Histopathologic Influences of Comorbid Smoking Status in Chronic Rhinosinusitis.

BACKGROUND

Smoking status has been established as a known irritant of the upper and lower respiratory tracts, leading to inflammation throughout the respiratory system. Tobacco smoking is one comorbidity encountered among chronic rhinosinusitis (CRS) patients. The histopathologic features of CRS and comorbid smoking status have yet to be determined by structured histopathology and may have important implications on disease management.

METHODS

Retrospective study of structured histopathology reports analyzing sinus tissue removed during functional endoscopic sinus surgery. Histopathology variables were compared among patients with CRS who were reported as never smokers, former smokers, or current smokers.

RESULTS

A total of 285 CRS patients were included: 173 never smokers, 85 former smokers, and 27 current smokers. When compared with former smokers, current smokers demonstrated increased basement membrane thickening (88.9% vs 67.1%, <.020). Compared with never smokers, former and current smokers collectively demonstrated increased hyperplastic changes (14.3% vs 6.9%,  < .035), increased squamous metaplasia (26.8% vs 17.3%,  < .040), and trends toward increased basement membrane thickening (72.3% vs 65.3%,  < .124) and increased fibrosis (47.3% vs 40.5%,  < .154).

CONCLUSION

Smoking status may influence histopathologic tissue-level changes in CRS disease. Interestingly, former and current smokers maintained few differences in histopathology. However, former and current smokers collectively demonstrated increased chronic inflammatory changes compared with never smokers. These findings suggest that the timing of smoking exposure has limited effect on the tissue level, rather exposure overall influences inflammatory change. These findings may have important implications on medical and surgical management of CRS disease and comorbid smoking status.