Pulmonary Toxicity and Environmental Contamination: Radicals, Electron Transfer, and Protection by Antioxidants

The pulmonary system is one of the main targets for toxicity. In the industrial age, there has been a large increase in atmospheric pollutants, including industrial products, particulates (asbestos and silica), cigarette smoke, ozone, nitrogen oxides, and substantial number of miscellaneous materials. In lung tissues, many adverse reactions result from exposure to these pollutants; some principal ones include asthma, chronic obstructive pulmonary disease (COPD), and cancer. The emphasis of this review is on three mechanisms by which many pulmonary toxicants, usually as derived metabolites, induce their effects: electron transfer (ET) (electron movement from one site to another), reactive oxygen species (ROS), and oxidative stress (OS), involving cellular insults. The preponderance of bioactive substances or their metabolites have chemical groups that we believe may play an important role in the physiological responses connected with induction of pulmonary toxicity. Such chemical functionalities include quinones (or their phenolic precursors), metal complexes (or complexors), aromatic nitro compounds (or reduced hydroxylamine and nitroso derivatives), and conjugated imines (or iminium species). © 2009 Springer-Verlag US.