco Helen Diller Comprehensive Cancer Center, San Francisco, California, USA
                Author notes
                Address correspondence to R. Seiler, Environmental Sciences Graduate Program, University of Nevada, Reno, P.O. Box 1025, Carson City, NV 89702 USA. Telephone: (775) 720-7764. E-mail: rlseiler@ 123456juno.com
                Article
                ehp.1104607
                10.1289/ehp.1104607
                3440115
                22538346
                17cb5bd8-aa0c-442f-8fc1-5aaa02452e1e
                Copyright @ 2012

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 October 2011
                : 26 April 2012
                Categories
                Review

                Public health
                fallon,polonium-210,human health,cigarettes,drinking water,ovary,lead-210,leukemia
                Public health
                fallon, polonium-210, human health, cigarettes, drinking water, ovary, lead-210, leukemia

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