J.P. Day

Accelerator mass spectrometry of plutonium isotopes

The feasibility of measuring plutonium isotope ratios by accelerator mass spectrometry has been demonstrated. Measurements on a test sample of known composition and on a blank showed that isotope ratios could be determined quantitatively, and that the present limit of detection by AMS is ∼ 106 atoms of plutonium. For 239Pu, this limit is at least two orders of magnitude lower than that practicable by alpha-spectrometry. In addition, 240Pu239Pu ratios were measured for four samples for which the combined activity of the two isotopes had been determined previously by alpha-counting. All measurements of plutonium isotope ratios entailed injection of PuO− into the 14UD accelerator operating at 3.5 MV, gas stripping, and analysis of the 7+ charge state after acceleration. Plutonium ions at 28 MeV were detected in a longitudinal-field ionisation chamber with an energy resolution of 3%. Using uranium oxide as a surrogate for plutonium oxide, it was shown that UO− was the predominant negative ion and that the probability for its formation and extraction was 0.3%.

Kinetics of uptake and elimination of silicic acid by a human subject: A novel application of 32Si and accelerator mass spectrometry

Silicon is possibly important in human physiology in protecting against the toxic effects of aluminium, but the kinetics of uptake and excretion of silicic acid, the bioavailable form, are not well characterised. We have used 32Si as a tracer in a human uptake experiment to determine a gastrointestinal uptake factor for silicic acid, and to elucidate the kinetics of renal elimination. Urine collections were made for extending intervals from 2 to 12 h over 2 days following ingestion by a single human subject of a neutral silicic acid solution containing tracer levels of 32Si (t1/2 approximately 150 y). Silicon was isolated as SiO2 and the 32Si content determined by accelerator mass spectrometry (AMS), using a gas-filled magnet technique to eliminate a prolific isobaric interference from 32S. Silicon uptake appears to have been essentially complete within 2 h of ingestion. Elimination occurred by two simultaneous first-order processes with half-lives of 2.7 and 11.3 h, representing around 90% and 10%, respectively, of the total output. The rapidly eliminated 32Si was probably retained in the extracellular fluid volume, whilst the slower component may represent intracellular uptake and release. Elimination of absorbed 32Si was essentially complete after 48 h and was equivalent to 36% of the ingested dose. This establishes only a lower limit for gastrointestinal absorption as, although there was no evidence for longer term retention of additional 32Si, the possibility could not be excluded by these results.

Uptake by man of aluminium in a public water supply

1 After overnight fasting, two young male adults each received a single oral dose of 100 Bq 26Al in tap water. Coincidence gamma-ray spectrometry and accelerator mass spectrometry were used to determine the 26Al content of excretion collections and of blood samples. 2 Close to 100% of the intake was recovered in faeces during the first 7 days. Gastro-intestinal uptake, determined by comparing urinary excretion with patterns previously established following intravenous administration of 26Al, averaged 0.22% in the two subjects. 3 Uptake fractions based on comparisons of blood concentration following ingestion and injection were much lower, but were judged to be unreliable. It is concluded that aluminium present in most water supplies is unlikely to contribute as much as 1% of a typical daily uptake of 10 mg from food.

THE INFLUENCE OF DISSOLVED SILICATE ON THE PHYSIOLOGICAL CHEMISTRY OF ALUMINIUM, STUDIED IN HUMANS USING TRACER 26AL AND ACCELERATOR MASS SPECTROMETRY

Abstract Trace quantities of aluminium, spiked with 26 Al, were administered twice, to each of two subjects, in citrate-containing drinks (4 or 50 mmol/l). Silicate (0.5 mmol/l), in the form of a Si-rich natural mineral water, was added to the dose on the second occasion for each subject. Al-uptake and excretion were determined from AMS measurement of 26 Al in blood plasma (whole plasma and the low molecular weight fraction) and urine for up to 7 days. Citrate markedly enhanced Al uptake, as previously observed. A major effect of silicate was to enhance the rate of Al elimination, probably through an increase in the LMW plasma fraction (5% with no Si; 7.5% with Si). Aluminium uptake appeared to be only slightly affected by Si, and showed opposite effects depending on citrate concentration. With low citrate, Si marginally increased Al uptake, whilst with high citrate, Al uptake appeared to be reduced by the presence of Si.

Uptake of 26-Al and 67-Ga into brain and other tissues of normal and hypotransferrinaemic mice

Aluminium uptake from blood into tissues of control and homozygous hypotransferrinaemic (hpx/hpx) mice, following continuous intravenous infusion of Al and Ga, has been compared with that of gallium, a proposed tracer for aluminium. Al uptake into tissues of control (hpx/+ and +/+) mice occurred in the order (expressed as a space): bone 464.7ml 100g; renal cortex 102.9ml 100g; liver 13.0ml 100g; spleen 8.4ml 100g and brain 0.8ml 100g. Ga uptakes were similar in liver, spleen and brain, but smaller in the renal cortex and bone, at one-third and one-fifth of the values for Al, respectively. In the hypotransferrinaemic mice, uptake of Ga into all tissues was increased, especially in renal cortex (ninefold) and bone (twentyfold) as compared with the controls. Increases in Ga uptakes into cerebral hemisphere, cerebellum and brain stem of the hypotransferrinaemic mice were 3.8, 4.2 and 2.8 fold, respectively. Al uptake into tissues of the hypotransferrinaemic mice was similar to control values except in bone where it was three times greater. Pre-treatment of control animals with the anti-transferrin receptor antibody, RI7 208, enhanced Ga uptake in all tissues, the effect being greatest in renal cortex (tenfold) and bone (ninefold). Ga uptakes into cerebral hemisphere, cerebellum and brain stem in the mice pre-treated with RI7 208 were 6.4, 6 and 10 times greater than in untreated mice, respectively. No influence of antibody on Al uptake into mouse tissues was observed except in spleen where it was three times greater than in untreated mice. Hence, transport of aluminium and gallium into mouse tissues is not similar under all conditions. Non-transferrin mediated transport of each metal can occur into all tissues, especially in renal cortex and bone, where gallium may be a suitable marker for aluminium.

Determination of Aluminium-26 in Biological Materials by Accelerator Mass Spectrometry

Studies of the biological chemistry of aluminium can gain significantly from the use of the long-lived isotope 26Al as a tracer, although the cost of the isotope often precludes its determination by radiochemical counting techniques. Accelerator mass spectrometry (AMS) provides an ultra-sensitive method of determination, free from isobaric interference from atomic (26Mg) or molecular species. The source materials for AMS can be aluminium oxide or phosphate, both of which can be readily prepared at a sufficient level of purity from biological substrates. Natural aluminium (27Al, 100%) is added to the preparations as a chemical yield monitor and to provide the reference for the isotope ratio measurement. 26Al/27Al ratios can be determined over the range 10(-14)-10(-7), implying a limit of detection for 26Al of around 10(-18) g. The precision of measurement and long-term reproducibility are < 5% and < 7% (RSD), respectively. Chemical methodologies for routine measurements on blood and urine samples have been developed.

Accelerator mass spectrometry of 99Tc

Abstract The measurement of low levels of 99Tc (T 1/2 =213 ka ) by accelerator mass spectrometry (AMS) is reported for the first time. Because there are no stable isotopes of technetium, the 99Tc content of a sample is determined from the ratio of 99Tc to a known trace amount of 103Rh. High-purity aluminium oxide constitutes the bulk of each sample. The contribution from the 99Ru isobar may be quantified and subtracted using 101Ru. In contrast to conventional AMS in which at least one isotope is measured as a beam current, here all three isotopes, 99Tc, 101Ru and 103Rh, are counted ion-by-ion in a propane-filled ionization chamber. This ionization chamber permits partial, but not complete, separation of 99Tc from 99Ru ions. The technique has been validated using a series of standards, as well as a set of five seaweed samples from an inter-laboratory comparison exercise. In addition, the technique has been used to measure the relative intensities of the Tc− and TcOm− (m=1–4) negative ions from a Cs sputter ion source.

AMS measurements to study uptake and distribution of 26Al in mice and the role of the transferrin receptor in aluminium absorption mechanisms

Abstract We report the use of a 20 MV tandem Van de Graaff accelerator and accelerator mass spectrometry (AMS) to measure the distribution and uptake mechanisms of 26 Al in vivo in mice. The influence of antibodies against the transferrin receptor and of hypotransferrinaemia (mice with virtual absence of circulating transferrin) were studied with regard to the uptake of 26 Al from infusion with aluminium citrate. In both hypotransferrinaemic and antibody-treated mice, uptake of 26 Al was similar to control values in all tissues except spleen and muscle for the antibody-treated mice and bone for the hypotransferrinaemic mice. It appears that non-transferrin mediated transport of aluminium can occur into tissues and that transport of the metal bound to citrate and other low molecular weight complexes may be important. Generally, the uptake of aluminium into control tissue follows the order bone (femur) > renal cortex > skeletal muscle ≈ liver > spleen > brain. Comparisons with the uptake and distribution of the radiotracer analogue of aluminium, (Ga-67) were made.