Nanoparticles are defined as primary particles with at least one dimension 1,2]. Like other nanoparticles, CDNP agglomerate readily and move into the accumulation mode which decreases the particle number but probably leaves the surface area dose unaffected. NP have the ability to cause inflammation and also, in the case of insoluble CDNP, have potential to escape from the site of deposition in the lungs and translocate to the blood and to other target organs [13]. The exemplar CDNP discussed here (Table 1) include welding fume and nanoparticulate carbon black, which are both occupational hazards, coal fly-ash which is an environmental hazard and diesel soot which is both an environmental and an occupational hazard. CDNP are primary in the sense that they arise directly from the combustion process, although their chemistry may change with aging as the particles undergo chemical interactions with components of the ambient air pollution cloud. The process of burning concentrates metals, due to combustion and hence degradation of the organic fraction to a degree that is dependent on the efficiency of the combustion. At the same time pyrolysis chemistry generates other complex organic molecules, some of which may persist along with elemental carbon nanoparticles. Nanoparticles also form from atmospheric chemistry e.g. sulphate and nitrate nanoparticles but these will not be discussed here as they are not derived directly from combustion. The combustion materials and the mode of combustion will ultimately determine the characteristics of the CDNP, including chemical composition, particle size and particle solubility. The large surface area of CDNP presents maximal opportunity for dissolution of soluble species from the surface of the insoluble core. For insoluble NP, the large surface area provides a surface on which catalytic chemistry can occur that favours the formation of free radicals. These free radicals are responsible for driving oxidative stress, the underlying mechanism that promotes an inflammatory response to CDNP. For a range of low toxicity, low solubility particle types the surface area alone is the driver for lung inflammation following instillation in rats [14]. CDNP may be soluble and release transition metals or organics as their primary pro-inflammatory mechanism. Both transition metals and organics can undergo complex cyclical chemical reactions in the milieu of the lungs that lead to the production of free radicals such as superoxide anion or hydroxyl radical [15-17]. By contrast low toxicity insoluble particles cause inflammation because of their surfaces; some types of CDNP have both soluble components and an insoluble core.
As detailed in this review, exposure to CDNP of various types is associated with a range of adverse health effects including fibrosis, chronic inflammatory lung disease, metal fume fever and cancer. These endpoints are found across a number of exposure conditions and to different kinds of CDNP but are not unique for CDNP.
This paper examines the evidence for harmful effects of CDNP and puts these in the context of a unifying hypothesis based on observations that the generic ability of CDNPs to cause inflammation is via oxidative stress and activation of redox-sensitive transcription factors that can lead to the adverse health effects listed below. The ability of CDNP and their associated metals to translocate to the blood and the brain are also discussed. These unusual toxic properties unite these materials and suggest that they can usefully be seen as a group of particulate lung toxins that act through similar pathways.
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