Monday, September 26, 2005

Fine Particles and Acute Inflammation Effects at 10 ug

BrooklynDodger fears prior posting of this clinical study of ultrafine particle effects. Nevertheless, it goes up again, and will likely appear yet another time when the technical report to the Health Effects Institute appears in a peer reviewed journal.

BrooklynDodger also neglected to return to the original to see where the investigators got the ultrafine particles or how they adjusted the concentration or followed agglomeration. Since these are 0.1 micron in diameter at less, they could also be called “nanoparticles,” a jazzier name. As carbon particles, these would formerly be thought inert.

Bottom line is that 10 ug/M3 for 2 hours is an effect level for various circulating cellular indications of inflammation. Some in asthmatics only, some in healthy volunteers as well.

BrooklynDodger notes that Gunter Oberdorster and the laboratory at the University of Rochester have emerged as major authorities on this subject.

Res Rep Health Eff Inst. 2004 Dec;(126):1-47;
Effects of exposure to ultrafine carbon particles in healthy subjects and subjects with asthma.Frampton MW, Utell MJ, Zareba W, Oberdorster G, Cox C, Huang LS, Morrow PE, Lee FE, Chalupa D, Frasier LM, Speers DM, Stewart J.University of Rochester Medical Center, NY 14642-8692, USA. mark_frampton@urmc.rochester.eduUltrafine particles (UFP; less than 0.1 microm in aerodynamic diameter) may contribute to the health effects of particulate matter (PM) because of a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity and the potential to cross the epithelium and enter the systemic circulation. Three clinical exposure studies: healthy subjects breathing filtered air and UFP (10 microg/m3) at rest; healthy subjects breathing air and UFP (10 and 25 microg/m3) with intermittent exercise; and subjects with mild asthma breathing air and UFP (10 microg/m3) with intermittent exercise. All exposures were for 2 hours. For healthy subjects, the fractional deposition of UFP at rest was 0.66 by particle number. Deposition further increased during exercise (0.83). Asthmatic subjects showed higher UFP deposition than did healthy subjects when breathing at rest (0.76 +/- 0.05). Breathing 25 microg/m3 UFP with exercise (UPDOSE) was associated with reductions in blood monocytes and activation of T lymphocytes in healthy females. In asthmatic subjects, breathing 10 microg/m3 UFP was associated with reduced numbers of blood eosinophils and CD4+ T lymphocytes. Monocyte expression of intercellular adhesion molecule-1 (ICAM-1) was reduced in a concentration-related manner (P = 0.001). In the UPASTHMA group, CD11b expression was reduced on monocytes and eosinophils, and ICAM-1 expression was reduced on polymorphonuclear leukocytes (PMNs). ECG analyses of UPDOSE subjects showed transient reductions in parasympathetic influence on heart rate variability and a reduced repolarization (QT) interval. In UPASTHMA subjects, ECG analyses showed decreased QT variability, but no effect on the QT interval. There were no significant effects in any of the studies on symptoms, pulmonary function, or markers of airway inflammation. The observed subtle changes in leukocyte subsets and adhesion molecule expression are consistent with effects on vascular endothelial function. We also found effects [in an adverse direction] on heart rate variability and on cardiac repolarization in healthy subjects.

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