The mechanisms underlying GC resistance in smoking asthmatics are incompletely understood but are thought to include noneosinophilic (often neutrophilic) airway inflammation [Chalmers, 2001], impaired corticosteroid receptor function, and/or reduced histone deacetylase activity [Adcock, 2008]. In support of these effects of smoking on asthma, animal models show that smoking can increase inflammation in allergic models of asthma and can affect steroid responsiveness.