Particulate matter (PM) is a complex mixture of different particle types, much of which are unlikely to cause any adverse effects and so the hypothesis has arisen that a sub-component(s) of PM drives the adverse effects. Much research has been, and is being, undertaken to test various hypotheses regarding which of the components in fact drives adverse effects. Combustion has been recognised as a potential source of harmful particles as well as gaseous pollutants [1,2]. Epidemiological studies do not readily allow associations of adverse effects with sub-components of PM, dependent as they usually are on mass measures of PM. However several epidemiological studies have been able to identify combustion-derived particles as an important component in driving adverse effects of PM [3-7]. Toxicology can more readily study the components of PM and there has been considerable amount of research demonstrating the toxicity of combustion-derived particles such as diesel soot [8,9], welding fume , carbon black  and nanoparticles coal fly-ash . The workplace is also a site of exposure to combustion-derived nanoparticles as in the case of welding fume and in the manufacture of carbon black. We focus here on the toxicology of combustion-derived nanoparticles (CDNP) produced in a range of situations because reports on their mechanisms of toxicity suggest similarities.
CDNP present a diverse group of materials which gain commonality because of their origin in combustion processes and their demonstrated toxicity in various models. We have attempted to be systematic and have described the CDNP in terms of their physicochemistry then their adverse effects and finally their molecular toxicology; however there are gaps of various sizes in the available information and so we fall short of a truly systematic approach. We feel that this review is timely because the molecular toxicology of these materials is becoming better understood and the final common pathways of oxidative stress-mediated inflammation are now considered to underlie the effects of a range of CDNP. This is outlined in Figure 1 where the link between oxidative stress and inflammation is shown. In addition we review the evidence that CDNP and their components can migrate, from their site of deposition in the lungs, to other target organs.