Asthma is a complex entity and one of the most common disorders in the world, affecting much of the workforce [1]. Asthma prevalence in children and adults has shown an increasing trend in the last decades [2], [3], which makes this disorder a major public health concern. Nevertheless, the mechanisms for the high incidence are not yet completely understood. In this regard, epidemiological studies focused on occupational asthma may contribute to unravelling the complexity of the disorder and the agents related to its onset and development. Work-related asthma has been classified as comprising two main entities: sensitiser-induced asthma and irritant-induced asthma (IIA) [4]. The first involves a specific immunological response to a workplace sensitiser. These sensitisers are high-molecular-weight agents acting via the production of specific IgE antibodies or low-molecular-weight chemicals acting via other, hitherto less clarified immunological pathways [5]–[8]. The term IIA refers to asthma caused by exposure to agents that, when inhaled, act as respiratory irritants in the absence of sensitisation [9], [10]. In the 1980s, Brooks et al. [11] described reactive airway dysfunction syndrome. This diagnosis required very strict criteria that restricted the syndrome to the onset of asthma-like symptoms within 24 h after a single, very high exposure to an irritant agent. However, further studies suggested that repeated exposure to lower levels of irritants may also play a role in the onset …