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Effects of early low-level lead exposure on human brain structure, organization and functions

Published online by Cambridge University Press:  28 September 2010

K. M. Cecil*
Affiliation:
Cincinnati Children’s Environmental Health Center at Cincinnati Children’s Hospital Medical Center, Departments of Radiology, Pediatrics, Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH, USA
*
*Address for correspondence: K. M. Cecil, PhD, Professor, Radiology, Pediatrics, Neuroscience & Environmental Health, Cincinnati Children’s Hospital Medical Center, Department of Radiology, MLC 5033, 3333 Burnet Avenue, Cincinnati, OH 45229, USA. (Email kim.cecil@chmcc.org)

Abstract

Advanced neuroimaging techniques offer unique insights into how childhood lead exposure impacts the brain. Volumetric magnetic resonance imaging affords anatomical information about the size of global, regional and subcomponent structures within the brain. Diffusion tensor imaging provides information about white matter architecture by quantitatively describing how water molecules diffuse within it. Proton magnetic resonance spectroscopy generates quantitative measures of neuronal, axonal and glial elements via concentration levels of select metabolites. Functional magnetic resonance imaging infers neuronal activity associated with a given task performed. Employing these techniques in the study of the Cincinnati Lead Study, a relatively homogeneous birth cohort longitudinally monitored for over 30 years, one can non-invasively and quantitatively explore how childhood lead exposure is associated with adult brain structure, organization and function. These studies yield important findings how environmental lead exposure impacts human health.

Type
Themed Content: Role of Environmental Stressors in the Developmental Origins of Disease
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

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References

1.Al Khayat, A, Menon, NS, Alidina, MR. Acute lead encephalopathy in early infancy – clinical presentation and outcome. Ann Trop Paediatr. 1997; 1, 3944.CrossRefGoogle Scholar
2.Atre, AL, Shinde, PR, Shinde, SN, et al. Pre- and posttreatment MR imaging findings in lead encephalopathy. AJNR Am J Neuroradiol. 2006; 27, 902903.Google ScholarPubMed
3.Mani, J, Chaudhary, N, Kanjalkar, M, Shah, PU. Cerebellar ataxia due to lead encephalopathy in an adult. J Neurol Neurosurg Psychiatr. 1998; 65, 797.CrossRefGoogle ScholarPubMed
4.Tuzun, M, Tuzun, D, Salan, A, Hekimoglu, B. Lead encephalopathy: CT and MR findings. J Comput Assist Tomogr. 2002; 26, 479481.CrossRefGoogle ScholarPubMed
5.Staudinger, KC, Roth, VS. Occupational lead poisoning. Am Fam Physician (Review) 1998; 57, 719726.Google ScholarPubMed
6.Bellinger, DC, Stiles, KM, Needleman, HL. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics. 1992; 90, 855861.CrossRefGoogle ScholarPubMed
7.Canfield, RL, Gendle, MH, Cory-Slechta, DA. Impaired neuropsychological functioning in lead-exposed children. Dev Neuropsychol. 2004; 26, 513540.CrossRefGoogle ScholarPubMed
8.Canfield, RL, Henderson, CR Jr, Cory-Slechta, DA, et al. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. 2003; 348, 15171526.CrossRefGoogle ScholarPubMed
9.Dietrich, KN, Berger, OG, Succop, PA, Hammond, PB, Bornschein, RL. The developmental consequences of low to moderate prenatal and postnatal lead exposure: intellectual attainment in the cincinnati lead study Cohort following school entry. Neurotoxicol Teratol. 1993; 15, 3744.CrossRefGoogle ScholarPubMed
10.Needleman, HL, Gatsonis, CA. Low-level lead exposure and the IQ of children. A meta-analysis of modern studies. JAMA. 1990; 263, 673678.CrossRefGoogle ScholarPubMed
11.Wright, JP, Dietrich, KN, Ris, MD, et al. Association of prenatal and childhood blood lead concentrations with criminal arrests in early adulthood. PLoS Med. 2008; 5, e101.CrossRefGoogle ScholarPubMed
12.Ashburner, J, Friston, KJ. Voxel-based morphometry – the methods. Neuroimage. 2000; 11, 805821.CrossRefGoogle ScholarPubMed
13.Le Bihan, D, Mangin, JF, Poupon, C, et al. Diffusion tensor imaging: concepts and applications. J Magn Reson Imaging. 2001; 13, 534546.CrossRefGoogle ScholarPubMed
14.Beaulieu, C. The basis of anisotropic water diffusion in the nervous system – a technical review. NMR Biomed. 2002; 15, 435455.CrossRefGoogle ScholarPubMed
15.Kim, JH, Budde, MD, Liang, HF, et al. Detecting axon damage in spinal cord from a mouse model of multiple sclerosis. Neurobiol Dis. 2006; 21, 626632.CrossRefGoogle ScholarPubMed
16.Kinoshita, Y, Ohnishi, A, Kohshi, K, Yokota, A. Apparent diffusion coefficient on rat brain and nerves intoxicated with methylmercury. Environ Res. 1999; 80, 348354.CrossRefGoogle ScholarPubMed
17.Song, S-K, Sun, S-W, Ju, W-K, et al. Diffusion tensor imaging detects and differentiates axon and myelin degeneration in mouse optic nerve after retinal ischemia. Neuroimage. 2003; 20, 17141722.CrossRefGoogle ScholarPubMed
18.Partridge, SC, Mukherjee, P, Henry, RG, et al. Diffusion tensor imaging: serial quantitation of white matter tract maturity in premature newborns. Neuroimage. 2004; 22, 13021314.CrossRefGoogle ScholarPubMed
19.Song, S-K, Sun, S-W, Ramsbottom, MJ, et al. Dysmyelination revealed through MRI as increased radial (but Unchanged Axial) diffusion of water. Neuroimage. 2002; 17, 14291436.CrossRefGoogle ScholarPubMed
20.Song, S-K, Yoshino, J, Le, TQ, et al. Demyelination increases radial diffusivity in corpus callosum of mouse brain. Neuroimage. 2005; 26, 132140.CrossRefGoogle ScholarPubMed
21.Suzuki, Y, Matsuzawa, H, Kwee, IL, Nakada, T. Absolute eigenvalue diffusion tensor analysis for human brain maturation. NMR Biomed. 2003; 16, 257260.CrossRefGoogle ScholarPubMed
22.Dietrich, KN, Succop, PA, Berger, OG, Hammond, PB, Bornschein, RL. Lead exposure and the cognitive development of urban preschool children: the cincinnati lead study cohort at age 4 years. Neurotoxicol Teratol. 1991; 13, 203211.CrossRefGoogle ScholarPubMed
23.Cecil, KM, Brubaker, CJ, Adler, CM, et al. Decreased brain volume in adults with childhood lead exposure. PLoS Med. 2008; 5, e112.CrossRefGoogle ScholarPubMed
24.Brubaker, CJ, Dietrich, KN, Lanphear, BP, Cecil, KM. The influence of age of lead exposure on adult gray matter volume. Neurotoxicology. 2010; 31, 259266.CrossRefGoogle ScholarPubMed
25.Cecil, KM, Dietrich, KN, Altaye, M , et al. Proton magnetic resonance spectroscopy in adults with childhood lead exposure. EHP (in press).Google Scholar
26.Brubaker, CJ, Schmithorst, VJ, Haynes, EN, et al. Altered myelination and axonal integrity in adults with childhood lead exposure: a diffusion tensor imaging study. Neurotoxicology. 2009; 30, 867875.CrossRefGoogle ScholarPubMed
27.Yuan, W, Holland, SK, Cecil, KM, et al. The impact of early childhood lead exposure on brain organization: a functional magnetic resonance imaging study of language function. Pediatrics. 2006; 118, 971977.CrossRefGoogle ScholarPubMed
28.Toscano, CD, Guilarte, TR. Lead neurotoxicity: from exposure to molecular effects. Brain Res Rev. 2005; 49, 529554.CrossRefGoogle ScholarPubMed
29.Guilarte, TR, Miceli, RC, Jett, DA. Neurochemical aspects of hippocampal and cortical Pb2+ neurotoxicity. Neurotoxicology. 1994; 15, 459466.Google ScholarPubMed
30.Deng, W, Poretz, RD. Lead exposure affects levels of galactolipid metabolic enzymes in the developing rat brain. Toxicol Appl Pharmacol. 2001; 172, 98107.CrossRefGoogle ScholarPubMed
31.Zawia, NH, Harry, GJ. Exposure to lead-acetate modulates the developmental expression of myelin genes in the rat frontal lobe. Int J Dev Neurosci. 1995; 13, 639644.CrossRefGoogle ScholarPubMed
32.Toews, AD, Blaker, WD, Thomas, DJ, et al. Myelin deficits produced by early postnatal exposure to inorganic lead or triethyltin are persistent. J Neurochem. 1983; 41, 816822.CrossRefGoogle ScholarPubMed
33.Toews, AD, Krigman, MR, Thomas, DJ, Morell, P. Effect of inorganic lead exposure on myelination in the rat. Neurochem Res. 1980; 5, 605616.CrossRefGoogle ScholarPubMed
34.Deng, W, Poretz, RD. Protein kinase C activation is required for the lead-induced inhibition of proliferation and differentiation of cultured oligodendroglial progenitor cells. Brain Res. 2002; 929, 8795.CrossRefGoogle ScholarPubMed
35.Dabrowska-Bouta, B, Struzynska, L, Walski, M, Rafalowska, U. Myelin glycoproteins targeted by lead in the rodent model of prolonged exposure. Food Chem Toxicol. 2008; 46, 961966.CrossRefGoogle ScholarPubMed
36.Dabrowska-Bouta, B, Sulkowski, G, Bartosz, G, Walski, M, Rafalowska, U. Chronic lead intoxication affects the myelin membrane status in the central nervous system of adult rats. J Mol Neurosci. 1999; 13, 127139.CrossRefGoogle ScholarPubMed
37.Selvin-Testa, A, Loidl, CF, Lopez-Costa, JJ, Lopez, EM, Pecci-Saavedra, J. Chronic lead exposure induces astrogliosis in hippocampus and cerebellum. Neurotoxicology. 1994; 15, 389401.Google ScholarPubMed
38.Struzynska, L, Bubko, I, Walski, M, Rafalowska, U. Astroglial reaction during the early phase of acute lead toxicity in the adult rat brain. Toxicology. 2001; 165, 121131.CrossRefGoogle ScholarPubMed
39.Struzynska, L, Dabrowska-Bouta, B, Koza, K, Sulkowski, G. Inflammation-like glial response in lead-exposed immature rat brain. Toxicol Sci. 2007; 95, 156162.CrossRefGoogle ScholarPubMed