Studies of the inflammatory processes in asthma and in COPD have been hindered by the imprecise definitions of these diseases, the uncertainty as to the location of the relevant inflammatory sites for these diseases within the lungs, and the difficulties in relating observed histopathologic changes to the effects of particular proinflammatory leukocytes or their products. Circumstantial evidence exists implicating neutrophils, eosinophils, mast cells, and monocytes in asthma pathogenesis based on increased numbers and activation of these cells in blood, BAL fluid, or biopsy material, and the propensity of these cells to release products causing tissue damage. There is increasing evidence that the accumulation and activation of these cells is orchestrated by lymphokines elaborated by sensitized T lymphocytes. In COPD, attention has been focused on the secretion of proteases by infiltrating neutrophils and macrophages, although there is no incontrovertible evidence that these are relevant to the disease pathogenesis in the majority of patients with normal serum concentrations of protease inhibitors. In the future, studies of the functions of inflammatory cells actually at the sites of inflammation using the techniques of immunocytochemistry and molecular biology may provide further information as to the role of these cells in the inflammatory processes associated with asthma and COPD.