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Published online before print September 13, 2006, doi:10.1212/01.wnl.0000239836.26142.c5)
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 Volume 67, Number 9, November 14, 2006
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Received February 22, 2006
Accepted July 17, 2006

Environmental lead exposure and cognitive function in community-dwelling older adults

R. A. Shih PhD, T. A. Glass PhD, K. Bandeen-Roche PhD, M. C. Carlson PhD, K. I. Bolla PhD, A. C. Todd PhD, and B. S. Schwartz MD, MS*

From the Departments of Mental Health (R.A.S., M.C.C.), Epidemiology (T.A.G., B.S.S.), Biostatistics (K.B.-R.), and Environmental Health Sciences (K.I.B., B.S.S.), Johns Hopkins Bloomberg School of Public Health, and Departments of Medicine (B.S.S.) and Neurology (K.I.B.), Johns Hopkins Medical Institutions, Baltimore, MD; and Department of Community and Preventive Medicine (A.C.T.), Mount Sinai School of Medicine, New York, NY. R.A.S. is currently at the Division of Epidemiology, Statistics, and Prevention Research, National Institute of Child Health and Human Development, Rockville, MD.


* To whom correspondence should be addressed. E-mail: bschwart{at}jhsph.edu.

Abstract-- Objective: To determine if long-term exposure to high levels of lead in the environment is associated with decrements in cognitive ability in older Americans. Methods: We completed a cross-sectional analysis using multiple linear regression to evaluate associations of recent (in blood) and cumulative (in tibia) lead dose with cognitive function in 991 sociodemographically diverse, community-dwelling adults, aged 50 to 70 years, randomly selected from 65 contiguous neighborhoods in Baltimore, MD. Tibia lead was measured with 109Cd induced K-shell X-ray fluorescence. Seven summary measures of cognitive function were created based on standard tests in these domains: language, processing speed, eye-hand coordination, executive functioning, verbal memory and learning, visual memory, and visuoconstruction. Results: The mean (SD) blood lead level was 3.5 (2.2) µg/dL and tibia lead level was 18.7 (11.2) µg/g. Higher tibia lead levels were consistently associated with worse cognitive function in all seven domains after adjusting for age, sex, APOE-{varepsilon}4, and testing technician (six domains p ≤ 0.01, one domain p ≤ 0.05). Blood lead was not associated with any cognitive domain. Associations with tibia lead were attenuated after adjustment for years of education, wealth, and race/ethnicity. Conclusions: Independent of recent lead dose, retained cumulative dose resulting from previous environmental exposures may have persistent effects on cognitive function. A portion of age-related decrements in cognitive function in this population may be associated with earlier lead exposure.




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