To investigate the effect of aluminum and silica in drinking water on the risk of dementia and AD the authors analyzed data from a large prospective cohort (Paquid) including 3,777 subjects aged 65 years and over, living at home in 75 civil parishes in Gironde and Dordogne in southwestern France. The subjects were followed up for eight years with an active search for incident cases of dementia or AD. Mean exposure to aluminum and silica in drinking water was estimated in each area. We analyzed 2,698 non-demented subjects at baseline, and for whom components of drinking water and covariates were available. 253 incident cases of dementia including 182 AD were identified. The relative risk of dementia adjusted for age, gender, educational level, place of residence and wine consumption was 2.03 (95 percent CI 1.23–3.34) for subjects exposed to aluminum concentration greater than 0.1 mg/l. This result was confirmed for AD (adjusted relative risk=2.20, 95 percent CI 1.24–3.89). Inversely, the adjusted relative risk of dementia for subjects exposed to silica (≥ 11.25 mg/l) was 0.75 (95 percent CI 0.58–0.96). These findings support the hypothesis that aluminum in drinking water is a risk factor for AD.
Although much effort has been devoted to identifying the genetic determinants of Alzheimer’s disease (AD), it is likely that certain environmental factors play a role in this disease. Because of its proven neurotoxicity, aluminum may be one such factor. Although the hypothesis of a link between aluminum and AD has been supported by several biological findings, uncertainty still prevails. Dialysis encephalopathy6 is one of the main observations in favour of the neurotoxicity of aluminum because it proves that aluminum is able to reach the brain and induce neurofibrillary degeneration and neuronal death. Several epidemiological studies have reported an association between exposure to aluminum and dementia, most studying aluminum from drinking water, but some from other sources. Another hypothesis has been proposed by Birchall on the role of silicon in water as a protective factor against aluminum toxicity. However, there is much controversy regarding these findings and their interpretation, in particular owing to recently published epidemiological studies which failed to find an association. In previous papers we have shown that baseline cognitive performances of subjects in the Paquid cohort were correlated with levels of aluminum and silica in drinking water. Here we present results for incident dementia and Alzheimer’s disease based on 8 years of follow-up.
MATERIALS AND METHODS Sample The Paquid cohort was designed to study prospectively a representative random sample of 3,777 people aged 65 years or older at baseline, and living at home in one of 75 randomized rural or urban parishes of the administrative areas of Gironde or Dordogne. Subjects were randomly selected from electoral rolls and baseline data were collected in 1988–1989. Subjects were then re-evaluated 1, 3, 5 and 8 years after the initial visit to diagnose incident cases of dementia. The general methodology of Paquid has been described fully elsewhere. Measure of dementia and AD In brief, prevalent and incident cases of dementia were detected by a two-step procedure. First, all participants underwent a 1-hour home interview and a psychometric evaluation with a trained psychologist who systematically completed a standardized questionnaire designed to obtain the A (memory impairment), B (impairment of at least one other cognitive function) and C (interference with social and professional life) criteria for dementia according to the DSM-III-R. Second, subjects positive for these criteria were examined by a senior neurologist who confirmed the diagnosis and applied the NINCDS-ADRDA criteria for AD and the Hachinski score for vascular dementia to document the diagnosis of dementia and its etiology: probable or possible AD or other type of dementia. Measure of exposure A specific study (ALMA) was started in 1990 to examine the relationship between aluminum in drinking water and Alzheimer’s Disease for the Paquid subjects. After investigation of the water distribution network, the sample was divided into 78 drinking water areas. Two surveys were carried out in 1991 to measure pH and concentrations of aluminum, calcium, and fluorine in each water supply, and to study the variability of the measurements. These data were described in detail by Jacqmin et al. Then all the results of the chemical analyses of drinking water (including silica) carried out by the sanitary administration between 1991 and 1994 were collected. Therefore, for each drinking water area, we computed a weighted mean of all the measures of each drinking water component. The weighting took into account the length of the period of use of each water supply over the previous 10 years (1981–1991) and the relative contribution of each water supply. The present study is based on 70 areas for which measurements were available. Statistical analysis A Cox proportional hazard model with delayed entry was performed to estimate relative risks (RR) and to adjust for covariates. Age was taken as the basic time scale in the analysis, so that the risk of dementia or AD at a given age could be modelled. For the analyses we considered only subjects free of dementia at entry into the cohort. In a previous analysis we observed that the proportional hazards assumption was violated for gender, so we chose to perform a stratified analysis. The main risk factors under consideration were aluminum as a quantitative variable or as a binary variable with the threshold of 0.1 mg per liter already used in previous studies, and silica as a binary variable with 11.25 mg/l (the median in our sample) as the cut-off. We adjusted for potential confounders: educational level (with vs without a primary school diploma), wine consumption (non-drinkers or mild drinkers vs moderate or heavy drinkers) and place of residence (rural vs urban). Adjustment for baseline cognitive status measured by the Mini Mental State Examination (MMSE) scores was done in a complementary analysis (MMSE was available for 2,658 subjects). We then examined separately the effect of mineral water consumption (daily consumption of mineral water vs no or occasional consumption). This information was collected only at the 3-year follow-up visit. Thereafter, we examined the sub-sample of non-demented subjects who were visited at that follow-up, and we used incident cases of dementia between the 3-year and 8-year follow-up visits.
RESULTS
Among the 3,777 subjects who initially agreed to participate, 3,675 were non-demented at the first visit. The measurements of water and adjustment covariates were available for 3,401 subjects unaffected at the initial visit. Among the 3,401 subjects, 703 (20.6 percent) did not participate in the follow-up because they had died (n=383, 11.3 percent), were lost to follow-up (n=4, 0.1 percent) or refused the follow-up procedure (n=316, 9.3 percent). At least one complete follow-up evaluation was performed in 2,698 subjects (79.3 percent). The percentage of deaths before the investigation between exposed and non-exposed to aluminum subjects (13.9 percent vs 11.2 percent, p=0.42) were not significantly different; nor refusals (12.7 percent vs 9.3 percent, p=0.27).
At baseline, 91 percent of the individuals had stayed more than 10 years in the same parish, and the mean length of residence in the same parish was 41 years. During the 8-year follow-up of these subjects, 253 subjects were diagnosed with dementia and 182 (72.0 percent) were classified as having Alzheimer’s disease (probable or possible). The incidence rate for all causes of dementia and Alzheimer’s disease was estimated as 1.69 per 100 person-years and 1.22 per 100 person-years, respectively.
Aluminum levels in water supplies ranged from 0.001 to 0.459 mg/l with a median value of 0.009 mg/l, and 63 subjects were exposed to more than 0.1 mg/l. Silica levels in water ranged from 4.2 to 22.4 mg/l and were inversely related to aluminum concentrations, but this negative correlation was weak in our study (Spearman rank correlation coefficient.
The results of the analyses suggest that the risk of dementia was higher for subjects living in parishes where the mean aluminum concentrations exceeded 0.1 mg/l than for those living in areas where concentrations were less than 0.1 mg/l (RR non-parametrically adjusted for age and gender < 0.001, model 1). Conversely, higher silica concentrations (≥ 11.25 mg/l) were associated with a reduced risk of dementia (RR non-parametrically adjusted for age and gender 0.71, p = 0.007, model 2). After additional adjustment for educational level, wine consumption and place of residence, aluminum and silica concentrations remained associated with dementia (RR for aluminum 2.03, p = 0.006; RR for silica 0.75, p = 0.023, model 3). There was no significant interaction between aluminum and silica concentrations (likelihood ratio = 0.48). Results of model 3 were not significantly changed after adjustment for baseline MMSE (RR for aluminum 2.08, p = 0.005; RR for silica 0.74. The pH level was not associated with dementia and the interaction between aluminum and pH was not significant.
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