Inhalation of Ultrafine Particles Alters Blood Leukocyte Expression of Adhesion Molecules in Humans

Abstract

Ultrafine particles (UFPs; aerodynamic diameter < 100 nm) may contribute to the respiratory and cardiovascular morbidity and mortality associated with particulate air pollution. We tested the hypothesis that inhalation of carbon UFPs has vascular effects in healthy and asthmatic subjects, detectable as alterations in blood leukocyte expression of adhesion molecules. Healthy subjects inhaled filtered air and freshly generated elemental carbon particles (count median diameter ~ 25 nm, geometric standard deviation ~ 1.6), for 2 hr, in three separate protocols: 10 μg/m3 at rest, 10 and 25 μg/m3 with exercise, and 50 μg/m3 with exercise. In a fourth protocol, subjects with asthma inhaled air and 10 μg/m3 UFPs with exercise. Peripheral venous blood was obtained before and at intervals after exposure, and leukocyte expression of surface markers was quantitated using multiparameter flow cytometry. In healthy subjects, particle exposure with exercise reduced expression of adhesion molecules CD54 and CD18 on monocytes and CD18 and CD49d on granulocytes. There were also concentration-related reductions in blood monocytes, basophils, and eosinophils and increased lymphocyte expression of the activation marker CD25. In subjects with asthma, exposure with exercise to 10 μg/m3 UFPs reduced expression of CD11b on monocytes and eosinophils and CD54 on granulocytes. Particle exposure also reduced the percentage of CD4+ T cells, basophils, and eosinophils. Inhalation of elemental carbon UFPs alters peripheral blood leukocyte distribution and expression of adhesion molecules, in a pattern consistent with increased retention of leukocytes in the pulmonary vascular bed.

Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung

“…TNF-a could not be detected in BALF. IL-1b showed a mild but not significant increase from 1 UFCP did not cause any detectable changes in airway inflammation [15]; however, they caused alterations in the expression pattern of adhesion molecules on blood cells, indicating increased retention of leukocytes in the pulmonary vascular bed [24]. The present study provides evidence that inhalation of elemental carbon particles at doses .40-fold above environmental relevant doses induces mild pro-inflammatory processes within 24 h of exposure.…”

Promoting effects of nanoparticles/materials on sensitive lung inflammatory diseases

“…Nanoparticles have enhanced capacity to produce reactive oxygen species, and, consequently, have widespread toxicity [18][19][20]. Consistent with these in vitro and in vivo reports, nanoparticle exposure also reportedly influences cardiopulmonary systems with or without predisposing diseases in human studies [21,22]. On the other hand, development of nanotechnology has increased the risk of types of particles other than combustion-derived particles in the environment, namely engineered nanomaterials [23].…”

Particulate Matter Air Pollution and Cardiovascular Disease

“…390 Conversely, decreases in blood monocytes, basophils, eosinophils, and CD54 and CD18 adhesion molecule expression on monocytes after exposure to ultrafine carbon (10 to 50 g/m 3 ) among exercising asthmatic individuals and healthy adults have also been reported. 391 The authors suggested in the latter study that these results may represent the sequestration of these cells in tissue compartments such as the lung or vasculature, where there may be selective expression of the corresponding receptors for these ligands. 362 However, other recent human clinical studies have found no association between peripheral blood cell counts and exposure to fine PM or UFPs such as zinc oxide, 392 ultrafine carbon, 393 or diesel exhaust.…”