PULMONARY TISSUE ACCESS OF ULTRAFINE PARTICLES

被引：93

作者：

FERIN, J

OBERDORSTER, G

SODERHOLM, SC

GELEIN, R

机构：

[1] Environmental Health Sciences Center, Department of Biophysics, University of Rochester School of Medicine and Dentistry, Rochester

来源：

JOURNAL OF AEROSOL MEDICINE-DEPOSITION CLEARANCE AND EFFECTS IN THE LUNG | 1991年 / 4卷 / 01期

关键词：

ULTRAFINE PARTICLES; TITANIUM DIOXIDE; ALUMINUM OXIDE; PARTICLE TRANSLOCATION; INFLAMMATION; PHAGOCYTOSIS; FREE CELL RESPONSE; LUNG CLEARANCE;

D O I：

10.1089/jam.1991.4.57

中图分类号：

R1 [预防医学、卫生学];

学科分类号：

1004 ; 120402 ;

摘要：

Rats were exposed to different sizes of TiO2 or Al2O3 particles by intratracheal instillation or by aerosol inhalation. The lungs were analyzed at days 1, 29 and 59 or 60 after exposure for TiO2 and Al2O3 content and for the lung's free cell responses. An extensive lung lavage was used in an attempt to distinguish between the particles retained in the alveoli and airways and particles translocated into the pulmonary tissue itself. After intratracheal instillation of 500-mu-g, particles of TiO2 and Al2O3 with a primary particle diameter of approximately 20 nm were translocated into the pulmonary tissue from the alveoli to a greater extent than particles with 250-500 nm diameter. The enhanced translocation resulted in an increase of particle content in the hilar lymph nodes. This was accompanied by an acute inflammatory response as indexed by the abnormal abundance of polymorphonuclear leukocytes. After 10 similar inhalation exposures, no difference in translocation of ultrafine (approximately 20 nm) and larger (approximately 250 nm) TiO2 particles could be observed, indicating the importance of particle delivery rates. Phagocytosis of particles by alveolar macrophages in the alveoli appears to be the mechanism which prevents the rapid translocation of particles from the alveoli into the pulmonary tissue.

引用

页码：57 / 68

页数：12

共 28 条

[1] Adamson I.Y.R., Bowden D.H., Adaptive responses of pulmonary macrophage system to carbon, Laborat. Invest., 38, pp. 430-438, (1978)
[2] Adamson I.Y.R., Bowden D., Dose response of the pulmonary macrophagic system to various particulates and its relationship to transepithelial passage of free particles, Exp. Lung Res., 2, pp. 165-175, (1981)
[3] Adamson I.Y.R., Letorneau H.L., Bowden D.H., Enhanced macrophage-fibroblast interactions in the pulmonary interstitium increases fibrosis after silica injection to monocyte depleted mice, Am. J. Path, 134, pp. 411-418, (1989)
[4] Threshold Limit Values and Biological Exposure Indices for 1988–1989, (1988)
[5] Bellmann B., Muhle H., Creutzenberg O., Mermelstein R., Recovery behaviour after dust overloading of lungs in rats, J. Aerosol Sci, 21, pp. 377-380, (1990)
[6] Brody A.R., Roe M.W., Evans J.N., Davis G.S., Deposition and translocation of inhaled silica in rats, Laborat. Invest., 47, pp. 533-542, (1982)
[7] Brody A.R., Roe M.W., Deposition pattern of inorganic particles at the alveolar level in the lungs of rats and mice, Am. Rev. Respir. Dis., 128, pp. 724-729, (1983)
[8] Brody A.R., Hill L.A., Warheit D.B., Induction of early alveolar injury by inhaled asbestos and silica, Fed. Proc., 44, pp. 2596-2601, (1985)
[9] Dethloff L.A., Lehnert B.E., Compartmental origin of pulmonary macrophages harvested from mechanically disrupted lung tissue, Exp. Lung Res., 13, pp. 361-383, (1987)
[10] Ferin J., Feldstein M.L., Pulmonary clearance and hilar lymph node content in rats after particle exposure, Environ. Res., 16, pp. 342-352, (1978)

← 1 2 3 →