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BALTIMORE -- Cognitive function in adults as well as children can be impaired by cumulative exposure to lead in the environment, researchers here have found.
BALTIMORE, Sept. 14 -- A lifetime of exposure to lead can weigh down the minds of older adults, researchers here have found, adding two to six years to the normal cognitive effects of aging.
A study of community-dwelling adults ranging in age from 50 to 70 showed that higher lead levels in the tibia, a measure of cumulative lead exposure, were associated with worse performance in seven cognitive domains revealed a study reported in an early online release in Neurology.
These cognitive domains were learning, memory and visual-motor tasks, said Brian Schwartz, M.D., of the Johns Hopkins Bloomberg School of Public Health, and colleagues.
"The analysis showed the effect of community lead exposure was equivalent to two to six years of aging," said Dr. Schwartz and colleagues. "If lead is associated with lower cognitive performance, this may suggest possible treatment and prevention options for older adults."
The negative effects of lead exposure on cognitive function in children under the age of six are well documented, and measurable lead levels are found in all individuals, the authors noted.
"Population-based studies in the 1970s documented average population blood lead levels exceeding 15 to 20 ?g/dL," they wrote. "This past widespread use has led to lifetime cumulative doses in most older Americans, who are now entering a period of life when age-related decline in cognitive function is prevalent."
Because lead accumulates in bone and has a clearance half-life of about 20 to 30 years from cortical bone, it can be measured non-invasively with x-ray fluorescence techniques. In contrast, lead levels in blood generally indicate recent exposure.
The authors looked at a diverse population of 991 community-dwelling adults from the ages of 50 to 70 who were randomly selected from 65 contiguous neighborhoods in Baltimore.
They measured lead levels in the tibias of the participants with 109Cd-induced K-shell x-ray fluorescence, and assessed their cognitive function with standards tests for language, processing speed, eye-hand coordination, executive functioning, verbal memory and learning, visual memory, and visuoconstruction.
The investigators performed a cross-sectional analysis using multiple linear regression to evaluate associations of recent and cumulative lead exposure with cognitive function.
They found that the mean blood lead level was 3.5 (standard deviation 2.2) ?g/dL, and that the mean tibia lead level was 18.7 (11.2) ?g/g.
Higher levels of lead in the tibias of the participants, but not in their blood, were consistently and significantly associated with worse cognitive function in all seven domains tested, after adjustment for age, gender, the presence of the Alzheimer's-prone genotype APOE-E4, and the testing technician (six domains P<0.01, one domain P<0.05).
In multivariate models, the association between tibial lead levels and impaired cognitive function was attenuated by years of education, household income, and race/ethnicity.
The authors speculated that the effect could be due to lead exposure in early life leading to lower educational achievement and less remunerative occupations, or to unmeasured factors such as cardiovascular health that could be related to race or ethnicity and might modify the effect of lead on cognition.
They also considered that "it is possible that higher tibia lead levels are associated with lower secondary school quality or innate intellectual ability, and that the association of tibia lead with lower cognitive function is explained by its association with these other factors."
It's also possible, they noted, that the race/ethnicity might be more closely correlated with lifetime lead dose than tibial lead measures.
The authors proffered several possible explanations for the neurotoxic effects of cumulative lead exposure.
"Lead may alter energy metabolism in mitochondria and synaptosomes," they wrote, "and can interfere with several calcium-dependent processes, including the activity of protein kinase C. Recent evidence also suggests that lead accumulates in myelin, inhibits integral enzymes there, and may contribute to ultrastructural changes, or other changes in myelin. This last finding is particularly relevant given increasing interest in the myelin hypothesis of neurodegenerative diseases."