Combustion-derived nanoparticles: A review of their toxicology following inhalation exposure

被引:643
作者
Donaldson, Ken [1 ]
Tran, Lang [2 ]
Jimenez, Luis Albert [1 ]
Duffin, Rodger [1 ]
Newby, David E. [3 ]
Mills, Nicholas [3 ]
MacNee, William [1 ]
Stone, Vicki [4 ]
机构
[1] Univ Edinburgh, Queens Med Res Inst, ELEGI Colt Lab, 47 Little France Crescent, Edinburgh EH16 4TJ, Midlothian, Scotland
[2] Inst Occupat Med, Edinburgh EH14 4AP, Midlothian, Scotland
[3] Univ Edinburgh, Div Med & Radiol Sci, Cardiovasc Res, Edinburgh EH16 4SU, Midlothian, Scotland
[4] Napier Univ, Sch Life Sci, Edinburgh EH10 5DT, Midlothian, Scotland
关键词
D O I
10.1186/1743-8977-2-10
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
This review considers the molecular toxicology of combustion-derived nanoparticles (CDNP) following inhalation exposure. CDNP originate from a number of sources and in this review we consider diesel soot, welding fume, carbon black and coal fly ash. A substantial literature demonstrates that these pose a hazard to the lungs through their potential to cause oxidative stress, inflammation and cancer; they also have the potential to redistribute to other organs following pulmonary deposition. These different CDNP show considerable heterogeneity in composition and solubility, meaning that oxidative stress may originate from different components depending on the particle under consideration. Key CDNP-associated properties of large surface area and the presence of metals and organics all have the potential to produce oxidative stress. CDNP may also exert genotoxic effects, depending on their composition. CDNP and their components also have the potential to translocate to the brain and also the blood, and thereby reach other targets such as the cardiovascular system, spleen and liver. CDNP therefore can be seen as a group of particulate toxins unified by a common mechanism of injury and properties of translocation which have the potential to mediate a range of adverse effects in the lungs and other organs and warrant further research.
引用
收藏
页数:14
相关论文
共 131 条
[101]   Mechanisms of genotoxicity of particles and fibers [J].
Schins, RPF .
INHALATION TOXICOLOGY, 2002, 14 (01) :57-78
[102]   INCREASED MORTALITY IN PHILADELPHIA ASSOCIATED WITH DAILY AIR-POLLUTION CONCENTRATIONS [J].
SCHWARTZ, J ;
DOCKERY, DW .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1992, 145 (03) :600-604
[103]   WHAT ARE PEOPLE DYING OF ON HIGH AIR-POLLUTION DAYS [J].
SCHWARTZ, J .
ENVIRONMENTAL RESEARCH, 1994, 64 (01) :26-35
[104]   THE RESPIRATORY HEALTH OF WELDERS [J].
SFERLAZZA, SJ ;
BECKETT, WS .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1991, 143 (05) :1134-1148
[105]   Inhaled particulate matter causes expression of nuclear factor (NF)-κB-related genes and oxidant-dependent NF-κB activation in vitro [J].
Shukla, A ;
Timblin, C ;
BeruBe, K ;
Gordon, T ;
McKinney, W ;
Driscoll, K ;
Vacek, P ;
Mossman, BT .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2000, 23 (02) :182-187
[106]   Interleukin-8 levels in human lung epithelial cells are increased in response to coal fly ash and vary with the bioavailability of iron, as a function of particle size and source of coal [J].
Smith, KR ;
Veranth, JM ;
Hu, AA ;
Lighty, JS ;
Aust, AE .
CHEMICAL RESEARCH IN TOXICOLOGY, 2000, 13 (02) :118-125
[107]  
Sorahan T, 2001, AM J IND MED, V39, P158, DOI 10.1002/1097-0274(200102)39:2<158::AID-AJIM1003>3.0.CO
[108]  
2-L
[109]   Quinoid redox cycling as a mechanism for sustained free radical generation by inhaled airborne particulate matter [J].
Squadrito, GL ;
Cueto, R ;
Dellinger, B ;
Pryor, WA .
FREE RADICAL BIOLOGY AND MEDICINE, 2001, 31 (09) :1132-1138
[110]   Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2B) in vitro [J].
Steerenberg, PA ;
Zonnenberg, JAJ ;
Dormans, JAMA ;
Joon, PNT ;
Wouters, IM ;
van Bree, L ;
Scheepers, PTJ ;
Van Loveren, H .
EXPERIMENTAL LUNG RESEARCH, 1998, 24 (01) :85-100