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The susceptibility to develop non-communicable diseases, like cardiovascular disease and cancer, depends on an interplay between the genes and the environment. Extrinsic factors, such as maternal stress hormones, dietary constituents, and endocrine disruptive chemicals, are known to affect fetal development and later disease phenotypes. Many of these factors have been shown to modify the epigenetic landscape during development, with a consequent change in the adult phenotype. Whether fetal exposure to adverse conditions leads to the epigenetic changes underlying non-communicable diseases in humans is an intensively studied question. In this chapter, we discuss the possible involvement of environmental factors, in particular endocrine disruptive chemicals, in shaping human health and risk of disease through epigenetic mechanisms. We start by describing different mechanisms to code epigenetic information and then move on to discussing how early life influences can affect this coding and what kind of consequences it can have on the phenotype level. Finally, we will describe the mechanistic principles by which endocrine disruptors could affect the epigenetic machinery.

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