The
particulate matter present in air pollution is a
complex mixture of solid and liquid particles that vary in size, origin, and composition, among which are
polycyclic aromatic hydrocarbons (PAHs). Although exposure to PAHs has become an important risk factor for
cardiovascular disease, the mechanisms by which these compounds contribute to increased cardiovascular risk have not been fully explored. The aim of the present study was to evaluate the effects of PAH exposure on systemic pro-inflammatory
cytokines and markers of endothelial dysfunction. An intervention was designed using a murine model composed of twenty BALB/c male mice separated into controls and three groups exposed to a mixture of
phenanthrene,
fluoranthene, and
pyrene using three different concentrations. The serum levels of the inflammatory
cytokines and gene expression of adhesion molecules located on endothelial cells along with inflammatory markers related to PAH exposure in aortic tissue were determined. Furthermore, the expression of the
ICAM-1 and
VCAM-1 proteins was evaluated. The data showed significant differences in
IL-6 and IFN-γ in the serum. In the gene expression, significant differences for
ICAM-1,
VCAM-1, and
E-Selectin were observed. The results suggest that
phenanthrene,
fluoranthene, and
pyrene, present in air pollution, stimulate the increase in serum inflammatory
cytokines and the expression of markers of endothelial dysfunction in the murine model studied, both relevant characteristics associated with the onset of disease
atherosclerosis and
cardiovascular disease.