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Plasma Homocysteine, Particulate Air Pollution, and Oxidative Stress-Related Genes-A Gene-Environment Interaction

Ren, Cizao*; Park, Sung†; Vokonas, Pantel‡; Sparrow, David‡; Wilker, Elissa§; Baccarelli, Andrea¶; Suh, Helen*; Tucker, Katherine**; Wright, Robert††; Schwartz, Joel*

doi: 10.1097/01.ede.0000362353.43658.7a
Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25-29, 2009: Oral Presentations

*Exposure, Epidemiology, and Risk Program, Harvard School of Public Health, Boston, MA, United States; †Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, United States; ‡Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA, United States; §Environmental and Occupational Medicine and Epidemiology Program, Harvard School of Public Health, Boston, MA, United States; ¶Department of Environmental and Occupational Health,University of Milan, Milan, Italy; **Dietary Assessment and Epidemiology Research Program, Tufts University, Boston, MA, United States; and ††Department of Pediatrics, Children's Hospital, Boston and Department of Environmental Health, Harvard School of Public Health, Boston, MA, United States.

Abstracts published in Epidemiology have been reviewed by the organizations of Epidemiology. Affliate Societies at whose meetings the abstracts have been accepted for presentation. These abstracts have not undergone review by the Editorial Board of Epidemiology.

ISEE-0468

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Background and Objective:

High total plasma homocysteine (tHcy) is a risk factor for human health. Ambient particulate matter is also associated with cardiovascular events and, recently, with tHcy. However, the biological mechanisms are not fully understood. One of the putative pathways is through oxidative stress. We used repeated measures data from the Normative Aging Study to examine whether the associations of PM2.5 and black carbon (BC) with tHcy were modified by a broad set of genetic polymorphisms related to oxidative stress, including HFE H63D, C282Y, CAT (rs480575, rs1001179, rs2284367 and rs2300181), NQO1 (rs1800566), GSTP1 (wild vs non-wild), GSTM1, GSTT1 (deletion vs non-deletion) and HMOX-1 (any short vs both long) genotypes.

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Methods:

PM2.5, BC, tHcy and other covariates were repeatedly measured between 1995 and 2006. We fit mixed models in R to examine the association of pollution with tHcy and the effect modifications by individual genotypes adjusting for covariates.

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Results:

Interquartile ranges (IQR) increases in PM2.5 and BC of 7-day moving averages were associated with 1.05% (95% confidence interval (CI): −0.01%, 2.11%) (P = 0.089) and 2.40% (95% CI: 1.00%, 3.83%) (P = 0.007) increases in tHcy (natural log), respectively. GSTT1 and HFE C282Y significantly modified effects of BC on tHcy, and HFE C282Y and CAT (rs2300181) significantly modified effects of PM2.5 on tHcy. Several gene polymorphisms marginally modified effects of PM2.5 and BC. All genes with significant interactions with particulate air pollution had marginally significant main effects on tHcy.

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Conclusion:

Effects of PM2.5 and BC on tHcy appeared to be mediated by genes related to oxidative stress pathways.

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