PM2.5 exposure and DLEC1 promoter methylation in Taiwan Biobank participants

Ying-Hsiang Chou,Oswald Ndi Nfor,Yeu-Sheng Tyan,Pei-Hsin Chen,Chao-Yu Shen,Disline Manli Tantoh,Yung-Po Liaw,Shu-Yi Hsu,Chien-Ning Huang,Ming-Chi Wu

doi:10.1186/s12199-020-00909-x

Abstract

BackgroundParticulate matter (PM) < 2.5 μm (PM2.5) or fine PM is a serious public health concern. It affects DNA methylation and heightens carcinogenesis. Deleted in lung and esophageal cancer 1 (DLEC1) is a tumor suppressor gene. However, aberrant methylation of the gene is associated with several cancers. We evaluated the association between PM2.5 and DLEC1 promoter methylation in Taiwanese adults based on regular outdoor exercise.MethodsWe obtained DNA methylation and exercise data of 496 participants (aged between 30 and 70 years) from the Taiwan Biobank (TWB) database. We also extracted PM2.5 data from the Air Quality Monitoring Database (AQMD) and estimated participants’ exposure using residential addresses.ResultsDLEC1 methylation and PM2.5 were positively associated: beta coefficient (β) = 0.114 × 10−3; p value = 0.046. The test for interaction between exercise and PM2.5 on DLEC1 methylation was significant (p value = 0.036). After stratification by exercise habits, PM2.5 and DLEC1 methylation remained significantly associated only among those who exercised regularly (β = 0.237 × 10−3; p value = 0.007). PM2.5 quartile-stratified analyses revealed an inverse association between regular exercise and DLEC1 methylation at PM2.5 < 27.37 μg/m3 (β = − 5.280 × 10−3; p value = 0.009). After combining exercise habits and PM2.5 quartiles, one stratum (i.e., regular exercise and PM2.5 < 27.37 μg/m3) was inversely associated with DLEC1 methylation (β = -5.160 × 10−3, p value = 0.007).ConclusionsWe found significant positive associations between PM2.5 and DLEC1 promoter methylation. Regular exercise at PM2.5 < 27.37 μg/m3 seemingly regulated DLEC1 promoter methylation.

Highlights

PM2.5 induces the generation of reactive oxygen species (ROS) which have detrimental effects [1], like immune response stress, inflammatory injury, Deoxyribonucleic acid (DNA) damage, and oxidative stress that enhance cancer formation [1,2,3]
We evaluated the association between PM2.5 and Deleted in lung and esophageal cancer 1 (DLEC1) promoter methylation in relation to exercise among Taiwan Biobank (TWB) participants
PM2.5 was significantly associated with hypermethylation or higher levels (β = 0.114 × 10−3; p value = 0.046) while age was significantly associated with hypomethylation or lower levels of DLEC1 promoter methylation: β = − 0.206 × 10−3; p value = < 0.001 (Table 2)

Summary

Introduction

PM2.5 induces the generation of reactive oxygen species (ROS) which have detrimental effects [1], like immune response stress, inflammatory injury, DNA damage, and oxidative stress that enhance cancer formation [1,2,3]. PM2.5 is a critical public health issue that accounts for DNA methylation is an epigenetic change that integrates the interactions between genes and the environment [10]. Abnormal patterns of this epigenetic marker are promising diagnostic and prognostic tumor markers. In a study where exercise-induced immunologic benefits attenuated the detrimental effects of air pollution on the lungs, DNA methylation was a marker of such benefits [18]. Particulate matter (PM) < 2.5 μm (PM2.5) or fine PM is a serious public health concern It affects DNA methylation and heightens carcinogenesis. We evaluated the association between PM2.5 and DLEC1 promoter methylation in Taiwanese adults based on regular outdoor exercise

Methods

Results

Discussion

Conclusion