US EPA

156111 

Journal Article 

Reactive oxygen species in pulmonary inflammation by ambient particulates 

Tao, F; Gonzalez-Flecha, B; Kobzik, L 

2003 

Yes 

Free Radical Biology and Medicine
ISSN: 0891-5849
EISSN: 1873-4596 

35 

4 

327-340 

12899936 

10.1016/S0891-5849(03)00280-6 

WOS:000184488400001 

Exposure to ambient air pollution particles (PM) has been
associated with increased cardiopulmonary morbidity and mortality, particularly in individuals
with pre-existing disease. Exacerbation of pulmonary inflammation in susceptible people (e.g.,
asthmatics, COPD patients) appears to be a central mechanism by which PM exert their toxicity.
Health effects are seen most consistently with PM with aerodynamic diameter < 2.5 mum (PM2.5),
although 10 mum < PM < 2.5 mum can also be toxic. Through its metal, semi-quinone,
lipopolysaccaride, hydrocarbon, and ultrafine constituents, PM may exert oxidative stress on
cells in the lung by presenting or by stimulating the cells to produce reactive oxygen (ROS). In
vivo, PM increase cytokine and chemokine release, lung injury, and neutrophil influx. In vitro
analysis of PM effects on the critical cellular targets, alveolar macrophages, epithelial cells,
and neutrophils, demonstrates PM- and oxidant-dependent responses consistent with in vivo data.
These effects have been observed with PM samples collected over years as well as concentrated
PM2.5 (CAPs) collected in real time. Oxidative stress mediated by ROS is an important mechanism
of PM-induced lung inflammation. (C) 2003 Elsevier Inc. 

free radicals; oxidative stress; ambient air particles; alveolar macrophages; epithelial cells; nentrophils