Clear guidelines for the treatment of occupational COPD are currently lacking. 26 Physicians should work with patients and employers to eliminate respiratory exposures. Primary prevention strategies include identification of workplace hazards and use of personal protective equipment, and secondary prevention focuses on medical surveillance with the use of symptom questionnaires. 26 , 27 Family physicians should encourage and support smoking cessation. There is no evidence that the use of inhaled corticosteroids, long-acting beta agonists, or leukotriene modifiers changes the prognosis of occupational COPD. 27
Theophylline down-regulates inflammatory and immune cell function in vitro and in vivo in animals with airway inflammation [ 16,17 ]. In patients with allergic asthma, it attenuates the late phase increase in airway obstruction and airway responsiveness to histamine, decreases allergen-induced migration of activated eosinophils into the bronchial mucosa, and decreases the sputum eosinophil count [ 8,9,18 ]. Moreover, withdrawal of theophylline from patients with severe chronic asthma receiving high-doses of inhaled glucocorticoid therapy results in increased symptoms of asthma accompanied by an increase in the number of activated cytotoxic T-lymphocytes in the bronchial mucosa and an increase in helper T-lymphocytes in the airway epithelium [ 7 ]. The reduction in nocturnal worsening of lung function when theophylline is used is associated with both a decrease in the percentage of neutrophils and a decrease in stimulated leukotriene B4 from macrophages in early morning bronchoalveolar lavage fluid [ 19 ]. An in depth review of in vitro and in vivo studies demonstrating the immunomodulatory, anti-inflammatory, and glucocorticoid-sparing effects of theophylline has been published [ 20 ].