Leukocyte counts in hypertonic saline-induced sputum in subjects with occupational asthma.

We measured markers of eosinophilic inflammation in the blood and in the sputum induced by hypertonic saline (HS) inhalation of 24 subjects with occupational asthma who were still exposed to high molecular weight compounds (HMWCs, n = 8) or to low molecular weight compounds (LMWCs, n = 16); all subjects were symptomatic and showed bronchial hyperresponsiveness to methacholine at the time of study. Sputum cell counts were also measured in 14 normal subjects and in 24 subjects with non-occupational asthma with asthma severity similar to that of occupational asthmatics. Both occupational and non-occupational asthmatic subjects showed higher neutrophil percentages in HS-induced sputum than normal subjects, asthmatics with LMWC-induced asthma showing the highest values. Eosinophil percentages in HS-induced sputum were higher in non-occupational asthmatics and in asthmatics with HMWC-induced asthma than in normal subjects and in subjects with occupational asthma due to LMWCs. No difference in bronchial responsiveness, peak expiratory flow variability and serum eosinophil cationic protein (ECP) levels were observed among the different asthma groups. Although sputum eosinophil percentages significantly correlated with blood eosinophil percentages, sputum allowed the detection of a higher number of subjects with eosinophilic inflammation than blood. Serum ECP levels were normal in most asthmatic subjects. A significant correlation between sputum eosinophil percentages and bronchial hyperresponsiveness to HS was observed. Despite a similar degree of functional abnormalities, subjects with asthma due to LMWCs and still exposed to the occupational sensitizer showed a lower degree of eosinophilic inflammation and a higher degree of neutrophilic inflammation in the airways than subjects with occupational asthma due to HMWCs or non-occupational asthmatics. Furthermore, sputum eosinophil counts detect, better than blood indices, the degree of airway inflammation in both occupational and non-occupational asthma.