Abstract Shilnikova, N. S., Preston, D. L., Ron, E., Gilbert, E. S., Vassilenko, E. K., Romanov, S. A., Kuznetsova, I. S., Sokolnikov, M. E., Okatenko, P. V., Kreslov, V. V. and Koshurnikova, N. A. Cancer Mortality Risk among Workers at the Mayak Nuclear Complex. Radiat. Res. 159, 787–798 (2003). At present, direct data on risk from protracted or fractionated radiation exposure at low dose rates have been limited largely to studies of populations exposed to low cumulative doses with resulting low statistical power. We evaluated the cancer risks associated with protracted exposure to external whole-body γ radiation at high cumulative doses (the average dose is 0.8 Gy and the highest doses exceed 10 Gy) in Russian nuclear workers. Cancer deaths in a cohort of about 21,500 nuclear workers who began working at the Mayak complex between 1948 and 1972 were ascertained from death certificates and autopsy reports with follow-up through December 1997. Excess relative risk models were used to estimate solid cancer and leukemia risks associated with external γ-radiation dose with adjustment for effects of plutonium exposures. Both solid cancer and leukemia death rates increased significantly with increasing γ-ray dose (P < 0.001). Under a linear dose–response model, the excess relative risk for lung, liver and skeletal cancers as a group (668 deaths) adjusted for plutonium exposure is 0.30 per gray (P < 0.001) and 0.08 per gray (P < 0.001) for all other solid cancers (1062 deaths). The solid cancer dose–response functions appear to be nonlinear, with the excess risk estimates at doses of less than 3 Gy being about twice those predicted by the linear model. Plutonium exposure was associated with increased risks both for lung, liver and skeletal cancers (the sites of primary plutonium deposition) and for other solid cancers as a group. A significant dose response, with no indication of plutonium exposure effects, was found for leukemia. Excess risks for leukemia exhibited a significant dependence on the time since the dose was received. For doses received within 3 to 5 years of death the excess relative risk per gray was estimated to be about 7 (P < 0.001), but this risk was only 0.45 (P = 0.02) for doses received 5 to 45 years prior to death. External γ-ray exposures significantly increased risks of both solid cancers and leukemia in this large cohort of men and women with occupational radiation exposures. Risks at doses of less than 1 Gy may be slightly lower than those seen for doses arising from acute exposures in the atomic bomb survivors. As dose estimates for the Mayak workers are improved, it should be possible to obtain more precise estimates of solid cancer and leukemia risks from protracted external radiation exposure in this cohort.

OBJECTIVES: To summarise and to facilitate comparison of three major studies of electric utility workers that examined the relation between quantitative measurements of occupational exposure to magnetic fields and risk of brain cancer and leukaemia. These studies have been interpreted as providing conflicting evidence. METHODS: A common analytical approach was applied to data from the five cohorts included in the three studies based on original data from four of the cohorts, and published data from one additional cohort. A nested case-control design with conditional logistic regression was used to estimate the relative risk/10 microtesla-years (microT-years) for each of the contributing cohorts and for the combined data. The homogeneity of these estimates among the studies was also evaluated. RESULTS: Apparent inconsistencies in the findings of these studies can be explained by statistical variation. Overall, the studies suggest a small increase in risk of both brain cancer and leukaemia. Different methodological choices had little impact on the results. Based on a combined analysis of data from all five studies, the relative risk/10 microT-years was 1.12 (95% confidence interval (95% CI) 0.98 to 1.28) for brain cancer, and 1.09 (95% CI 0.98 to 1.21) for leukaemia. CONCLUSIONS: The combined estimates seem to provide the best summary measures of the data from all studies. However, fluctuations in risks among studies may reflect real differences, and the exposure measurements in different studies may not be entirely comparable.

The rhizosphere fortuitously enhances the population numbers and activity of certain microorganisms that degrade xenobiotic soil contaminants. This review examines the ecology of degrader microorganisms in the rhizosphere, and summarizes prior research that has examined the influence of plants on biodegradation of chlorobenzoates, chlordane, polychlorinated biphenyls (PCBs), and the herbicide atrazine. Degradation rates of most xenobiotics examined to dale are not significantly influenced by the presence of a rhizosphere. However; a major benefit of the rhizosphere may be to harbor certain degrader organisms at higher cell numbers, thereby shortening the acclimation period. Another benefit may be enhanced transfer of degradative plasmids, or in some instances, enhanced cometabolism of compounds which can not be directly utilized as substrates for microbial growth.

Using data on 3117 rats exposed by inhalation to radon, radon progeny and uranium ore dust, the hazard function (or age-specific risk) for lung tumor incidence was modeled as a function of exposure, exposure rate and other factors. The overall estimate of lifetime risk was 237 cases per 10(6) rats per WLM (237 per 10(6) WLM), reasonably comparable to estimates obtained from data for humans. The data below 1000 WLM (20-640 WLM) were consistent with linearity with positive excess risks at all levels; however, evidence of statistically significant excess risk was limited to exposures of 80 WLM or greater. Evidence for an inverse exposure-rate effect was limited primarily to cumulative exposures exceeding 1000 WLM (1280-10,240 WLM) and to comparison of results at 100 and 1000 WL. Even at these levels, the possibility that the effect might be explained by time since last exposure or by heterogeneity across experiments could not be entirely excluded. The inverse exposure-rate effect was strongest for epidermoid and adenosquamous tumors, and the only indication of such an effect at exposures below 1000 WLM was modest evidence (P=0.024) in analyses limited to these tumors. When all lung tumors, or all malignant lung tumors, were included, there was no evidence of such an effect below 1000 WLM. These data support the viewpoint that the inverse exposure-rate effect is primarily a high-dose phenomenon.

This paper describes an approach to quantifying errors in recorded estimates of external radiation dose obtained from personal dosimeters and applies the approach to dose estimates of workers at the Hanford site. Because a major objective of this evaluation is to provide the information needed for adjusting epidemiologic dose-response analyses of worker data for errors in dose estimates, the paper addresses the extent that errors for different workers are correlated, focuses on recorded doses as estimates of organ doses, and focuses on recorded doses as estimates of organ doses, and gives consideration to both annual and cumulative doses. The evaluation emphasizes errors resulting from the fact that dosimeters are limited in their ability to respond accurately to all radiation energies to which workers are exposed or to radiation coming from all directions. For each of several sources of error, systematic bias factors are estimated for two energy ranges (100--300 keV and 300--1,000 keV), two geometries (anterior-posterior and rotational), and four calendar year periods. These are then combined using information provided by health physicists on energies and geometries in Hanford exposure environments. Except for the period before 1958, deep dose, the objective of modern dosimetry systems, was found to be fairly accurately estimated. Lung dose was found to be overestimated by about 10%, and bone marrow dose was found to be overestimated by about 50%. However, many aspects of this evaluation relied heavily on subjective judgments, and, thus, these factors are subject to considerable uncertainty. Estimates of uncertainty in the bias factors and uncertainty reflecting random error are provided.

Since 1978 follow-up studies of plant-specific and combined populations involving similar to 360,000 current and former employees of the U.S. Department of Energy (DOE) and predecessor agencies and their contractors at 40 or more sites nationwide have been conducted by DOE contract epidemiologists as part of the Health and Mortality Study of Atomic Workers. Among these populations, death rates to date for all causes of death combined and for most specific disease categories generally have been found to be similar to or lower than those in the U.S. population. No consistent pattern of increases in site-specific cancer mortality has been identified thus far across the populations studied. Although statistical associations have been demonstrated between certain cancer increases and employees' occupational radiation exposure, it is premature to draw conclusions about the contribution to their causation of occupational exposure to potentially hazardous agents given the generally low mortality and other study limitations. A summary review is presented of completed and ongoing studies in this series.

When setting standards for protection against ionising radiation it has been usual to extrapolate from experience with high-dose short-term exposure-studies based on atom bomb survivors and patients exposed to radiation therapeutically. Those who work in the nuclear industry are exposed to low-level predominantly gamma radiation for longer periods, and provide an alternative direct source of information. We have combined mortality data from seven cohort studies on nearly 96 000 nuclear industry workers monitored for external radiation in Canada, UK, and USA to assess directly the carcinogenic effects of protracted low-dose exposure to ionising radiation.The excess relative risk for death from leukaemia, excluding chronic lymphocytic leukaemia, was 2.2 per Sv (90% Cl 0.1 to 5.7). This estimate is intermediate between the linear estimate of 3.7 per Sv and the linear-quadratic estimate (as used in recent leukaemia risk assessments) of 1.4 per Sv derived from Japanese atomic bomb survivors' data. The excess relative risk for death from all cancers, excluding leukaemia, was -0.07 per Sv (90% Cl -0.4 to 0.3). This estimate is consistent with a range of risks varying from negative to nearly twice those estimated from atomic bomb survivors (0.18 per Sv).These are the most precise direct estimates so far made of carcinogenic risk after protracted exposure to low-dose ionising radiation. They provide little evidence that the estimates that form the basis of current radiation protection recommendations are appreciably in error.

Journal Article RE: “DOES NONDIFFERENTIAL MISCLASSIFICATION OF EXPOSURE ALWAYS BIAS A TRUE EFFECT TOWARD THE NULL VALUE?” Get access Petra Peeters Petra Peeters Department of Epidemiology University of Epidemiology University of UtrechtRadboudkwartier 261 3511 CK Utrecht The Netherlands Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 134, Issue 4, 15 August 1991, Pages 439–440, https://doi.org/10.1093/oxfordjournals.aje.a116107 Published: 15 August 1991

Currently, several epidemiologic studies of workers who have been exposed occupationally to low levels of radiation are being conducted. They include studies of workers in the United States, Great Britain, and Canada involved in the production of both defense materials and nuclear power. This paper focuses on studies evaluating the possible adverse effects that result from external exposure to radiation.

Epidemiologic studies of workers exposed occupationally to protracted low doses of radiation provide a direct assessment of health effects resulting from such exposure and thus supplement information provided by studies of populations exposed at high doses of radiation and high dose rates. Analyses based on combined data from several studies can be expected to provide a more thorough assessment of low dose occupational studies and more precise risk estimates than can be obtained from any single study. Statistical methods for conducting such combined analyses are discussed, and different approaches, such as basing analyses on various levels of aggregation of exposure data, are compared and evaluated. Emphasis is given to methods for obtaining risk estimates and confidence limits that can be appropriately compared with estimates that form the basis for current radiation protection standards; these estimates have been obtained through extrapolation from high dose data. Methods are illustrated using combined data on workers at three US Department of Energy facilities: the Hanford Site, Richland, Washington; the Oak Ridge National Laboratory, Oak Ridge, Tennessee; and the Rocky Flats Nuclear Weapons Plant, Denver, Colorado.

Inhaled plutonium is a potent carcinogen in both dogs and rats. Young adult beagle dogs and Wistar rats, in lifespan studies designed to examine the relationship between dose and lungtumor incidence, were given a single exposure to high-fired 239PuO2 (AMAD values, 2.3 μm and 1.6 μm, respectively). Dosimetry and histopathology have been completed on 122 of 136 dogs and on 1436 of 3192 rats, including most animals with lung doses > 1 Gy (100 rad). Initial lung depositions (ILD) ranged from 1.073 to 1850 Bq g−1 (0.029 to 50 nCi g−1) for dogs and 10.36 to 2775 Bq g−1 (0.28 to 75 nCi g−1) for rats. About 80% of the ILD in rats was cleared with a half time of 200 d. Lung clearance in dogs was described by a single exponential function with a half time of 1100 d. Final lung doses ranged from 0.1 Gy (10 rad) to 60 Gy (6000 rad) in dogs and 0.06 Gy (6 rad) to 25 Gy (2500 rad) in rats. In dogs, about 40% and 20% of the ILD were present in thoracic lymph nodes and liver, respectively, by 5 to 15 y after exposure; <0.05% of the ILD was present in either tissue of rats at 1.5 y. Median survival of control dogs was about 14 y; for control rats it was 2.2 y. Significant life-shortening was observed only in groups of dogs or rats with lung doses of 10 Gy (1000 rad). Early deaths from radiation pneumonitis were infrequent in both species at lung doses of 20 Gy (2000 rad). Maximum percentage of animals with lung tumors was 80 to 90% at about 10 Gy (1000 rad) in rats and 25 Gy (2500 rad) in dogs, with a rapid increase between 1 Gy (100 rad) and 10 Gy (1000 rad). Percentage of animals with tumors was similar in dogs and rats despite large differences in the fate of inhaled 239PuO2 in the two species. This suggested that total accumulated dose to the lung is a useful dosimetric parameter in estimating lung-tumor risk for humans.

The effects of occupational exposure to low level ionizing radiation at the Hanford plant in southeastern Washington were investigated. Death rates were related to exposure status. To provide perspective, the rates were also compared with the death rates of the US population. (ACR)

Data from epidemiological studies of humans exposed to potentially harmful substances are usually analyzed using methods that account for the dependence of risks on time-related factors such as age and follow-up period. Recently developed statistical procedures allow modeling of the age-specific risks as a function of dose as well as factors such as age at exposure, time since exposure, exposure duration, and dose rate. These procedures potentially allow more rigorous inferences and clearer understanding of the patterns of risk observed in epidemiological studies than has been available in the past. Statistical procedures that consider time-related factors can also be applied to laboratory animal data, providing information that is useful for the problems involved in extrapolating from animal studies to humans. By applying such procedures to data on exposure to the same substance in different species (including humans) or to different substances in the same species, better understanding of the relationship of risks across species and across substances can be achieved. In addition, such statistical procedures allow appropriate treatment of exposure that is accumulated over time and lead to improved understanding of patterns of risk over time. The approach is illustrated using data from a lifespan study of beagle dogs exposed to inhaled Pu.

A major objective of studying populations exposed to low levels of radiation is provision of direct assessment of the adequacy of estimates of health risks obtained by extrapolation of data on populations exposed at high levels. Meeting this objective requires the use of statistical methods that fully utilize available exposure measurements, and that consider the extensive body of prior knowledge regarding radiation-induced health effects. This paper describes various methods of analysis and illustrates the methods with data on workers at the Hanford Site. Special problems are discussed, with attention to comparability of estimates and confidence limits with those obtained from extrapolation.