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Abstract. Aluminium is involved in the etiology of several complications of chronic renal failure and has been firmly established as having toxic effects on bone tissue. We have measured plasma aluminium together with serum osteocalcin, procollagen I C-terminal peptide and total alkaline phosphatase activity in healthy subjects and in a group of subjects who consumed aluminium-containing and non-aluminium containing antacid preparations, with normal renal function. Age-related healthy reference ranges for plasma aluminium are presented and the effects of chronic antacid consumption on plasma aluminium and biochemical markers of bone formation investigated.In 172 healthy subjects the mean plasma aluminium concentration was 4.4k2.9 p g L-', men having a significantly greater circulating aluminium load than women (5-4k2.8 p g L-' vs. 4.0f2.8 p g L-' respectively (P = 0.0039)). Older men were found to have significantly higher plasma aluminium levels than younger men. Increased plasma aluminium was seen in subjects taking antacids although this was not associated with significant changes in most indices of bone formation.

Radiation-induced segregation of phosphorus has been studied in nickel and Fe-15Cr-Ni alloys, with nickel content varying from 15 to 70 atomic%, using accelerator based techniques and secondary ion mass spectrometry. Experiments in pure nickel demonstrated that phosphorus segregates by an interstitial mechanism. The similarity of segregation in nickel and Fe-15Cr-Ni alloys suggests that this conclusion also applies to the alloys. We have confirmed that manganese segregates by solute-vacancy exchanges. Phosphorus, manganese, and silicon segregation in the alloys was found to be strongly dependent on nickel content. The composition dependence was, however, similar for all the solutes, independent of mechanism. Segregation was a minimum for nickel contents about 45 atomic%. Possible explanations for this are discussed.

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