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大气颗粒物对人支气管上皮细胞的生物学效应。与柴油废气颗粒物的比较。

Biological effects of atmospheric particles on human bronchial epithelial cells. Comparison with diesel exhaust particles.

作者信息

Baulig Augustin, Sourdeval Matthieu, Meyer Martine, Marano Francelyne, Baeza-Squiban Armelle

机构信息

Laboratoire de Cytophysiologie et Toxicologie cellulaire, Université Paris 7, 2 place Jussieu, Tour 53-54, 3e étage, case courrier 7073, 75251 Paris 05, France.

出版信息

Toxicol In Vitro. 2003 Oct-Dec;17(5-6):567-73. doi: 10.1016/s0887-2333(03)00115-2.

DOI:10.1016/s0887-2333(03)00115-2
PMID:14599446
Abstract

Epidemiological studies have associated the increase of respiratory disorders with high levels of ambient particulate matter (PM) levels although the underlying biological mechanisms are unclear. PM are a complex mixture of particles with different origins but in urban areas, they mainly contain soots from transport like Diesel exhaust particles (DEP). In order to determine whether PM biological effects can be explained by the presence of DEP, the effects of urban PM, DEP and carbon black particles (CB) were compared on a human bronchial epithelial cell line (16-HBE14o-). Two types of PM were used : reference material (RPM) and PM with an aerodynamic diameter < or =2.5 microm collected in Paris with a high volume sampler (VPM). From 10 to 30 microg/cm2, cell viability was never modified whatever the particles. However, DEP and to a lower extent PM inhibited cell proliferation, induced the release of a pro-inflammatory cytokine, GM-CSF, and generated a pro-oxidant state as shown by the increased intracellular peroxides production. By contrast, CB never induced such effects. Nevertheless CB are more endocytosed than DEP whereas PM are the less endocytosed particles. In conclusion, PM induced to a lower extent the same biological effects than DEP in 16-HBE cells suggesting that particle characteristics should be thoroughly considered in order to clearly correlate adverse effects of PM to their composition and to clarify the role of DEP in PM effects.

摘要

流行病学研究已将呼吸系统疾病的增加与高浓度的环境颗粒物(PM)联系起来,尽管其潜在的生物学机制尚不清楚。PM是一种由不同来源的颗粒组成的复杂混合物,但在城市地区,它们主要包含来自交通的烟尘,如柴油尾气颗粒(DEP)。为了确定PM的生物学效应是否可以用DEP的存在来解释,我们比较了城市PM、DEP和炭黑颗粒(CB)对人支气管上皮细胞系(16-HBE14o-)的影响。使用了两种类型的PM:参考物质(RPM)和用大容量采样器在巴黎收集的空气动力学直径≤2.5微米的PM(VPM)。在10至30微克/平方厘米的浓度范围内,无论何种颗粒,细胞活力均未改变。然而,DEP以及程度稍低的PM抑制细胞增殖,诱导促炎细胞因子GM-CSF的释放,并产生促氧化状态,如细胞内过氧化物生成增加所示。相比之下,CB从未诱导出此类效应。然而,CB比DEP更容易被内吞,而PM是最不容易被内吞的颗粒。总之,在16-HBE细胞中,PM诱导的生物学效应程度低于DEP,这表明为了明确将PM的不良反应与其组成相关联并阐明DEP在PM效应中的作用,应充分考虑颗粒特性。

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