Subchronic pulmonary toxicity of ambient particles containing cement production–related elements

Eun Jung Park, Mi Jin Yang, Min Sung Kang, Young Min Jo, Cheolho Yoon, Yunseo Lee, Dong Wan Kim, Gwang Hee Lee, Ik Hwan Kwon, Jin Bae Kim

Research output: Contribution to journalArticlepeer-review


Chronic respiratory disease is among the most common non-communicable diseases, and particulate materials (PM) are a major risk factor. Meanwhile, evidence of the relationship between the physicochemical characteristics of PM and pulmonary toxicity mechanism is still limited. Here, we collected particles (CPM) from the air of a port city adjacent to a cement factory, and we found that the CPM contained various elements, including heavy metals (such as arsenic, thallium, barium, and zirconium) which are predicted to have originated from a cement plant adjacent to the sampling site. We also delivered the CPM intratracheally to mice for 13 weeks to investigate the pulmonary toxicity of inhaled CPM. CPM-induced chronic inflammatory lesions with an increased total number of cells in the lung of mice. Meanwhile, among inflammatory mediators measured in this study, levels of IL-1β, TNF-α, CXCL-1, and IFN-γ were elevated in the treated group compared with the controls. Considering that the alveolar macrophage (known as dust cell) is a professional phagocyte that is responsible for the clearance of PM from the respiratory surfaces, we also investigated cellular responses following exposure to CPM in MH-S cells, a mouse alveolar macrophage cell line. CPM inhibited cell proliferation and formed autophagosome-like vacuoles. Intracellular calcium accumulation and oxidative stress, and altered expression of pyrimidine metabolism- and olfactory transduction-related genes were observed in CPM-treated cells. More interestingly, type I-LC3B and full-length PARP proteins were not replenished in CPM-treated cells, and cell cycle changes, apoptotic and necrotic cell death, and caspase-3 cleavage were not significantly detected in cells exposed to CPM. Taken together, we conclude that dysfunction of alveolar macrophages may contribute to CPM-induced pulmonary inflammation. In addition, given the possible transformation of heart tissue observed in CPM-treated mice, we suggest that further study is needed to clarify the systemic pathological changes and the molecular mechanisms following chronic exposure to CPM.

Original languageEnglish
Pages (from-to)116-128
Number of pages13
JournalToxicology Reports
Publication statusPublished - 2023 Dec

Bibliographical note

Publisher Copyright:
© 2023 The Authors


  • Autophagy
  • Cement
  • Multinucleated macrophages
  • Particulate materials
  • Pulmonary inflammation

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis


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