Published ahead of print on June 30, 2004, doi:10.1164/rccm.200403-423OC
Am. J. Respir. Crit. Care Med., Volume 170, Number 8, October 2004, 898-903
A more recent version of this article appeared on October 15, 2004
Submitted on March 30, 2004
Accepted on June 28, 2004
Metal Rich Ambient Particles (PM2.5) Cause Airway Inflammation in Healthy Subjects
Frank Schaumann1, Paul J.A. Borm2, Andreas Herbrich1, Johannes Knoch1, Mike Pitz3, Roel P.F. Schins2, Birgit Luettig1, Jens M Hohlfeld1, Joachim Heinrich2, and Norbert Krug1*
1 Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany,
2 Institut fuer Umweltmedizinische Forschung (IUF), Duesseldorf, Germany,
3 Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Germany
* To whom correspondence should be addressed. E-mail: krug{at}item.fhg.de.
Epidemiological studies have shown an increased prevalence of allergic asthma in children living in a German smelter area (Hettstedt) compared to a cohort who live in a non-industrialized area (Zerbst). However, it is not known whether ambient particles (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. Both PM2.5 from 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 % versus Zerbst: 4.3%), without influencing the expression of surface activation markers on monocytes and alveolar macrophages. Oxidant radical generation of BAL cells and cytokine concentration (IL-6 and TNF- ) in BAL 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, monocytes, oxidants, bronchoscopy
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