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American Journal of Epidemiology Advance Access originally published online on February 7, 2008
American Journal of Epidemiology 2008 167(7):807-813; doi:10.1093/aje/kwm378
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American Journal of Epidemiology © The Author 2008. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Single Nucleotide Polymorphisms in Inflammation-related Genes and Mortality in a Community-based Cohort in Washington County, Maryland

Lisa Gallicchio1,2, Howard Chang3, Dana K. Christo2, Lucy Thuita2, Han-Yao Huang2, Paul Strickland4, Ingo Ruczinski3, Sandra C. Hoffman2 and Kathy J. Helzlsouer1,2

1 Prevention and Research Center, Weinberg Center for Women's Health and Medicine, Mercy Medical Center, Baltimore, MD
2 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
3 Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
4 Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

Correspondence to Dr. Lisa Gallicchio, Prevention and Research Center, Weinberg Center for Women's Health and Medicine, Mercy Medical Center, 227 St. Paul Place, Sixth Floor, Baltimore, MD 21202 (e-mail: Lgallic{at}mdmercy.com).

Received for publication August 24, 2007. Accepted for publication November 30, 2007.

The purpose of this study was to examine the associations between single nucleotide polymorphisms (SNPs) in genes controlling inflammatory processes and mortality. Data were analyzed from 9,933 individuals who participated in two large community-based cohort studies conducted in Washington County, Maryland, in 1974 and 1989, designated "CLUE I" and "CLUE II," respectively. DNA from blood collected in 1989 was genotyped for 47 SNPs in 23 inflammation-related genes, including interferon-{gamma} (IFN{gamma}), lymphotoxin-{alpha} (LT{alpha}), tumor necrosis factor-{alpha} (TNF{alpha}), C-reactive protein (CRP), peroxisome proliferator-activated receptor (PPAR), and the human endothelial nitric oxide synthase (eNOS). All participants were followed from 1989 to the date of death or to June 20, 2005. The results showed no observable patterns of association for the SNPs and the all-cause and cause-specific mortality outcomes, although statistically significant associations were observed between at least one mortality outcome and SNPs in eNOS (reference SNP (rs) 1799983), PPARG (rs4684847), CRP (rs2794521), IFN{gamma} (rs2069705), TNF{alpha} (rs1799964), and LT{alpha} (rs2229094). Additionally, three of the four examined CRP SNPs were strongly associated with CRP serum concentration among those with CRP measurements. The authors' findings from this community-based prospective cohort study suggest that the selected SNPs are not associated with overall or cause-specific death, although CRP genotypes may be associated with systemic inflammation.

cohort studies; C-reactive protein; inflammation; mortality; neoplasms; polymorphism, genetic

Abbreviations: CRP, C-reactive protein; ICD, International Classification of Diseases; IL, interleukin; rs, reference single nucleotide polymorphism; SNP, single nucleotide polymorphism


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