Pregnant CD1 mice were exposed or sham-exposed from day 0 to day 17 of gestation to a 50 Hz sinusoidal magnetic field at 20 mT (rms). Preimplantation and postimplantation survival were assessed and fetuses examined for the presence of gross external, internal, and skeletal abnormalities. There were no statistically significant field-dependent effects on preimplantation or postimplantation survival, sex ratio, or the incidence of fetuses with internal or skeletal abnormalities. Magnetic field exposure was, however, associated with longer and heavier fetuses at term, with fewer external abnormalities. The results lend no support to suggestions of increased rates of spontaneous abortion or congenital malformation following prenatal exposure to power frequency magnetic fields.

From studies of the atomic bomb survivors, it is well known that ionizing radiation causes several forms of leukemia. However, since the specific mechanism behind this process remains largely unknown, it is difficult to extrapolate carcinogenic effects at acute high-dose exposures to risk estimates for the chronic low-dose exposures that are important for radiation protection purposes. Recently, it has become clear that the induction of acute myeloid leukemia (AML) in CBA/H mice takes place through two key steps, both involving the Sfpi1 gene. A similar mechanism may play a role in human radiation-induced AML. In the present paper, a two-mutation carcinogenesis model is applied to model AML in several data sets of X-ray- and neutron-exposed CBA/H mice. The models obtained provide good fits to the data. A comparison between the predictions for neutron-induced and X-ray-induced AML yields an RBE for neutrons of approximately 3. The model used is considered to be a first step toward a model for human radiation-induced AML, which could be used to estimate risks of exposure to low doses.

The rear halves of the bodies of anaesthetized male C3H mice were exposed for 30 min to 2.45 GHz microwave radiation and the effects on the testes were compared to those produced by direct heating. Effects were observed which are consistent with the hypothesis that heat damage is the primary effect of microwave exposure. Damage measured six days after exposure ranged in severity from depletion of the spermatocytes to extensive necrosis of the germinal epithelium. Temperature-sensitive probes implanted in the testes revealed a threshold effect for depletion of the spermatocytes of approximately 39 degrees C and an LD50 6 (50 per cent cell death after 6 days) of about 41 degrees C after microwave exposure or direct heating. The corresponding effective threshold effect and LD50 6 expressed in terms of absorbed microwave power were 20 W kg-1 and 30 W kg-1. However, it is probable that a conscious animal is better able to regulate testicular temperature and hence adjust to higher dose-rates.

These results show that G361 malignant melanoma cells have lost the ability to regulate the cell cycle at the G1/S checkpoint and are more sensitive than melanocytes to cell killing by UVC and UVB but not UVA radiation. Similarly, exposure of these melanoma cells to UVC and UVB, and to a much lesser extent UVA, induced chromatid aberrations. UVA nevertheless induced strong cell cycle delays in both cell types, indicating that UVA exposure can significantly affect genome metabolism.

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