Particle clearance

To enhance lipid particle clearance by acting as a cofactor for the lipoprotein lipase enzyme... 

Hofmann, W. and Sturm, R., Stochastic model of particle clearance in human bronchial airways, J. Aerosol. Med. 17, 1, 73, 2004. 

Fig. 8. Attractive force between equal-sized, equally and oppositely charged spheres at various particle clearances.

Mucus flows in the bronchial airways have not been directly measured. The measurements of particle clearance for radioactively tagged particles depend on a mixture of deposition sites and mucus flow rates. However, such measurements have shown reproducibility in the individual and a large variation among individuals. ... 

The tracheobronchial or conducting airways, which provide the channels for gas transport but have no gas-exchange function. Their surface is ciliated to provide a particle clearance mechanism called mucociliary clearance. 

Bohning, D.E., Atkins, H.,L. Cohn, S.H. (1982) Long term particle clearance in man normal and impaired. Annals of Occupational Hygiene, 26, 259-71. 

S. M. Moghimi and S. S. Davis, Innovations in avoiding particle clearance from blood by Kupffer cells Cause for reflection, Crit. Rev. Ther. Drug Carrier Syst. 77 31-59 (1994). 

Wolff RK. Griffith WC. Henderson RF. et al. 1989a. Effects of repeated inhalation exposures to 1-nitropyrene. benzo(a)pyrene, GspQs particles, and SO2 alone and in combinations on particle clearance, bronchoalveolar lavage fluid composition, and histopathology. J Toxicol Environ Health 27(1) 123-138. 

The rhombohedral lattice arrangement gives the maximum concentration for a given interparticle spacing. This is assumed in arriving at the relation between the average inter-particle clearance C and the porosity. This relation is... 

Kennedy CH, Barr EB, Maples KR and Snipes MB (1995) Particle clearance and histopathology in lungs ofF344/N rats and B6C3F, mice inhaling nickd oxide or nickel sulfate. Fund Appl Toxicol 28 232- 244. 

Y. Kitasako, S. Shibata, J. Tagami, Migration and particle clearance from hard-setting Ca(OH)j and self-etching adhesive resin following direct pulp capping. Am. J. Dent. 19 (2006) 370-375. 

According Co Juliano (82), several mechanisms can be held responsible for the particle clearance ... 

Clearance of foreign materials (particles) from the lung and airways depends on the function of macrophages, ciliated cells and secretory cells, and on the physical and chemical properties of the alveolar cells. All these are affected by ozone exposure. Single acute exposure of animals and humans to ozone concentrations less than 0.6 ppm have been shown to accelerate clearance of particles from the tracheobronchial tree whereas acute exposures to ozone levels greater than 0.6 ppm caused a delay in particles clearance [79, 261]. Repeated exposures (2 h daily for 14 days) to 0.1 ppm ozone gave rise to acceleration in alveolar clearance of latex particles but had no effect on tracheobronchial clearance. These results, related to morphological studies, are consistent with certain adaptation [278-283]. 

Let us first consider particle clearance from the respiratory tract when exposure concentrations are lower than those that elicit pathological alterations. Clearance at low-exposure concentrations involves interplay between mechanical and biological mechanisms. In all regions of the respiratory tract, macrophages are present that begin engulfing particles as soon as they are deposited. Both the free particles and those that are engulfed are available for mechanical removal. 

With prolonged exposure to particulate matter at sufficiently high concentrations, the particulate matter continuously deposited in the alveolar spaces can trigger a sustained inflammatory reaction. The inflammation can alter particle clearance, initially increase the rate of clearance, and then later canse inhibition of clearance. This, in turn, intensifies the inflammatory reaction, which further impairs clearance and enhances the rate of particle accumulation in the alveolar region. Some of these particles are found in the interstitial areas and others in the alveolar spaces, where aggregates of macrophages, particles, and proteinaceous material may be observed. Adjacent epithelial cells become hypertrophic, hyperplastic, and occasionally, metaplastic. Freqnently, bronchiolar epithelium may appear to be extending down into the alveoli. This pattern of particle-indnced overload disease has been described in detail in rats chronically exposed to diesel exhaust or carbon black particles (39,40). The extent to which similar lesions are produced in humans exposed to similar levels of diesel soot or carbon black is not well understood. 

Oberdorster G, Ferrin J, Morrow PE. Volumetric loading of alveolar macrophages (AM) a possible basis for diminished AM-mediated particle clearance. Exp Lung Res 1992 18 87-104. 

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