• chronic rhinosinusitis;
  • smoking;
  • biomarkers;
  • inflammation;
  • asthma;
  • Staphylococcus aureus


Smoking negatively affects postoperative evolution in patients with chronic rhinosinusitis (CRS); however, the mechanism remains incompletely described. In the lung, smoking increases expression of proinflammatory genes and is associated with an elevation of inflammatory serum markers. Our objective is to determine the impact of smoking on these biomarkers in CRS.


Two existing populations of patients previously phenotyped for genetic association studies (206 patients with refractory CRS and 408 patients with CRS and nasal polyposis) were stratified according to self-reported smoking status and available serum biomarkers (complete blood count [CBC], total immunoglobulin E [IgE]). Asthma and bacterial cultures were evaluated.


Active smoking was low in both groups (genetics of chronic rhinosinusitis 1 [GCRS1]: 11.2%; genetics of chronic rhinosinusitis 2 [GCRS2]: 9.4%). Total white blood cell (WBC) count was significantly higher in active smokers than in those who had never smoked and ex-smokers. Serum eosinophilia and prevalence of self-reported asthma was lower in active smokers than never-smokers. In the GCRS2 population, endoscopically-collected cultures trended toward a lower recovery rate of Staphylococcus aureus in smokers (p = 0.07). Never-smokers and ex-smokers had similar levels of WBCs and eosinophils.


Our study reveals that active tobacco smoking is associated with increases in markers of systemic inflammation in patients with CRS. The proinflammatory effect of smoking seems not only to act locally on sinus mucosa as previously described, but may also influence levels of inflammatory biomarkers systemically, suggesting that smoking-induced changes have profound implications for health. Nevertheless, these changes may be potentially reversible; thus smoking cessation in CRS patients is strongly advised, and may have an impact on response of CRS to therapy.