EBRC Consulting GmbH, Raffaelstr. 4, 30177, Hannover, Germany.
Fraunhofer Institute for Toxicology and Experimental Medicine (Fh-ITEM), Nikolai Fuchs Strasse 1, 30625, Hannover, Germany.
Regul Toxicol Pharmacol. 2022 Apr;130:105129. doi: 10.1016/j.yrtph.2022.105129. Epub 2022 Feb 4.
Lung cancer following inhalation in rodents is a major concern regarding exposure to cobalt substances. However, little information is available on adverse effects and toxicity following long-term inhalation exposure to poorly soluble cobalt substances with low bioavailability. Thus, the present study focused on pulmonary effects of the poorly soluble tricobalt tetraoxide (5, 20, 80 mg/m³) in a 28-day inhalation exposure study. Lung weights increased with increasing exposures. Bronchoalveolar lavage fluid analysis and histopathology revealed lung tissue inflammation at the mid-dose with increasing severity in the high-dose group and post-exposure persistency. Markers for cellular damage and cell proliferation were statistically significantly increased. No increase in 8-OH-dG lesions was observed, indicating an absence of oxidative DNA lesions. The primary effect of inhaled CoO particles is inflammation of the respiratory tract strongly resembling responses of inhaled "inert dust" substances, with a NOAEC of 5 mg/m³ under the conditions of this test.
吸入式钴物质对啮齿动物肺癌的影响是人们关注的主要问题。然而，对于长期吸入低生物利用度的难溶性钴物质的不良影响和毒性，目前还知之甚少。因此，本研究集中于在为期 28 天的吸入暴露研究中，研究肺部对难溶性三氧化二钴（5、20、80mg/m³）的影响。肺重量随暴露量的增加而增加。支气管肺泡灌洗分析和组织病理学显示，中剂量组的肺组织炎症随着高剂量组的加重而加重，且在暴露后持续存在。细胞损伤和细胞增殖的标志物显著增加。8-OH-dG 损伤未见增加，表明不存在氧化 DNA 损伤。吸入 CoO 颗粒的主要作用是强烈模仿呼吸道炎症对吸入“惰性粉尘”物质的反应，在该试验条件下，NOAEC 为 5mg/m³。
