Scholarlink

Background <p>Tin mine dust (MD), a by-product of tin mining and rock drilling, is a significant contributor to miners’ pneumoconiosis. This aerosolized dust is a complex mixture of mineral components, including potentially toxic heavy metals such as arsenic, which may contribute to the development of pneumoconiosis and lung cancer. This study investigates the inhalation toxicity of tin MD samples on pulmonary cells using an Air-Liquid Interface (ALI) exposure model.</p> Results <p>MD-A was characterized by high arsenic content, exceeding 30%. In contrast, the elemental composition of MD-B and MD-C was predominantly composed of calcium, magnesium, and aluminum. In the toxicity study, key toxicological endpoints (cell viability, cytotoxicity, pro-inflammatory markers, and cell barrier function) were systematically assessed, and real-time monitoring of the cell-delivered MD particles (MD-A, MD-B, MD-C, and silica) concentrations was achieved using QCM. MD-A significantly enhanced the proliferation ability of 16HBE and Calu-3 cells compared to other particulate matters, indicating arsenic-containing MD promotes cell proliferation. MD-A resulted in an increase in IL-1β mRNA expression in 16HBE cells; elevations in IL-1β, IL-6, IL-8, TNF-α, and CCL2 mRNA were observed in Calu-3 cells. Additionally, treatment with four different particles significantly increased the mRNA expression of MUC5AC in both cell types. Immunofluorescence staining demonstrated alterations in the typical morphology of epithelial cells exposed to arsenic-containing MD and silica particles. In this study, it was shown that four types of particles delivered via suspension to the same in vitro model can induce differing levels of cytotoxicity and proinflammatory responses. The differences in results underscore the specific effects of the inherent physicochemical attributes of particles on biological interactions.</p> Conclusions <p>Under identical particle size conditions, in vitro studies on inhalation toxicity reveal that the chemical composition of particulate matter causes varying degrees of toxic damage to cells. This study utilizes an advanced in vitro method to assess the inhalation hazards of tin MD particles by integrating the ALICE system. The chemical complexity of tin MD, particularly its significant arsenic content, requires special attention and thorough evaluation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Inhalation toxicity of arsenic-containing mine dust in an air-liquid interface bronchial epithelial model

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月27日

查看全文
  • Xiaoli Ji,
  • Yanping Li,
  • Shuyi Gu,
  • Zhen Min,
  • Daoyuan Sun,
  • Ziren Zhang,
  • Wenkang Jiang,
  • Jingbo Zhang

摘要

Background

Tin mine dust (MD), a by-product of tin mining and rock drilling, is a significant contributor to miners’ pneumoconiosis. This aerosolized dust is a complex mixture of mineral components, including potentially toxic heavy metals such as arsenic, which may contribute to the development of pneumoconiosis and lung cancer. This study investigates the inhalation toxicity of tin MD samples on pulmonary cells using an Air-Liquid Interface (ALI) exposure model.

Results

MD-A was characterized by high arsenic content, exceeding 30%. In contrast, the elemental composition of MD-B and MD-C was predominantly composed of calcium, magnesium, and aluminum. In the toxicity study, key toxicological endpoints (cell viability, cytotoxicity, pro-inflammatory markers, and cell barrier function) were systematically assessed, and real-time monitoring of the cell-delivered MD particles (MD-A, MD-B, MD-C, and silica) concentrations was achieved using QCM. MD-A significantly enhanced the proliferation ability of 16HBE and Calu-3 cells compared to other particulate matters, indicating arsenic-containing MD promotes cell proliferation. MD-A resulted in an increase in IL-1β mRNA expression in 16HBE cells; elevations in IL-1β, IL-6, IL-8, TNF-α, and CCL2 mRNA were observed in Calu-3 cells. Additionally, treatment with four different particles significantly increased the mRNA expression of MUC5AC in both cell types. Immunofluorescence staining demonstrated alterations in the typical morphology of epithelial cells exposed to arsenic-containing MD and silica particles. In this study, it was shown that four types of particles delivered via suspension to the same in vitro model can induce differing levels of cytotoxicity and proinflammatory responses. The differences in results underscore the specific effects of the inherent physicochemical attributes of particles on biological interactions.

Conclusions

Under identical particle size conditions, in vitro studies on inhalation toxicity reveal that the chemical composition of particulate matter causes varying degrees of toxic damage to cells. This study utilizes an advanced in vitro method to assess the inhalation hazards of tin MD particles by integrating the ALICE system. The chemical complexity of tin MD, particularly its significant arsenic content, requires special attention and thorough evaluation.