Atelectasis due to decreased surfactant in lungs
Long-term exposure to excessive oxygen will lead to damage in pulmonary tissue. This damage resembles the same damage which is seen in patients with Acute Respiratory Distress Syndrome (ARDS). In these patients surfactant specific proteins are damaged by proteolysis. This proteolysis is caused by the neutrophil elastase enzyme, after a massive influx of activated neutrophils. 

The damage done by exposure to excessive oxygen is thought to be done by Reactive Oxygen Species (ROS). 


  Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen...


These ROS can cause oxidative damage to DNA, RNA and proteins. They can form covalent bonds between molecules in the surfactant, thus inactivating them. Damaging of molecules can lead to cellular damage, causing ROS-mediated necrosis or apoptosis. Therefore there will be less surfactant production possible. 

Also interestingly: 


  An important feature of pulmonary oxygen toxicity is that it is almost impossible to distinguish from damage caused by other lung injury processes. Consequently, it is unclear whether deterioration of lung function during high concentration oxygen therapy is due to worsening of the primary disease process or to oxygen-free radical-induced damage; the administration of high concentration oxygen may be perpetuating lung injury in some patients.


So in patients who undergo long-term 100% oxygen exposure, for example due to lung problems, the problems could be perpetuated or even worsened due to oxygen therapy and the oxidative stress caused by it.