Platelet Mitochondrial DNA Methylation as Epigenetic Biomarker of Short-Term Air Pollution Exposure in Healthy Subjects.

Huimin Sun,Yaxian Pang,Jianzhong Zhang,Yuxin Zheng,Rong Zhang,Jinglong Tang,Xin Li,Tsendmaa Bold,Tao Wang,Nan Kong,Yanting Li,Xue Cao,Teng Shi

doi:10.3389/fmolb.2021.803488

Huimin Sun, Yaxian Pang + Show 11 more

Open Access

https://doi.org/10.3389/fmolb.2021.803488

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Abstract

Air pollution exposure is now considered a growing concern for global public health. RNA or DNA methylation changes caused by air pollution may be related to the development of cardiovascular disease. To investigate the early biomarkers of air pollution exposure, a panel study of eight college students recorded after a business trip from Qingdao to Shijiazhuang and back to Qingdao was performed in this work. The concentration of PM2.5, PM10, SO2, NO2, and CO in Shijiazhuang was higher than that in Qingdao during the study period. The platelet count was positively correlated with air pollutants of 0–6 day moving averages (βPM2.5 = 88.90; βPM10 = 61.83; βSO2 = 41.13; βNO2 = 57.70; βCO = 62.99, respectively, for an IQR increased). Additionally, internal dose biomarkers 2-OHNa, 1-OHNa, 2-OHFlu, 2,3-OHPhe, and ∑PAHs were also significantly associated with platelet count in participants. Furthermore, PM2.5 and PM10 are positively linked with methylation of one CpG site at platelet mitochondrial gene CO2 (PM2.5 = 0.47; PM10 = 0.25, respectively, for an IQR increase). Both platelet counts and methylation levels returned to their pre-exposure levels after leaving the highly contaminated area. In short, this study investigated the relationship between platelet properties and air pollution exposure, revealing that short-term exposure to air pollution might increase the risk of thrombosis. Our research suggests that platelet count and mitochondrial DNA methylation of mtCO2 site 2 in platelets from healthy adults may be the novel biomarker for acute exposure to air pollution.

Highlights

According to the World Health Organization (WHO), air pollution causes approximately 7 million deaths annually (Kuehn, 2014), with cardiovascular illnesses accounting for the majority of these deaths (Brook et al, 2010; Miller and Xu, 2018)
Some evidence suggests that particulate matter (PM) in the air causes platelet activation through different pathways, such as endothelial cell damage
A prospective panel study was conducted to track a group of healthy young people who travelled from Qingdao to Shijiazhuang for 6 days

Summary

Introduction

According to the World Health Organization (WHO), air pollution causes approximately 7 million deaths annually (Kuehn, 2014), with cardiovascular illnesses accounting for the majority of these deaths (Brook et al, 2010; Miller and Xu, 2018). Numerous epidemiological studies have shown that air pollution affects prothrombosis, elevating platelet activation markers (Baccarelli et al, 2007; Devlin et al, 2012; Poursafa and Kelishadi, 2010). Previous epidemiological studies only focused on a Platelet Mitochondrial DNA Methylation few biomarkers of platelet activation (such as sCD40L) and paid less attention to platelet characteristics and DNA methylation changes of platelet mitochondria (Poursafa and Kelishadi, 2010). Some evidence suggests that particulate matter (PM) in the air causes platelet activation through different pathways, such as endothelial cell damage. Animal studies have shown a shift in the balance between platelet activation, coagulation, and fibrinolysis to pro-coagulation and anti-fibrinolysis states after exposure to air pollutants (Dobrakowski et al, 2016; Daiber et al, 2017). The effect of acute air pollution on platelet changes in healthy people is still controversial (Li et al, 2018a; Lin et al, 2019); due to the limitation of methods, there are few studies to explore the epigenetic effects of air pollution on platelet genes in the general population

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