Diesel exhaust (DE) is associated with triggering acute myocardial infarction. Furthermore, DE can induce and exacerbate hypersensitivity responses, amplify the production of a variety of chemokines and cytokines, facilitate interactions between inflammatory cells and act as allergen transporter. Therefore Kounis syndrome Type I which includes patients with normal coronary arteries, and Type II variant which applies to individuals with quiescent preexisting atheromatous disease can be the result of these hypersensitivity processes.