Chapter 11: Mechanism of Action of Combustion-derived Nanoparticles
Published:16 Oct 2015
K. Donaldson, A. Hunter, C. Poland, and S. Smith, in Toxicology, Survival and Health Hazards of Combustion Products, ed. D. A. Purser, R. L. Maynard, and J. C. Wakefield, The Royal Society of Chemistry, 2015, ch. 11, pp. 361-381.
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Combustion-derived nanoparticles (CDNP) are exemplified by diesel exhaust particles (DEP) and DEP have been studied extensively as to their mechanism of adverse action. These adverse actions include effects on the lungs in exacerbating existing airways disease and adverse effects in cardiovascular disease. Toxicologists seek to link particle structure to toxicity and studies have shown that DEP and other CDNP have components capable of causing oxidative stress in the lungs following deposition, i.e., the carbon core, metals and a range of organics. Oxidative stress can be measured in cells in culture and in tissues from animals and humans exposed to DEP and other CDNP. Oxidative stress is linked to inflammation by well-recognised signalling pathways and pro-inflammatory effects are induced in cells, animals and humans exposed to CDNP. Inflammation is an underlying mechanism in the major pulmonary effects of DEP and particulates in human populations. Oxidative stress and inflammation are known to be involved in atherosclerosis development and in their destabilisation and rupture, leading to heart attacks and strokes. Wood-smoke appears to be less potent than DEP in causing pulmonary oxidative stress and inflammation and impacts little on the cardiovascular system. Difference in composition between DEP and wood-smoke can reasonably explain the differences in potency between DEP and wood-smoke, and this suggests that CDNP from various sources will have different potency depending on their composition.