As discussed above, NP of various types are reported to gain access to the blood. Stuart showed in 1970 that the liver and the spleen turn black following the instillation of carbon particle into the blood because the spleen and the liver have sinusoidal phagocytes which are in contact with the blood – the 'littoral' macrophages [119]. There is existing evidence that particles can gain access to the blood since coalworkers, who receive considerable exposure to particles, show greater numbers of particles in their spleen and liver at autopsy than non-coalworkers [120]. The amount of particulate in the spleen and liver, which can be assumed to have travelled via the blood, was greater in coalworkers with more severe lung disease, suggesting that inflamed/damaged lungs may be more susceptible to egress of particles into the blood than normal lungs. The normal function of the littoral macrophages of the spleen and liver is probably to 'sample' for antigens and xenobiotics in the blood and to quickly remove any bacteria that gain access to the blood. We may therefore anticipate that any NP that gain access to the blood will be taken up by these littoral macrophages in the spleen and the liver. Particles may also reach hepatocytes and other spleen cells with consequences that are presently unknown. However, in line with the above arguments pertaining to the potential role of NP in the adverse effects of PM10, we may anticipate that increases in acute phase proteins during periods of high PM [121] could be due to direct particle effects on the liver, the primary source of acute phase proteins [122]. In the single study that has so far been published concerning the effects of bloodborne NP on liver function of healthy mice, CDNPs induce platelet accumulation in the hepatic microvasculature that was associated with pro-thrombotic changes on the endothelial surface of hepatic microvessels. [123]. The accumulation of particles in the liver exerted a strong pro-coagulatory effect but did not trigger an inflammatory reaction. The effects of a particle burden on the spleen are unknown but could include adjuvant effects as observed with diesel particles and antigens in the lung [124].