[en] The claim that the results of the latest radiation epidemiological investigations have forced a completely new assessment of radiation risks is considered critically. There is a discussion of the additional risk to which a single person exposed to radiation is exposed of suffering from cancer as a consequence of this exposure to radiation. (DG)

[en] A major public heath concern today is the understanding of health risks related to exposure to mutagenic/genotoxic agents. The majority of reasonably well characterized environmental carcinogens through damage that they, or their metabolites, cause to DNA. Mutagenic chemicals in our environment, particularly those released through human activities, have become a major public health issue. Using incidence or mortality data to characterize the health effects of mutagenic carcinogens is difficult because of the decade long latency between exposure and effect. Methods have been needed for identifying and characterizing hazardous exposures at the time of their occurrence, so that the risks associated with current exposure conditions can be estimated. One promising approach is to use biological markers as surrogates for health outcomes studying exposed populations. Biomarkers are parameters that can be measured in specimens of body fluids cells or other sources obtained from individuals in study populations; The biomarkers typically classified as measuring exposure, effects of exposure, or susceptibility to exposure. For cancer, biomarkers are events on continuum beginning with external exposure to an agent, through internal dose and tissue-specific dose, to functional changes, and, finally, clinical expression of disease. The development of convenient biomarkers f DNA damage caused by exposure to hazardous substances is important in identifying the segment of population who are at high risk of developing cancer. Therefore, there is need to develop and assess biomarkers related environmental pollution. These biomarkers could provide valuable qualitative and quantitative information about the potential biological significance of the persistent DNA damage in humans. So far very little work has be done in Pakistan on the effects of industrial pollution on workers/general public. No facility to detect genotoxic agents in the environment is available in the country. Therefore, development in these areas to an international standard is required so that it can fulfill the demands in, environmental and occupational health sectors for the coming years. At NIBGE, Faisalabad, genetic toxicity of environmental other samples is being conducted using different tests. Moreover, a couple of environmental genotoxic risk assessment studies on workers exposed to hazardous agents at their workplace have also been carried out using different biomarkers. (author)

[en] New information is available concerning the carcinogenic effects of radiation and the implications for risk assessment and risk management. This information comes from further follow-up of the epidemiological studies of the Japanese atomic bomb survivors, patients irradiated medically for cancer and allied conditions, and workers exposed in various occupations. In the Japanese atomic bomb survivors the carcinogenic risks are estimated to be somewhat higher than previously, due to the reassessment of the atomic-bomb dosimetry, further follow-up with increase in the number of excess cancer deaths, particularly in survivors irradiated early in life, and changes in the methods of analysis to compute the age-specific risks of cancer. Because of the characteristics of the atomic bomb survivor series as regards sample size, age and sex distribution, duration for follow-up, person-years at risk, and type of dosimetry, the mortality experience of the atomic bomb survivors was selected by the UNSCEAR Committee and the BEIR V Committee as the more appropriate basis for projecting risk estimates for the general population. In the atomic bomb survivors, the dose-effect relationship for overall cancer mortality other than leukemia is consistent with linearity below 3 Gy, while the dose-effect relationship for leukemia, excluding chronic lymphatic leukemia, conforms best to a linear-quadratic function. The shape of the dose-incidence curve at low doses still remains uncertain, and the data do not rule out the possible existence of a threshold for an neoplasm. The excess relative risk of mortality from all cancers combined is estimated to be 1.39 per Gy (shielded kerma), which corresponds to an absolute risk of 10.0 excess cancer deaths per 10,000 PYGy; the relative risks is 1.41 at 1 Gy (organ-absorbed dose), and an absolute risk of 13.07 excess cancer deaths per 10,000 PYGy. 19 refs

[en] This paper studies the mortality rate experienced by over 23000 A-bomb survivors in Nagasaki between September 1945 and 1950 when the RERF-ABCC initiated the follow-up of the large LSS cohort. The study is based on the data of the 10-year House Reconstruction Survey. As expected, these data show an increasing mortality rate with increasing proximity to the hypocenter of the bomb. What was not anticipated was a higher morality rate in the 1400-1699m band than in the closer distance interval of 1200-1399m. This suggests a possible selective survival among A-bomb survivors. Whether this affects the cancer risk estimates has not as yet been determined. (author)

[en] A diffusion model for the latent period distribution function prior to malignancy is constructed from the assumption that the latency arises from the time required for a series of discrete changes in cell character akin to tumour progression. With the further assumption that frequency of cell character changes is determined by the mitotic rate since the changes originate from abnormalities in mitosis or DNA replication it is readily demonstrated that the probable location of a cell in the deviant character space is described by the diffusion equation. The general properties of this equation and its solutions indicate that the risk of malignancy is partially determined by the number of exposed cells and that the mean latent period is inversely correlated to dose rate. It is also deduced that the latent period following short exposures is independent of the dose to first order. The dependence of the diffusion coefficient upon the mitotic index implies an age dependency of the latent period as illustrated by the incidence of leukaemia following pre-natal X-irradiation. The latent period distributions observed for the available high dose data may be used to define the shape of the Green's function for computation of the time and age variation of risk in the occupational situation. A computed example for leukaemia is given. Finally some simple models have been computed and compared to the available data

[en] This paper is a high-level overview of managing risks to workers, public, and the environment. It discusses the difference between a model and a hypothesis. The need for models in risk assessment is justified, and then it is shown that radiation risk models that are useable in risk management are highly simplistic. The weight of evidence is considered for and against the linear non-threshold (LNT) model for carcinogenesis and heritable ill-health that is currently the basis for radiation risk management. Finally, uses and misuses of this model are considered. It is concluded that the LNT model continues to be suitable for use as the basis for radiation protection

[en] The scientific basis for compensation of persons developing cancer who have a documented history of exposure to radiation or other carcinogens is an important legal issue. The measure Relative Attributable Risk (RAR) has been proposed as a basis for determining eligibility for compensation. The purpose of this report is to present results of an analysis of the magnitude and sources of uncertainty in the RAR measure. The range of 1/10⁶/rad-year to 6/10⁶/rad-year was chosen as a reasonable range of excess-risk estimates for thyroid cancer based on published estimates. The use of such a range in risk estimates produces very wide variability in RAR estimates. Uncertainty in underlying incidence levels and in dosimetry are other major factors contributing to large variability in estimated RAR levels

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[en] Analyses of data from epidemiological studies of persons exposed to radiation have usually been based on the assumption that doses are measured without error. This paper begins with a general discussion of measurement error, followed by discussion of approaches for handling both random and systematic error. However, dose measurement error is only one of many sources of uncertainty that have not usually been fully accounted for in epidemiological analyses. At the end of the paper, brief consideration is given to the general problem of quantifying uncertainties from several different sources. (Author)