-Every year more than 13 million deaths worldwide are due to environmental pollutants, and approximately 24% of diseases are caused by environmental exposures that might be averted through preventive measures. Out of all these environmental chemicals, effects of air pollution is responsible for death of 3.3 million people prematurely worldwide -a figure that could double by 2050 if emissions continue to rise at the current rate. Increasing number of evidences has linked environmental pollutants with epigenetic variations, including changes in DNA methylation status, histone modifications and other factors like incorporation of miRNAs, nucleosome remodeling, etc. These entire mechanisms are likely to play important roles in disease aetiology, and their modifications, thus providing further understanding of disease aetiology, as well as biomarkers for these exposures to environmental chemicals and/or prediction of the risk for the disease. In this, we had tried to summarize the different epigenetic alterations related to environmental chemical exposures, and propose the probable mechanisms of action behind such epigenetic changes. We will also focus onopportunities, challenges and further directions for future epidemiology research in environmental epigenomics. Further studies are needed in this regard to solve methodological and practical challenges, including uncertainties about stability over time of epigenomic changes induced by the environment, tissue specificity of epigenetic alterations, validation of laboratory methods, and adaptation of bioinformatic and biostatistical methods to high-throughput epigenomics. Moreover, there are several reports of epigenetic modifications arising from environmental chemical exposures, but most have not been directly linked to disease endpoints.
CITATION STYLE
Ranjan, S., & Sharma, P. K. (2016). Effect of Environmental Chemical Exposures on Epigenetics of Diseases: A Systematic Review. International Journal of Life-Sciences Scientific Research, 2(4). https://doi.org/10.21276/ijlssr.2016.2.4.11
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