Clinical and functional characteristics of chronic obstructive pulmonary disease among smokers and never-smokers: a retrospective cross-sectional observational study at a specialist center in Guayaquil, Ecuador, 2023–2025

Abstract Background Chronic obstructive pulmonary disease (COPD) also occurs in people who have never smoked, particularly in settings where pulmonary tuberculosis and household biomass exposure remain common. We aimed to compare clinical and functional characteristics of smokers and never-smokers with established COPD and to determine whether tuberculosis and biomass exposure were independently associated with post-bronchodilator lung function. This retrospective cross-sectional study included 156 adults with spirometry-confirmed COPD treated at a specialist respiratory center in Guayaquil, Ecuador, during 2023–2025. Results Eighty-two participants (52.6%) were never-smokers and 74 (47.4%) were smokers. Never-smokers had a lower mean age than smokers (64.9 ± 13.9 vs. 70.9 ± 12.7 years; p = 0.005) and were more frequently female (54.9% vs. 24.3%; p < 0.001). Prior pulmonary tuberculosis (74.4% vs. 33.8%; OR 5.69, 95% CI 2.85–11.37) and biomass exposure (34.1% vs. 14.9%; OR 2.97, 95% CI 1.35–6.52) were more common among never-smokers. Unadjusted post-bronchodilator FEV₁ was lower in never-smokers (58.1 ± 19.7% vs. 67.0 ± 24.3% predicted; mean difference − 8.88% points, 95% CI − 15.92 to − 1.83; p = 0.014). Across seven mutually exclusive exposure patterns, FEV₁ differed overall (ANOVA p = 0.011; Kruskal–Wallis sensitivity p = 0.007). In multivariable linear regression with HC3 robust standard errors, smoking status was not independently associated with FEV₁ (β = 0.56, 95% CI − 8.70 to 9.83; p = 0.906). In the overall cohort, prior tuberculosis (β=−10.00, 95% CI − 19.80 to − 0.20; p = 0.045) and biomass exposure (β=−10.49, 95% CI − 19.72 to − 1.26; p = 0.026) were associated with lower FEV₁ after multivariable adjustment. Prior tuberculosis was also associated with GOLD grade 3–4 airflow obstruction in a secondary adjusted model (aOR 2.61, 95% CI 1.04–6.58; p = 0.041). Conclusions In this specialist COPD cohort, never-smokers had a distinct exposure profile characterized by substantially more previous pulmonary tuberculosis and biomass exposure. The unadjusted difference in FEV₁ by smoking status was attenuated after adjustment, and smoking status was not independently associated with FEV₁. In analyses of the overall cohort, prior tuberculosis and biomass exposure were associated with lower FEV₁; these associations should not be interpreted as evidence of causality or as demonstrating a tuberculosis-specific effect among never-smokers. These findings support systematic assessment of non-tobacco respiratory exposures in patients with COPD and warrant confirmation in larger prospective studies.