INTRODUCTION: Severe eosinophilic asthma is characterised by frequent exacerbations and a relative insensitivity to steroids., Experimentally, smoking may induce eosinophilic airway inflammation, but the impact in patients with severe asthma is not clear.

OBJECTIVE: To investigate the association between smoking exposure in patients with severe asthma, and eosinophilic inflammation and activation, as well as airway autoimmunity and steroid responsiveness.

METHODS: Patients with severe asthma according to ERS/ATS criteria were assessed with sputum samples, analysed by cell differential count, and for the presence of free eosinophil granules (FEGs), autoantibodies against eosinophil peroxidase (EPX) and macrophage receptor with collagenous structure (MARCO). A subgroup of patients with eosinophilic airway inflammation was re-assessed after a 2-weeks course of prednisolone.

RESULTS: A total of 132 severe asthmatics were included in the study; 39 patients (29.5%) had ≥10 pack years of smoking history; 36 (27.3%) were former smokers and 3 (2.3%) current smokers, and 93 (70.5%) had <10 pack years exposure. Eosinophilic airway inflammation was more prevalent among patients with ≥10 pack years (66.7%), compared to patients with <10 pack years (38.7%, p=0.03), as was the level of FEGs (p=0.001) and both anti-EPX and anti-MARCO(p<0.05 and p<0.0001, respectively). Omitting current smokers did not affect these associations. Furthermore, prednisolone reduced, but did not normalise, sputum eosinophils in patients with a ≥10 pack years smoking history.

CONCLUSION: In patients with severe asthma, a former smoking history is associated with eosinophilic airway inflammation and activation, relative insensitivity to steroids, as well as airway autoimmunity.