Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM₁₀)

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.