Nitrogen dioxide (NO2), a gaseous air pollutant and reactive nitrogen species, has been widely studied using epidemiological methods and exposure has been associated with conditions such as respiratory disease, cardiovascular disease, and cancer. However, its toxicological mechanism is not fully understood. Pulmonary surfactant, the upper layer of the lung lining fluid, is the first point of contact for inhaled pollutants in the lung and therefore has been the subject of a number of investigations studying the effect of foreign particles on the lung. This thesis builds on this body of work, adapting existing biomolecular models of pulmonary surfactant to study the effect of NO2 on surfactant using computational chemistry methods that have been previously used to study air-water interfaces. Classical molecular dynamics simulations were run on atomistic-scale models of the PS monolayer to characterize the orientation with which NO2 interacted with biomolecules in the model. These simulations provided information about possible fields of reactivity between NO2 and biomolecules in the model, which was further explored using ab initio molecular dynamics simulations. Specifically, three pathways for the first step of the reaction between NO2 and two functional groups–the hydroxyl group of cholesterol and the thiol group of cysteine in surfactant protein B–were explored, and free energy surfaces were computed as a metric of the favorability of the selected reactions. Our classical molecular dynamics simulations established the feasibility of NO2 traversing the monolayer, allowing the gas molecules to interact with functional groups located far from the surface. The three-dimensional trajectories from these simulations were used to compute several metrics of adsorption between NO2 and the two functional groups of interest, and no significant difference between the groups was observed. In our ab initio molecular dynamics simulations, hydrogen abstraction from both the hydroxyl group in cholesterol and the thiol group in cysteine by NO2 was observed, yielding HONO(+) and alkoxy or thiolate anions, respectively. However, only the cysteine thiol pathway was found to be energetically spontaneous. Our findings provide computational validation for initial steps of toxicological pathways experimentally observed by others, but further benchmarking by additional computations and experimental work is required. Future work should explore the health implications of HONO(+) and of the functional group modifications observed to yield additional insight into the molecular mechanism by which NO2 impacts health.