Demonstration of lightweight gamma spectrometry systems in urban environments

Urban areas present highly complex radiation environments; with small scale features resulting from different construction materials, topographic effects and potential anthropogenic inputs from past industrial activity or other sources. Mapping of the radiation fields in urban areas allows a detailed assessment of exposure pathways for the people who live and work there, as well as locating discrete sources of activity that may warrant removal to mitigate dose to the general public. These areas also present access difficulties for radiometric mapping using vehicles or aircraft. A lightweight portable gamma spectrometry system has been used to survey sites in the vicinity of Glasgow to demonstrate the possibilities of radiometric mapping of urban areas, and to investigate the complex radiometric features such areas present. Variations in natural activity due to construction materials have been described, the presence of 137Cs used to identify relatively undisturbed ground, and a previously unknown NORM feature identified. The effect of topographic enclosure on measurements of activity concentration has been quantified. The portable system is compared with the outputs that might be expected from larger vehicular or airborne systems. For large areas airborne surveys are the most cost effective approach, but provide limited spatial resolution, vehicular surveys can provide sparse exploratory data rapidly or detailed mapping of open areas where off-road access is possible. Backpack systems are ideally suited to detailed surveys of small areas, especially where vehicular access is difficult

Low-Dose Cancer Risk Modeling Must Recognize Up-Regulation Of Protection

Ionizing radiation primarily perturbs the basic molecular level proportional to dose, with potential damage propagation to higher levels: cells, tissues, organs, and whole body. There are three types of defenses against damage propagation. These operate deterministically and below a certain impact threshold there is no propagation. Physical-static defenses precede metabolic-dynamic defenses acting immediately: scavenging of toxins; - molecular repair, especially of DNA; - removal of damaged cells either by apoptosis, necrosis, phagocytosis, cell differentiation-senescence, or by immune responses, - followed by replacement of lost elements. Another metabolic-dynamic defense arises delayed by up-regulating immediately operating defense mechanisms. Some of these adaptive protections may last beyond a year and all create temporary protection against renewed potentially toxic impacts also from non-radiogenic endogenous sources. Adaptive protections have a maximum after single tissue absorbed doses around 100 to 200 mSv and disappear with higher doses. Low dose rates initiate maximum protection likely at lower cell doses delivered repetitively at certain time intervals. Adaptive protection preventing only about 2 – 3 % of endogenous life-time cancer risk would fully balance a calculated induced cancer risk at about 100 mSv, in agreement with epidemiological data and concordant with an hormetic effect. Low-dose-risk modeling must recognize up-regulation of protection

An Examination of Radiation Hormesis Mechanisms Using a Multistage Carcinogenesis Model

A multistage cancer model that describes the putative rate-limiting steps in carcinogenesis is developed and used to investigate the potential impact on cumulative lung cancer incidence of the hormesis mechanisms suggested by Feinendegen and Pollycove. In the model, radiation and endogenous processes damage the DNA of target cells in the lung. Some fraction of the misrepaired or unrepaired DNA damage induces genomic instability and, ultimately, leads to the accumulation of malignant cells. The model explicitly accounts for cell birth and death processes, the clonal expansion of initiated cells, malignant conversion, and a lag period for tumor formation. Radioprotective mechanisms are incorporated into the model by postulating dose and dose-rate-dependent radical scavenging. The accuracy of DNA damage repair also depends on dose and dose rate. As currently formulated, the model is most applicable to low-linear-energy-transfer (LET) radiation delivered at low dose rates. Sensitivity studies are conducted to identify critical model inputs and to help define the shapes of the cumulative lung cancer incidence curves that may arise when dose and dose-rate-dependent cellular defense mechanisms are incorporated into a multistage cancer model. For lung cancer, both linear no-threshold (LNT-), and non-LNT-shaped responses can be obtained. If experiments demonstrate that the effects of DNA damage repair and radical scavenging are enhanced at least three-fold under low-dose conditions, our studies would support the existence of U-shaped responses. The overall fidelity of the DNA damage repair process may have a large impact on the cumulative incidence of lung cancer. The reported studies also highlight the need to know whether or not (or to what extent) multiply damaged DNA sites are formed by endogenous processes. Model inputs that give rise to U-shaped responses are consistent with an effective cumulative lung cancer incidence threshold that may be as high as 300 mGy (4 mGy per year for 75 years) for low-LET radiation