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A vision for greater use of experimental models to evaluate the role of genetic variability in environmental health and toxicology (Festing 2001) was outlined at the same time as the revolution in genome sequencing of humans and other species was taking place (Lander et al. 2001; Venter et al. 2001; Waterston et al. 2002). The Genes, Environment and Health Initiative established by the US Department of Health and Human Services and the National Institutes of Health in 2006 laid the foundation for investigating the interactions between environmental and genetic underpinnings of human disease by funding development of tools for genetic analysis and exposure biology. Several years later, the landmark study that sequenced the genomes of 15 mouse inbred strains (Frazer et al. 2007) opened the opportunity to link genetic variants to disease traits using the mouse, one of the principal experimental models in environmental health sciences and toxicology. Further analyses (Yang et al. 2007) revealed significant identity by descent between the homozygous inbred strains and the dominant contribution of laboratory-derived strains from Mus musculus domesticus. New population-based models have been created based on and aided by this refined understanding of mouse genetics (Churchill et al. 2012; Threadgill and Churchill 2012). Many studies have been published in the decade since that demonstrate the value of population-based testing and the power of genetics as an important dimension of environmental health science and toxicology (Harrill and McAllister 2017; Rusyn et al. 2010). This Special Issue of Mammalian Genome highlights a variety of topics broadly unified by the interest in the combined role of genetics and environment relevant to human disease outcomes. Population-based studies aiming to understand the relationship between inter-individual variation and environmental stressors are now being conducted in humans (Daly and Day 2012; Kwo and Christiani 2017), rodents (Rusyn et al. 2010), and other model organisms (Anholt and Mackay 2018). Importantly, many recent studies were designed to translate findings in model organisms to human disease susceptibility and draw mechanistic linkages that may help identify individuals who are sensitive to environmental exposures. For example, Jerry et al. (2018) demonstrate how quantitative trait loci (QTL) identified in studies of susceptibility to mammary tumors in estrogen-treated rats, together with surrogate biomarkers in humans, help explain gene by environment interactions and breast cancer risk posed by environmental xenoestrogens and endogenous estrogens. Anholt and Mackay (2018) use the model of D. melanogaster to highlight the opportunities to study environmental exposures and complex traits in a non-mammalian model organism. Despite major differences in genetic architecture and transcriptomes between flies and humans, the authors posit that the genetic underpinnings of complex traits can be represented as simplified gene networks in D. melanogaster on which human orthologues can be superimposed to provide blueprints for subsequent studies on analogous traits in human populations. Several reviews in this special issue demonstrate the role of inter-individual variability in health and disease associated with infections, lifestyle, and dietary factors. Verhein et al. (2018) review human, rodent, and in vitro association studies that identified biologically plausible gene candidates for susceptibility to pulmonary infections and disease severity, as well as how knowledge of these susceptibility factors can aid in novel strategies to prevent and treat disease that contributes to global morbidity and mortality attributed to respiratory infections. Vellers et al. (2018) used exercise * Ivan Rusyn IRusyn@cvm.tamu.edu

Introduction to mammalian genome special issue: the combined role of genetics and environment relevant to human disease outcomes