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Camelford Water Poisoning Accident; Serial Neuropsychological Assessments and Further Observations on Bone Aluminium

Department of Clinical Neuropsychology, Atkinson Morley's Hospital, Copse Hill, London SW20 ONE

A.J. Freemont

Department of Rheumatology Pathology Laboratories, University of Manchester, Oxford Road, Manchester M13 9PT

A. Herxheimer

Department of Clinical Pharmacology and Therapeutics, Charing Cross and Westminster Medical School, Fulham Palace Road, London W6 8RF

J. Denton

Department of Rheumatology Pathology Laboratories, University of Manchester, Oxford Road, Manchester M13 9PT

A.P. Taylor

Robens Institute, University of Surrey, Guildford, Surrey GU2 5XH

M. Pazianas

Divisions of Biochemical and Physiological Medicine, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK

A.R.C. Cummin

Divisions of Biochemical and Physiological Medicine, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK

J.B. Eastwood

Divisions of Biochemical and Physiological Medicine, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK

The serial cognitive assessment of ten individuals made between 8 and 26 months after the water at Camelford in Cornwall was accidentally contaminated with aluminium sulphate, showed consistent evidence of impairment of information processing and memory. There was no obvious relationship between these impairments and measurements of anxiety and depression.

Serial bone biopsies in two individuals showed that the aluminium which was present 6 and 7 months after the accident had disappeared by 19 months. In the eight individuals biopsied 12-17 months after the accident the bone showed no stainable aluminium.

Thus, aluminium deposited in the bone of normal individuals can disappear within 18 months. After an accident such as that at Camelford important evidence of toxicity is likely to be missed if an investigation is delayed. The abnormal neuropsychological findings indicate cognitive impairment, but whether this was caused by an acute episode of brain damage, or other causes such as the psychological effects of stress resulting from the accident, is uncertain.

Human & Experimental Toxicology, Vol. 12, No. 1, 37-42 (1993)
DOI: 10.1177/096032719301200108


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