Combustion is considered a source of toxic chemicals and particles  and this review has focused solely on the toxicology of the particulate component. Emanating, as they do, from very diverse combustion scenarios, CDNP have received variable and piecemeal research attention. This review has used diesel soot, welding fume, carbon black and fly-ash as exemplar CDNP to demonstrate that different CDNP in fact have many properties in common that suggest that they can be viewed as a coherent class of particulate toxins. They are unified by their combustion origin, small size, universal mechanism of injury and common properties of translocation which have the potential to mediate a range of adverse effects in the lungs and other organs. Notably, the CDNP studied here all have the potential to cause oxidative stress as an integral part of their pathogenic mechanism. This oxidative stress can cause inflammation and its local and systemic acute and chronic sequelae, as well as causing oxidative adducts in epithelium that can contribute to carcinogenesis. CDNP originating from any source can therefore be considered a potential hazard to the lungs and other systems through the pathways of oxidative stress, inflammation and carcinogenesis. This is summarised in Figure 4 where the link between oxidative stress and inflammation-related effects are shown along with carcinogenic effects of oxidative stress.
Of course the temperature, conditions and substrate for combustion mean that there is considerable heterogeneity in composition between, for example, welding fume and diesel soot. Therefore the key oxidative stress event may originate from different components depending on the particle under consideration. Components that may cause oxidative stress include CDNP-associated surfaces, metals or organics; this oxidative stress then acts through oxidative stress-responsive signalling pathways to affect responses such as inflammation and proliferation. In addition, oxidative stress can also cause oxidative genotoxic DNA adducts such as 8-OH-dG whilst bulky PAH-derived adducts may also form. Both adduct types can lead to mutation. Different components of CDNP may interact to enhance the level of oxidative stress, as in the case of metals and organics interacting in the redox-cycling of quinoid organics  or CDNP surfaces and transition metals interacting additively in their ability to cause inflammation .
In addition to the local inflammatory effects of CDNP at their sites of deposition they have the potential to translocate away from their site of deposition to the blood and brain. Bloodborne particles will be delivered to the cardiovascular system, spleen and liver. The cardiovascular system has emerged as a target for the effects of PM10 [104, 135] and it is likely that the CDNP in PM in fact mediate this effect [3-6]. They may do this through causing inflammation in the lungs which then impacts on inflammatory processes in the atheromatous plaques that govern their stability and development. Inflammation in the lungs may also affect the thrombotic potential of the blood. Alternatively, direct effects of bloodborne particles on the endothelium, clotting system and on atheromatous plaques could be responsible. Bloodborne CDNP may deposit in the spleen, liver and heart and in these situations they may have numerous additional adverse effects.
Combustion is a ubiquitous in the modern world and the generation of CDNP is correspondingly omnipresent. Much research emphasis has been placed on traffic-derived CDNP in PM and rightly so as they are the source of most CDNP in our cities where the greatest potential for human exposure exists. However it is also clear that there is considerable potential for mixed exposures to occur in specific scenarios, e.g. a welder working in a busy street. The interactions between different particle types are unknown but the common pathway of oxidative stress means that there is potential for additive or synergistic effects. Furthermore the involvement of oxidative stress in a number of chronic diseases such as asthma, COPD and coronary artery disease argues a powerful case for existence of susceptible populations, already well-studied in the adverse effects of PM.
CDNP represent an interesting and ubiquitous category of pathogenic particles whose adverse effects are substantial and additions to the list of candidate CDNP are to be anticipated. More research is warranted into the effects of CDNP at numerous levels from factors dictating their translocation between organs and tissue to their effect in sub-cellular signalling. Viewing CDNP as a class of particles with common origins and a strong hypothesis-based understanding of their toxic mechanisms should provide impetus and direction to research on existing and new CDNP, leading to a greater understanding.