Lead, genetic susceptibility, and risk of adult brain tumors
-
2006/12/01
Details
-
Personal Author:Black PM ; Fine HA ; Inskip PD ; Linet MS ; Loeffler J ; Rajaraman P ; Rothman N ; Samet JM ; Schwartz BS ; Selker RG ; Shapiro WR ; Stewart PA ; Yeager M ; Zahm SH
-
Description: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 microg/m3-y, 50 to 99 microg/m3-y, and >or=100 microg/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. [Description provided by NIOSH]
-
Subjects:
-
Keywords:
-
ISSN:1055-9965
-
Document Type:
-
Funding:
-
Genre:
-
Place as Subject:
-
CIO:
-
Topic:
-
Location:
-
Volume:15
-
Issue:12
-
NIOSHTIC Number:nn:20037671
-
Citation:Cancer Epidemiol Biomark Prev 2006 Dec; 15(12):2514-2520
-
Contact Point Address: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
-
Email:rajarama@mail.nih.gov
-
CAS Registry Number:
-
Federal Fiscal Year:2007
-
Performing Organization:Johns Hopkins University
-
Peer Reviewed:True
-
Start Date:20050701
-
Source Full Name:Cancer Epidemiology, Biomarkers & Prevention
-
End Date:20280630
-
Collection(s):
-
Main Document Checksum:urn:sha-512:92406c6ca1b23676ca4bfb7e47308f27a17afacb0df100891c87252dca1eed8e86478ee8dc7bc8e82c8a0ffeceb3a07090c720a93057ff60f96efca41f4cbb19
-
Download URL:
-
File Type:
ON THIS PAGE
CDC STACKS serves as an archival repository of CDC-published products including
scientific findings,
journal articles, guidelines, recommendations, or other public health information authored or
co-authored by CDC or funded partners.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
You May Also Like