Mechanisms of Heightened Airway Sensitivity and Responses to Inhaled SO(2) in Asthmatics

Sulfur dioxide (SO(2)) is a problematic inhalable air pollutant in areas of widespread industrialization, not only in the United States but also in countries undergoing rapid industrialization, such as China, and it can be a potential trigger factor for asthma exacerbations. It is known that asthmatics are sensitive to the effects of SO(2); however, the basis of this enhanced sensitivity remains incompletely understood. A PubMed search was performed over the course of 2014, encompassing the following terms: asthma, airway inflammation, sulfur dioxide, IL-10, mouse studies, and human studies. This search indicated that biomarkers of SO(2) exposure, SO(2) effects on airway epithelial cell function, and animal model data are useful in our understanding of the body’s response to SO(2), as are SO(2)-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties. While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO(2). Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO(2) inhalation, supporting the idea that asthmatics are predisposed to SO(2) sensitivity, leading to asthma exacerbations and airway dysfunction.