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1.  An iron-dependent and transferrin-mediated cellular uptake pathway for plutonium 
Nature chemical biology  2011;7(8):560-565.
Plutonium is a toxic synthetic element with no natural biological function, but it is strongly retained by humans when ingested. Using small angle X-ray scattering, receptor binding assays, and synchrotron X-ray fluorescence microscopy we find that rat adrenal gland (PC12) cells can acquire plutonium in vitro through the major iron acquisition pathway, receptor-mediated endocytosis of the iron transport protein serum transferrin; however only one form of the plutonium-transferrin complex is active. Low-resolution solution models of plutonium-loaded transferrins derived from small angle scattering demonstrate that only transferrin with plutonium bound in the protein’s C-terminal lobe and iron bound in the N-lobe (PuCFeNTf) adopts the proper conformation for recognition by the transferrin receptor protein. Although the metal binding site in each lobe contains the same donors in the same configuration and both lobes are similar, the differences between transferrin’s two lobes act to restrict, but not eliminate, cellular Pu uptake.
PMCID: PMC3462652  PMID: 21706034
2.  Plutonium Uptake and Distribution in Mammalian Cells: Molecular vs Polymeric Plutonium 
To study the cellular responses to molecular and polymeric forms of plutonium using PC12 cells derived from rat adrenal glands.
Materials and methods
Serum starved PC12 cells were exposed to polymeric and molecular forms of plutonium for three hours. Cells were washed with 10 mM EGTA, 100 mM NaCl at pH 7.4 to remove surface sorbed plutonium. Localization of plutonium in individual cell was quantitatively analyzed by synchrotron X-ray fluorescence (XRF) microscopy.
Molecular plutonium complexes introduced to cell growth media in the form of NTA, citrate, or transferrin complexes were taken up by PC12 cells, and mostly co-localized with iron within the cells. Polymeric plutonium prepared separately was not internalized by PC12 cells but it was always found on the cell surface as big agglomerates; however polymeric plutonium formed in situ was mostly found within the cells as agglomerates.
PC12 cells can differentiate molecular and polymeric forms of plutonium. Molecular plutonium is taken up by PC12 cells and mostly co-localized with iron but aged polymeric plutonium is not internalized by the cells.
PMCID: PMC3679905  PMID: 21770702
PC12 Cells; plutonium polymer; molecular plutonium; X-ray fluorescence microscopy
3.  Lung Cancer Risks from Plutonium: An Updated Analysis of Data from the Mayak Worker Cohort 
Radiation research  2013;179(3):332-342.
Workers at the Mayak nuclear facility in the Russian Federation offer a unique opportunity to evaluate health risks from exposure to inhaled plutonium. Risks of mortality from lung cancer, the most serious carcinogenic effect of plutonium, were evaluated in 14,621 Mayak workers who were hired in the period from 1948–1982, followed for at least 5 years, and either monitored for plutonium or never worked with plutonium. Over the follow-up period from 1953–2008, there were 486 deaths from lung cancer, 446 of them in men. In analyses that were adjusted for external radiation dose and smoking, the plutonium excess relative risk (ERR) per Gy declined with attained age and was higher for females than for males. The ERR per Gy for males at age 60 was 7.4 (95% CI: 5.0–11) while that for females was 24 (95% CI: 11–56). When analyses were restricted to plutonium doses <0.2 Gy, the ERR per Gy for males at age 60 was similar: 7.0 (95% CI: 2.5–13). Of the 486 lung cancer deaths, 105 (22%) were attributed to plutonium exposure and 29 (6%) to external exposure. Analyses of the 12,708 workers with information on smoking indicated that the relationship of plutonium exposure and smoking was likely sub-multiplicative (P = 0.011) and strongly indicated that it was super-additive (P < 0.001). Although extensive efforts have been made to improve plutonium dose estimates in this cohort, they are nevertheless subject to large uncertainties. Large bioassay measurement errors alone are likely to have resulted in serious underestimation of risks, whereas other sources of uncertainty may have biased results in ways that are difficult to predict.
PMCID: PMC3661277  PMID: 23391147
4.  Plutonium from Above-Ground Nuclear Tests in Milk Teeth: Investigation of Placental Transfer in Children Born between 1951 and 1995 in Switzerland 
Environmental Health Perspectives  2008;116(12):1731-1734.
Occupational risks, the present nuclear threat, and the potential danger associated with nuclear power have raised concerns regarding the metabolism of plutonium in pregnant women.
We measured plutonium levels in the milk teeth of children born between 1951 and 1995 to assess the potential risk that plutonium incorporated by pregnant women might pose to the radiosensitive tissues of the fetus through placenta transfer.
We used milk teeth, whose enamel is formed during pregnancy, to investigate the transfer of plutonium from the mother’s blood plasma to the fetus. We measured plutonium using sensitive sector field inductively coupled plasma mass spectrometry techniques. We compared our results with those of a previous study on strontium-90 (90Sr) released into the atmosphere after nuclear bomb tests.
Results show that plutonium activity peaks in the milk teeth of children born about 10 years before the highest recorded levels of plutonium fallout. By contrast, 90Sr, which is known to cross the placenta barrier, manifests differently in milk teeth, in accordance with 90Sr fallout deposition as a function of time.
These findings demonstrate that plutonium found in milk teeth is caused by fallout that was inhaled around the time the milk teeth were shed and not from any accumulation during pregnancy through placenta transfer. Thus, plutonium may not represent a radiologic risk for the radiosensitive tissues of the fetus.
PMCID: PMC2599771  PMID: 19079728
fetus exposure; milk teeth; nuclear bomb test fallout; placenta transfer; plutonium; plutonium metabolism
5.  Biomimetic Actinide Chelators: An Update on the Preclinical Development of the Orally Active Hydroxypyridonate Decorporation Agents 3,4,3-LI(1,2-HOPO) and 5-LIO(Me-3,2-HOPO) 
Health physics  2010;99(3):401-407.
The threat of a dirty bomb or other major radiological contamination presents a danger of large-scale radiation exposure of the population. Because major components of such contamination are likely to be actinides, actinide decorporation treatments that will reduce radiation exposure must be a priority. Current therapies for the treatment of radionuclide contamination are limited and extensive efforts must be dedicated to the development of therapeutic, orally bioavailable, actinide chelators for emergency medical use. Using a biomimetic approach based on the similar biochemical properties of plutonium(IV) and iron(III), siderophore-inspired multidentate hydroxypyridonate ligands have been designed and are unrivaled in terms of actinide-affinity, selectivity and efficiency. A perspective on the preclinical development of two hydroxypyridonate actinide decorporation agents, 3,4,3-LI(1,2-HOPO) and 5-LIO(Me-3,2-HOPO), is presented. The chemical syntheses of both candidate compounds have been optimized for scale-up. Baseline preparation and analytical methods suitable for manufacturing large amounts have been established. Both ligands show much higher actinide-removal efficacy than the currently approved agent, diethylenetriaminepentaacetic acid (DTPA), with different selectivity for the tested isotopes of plutonium, americium, uranium and neptunium. No toxicity is observed in cells derived from three different human tissue sources treated in vitro up to ligand concentrations of 1 mM, and both ligands were well tolerated in rats when orally administered daily at high doses (> 100 μmol kg−1 day−1) over 28 days under good laboratory practice (GLP) guidelines. Both compounds are on an accelerated development pathway towards clinical use.
PMCID: PMC2921233  PMID: 20699704
Actinides; Chelation; Internal Contamination; DTPA; Toxicology
Health physics  2010;99(4):464-470.
The purpose was to obtain quantitative data on plutonium microdistribution in different structural elements of human bone tissue for local dose assessment and dosimetric models validation. A sample of the thoracic vertebra was obtained from a former Mayak worker with a rather high plutonium burden. Additional information was obtained on occupational and exposure history, medical history, and measured plutonium content in organs. Plutonium was detected in bone sections from its fission tracks in polycarbonate film using neutron-induced autoradiography. Quantitative analysis of randomly selected microscopic fields on one of the autoradiographs was performed. Data included fission fragment tracks in different bone tissue and surface areas. Quantitative information on plutonium microdistribution in human bone tissue was obtained for the first time. From these data, quantitative relationship of plutonium decays in bone volume to decays on bone surface in cortical and trabecular fractions were defined as 2.0 and 0.4, correspondingly. The measured quantitative relationship of decays in bone volume to decays on bone surface does not coincide with recommended models for the cortical bone fraction by the International Commission on Radiological Protection. Biokinetic model parameters of extrapulmonary compartments might need to be adjusted after expansion of the data set on quantitative plutonium microdistribution in other bone types in human as well as other cases with different exposure patterns and types of plutonium.
PMCID: PMC2941237  PMID: 20838087
plutonium; skeleton; neutron-induced autoradiography
7.  Lung, liver and bone cancer mortality in Mayak workers 
Workers at the Mayak nuclear facility in the Russian Federation offer the only adequate human data for evaluating cancer risks from exposure to plutonium. Risks of mortality from cancers of the lung, liver and bone, the organs receiving the largest doses from plutonium, were evaluated in a cohort of 17,740 workers initially hired 1948–1972 using, for the first time, recently improved individual organ dose estimates. Excess relative risk (ERR) models were used to evaluate risks as functions of internal (plutonium) dose, external (primarily gamma) dose, gender, attained age and smoking. By December 31, 2003, 681 lung cancer deaths, 75 liver cancer deaths and 30 bone cancer deaths had occurred. Of these 786 deaths, 239 (30%) were attributed to plutonium exposure. Significant plutonium dose-response relationships (p < 0.001) were observed for all 3 endpoints, with lung and liver cancer risks reasonably described by linear functions. At attained age 60, the ERRs per Gy for lung cancer were 7.1 for males and 15 for females; the averaged-attained age ERRs for liver cancer were 2.6 and 29 for males and females, respectively; those for bone cancer were 0.76 and 3.4. This study is the first to present and compare dose-response analyses for cancers of all 3 organs. The unique Mayak cohort with its high exposures and well characterized doses has allowed quantification of the plutonium dose-response for lung, liver and bone cancer risks based on direct human data. These results will play an important role in plutonium risk assessment.
PMCID: PMC4020282  PMID: 18528867
lung cancer; liver cancer; bone cancer; plutonium; ionizing radiation; nuclear workers
8.  A Proteomic Approach to Identification of Plutonium Binding Proteins in Mammalian Cells 
Journal of proteomics  2011;75(5):1505-1514.
Plutonium can enter the body through different routes and remains there for decades; however its specific biochemical interactions are poorly defined. We, for the first time, have studied plutonium-binding proteins using a metalloproteomic approach with rat PC12 cells. A combination of immobilized metal ion chromatography, 2D gel electrophoresis, and mass spectrometry were employed to analyze potential plutonium-binding proteins. Our results show that several proteins from PC12 cells show affinity towards Pu4+-NTA (plutonium bound to nitrilotriacetic acid). Proteins from seven different spots in the 2D gel were identified. In contrast to the previously known plutonium-binding proteins transferrin and ferritin, which bind ferric ions, most identified proteins in our experiment are known to bind calcium, magnesium, or divalent transition metal ions. The identified plutonium interacting proteins also have functional roles in downregulation of apoptosis and other pro-proliferative processes. MetaCore analysis based on this group of proteins produced a pathway with a statistically significant association with development of neoplastic diseases.
PMCID: PMC3688465  PMID: 22146473
PC12 cells; 2-D gel electrophoresis; proteomics; plutonium-binding proteins; IMAC; anti-apoptotic; GO process
9.  Cancer mortality in relation to monitoring for radionuclide exposure in three UK nuclear industry workforces. 
British Journal of Cancer  1998;78(9):1224-1232.
Cancer mortality in 40,761 employees of three UK nuclear industry facilities who had been monitored for external radiation exposure was examined according to whether they had also been monitored for possible internal exposure to tritium, plutonium or other radionuclides (uranium, polonium, actinium or other unspecified). Death rates from cancer were compared both with national rates and with rates in radiation workers not monitored for exposure to any radionuclides. Among workers monitored for tritium exposure, overall cancer mortality was significantly below national rates [standardized mortality ratio (SMR) = 83, 165 deaths; 2P = 0.02] and none of the cancer-specific death rates was significantly above either the national average or rates in non-monitored workers. Although the overall death rate from cancer in workers monitored for plutonium exposure was also significantly low relative to national rates (SMR = 89, 581 deaths; 2P = 0.005), mortality from pleural cancer was significantly raised (SMR = 357, nine deaths; 2P = 0.002); none of the rates differed significantly from those of non-monitored workers. Workers monitored for radionuclides other than tritium or plutonium also had a death rate from all cancers combined that was below the national average (SMR = 86, 418 deaths; 2P = 0.002) but prostatic cancer mortality was raised both in relation to death rates in the general population (SMR = 153, 37 deaths; 2P = 0.02) and to death rates in radiation workers who had not been monitored for exposure to any radionuclide [rate ratio (RR) = 1.65; 2P = 0.03]. Mortality from cancer of the lung was also significantly increased in workers monitored for other radionuclides compared with those of radiation workers not monitored for exposure to radionuclides (RR = 1.31, 164 deaths; 2P = 0.01). For cancers of the lung, prostate and all cancers combined, death rates in monitored workers were examined according to the timing and duration of monitoring for radionuclide exposure, with rates of radiation workers not monitored for any radionuclide forming the comparison group. In tritium-monitored workers, RRs for prostatic cancer varied significantly according to the number of years in which they were monitored (2P = 0.03). In workers monitored for plutonium exposure, RRs for all cancers combined increased with the number of years in which they were monitored (2P = 0.04) and with the number of years since first monitoring (2P = 0.0003). There was little suggestion of systematic variation in RRs for workers monitored for other radionuclides in relation to the timing or duration of monitoring, nor did it appear that their raised rates of cancer of the lung and prostate were explained by external radiation dose. These analyses of cancer mortality in relation to monitoring for radionuclide exposure reported in a large cohort of nuclear industry workers suggest that certain patterns of monitoring for some radionuclides may be associated with higher death rates from cancers of the lung, pleura, prostate and all cancers combined. Some of these findings may be due to chance. Moreover, because of the paucity of related data and lack of information about other possible exposures, such as whether plutonium workers are more likely to be exposed to asbestos, firm conclusions cannot be drawn at this stage. Further investigations of the relationship between radionuclide exposure and cancer in nuclear industry workers are needed.
PMCID: PMC2063005  PMID: 9820185
10.  Plutonium release from Fukushima Daiichi fosters the need for more detailed investigations 
Scientific Reports  2013;3:2988.
The contamination of Japan after the Fukushima accident has been investigated mainly for volatile fission products, but only sparsely for actinides such as plutonium. Only small releases of actinides were estimated in Fukushima. Plutonium is still omnipresent in the environment from previous atmospheric nuclear weapons tests. We investigated soil and plants sampled at different hot spots in Japan, searching for reactor-borne plutonium using its isotopic ratio 240Pu/239Pu. By using accelerator mass spectrometry, we clearly demonstrated the release of Pu from the Fukushima Daiichi power plant: While most samples contained only the radionuclide signature of fallout plutonium, there is at least one vegetation sample whose isotope ratio (0.381 ± 0.046) evidences that the Pu originates from a nuclear reactor (239+240Pu activity concentration 0.49 Bq/kg). Plutonium content and isotope ratios differ considerably even for very close sampling locations, e.g. the soil and the plants growing on it. This strong localization indicates a particulate Pu release, which is of high radiological risk if incorporated.
PMCID: PMC3798882  PMID: 24136192
11.  Solid cancer incidence other than lung, liver and bone in Mayak workers: 1948–2004 
British Journal of Cancer  2013;109(7):1989-1996.
Cancer incidence in the Mayak Production Association (PA) cohort was analysed to investigate for the first time whether external gamma-ray and internal plutonium exposure are associated with raised incidence of solid cancers other than lung, liver and bone (other solid cancers).
The cohort includes 22 366 workers of both sexes who were first employed between 1948 and 1982. A total of 1447 cases of other solid cancers were registered in the follow-up period until 2004. The Poisson regression was used to estimate the excess relative risk (ERR) per unit of cumulative exposure to plutonium and external gamma-ray.
A weak association was found between cumulative exposure to external gamma-ray and the incidence of other solid cancers (ERR/Gy=0.07; 95% confidence intervals (CIs): 0.01–0.15), but this association lost its significance after adjusting for internal plutonium exposure. There was no indication of any association with plutonium exposure for other solid cancers. Among 16 individual cancer sites, there was a statistically significant association with external exposure for lip cancer (ERR/Gy=1.74; 95% CI: 0.37; 6.71) and with plutonium exposure for pancreatic cancer (ERR/Gy=1.58; 95% CI; 0.17; 4.77).
This study of Mayak workers does not provide evidence of an increased risk of other solid cancers. The observed increase in the risk of cancer of the lip and pancreas should be treated with caution because of the limited amount of relevant data and because the observations may be simply due to chance.
PMCID: PMC3790189  PMID: 24022197
cancer incidence; external gamma radiation; internal plutonium exposure; Mayak radiation workers
12.  Radiation Effects on Mortality from Solid Cancers Other than Lung, Liver, and Bone Cancer in the Mayak Worker Cohort: 1948–2008 
PLoS ONE  2015;10(2):e0117784.
Radiation effects on mortality from solid cancers other than lung, liver, and bone cancer in the Mayak worker cohort: 1948–2008. The cohort of Mayak Production Association (PA) workers in Russia offers a unique opportunity to study the effects of prolonged low dose rate external gamma exposures and exposure to plutonium in a working age population. We examined radiation effects on the risk of mortality from solid cancers excluding sites of primary plutonium deposition (lung, liver, and bone surface) among 25,757 workers who were first employed in 1948–1982. During the period 1948–2008, there were 1,825 deaths from cancers other than lung, liver and bone. Using colon dose as a representative external dose, a linear dose response model described the data well. The excess relative risk per Gray for external gamma exposure was 0.16 (95% CI: 0.07 – 0.26) when unadjusted for plutonium exposure and 0.12 (95% CI 0.03 – 0.21) when adjusted for plutonium dose and monitoring status. There was no significant effect modification by sex or attained age. Plutonium exposure was not significantly associated with the group of cancers analyzed after adjusting for monitoring status. Site-specific risks were uncertainly estimated but positive for 13 of the 15 sites evaluated with a statistically significant estimate only for esophageal cancer. Comparison with estimates based on the acute exposures in atomic bomb survivors suggests that the excess relative risk per Gray for prolonged external exposure in Mayak workers may be lower than that for acute exposure but, given the uncertainties, the possibility of equal effects cannot be dismissed.
PMCID: PMC4342229  PMID: 25719381
13.  Solid-phase extraction of plutonium in various oxidation states from simulated groundwater using N-benzoylphenylhydroxylamine 
Solid-phase extraction of plutonium in different individual and mixed oxidation states from simulated groundwater (pH 8.5) was studied. The extraction of plutonium species was carried out in a dynamic mode using DIAPAK C16 cartridges modified by N-benzoylphenylhydroxylamine (BPHA). It was shown that the extent of recovery depends on the oxidation state of plutonium. The extraction of Pu(IV) was at the level of 98–99% regardless of the volume and flow-rate of the sample solution. Pu(V) was extracted by 90–95% and 75–80% from 10- and 100-mL aliquots of the samples, respectively, whereas the extraction of Pu(VI) did not exceed 45–50%. An equimolar mixture of Pu(IV), Pu(V), and Pu(VI) was extracted by 74%. The distribution coefficients (Kd) and kinetic exchange capacities (S) of plutonium in various oxidation states were measured. It was found that during the sorption process, Pu(V) was reduced to Pu(IV) by 80–90% after an hour-long contact with the solid phase. Pu(VI) is reduced to Pu(V) by 34% and to Pu(IV) by 55%. In the case of mixed-valent solution of plutonium, only Pu(V) and Pu(IV) were found in the effluents.
PMCID: PMC4514682
Solid-phase extraction; Plutonium; N-benzoylphenylhydroxylamine; Groundwater
14.  Sub-micron Hard X-ray Fluorescence Imaging of Synthetic Elements 
Analytica chimica acta  2012;722:21-28.
Synchrotron-based X-ray fluorescence microscopy (SXFM) using hard X-rays focused into sub-micron spots is a powerful technique for elemental quantification and mapping, as well as microspectroscopic measurement such as μ-XANES (X-ray absorption near edge structure). We have used SXFM to image and simultaneously quantify the transuranic element plutonium at the L3 or L2 edge as well as lighter biologically essential elements in individual rat pheochromocytoma (PC12) cells after exposure to the long-lived plutonium isotope 242Pu. Elemental maps reveal that plutonium localizes principally in the cytoplasm of the cells and avoids the cell nucleus, which is marked by the highest concentrations of phosphorus and zinc, under the conditions of our experiments. The minimum detection limit under typical acquisition conditions for an average 202 μm2 cell is 1.4 fg Pu/cell or 2.9 × 10−20 moles Pu/μm2, which is similar to the detection limit of K-edge SXFM of transition metals at 10 keV. Copper electron microscopy grids were used to avoid interference from gold X-ray emissions, but traces of strontium present in naturally occurring calcium can still interfere with plutonium detection using its Lα X-ray emission.
PMCID: PMC3688452  PMID: 22444530
15.  Effect of inhaled plutonium dioxide on development of urethan-induced pulmonary adenomas. 
British Journal of Cancer  1977;35(4):433-438.
Mice were exposed to plutonium dioxide (PuO2) aerosols 2 weeks before or after urethan injection. Both exposures reduced the number and size of adenomas. The incidence of arrested metaphases showed no consistently significant differences between plutonium-exposed and mock-exposed animals. The results are discussed in relation to recent electron microscopic evidence of degenerative changes in the type II epithelial cells of the mouse lung following PuO2 inhalation. It is concluded that damage at the cellular level may account for the observed reduction in growth of pulmonary adenomas in mice whose lungs contained plutonium particles.
PMCID: PMC2025349  PMID: 857826
16.  Methodology Using a Portable X-Ray Fluorescence Device for On-Site and Rapid Evaluation of Heavy-Atom Contamination in Wounds: A Model Study for Application to Plutonium Contamination 
PLoS ONE  2014;9(7):e101966.
Workers decommissioning the Fukushima-Daiichi nuclear power plant damaged from the Great East Japan Earthquake and resulting tsunami are at risk of injury with possible contamination from radioactive heavy atoms including actinides, such as plutonium. We propose a new methodology for on-site and rapid evaluation of heavy-atom contamination in wounds using a portable X-ray fluorescence (XRF) device. In the present study, stable lead was used as the model contaminant substitute for radioactive heavy atoms. First, the wound model was developed by placing a liquid blood phantom on an epoxy resin wound phantom contaminated with lead. Next, the correlation between the concentration of contaminant and the XRF peak intensity was formulated considering the thickness of blood exiting the wound. Methods to determine the minimum detection limit (MDL) of contaminants at any maximal equivalent dose to the wound by XRF measurement were also established. For example, in this system, at a maximal equivalent dose of 16.5 mSv to the wound and blood thickness of 0.5 mm, the MDL value for lead was 1.2 ppm (3.1 nmol). The radioactivity of 239Pu corresponding to 3.1 nmol is 1.7 kBq, which is lower than the radioactivity of 239Pu contaminating puncture wounds in previous severe accidents. In conclusion, the established methodology could be beneficial for future development of a method to evaluate plutonium contamination in wounds. Highlights: Methodology for evaluation of heavy-atom contamination in a wound was established. A portable X-ray fluorescence device enables on-site, rapid and direct evaluation. This method is expected to be used for evaluation of plutonium contamination in wounds.
PMCID: PMC4092075  PMID: 25010749
17.  AMS of the Minor Plutonium Isotopes 
VERA, the Vienna Environmental Research Accelerator, is especially equipped for the measurement of actinides, and performs a growing number of measurements on environmental samples. While AMS is not the optimum method for each particular plutonium isotope, the possibility to measure 239Pu, 240Pu, 241Pu, 242Pu and 244Pu on the same AMS sputter target is a great simplification. We have obtained a first result on the global fallout value of 244Pu/239Pu = (5.7 ± 1.0) × 10−5 based on soil samples from Salzburg prefecture, Austria. Furthermore, we suggest using the 242Pu/240Pu ratio as an estimate of the initial 241Pu/239Pu ratio, which allows dating of the time of irradiation based solely on Pu isotopes. We have checked the validity of this estimate using literature data, simulations, and environmental samples from soil from the Salzburg prefecture (Austria), from the shut down Garigliano Nuclear Power Plant (Sessa Aurunca, Italy) and from the Irish Sea near the Sellafield nuclear facility. The maximum deviation of the estimated dates from the expected ages is 6 years, while relative dating of material from the same source seems to be possible with a precision of less than 2 years. Additional information carried by the minor plutonium isotopes may allow further improvements of the precision of the method.
PMCID: PMC3617651  PMID: 23565016
Minor plutonium isotopes; Plutonium dating; Environmental plutonium; AMS
18.  Emergence of californium as the second transitional element in the actinide series 
Nature Communications  2015;6:6827.
A break in periodicity occurs in the actinide series between plutonium and americium as the result of the localization of 5f electrons. The subsequent chemistry of later actinides is thought to closely parallel lanthanides in that bonding is expected to be ionic and complexation should not substantially alter the electronic structure of the metal ions. Here we demonstrate that ligation of californium(III) by a pyridine derivative results in significant deviations in the properties of the resultant complex with respect to that predicted for the free ion. We expand on this by characterizing the americium and curium analogues for comparison, and show that these pronounced effects result from a second transition in periodicity in the actinide series that occurs, in part, because of the stabilization of the divalent oxidation state. The metastability of californium(II) is responsible for many of the unusual properties of californium including the green photoluminescence.
The chemistry of the post-plutonium actinides is thought to resemble lanthanides in that bonding is primarily ionic. Here, the authors show that a californium(III) complex displays significantly different properties to those predicted for the free ion owing to a second break in actinide periodicity.
PMCID: PMC4410632  PMID: 25880116
19.  Characterization of 241Pu occurrence, distribution, and bioaccumulation in seabirds from northern Eurasia 
The paper presents unique data of plutonium 241Pu study in seabirds from northern Eurasia, permanently or temporally living at the southern Baltic Sea coast. Together, ten marine birds species were examined, as follows: three species that permanently reside at the southern Baltic, four species of wintering birds, and three species of migrating birds; 366 samples were analyzed. The obtained results indicated plutonium was non-uniformly distributed in organs and tissues of analyzed seabirds. The highest 241Pu content was found in the digestion organs and feathers, the lowest in muscles. Also, the internal radiation doses from 241Pu were evaluated.
PMCID: PMC4432091  PMID: 25529493
Plutonium 241Pu; 241Pu/239+240Pu activity ratio; Seabirds; Baltic Sea; Eurasia; Bioaccumulation
20.  241Pu in the biggest Polish rivers 
In the paper the results of 241Pu activity concentration determination in the biggest Polish rivers are presented. The analysis of more than 100 river water samples showed the Vistula and the Odra as well as three Pomeranian Rivers are important sources of 241Pu in the southern Baltic Sea. There were differences in 241Pu activities depending on season and sampling site and the plutonium contamination came mainly from the global atmospheric fallout as well as the Chernobyl accident, which is confirmed by plutonium activity ratios of 241Pu/239+240Pu and 238Pu/239+240Pu.
PMCID: PMC4516142
Plutonium 241Pu; 241Pu/239+240Pu activity ratio; Rivers; Inflow; Baltic Sea
21.  The Russian radiation legacy: its integrated impact and lessons. 
Environmental Health Perspectives  1997;105(Suppl 6):1385-1391.
Information about the consequences of human exposure to radiation in the former Soviet Union has recently become available. These data add new insights and provide possible answers to several important questions regarding radiation and its impact on occupational and public health. The 1986 Chernobyl accident initiated a major and early increase in childhood thyroid cancer that resulted from ingestion of iodine-131 (131I) by young children living in the most heavily contaminated areas of Belarus, Ukraine, and Russia. No significant additional cancer or other adverse medical effects have yet been reported in the affected populations and among clean-up workers. Major psychological stress independent of radiation dose has been observed in those people thought to be exposed. During the early days of the atomic energy program in the former Soviet Union, some unfortunate events occurred. The country's first atomic test in Semipalatinsk in 1949 exposed over 25,000 people downwind from the blast to significant doses of fission products, especially 131I. During the late 1940s and the early 1950s nuclear material production facilities were developed near Chelyabinsk in the South Ural Mountains, which resulted in major releases into the environment and significant overexposures for thousands of workers and nearby populations. Chronic radiation sickness was observed early in exposed workers, and increases in leukemia and other cancers were also reported. The series of plutonium inhalation-related lung cancers and fatalities among workers exposed in that first decade appears to be unique. Long-term consequences of chronic radiation sickness and four decades of follow-up are being described for the first time. Villagers downstream from the plant consumed high levels of 137Cs and 90Sr and, it is reported, manifested increases in leukemia from internal and external exposures. Although the 40-year databases for retrospective dosimetry epidemiology studies are just beginning to be integrated and evaluated, preliminary evaluations suggest that there may be graded, significant dose-rate amelioration factors for cancer and leukemia risks in workers and the general population relative to the risk data on the Japanese atomic bomb survivors. Even for plutonium-induced lung cancers in workers, such a dose-rate effect may be evident. These experiences give us insight into the consequences of protracted radiation at high and low doses and rates. If these findings are validated and confirmed, they can provide information that reduces some of the uncertainties in retrospective radiation dosimetry and radiation risk estimates (especially for low-level, chronic exposures) for activities related to medicine as well as the handling of nuclear materials and nuclear facility decommissioning, decontamination, and demilitarization.
PMCID: PMC1469939  PMID: 9467049
22.  Alterations in the K-ras and p53 genes in rat lung tumors. 
Environmental Health Perspectives  1997;105(Suppl 4):901-906.
Activation of the K-ras protooncogene and inactivation of the p53 tumor suppressor gene are events common to many types of human cancers. Molecular epidemiology studies have associated mutational profiles in these genes with specific exposures. The purpose of this paper is to review investigations that have examined the role of the K-ras and p53 genes in lung tumors induced in the F344 rat by mutagenic and nonmutagenic exposures. Mutation profiles within the K-ras and p53 genes, if present in rat lung tumors, would help to define some of the molecular mechanisms underlying cancer induction by various environmental agents. Pulmonary adenocarcinomas or squamous cell carcinomas were induced by tetranitromethane (TNM), 4-methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK), beryllium metal, plutonium-239, X-ray, diesel exhaust, or carbon black. These agents were chosen because the tumors they produced could arise via different types of DNA damage. Mutation of the K-ras gene was determined by approaches that included DNA transfection, direct sequencing, mismatch hybridization, and restriction fragment length polymorphism analysis. The frequency for mutation of the K-ras gene was exposure dependent. Only two agents, TNM and plutonium, led to mutation frequencies of > 10%. In both cases, the transition mutations formed could have been derived from deamination of cytosine. The identification of non-ras transforming genes in rat lung tumors induced by mutagenic and nonmutagenic exposures such as NNK and beryllium would help define some of the mechanisms underlying cancer induction by different types of DNA damage. Alteration in the p53 gene was assessed by immunohistochemical analysis for p53 protein and single-strand conformation polymorphism (SSCP) analysis of exons 4 to 9. None of the 93 adenocarcinomas examined was immunoreactive toward the anti-p53 antibody CM1. In contrast, 14 to 71 squamous cell carcinomas exhibited nuclear p53 immunoreactivity with no correlation to type of exposure. However, SSCP analysis only detected mutations in 2 of 14 squamous cell tumors that were immunoreactive, suggesting that protein stabilization did not stem from mutations within the p53 gene. Thus, the p53 gene does not appear to be involved in the genesis of most rat lung tumors.
PMCID: PMC1470039  PMID: 9255578
23.  Mortality of employees of the Atomic Weapons Establishment, 1951-82. 
BMJ : British Medical Journal  1988;297(6651):757-770.
A total of 22,552 workers employed by the Atomic Weapons Establishment between 1951 and 1982 were followed up for an average of 18.6 years. Of the 3115 who died, 865 (28%) died of cancer. Mortality was 23% lower than the national average for all causes of death and 18% lower for cancer. These low rates were consistent with the findings in other workforces in the nuclear industry and reflect, at least in part, the selection of healthy people to work in the industry and the disproportionate recruitment of people from the higher social classes. At some time during their employment 9389 (42%) of the workers were monitored for exposure to radiation, the average cumulative whole body exposure to external radiation being 7.8 mSv. Their mortality was generally similar to that of other employees, even when exposures were lagged by 10 years. The rate ratio after a 10 year lag in workers with a radiation record compared with other workers was 1.01 (95% confidence interval 0.92 to 1.10) for all causes of death and 1.06 (0.89 to 1.27) for all malignant neoplasms. The only significant differences were for prostatic cancer (rate ratio 2.23; 95% confidence interval 1.13 to 4.40) and for cancers of ill defined and secondary sites (rate ratio 2.37; 1.23 to 4.56). Cancers of lymphatic and haemopoietic tissues were notable for their low occurrence in the study population, with only four deaths from leukaemia and two from multiple myeloma in workers with a radiation record, 9.16 and 3.55 deaths respectively being expected on the basis of national rates. Among workers who had a radiation record 3742 (40%) were also monitored for possible internal exposure to plutonium, 3044 (32%) to uranium, 1562 (17%) to tritium, 638 (7%) to polonium, and 281 (3%) to actinium. In these workers mortality from malignant neoplasms as a whole was not increased, but after a 10 year lag death rates from prostatic and renal cancers were generally more than twice the national average, these excesses arising in a small group of workers monitored for exposure to multiple radionuclides. Though mortality from lung cancer in workers monitored for exposure to plutonium was below the national average, it was some two thirds higher than in other radiation workers, the excess being of borderline statistical significance. Mortality from malignant neoplasms as a whole showed a weak and non-significant increasing trend with increasing level of cumulative whole body exposure to external radiation. When the exposures were lagged by 10 years the trend became stronger and significant, the estimated increase in relative risk per 10 mSv being 7.6% (95% confidence interval 0.4% to 15.3%). This trend was confined almost entirely to workers who were also monitored for exposure to radionuclides (p<0.001), the main contributions coming from lung cancer and prostatic cancer. Exposures of the lung and prostate from internal sources of radiation were not quantified, except for the contribution from tritium. It was therefore not possible to assess the extent to which the associations were due to internally deposited radionuclides rather than external exposure. The finding for prostatic cancer taken in conjunction with the results of other studies suggest a specific occupational hazard in a small group of workers in the nuclear industry who had comparatively high exposures to external radiation and who were also monitored for internal exposure to multiple radionuclides. Research is needed to discover whether any of the radionuclides and other substances concerned are concentrated in the prostate. The occurrence of lung cancer in this workforce requires further investigation taking into account smoking habits and tissue doses from inhaled radionuclides.
PMCID: PMC1834407  PMID: 3142540
24.  Plutonium(IV) Reduction by the Metal-Reducing Bacteria Geobacter metallireducens GS15 and Shewanella oneidensis MR1▿  
Applied and Environmental Microbiology  2007;73(18):5897-5903.
The bacterial reduction of actinides has been suggested as a possible remedial strategy for actinide-contaminated environments, and the bacterial reduction of Pu(VI/V) has the potential to produce highly insoluble Pu(IV) solid phases. However, the behavior of plutonium with regard to bacterial reduction is more complex than for other actinides because it is possible for Pu(IV) to be further reduced to Pu(III), which is relatively more soluble than Pu(IV). This work investigates the ability of the metal-reducing bacteria Geobacter metallireducens GS15 and Shewanella oneidensis MR1 to enzymatically reduce freshly precipitated amorphous Pu(IV) (OH)4 [Pu(IV)(OH)4(am)] and soluble Pu(IV)(EDTA). In cell suspensions without added complexing ligands, minor Pu(III) production was observed in cultures containing S. oneidensis, but little or no Pu(III) production was observed in cultures containing G. metallireducens. In the presence of EDTA, most of the Pu(IV)(OH)4(am) present was reduced to Pu(III) and remained soluble in cell suspensions of both S. oneidensis and G. metallireducens. When soluble Pu(IV)(EDTA) was provided as the terminal electron acceptor, cell suspensions of both S. oneidensis and G. metallireducens rapidly reduced Pu(IV)(EDTA) to Pu(III)(EDTA) with nearly complete reduction within 20 to 40 min, depending on the initial concentration. Neither bacterium was able to use Pu(IV) (in any of the forms used) as a terminal electron acceptor to support growth. These results have significant implications for the potential remediation of plutonium and suggest that strongly reducing environments where complexing ligands are present may produce soluble forms of reduced Pu species.
PMCID: PMC2074912  PMID: 17644643
25.  Consequences of the nuclear power plant accident at Chernobyl. 
Public Health Reports  1991;106(1):32-40.
The Chernobyl Nuclear Power Plant accident, in the Ukrainian Soviet Socialist Republic (SSR), on April 26, 1986, was the first major nuclear power plant accident that resulted in a large-scale fire and subsequent explosions, immediate and delayed deaths of plant operators and emergency service workers, and the radioactive contamination of a significant land area. The release of radioactive material, over a 10-day period, resulted in millions of Soviets, and other Europeans, being exposed to measurable levels of radioactive fallout. Because of the effects of wind and rain, the radioactive nuclide fallout distribution patterns are not well defined, though they appear to be focused in three contiguous Soviet Republics: the Ukrainian SSR, the Byelorussian SSR, and the Russian Soviet Federated Socialist Republic. Further, because of the many radioactive nuclides (krypton, xenon, cesium, iodine, strontium, plutonium) released by the prolonged fires at Chernobyl, the long-term medical, psychological, social, and economic effects will require careful and prolonged study. Specifically, studies on the medical (leukemia, cancers, thyroid disease) and psychological (reactive depressions, post-traumatic stress disorders, family disorganization) consequences of continued low dose radiation exposure in the affected villages and towns need to be conducted so that a coherent, comprehensive, community-oriented plan may evolve that will not cause those already affected any additional harm and confusion.
PMCID: PMC1580196  PMID: 1899937

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