Airborne Particulate Matter and Increased Risk of Lung Cancer- Mechanisms of Carcinogenesis by Reactive Oxygen Species and the Role of Oxidative Stress

Urban air pollution has been one of the most important pollution problem for many decades. Airborne particulate matter (PM) from combustion sources is considered the most important air pollutants for adverse health effects to humans, especially for acute and chronic respiratory diseases and lung cancer. Airborne particles contain a number of toxic and carcinogenic substances as well as persistent free radicals entering the lung's alveoli. PM in the lungs can generate free radicals and reactive oxygen species (ROS), initiating mechanisms of oxidative stress, inflammation and mutagenic damage to cellular DNA. These conditions lead progressively to increased morbidity and mortality as well as to increased risk of lung cancer. In the last decades a number of studies investigated PM size focusing to PM with aerodynamic diameter below l0 μm (ΡM10 and ΡΜ2.5), transition metals, polycyclic aromatic hydrocarbons (ΡΑΗ), stable quinoids αnd carcinogenic nitropyrenes. ROS generated by PM are linked to the pathogenesis of pulmonary oxidative damage, lipid peroxidation, damages to enzymes and cellular DNA. In our experimental study we investigated ROS generation by airborne PM (exhaust soot diesel and gasoline) by Electron Paramagnetic Resonance (EPR) and persistent free radicals characteristic to a mixture of semiquinone radicals. Also, we examined by EPR the formation of oxidative damage to guanosine nucleobase. by PM in aqueous phosphate buffer (pH 7.4) and the formation of the cancer biomarker 8-hydroxy-2'-deoxyguanosine.