Proton magnetic resonance spectroscopy in adults with childhood lead exposure.
BACKGROUND
Childhood lead exposure adversely affects neurodevelopment. However, few studies have examined changes in human brain metabolism that may underlie known adverse cognitive and behavioral outcomes.


OBJECTIVE
We examined the association between mean childhood blood lead levels and in vivo brain metabolite concentrations as adults, determined by proton magnetic resonance spectroscopy (MRS) in a birth cohort with documented low-to-moderate lead exposure.


METHODS
Adult participants from the Cincinnati Lead Study [n = 159; mean age (± SD), 20.8 ± 0.9 years] completed a quantitative, short-echo proton MRS protocol evaluating seven regions to determine brain concentrations of N-acetyl aspartate (NAA), creatine and phosphocreatine (Cr), cholines (Cho), myo-inositol, and a composite of glutamate and glutamine (GLX). Correlation and multiple linear regression analyses were conducted.


RESULTS
Mean childhood blood lead levels were associated with regionally specific brain metabolite concentrations adjusted for age at imaging and Full-Scale intelligence quotient. Adjusted analyses estimated for a unit (micrograms per deciliter) increase in mean childhood blood lead concentrations, a decrease of NAA and Cr concentration levels in the basal ganglia, a decrease of NAA and a decrease of Cho concentration levels in the cerebellar hemisphere, a decrease of GLX concentration levels in vermis, a decrease of Cho and a decrease of GLX concentration levels in parietal white matter, and a decrease of Cho concentration levels in frontal white matter.


CONCLUSIONS
Gray-matter NAA reductions associated with increasing childhood blood lead levels suggest that sustained childhood lead exposure produces an irreversible pattern of neuronal dysfunction, whereas associated white-matter choline declines indicate a permanent alteration to myelin architecture.
Cincinnati Children's Environmental Health Center at Cincinnati Children's Hospital Medical Center, Ohio 45229, USA. kim.cecil@chmcc.org
Kim M
KM
Cecil
Kim N
KN
Dietrich
Mekibib
M
Altaye
John C
JC
Egelhoff
Diana M
DM
Lindquist
Christopher J
CJ
Brubaker
Bruce P
BP
Lanphear
D000293:Adolescent; D000328:Adult; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D004781:Environmental Exposure / Q000032:analysis / Q000706:statistics & numerical data; D004785:Environmental Pollutants / Q000097:blood / Q000633:toxicity*; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007854:Lead / Q000097:blood / Q000633:toxicity*; D008137:Longitudinal Studies; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D011522:Protons; D055815:Young Adult
D004785:Environmental Pollutants; D011522:Protons; D007854:Lead