Abstract

The long-term effects of professional exposure to radon are well-known. They result from the combined action on the lung epithelia of α-radiation due to radon inhalation and deposition in the lung of its decay products and external γ-radiation from uranium, thorium and their progeny. According to the guidelines applied by the USEPA and recommended by the ICRP, the maximal exposure in uranium mines may not exceed 4 WLM/y ; this exposure corresponds to an annual dose of 20 mSv. In most western uranium mines, miners' exposure is below this threshold. However, there is no good biological indicator of the early lung toxicity of irradiation. The animal model described in this paper considers exposure levels in the range of the professional exposure of miners that can be observed in some habitations in regions of particularly high natural background. Fifty-one Sprague-Dawley rats were exposed in a highly natural radioactive area in Lodeve (France) to external chronic low dose rate irradiation (16.5 µGy/h) and chronic exposure to radon (1650 Bq/m³). A control group (51 animals) was installed nearby, exposed to a background external radiation field (0.34 µGy/h) and atmospheric radon (64 Bq/m³). The biological effects were assessed on the parents F0 (for 17 months) and first generation F1 (14 months). For the exposed F0 and F1 group, the cumulative external dose was respectively 179 mGy and 175 mGy. The mean estimated dose from radon exposure was 2.74 WLM per year. DNA damage in alveolar macrophages was quantified using alkaline comet assay. Early modifications in DNA of pulmonary macrophages were detected by the comet assay which could be a suitable tool for the monitoring of people occupationally exposed to external low doses rates of irradiation and radon.

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