Abstract
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.
Declaration of interest: The authors report no financial conflicts of interest.