Pulmonary response to glass fiber by inhalation exposure.
Pulmonary response to glass fiber by inhalation exposure.
复制标题
吸入暴露对玻璃纤维的肺部反应。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
R. S. Waritz
中科院分区：
文献类型：
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作者：
K. P. Lee;C. Barras;F. D. Griffith;R. S. Waritz
大鼠、仓鼠和豚鼠暴露于空气中重量浓度为 0.42 毫克的玻璃纤维。每升，每天 6 小时，每周 5 天，持续 90 天。大于5微米的尘粒数量。长度为每升 0.73 x 10(6)，平均直径约为 1.2 微米。大多数颗粒小于 2 微米。尺寸上，只有 15% 的灰尘颗粒具有纤维状形状。很少有纤维长度超过 10 微米。肺部反应的特征是吸入90天时出现肺泡蛋白沉积的巨噬细胞反应。光和超微结构的改变与其他实验或人类肺泡蛋白沉积症相似。肺泡蛋白沉积症在暴露后 1 年消失，但局灶性尘埃细胞积聚和增殖的颗粒性肺细胞在整个 2 年恢复期持续存在。在灰尘沉积区域没有发现明显的纤维化或基质变化。在仓鼠和豚鼠中，大多数铁质身体是由纤维形成的，而不是由微小的灰尘颗粒形成的。气管支气管淋巴结明显肿胀并充满灰尘细胞。
Rats, hamsters, and guinea pigs were exposed to airborne glass fiber at a gravimetric concentration of 0.42 mg. per liter for 6 hours per day, 5 days per week for 90 days. The number of dust particles greater than 5 micron. in length was 0.73 x 10(6) per liter with an average diameter of approximately 1.2 micron. Most particles were less than 2 micron. in size and only 15% of the dust particles had a fibrous shape. Few fibers were longer than 10 micron. The pulmonary response was characterized by macrophage reaction with alveolar proteinosis at 90 days of inhalation. The light and ultrastructural alterations were similar to the other experimental or human alveolar proteinosis. The alveolar proteinosis disappeared at 1-year postexposure, but focal dust cell accumulation with proliferating granular pneumocytes persisted throughout the 2-year recovery period. No significant fibrosis or stromal changes were found in the dust-deposited areas. In hamsters and guinea pigs, most ferruginous bodies were developed from fibrous fibers but not from tiny dust particles. The tracheobronchial lymph nodes were markedly swollen and laden with dust cells.