Environmental lead exposure and neurobehavioral functioning in a population-based sample of adults

Lead's neurotoxic effects in older adults is a public health concern because (1) older adults had more opportunity for exposures when lead was widely used, (2) older adults have had more time to accumulate lead in their bones, and (3) cognitive aging may be particularly sensitive to lead. Given the historical and persistent disparities in exposure by socioeconomic and racial/ethnic subgroups, it is imperative to examine the effects of both recent and cumulative lead dose on neurobehavior in these subgroups.; This thesis presents the first large study of a socio-demographically diverse, population-based sample of urban-dwelling adults. In multiple linear regression models, higher tibia lead levels were associated with poorer performance in tests of language, visual and verbal memory, visuoconstruction, motor speed, and executive functioning, even after adjusting for age, sex, Apolipoprotein E epsilon4 status, blood lead, and testing technician.; We extended this line of research to examine whether the persistent effects of lead were indicative of mild cognitive impairment (MCI), which may herald the onset of dementia. In a cross-sectional logistic regression, the 2nd, 3rd, and 4th quartiles of tibia lead were significantly associated with an 84%, 94%, and 93% increase in odds for MCI, respectively, compared to the lowest tibia lead quartile.; Adjustment for race/ethnicity, education, wealth, and chronic conditions substantially reduced the tibia lead association with neurobehavioral outcomes and MCI. Using path analysis modeling, we modeled mediating and correlated pathways to explain race-associated differences in five domains of cognitive functioning. Accounting for individual-level factors explained up to 37% of the total effect of race/ethnicity. Race-stratified analyses indicated heterogeneity in the relative importance of covariates, suggesting the race-associated differences in cognition operated through different pathways.; We provide compelling evidence for a chronic effect of cumulative lead dose on neurobehavior, independent of low, recent lead dose from ongoing external and endogenous sources of lead exposure. Future analyses should examine the potential progressive effects of cumulative lead dose on accelerated cognitive declines, which may be indicative of pre-clinical dementia. The complex causal relationships surrounding cognitive functioning in late life require methodical modeling techniques to clarify the consequences of lead's neurotoxic effects.