Abstract

Background.Chronic obstructive pulmonary disease (COPD) is an inflammatory disease with predominant involvement of neutrophils, macrophages and CD8+ lymphocytes. Eosinophilic airway inflammations are reported in stable state and during acute exacerbations of tobacco smoke-associated COPD (TS-COPD). Women exposed to biomass fuel smoke are known to have eosinophils in sputum. However, little is known about the sputum cellular inflammatory profile in biomass fuel smoke-associated COPD (BMS-COPD). We therefore aimed to compare the sputum cellular inflammatory profile in tobacco smoke- and biomass smoke-associated COPD.Methods.The study was conducted in a tertiary care hospital in Goa, India. A total of 113 patients with stable COPD reporting to the outpatient pulmonary clinic were recruited. All participants were ≥ 40 years of age. Sputum induction studies were performed by the method of Pizzichini et al. after baseline subject characterization. Significant eosinophilia was defined as induced sputum eosinophils ≥ 3%.Results.There were 85 TS-COPD and 28 BMS-COPD patients. The mean age [standard deviation (SD)] was 64.7 (7.8) and 63.0 years (8.3), p = 0.32 in TS and BMS-COPD, respectively. Eighteen subjects (21.1%) were female smokers. The smoking pack-year median [interquartile range (IQR)] was 36 (20, 58) and hour-years of biomass smoke exposure mean (SD) was 192.4 (61). The TS-COPD and BMS-COPD cases showed a post-bronchodilator forced expiratory volume in one second (FEV1%) mean (SD) of 57.9 (17.1), and 62.6 (19.4), p= 0.22, respectively. Both groups had similar symptoms and severity of disease. Induced sputum total cell count per gram of sputum × 106 mean (SD) was 3.05 (1.53) for TS-COPD, and 2.55(1.37) for BMS-COPD p=0.12. The neutrophils % mean (SD) was 86.4 (16.5) and 87.9 (10.2), p = 0.64; eosinophils % median (IQR) was 2.5 (1, 10) and 8 (2, 12.8), p = 0.07; lymphocytes % median (IQR) was 0 (0, 0.75) and 0 (0, 1) p = 0.13; macrophages % median (IQR) was 2.5 (0.75, 5.7) and 1 (0, 4.7) p = 0.13; and significant eosinophilia (eosinophils ≥3%) was 42 (49.4%) and 20 (71%), p=0.04, for TS-COPD and BMS-COPD, respectively.Conclusions.For similar severity of disease and clinical symptoms, significant eosinophilic inflammation was observed in stable BMS-COPD, while both groups had similar neutrophilic inflammation.Participant Consent.Obtained.Ethics Approval.The study was approved by the Institutional Ethics Committee of the Goa Medical College, Goa, India.Competing Interests.The authors declare no competing financial interests.

Highlights

  • Chronic obstructive pulmonary disease (COPD) is a common disorder and is currently the third leading cause of death worldwide.[1]

  • The neutrophils % mean (SD) was 86.4 (16.5) and 87.9 (10.2), p = 0.64; eosinophils % median (IQR) was 2.5 (1, 10) and 8 (2, 12.8), p = 0.07; lymphocytes % median (IQR) was 0 (0, 0.75) and 0 (0, 1) p = 0.13; macrophages % median (IQR) was 2.5 (0.75, 5.7) and 1 (0, 4.7) p = 0.13; and significant eosinophilia was 42 (49.4%) and 20 (71%), p=0.04, for tobacco smoke-associated COPD (TS-COPD) and BMS-COPD, respectively

  • Significant eosinophilia 42 (49.4%), 20 (71%), p=0.04 was noted in TS-COPD and BMS-COPD cases, respectively

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is a common disorder and is currently the third leading cause of death worldwide.[1]. About 20-40% of patients with tobacco smoke-associated COPD (TS-COPD) have eosinophils in induced sputum during acute exacerbations and during clinical stability.[5,6,7,8] Inflammation is. Little is known about the sputum cellular inflammatory profile in biomass fuel smoke-associated COPD (BMS-COPD). The TS-COPD and BMS-COPD cases showed a post-bronchodilator forced expiratory volume in one second (FEV1%) mean (SD) of 57.9 (17.1), and 62.6 (19.4), p= 0.22, respectively Both groups had similar symptoms and severity of disease. For similar severity of disease and clinical symptoms, significant eosinophilic inflammation was observed in stable BMS-COPD, while both groups had similar neutrophilic inflammation.

Methods
Results
Conclusion

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