This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rajaraman, P. Articles by Inskip, P. D. Search for Related Content PubMed PubMed Citation Articles by Rajaraman, P. Articles by Inskip, P. D.

Lead, Genetic Susceptibility, and Risk of Adult Brain Tumors

¹ Division of Cancer Epidemiology and Genetics, ² Core Genotyping Facility, and ³ Neuro-Oncology Branch, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland; ⁴ Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; ⁵ Brigham and Women's Hospital, Boston, MA; ⁶ Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts; ⁷ Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona; and ⁸ Western Pennsylvania Hospital, Pittsburgh, Pennsylvania

Requests for reprints: Preetha Rajaraman, Radiation Epidemiology Branch, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, EPS Room 7085, Bethesda, MD 20892-7238. Phone: 301-496-8847; Fax: 301-402-0207. E-mail: rajarama{at}mail.nih.gov

Background: Although few etiologic factors for brain tumors have been identified, limited data suggest that lead may increase the risk of brain tumors, particularly meningioma. The ALAD G177C polymorphism affects the toxicokinetics of lead and may confer genetic susceptibility to adverse effects of lead exposure.

Methods: We examined occupational exposure to lead and risk of brain tumors in a multisite, hospital-based, case-control study of 489 patients with glioma, 197 with meningioma, and 799 non-cancer controls frequency matched on hospital, age, sex, race/ethnicity, and residential proximity to hospital. ALAD genotype was assessed by a Taqman assay for 355 glioma patients, 151 meningioma patients, and 505 controls. Exposure to lead was estimated using a rigorous questionnaire-based exposure assessment strategy incorporating lead measurement and other occupational data abstracted from published articles and reports.

Results: Increased risk of meningioma with occupational lead exposure (estimated by odds ratios and 95% confidence intervals) was most apparent in individuals with the ALAD2 variant allele, for whom risk increased from 1.1 (0.3-4.5) to 5.6 (0.7-45.5) and 12.8 (1.4-120.8) for estimated cumulative lead exposures of 1 to 49 µg/m³-y, 50 to 99 µg/m³-y, and 100 µg/m³-y, respectively, compared with unexposed individuals (two-sided P trend = 0.06). This relationship became stronger after excluding occupational lead exposures characterized by a low confidence level or occurring in the 10 years before meningioma diagnosis. Occupational lead exposure was not associated with glioma risk.

Conclusions: Although our results indicate that lead may be implicated in meningioma risk in genetically susceptible individuals, these results need to be interpreted with caution given the small numbers of exposed cases with a variant genotype. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2514–20)

This article has been cited by other articles:

				M.-C. Rousseau, M.-E. Parent, L. Nadon, B. Latreille, and J. Siemiatycki Occupational Exposure to Lead Compounds and Risk of Cancer among Men: A Population-based Case-Control Study Am. J. Epidemiol., November 1, 2007; 166(9): 1005 - 1014. [Abstract] [Full Text] [PDF]