Purpose of review: It has been demonstrated that particulate air pollutants such as diesel exhaust particles (DEPs) are associated with allergic respiratory disorders, including asthma and allergic rhinitis. Recent in-vivo and in-vitro studies strongly suggest that DEPs induce both anti-inflammatory and proinflammatory products by activating their transcription. If pollutants are to be controlled in the environment in a cost-effective manner, it is important that the molecular target(s) of DEP-induced responses be elucidated. Bronchial epithelial cells are the key regulators of airway inflammation, and therefore it is crucial to clarify the cellular and molecular mechanisms that are active in these cells. It is also important to compare responses to DEP exposure between healthy and susceptible populations.
Recent findings: Studies have shown that DEPs activate several signalling pathways such as mitogen-activated protein kinases and transcription factors, in particular nuclear factor-kappa and activator protein-1, in human bronchial epithelial cells; these effects are thought to occur via production of reactive oxygen species. Antioxidants effectively reduce the allergic inflammatory effects of DEPs both in vitro and in mice.
Summary: Host responses to DEPs are regulated by a balance between antioxidants and proinflammatory responses. DEP-induced oxidants play a key role in proinflammatory reactions. Recent human studies suggest that chemoprevention against DEP-induced adverse effects in susceptible individuals is possible.