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NEUROLOGY 1996;46:401-405
© 1996 American Academy of Neurology

Risk for neuropathologically confirmed Alzheimer's disease and residual aluminum in municipal drinking water employing weighted residential histories

D.R.C. McLachlan, MD, C. Bergeron, MD, J. E. Smith, BSc, D. Boomer, PhD and S. L. Rifat, PhD

From the Departments of Physiology and Medicine (Dr. McLachlan), Pathology (Dr. Bergeron), and Preventive Medicine and Biostatistics (J. Smith and Dr. Rifat), University of Toronto, and the Ontario Ministry of Environment and Energy, Drinking Water Section (Dr. Boomer), Toronto, ON, Canada.
Supported by the Alzheimer Association of Ontario and the Ontario Mental Health Foundation.
Received April 26, 1995. Accepted in final form May 31, 1995.
Address correspondence and reprint requests to Dr Rifat, 69 Yonge Street, Suite 1004, Toronto, ON, Canada, M5E 1K3.

We investigated a possible relation between aluminum concentration ([Al]) in public drinking water and Alzheimer's disease (AD), with AD cases and controls defined on the basis of strict neuropathologic criteria.Using the case/control odds ratio as an estimate of relative risk and [Al] more than equals to 100 mu g/L as the cutoff point, elevated risks for histopathologically verified AD were associated with higher [Al]. Comparing all AD cases with all non-AD controls, and using the [Al] of public drinking water at last residence before death as the measure of exposure, the estimated relative risk associated with [Al] more than equals to 100 mu g/L was 1.7 (95% CI: 1.2-2.5). Estimating aluminum exposure from a 10-year weighted residential history resulted in estimates of relative risk of 2.5 or greater. The public health implications of the observed relationship between [Al] in drinking water and AD prevalence in the population depend in large measure on population exposure characteristics. In Ontario, it is estimated that 19% of the population was exposed to residual [Al] greater than or equal to 100 mu g/L. Based on the estimated relative risk and the assumption of causality, this translates to an etiologic fraction of 0.23. Although the potential contributions of confounding and mitigating factors are not defined in this report, the merit of limiting residual aluminum in drinking water supplies deserves serious attention.

NEUROLOGY 1996;46: 401-405




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