Abstract 15898: Toll-Like Receptor 2 Methylation and Dietary Flavonoid Intake Modify the Association Between Fine Particle Exposure and Cardiac Autonomic Dysfunction: The Normative Aging Study
Introduction: Short-term exposure to fine particles (PM2.5) is associated with reduced heart rate variability (HRV), a strong predictor of cardiac mortality among the elderly. Identifying modifiable factors that confer susceptibility is essential for personalized intervention. We evaluated whether Toll-Like Receptor 2 (TLR2) methylation [[Unable to Display Character: –]] a reversible epigenetic process affecting immunoregulation [[Unable to Display Character: –]] modified the effect of PM2.5 on HRV, and investigated the impact of flavonoid and folic acid intake on TLR2 methylation.
Methods: We collected longitudinal measures of HRV and PM2.5 over 11 years among 573 elderly men from the Normative Aging Study. TLR2 methylation was analyzed using bisulfite-treated Pyrosequencing from 500 participants. Harvard Food Frequency Questionnaire was administrated to assess average daily flavonoid and folic acid intake in the past year.
Results: Every 10 μg/m3 increase in 48 hours PM2.5 moving average was associated with 7.23% (95% CI, 2.95%, 11.33%; P = 0.03) and 13.88% (95% CI, 1.39%, 24.79%; P = 0.04) reduction in the standard deviation of normal-to-normal intervals (SDNN) and low frequency (LF), respectively. TLR2 hypermethylation exacerbated the post-exposure SDNN, LF, and high frequency (HF) reduction (Pglobal = 0.03, 0.05, 0.04, respectively). Every 10-fold increase in flavonoid intake was associated with 0.41 %5mC lower in TLR2 methylation (95% CI, 0.04, 0.78; P = 0.03). High flavonoid intake weakened the association between PM2.5 and LF by lessening 33.01% (95% CI, 1.56, 74.22; P = 0.04) LF reduction per 10 μg/m3 increase in PM2.5, compared to the low intake group. Folic acid intake was not associated with TLR2 methylation.
Conclusion: TLR2 hypermethylation confers the vulnerability to post-exposure HRV decline of the elderly when confronted with air pollution peaks, while high flavonoid intake emolliates the hazardous effect of pollution, likely through regulating TLR2 methylation.
Author Disclosures: J. Zhong: None. E. Colicino: None. X. Lin: None. A. Mehta: None. I. Kloog: None. A. Zanobetti: None. H. Byun: None. M. Bind: None. L. Cantone: None. D. Prada: None. L. Tarantini: None. D. Sparrow: None. P. Vokonas: None. J. Schwartz: None. A. Baccarelli: None.
- © 2014 by American Heart Association, Inc.