Public Health - Environmental Health Science
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Epigenetic mechanism for toxic haze-exposed fetal origin of adult disease in China
This project aims to determine the toxic haze, which is a major, global health threat to billions of people in many countries (especially in China and India), in affecting epigenetic patterns of new born babies for future disease pathogenesis. Both epidemiological and animal studies demonstrate that exposure of PM2.5 (particulate matter with a diameter of 2.5 micrometers) is implicated in the pathogenesis of asthma, obesity and type 2 diabetes (T2D). For T2D solely, the number of T2D patients has skyrocketed in China, coinciding with the existence of toxic haze in the past decade. Mounting evidence reveals that gestation and early childhood are periods of enhanced vulnerability to air pollution, resulting in increased risk to many diseases in adulthood. A phenomenon is termed as “fetal origin of adult disease (FOoAD).” The Gap: It remains to be determined how exposure to air pollutants during early development contributes to the pathogenesis of adult disease. To test our hypothesis, we will collect cord blood from newborn babies who are exposed to air pollution in Shanghai city and who are not exposed to air pollution in Zhoushan city. We will then check methylation status of a target gene (Gipr; putatively imprinted) and other genomic regions using conventional bisulfite sequencing or reduced representative bisulfite sequencing. The resulted changes in DNA methylation will be correlated with expression changes for mechanistic insights of disease pathogenesis. Recruited subjects and their corresponding data of changes of methylation and RNA transcripts will be used for future studies and NIH grant applications.