Inflammatory effects of coarse and fine particulate matter in relation to chemical and biological constituents

被引:291
作者
Schins, RPF
Lightbody, JH
Borm, PJA
Shi, TM
Donaldson, K
Stone, V
机构
[1] Univ Dusseldorf, IUF, D-40225 Dusseldorf, Germany
[2] Napier Univ, Sch Life Sci, Edinburgh EH14 1DJ, Midlothian, Scotland
[3] Univ Edinburgh, Resp Med Unit, ELEGI Colt Labs, Edinburgh, Midlothian, Scotland
关键词
PM10; PM2.5; coarse particles; fine particles; lung inflammation; particle composition; endotoxin; metals; electron paramagnetic resonance; whole blood; tumor necrosis factor alpha; interleukin-8;
D O I
10.1016/j.taap.2003.10.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
There is conflicting evidence in the literature as to the predominant mechanism and also the compositional element(s) that drives the pulmonary inflammatory response of ambient particulate matter (PM). We have investigated the inflammogenic potential of coarse (2.5 - 10 mum) and fine (<2.5 mum) PM from both a rural and an industrial location in Germany, using bronchoalveolar lavage (BAL) of rat lungs 18 h post intratracheal instillation with PM. Irrespective of the sampling location, the coarse fraction of PM10 but not its fine counterpart caused neutrophilic inflammation in rat lungs, in the absence of any severe pulmonary toxicity as indicated by the lack of an increase in lavage protein and lactate dehydrogenase levels. The rural sample of coarse PM also caused a significant increase in the tumor necrosis factor a (TNFalpha) content as well as glutathione depletion in the BAL fluid. The contrasting inflammatory responses of the different samples could not be explained by differences in the concentrations of soluble Fe, Cu, V, Ni, Cr, or Al or by the OH generating capacities of the PM suspensions. However, the effects of the different PM samples were clearly associated with their endotoxin content, as well as their ability to induce interleukin (IL)-8 and TNFalpha from whole blood in vitro. In conclusion, on an equal mass basis, coarse but not fine PM samples from our sampling campaign induced an inflammatory reaction in the lung in the absence of gross cellular lung damage, following intratracheal instillation. Our data also indicate, in accordance with previous independent in vitro observations, that endotoxin or related contaminants may play a role in these in vivo effects. (C) 2003 Elsevier Inc. All rights reserved.
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页码:1 / 11
页数:11
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