Engineered Stone (ES) silicosis, a serious occupational health problem and is highly prevalent due to the introduction of new materials for kitchen countertops and bathrooms. It is unknown what metabolic processes take place in the lungs and adenopathies, and how they relate to systemic inflammation. Thus, the objective of this study was to evaluate the metabolic activity of lymph nodes and lung lesions in patients with ES-related complicated silicosis and look into how these metabolic activities relate to particular biomarkers, systemic inflammatory indices, and peripheral blood lymphocyte subpopulations.
This study included patients with complex silicosis. The patients had all been engaged in finishing and installing engineered stone for at least 5 years, and they had all been away from these working circumstances for at least 7 years. Blood samples, pulmonary function tests, positron emission tomography/computed tomography employing 18F-fluorodeoxyglucose (18F-FDG PET/CT), and clinical data measures were all carried out.
The patients were 44 ± 5.4 years old on average. Additionally, the average number of years from exposure cessation was 11.6 ± 1.6 years, and the average exposure length was 10.94 ± 3.2 years. The average maximum standardized uptake value (SUVmax) of significant opacities was 6.32 ± 3.
Hypermetabolic mediastinal lymphadenopathies were seen in all of the patients, and extrathoracic lymphadenopathies were seen in 88.2% of the patients. Fibrinogen (ρ = 0.717, P = 0.001), the lymphocyte-to-monocyte ratio (ρ = -0.506, P = 0.038), the systemic inflammatory response index (ρ = 0.559, P = 0.02), and CD4+NKT cells were all associated with the SUVmax of the big opacities. Years after the end of silica exposure, large regions of lung opacity and lymphadenopathies showed elevated metabolic activity.
Overall, even years after exposure has stopped, ES silicosis causes severe metabolic activity in the lungs as well as in thoracic and extrathoracic lymphadenopathies. Given that silica is a Group 1 carcinogen and may cause lung cancer to coexist, it's critical to comprehend the topographic distribution of hypermetabolic lymphadenopathy linked to silica exposure in order to prevent PET from overstaging neoplastic processes.
Source:
León-Jiménez, A., Rodríguez-Rubio Corona, J., Jiménez-Gómez, G., Piñero Fernández-Reyes, M. L., Hidalgo-Molina, A., Pajares-Vinardel, M., Conde-Sánchez, M. Á., Campos-Caro, A., & Sanchez-Morillo, D. (2025). High metabolic activity in positron emission tomography and systemic inflammation occurring years after exposure cessation in engineered stone silicosis. Scientific Reports, 15(1), 25364. https://doi.org/10.1038/s41598-025-10562-5
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