Dust related systemic syndrome in miners: an integrative concept of pathogenesis (comprehensive morphological, experimental, and immunohistochemical study)

Introduction. The accumulated clinical and morphological data indicate that dust related pathology in miners is not limited to isolated pulmonary fibrosis but represents a systemic process involving damage to the cardiovascular system, liver, kidneys, and brain. The absence of a unified concept uniting these changes hinders the development of early diagnosis and prevention.

The study aims to substantiate the introduction of the concept of “dust systemic syndrome” as a new clinical pathogenetic entity based on a comprehensive analysis of morphological, experimental, and immunohistochemical data.

Material and methods. The lungs, heart, liver, kidneys, and brain of 80 Kuzbass miners with varying work experience (from 1 to 30 years) and 40 individuals from the control group were examined. The scientists have conducted an experiment on 90 rats to model anthracosilicosis (intratracheal administration of coal dust for 1–12 weeks); they have used histological, morphometric, and immunohistochemical methods (NAM-56, Ki-67, vimentin, α-SMA, CD31).

Results. For the first time, the synchronous progression of structural changes in all studied organs, correlating with the duration of occupational exposure to coal dust, has been experimentally and morphologically proven. The authors identified universal pathological processes: systemic endothelial dysfunction (endotheliosis), hypertrophy of vascular smooth muscle cells, progressive perivascular fibrosis, and dystrophy of parenchymal cells. Immunohistochemical verification confirmed the activation of epithelial mesenchymal and endothelial mesenchymal transformation as key mechanisms of fibrogenesis. The experiment confirmed the etiological role of dust and the step by step nature of lesion development.

Limitations. The study has a number of limitations related to its retrospective design, the regional sample (Kuzbass), and the use of autopsy material from victims of man made disasters; it requires careful interpretation and may limit the direct extrapolation of the results. The experimental model in rats, despite the reproducibility of key pathogenetic mechanisms, does not fully reflect the chronic inhalation exposure of humans to dust. These limitations determine the need for further prospective studies with in vivo assessment of biomarkers of systemic endothelial damage and fibrogenesis in various coal mining regions.

Conclusion. The data obtained allow us to classify dust pathology as a systemic dust syndrome, a generalized process characterized by persistent macrophage inflammation, systemic endothelial dysfunction, and activation of epithelial-mesenchymal and endothelial-mesenchymal transformation, which leads to fibrous remodeling of all visceral organs. The introduction of the term "dust systemic syndrome" is justified morphologically and experimentally and opens up new prospects for early diagnosis and pathogenetic therapy.

Ethics. The study of the archived autopsy material was conducted in accordance with Order No. 207n of the Ministry of Health of Russia dated April 14, 2025, which does not require obtaining informed consent. The animal experiments were carried out in accordance with national and international standards (Orders No. 708n, No. 199n; Guide for the Care and Use of Laboratory Animals, 1996). The research protocol was approved by the local Ethics Committee of the Federal State Budgetary Scientific Institution "Research Institute for Complex Problems of Hygiene and Occupational Diseases” (meeting protocol No. 4, § 2 dated November 18, 2021).

Contributions:
Bondarev O.I. — data collection and processing, statistical analysis, writing the text;
Filimonov S.N. — data processing, editing;
Zhukova A.G. — data collection and data processing;
Gorokhova L.G. — data collection and data processing;
Bugaeva M.S. — data collection and data processing.

Funding. The study had no funding.

Conflict of interest. The authors declare no conflict of interest.

Received: 17.06.2026 / Accepted: 24.08.2026 / Published: 11.09.2026

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