Exp Mol Med.
2011 Jun;43(6):374-378. 10.3858/emm.2011.43.6.041.
Polymorphisms in genes involved in innate immunity and susceptibility to benzene-induced hematotoxicity
- Affiliations
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- 1Division of Cancer Epidemiology and Genetics, NCI, NIH, DHHS, Bethesda, MD 20892, USA. hosgoodd@mail.nih.gov
- 2School of Public Health, University of California, Berkeley, CA 94720, USA.
- 3Department of Environmental Health, Korea National Open University, Seoul 110-791, Korea.
- 4Institute for Risk Assessment Sciences, Utrecht University; Julius Center, University Medical Center Utrecht, Utrecht, Netherlands.
- 5Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
- KMID: 1107379
- DOI: http://doi.org/10.3858/emm.2011.43.6.041
Abstract
- Benzene, a recognized hematotoxicant and carcinogen, can damage the human immune system. We studied the association between single nucleotide polymorphisms (SNPs) in genes involved in innate immunity and benzene hematotoxicity in a cross-sectional study of workers exposed to benzene (250 workers and 140 controls). A total of 1,236 tag SNPs in 149 gene regions of six pathways were included in the analysis. Six gene regions were significant for their association with white blood cell (WBC) counts (MBP, VCAM1, ALOX5, MPO, RAC2, and CRP) based on gene-region (P < 0.05) and SNP analyses (FDR < 0.05). VCAM1 rs3176867, ALOX5 rs7099684, and MPO rs2071409 were the three most significant SNPs. They showed similar effects on WBC subtypes, especially granulocytes, lymphocytes, and monocytes. A 3-SNP block in ALOXE3 (rs7215658, rs9892383, and rs3027208) showed a global association (omnibus P = 0.0008) with WBCs even though the three SNPs were not significant individually. Our study suggests that polymorphisms in innate immunity genes may play a role in benzene-induced hematotoxicity; however, independent replication is necessary.
MeSH Terms
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Adult
Arachidonate 5-Lipoxygenase/genetics/*metabolism
Benzene/toxicity
Cell Count
Cross-Sectional Studies
Female
Genetic Association Studies
Genetic Predisposition to Disease
Hematologic Diseases/chemically induced/genetics/*metabolism/pathology
Humans
Immunity, Innate/genetics
Leukocytes/*drug effects/metabolism/pathology
Male
Occupational Exposure/adverse effects
Peroxidase/genetics/*metabolism
Polymorphism, Single Nucleotide
Vascular Cell Adhesion Molecule-1/genetics/*metabolism
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