Pre- and Early Postnatal Lead Exposure, Late Adulthood Cognitive Function, and Modification by Cognitive Stimulating Activities
Marc Weisskopf1, Ruby Hickman1, Joyce Lin1, Kaleigh McAlaine1, Tracy Punshon2, Brian Jackson2, Felicitas Bidlack3, Laura Germine4, Scott Bartell5, Joseph Mangano6
1Harvard TH Chan School of Public Health, 2Dartmouth College, 3Forsyth Institute, 4Albert Einstein College of Medicine, 5UC Irvine, 6Radiation and Public Health Project
Objective:
To assess whether pre and early postnatal lead exposure—as measured in deciduous teeth—is a risk factor for worse late adulthood cognition and whether associations vary by level of early life cognitively stimulating activities (ELCSA).
Background:
Early-life exposure to lead has been associated with late-life Alzheimer’s-like pathology in animal models and neurodevelopmental impacts in children. Research into associations with late-life cognition in humans have been limited. Further, in animal studies, enriched environments appear to protect against adverse effects of lead exposure, but there has been limited exploration of this in humans.
Design/Methods:
We recontacted original St. Louis Baby Tooth Survey participants who donated deciduous (baby) teeth between 1958-1972. 715 baby teeth were sectioned and lead concentrations in primary dentin—reflecting in utero through early postnatal months exposure—were assessed using laser ablation inductively coupled plasma mass spectrometry. We assessed cognition in late adulthood (mean age: 62) via a computerized battery of cognitive tests through TestMyBrain.org. We used adjusted weighted generalized estimating equations to estimate associations between lead exposure and cognition. We examined modification by early-life cognitively stimulating activities assessed using the Rush Alzheimer’s Disease Center Lifetime Cognitive Activity scales.
Results:
Per 1 part per million (ppm) higher second trimester tooth lead concentration, composite cognition was 0.07 standard deviations (sd) (95% CI: -0.15, 0.02) lower and was modified by cognitively stimulating activities (Interaction p=0.001). For those with low ELCSA (bottom 24%), per 1ppm higher second trimester lead adulthood cognitive function was 0.34 (95% CI: -0.52, -0.16) sd lower, while the association among those with high cognitively stimulating activities was null (-0.02; 95% CI: -0.12, 0.07).
Conclusions:
Early-life lead exposure was associated with late adulthood cognitive function and was modified by cognitively stimulating activities. Our work supports the hypothesis that engaging in cognitively stimulating activities could mitigate against deleterious effects of lead on later adulthood cognitive function.
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