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

Ken Donaldson1 email, Lang Tran2 email, Luis Albert Jimenez1 email, Rodger Duffin1 email, David E Newby3 email, Nicholas Mills3 email, William MacNee1 email and Vicki Stone4 email

ELEGI Colt Laboratory, Queens Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK

Institute of Occupational Medicine, Research Park North, Riccarton, Edinburgh EH14 4AP, UK

Cardiovascular Research, Division of Medical and Radiological Sciences, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh EH16 4SU, UK

Napier University, School of Life Sciences, 10 Colinton Rd, Edinburgh EH10 5DT, UK

author email corresponding author email

Particle and Fibre Toxicology 2005, 2:10doi:10.1186/1743-8977-2-10

Published: 21 October 2005

Abstract

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.


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