There has been a marked increase in the global prevalence, morbidity, and mortality of asthma, and its associated economic burden has also grown over the last 40 years. Approximately 300 million people worldwide currently have asthma, and its prevalence increases by 50% every decade. Airway inflammation is the most proximate cause of the recurrent episodes of airflow limitation in asthma. Recent research has revealed that numerous biologically active proinflammatory mediators are responsible for the pathogenesis of asthma. Among these mediators, there is increasing evidence that endogenous or exogenous reactive oxygen species (ROS) and reactive nitrogen species (RNS) are responsible for the airway inflammation of asthma. Many reports have shown that there is an excessive production of ROS and RNS in the airways of asthmatic individuals compared with healthy subjects. Excessively produced ROS and RNS have been reported to lead to airway inflammation, airway hyper-responsiveness, airway microvascular hyperpermeability, tissue injury, and remodeling in animal models and human studies. Although human lungs have a potent antioxidant system, excessive oxidative and nitrative stress leads to an imbalance of oxidants/antioxidants. This review describes the rapidly accruing data linking oxidative and nitrative events to the pathogenesis of bronchial asthma.