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Published ahead of print on June 30, 2004, doi:10.1164/rccm.200403-423OC
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American Journal of Respiratory and Critical Care Medicine Vol 170. pp. 898-903, (2004)
© 2004 American Thoracic Society
doi: 10.1164/rccm.200403-423OC

Metal-rich Ambient Particles (Particulate Matter2.5) Cause Airway Inflammation in Healthy Subjects

Frank Schaumann, Paul J. A. Borm, Andreas Herbrich, Johannes Knoch, Mike Pitz, Roel P. F. Schins, Birgit Luettig, Jens M. Hohlfeld, Joachim Heinrich and Norbert Krug

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover; Institut für Umweltmedizinische Forschung, Duesseldorf; and GSF-National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg, Germany

Correspondence and requests for reprints should be addressed to Norbert Krug, M.D., Fraunhofer Institute of Toxicology and Experimental Medicine, Nikolai-Fuchs-Str. 1, Hannover 30625, Germany. E-mail: krug{at}item.fraunhofer.de

Epidemiologic studies have shown an increased prevalence of allergic asthma in children living in a German smelter area (Hettstedt) compared with a cohort who live in a nonindustrialized area (Zerbst). However, it is not known whether ambient particles (particulate matter2.5 [PM2.5]) from these areas induce distinct lung inflammation, which might be an explanation for this difference. Therefore, 100 µg of PM2.5 suspensions, collected simultaneously in the two areas, were instilled through a bronchoscope into contralateral lung segments of 12 healthy volunteers. PM2.5 from both Hettstedt and Zerbst increased the number of leukocytes in the bronchoalveolar lavage performed 24 hours later. PM2.5 from Hettstedt, but not Zerbst, induced a significant influx of monocytes (Hettstedt: 7.0% vs. Zerbst: 4.3%) without influencing the expression of surface activation markers on monocytes and alveolar macrophages. Oxidant radical generation of bronchoalveolar lavage cells and cytokine concentration (interleukin-6 and tumor necrosis factor-{alpha}) in bronchoalveolar lavage fluid was significantly increased after instillation of Hettstedt PM2.5. We conclude that environmentally relevant concentrations of PM2.5 from the smelter area induced distinct airway inflammation in healthy subjects with a selective influx of monocytes and increased generation of oxidant radicals. The higher concentration of transition metals in PM2.5 from Hettstedt might be responsible for this increased inflammation.

Key Words: air pollution, bronchoscopy • monocytes • oxidants




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