Long term depleted uranium exposure in Gulf War I veterans does not cause elevated numbers of micronuclei in peripheral blood lymphocytes

Depleted uranium (DU) is a high density heavy metal that has been used in military munitions since the 1991 Gulf War. DU is weakly radioactive and chemically toxic. Long term exposure can cause adverse health effects. This study assessed genotoxic effects in DU exposed Gulf War I veterans as a function of uranium (U) body burden. Levels of urine U were used to categorize the cohort into low and high exposure groups. Exposure to DU occurred during friendly fire incidents in 1991 involving DU munitions resulting in inhalation and ingestion exposure to small particles of DU and soft tissue DU fragments from traumatic injuries. All of these Veterans are enrolled in a long term health surveillance program at the Baltimore Veterans Administration Medical Center. Blood was drawn from 35 exposed male veterans aged 36-59 years, then cultured and evaluated for micronuclei (MN) using the cytokinesis block method. The participants were divided into two exposure groups, low and high, based on their mean urine uranium (uU) concentrations. Poisson regression analyses with mean urine U concentrations, current smoking, X-rays in the past year and donor age as dependent variables revealed no significant relationships with MN frequencies. Our results indicate that on-going systemic exposure to DU occurring in Gulf War I Veterans with DU embedded fragments does not induce significant increases in MN in peripheral blood lymphocytes compared to MN frequencies in Veterans with normal U body burdens.     

Depleted uranium is not toxic to rat brain endothelial (RBE4) cells

Studies on Gulf War veterans with depleted uranium (DU) fragments embedded in their soft tissues have led to suggestions of possible DU-induced neurotoxicity. We investigated DU uptake into cultured rat brain endothelial cells (RBE4). Following the determination that DU readily enters RBE4 cells, cytotoxic effects were analyzed using assays for cell volume increase, heat shock protein 90 (Hsp90) expression, 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) reduction, and lactate dehydrogenase (LDH) activity. The results of these studies show that uptake of the U₃O₈ uranyl chloride form of DU into RBE4 cells is efficient, but there are little or no resulting cytotoxic effects on these cells as detected by common biomarkers. Thus, the present experimental paradigm is rather reassuring and provides no indication for overt cytotoxicity in endothelial cells exposed to DU.     

Problems in the biological monitoring of chromium(VI) exposed individuals

The usefulness of currently available techniques for the biological monitoring of chromium(VI) exposed individuals is reviewed. Chromium levels in body fluids, such as urine and blood plasma, are reliable markers of exposure to chromium in oxidation states (VI) and (III) and provide a measure of the internalized dose of chromium. These markers are sufficiently sensitive to be useful in most occupational settings encountered today. In contrast, the majority of cytogenetic surveillance studies among chromium platers, ferrochromium workers and stainless steel welders using the manual metal arc (MMA) method have yielded negative or inconclusive results. As a marker for genotoxicity, the number of sister chromatid exchanges in blood lymphocytes proved to be relatively insensitive towards exposure to chromium(VI). There were however significant increases in rare chromosome aberrations among MMA stainless steel welders, although the reported levels of all aberrations combined were similar to those observed among control groups of many other studies. The relative lack of success of cytogenetic surveillance studies using blood lymphocytes is surprising in view of the strong genotoxicity of chromium(VI). A possible explanation comes from recent studies which showed that the differences in chromium lymphocyte levels between exposed and controls were disproportionately small. Another factor which complicates attempts to correlate genotoxic effects in lymphocytes with the processes giving rise to cancers of the respiratory system is the toxicokinetics of inhaled chromium(VI). Only small fractions of the total inhaled dose are distributed in the body while the bulk of chromium(VI) deposited in the lungs remains there for very long periods of time. The vast majority of lymphocytes will therefore come into contact with chromium(VI) not while travelling through the supporting tissues of the lungs but during their migration through the blood. There they take up chromium(VI) that has leached from the lungs. Blood lymphocytes therefore seem to be inappropriate for the monitoring of the biologically effective dose, and of early biological effects arising from exposure to chromium(VI). Thus there is an urgent need to develop techniques which would allow the non-invasive monitoring of internalized doses of chromium in the lung.     

Problems in the biological monitoring of chromium(VI) exposed individuals

The usefulness of currently available techniques for the biological monitoring of chromium(VI) exposed individuals is reviewed. Chromium levels in body fluids, such as urine and blood plasma, are reliable markers of exposure to chromium in oxidation states (VI) and (III) and provide a measure of the internalized dose of chromium. These markers are sufficiently sensitive to be useful in most occupational settings encountered today. In contrast, the majority of cytogenetic surveillance studies among chromium platers, ferrochromium workers and stainless steel welders using the manual metal arc (MMA) method have yielded negative or inconclusive results. As a marker for genotoxicity, the number of sister chromatid exchanges in blood lymphocytes proved to be relatively insensitive towards exposure to chromium(VI). There were however significant increases in rare chromosome aberrations among MMA stainless steel welders, although the reported levels of all aberrations combined were similar to those observed among control groups of many other studies. The relative lack of success of cytogenetic surveillance studies using blood lymphocytes is surprising in view of the strong genotoxicity of chromium(VI). A possible explanation comes from recent studies which showed that the differences in chromium lymphocyte levels between exposed and controls were disproportionately small. Another factor which complicates attempts to correlate genotoxic effects in lymphocytes with the processes giving rise to cancers of the respiratory system is the toxicokinetics of inhaled chromium(VI). Only small fractions of the total inhaled dose are distributed in the body while the bulk of chromium(VI) deposited in the lungs remains there for very long periods of time. The vast majority of lymphocytes will therefore come into contact with chromium(VI) not while travelling through the supporting tissues of the lungs but during their migration through the blood. There they take up chromium(VI) that has leached from the lungs. Blood lymphocytes therefore seem to be inappropriate for the monitoring of the biologically effective dose, and of early biological effects arising from exposure to chromium(VI). Thus there is an urgent need to develop techniques which would allow the non-invasive monitoring of internalized doses of chromium in the lung.     

Experimental validation of non-invasive and fluid density independent methods for the determination of local wave speed and arrival time of reflected wave

The relationship between the vessel diameter (D) and fluid velocity (U) in arteries and flexible tubes has been recently characterized as linear in the absence of wave reflections. This relationship allowed for determining local wave speed (C(DU)) using the lnDU-loop method. Using C(DU), it was possible to separate U and D waveforms into their forward and backward components. It was also possible to calculate wave intensity (dI(DU)), using D and U, from which the arrival time of reflected wave (Trw(DU)) could be determined. These techniques are fluid density independent and require only non-invasive measurements of D and U. In this work we experimentally validate the relative accuracy of these new techniques in vitro, by comparing their results of C(DU) and Trw(DU) to those determined by the established techniques, PU-loop and wave intensity analysis, C and Trw, respectively. We generated a single semi-sinusoidal wave in long flexible tubes, and simultaneously measured pressure (P), D, and U at the same site. Sequentially in time, we repeated this experiment at three sites along each of the flexible tubes, which were made of different materials and sizes, and three fluids of different densities. C(DU) compared well with that C and likewise Trw(DU) was very similar to Trw. Varying fluid density did not appreciably change the difference between the results of the two techniques. We conclude that the new techniques for determining C(DU) and Trw(DU), although independent of density, provide relatively accurate estimates of wave speed and arrival times of reflected waves in vitro. The new techniques require only non-invasive measurements of D and U, and further in vivo validation is required to establish its advantage in the clinical setting.     

Cancer risk and all-cause mortality among Norwegian military United Nations peacekeepers deployed to Kosovo between 1999 and 2011

ObjectiveMedia reports of leukaemia and other cancers among European United Nations (UN) peacekeepers who served in the Balkans, and a scientific finding of excess Hodgkin lymphoma among Italian UN peacekeepers who served in Bosnia, suggested a link between cancer incidence and depleted uranium (DU) exposure. This spurred several studies on cancer risk among UN peacekeepers who served in the Balkans. Although these studies turned out to be negative, the debate about possible cancers and other health risks caused by DU exposure continues. The aim of the present study was to investigate cancer incidence and all-cause mortality in a cohort of 6076 (4.4% women) Norwegian military UN peacekeepers deployed to Kosovo between 1999 and 2011.MethodsThe cohort was followed for cancer incidence and mortality from 1999 to 2011. Standardised incidence ratios for cancer (SIR) and mortality ratios (SMR) were calculated from national rates.ResultsSixty-nine cancer cases and 38 deaths were observed during follow-up. Cancer incidence in the cohort was similar to that in the general Norwegian population. No cancers in the overall cohort significantly exceeded incidence rates in the general Norwegian population, but there was an elevated SIR for melanoma of skin in men of 1.90 (95% confidence interval [CI] 0.95–3.40). A fivefold increased incidence of bladder cancer was observed among men who served in Kosovo for ≥1 year, based on 2 excess cases (SIR = 5.27; 95% CI 1.09–15.4). All-cause mortality was half the expected rate (SMR = 0.49; 95% CI 0.35–0.67).ConclusionOur study did not support the suggestion that UN peacekeeping service in Kosovo is associated with increased cancer risk.     

Leukemic transformation of hematopoietic cells in mice internally exposed to depleted uranium

Depleted uranium (DU) is a dense heavy metal used in military applications. During military conflicts, US military personnel have been wounded by DU shrapnel. The health effects of embedded DU are unknown. Published data from our laboratory demonstrated that DU exposure in vitro can transform immortalized human osteoblast cells (HOS) to the tumorigenic phenotype. Results from our laboratory have also shown that DU is genotoxic and mutagenic in cultured human cells. Internalized DU could be a carcinogenic risk and concurrent alpha particle and heavy metal toxic effects complicate this potential risk. Anecdotal reports have suggested that DU can cause leukemia. To better assess this risk, we have developed an in vivo leukemogenesis model. This model involves using murine hematopoietic cells (FDC-P1) that are dependent on stimulation by granulocyte-macrophage colony stimulating factor (GM-CSF) or interleukin 3 (IL-3) and injected into mice to produce myeloid leukemia. Although immortalized, these cells are not tumorigenic on subcutaneous inoculation in mice. Intravenous injection of FDC-P1 cells into DU-implanted DBA/2 mice was followed by the development of leukemias in 76% of all mice implanted with DU pellets. In contrast, only 12% of control mice developed leukemia. Karyotypic analysis confirmed that the leukemias originated from FDC-P1 cells. The growth properties of leukemic cells from bone marrow, spleen, and lymph node were assessed and indicate that the FDC-P1 cells had become transformed in vivo. The kidney, spleen, bone marrow, muscle, and urine showed significant elevations in tissue uranium levels prior to induction of leukemia. These results demonstrated that a DU altered in vivo environment may be involved in the pathogenesis of DU induced leukemia in an animal model.     

Elevated expression of ERK 2 in human tumor cells chronically treated with PD98059

We examined the effect of chronic exposure of tumor cells to a mitogen-activated protein kinase/extracellular signal-regulated kinases (ERK) kinase inhibitor, PD98059, on cell proliferation was investigated. Human renal carcinoma cells (ACHN) and prostatic carcinoma cells (DU145) were cultured in the presence of PD98059 for more than 4 weeks (denoted ACHN (PD) cells and DU145 (PD) cells, respectively) and proliferation and signal transduction pathways were examined. PD98059 significantly inhibited the proliferation of parental cells. However, PD98059 failed to inhibit proliferation of ACHN (PD) and DU145 (PD) cells significantly. Expression of ERK 1 and 2 was elevated in these cells. These phenotypes were reversible. Downregulation of ERK 2, but not ERK 1, by small interfering RNA significantly inhibited the proliferation of ACHN (PD) and DU145 (PD) cells. Taken together, chronic exposure of tumor cells to PD98059 induced elevated expression of ERK 2, which was associated with decreased sensitivity of cellular proliferation to PD98059.     

Microarray gene expression profiling of a human glioblastoma cell line exposed in vitro to a 1.9 GHz pulse-modulated radiofrequency field

The widespread use of mobile phones has led to public concerns about the health effects associated with exposure to radiofrequency (RF) fields. The paramount concern of most persons relates to the potential of these fields to cause cancer. Unlike ionizing radiation, RF fields used for mobile telecommunications (800-1900 MHz) do not possess sufficient energy to directly damage DNA. Most rodent bioassay and in vitro genotoxicity/mutation studies have reported that RF fields at non-thermal levels have no direct mutagenic, genotoxic or carcinogenic effects. However, some evidence has suggested that RF fields may cause detectable postexposure changes in gene expression. Therefore, the purpose of this study was to assess the ability of exposure to a 1.9 GHz pulse-modulated RF field for 4 h at specific absorption rates (SARs) of 0.1, 1.0 and 10.0 W/kg to affect global gene expression in U87MG glioblastoma cells. We found no evidence that non-thermal RF fields can affect gene expression in cultured U87MG cells relative to the nonirradiated control groups, whereas exposure to heat shock at 43 degrees C for 1 h up-regulated a number of typical stress-responsive genes in the positive control group. Future studies will assess the effect of RF fields on other cell lines and on gene expression in the mouse brain after in vivo exposure.     

Residential Treatment for Combat-Related Posttraumatic Stress Disorder: Identifying Trajectories of Change and Predictors of Treatment Response

Background

Combat-related posttraumatic stress disorder (PTSD) can be a difficult condition to treat and has been associated with serious medical and economic issues among U.S. military veterans. Distinguishing between treatment responders vs. non-responders in this population has become an important public health priority. This study was conducted to identify pre-treatment characteristics of U.S. veterans with combat-related PTSD that might contribute to favorable and unfavorable responses to high value treatments for this condition.

Method

This study focused on 805 patients who completed a VHA PTSD residential program between 2000 and 2007. These patients completed the PTSD Clinical Checklist at pre-treatment, post-treatment, and a four-month follow-up assessment. Latent growth curve analysis (LCGA) was incorporated to determine trajectories of changes in PTSD across these assessments and whether several key clinical concerns for this population were associated with their treatment responses.

Study Findings

LCGA indicated three distinct trajectories in PTSD outcomes and identified several clinical factors that were prospectively linked with changes in veterans'' posttraumatic symptomatology. When compared to a group with high PTSD symptom severity that decreased over the program but relapsed at follow-up (41%), the near half (48.8%) of the sample with an improving trajectory had less combat exposure and superior physical/mental health. However, when compared to a minority (10.2%) with relatively low symptomatology that also remained somewhat stable, patients in the improving group were younger and also reported greater combat exposure, poorer physical/mental health status, and more problems with substance abuse before the start of treatment.

Conclusions

Findings suggest that veterans are most likely to benefit from residential treatment in an intermediate range of symptoms and risk factors, including PTSD symptom severity, history of combat exposure, and comorbid issues with physical/mental health. Addressing these factors in an integrative manner could help to optimize the effectiveness of treatments of combat-related PTSD in many cases.     

A comparison of intraperitoneal and oral gavage administration in comet assay in mouse eight organs

One of the important advantages of the comet assay is its ability to detect genotoxicity in many different organs. Since the exposure route of the test compounds is likely to influence the genotoxicity detected in a given organ, it is an important factor to consider when conducting the assay. In this study, we compared the effects of numerous model compounds on eight organs when administered to mice by intraperitoneal (i.p.) injection and oral (p.o.) gavage.Groups of four mice were treated once i.p. or p.o. at the identical proportion of LD50 for each route, and the stomach, colon, liver, kidney, bladder, lung, brain, and bone marrow were sampled 3, 8, and 24h after treatment. For 19 of the 20 tested mutagens with various modes of action, genotoxicity in some organs varied with treatment route; only the genotoxicity of methyl methane sulfonate was not affected. Treatment route, however, did not produce a qualitative difference in the genotoxicity of promutagens at the sites of conversion to ultimate mutagens, with aromatic hydrocarbons as the exception. When chemicals with positive responses in at least one organ were considered to be comet assay-positive, the administration route made no difference. Since azo reduction is mediated by azo reductase synthesized in the gastrointestinal wall and by gut microflora and i.p.-administered azo dyes bypass their activation site (colon), the administration route is expected to make a difference in their in vivo genotoxicity. Direct-acting mutagens are expected to affect the mucosa of the gastrointestinal tract when given p.o. For those mutagens, however, the administration route did not make a qualitative difference in gastrointestinal tract genotoxicity. Moreover, although the gastrointestinal mucosa is the first site to be exposed to p.o. administered agents, the peak times in the stomach tended to be the same as in most other organs. Based on those results, we concluded that the genotoxicity at high exposures was due to a systemic effect, and that both routes are acceptable for the comet assay when the liver and gastrointestinal organs are sampled, so long as appropriate dose levels for systemic exposure are selected for each route.     

The impact of the 1991 Gulf War on the mind and brain: findings from neuropsychological and neuroimaging research

Many veterans of the 1991 Gulf War (GW) have complained of somatic and cognitive symptoms that may be neurological in nature. However, whether or not changes in brain function are associated with GW service continues to be debated. Studies of GW veterans using objective, performance-based neuropsychological measures have yielded inconsistent findings, with those indicating deficits among GW veterans typically revealing only relatively mild levels of neuropsychological impairment. Further, performances on objective neuropsychological tasks show little correspondence to subjective perceptions of cognitive functioning. Although preliminary magnetic resonance spectroscopy (MRS) studies demonstrate reduced N-acetylaspartate-to-creatine (NAA/Cr) ratio in select brain regions among GW veterans who report health concerns, this work requires further replication with larger, more representative samples. There is no evidence from neuroimaging studies of a non-specific effect of GW service or of changes in brain structure or function related to health status when conventional radiological methods are used. Owing to the paucity of objective exposure, baseline health data, and the now significant time elapsed since the GW, aetiological issues may never be fully resolved. Therefore, research addressing clinical management of GW veterans with neuropsychological dysfunction and neuroimaging abnormalities may prove more fruitful than exclusive focus on aetiology.     

Comparison of hair, nails and urine for biological monitoring of low level inorganic mercury exposure in dental workers.

Creatinine-corrected urine mercury measurements in spot urine samples are routinely used in monitoring workers exposed to inorganic mercury. However, mercury measurement in other non-invasive biological material has been used in some epidemiological studies. Dentists and dental nurses remain a group of workers with potential exposure to inorganic mercury through their handling of mercury-containing amalgam, although changes in work practices have reduced the current, likely exposure to mercury. Therefore, dental workers remain an occupational cohort in whom the value of using different biological media to identify exposure to low level inorganic mercury can be investigated. Samples of head hair, pubic hair, fingernails, toenails and urine were analysed for mercury content from a cohort of UK dentists (n=167) and a socioeconomically similar reference population (n=68) in whom any mercury exposure was primarily through diet. The mercury content in all biological material was significantly higher in the dental workers than in the control population (p<0.0001). The geometric mean and 90th percentile mercury concentrations in the urine samples from dentists were 1.7 and 7.3 micromol mol(-1) creatinine, respectively, with only one sample having a value at around the UK's Health and Safety Executive biological monitoring health guidance level of 20 micromol mol(-1) creatinine. Receiver operator characteristic analyses suggested that the ability of the biological material to discriminate between dentists and referents were fingernails>urine approximately equal to toenails>pubic hair approximately equal to head hair. Further investigation is warranted as to why fingernails appear to be such a good discriminator, possibly reflecting some contribution of direct finger contact with amalgam or contaminated surfaces rather than systemic incorporation of mercury into growing nails. Good correlation between head hair and pubic hair mercury levels in all subjects was obtained (r=0.832), which was significantly improved when hair samples weighing <10 mg were excluded (r=0.868). Therefore, under these exposure conditions and using the described pre-analytical washing steps, there is little influence from atmospheric contamination on the level of mercury content of head hair. The choice of non-invasive biological materials for mercury analysis depends on a number of considerations. These include the toxicokinetics of urinary mercury excretion, the growth rates of hair and nail, the nature and time-frame of exposure, and the fact that urine mercury may not reflect the body burden level from dietary methyl mercury. However, the data from this study suggests that urine mercury remains the most practical and sensitive means of monitoring low level occupational exposure to inorganic mercury.     

Brain accumulation of depleted uranium in rats following 3- or 6-month treatment with implanted depleted uranium pellets

Depleted uranium (DU) is used to reinforce armor shielding and increase penetrability of military munitions. Although the data are conflicting, DU has been invoked as a potential etiological factor in Gulf War syndrome. We examined regional brain DU accumulation following surgical implantation of metal pellets in male Sprague-Dawley rats for 3 or 6 mo. Prior to surgery, rats were randomly divided into five groups: Nonsurgical control (NS Control); 0 DU pellets/20 tantalum (Ta) pellets (Sham); 4 DU pellets/16 Ta pellets (Low); 10 DU pellets/10 Ta pellets (Medium); 20 DU pellets/0 Ta pellets (High). Rats were weighed weekly as a measure of general health, with no statistically significant differences observed among groups in either cohort. At the conclusion of the respective studies, animals were perfused with phosphate-buffered saline, pH 7.4, to prevent contamination of brain tissue with DU from blood. Brains were removed and dissected into six regions: cerebellum, brainstem (pons and medulla), midbrain, hippocampus, striatum, and cortex. The uranium content was measured in digested samples as its ²³⁸U isotope by high-resolution inductively coupled plasma-mass spectrometry. After 3 mo postimplantation, DU significantly accumulated in all brain regions except the hippocampus in animals receiving the highest dose of DU (p<0.05). By 6 mo, however, significant accumulation was measured only in the cortex, midbrain, and cerebellum (p<0.01). Our data suggest that DU implanted in peripheral tissues can preferentially accumulate in specific brain regions.     

Post-traumatic Stress Disorder in children and adolescents: from Sigmund Freud's "trauma" to psychopathology and the (Dys)metabolic syndrome.

Post-traumatic Stress Disorder (PTSD) is an anxiety syndrome that develops after exposure to traumatic life events. Symptoms include re-experience of the initial trauma, avoidance of stimuli associated with the trauma and symptoms of excessive arousal. Neuroendocrine studies in adults with PTSD have demonstrated that basal cerebrospinal fluid (CSF) CRH levels are elevated and urinary cortisol levels are variable--low in the majority of cases--whereas other studies demonstrate no differences in urinary and plasma cortisol concentrations. Urinary catecholamine excretion is higher in PTSD patients than those of control subjects and other psychiatric disorders. Children may differ from adults in their psychologic and physiologic responses to severe stressors. Also, exposure to stress during critical periods of development may have irreversible effects on behavioral maturation and may affect specific vulnerable brain areas, altering CNS development. Similar to findings in adult studies, PTSD in children is characterized by increased sympathetic nervous system (SNS) activity, as indicated by elevated norepinephrine levels in the periphery. High cortisol levels in urine or saliva have been reported in most studies of childhood PTSD, while prospective longitudinal studies concerning the natural history of neuroendocrine changes in pediatric PTSD after an acute stressor are limited. The identification of neurobiologic changes in response to early adverse experiences is of major importance for the prognosis, prevention, management, and treatment of children and adolescents at risk for or suffering from PTSD.     

Significance of tissue fragments in voided urine specimens

OBJECTIVE: To determine the diagnostic significance of tissue fragments in voided urine specimens. STUDY DESIGN: We reviewed all the voided urine specimens collected and processed by the Millipore filter technique (Bedford, Massachusetts, U.S.A.) at our institution between January 1, 1997, and December 31, 1998, and the corresponding biopsies obtained within 120 days after urine examination. The type and number of tissue fragments were correlated with the histologic diagnosis and clinical features; the results were compared to those from a recently published study. RESULTS: Of the 2,553 voided urine specimens examined, 174 (7%) had corresponding biopsies. Cell groups (tissue fragments) consisting of either flat sheets or three-dimensional structures were significantly more common (57%) (chi 2 P < .005) in urine specimens with biopsies revealing urothelial malignancies than in negative biopsies (6%). Three-dimensional groups were also statistically more common in cases with invasive transitional cell carcinoma. Proper identification of tissue fragments was highly significant and correlated with urothelial neoplastic changes. CONCLUSION: The results of the present investigation using the Millipore filter technique for voided urine cytology processing, differed from those of a recently published study that employed cytocentrifugation. Tissue fragments, to be differentiated from groups, clumps or clusters that often result from centrifugation and other concentration artifacts, were strongly associated with urothelial neoplasia, uncommonly with nonneoplastic disease processes affecting the urinary tract but always with urothelial disease.     

Neurotoxicity of depleted uranium

Depleted uranium (DU) is a byproduct of the enrichment process of uranium for its more radioactive isotopes to be used in nuclear energy. Because DU is pyrophoric and a dense metal with unique features when combined in alloys, it is used by the military in armor and ammunitions. There has been significant public concern regarding the use of DU by such armed forces, and it has been hypothesized to play a role in Gulf War syndrome. In light of experimental evidence from cell cultures, rats, and humans, there is justification for such concern. However, there are limited data on the neurotoxicity of DU. This review reports on uranium uses and its published health effects, with a major focus on in vitro and in vivo studies that escalate concerns that exposure to DU might be associated with neurotoxic health sequelae.     

Ecological Risk Assessment of Radiological Exposure to Depleted Uranium in Soils at a Weapons Testing Facility

The potential for unacceptable risks to biota from radiological exposure to depleted uranium (DU) in soils was evaluated at two sites where DU weapons testing had been conducted in the past. A screening risk assessment was conducted to determine if measured concentrations of DU-associated radionuclides in site soils exceed radionuclide levels considered protective of biota. While concentrations of individual radionuclides did not exceed acceptable levels, total radionuclide concentrations could result in potentially unacceptable doses to exposed biota. Thus, a receptor-specific assessment was conducted to estimate external and internal radiological doses to vegetation and wildlife known or expected to occur at the sites. Wildlife evaluated included herbivores, omnivores, and top-level predators. Internal dose estimates to wildlife considered exposure via fugitive dust inhalation and soil and food ingestion; root uptake was the primary exposure route evaluated for vegetation. Total doses were compared with acceptable dose levels of 1.0 and 0.1 rad/day for vegetation and wildlife, respectively, with potentially unacceptable risks indicated for doses exceeding these levels. All estimated doses were below or approximated acceptable levels, typically by an order of magnitude or more. These results indicate that current levels of DU in soils do not pose unacceptable radiological risks to biota at the sites evaluated.