This study investigated health risks in workers residing and working in terrains contaminated by low ionizing radiation doses which originated from ammunition containing depleted uranium (DU). The studied population was composed of two test groups (T-I, T-II) who were occasionally exposed to DU, and two referent (R-I, R-II) groups not exposed at any time to DU. All of them were evaluated for the following: complete clinical examination and blood count, presence of immature forms and blasts, leukocyte alkaline phosphatase activity and cytogenetic tests. The probability of onset of the characteristic complete biomarkers--chromosomal aberrations, was analyzed using logarithmic function of the Poisson regression. The estimated function of the density of probabilities of Poisson distribution of the chromosomal aberrations in the test group T-II was drastically different from the corresponding distribution of the referent group R-I and to a somewhat lesser extent from the group R-II; Wilcoxon test exactly confirms the presence of a significant difference between the reference group R-II and test group T-II, p < 0.05. The damages to chromosomes and cells were highest in the test group T-II of workers additionally occupationally exposed to DU. The group of workers T-I, who had been exposed to DU working on contaminated terrain, have had certain risks of cell and chromosome damages, and that risk was not greater than the risk to the referent group R-II of workers occupationally exposed to ionizing radiation.

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Occupational exposure to low doses of ionizing radiation is a particularly delicate subject for investigation, due to the cumulative effects of chronic exposure. It is extremely important to consider and to measure the biological response to given conditions of exposure. The aim of this study was to establish possible recovery from DNA damage in subjects professionally exposed to radiation in their working area by examinations for chromosomal aberrations (CA) at two different times. The first group (I) was composed of 30 professionally exposed subjects in whom unstable CA (dicentrics, ring, acentric fragments, chromatid, chromosomal breaks, and chromatid interchanges) were identified at time zero. After removal from the radiation area, they were re-examined 9 months later. The second group (II) contained 64 healthy individuals, not professionally exposed to ionizing radiation or other known mutagenic agents. In the group of exposed individuals, five (16.67%) subjects exhibited permanent unstable CAs, even after 9 months absence from the radiation. When the nonexposed and exposed groups were compared, an increase of unstable aberrations (p < 0.05) was observed in the exposed group. Nevertheless, a statistically significant decrease of dicentrics, acentric fragments, and ring frequencies was observed in exposed individuals after 9 months away from the radiation area. However, chromatid and isochromatid break frequencies increased slightly but not significantly after 9 months. The detected CAs corresponded to the total effective doses of radiation measured in our subjects. The existence of CAs in some individuals even after absence from the radiation area suggests that the time necessary for the damaged DNA to recover is extremely variable and indicates interindividual differences in radiosensitivity as well as differences in the cellular-reparation response.

This paper analyzes the effects of x rays on workers exposed to radiation. In particular, this paper documents the emergence and frequency of non-specific chromosomal lesions with characteristic chromosomal aberrations and the number of damaged lymphocytes before, during, and after occupational exposure. Chromosomal changes were analyzed taking into consideration duration of exposure, dose, age, and sex. Correlation between aberrations and absorbed doses of x rays measured by thermoluminescence dosimeters is shown, as well as correlation between chromosomal lesions and damaged cells and the frequency of chromosomal aberrations. Chromosomal aberrations of karyotype diminish after exposures cease, but the number of non-specific lesions in karyotype do not decrease during the same period. The duration of exposure and age are not significant predictors of analyzed aberrations and lesions.

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