Cardiovascular disease (CVDs) is the major cause of morbidity, mortality, and health care costs in the United States, and around the world. Atherosclerosis is the common cause of CVDs, and it results from the build-up of plaques (e.g., fat, cholesterol, etc.) within the arterial walls, narrowing the arterial lumen, and restricting the amount of blood flow. Vascular cells are central players in maintaining homeostatic balance and mediating pathogenic processes in the cardiovascular system. These cells determine the diameter, permeability and flow rate in blood vessels. As regulators of leukocyte extravasation during inflammation, vascular cells including endothelial cells and macrophages are among the key components of the development of atherosclerosis. Among the various risk factors of atherosclerosis, environmental chemical exposures, has recently been recognized as a potential contributor towards human atherosclerotic development. The Jia molecular Toxicology lab at UNC-Greensboro is focused on investigating environmental chemical-induced vascular inflammation and injury. We have a special interest in understanding the possible signaling mechanisms involved, and the amelioration of toxicity associated with oxidative stress and inflammation. The environmental chemicals of interest include Benzo[a]pyrene -1,6-quinone (BP-1,6-Q), acrolein and microplastics and nanoplastics (M-NPLs). In line with this research, funded by the NIH, we are also actively investigating the molecular mechanism(s) of the pharmacological agents/novel bioactive compounds that target and reduce toxic chemical-mediated cardiovascular inflammation. Our approaches include cell- and molecular biology techniques and physiologically relevant animal models.