This report describes a whole body donation from a person with a documented occupational intake of uranium. USTUR Case 1002 was an adult male who died from an acute cerebellar infarct at the age of 83. He worked as a power operator, utility operator, and metal operator for 28 years in a facility that processed and handled radioactive materials. Although he suffered a number of burns from hot metal and acids, cuts, abrasions, and puncture wounds during his many years of work, there were no corresponding health physics or medical records to indicate that these occurrences needed or required excision or decontamination due to the suspicion of the deposition of radioactive material. Over the course of his employment, USTUR Case 1002 submitted numerous urine samples for uranium, plutonium, and fission product analysis. The highest single uranium value measured during this time period was approximately 30 microg L(-1) recorded during the second year of his employment. A urinary bioassay sample taken before termination of employment measured 4.3 microg L(-1). The mean urinary uranium concentration per liter per year calculated from the employee's bioassay records covering the first eleven years of monitoring averaged less than 3 microg L(-1). The ratio of 234/238U activity in the lung tissue was about 1, the same as that found in natural uranium. The highest concentration of uranium was found in a tracheobronchial lymph node. The uranium content in the various tissues of the body followed a rank order lung > skeleton > liver > kidney. Concentration of uranium in the kidney tissue was approximately 1.98 ng g(-1), about 3 orders of magnitude less than the generally accepted threshold level for permanent kidney damage of 3 microg U g(-1) and roughly equal to the 1.4 ng g(-1) reported for Reference Man. The autopsy disclosed findings not uncommon in the aged: severe atherosclerosis, areas of sclerotic kidney glomeruli with stromal fibrous scarring, and moderate to severe arterionephrosclerosis. Lung sections contained parenchymal areas of acute vascular congestion and a mild degree of anthracosis.

We analyzed six different tissue DNA samples from a leukemic individual who received an injection of Thorotrast for alterations in proto-oncogene or tumor-suppressor gene structure. Our examination of the DNA indicated an alteration of the c-fms gene in the blood sample from this individual. This locus showed a deletion in which the 3' end of the deleted region maps between exons 11 and 12. In this particular case, the type of leukemia is unknown but myeloid leukemia is a neoplasm associated with individuals injected with Thorotrast. It is possible that the alteration in the c-fms gene of this individual is a consequence of the radiation exposure. No apparent alterations in the c-mos gene were observed in any of the tissues from the individual. This is in contrast to previous studies that described alterations in methylation patterns associated with the c-mos locus in radium-exposed individuals. A number of the individuals exposed to radium also had alterations of the retinoblastoma gene while no such alterations were observed in any tissue DNA samples from this Thorotrast case. It is possible that our inability to detect alterations of the c-mos and retinoblastoma gene may be attributable to the nature of alpha-emitting radionuclides or their distribution, or to the limited set of tissues available for analysis.

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Results are presented of postmortem human tissue sampling and analysis for plutonium of Hanford Site workers, residents of the nearby Tri-Cities, and individuals residing farther away from the Hanford Site for the period 1970-1975. The majority of Hanford Site workers and nearby residents coming to autopsy had tissue concentrations of plutonium no larger than those who lived farther away from Hanford and whose likely source of plutonium was limited to nuclear weapons testing fallout. Thus, Hanford operations up to that time apparently had made no significant addition to plutonium in those individuals sampled postmortem.