Cardiac Autonomic Dysfunction: Particulate Air Pollution Effects Are Modulated by Epigenetic Immunoregulation of Toll‐like Receptor 2 and Dietary Flavonoid Intake

In the article by Zhong et al, “Cardiac Autonomic Dysfunction: Particulate Air Pollution Effects Are Modulated by Epigenetic Immunoregulation of Toll‐like Receptor 2 and Dietary Flavonoid Intake,” which published online January 27, 2015, and appeared in the January 2015 issue of the journal (J Am Heart Assoc. 2015;4:e001423 doi: 10.1161/JAHA.114.001423), the second affiliation of the tenth author (Diddier Prada) was not included. The affiliation “Unidad de Investigación Biomédica en Cáncer del Instituto Nacional de Cancerología – Instituto de Investigaciones Biomédicas‐UNAM, Mexico City, Mexico (D.P.)” has been added to the article.

Figure 3 originally contained incorrect labels for the regression lines. The solid, medium‐dashed, dashed, and dotted line presenting PM2.5‐HRV relationship is now correctly labeled with TLR2 methylation level at the midpoints of Q4, Q3, Q2, and Q1, respectively.

Figure 3.

The effect of particulate matter with aerodynamic diameter <2.5 μm (PM _2.5) exposure on heart rate variability (HRV) at different mean Toll‐like receptor 2 (TLR2) methylation levels, Normative Aging Study, 2000–2011 (N=500). log₁₀ HR indicates log₁₀‐transformed heart rate; log₁₀rMSSD, log₁₀‐transformed root mean square of the successive differences; log₁₀ SDNN, log₁₀‐transformed standard deviation of normal‐to‐normal intervals; log₁₀ LF, log₁₀‐transformed low‐frequency power (0.04 to 0.15 Hz); log₁₀ HF, log₁₀‐transformed high‐frequency power (0.15 to 0.4 Hz); Q1, Q2, Q3, and Q4 indicate the first, second, third, and fourth quartiles. The association of PM _2.5 with rMSSD, SDNN, LF, and HF is modified by mean TLR2 methylation levels, as indicated by the different slopes. The 4 lines in each figure represent the relationship between PM _2.5 and HRV when the mean TLR2 methylation level is at the midpoints of each quartile. If there was no effect modification, the 4 lines would be the same. The P _global for interaction was based on a global test for effect modification by position‐specific methylation. Interaction terms between each of the 5 TLR2 positions and PM _2.5 were included in the model, and these 5 interaction terms were tested jointly for effect modification using a Wald test (global test). Results were adjusted for age; body mass index; fasting glucose level; hypertension; smoking status; alcohol consumption; physical exercise; household income; the use of calcium channel blocker, β‐blocker, and angiotensin‐converting enzyme inhibitor; room temperature; outdoor apparent temperature; season; weekday; and visit date.

Figure 3 originally contained incorrect labels for the regression lines. The solid, medium‐dashed, dashed, and dotted line presenting PM2.5‐HRV relationship is now correctly labeled with TLR2 methylation level at the midpoints of Q4, Q3, Q2, and Q1, respectively. The correct Figure 3 is presented here.

The authors regret these errors.

The online version of the article has been updated and is available at http://jaha.ahajournals.org/content/4/1/e001423.

J Am Heart Assoc. 2016;5:e002008 doi: 10.1161/JAHA.115.002008