Many noncommunicable diseases, such as atherosclerosis and other cardiometabolic diseases, are defined as inflammatory diseases, which suggests that multifactorial interactions linked to exacerbated disease pathology include pro-inflammatory chemical and nonchemical stressor. Recent data suggest that genetic and lifestyle factors are independently associated with susceptibility to cardiovascular diseases (Khera et al., 2016;Satija et al., 2018;Tong, 2016). Thus, potential biological interactions between chemical and nonchemical stressors and buffers and other lifestyle factors will determine disease outcome. Chemical stressors include environmental pollutants with pro-oxidant and pro-inflammatory properties, such as air pollutants, both gaseous and particulate matter, and persistent organic pollutants, such as dioxinlike polychlorinated biphenyls (PCBs). Many persistent organic pollutants also have an affinity for the aryl hydrocarbon receptor (AhR).AhR ligands lead to induction of cytochrome P450s and free radical formation, followed by inflammation. For example, dioxin-like PCBs can increase endothelial cell dysfunction, activation, and inflammation (e.g., increased adhesion molecule expression and cytokine production)