Ronald L. Kathren

NORM sources and their origins

Naturally Occurring Radioactive Materials, often referred to by the acronym NORM, are and always have been a part of our world. Our planet and its atmosphere contain many different naturally occurring radioactive species, and it and virtually everything, living or inanimate, contains NORM. In the history of mankind, knowledge of the existence of radioactivity is very recent, even when considered within the span of recorded history. Indeed, the discovery of radioactivity and hence NORM is barely a century old, dating back to the final years of the nineteenth century.

Pathway to a Paradigm: The Linear Nonthreshold Dose-response Model in Historical Context

This paper traces the evolution of the linear nonthreshold dose-response model and its acceptance as a paradigm in radiation protection practice and risk analysis. Deterministic effects such as skin burns and even deep tissue trauma were associated with excessive exposure to x rays shortly after their discovery, and carcinogenicity was observed as early as 1902. Still, it was not until 1925 that the first protective limits were suggested. For three decades these limits were based on the concept of a tolerance dose which, if not exceeded, would result in no demonstrable harm to the individual and implicitly assumed a threshold dose below which radiation effects would be absent. After World War II, largely because of genetic concerns related to atmospheric weapons testing, radiation protection dose limits were expressed in terms of a risk based maximum permissible dose which clearly implied no threshold. The 1927 discovery by Muller of x-ray induced genetic mutations in fruit flies, linear with dose and with no apparent threshold, was an important underpinning of the standards. The linear nonthreshold dose-response model was originally used to provide an upper limit estimate of the risk, with zero being the lower limit, of low level irradiation since the dose-response curve could not be determined at low dose levels. Evidence to the contrary such as hormesis and the classic studies of the radium dial painters notwithstanding, the linear nonthreshold model gained greater acceptance and in the centennial year of the discovery of x rays stands as a paradigm although serious questions are beginning to be raised regarding its general applicability. The work includes a brief digression describing the work of x-ray protection pioneer William Rollins and concludes with a recommendation for application of a de minimis dose level in radiation protection.

Uranium in the tissues of an occupationally exposed individual

Uranium concentrations were radiochemically determined in samples of lung, kidney, liver and bone collected at autopsy from an occupationally exposed individual. Levels of U in these tissues were clearly in excess of those expected from environmental exposure. Deposition followed the pattern: skeleton greater than liver greater than kidney, with ratios of 63:2.8:1. The data suggest there is an important long-term storage depot in the skeleton, but the fraction transferred to this compartment, as proposed by ICRP 30, may be too small. In vivo chest counts obtained over about a 10-y period prior to death indicated about a factor of 2 greater in total U content and 235U enrichment than deposition estimates made at autopsy for the lungs and associated lymph nodes.

Acute accidental inhalation of U: a 38-year follow-up

The intake and deposition of U in three men accidentally exposed to soluble natural U compounds in an explosion in 1944 were reevaluated 38 y later by the U.S. Uranium Registry. The initial lung depositions were estimated to be about 40-50 mg of U based on the fragmentary urinary excretion data obtained shortly after the accident. The initial long-term bone deposition was estimated from individual excretion curves and was 410 micrograms (5.2 Bq) in the highest exposed individual, which resulted in an integrated 40-y dose equivalent to the bone surfaces approximately 2 mSv (200 mrem). Medical and health physics examinations of two of the men 38 y after the accident revealed no detectable deposition of U nor any physical findings attributable to U exposure. One of the exposed individuals showed an altered clearance pattern for U shortly after the accident, possibly from pulmonary edema associated with concomitant exposure to acid fumes.

ACUTE CHEMICAL TOXICITY OF URANIUM

Although human experience with uranium spans more than 200 years, the LD50 for acute intake in humans has not been well established. Large acute doses of uranium can produce death from chemical toxicity in rats, guinea pigs, and other small experimental animals, with variation in sensitivity among species. However, there has never been a death attributable to uranium poisoning in humans, and humans seem to be less sensitive to both acute and chronic toxic effects of uranium than other mammalian species studied. Highly relevant data on uranium toxicity in humans are available from the experience of persons administered large doses of uranium for therapy of diabetes and from acute accidental inhalation intakes. Although the data on which to establish oral and inhalation acute LD50 for uranium in humans are sparse, they are adequate to conclude that the LD50 for oral intake of soluble uranium compounds exceeds several grams of uranium and is at least 1.0 g for inhalation intakes. For intakes of uranium compounds of lesser solubility, acute LD50 values are likely to be significantly greater. It is suggested that 5 g be provisionally considered the acute oral LD50 for uranium in humans. For inhalation intakes of soluble compounds of uranium, 1.0 g of uranium is proposed as the provisional acute inhalation LD50.

A sensitive method for the determination of uranium in biological samples utilizing kinetic phosphorescence analysis (KPA)

Kinetic phosphorescence analysis is a technique that provides rapid, precise and accurate determination of uranium concentration in aqueous solutions. This technique utilizes a laser source to excite an aqueous solution of uranium, and measures the emission luminescence intensity over time to determine the luminescence decay profile. The lifetime of the luminescence decay profile and the linearity of the log luminescence intensity versus time profile are indications of the specificity of the technique for uranium determination. The luminescence intensity at the onset of decay (the initial luminescence intensity), which is the luminescence intensity at time zero after termination of the laser pulse used for excitation, is proportional to the uranium concentration in the sample. Calibration standards of known uranium concentrations are used to construct the calibration curve between the initial luminescence intensity and uranium concentration. This calibration curve is used to determine the uranium concentration of unknown samples from their initial luminescence intensity. We developed the sample preparation method that allows the determination of uranium concentrations in urine, plasma, kidney, liver, bone spleen and soft tissue samples. Tissue samples are subjected to dry-ashing in a muffle furnace at 600 degrees C and wet-ashing with concentrated nitric acid and hydrogen peroxide twice to destroy the organic component in the sample that may interfere with uranium determination by KPA. Samples are then solubilized in 0.82 M nitric acid prior to analysis by KPA. The assay calibration curves are linear and cover the range of uranium concentrations between 0.05 micrograms l-1 and 1000 micrograms l-1 (0.05-1000 ppb). The developed sample preparation procedures coupled with the KPA technique provide a specific, sensitive, precise and accurate method for the determination of uranium concentration in tissue samples. This method was used to quantify uranium in different tissue samples obtained over a period of 90 days following a single intraperitoneal uranium dose of 0.1 mg kg-1 in rats.

Partitioning of 238Pu, 239Pu and 241Am in skeleton and liver of U.S. Transuranium Registry autopsy cases.

The content of 238Pu, 239Pu and 241Am in the liver and skeleton was estimated from radiochemical analysis of human liver and bone samples obtained at autopsy from former actinide workers whose occupational histories were suggestive of chronic inhalation exposures, with minor skin contamination and wounds documented in a few individuals. For times estimated to be several years to a few decades post intake, 75.8 +/- 15.3% of the total 241Am in the skeleton and liver was found in the skeleton (25 cases) as compared with 63.4 +/- 24.1% for 238Pu (36 cases) and 53.2 +/- 18.2% for 239Pu (43 cases). These differences are significant at the 95% confidence level. Of these cases, 34 included data on both 238Pu and 239Pu and were divided into high and low activity subgroups. The difference in the fractionation of the two Pu isotopes was apparent only in the low activity subgroup, suggesting that the difference observed between the Pu isotopes may be an artifact of the data. The different partitioning of these three nuclides suggests that the ALIs for 238Pu and 241Am may be high by about 25-50% if only the dose to bone is considered and may be high by 12-13%, based on the weighted committed dose equivalent in target organs or tissues.

Modified biokinetic model for uranium from analysis of acute exposure to UF6.

Urinalysis measurements from 31 workers acutely exposed to uranium hexafluoride (UF6) and its hydrolysis product UO2F2 (during the 1986 Gore, Oklahoma UF6-release accident) were used to develop a modified recycling biokinetic model for soluble U compounds. The model is expressed as a five-compartment exponential equation: yu(t) = 0.086e-2.77t + 0.0048e-0.116t + 0.00069e-0.0267t + 0.00017 e-0.00231t + 2.5 x 10(-6) e-0.000187t, where yu(t) is the fractional daily urinary excretion and t is the time after intake, in days. The excretion constants of the five exponential compartments correspond to residence half-times of 0.25, 6, 26, 300, and 3,700 d in the lungs, kidneys, other soft tissues, and in two bone volume compartments, respectively. The modified recycling model was used to estimate intake amounts, the resulting committed effective dose equivalent, maximum kidney concentrations, and dose equivalent to bone surfaces, kidneys, and lungs.

Six-year follow-up of an acute 241Am inhalation intake.

Abstract— A 38-y-old Caucasian male who suffered an acute accidental inhalation intake of 6.3 kBq of 241Am was monitored over 2,135 d using periodic in vivo measurements of the activity in the lungs, liver, and skeleton. Lung clearance was described by a two-compartment exponential model with half-times of 110 d and 10,000 d. The observed uptake of 241Am in the liver (72 Bq) and skeleton (170 Bq) was significantly greater than predicted by the ICRP models for liver (5 Bq) and skeleton (8 Bq). The half-time in the liver was approximately 850 d. Estimates of skeletal activity based on head, wrist, and knee counts generally agreed within 25% over the course of the monitoring period. The half-time in the skeleton was approximately 20,000 d.

Changes in soft tissue concentrations of plutonium and americium with time after human occupational exposure

Concentrations of 239 + 240Pu and 241Am in human soft tissues (testes, thyroid gland, kidneys, spleen, heart, skeletal muscle, brain, and pancreas) were compared to those in livers of the same subjects. The subjects were volunteer donors with occupational exposures to plutonium and americium autopsied as part of the United States Transuranium and Uranium Registries program. The temporal distributions of tissue-to-liver ratios were compared to liver uptake fractions assumed on the basis of current models to estimate the initial uptake fractions for each tissue studied. Regressions of the ratios were used to compare tissue retention half-times to those of the liver. Effective half-times for plutonium and americium in the tissues studied were similar to those for the liver with three exceptions: (1) the clearance half-time for plutonium in kidneys is shorter than that of liver; (2) the retention half-time for plutonium in testes is longer than that of liver; and (3) the retention half-time for americium in skeletal muscle was longer than in the liver. Next to liver, the greatest initial uptake of systemic actinides was in skeletal muscle and the greatest initial concentrations were in the spleen. The uptake fraction of plutonium in the testes proposed by the ICRP was verified.