Effects of dust exposure on IGF1 and autophagy related to coal workers' pneumoconiosis.

OBJECTIVE: To analyze the correlated factors of pneumoconiosis in coal miners, and explore the potential regulatory mechanism of insulin-like growth factor 1 (IGF1) in pneumoconiosis progression, so as to provide scientific evidence for the prevention and clinical treatment of coal workers' pneumoconiosis. METHODS: Clinical data of 2028 employees from a coal mining enterprise in Tangshan City, Hebei Province during 2023-2024 were retrospectively analyzed to screen the risk indicators of coal workers' pneumoconiosis. A SiO₂-induced macrophage injury cell model was established to simulate pneumoconiosis-related pathological changes. The expression levels of inflammatory cytokines (IL-6, IL-1β), polypeptide growth factor (IGF1), autophagy marker proteins (LC3, P62) and intracellular signaling kinases (PI3K, AKT, mTOR) were detected. Logistic regression analysis was applied to identify pneumoconiosis correlated factors, and bioinformatics analysis was performed to clarify the regulatory relationship between dust exposure, IGF1 expression and cellular autophagy activity. RESULTS: Early initial working age, long dust exposure duration, smoking, elevated white blood cell count and increased AST/ALT ratio were key correlated factors for pneumoconiosis. The coal worker pneumoconiosis group presented enhanced inflammatory response, upregulated IGF1 expression and altered autophagy-related protein expression activity. Consistent with the observational trends observed in human subjects, in vitro cellular assays demonstrated that SiO₂ stimulation was accompanied by elevated inflammatory response and IGF1 abundance, altered autophagy-related protein expression, and a rise in activity of the PI3K/AKT/mTOR kinase signaling cascade. CONCLUSION: Age, early initial working age, prolonged dust exposure, smoking, elevated white blood cell count and increased AST/ALT ratio are correlated factors for coal workers' pneumoconiosis. Synchronous alterations in IGF1 upregulation, elevated phosphorylation levels of PI3K and AKT, and abnormal expression of autophagy-related markers were observed in pneumoconiosis patients and silica-stimulated macrophages, revealing correlative molecular links among these molecules in pneumoconiosis progression.