© 2006 American Thoracic Society
Nonspecific Triggers Also Provoke Occupational AsthmaFrom the Authors:We thank Dr. Piligian and colleagues for their interest in our article (1). We would make two comments. First, we wish to emphasize that the definition of occupational asthma (OA) should be limited to those conditions in which asthma is caused by occupation (2). In patients with OA, the experience of exacerbation of OA by nonspecific stimuli is a common observation, since nonspecific airway hyperresponsiveness usually persists (3). However, it does not mean that nonspecific triggers provoke OA, as indicated in the title to Dr. Piligian and colleagues' letter. We believe that, in the literature, there is a lack of data on the persistence of OA due to nonspecific environmental/exogenous stimuli or to intrinsic ongoing pathologic process, and we agree that more investigations on this issue are needed. Second, results from the published literature contradict Dr. Piligian and colleagues' conclusion that concomitant sensitization to ubiquitous allergens is frequent in patients with OA. Although Piligian cites the study by Maghni and colleagues (4) to demonstrate that concomitant sensitization to ubiquitous allergens is frequent in patients with OA, these authors showed that failure to improve after cessation of exposure to an agent causing OA is associated with airway inflammation and that new sensitization to a ubiquitous allergen after removal from exposure can be excluded. In fact, among the 54 workers without evidence of atopy at the time of diagnosis, in whom skin tests to common aeroallergens were repeated, only three subjects (5.5%) developed skin reactivity to one common allergen (4). Similarly, Perfetti and colleagues showed that subjects with OA are unlikely to develop IgE-dependent sensitization to common inhalants after removal from exposure to occupational agents (5). It thus seems that atopic status does not increase even years after the diagnosis of OA (5). Although a single study suggested that, in some subjects, new sensitizations to specific and common allergens may occur simultaneously (6), this result needs to be replicated by others. Clearly, the term "sensitization" should not be used interchangeably to describe asthma. We agree entirely with the authors' comment that reassignment to a different work setting is certainly the most appropriate way to manage OA, since it prevents worsening of the disease. Unfortunately, this solution may be associated with reduced income or a job that requires fewer qualifications (7). In addition, if Piligian and colleagues believe that the persistence of OA is due to nonspecific airborne environmental triggers, we are perplexed by their recommendation that cessation of specific exposure by relocation to another job will avoid the persistence of symptoms. In summary, because of the difficulty of elucidating the relative contributions of airway inflammation and remodeling to the chronicity of OA, since both are associated with the persistence of asthmatic symptoms and of nonspecific airway hyperresponsiveness, further work in this area is required. Clinical research performed in a busy urban occupational medicine clinic could be useful to clarify this important issue in OA.
University of Ferrara, Ferrara, Italy
University of Padova, Padova, Italy
University of Modena, Modena, Italy FOOTNOTES Conflict of Interest Statement: None of the authors have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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