An Overview of the Environmental Genome Project

Understanding the causes of common diseases such as cancer, asthma, diabetes, hypertension, and atherosclerosis, which have high population prevalence, is a significant priority for public health research and a major goal in biomedical studies. The influences on susceptibility to common disease are thought to arise from multiple factors, each conferring a low level of relative risk for disease. These low levels of disease risk probably reflect interactions between genotypes at multiple loci (epistasis), interactions between genotypes and environment, and more stochastic epigenetic events such as methylation (Belinsky 2004; Berwick 2000; Hayward 2003; Hegele 1997). Because the risk of any given effect is small (Lander and Schork 1994; Moffatt and Cookson 1999; Pritchard and Cox 2002; Reich and Lander 2001; Risch and Merikangas 1996), detecting these influences will require larger sample sizes, making populationbased association studies more practical for tracing the underlying genetic risks (Risch and Merikangas 1996). Association studies will also be key for exploring genetic links to environmental exposures (Bell and Taylor 1997). In 1997 Dr. Kenneth Olden, director of the National Institute of Environmental Health Sciences (NIEHS), convened a historic conference titled “The Environmental Genome Project” held 17–18 October 1997 in Bethesda, Maryland. This symposium explored the feasibility of the Environmental Genome Project (EGP) and generated significant discussion. The EGP is designed to explore the relationship between common genetic polymorphisms and environmentally induced disease in human populations E s s a y o n The Environmental Genome Project