CHRONIC INHALATION EXPOSURE OF WISTAR RATS AND 2 DIFFERENT STRAINS OF MICE TO DIESEL-ENGINE EXHAUST, CARBON-BLACK, AND TITANIUM-DIOXIDE
CHRONIC INHALATION EXPOSURE OF WISTAR RATS AND 2 DIFFERENT STRAINS OF MICE TO DIESEL-ENGINE EXHAUST, CARBON-BLACK, AND TITANIUM-DIOXIDE
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DOI：
10.3109/08958379509015211
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发表时间：
1995-05-01
影响因子：
2.1
通讯作者：
LEVSEN, K
中科院分区：
文献类型：
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作者：
HEINRICH, U;FUHST, R;LEVSEN, K
将Wistar大鼠暴露于柴油发动机废气、炭黑（Printex 90，Degussa，FRC）和超细TiO 2（P25，Degussa，FRG）2年，随后在清洁空气中保持6个月。在实验过程中，炭黑和TiO 2的颗粒暴露浓度增加，以达到与柴油机烟灰暴露大鼠中发现的颗粒肺负荷相似的颗粒肺负荷。柴油机烟灰、炭黑和TiO 2的平均颗粒暴露浓度分别为7、11.6和10 mg/m3。这些大鼠的肺部肿瘤发生率随着累积颗粒暴露量（mg/m（3）x h）的增加而增加，与所使用的颗粒类型无关。暴露于2.5 mg/m3的柴油烟尘也诱导肺肿瘤发生率显著增加，但0.8 mg/m3的柴油烟尘没有。通过这项研究，可以证明，柴油机烟尘的碳核心是主要负责柴油机排气相关的肺肿瘤的发生，柴油机烟尘连接的多环芳烃（PAH）和NO2-PAH的作用可能是次要的在大鼠肺。超细碳和TiO 2颗粒的团聚体似乎特别适合主要对肺泡巨噬细胞和肺泡肺颗粒清除产生毒性作用。尽管在使用的最低柴油烟尘暴露浓度（0.8 mg/m3）下也观察到了这种肺毒性效应，但在这组大鼠中未检测到肺肿瘤发生率增加。该结果是否意味着如Bostal（1986）已经讨论的颗粒相关肺肿瘤诱导机制的阈值，或者是否由于统计学原因根本没有观察到肿瘤效应，需要进一步研究超细不溶性颗粒在肺中的可能作用模式。在与大鼠相同的暴露环境（高柴油烟灰炭黑，TiO 2）中饲养的NMRI小鼠没有显示出肺肿瘤发生率增加。此外，在NMRI和暴露于含4.5 mg/m3柴油烟尘的柴油废气或相同废气稀释但不含烟尘颗粒的C57 BL/6 N小鼠中，均未出现治疗相关的肿瘤反应。C57 BL/6 N小鼠暴露24个月，随后在清洁空气中再保持6个月。C57 BL/6 N小鼠的平均存活时间和每克肺湿重的颗粒负荷与暴露于7 mg/m3柴油烟尘的大鼠非常相似。
Wistar rats were exposed for 2 yr to diesel engine exhaust, carbon black (Printex 90, Degussa, FRC), and ultrafine TiO2 (P25, Degussa, FRG) and were subsequently kept in clean air for 6 mo. Particle exposure concentration was increased during the course of the experiment for carbon black and TiO2 to reach particle lung loads similar to those found in the diesel soot-exposed rats. The average particle exposure concentrations for diesel soot carbon black, and TiO2 were 7, 11.6, and 10 mg/m(3), respectively. Lung tumor rates in these rats increased with increasing cumulative particle exposure (mg/m(3) x h) independent of the type of particle employed. The exposure to 2.5 mg/m(3) diesel soot also induced a significantly increased lung tumor rate, but 0.8 mg/m(3) diesel soot did not. With this study, it could be demonstrated that the carbon core of diesel soot is mainly responsible for the occurrence of diesel engine exhaust-related lung tumors; the role of diesel soot-attached polycyclic aromatic hydrocarbons (PAH) and NO2-PAH is probably of minor importance in the rat lung. Agglomerates of ultrafine carbon and TiO2 particles seem particularly suited to exert toxic effects primarily on alveolar macrophages and alveolar lung particle clearance. Although such lung toxic effects were also seen with the lowest diesel soot exposure concentration (0.8 mg/m(3)) used, no increased lung tumor rate was detected in this group of rats. Whether this result implies a threshold for the particle-related lung tumor induction mechanism as already discussed by Vostal (1986) or whether the tumor effect was simply not observed because of statistical reasons needs further research on the possible mode of action of ultrafine insoluble particles in the lung. NMRI mice that were kept in the same exposure atmospheres (high diesel soot carbon black, TiO2) as the rats did not show an increased lung tumor rate. Furthermore, there was no treatment-related tumor response in NMRI nor in C57BL/6N mice exposed to diesel exhaust containing 4.5 mg/m(3) diesel soot or to the same exhaust dilution but devoid of soot particles. C57BL/6N mice were exposed for 24 mo and were subsequently kept in clean air for another 6 mo. Not only the average survival lime but also the particle load per gram lung wet weight of the C57BL/6N mice was very similar to rats exposed to 7 mg/m(3) diesel soot.