Molecular Markers Associated with the Biological Response to Aromatic Hydrocarbons from Urban Air in Humans

Morbidity and mortality attributable to air pollution continue to be a growing problem in several parts of the world. Both epidemiologic and clinical studies have demonstrated a strong link between exposure to particulate matter (PM) and adverse effects on health. From the PM generated in the atmospheres of several countries, the respirable fraction of PM2.5 (PM2.5) and diesel exhaust particles (DEP) represent some of the largest products of vehicularand industrial-emitted airborne PM that can persist in the air, where they are readily inhaled and deposited throughout the respiratory tract. PM2.5 and DEP have been associated with cardiac and pulmonary alterations. Also, exposure to DEP has been associated with lung cancer, pulmonary inflammation, an increased susceptibility to respiratory infections and the exacerbation of asthma and chronic obstructive pulmonary diseases. Furthermore, the effect of tobacco and its smoke, a complex mixture, represents another source of polycyclic aromatic hydrocarbons (PAH). The three, PM2.5, DEP and tobacco smoke, are the main foci of several studies that evaluate the principal effects of PAH, and represent the via to/source of PAH exposure. Normally, black carbon particles, also products of incomplete fuel combustion, act as condensation nuclei for organic chemicals, such as aromatic aliphatic compounds, including PAH, but they are not considered in this chapter. Rather, this chapter will centre on a molecular description of the cellular responses (AHR pathway) after exposure to PAH from urban air, including relatively new markers, microRNAs and their utility as new biomarkers of exposure to PAH. We propose the use of lung tissue embedded in paraffin as a source of biological material to perform any kind of study: retrospective and prospectives. First, however, an important general description of PAH, its main sources and its concentrations in urban air and their metabolism will be presented in order to contextualize the main objective of this study of molecular markers associated with PAH exposure.