Melinda C Power1, Susan Korrick2, Eric J Tchetgen Tchetgen3, Linda H Nie4, Francine Grodstein5, Howard Hu6, Jennifer Weuve7, Joel Schwartz8, Marc G Weisskopf9. 1. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. Electronic address: melindacpower@gmail.com. 2. Department of Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Division of Network Medicine, Department of Medicine at Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. Electronic address: resak@channing.harvard.edu. 3. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Biostatistics, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. Electronic address: etchetge@hsph.harvard.edu. 4. Purdue University, School of Health Sciences, College of Health and Human Sciences, 700 W. State Street, West Lafayette, IN 47907, USA. Electronic address: hnie@purdue.edu. 5. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Division of Network Medicine, Department of Medicine at Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. Electronic address: phfrg@channing.harvard.edu. 6. Department of Environmental Health Sciences at the University of Michigan School of Public Health, 1415 Washington Heights, Ann Arbor, MI 48109, USA. Electronic address: howard.hu@utoronto.ca. 7. Department of Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Institute of Healthy Aging and Department of Internal Medicine, Rush University Medical Center, 1653 W. Congress Parkway, Chicago, IL 60612, USA. Electronic address: jweuve@hsph.harvard.edu. 8. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. Electronic address: joel@hsph.harvard.edu. 9. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Department of Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. Electronic address: mweissko@hsph.harvard.edu.
Abstract
BACKGROUND: Higher long-term cumulative lead exposure predicts faster cognitive decline in older men, but evidence of an association in women is lacking. OBJECTIVE: To determine if there is an association between lead exposure and cognitive decline in women. METHODS: This study considers a sample of 584 women from the Nurses' Health Study who live in or near Boston, Massachusetts. We quantified lead exposure using biomarkers of lead exposure assessed in 1993-2004 and evaluated cognitive decline by repeated performance on a telephone battery of cognitive tests primarily assessing learning, memory, executive function, and attention completed in 1995-2008. All cognitive test scores were z-transformed for use in analyses. We used linear mixed models with random effects to quantify the association between each lead biomarker and change in cognition overall and on each individual test. RESULTS: Consideration of individual tests showed greater cognitive decline with increased tibia lead concentrations, a measure of long-term cumulative exposure, for story memory and category fluency. The estimated excess annual decline in overall cognitive test z-score per SD increase in tibia bone lead concentration was suggestive, although the confidence intervals included the null (0.024 standard units, 95% confidence interval: -0.053, 0.004 - an additional decline in function equivalent to being 0.33 years older). We found little support for associations between cognitive decline and patella or blood lead, which provide integrated measures of exposure over shorter timeframes. CONCLUSIONS: Long-term cumulative lead exposure may be weakly associated with faster cognitive decline in community-dwelling women, at least in some cognitive domains.
BACKGROUND: Higher long-term cumulative lead exposure predicts faster cognitive decline in older men, but evidence of an association in women is lacking. OBJECTIVE: To determine if there is an association between lead exposure and cognitive decline in women. METHODS: This study considers a sample of 584 women from the Nurses' Health Study who live in or near Boston, Massachusetts. We quantified lead exposure using biomarkers of lead exposure assessed in 1993-2004 and evaluated cognitive decline by repeated performance on a telephone battery of cognitive tests primarily assessing learning, memory, executive function, and attention completed in 1995-2008. All cognitive test scores were z-transformed for use in analyses. We used linear mixed models with random effects to quantify the association between each lead biomarker and change in cognition overall and on each individual test. RESULTS: Consideration of individual tests showed greater cognitive decline with increased tibia lead concentrations, a measure of long-term cumulative exposure, for story memory and category fluency. The estimated excess annual decline in overall cognitive test z-score per SD increase in tibia bone lead concentration was suggestive, although the confidence intervals included the null (0.024 standard units, 95% confidence interval: -0.053, 0.004 - an additional decline in function equivalent to being 0.33 years older). We found little support for associations between cognitive decline and patella or blood lead, which provide integrated measures of exposure over shorter timeframes. CONCLUSIONS: Long-term cumulative lead exposure may be weakly associated with faster cognitive decline in community-dwelling women, at least in some cognitive domains.
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