Epigenetics and chemical exposures

Seminal epidemiological studies led by Barker, Hales and collaborators identifying links between low birth weight and subsequent risk of traditionally adult-onset diseases such as cardiovascular disease and type 2 diabetes led to the concept of what is now termed the Developmental Origins of Health and Disease (DOHaD). This suggests that suboptimal exposures in early life (including the in utero period) permanently influence the structure, physiology, biochemistry and molecular biology of our organ systems and therefore our long-term health. Although the initial epidemiological observations almost 40 years ago focussed on the consequences of nutrient restriction during early life on long-term cardiometabolic health, the DOHaD field has now established a much broader spectrum of suboptimal exposures (including chemicals and environmental toxins) that affect a wide range of health outcomes (including certain forms of cancer and mental health). Epigenetic processes are thought to play an important mechanistic role in mediating the effects of a suboptimal in utero environment on long-term health. This includes changes in DNA methylation and histone modifications that regulate gene expression without affecting the DNA sequence. This special issue focuses on current knowledge on the impact of chemical exposures, such as heavy metals and endocrine disruptors, on the epigenome and long-term health outcomes, including mental health disorders, cardiovascular and neurodegenerative diseases.