Advances in the study of silicosis calcification have been slower. Zhang Zhiyong, such as occurred sooner, indicates a better prognosis. Scholars have confirmed through electron probe examination that a large number of calcified silicotic nodules contain silica dust enclosed within these calcified nodules, resulting in areas becoming dead zones. Animal experimental research suggests that silica dust cannot repeatedly harm other non-damaged lung tissue, thereby improving the prognosis. However, not all studies agree that calcification is a stable indicator of silicosis conditions.
Point England contains the following: ① Silicotic nodule calcification determines whether the silicon nodules will collapse, rather than determining if calcium will be present or not. Under experimental conditions, after intravenous injection of Tong calcium, macrophage function is stimulated, and silicosis changes for the worse. ② Silicotic nodule necrosis occurs before calcification, and nodular calcification happens after silica dust has already disintegrated macrophages which are released. On the other hand, microscopic examination of the edges of calcified nodules or around the alveoli near the nodules commonly reveals a large number of phagocytic macrophages exposed to silica dust, and alveoli free of macrophages still have quartz particles engulfed by new macrophages, providing a complementary description of calcified silicotic nodules, thus allowing the condition to continue expanding. ④ CaSiO3 solubility Ca(PO4)2. From a theoretical point of view, if the solution simultaneously contains Ca, SiO3, and PO4 three ions, Ca3(PO4)2 precipitate will form first. Therefore, neither experimental results nor theoretical arguments support the idea that silicotic nodule calcification can prevent the development of silicosis.