ABSTRACT

Occupational eosinophilic bronchitis is regarded as a variant syndrome of occupational asthma (OA) because respiratory symptoms, predominantly cough, are associated with changes in sputum eosinophil counts related to the exposure to a specific agent present at the workplace. The pathophysiological mechanisms involved in the development of occupational eosinophilic bronchitis remain largely incertain. Non-occupational, non-asthmatic eosinophilic bronchitis (NAEB) and asthma share common pathophysiologic features but NAEB is characterized by a lower degree of airway wall thickening, lower numbers of mast cells infiltrating the airway smooth muscle, lower levels of sputum interleukin (IL)-13 and higher sputum concentrations of prostaglandin (PG)E2 compared to asthma. A number of high-molecular-weight(HMW) and low-molecular-weight (LMW) workplace sensitizing agents have been documented as causing occupational eosinophilic bronchitis in case reports. The prevalence of occupational eosinophilic bronchitis remains unknown but in a recent multicenter retrospective analysis of 259 subjects who underwent specific inhalation challenges that were negative in terms of airway obstruction, 13% had a significant (≥3%) increase in sputum eosinophils after exposure (Wiszniewska M et al. JACI in practice, in press). Coughing is the characteristic symptom although other asthma-like symptoms are also present. Occupational eosinophilic bronchitis should be suspected in every adult with new-onset chronic cough or respiratory symptoms that are induced or worsened by their workplace In patients with ascertained occupational eosinophilic bronchitis, avoidance of exposure to the causal agent is by far the most sensible therapeutic option, although evidence supporting this approach is currently lacking.