Chemical- and Drug-Induced Asthma

Publication date: 2017
Source:Reference Module in Biomedical Sciences
Author(s): B.J. Kilburg-Basnyat, M.K. Selgrade, K.M. Gowdy
Each year, approximately 300 million people worldwide are diagnosed with asthma, and more than 250,000 deaths annually are attributed to asthma. However, the sources and mechanisms behind the development of asthma are diverse. High-molecular-weight proteins, including detergent enzymes and common allergens, contribute to an immunoglobulin E (IgE)-mediated atopic asthma response. Low-molecular-weight chemicals typically are haptens that form hapten–protein complexes resulting in IgE-mediated or IgE-independent immune-mediated asthma. Hapten–protein exposures typically occur at the workplace and can include acid anhydrides, isocyanates, as well as others. Irritant-induced asthma typically results from a single, accidental exposure to a highly concentrated irritant in the workplace that induces pulmonary damage by releasing proinflammatory mediators that lead to asthma. Additionally, ingestion of certain medications including aspirin, β-blockers, or angiotensin-converting enzyme inhibitors can cause drug-induced asthma by enzymatic reactions leading to the production of proinflammatory mediators and modulation of smooth muscle function. Overall, the diversity of asthma makes this prevalent lung disease difficult to diagnose and manage. This article compares and contrasts phenotypes, mechanisms, and possible treatments for these differing types of drug- and chemical-induced asthma that are currently understudied.



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