The Role of Stable Free Radicals, Metals and PAHs of Airborne Particulate Matter in Mechanisms of Oxidative Stress and Carcinogenicity

Abstract

Ambient airborne particulate matter (PM) is considered as the most important pollutant for adverse health effects in the human respiratory system. PM is known to contain a large number of toxic and carcinogenic substances which in the lung’s alveoli cause oxidative stress, inflammation and cytotoxic damage leading to malignant neoplasms. Studies in recent years focused on transition metals, polycyclic aromatic hydrocarbons (PAH), stable quinoid and carbonaceous radicals. In the presence of oxygen and through redox reactions PM promote the production of reactive oxygen species (ROS), especially hydroxyl radicals (HO•), which are linked to lipid peroxidation and oxidative damage to peptides and cellular and mitochondrial DNA. In this study we investigated the most important mechanisms of ROS generation from airborne traffic-related PM, and exhaust soot from diesel and gasoline vehicles (DEP, GEP). Using Electron Paramagnetic Resonance (EPR) we examined the presence of persistent quinoid free radicals and we studied the direct production of superoxide anion (O2•− ), hydrogen peroxide (H2O2) and the damaging hydroxyl radicals (HO•) by PM extracts. Also, we examined by EPR the formation of oxidative damage to guanosine nucleobase by PM in aqueous phosphate buffer (pH 7.4). Experimental evidence shows that redox-active transition metals, persistent redox-cycling quinoids, and PAHs contained in the PM act synergistically, producing ROS. These ROS are considered the main mechanisms for the cytotoxic and carcinogenic potential of PM, leading to oxidative stress, pulmonary tissue injuries and DNA damage.