title: Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.
abstract: Seventy-one-year-old identical twin brothers with chronic lead poisoning were identified from an occupational medicine clinic roster. Both were retired painters, but one brother (J.G.) primarily removed paint and had a history of higher chronic lead exposure. Patella and tibia bone lead concentrations measured by K-X-ray fluorescence in each brother were 5-10 times those of the general population and about 2.5 times higher in J.G. than in his brother (E.G.). Magnetic resonance spectroscopy (MRS) studies examined N-acetylaspartate:creatine ratios, a marker of neuronal density. Ratios were lower in J.G. than in his brother. Scores on neurocognitive tests that assess working memory/executive function were below expectation in both twins. Short-term memory function was dramatically worse in J.G. than in his brother. These results demonstrate some of the more subtle long-term neurologic effects of chronic lead poisoning in adults. In particular, they suggest the presence of frontal lobe dysfunction in both twins, but more dramatic hippocampal dysfunction in the brother with higher lead exposure. The MRS findings are consistent with the hypothesis that chronic lead exposure caused neuronal loss, which may contribute to the impairment in cognitive function. Although a causal relation cannot be inferred, the brothers were genetically identical, with similar life experiences. Although these results are promising, further study is necessary to determine whether MRS findings correlate both with markers of lead exposure and tests of cognitive function. Nevertheless, the results point to the potential utility of MRS in determining mechanisms of neurotoxicity not only for lead but also for other neurotoxicants as well.
authors.affiliation: Department of Environmental Health, Occupational Health Program, Harvard School of Public Health, Landmark Center, 401 Park Drive, PO Box 15697, Boston, MA 02215, USA. mweissko@hsph.harvard.edu
authors.forename: Marc G
authors.initials: MG
authors.lastname: Weisskopf
authors.forename: Howard
authors.initials: H
authors.lastname: Hu
authors.forename: Robert V
authors.initials: RV
authors.lastname: Mulkern
authors.forename: Roberta
authors.initials: R
authors.lastname: White
authors.forename: Antonio
authors.initials: A
authors.lastname: Aro
authors.forename: Steve
authors.initials: S
authors.lastname: Oliveira
authors.forename: Robert O
authors.initials: RO
authors.lastname: Wright
mesh_terms: D000368:Aged; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001842:Bone and Bones / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002452:Cell Count; D003072:Cognition Disorders / Q000139:chemically induced* / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D004200:Diseases in Twins; D006801:Humans; D007854:Lead / Q000378:metabolism; D007855:Lead Poisoning / Q000378:metabolism* / Q000523:psychology*; D020265:Lead Poisoning, Nervous System, Adult / Q000378:metabolism / Q000523:psychology; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009474:Neurons / Q000187:drug effects; D009784:Occupational Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000523:psychology; D014430:Twins, Monozygotic
chemical_list: D007854:Lead; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine