Note: This article was originally published with an incorrect version of the Acknowledgments, which appeared on p. 218 of the print version. The correct version of the Acknowledgments appeared on pp. 1–2. The corrected article is available below.

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Human Health Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide

The chronic toxicity of aluminium, cadmium, mercury, and lead in birds: a review.

Renal osteodystrophy

Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

Metabolism and possible health effects of aluminum.

Aluminium poisoning: dialysis encephalopathy, osteomalacia, and anaemia.

Iliac bone aluminium was determined by neutron activation analysis in 34 patients with chronic renal failure and in eight control subjects. In 17 patients treated by haemodialysis there was a significant increase in the amount of aluminium (mean +/- SE = 152 +/- 30 ppm bone ash). In eight patients treated by haemodialysis and subsequent renal transplantation, bone aluminium was still significantly increased (92 +/- 4.5 ppm bone ash) but was less than in the haemodialysed patients. In some patients aluminium persisted in bone for many years after successful renal transplantation. There was no relationship between hyperparathyroidism and bone aluminium. Although no statistically significant relationship was found between the mineralisation status of bone and bone aluminium, patients dialysed for the longest periods tended to be those with the highest levels of aluminium, osteomalacia, and dialysis encephalopathy. In 20 rats given daily intraperitoneal injections of aluminium chloride for periods of up to three months, there was accumulation of aluminium in bone (163 +/- 9 ppm ash) to levels comparable to those obtained in the dialysis patients, and after about eight weeks osteomalacia developed. The increased bone aluminium and osteomalacia persisted after injections had been stopped for up to 49 days, although endochondral ossification was restored to normal. As a working hypothesis it is suggested that aluminium retained in the bone of the dialysis patients and the experimental animals interferes with normal mineralisation.

https://jcp.bmj.com/content/jclinpath/32/8/832.full.pdf

J H McCarthy

Papers

Bone aluminium in haemodialysed patients and in rats injected with aluminium chloride: relationship to impaired bone mineralisation.