Data from nine longitudinal studies showed a population attributable fraction for the occupational contribution to incident asthma of 16%. The main phenotypes of occupational asthma are: occupational asthma caused by high-molecular-weight (HMW) or low-molecular-weight (LMW) agents, irritant-induced asthma and occupational asthma-chronic obstructive pulmonary disease overlap. Among the variety of causative agents of occupational asthma, food-derived components are increasingly being reported, accounting for up to 25% cases of occupational asthma and/or occupational rhinitis. Recently, a specific inhalation challenge (SIC)-independent model has been developed to calculate the probability of occupational asthma diagnosis in workers exposed to HMW agents. In this model, work-specific sensitization, bronchial hyperresponsiveness, inhaled corticosteroid use, rhinoconjunctivitis and age 40 years or less were the most relevant predictive factors. Specific IgE measurements showed a pooled sensitivity of 0.74 and a specificity of 0.71 in the diagnosis of occupational asthma for HMW agents, while a lower sensitivity (0.28) and a higher specificity (0.89) was shown for LMW agents. Cessation of exposure to workplace sensitizers is the cornerstone of management of work-related conditions.
An early and precise diagnosis of occupational asthma is crucial, allowing appropriate management and implementation of preventive strategies.