This review focuses on the potential role that oxidative stress plays in the adverse effects of PM10. The central hypothesis is that the ability of PM10 to cause oxidative stress underlies the association between increased exposure to PM10 and both exacerbations of lung disease and lung cancer. Pulmonary inflammation may also underlie the cardiovascular effects seen following increased PM10, although the mechanisms of the cardiovascular effects of PM10 are not well understood. PM10 is a complex mix of various particle types and several of the components of PM10 are likely to be involved in the induction of oxidative stress. The most likely of these are transition metals, ultrafine particle surfaces, and organic compounds. In support of this hypothesis, oxidative stress arising from PM10 has been shown to activate a number of redox-responsive signaling pathways in lung target cells. These pathways are involved in expression of genes that play a role in responses relevant to inflammation and pathological change, including MAPKs, NF-κB, AP-1, and histone acetylation. Oxidative stress from particles is also likely to play an important role in the carcinogenic effects associated with PM10 and hydroxyl radicals from PM10 cause DNA damage in vitro.