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Lead, genetic susceptibility, and risk of adult brain tumors.

Abstract

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.

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  • Authors+Show Affiliations

    ,

    Division of Cancer Epidemiology Branch, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, EPS Room 7085, Bethesda, MD 20892-7238, USA. rajarama@mail.nih.gov

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    Source

    MeSH

    Adolescent
    Adult
    Aged
    Aged, 80 and over
    Arizona
    Brain Neoplasms
    Case-Control Studies
    Female
    Genetic Predisposition to Disease
    Genotype
    Glioma
    Humans
    Lead
    Male
    Massachusetts
    Meningioma
    Middle Aged
    Occupational Exposure
    Pennsylvania

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural

    Language

    eng

    PubMed ID

    17164378

    Citation

    Rajaraman, Preetha, et al. "Lead, Genetic Susceptibility, and Risk of Adult Brain Tumors." Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, vol. 15, no. 12, 2006, pp. 2514-20.
    Rajaraman P, Stewart PA, Samet JM, et al. Lead, genetic susceptibility, and risk of adult brain tumors. Cancer Epidemiol Biomarkers Prev. 2006;15(12):2514-20.
    Rajaraman, P., Stewart, P. A., Samet, J. M., Schwartz, B. S., Linet, M. S., Zahm, S. H., ... Inskip, P. D. (2006). Lead, genetic susceptibility, and risk of adult brain tumors. Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, 15(12), pp. 2514-20.
    Rajaraman P, et al. Lead, Genetic Susceptibility, and Risk of Adult Brain Tumors. Cancer Epidemiol Biomarkers Prev. 2006;15(12):2514-20. PubMed PMID: 17164378.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Lead, genetic susceptibility, and risk of adult brain tumors. AU - Rajaraman,Preetha, AU - Stewart,Patricia A, AU - Samet,Jonathan M, AU - Schwartz,Brian S, AU - Linet,Martha S, AU - Zahm,Shelia Hoar, AU - Rothman,Nathaniel, AU - Yeager,Meredith, AU - Fine,Howard A, AU - Black,Peter M, AU - Loeffler,Jay, AU - Shapiro,William R, AU - Selker,Robert G, AU - Inskip,Peter D, PY - 2006/12/14/pubmed PY - 2007/4/10/medline PY - 2006/12/14/entrez SP - 2514 EP - 20 JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JO - Cancer Epidemiol. Biomarkers Prev. VL - 15 IS - 12 N2 - 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. SN - 1055-9965 UR - https://www.unboundmedicine.com/medline/citation/17164378/Lead_genetic_susceptibility_and_risk_of_adult_brain_tumors_ L2 - http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=17164378 DB - PRIME DP - Unbound Medicine ER -