Not only did more than 2,753 individuals pass away the morning of September 11,2001, but there have been individuals suffering from mental and physical illness ever since. Thousands of individuals suffered from breathing complications, asthma, and lung cancer. Clinical trials on cancer patients, including a patient who was exposed to the World Trade Center Dust (WTCD), have seen a decrease in the progression of tumor growth with use of oral nicotinamide adenine dinucleotide (NADH). NADH is naturally occurring within a cell's mitochondria and aids in the production of adenosine triphosphate (ATP), the energy of the cell. NADH is an anti-aging, energy enhancing, substance that also reduces fatigue and successfully treats degenerative medical conditions. NADH is becoming a possible treatment for tumor regression but it is still unknown, on a cellular level, why NADH reacts with these cells to prevent further tumor growth. In this study, the amount of NADH produced by normal MRC-5 lung fibroblast cells will be compared to lung cells exposed to World Trade Center Dust (WTCD), using a Promega NAD/NADH-Glo Assay. The same cells will be evaluated to note the decline in Glutathione to determine the amount Reactive Oxidative Species ( ROS) brought on to lung cells by WTCD. ROS can decrease GSH levels by causing oxidative stress that leads to apoptosis. It is important for the cells to maintain high levels of reduced GSH and low levels of oxidized GSH. PROMEGA GSH Glo Glutathione assay will be used to determine if the toxic, mutagenic and apoptotic effects of WTC dust can be shown as the result of oxidative stress. The cells will be exposed to various concentrations of WTCD, ranging from 25-250 ppm. It is hypothesized that the cells with the highest concentrations of this toxic particulate matter will experience the most accumulation of oxidative stress, resulting in less NAD+, being reduced to NADH, within the mitochondria and simultaneous decrease in protective antioxidants as shown in changes in levels of Glutatione. This should allow correlations to be made on a more precise cellular mechanism between exposure to this WTCD, oxidative stress, and loss of mitochondrial function seen in the diseases of the exposed first responder population. Citation Format: Ann Marie DiLorenzo, Lara Seder, Rebekah Madrid, Eric Tobias, Jonathan Ortiz, Vern Gatson. Loss of mitochondrial function and increases in levels of oxidative stress pinpointed in human lung cell cultures exposed to particulate matter from September 11, 2001 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2447.