Non-Hodgkin lymphomas and ionizing radiation: case report and review of the literature.

Non-Hodgkin lymphoma (NHL) increased continuously since the last century in developed countries. While they are considered as disease in elder ages, a remarkable increasing incidence is also observed in German children and juveniles. The higher rates are interpreted by the changes in classification because diseases such as chronic lymphocytic leukaemia were also identified as NHL. Considerable rates of NHL were found in nuclear workers and liquidators of Chernobyl, i.e. in cases of low-dose chronical exposures. In Germany, we noticed three workers who developed NHL after decontamination of nuclear facilities. The bone marrow is generally considered as target organ for ionizing radiation, but NHL is obviously induced in the whole pool of lymphocytes. Therefore, the dosimetry in cases of typical occupational external and internal exposure must be revised. A high radiation sensitivity for NHL is a possible suspect and likely reason which may partly explain the continuous rise of the diseases in populations underlying the current increases of medical diagnostic exposure. NHL is also induced in children and juveniles with a history of diagnostic X-rays.

Genetic radiation risks: a neglected topic in the low dose debate.

OBJECTIVES: To investigate the accuracy and scientific validity of the current very low risk factor for hereditary diseases in humans following exposures to ionizing radiation adopted by the United Nations Scientific Committee on the Effects of Atomic Radiation and the International Commission on Radiological Protection. The value is based on experiments on mice due to reportedly absent effects in the Japanese atomic bomb (Abomb) survivors. METHODS: To review the published evidence for heritable effects after ionising radiation exposures particularly, but not restricted to, populations exposed to contamination from the Chernobyl accident and from atmospheric nuclear test fallout. To make a compilation of findings about early deaths, congenital malformations, Down's syndrome, cancer and other genetic effects observed in humans after the exposure of the parents. To also examine more closely the evidence from the Japanese A-bomb epidemiology and discuss its scientific validity. RESULTS: Nearly all types of hereditary defects were found at doses as low as one to 10 mSv. We discuss the clash between the current risk model and these observations on the basis of biological mechanism and assumptions about linear relationships between dose and effect in neonatal and foetal epidemiology. The evidence supports a dose response relationship which is non-linear and is either biphasic or supralinear (hogs-back) and largely either saturates or falls above 10 mSv. CONCLUSIONS: We conclude that the current risk model for heritable effects of radiation is unsafe. The dose response relationship is non-linear with the greatest effects at the lowest doses. Using Chernobyl data we derive an excess relative risk for all malformations of 1.0 per 10 mSv cumulative dose. The safety of the Japanese A-bomb epidemiology is argued to be both scientifically and philosophically questionable owing to errors in the choice of control groups, omission of internal exposure effects and assumptions about linear dose response.

'Lifestyle' and cancer rates in former East and West Germany: the possible contribution of diagnostic radiation exposures.

Breast and prostatic cancer as well as leukaemia in childhood have remarkably increased over some decades in the Federal Republic of Germany as well as in several other highly developed industrial nations. Such increase was much less or not observable in East Germany between 1960 and 1989 where diagnostic exposures were applied to a lesser extent. Low-level radiation can cause these diseases and the difference of cancer rates gives rise to renewed evaluation of current risk estimates. Risk factors for radiation-induced childhood leukaemia and breast cancer are derived from the literature, considering a higher relative biological effectiveness of diagnostic X rays in comparison to the A-bomb gamma rays in Hiroshima and Nagasaki. The prostate is not considered as radiation sensitive by the ICRP. But following a variety of low-level findings in the last two decades it was shown by Myles et al. in the UK that prostatic cancer is inducible by diagnostic X-ray procedures. From their study in men below the age of 60, a doubling dose of about 20 mSv can be estimated. Medical exposures of the considered tissues are taken from published data for East and West Germany. The difference in breast cancer mortality can be explained by diagnostic exposures. The contribution of these to prostatic cancer and childhood leukaemia must be regarded as relevant in current incidences. Reduction of diagnostic exposures would be an important measure for preventing several prominent cancer diseases.

The evidence of radiation effects in embryos and fetuses exposed to Chernobyl fallout and the question of dose response.

Current legal frameworks for radiation exposure limits are based on the risk models of the International Commission on Radiological Protection (ICRP). In Publication 90 (2003), ICRP presents a safe (threshold) dose range of up to 100 mSv for radiogenic effects resulting from in utero exposure and bases this conclusion on the findings in Hiroshima and Nagasaki. However, a variety of observations of congenital malformations, fetal loss, stillbirths and infant deaths, as well as of Down's syndrome and other health defects in children after the Chernobyl accident exposures suggest that the A-bomb survivor data are incomplete. The Chernobyl findings are generally marginalized or even denied because of the low values of the estimated human exposures and the inconsistency of the results with the accepted risk models. One explanation for the observations is that physical dosimetric models have underestimated the effective exposure. This possibility is supported by biological dosimetry in the contaminated regions. The assumptions about effects after in utero exposure by incorporated radionuclides need to be revised.

Pediatric CT research elevates public health concerns: low-dose radiation issues are highly politicized.

This article presents an analysis of issues related to low-dose radiation, with a focus on pediatric computed tomography (CT). It references several early studies that are seldom quoted in radiation research papers, then quantifies the excess lifetime fatal cancer yield attributable to an estimated 6.5 million pediatric abdominal CT scans. The authors highlight an important policy document issued jointly by the National Cancer Institute and the Society for Pediatric Radiology--specifically, its conclusion that a small dose from CT represents "a public health concern." Finally, the article identifies several contentious issues and proposes policy initiatives that, if implemented, could result in significant reductions of future radiogenic cancers and chronic injuries. The authors call for discussions between professional radiology societies and public interest health organizations, thereby involving all stakeholders.

Ionizing radiation and chronic lymphocytic leukemia.

The U.S. government recently implemented rules for awarding compensation to individuals with cancer who were exposed to ionizing radiation while working in the nuclear weapons complex. Under these rules, chronic lymphocytic leukemia (CLL) is considered to be a nonradiogenic form of cancer. In other words, workers who develop CLL automatically have their compensation claim rejected because the compensation rules hold that the risk of radiation-induced CLL is zero. In this article we review molecular, clinical, and epidemiologic evidence regarding the radiogenicity of CLL. We note that current understanding of radiation-induced tumorigenesis and the etiology of lymphatic neoplasia provides a strong mechanistic basis for expecting that ionizing radiation exposure increases CLL risk. The clinical characteristics of CLL, including prolonged latency and morbidity periods and a low case fatality rate, make it relatively difficult to evaluate associations between ionizing radiation and CLL risk via epidemiologic methods. The epidemiologic evidence of association between external exposure to ionizing radiation and CLL is weak. However, epidemiologic findings are consistent with a hypothesis of elevated CLL mortality risk after a latency and morbidity period that spans several decades. Our findings in this review suggest that there is not a persuasive basis for the conclusion that CLL is a nonradiogenic form of cancer.