Black smoke, unlike white smoke, contains a high concentration of carbon exhaust particles. The combustion of diesel fuel in the cylinders breaks down the long chain of carbon molecules to smaller and smaller molecular chains. When the exhaust leaves the engines the byproduct is a combination of carbon dioxide and water. If something goes wrong during combustion the chemical reaction taking place is not as robust, causing long tail hydrocarbons to be left completely intact and then expelled in the form of smog or soot. Partial burning of diesel fuel results in large carbon dioxide particles as well as greenhouse gasses which contribute to air pollution. The advent of the Selective Catalytic Converter, Diesel Exhaust Fluid and Diesel Particulate Filter all helped to regenerate exhaust back into the combustion chamber to further break down particulate matter. Diagnosing Causes of Diesel Smoke at Capital Reman ExchangeBlack smoke is the most common smoke color coming from a diesel engine and most likely indicates something is wrong during the combustion of the diesel fuel. When diagnosing the problem the first place to look at is the mixture of air and fuel flow into the cylinders. The engine could be delivering too much fuel, not enough fuel, too much air or simply not enough air.
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].
Various Artists Chains and Black Exhaust 2002
The genotoxic properties of various particle types has been the focus of several studies concerned with elucidating the role such properties play in particle-associated pathogenicity [34]. However, the mechanisms involved in particle-induced genotoxicity remain poorly understood as particles are uniquely complex compared with soluble genotoxic/carcinogenic compounds, due to their physical and chemical characteristics [125]. There is evidence that 3 of the 4 CDNP studied in this review (diesel, NPCB and welding fume) are carcinogenic in humans or rats [20, 38, 126, 127]. As mentioned earlier, DEP consist of a carbon core with adsorbed PAHs, quinones and transition metals. Genotoxicity, may therefore be caused by the direct (primary) interaction of PAHs which are known to cause DNA adduct formation [128] or alternatively via DNA strand breakage due to the production of reactive oxygen species generated by associated transition metals [8]. Carbon black particles are generally almost free of adsorbed organic compounds; however they have been shown to produce lung tumours in rats following chronic inhalation and instillation studies [127, 129]. This indirect (secondary) genotoxicity pathway involves the phenomenon of lung particle overload resulting in a chronic inflammation and hence excessive ROS production leading to DNA damage. Studies by Knaapen et al, have demonstrated that co-incubation of rat lung epithelial cells with activated neutrophils in vitro stimulate the formation of the oxidative DNA lesion 8-OH-dG [32]. Less research has been carried out on the genotoxic effects of welding fumes. Some of the major components of welding fumes include iron, manganese, chromium and in particular hexavalent chromium (CrVI) chromium which has been shown to increase levels of 8-OH-dG in rats after inhalation exposure [130]. Yu and co-workers showed that rats exposed for 30 days to manual metal arc stainless steel (MMA-SS) welding fumes, exhibited increased DNA damage as measured by the comet assay and immunohistochemistry for 8-OH-dG [131]. Studies investigating the genotoxic capacity of coal fly ash have shown a role for particulate size and iron release leading to radical generation and oxidative DNA damage [132, 133] as well as increased sister-chromatid exchange (SCE) frequencies in peripheral blood lymphocytes from workers occupationally exposed to coal fly ash [134]. 2ff7e9595c
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