Oxidative stress to the lung leads to cellular DNA damage as evidenced by the release of specific gene products known to regulate DNA base excision repair pathways such as p53 and p21 [29] [30] [31] . Alterations in pro-inflammatory mediators, transcription factors, and other related gene products are also observed [32] . This injury has been shown to be associated with features of both cellular necrosis and apoptosis [33] [34] [35] . The resultant cellular inflammation and death from oxidative stress has a dramatic impact on the outcome of patients in the clinical setting [7, 36] .