The following is a summary of “Impact of former smoking exposure on airway eosinophilic activation and autoimmunity in patients with severe asthma” published in the October 2022 issue of Respiratory by Klein et al.

Severe eosinophilic asthma has frequent flare-ups and doesn’t respond as well to steroids. Experiments show that smoking can cause eosinophilic airway inflammation, but it’s unclear what this means for people with severe asthma. The goal was to find out if there was a link between smoking and eosinophilic inflammation and activation, as well as airway autoimmunity and steroid responsiveness, in people with severe asthma. Patients with severe asthma, as defined by the European Respiratory Society and the American Thoracic Society, had their sputum samples looked at for free eosinophil granules (FEGs), autoantibodies against eosinophil peroxidase (EPX), and macrophage receptors with collagenous structures (MARCO).

After taking prednisolone for two weeks, a subgroup of patients with eosinophilic airway inflammation was looked at again. The study looked at 132 people with severe asthma. 39 (29.5%) of the patients had a smoking history of more than equal to 10 pack-years. Of these, 36 (27.3%) were former smokers, and 3 (2.3%) were current smokers. Another 93 (70.5%) had a smoking history of less than 10 pack years. Eosinophilic airway inflammation was more common in patients with 10 pack-years (66.7%) than in patients with less than 10 pack-years (38.7%, P=0.03). The same was true for the level of FEGs (P=0.001) and both anti-EPX and anti-MARCO (P<0.05 and P<0.0001, respectively).

Leaving out current smokers didn’t change these links. Also, prednisolone decreased the number of eosinophils in sputum, but it did not bring them back to normal in people who had smoked for more than equal to 10 pack years. A history of smoking is linked to eosinophilic airway inflammation and activation, a lack of response to steroids, and airway autoimmunity in people with severe asthma.