Disease risk is governed by a complex interaction of hereditary and environmental factors. The modern revolution in genetic sequencing has dramatically expanded our knowledge of inherited genetic factors, while simultaneously promoting a silent bias toward overestimating the contribution of genetics to disease risk. The importance of environmental contributions to psychiatric disorders is illustrated by genetic studies that clearly cannot account for the majority of disease risk [1, 2]. We are now approaching a tipping point in the technology available to measure the sum total of all environmental exposures, referred to as the “exposome”, which promises to represent the vast environmental space in equal proportion to the hereditary space [3].

A growing body of evidence links diverse elements of the environment to psychiatric disease. This includes environmental factors writ large, including local ecosystems, lifestyle choices, social factors, life experiences, and the physical environment; and the environment writ small, referring to exposures to toxic and non-toxic chemicals [3]. The vast majority of research on environmental exposures contributing to psychiatric disease focuses on individual candidate exposures and evaluates the effects relative to a small number of outcomes of a priori interest. While limited, this approach has yielded results of vast scientific importance. As an example, risk for autism and developmental delay has been linked to air pollution, heavy metals (such as lead), pesticides, phthalates, and polychlorinated biphenyls; medications such as valproic acid; and nutritional factors such as iron and folic acid [4].

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