CDNP are generated in a number of scenarios including internal combustion engines, large scale burning of coal for power generation and in industrial processes where they often could be produced along with larger particles. The CDNP considered here are described in Table 1 along with their salient effects in humans and animals.
Diesel exhaust particulate
Both petrol and diesel fuels undergo combustion in automobile engines and give rise to CDNP [18
] but diesel produces more particles per unit fuel than petrol and is by far the most-studied of the two regarding adverse health effects; therefore diesel CDNP are discussed here. Diesel fuel is a middle distillate of petroleum which contains paraffins, alkenes and aromatics[20
]. On combustion in automobile engines it produces low solubility carbon-centred nanoparticles with complex chemical and physical structure, containing sulphates and an organic fraction comprising unburnt fuel, lubricating oil and polycyclic aromatic hydrocarbons along with a range of other chemicals, which can condense on the particles [20
]. Singlet Diesel nanoparticles are 5–20 nm but readily form complexes chains and aggregates of 60 to 100 nm and larger [22
]. Diesel exhaust particles (DEP) are usually the most common CDNP in urban environmental air and in environmental particulate air pollution (PM10
) in conurbations generally; they also occur in an occupational setting. In the ambient environment the concentration of DEP in PM10
is likely to range from 5–30 μg/m3
while in occupational settings levels up to 1000 μg/m3
have been experienced [20
]. The adverse health effects of exposure to DEP have been extensively studied epidemiologically, in animals and in cells. Epidemiological studies have been reviewed and show that there is a strong link between occupational exposure to diesel soot and lung cancer [20
]. Animal studies generally support these findings and demonstrate that exposure to DEP and other nanoparticulate forms of carbon are carcinogenic [23
] but these findings are complicated by the issue of rat lung overload [24
]. Rat lung overload is a condition when very high lung surface area burden [25
] of low toxicity, low soluble particles leads to failure of clearance, rapid accumulation of dose with concomitant inflammation and proliferation, which culminates in fibrosis and cancer. Humans are unlikely to experience overload levels of diesel soot, even in occupational settings, and there is a question over whether overload can occur at all in humans. It is therefore unlikely that cancer associated with DEP-exposure in humans results from mechanism similar to rat lung overload. Exposure to DEP has also been shown to be highly inflammatory in rats and mice in non-overload conditions [26
] and to induce pro inflammatory effects on cells in vitro
]. The well-documented link between inflammation and lung cancer [32
] supports the idea that diesel exhaust may indeed be carcinogenic via an inflammatory pathway (see below).
Many studies have demonstrated profound adjuvant effects of diesel particles on development and intensity of allergic responses and these effects are mediated by direct effects of DEP on a wide range of cell types involved in allergy . These effects could also be mediated indirectly through inflammation and oxidative stress . The inflammatory effects of DEP appear to be driven by the particulate component i.e. the surface area effect  although the organic  and metal components  also appear to play a role in oxidative and pro-inflammatory effects and thereby affect pathogenicity.
Welding is an industrial technique that involves the joining of metal pieces using a filler metal. The filler metal is produced from an electrode wire that is consumed during the welding fusion process. High temperatures are involved, generating a welding fume as well as radiation, noise and gases [38
] but we focus her on the fume particles. The vaporized metal produced by the heat of the welding process oxidises to produce a fume containing particles of metal oxide such as aluminium, cadmium, chromium, and copper [38
], many of which are water soluble. The exact composition of the welding fume is determined by the metals involved in the weld and the composition of the electrode. Welding fume particles are comprised of a large proportion of nanoparticles [10
Exposure to welding fume has been associated with both pulmonary and systemic health endpoints reviewed in . These include decreases in pulmonary function, increased airway responsiveness, bronchitis, fibrosis, lung cancer and increased incidence of respiratory infection; in addition to these pulmonary effects metal fume fever is frequently observed in welders [38,39]. This systemic condition is considered to be caused by inhalation of zinc oxide fumes and it is characterised by acute onset of a flu-like illness accompanied by a dry cough, dyspnea, muscle aches, headaches and fever . Metal fume fever is usually experienced in the first periods of exposure and on Mondays, with the symptoms declining as the working week progresses. Welding fume has been studied in both animals and in cells in culture, and in both it produces marked pro-inflammatory effects [10,41,42]. These effects are driven largely by the transition metals [10,42,43] which undergo redox-cycling resulting in oxidative stress.
Nanoparticulate carbon black
Carbon black (CB) is a low solubility particle produced industrially from incomplete thermal decomposition of hydrocarbons [44
] in which the process is controlled to achieve pre-defined and reproducible particle sizes and properties suitable for a diverse range of industrial applications. Unlike the other CDNP described here NPCB is not accidentally produced, and is an industrial product but it clearly classifies as a CDNP. In thermal-oxidative processes such as the furnace black process, various types of hydrocarbon are sprayed into a natural gas-fired furnace and quenched with water to prevent complete burning [45
]. The carbon black particles so-formed are complex, with a degenerated graphitic crystallite structure and high power electron micrographs clearly show irregular layered graphitic plates. [44
]. The structure of carbon black is described as nodules, the roughly spherical primary structural elements, aggregates which comprise fused, connected particles and agglomerates, which are undispersed clusters of aggregates. CB has been studied extensively as to its toxicology, especially as an example of a low toxicity, low solubility particle not complicated by harmful levels of toxicologically-relevant organics or metals [23
]. In long-term animal studies CB was found to be a carcinogen although rat lung overload very likely plays a role in this affect [46
The smallest nodule-or particle-sized CB comprises primary particles in the low tens of nanonetres size range. CB with smallest primary particle sizes produces the highest optical density (jetness) compared to larger particle sizes, placing this material in demand for colouring enamels, acrylics and plastics, as well as inks and paints . This nanoparticulate CB (NPCB), as it has come to be known, comprises a portion of the overall CB industry. NPCB was able to cause detectable but low level pro-inflammatory effects in rats following 7 hours inhalation exposure  and also following instillation  and this appears to be a consequence of the high surface area area per unit mass . In cell studies NPCB has been shown to cause oxidative stress, pro-inflammatory gene transcription  stimulation of phagocytosis at low doses and inhibition at higher doses . In studies of the health status of individuals working in the carbon black industry there is evidence of abnormalities in chest radiographs and respiratory morbidity, but equivocal findings on lung cancer [50-52]. However, none of these studies analysed a worker population exposed solely to NPCB. NPCB has been used quite extensively in particle toxicology as a model particle and nanoparticles, so there is a considerable existing database on its toxicity in vitro and in vivo .
Coal fly ash
Pulverised coal combustion is a commonly-used and efficient method of coal burning in power stations. In pulverized coal power stations the pulverised coal is blown into the furnace and burned off producing a fly ash emission. This particulate emission is controlled by number or methodologies including electrostatic precipitators, filters scrubbers and mechanical collectors [12
]. However, these control measures are not 100% effective and some particles are released into the environment.
Toxicology studies have in general examined unfractionated pulverised coal fly ash (CFA) and these have shown generally low toxicity , however bioavailable iron has been reported to underlie an ability to generate oxidative stress [55,56]. Coal fly ash-exposed rats have been shown to exhibit increased susceptibility to infection , while a specially-prepared cloud of ultrafine (nanoparticulate) coal fly ash induced adverse effects on guinea pig lung function . A recent study systematically examined the effect of fractionated coal fly ash in pulmonary inflammation and a nanoparticle fraction was available . This study showed greatly enhanced potency of the nanoparticulate fraction compared to the fine and coarse fractions, as seen by enhanced ability to cause lung inflammation and kill macrophages in culture. The nanoparticle fraction was not especially enriched for toxic metals and the increased toxicity of this fraction may be a result of the high surface area, allowing redox reactions to take place.