Li, N., Xia, T. & Nel, A. E. The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. Free Radic. Biol. Med. 44, 1689-1699

Division of NanoMedicine, Department of Medicine, University of California, Los Angeles, CA 90095, USA.
Free Radical Biology and Medicine (Impact Factor: 5.74). 06/2008; 44(9):1689-99. DOI: 10.1016/j.freeradbiomed.2008.01.028
Source: PubMed


Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The proinflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered nanoparticles (NP) may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effects of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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    • "Particulate matter (PM) air pollution exposure is a known risk factor for the induction of inflammatory and oxidative stress responses1234, especially during the pregnancy period when increased levels of oxidative stress can be expected[5]. Mitochondria are the main intracellular source and target of reactive oxygen species (ROS) that are continually generated as by-products of mitochondrial respiration in the electron transport chain[6]. "

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    • "Dust inhalation for long periods emitted by coal mining and coal burning lead to several lung pathologies, such as bronchitis, asthma, cancer, fibrosis, emphysema and pneumoconiosis, triggering a chronic inflammatory process, which is activated and linked to increased ROS generation and therefore systemic OS[18]. Moreover, several prospective studies have suggested that air pollution may be responsible for increased risk of developing lung cancer and cardiovascular diseases, among others, linking these risks with PM exposure and with ROS overgeneration[27,29,30]. Similarly to the results found in the contamination related to coal mining extraction[1], our group found that coal combustion was also capable to induce a similar OS in the blood of subjects exposed directly (working closed to the burning area) or indirectly (working at the administration building, ca. "

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