Recent work by Oberdorster and colleagues has demonstrated the transfer of radiolabelled nanoparticulate carbon from the nose of rats directly into the brain [112]. It is postulated that this transfer occurs via the olfactory nerves which run from the roof of the nasal cavity in to the olfactory lobes of the brain. However, this part of the brain is well vascularised, providing a potential systemic portal of deposition. If size is the factor that drives these effects then there is some concern that CDNP may have the general property of tropism to the brain. A search of relevant terms showed no published studies pertaining to brain transfer of diesel or coal fly-ash. The best-studied of the CDNP in regard to brain transfer is welding fume. Rats exposed to stainless steel welding fume over 60 days showed accumulation of manganese in the blood and liver but, most importantly, also in various areas of the brain [113]. Erikson et al [114] showed that inhalation exposure to manganese sulphate and manganese phosphate produced oxidative stress in the brains of rats as shown by metallothienin and glutamine synthetase levels; this varied between sexes and with age. In a sub-chronic exposure study with manganese phosphate there was accumulation of Mn in the brain but there was no associated loss of neurons or neurobehavioural effects [115]. Studies of workers exposed to welding fume, however, show clear evidence of neurological disease [116] and Mn is implicated in these effects [117]. It is not known whether the welding fume particles themselves are transferred to the brain or only the soluble Mn and other metals. However, soluble metals are very rapidly lost from welding fume particles [10] and a soluble salt of Mn was more efficient than an insoluble Mn salt in gaining access to the brain following inhalation exposure in rats [118]. Further work is required to improve our understanding of the factors dictating the transfer of CDNP and their associated soluble contaminants to the brain.
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