Recent years have seen an explosion of animal models of cigarette smoke-induced chronic obstructive lung disease (COPD). Almost all of these have concentrated on the induction and prevention of emphysema. Neutrophils and neutrophil elastase, macrophages and macrophage-derived metalloproteases, lymphocytes, TNF-alpha, and oxidants have all been shown to play a role in the pathogenesis of emphysema in animal models, and interventions using either knockout mice or drugs have indicated possible preventive/therapeutic avenues. There is less in the way of models of smoke-induced small airway remodeling and almost nothing is known of its pathogenesis. Cigarette smoke has been shown to induce vascular remodeling and pulmonary hypertension in laboratory animals, and these mechanisms are beginning to be understood. A major limitation of existing animal models is that most produce relatively mild disease (no more severe than corresponding to the GOLD 2 stage of human COPD), and none of the models show the smoke-independent progressive disease seen in humans with GOLD 3 or 4 COPD. There are no models of cigarette smoke-induced chronic bronchitis in animals and there are no models of acute exacerbations of COPD.