Research interests 

My research is focussed upon epigenetics (mainly DNA methylation, but recently extending to RNA methylation) and environmental exposures (e.g. air pollution, diet, noise, stress, smoking, carcinogens, and endocrine disruptors) related to human diseases (e.g. CVD, obesity, and diabetes) and cancers (leukaemias and other solid cancers). I have extensive experience in the field of epigenetics, which began with my appointment to a postdoctoral position with Dr. Allen Yang at the Norris Cancer Center at the University of Southern California. There my work was predominantly focused on fundamental mechanisms in epigenetics, which has provided me with an excellent foundation for applying my knowledge to the study of health and disease. My research was highly translational and at the forefront of the field. This included being among the very first researchers to adopt the use of DNA methylation microarrays, which I utilized to demonstrate the tissue-specificity of DNA methylation patterns across 11 tissues from human autopsies, and to analyze DNA methylation changes in one of the first patients treated with the epigenetic drug Vidaza and developed a novel inhibitor of DNA methyltransferase. Further, I was the first to identify technical artifacts in methylation microarray data originating from SNPs, which has subsequently led to the exclusion of SNP-associated probes becoming an established aspect of analysis pipelines for Illumina Infinium microarrays.


My research in epigenetics continued when I was recruited to Dr. Andrea Baccarelli’s group at Harvard School of Public Health, where I also gained experience in epidemiology, public health, and environmental exposures. There my research predominantly focused upon the effect of air pollution upon the epigenome. My work demonstrated that the susceptibility of LINE-1 and Alu elements within the genome to the effects of particulate matter air pollution is dependent upon their evolutionary age. Further, I pioneered the study of the mitochondrial epigenome, which I have demonstrated to be affected by particulate matter air pollution and to be disrupted in cardiovascular disease


I currently work at the Human Nutrition Research Centre at Newcastle University, where I am studying the effects of diet on human health through DNA methylation changes. In 2015, soon after my move to Newcastle, I became involved in the development of large and newly-established population studies based in Tianjin, China along with two other co-PIs. The project title is Environmental and LifEstyle FActors iN metabolic health throughout life-course Trajectories (ELEFANT). Project ELEFANT consists of three cohorts that each cover a stage of the human life cycle: birth (Baby ELEFANT, = 48,762, a birth cohort with multiple collection points of data from mothers and babies); young adults (Young ELEFANT, n = 366,474, mean age = 30, a cross-sectional study with the potential for developing a longitudinal study in the future); and elderly adults (Elderly ELEFANT, n = 6,503, mean age = 68, longitudinal study). We have collected data on basic demographics, clinical measures, socio-economic status, exercise, occupational exposures, ambient air pollution exposures (hourly measurements from 27 monitoring stations since 2002), and questionnaire data (including stress, occupational exposures and family history of disease).

In tandem with these observational studies, I am continuing my mechanistic research into the maintenance of epigenetic patterns and their modification through environmental exposures. One of my PhD students in my laboratory is investigating the regional- and sequence-specificity of DNA methyltransferase (DNMT) isoforms through in vitro studies overexpressing 13 DNMT isoforms in cell lines in conjunction with epigenome-wide analysis of DNA methylation patterns. Another project is to investigate how mitochondrial DNA methylation patterns in platelets can be used to predict CVD risk using an in vitro system and samples from obese individuals. Further, my team have been examining how methyl donors (e.g. folate) and dietary polyphenolic compounds (which are known to inhibit DNMTs) modulate global DNA methylation patterns and influence epigenetic ageing. Together, my observational and mechanistic studies are designed to elucidate how the epigenome is modified through environmental exposures and lifestyle, and how these epigenomic patterns influence the risk of non-communicable diseases. In the medium term, this will help inform intervention approaches to reduce disease incidence.


  • Erythrocyte ghosts containing a desired gene for biocompatible gene systems’ Korea Patent, Registration Date; 27 December 2004

  • N4 modifications of pyrimidine analogs and uses thereof US 20080234223 A1, 2007


  • Epigenetic changes through airborne pollutants

...thus allowing for separate analysis of maternal and paternal alleles.[8]​

...thus allowing for separate analysis of maternal and paternal alleles.[8]

  • Environmental exposure, epigenetics and human health at Qingdao University (In Chinese)

  • Changes in DNA patterns linked to prenatal smoke exposure

​"During pregnancy, there is a natural process of methylation reprogramming where small chemical compounds are removed from the DNA bases and then reattached a short while later, so it's reasonable to think that an environmental exposure could alter DNA methylation during this period," says co-author Hyang-Min Byun.


  • Identification of novel early epigenetic changes in Chronic Lymphocytic Leukaemia

  • Platelet mitochondrial DNA methylation: New biomarker of particulate matter effects

  • Cardiovascular disease risk assessment for general population exposed to PM2.5 based on epigenetics method

  • Platelet mitochondrial epigenetics; markers of CVD predisposition in obese individuals

  • Diesel exhaust exposure and mitochondrial DNA methylation in the biomarker study of diesel exhaust in China

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