Exposome

The exposome encompasses the totality of human environmental (i.e. non-genetic) exposures from conception onwards, complementing the genome. It was first proposed by Dr. Christopher Wild, a cancer epidemiologist, in a 2005 article entitled "Complementing the Genome with an “Exposome”: The Outstanding Challenge of Environmental Exposure Measurement in Molecular Epidemiology". The concept of the exposome and how to assess it has led to lively discussions with varied views. Although at this stage it may not be possible to measure or model the full exposome, some recent European projects such as HELIX, EXPOsOMICS, and HEALS and the American initiative HERCULES have started to make first attempts.

In his 2005 article Wild stated, "At its most complete, the exposome encompasses life-course environmental exposures (including lifestyle factors), from the prenatal period onwards." The concept was first proposed to draw attention to the need for better and more complete environmental exposure data for causal research, in order to balance the investment, tools and knowledge in genetics. Wild also stated that even incomplete versions of the exposome could be of great use to field of epidemiology. Wild published a follow-up paper in 2012 where he outlines methods, including personal sensors, biomarkers and 'omics' technologies, to better define the exposome. He has described three overlapping domains within the exposome:

More recently, G.W. Miller and D. P. Jones proposed a revised definition of the exposome that explicitly incorporates the body's response to environmental influences and also includes the endogenous metabolic processes that can alter or process the chemicals to which humans are exposed. This definition is explained in greater depth in the new book by G.W. Miller entitled "The Exposome: A Primer" published by Elsevier in late 2013. This introductory text is the first book on the exposome and explores the gene versus environmental argument.

For complex disorders specific genetic causes appear to only account for 10-30% of the disease incidence, although as genomic approaches improve this percentage could increase. Environmental influences contribute to human disease, but unlike with genetics, there is no standard or systematic way to measure the influence of environmental exposures. Some studies, such as those by C. J. Patel et al into the interaction of genetic and environmental factors in the incidence of diabetes have demonstrated that environmental-wide association studies (EWAS, or exposome-wide association studies) may be feasible. However, it is not clear what data sets are most appropriate to represent the value of "E".

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