Abstract Rationale Fractional exhaled nitric oxide (FeNO) is a biomarker of type 2 airway inflammation but is suppressed by active smoking. The dynamics and timeline of FeNO recovery after smoking cessation remain poorly characterized in the general population. Methods We analyzed 13,474 adults aged 18-80 years from NHANES 2007-2012 with valid FeNO measurements and complete smoking histories. Smoking status was categorized as current, former, or never smoker. For current and former smokers, years since smoking initiation or cessation were calculated. FeNO was measured using the NIOX MINO analyzer at 50 mL/s per ATS/ERS standards. Associations between FeNO and smoking history were examined using unadjusted analyses and multivariable linear regression adjusted for age, sex, BMI, blood eosinophil count (BEC), asthma, and COPD. Predicted FeNO values were estimated via marginal effects. Stratified analyses were performed by BEC (≤300 or 300 cells/μL) and by disease status. Asthma was defined as self-reported physician-diagnosed asthma and COPD as post-bronchodilator FEV1/FVC 0.7 with ≥10 pack-years. Results Of the participants, 53.8% were never, 23.0% former, and 23.2% current smokers. Current smokers had the lowest FeNO (mean 11 ppb) and the highest prevalence of COPD (8.3%) and asthma (16.4%). Former smokers showed lower FeNO immediately after quitting, with gradual recovery to never-smoker levels after ∼7 years in unadjusted models (Figure 1A) and ∼4 years after adjustment (Figure 1B). FeNO declined progressively with smoking duration in current smokers, plateauing after ∼20 years in unadjusted (Figure 1A) and adjusted models (Figure 1B). Among those with BEC 150 cells/μL, recovery was slower (≈19 years) and the decline during active smoking steeper (Figure 1D) compared to those with BEC ≤ 150 cells/μL (Figure 1C). Pack-years strongly influenced FeNO suppression in current smokers but not in former smokers (Figure 1E). In disease-stratified analyses, FeNO was higher in asthma (both current and former smokers), whereas in COPD, FeNO was higher in former but lower in current smokers compared with participants without airway disease (Figure 1F). Conclusions FeNO suppression and recovery vary substantially by smoking intensity, eosinophil phenotype, and chronic airway disease status. These findings highlight the need for smoking history-specific reference ranges when interpreting FeNO in asthma and COPD to improve the detection of eosinophilic inflammation. This abstract is funded by: None
Abohalaka et al. (Fri,) studied this question.