Risk assessment after internal exposure to black sand from Camargue: uptake and prospective dose calculation.

Some beaches in the south of France present high levels of natural radioactivity mainly due to thorium (Th) and uranium (U) present in the sand. Risk assessment after internal exposure of members of the public by either inhalation or ingestion of black sand of Camargue was performed. This evaluation required some information on the human bioavailability of U and Th from this sand. In vitro assays to determine the solubility of U, Th and their progeny were performed either in simulated lung fluid, with the inhalable fraction of sand, or in both simulated gastric and intestinal fluids with a sample of the whole sand. The experimental data show that the bioavailability of these radionuclides from Camargue sand is low in the conditions of the study. Prospective dose assessment for both routes of intake show low risk after internal exposure to this sand.

Heterogeneous accumulation of uranium in the brain of rats.

Recent reports suggest that uranium can accumulate not only in known target organs, that is, kidneys or bones, but also in others such as central nervous system. In the present work, the accumulation of uranium in the brain of rats was studied after repeated exposure by inhalation, chronic exposure by ingestion and acute exposure by injection. For each route of administration, the amount of uranium entering the brain was low. The results showed different accumulation in the brain areas according to the route of intake. Injection gave a rather homogeneous distribution in the different brain areas, whereas both inhalation and ingestion yielded heterogeneous but specific accumulation. These differences in distribution suggest the operation of different mechanisms of delivery of uranium to the brain tissues.

Distribution and genotoxic effects after successive exposure to different uranium oxide particles inhaled by rats.

In nuclear fuel cycle facilities, workers may inhale airborne uranium compounds that lead to internal contamination, with various exposure scenarios depending on the workplace. These exposures can be chronic, repeated, or acute, and can involve many different compounds. The effect of uranium after multiple scenarios of exposure is unknown. The aim of this study, therefore, was to investigate the genotoxic and biokinetics consequences of exposure to depleted insoluble uranium dioxide (UO2) by repeated or acute inhalation on subsequent acute inhalation of moderately soluble uranium peroxide (UO4) in rats. The results show that UO2 repeated preexposure by inhalation increases the genotoxic effects of UO4 inhalation, assessed by comet assay, in different cell types, when UO4 exposure alone has no effect. At the same time, the study of UO4 bioaccumulation showed that the UO4 biokinetics in the kidneys, gastrointestinal tract, and excreta, but not in the lungs, were slightly modified by previous UO2 exposures. All these results show that both genotoxic and biokinetics effects of uranium may depend on preexposure and that repeated exposure induces a potentiation effect compared with acute exposure.

The effect of repeated inhalation on the distribution of uranium in rats.

For the assessment of doses after inhalation of airborne uranium compounds by workers, the International Commission on Radiological Protection (ICRP) developed compartmental models that are used to calculate reference dose coefficients and retention and excretion functions. It is assumed that each acute intake has no effect on the biokinetics of later intakes. Consequently, retention and excretion after multiple or chronic exposure are predicted using the same models as after acute exposure. This assumption was tested here on rats exposed to repeated inhalation of uranium dioxide (UO2). First, excretion and organ retention were determined after a single inhalation of UO2. The follow-up of incorporated activity was used to design a biokinetic model for uranium inhaled by rats. Second, the biokinetics of uranium were monitored in two experiments of repeated inhalations of uranium dioxide under different intake patterns. For these two experiments, the organs' retention and excretion after repeated UO2 inhalation were predicted using the biokinetic model and compared to the experimental measurement. Under the two sets of experimental conditions considered, the prediction of the biokinetic model based on acute exposure data was consistent with the biokinetics observed after repeated UO2 inhalations, with the possible exception of retention in the skeleton.

Genotoxic and inflammatory effects of depleted uranium particles inhaled by rats.

Depleted uranium (DU) is a radioactive heavy metal coming from the nuclear industry and used in numerous military applications. Uranium inhalation can lead to the development of fibrosis and neoplasia in the lungs. As little is known concerning the molecular processes leading to these pathological effects, some of the events in terms of genotoxicity and inflammation were investigated in rats exposed to DU by inhalation. Our results show that exposure to DU by inhalation resulted in DNA strand breaks in broncho-alveolar lavage (BAL) cells and in increase of inflammatory cytokine expression and production of hydroperoxides in lung tissue suggesting that the DNA damage was in part a consequence of the inflammatory processes and oxidative stress. The effects seemed to be linked to the doses, were independent of the solubility of uranium compounds and correlating with the type of inhalation. Repeated inhalations seemed to induce an effect of potentiation in BAL cells and also in kidney cells. Comet assay in neutral conditions revealed that DNA damage in BAL cells was composed partly by double strands breaks suggesting that radiation could contribute to DU genotoxic effects in vivo. All these in vivo results contribute to a better understanding of the pathological effect of DU inhalation.

Bioaccumulation and behavioural effects of depleted uranium in rats exposed to repeated inhalations.

Depleted uranium has numerous industrial and military uses. Contamination by inhalation of airborne compounds is probably the most important route of exposure. In humans, there are no data clearly demonstrating neurotoxicity of uranium, yet some experimental studies suggest a link between neurological toxicity and uranium exposure. In this work, the bioaccumulation of uranium in male rats after exposure to repeated depleted uranium dioxide inhalation (30 min inhalation at 197 mgm(-3), 4 days a week for 3 weeks) has been studied, together with the behavioural effects. The uranium concentrations in the brain 1 day after the end of the exposure period varied as follows: olfactory bulb>hippocampus>frontal cortex>cerebellum, subsequently decreasing rapidly. The spontaneous locomotion activity of exposed rats was increased 1 day post exposure and the spatial working memory was less efficient 6 days post exposure, compared with control rats. These data suggest that depleted uranium is able to enter the brain after exposure to repeated inhalation, producing behavioural changes.