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Vol. 2, No. 3-4, 2005
Issue release date: January 2006
Section title: Clinical and Epidemiological Aspects of ALS
Neurodegenerative Dis 2005;2:195–201
(DOI:10.1159/000089625)

Lead Exposure as a Risk Factor for Amyotrophic Lateral Sclerosis

Kamel F. · Umbach D.M. · Hu H. · Munsat T.L. · Shefner J.M. · Taylor J.A. · Sandler D.P.
aNational Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, N.C.; bHarvard Medical School and Harvard School of Public Health and cNew England Medical Center, Cambridge, Mass., and dSUNY Upstate Medical University, Syracuse, N.Y., USA

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Article / Publication Details

First-Page Preview
Abstract of Clinical and Epidemiological Aspects of ALS

Published online: 1/6/2006

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 3

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Background: The etiology of amyotrophic lateral sclerosis (ALS) likely involves an environmental component. We qualitatively assessed literature on ALS and lead exposure. Problems of study design make case reports and studies of lead in blood or tissues difficult to interpret. Most previous case-control studies found an association of ALS with self-reported occupational exposure to lead, with increased risks of 2- to >4-fold. However, these results may have been affected by recall bias. Objective: To address inconsistencies among published reports, we used both lead biomarkers and interview data to assess lead exposure, and we evaluated the role of genetic susceptibility to lead. Methods: We conducted a case-control study in New England in 1993–1996 with 109 ALS cases and 256 population-based controls. We measured blood and bone lead levels, the latter using X-ray fluorescence, and interviewed participants regarding sources of lead exposure. Results: In our study, ALS was associated with self-reported occupational lead exposure, with a dose response for cumulative days of exposure. ALS was also associated with blood and bone lead levels, with a 1.9-fold increase in risk for each µg/dl increment in blood lead and a 2.3- to 3.6-fold increase for each doubling of bone lead. A polymorphism in the δ-aminolevulinic acid dehydratase gene was associated with a 1.9-fold increase in ALS risk. Conclusion: These results, together with previous studies, suggest that lead exposure plays a role in the etiology of ALS. An increase in mobilization of lead from bone into blood may play a role in the acute onset of disease.


  

Author Contacts

Freya Kamel, PhD, MPH
Epidemiology Branch, National Institute of Environmental Health Sciences
PO Box 12233, MD A3-05
Research Triangle Park, NC 27709 (USA)
Tel. +1 919 541 1581, Fax +1 919 541 2511, E-Mail kamel@mail.nih.gov

  

Article Information

Number of Print Pages : 7
Number of Figures : 0, Number of Tables : 3, Number of References : 57

  

Publication Details

Neurodegenerative Diseases

Vol. 2, No. 3-4, Year 2005 (Cover Date: Released January 2006)

Journal Editor: Nitsch, R.M. (Zürich)
ISSN: 1660–2854 (print), 1660–2862 (Online)

For additional information: http://www.karger.com/NDD


Article / Publication Details

First-Page Preview
Abstract of Clinical and Epidemiological Aspects of ALS

Published online: 1/6/2006

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 3

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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