The observation that macrophages are increased in chronic obstructive pulmonary disease (COPD) and are associated with COPD severity has led to a large number of studies on macrophage function in COPD. These studies have provided evidence that these cells contribute to tissue injury through the release of various mediators, including proteases such as matrix metalloprotease-12. In addition, it was found that macrophages in COPD have an impaired ability to clear respiratory pathogens and apoptotic cells. Macrophage phagocytic function in COPD can be restored at least in part, as shown by in vitro studies. In a search to further understand this altered function of macrophages in COPD, several studies have used a range of markers to phenotype macrophages in COPD. Macrophages constitute a heterogeneous cell population, and, currently, proinflammatory M1 and anti-inflammatory M2 and M2-like cells are considered to represent the extremes of a pattern of macrophage polarization. In COPD, there is no clear evidence for a predominance of one of these phenotypes, and an intermediate phenotype may be present. Future studies are needed to establish the nature of this apparent COPD-specific macrophage subset, and to link macrophage dysfunction to COPD phenotypes.