I don't believe that there is an established threshold for oxygen free radical concentrations to produce damage to the lung epithelium.  My students have shown that cigrette smoke exposure, equivalent to a pack a day smoker, induced autophagy in ovarian granulosa cells in the absence of apoptosis. We suggest that dysregulation of reparative autophagy through chronic exposure to oxidative stress is a potential novel or alternative cell death pathway. Ongoing studies in my lab reveal that similar effects are seen in the lung epithelium. These are preliminary results that we hope to expand on for publication in the coming month. From this I encourage consideration of acute vs. chronic ROS exposure which likely will require different concentrations to induce adverse effects on the lung epithelium and thus will produce different threshold values. Moreover, the mechanisms may also be quite different in both scenarios.  

A possible quantification is the generation of nitrotirosine from tirosine and peroxinitrite.

It is not possible to evaluate directly the amount of radicals generated iin or autside cells.

Imunostaining of nitrotirosine is useful.

Dr F G Frunza