Castranova V, Bowman L, Shreve J M, Jones G S, Miles P R
J Toxicol Environ Health. 1982 Feb;9(2):317-25. doi: 10.1080/15287398209530164.
Samples of volcanic ash from Mount St. Helens were collected from Spokane, Washington, after the major eruption of May 18, 1980. The toxicity of ash to the lung was estimated by monitoring the effects of in vitro and in vivo exposure on various physiological parameters of isolated lung cells. Volcanic ash had little effect on O2 consumption of rabbit type II pneumocytes, O2 consumption or superoxide release of resting rat alveolar macrophages, or membrane integrity of rat alveolar macrophages. Ash also caused no significant lipid peroxidation in rat lung microsomes. However, volcanic ash did inhibit superoxide anion release from zymosan-stimulated rat alveolar macrophages. Since superoxide is an antibacterial substance, this result suggests that exposure to volcanic ash may adversely affect the ability of alveolar macrophages to protect the lung from infection.
1980年5月18日圣海伦斯火山大爆发后，从华盛顿州斯波坎采集了火山灰样本。通过监测体外和体内暴露对分离的肺细胞各种生理参数的影响，评估了火山灰对肺部的毒性。火山灰对兔II型肺细胞的氧气消耗、静息大鼠肺泡巨噬细胞的氧气消耗或超氧化物释放，以及大鼠肺泡巨噬细胞的膜完整性几乎没有影响。火山灰在大鼠肺微粒体中也未引起明显的脂质过氧化。然而，火山灰确实抑制了酵母聚糖刺激的大鼠肺泡巨噬细胞中超氧阴离子的释放。由于超氧化物是一种抗菌物质，这一结果表明，接触火山灰可能会对肺泡巨噬细胞保护肺部免受感染的能力产生不利影响。
