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76637 
Journal Article 
Chronic inhalation exposure of Wistar rats and two different strains of mice to diesel engine exhaust, carbon black, and titanium dioxide 
Heinrich, U; Fuhst, R; Rittinghausen, S; Creutzenberg, O; Bellmann, B; Koch, W; Levsen, K 
1995 
Yes 
Inhalation Toxicology
ISSN: 0895-8378
EISSN: 1091-7691 
7 
4 
533-556 
English 
WOS:A1995RA71300004 
The possible mechanism of diesel soot related lung tumors was investigated in female Wistar-rats, female NMRI-mice, and female C57BL/6N-mice. The animals were exposed for 18 hours a day, 5 days a week for up to 24 months in special whole body exposure chambers. Exposures were to diesel engine exhaust, carbon-black (1333864), and ultrafine titanium-dioxide (13463677) (TiO2). The average particle exposure concentrations for diesel soot, carbon black and TiO2 were 7, 11.6, and 10mg/m3, respectively. After that time the rats and C57BL/6N-mice were kept under clean air conditions for an additional 6 months. Regardless of the exposure, lung tumor rates increased with increasing cumulative particle exposure. The carbon core of diesel soot was primarily responsible for the occurrence of diesel engine exhaust related lung tumors and the role of diesel soot attached to polycyclic aromatic hydrocarbons (PAHs) and nitrogen-dioxide (10102440) attached to PAH is likely to be of only minor importance. Exposure to 0.8mg/m3 diesel soot did not cause any increased lung tumor rate, suggesting a threshold for the particle related lung tumor induction mechanism. NMRI-mice did not show an increased lung tumor rate on exposure to high diesel soot, carbon-black, or TiO2, and there was no treatment related tumor response in NMRI nor in C57BL/6N-mice exposed to 4.5mg/m3 diesel soot.