Open AccessEffects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability
Author(s) -
Byun HyangMin,
Colicino Elena,
Trevisi Letizia,
Fan Tianteng,
Christiani David C.,
Baccarelli Andrea A.
Publication year - 2016
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.116.003218
Subject(s) - medicine , dna methylation , mitochondrial dna , methylation , cardiology , dna , environmental health , genetics , gene , gene expression , biology
Background The mitochondrion is the primary target of oxidative stress in response to exogenous environments. Mitochondrial DNA (mt DNA ) is independent from nuclear DNA and uses separate epigenetic machinery to regulate mt DNA methylation. The mt DNA damage induced by oxidative stress can cause mitochondrial dysfunction and is implicated in human diseases; however, mt DNA methylation has been largely overlooked in environmental studies relating to human disease. The purpose of this study was to examine the association between exposure to fine metal‐rich particulates (particulate matter <2.5 µm in diameter [ PM 2.5 ]) from welding in a boilermaker union and blood mt DNA methylation in relation to heart rate variability. Methods and Results Forty‐eight healthy men were recruited on multiple sampling cycles at the Boilermaker Union Local 29, located in Quincy, Massachusetts. We measured personal PM 2.5 in the background ambient environment. We measured blood mt DNA methylation in the mt DNA promoter (D‐loop) and genes essential for ATP synthesis ( MT ‐ TF and MT ‐ RNR 1 ) by bisulfite pyrosequencing. All analyses were adjusted for demographics, type of job, season, welding‐work day, and mt DNA methylation experimental batch effect. The participants’ PM 2.5 exposure was significantly higher after a welding‐work day (mean 0.38 mg/m 3 ) than the background personal level (mean 0.15 mg/m 3 , P <0.001). Blood mt DNA methylation in the D‐loop promoter was associated with PM 2.5 levels (β=−0.99%, SE =0.41, P =0.02). MT ‐ TF and MT ‐ RNR 1 methylation was not associated with PM 2.5 exposure (β=0.10%, SE =0.45, P =0.82). Interaction of PM 2.5 exposure levels and D‐loop promoter methylation was significantly associated with markers of heart rate variability. Conclusions Blood mt DNA methylation levels were negatively associated with PM 2.5 exposure and modified the adverse relationships between PM 2.5 exposure and heart rate variability outcomes.