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 matter(2.5) [PM(2.5)]) from these areas induce distinct lung inflammation, which might be an explanation for this difference. Therefore, 100 microg of PM(2.5) suspensions, collected simultaneously in the two areas, were instilled through a bronchoscope into contralateral lung segments of 12 healthy volunteers. PM(2.5) from both Hettstedt and Zerbst increased the number of leukocytes in the bronchoalveolar lavage performed 24 hours later. PM(2.5) 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 PM(2.5). We conclude that environmentally relevant concentrations of PM(2.5) 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 PM(2.5) from Hettstedt might be responsible for this increased inflammation.

Background: Electrocautery, laser tissue ablation, and ultrasonic scalpel tissue dissection all generate a 'surgical smoke' containing ultrafine (<100 nm) and accumulation mode particles (< 1 μm). Epidemiological and toxicological studies have shown that exposure to particulate air

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The link between elevated concentrations of ambient particulate matter (PM) and increased mortality has been investigated in numerous studies. Here we analyzed the role of different particle size fractions with respect to total and cardio-respiratory mortality in Erfurt, Germany, between 1995 and 2001. Number concentrations (NC) of PM were measured using an aerosol spectrometer consisting of a Differential Mobility Particle Sizer and a Laser Aerosol Spectrometer to characterize particles between 0.01 and 0.5 and between 0.1 and 2.5 mm, respectively. We derived daily means of particle NC for ultrafine (0.01-0.1 mm) and for fine particles (0.01-2.5 mm). Assuming spherical particles of a constant density, we estimated the mass concentrations (MC) of particles in these size ranges. Concurrently, data on daily total and cardio-respiratory death counts were obtained from local health authorities. The data were analyzed using Poisson Generalized Additive Models adjusting for trend, seasonality, influenza epidemics, day of the week, and meteorology using smooth functions or indicator variables. We found statistically significant associations between elevated ultrafine particle (UFP; diameter: 0.01-0.1 mm) NC and total as well as cardio-respiratory mortality, each with a 4 days lag. The relative mortality risk (RR) for a 9748 cm À3 increase in UFP NC was RR ¼ 1.029 and its 95% confidence interval (CI) ¼ 1.003-1.055 for total mortality. For cardio-respiratory mortality we found: RR ¼ 1.031, 95% CI: 1.003-1.060. No association between fine particle MC and mortality was found. This study shows that UFP, representing fresh combustion particles, may be an important component of urban air pollution associated with health effects.