From dust to disease: Neopterin as a marker of silicosis in ceramic industry workers

Silicosis, caused by prolonged inhalation of respirable crystalline silica (RCS) dust leads to irreversible lung fibrosis. It has emerged as a major occupational health burden within the rapidly expanding ceramic industry, where workers are routinely exposed to high concentrations of RCS. Inadequate dust control practices, limited occupational surveillance, and poor regulatory enforcement further amplify the risk, contributing to an under-recognized yet substantial disease burden among ceramic workers. Silica-induced lung damage activates macrophages, stimulates IFN-γ-mediated immune pathways, and increases oxidative stress, all of which cause enhanced neopterin production. A number of studies suggest that neopterin has potential to be a marker of silicosis. We recruited 30 ceramic industry workers with silicosis and 29 healthy controls. Neopterin levels were measured in serum and urine using ELISA and UHPLC, respectively. Serum neopterin levels were found to be significantly higher in silicosis patients (4.37 ± 1.25 ng/mL) than healthy controls (1.82 ± 0.23 ng/mL). The urinary neopterin levels were observed to be 655.03 ± 244.14 μmol/mol creatinine in silicosis patients as compared to 354.17 ± 116.46 μmol/mol creatinine in healthy controls. ROC analysis demonstrated robust discriminatory performance of neopterin, with AUCs of 0.997 (cut-off 2.483 ng/mL) for serum and 0.903 (cut-off 488.06 μmol/mol creatinine) for urinary neopterin. As compared to healthy controls, silicosis patients exhibited >2-fold and > 1.5-fold increase in serum and urinary neopterin levels, respectively. This finding should be examined further in larger cohort, including other patient-control groups and silica-exposed non-silicosis workers.