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.