Gene inflammatory expression profiling in right versus left ventricles in young urbanites: what is the long‐term impact of myocardial inflammation in the setting of air pollution?

Abstract

Increased cardiac morbidity and mortality are associated with air pollution. Mexico City (MC) residents are exposed to high concentrations of fine particulate matter and endotoxin. South MC residents are exposed to higher endotoxin v North (Rosas 2007). SMC exposed mice had the highest CD14 and IL1beta mRNA in myocardium v N (Villarreal 2009). To test the hypothesis that residency within MC is a key factor for the degree of myocardial inflammation, we measured inflammatory mediator genes in autopsy samples from R and L ventricles of 6 South and 15 North age‐matched MC residents 18.5±5.2y. South residents had significant up‐regulation of CD14, IL1beta and TNFalpha v North (p<0.001). An anti‐inflammatory biventricular response was also present: IL10 (RV p=0.001, LV p=0.02). Increases in myocardial IL1beta and TNFalpha have been implicated in the pathogenesis of myocardial dysfunction and cardiomyocyte death in ischemia‐reperfusion injury, sepsis, chronic heart failure, etc. Exposure to polluted urban air is associated with myocardial inflammation in young people, the RV responds differently from the LV and endotoxin is a key player in the inflammatory response. Occult cardiotoxicity (Golomb et al., 2009) may be a deleterious effect in young urbanites and the long‐term impact of sustained myocardial inflammation is uncertain.