MYELOTOXICITY INDUCED IN B6C3F1 MICE BY METHYL ISOCYANATE INHALATION EXPOSURE

4天吸入暴露（6小时/天）对0、1和 3 ppm异氰酸甲酯（MIC）对雌性骨髓参数的影响 在接触后5、8、21天和1年对小鼠进行了检查。 MIC暴露与骨髓相关， 通过细胞减少，抑制多能干细胞（CFU-S）， 粒细胞-巨噬细胞祖细胞（CFU-C）和红系前体细胞 （CFU-E）。 造血参数恢复至 在1 ppm剂量组中，21天时正常，但在3 ppm剂量组中不正常 剂量组。 MIC是一种高活性化学物质， 直接作用于鼻粘膜上皮 腔和主要气道，并且没有组织学证据 一种系统效应。 对骨无明显影响 急性骨髓炎后1年小鼠骨髓细胞结构和CFU-C 以3和10 ppm的剂量暴露2小时。 最后，我谨指出， MIC暴露似乎导致衬里上皮细胞急性死亡 鼻道和主要气道的暂时性改变 骨髓参数可能与肺部 直接损伤或通过胸腺继发损伤。 这些 结果发表在《环境》杂志上。健康感知72，第143-148页， 1987.

The effects of a 4-day inhalation exposure (6 hr/day) to 0, 1 and 3 ppm methyl isocyanate (MIC) on bone marrow parameters in female mice were examined at 5, 8, 21 days and 1 year following exposure. The MIC exposure was associated with the bone marrow as evidenced by hypocellularity, suppression of pluripotent stem cells (CFU-S), granulocyte-macrophage progenitors (CFU-C) and erythroid precursors (CFU-E) in both dose groups. Hematopoietic parameters returned to normal by 21 days in the 1 ppm dose group, but not in the 3 ppm dose group. MIC is a highly reactive chemical that appears to exert its effect directly on the lining epithelium of the nasal cavity and major airways, and there was no histological evidence of a systemic effect. There was no significant effect on bone marrow cellularity and CFU-C in mice 1 year following acute exposure at the doses of 3 and 10 ppm for 2 hours. In conclusion, MIC exposure appears to cause acute cell death of lining epithelium of the nasal passages and major airways with transient alterations of bone marrow parameters that are likely related to the pulmonary injury either directly or secondary through the thymus. These results were publicated in Environ. Health Persp. 72, p. 143-148, 1987.