Introduction: Patients with SA silicosis present a rapid progression from simple silicosis (SS) to
complicated (SC). Classification is based on radiology, but limited studies are available that
have explored biomarkers and systemic inflammatory indices from routine clinical tests.

Material and methods: Observational study of patients with SA silicosis under follow-up at our
center recording biomarker levels according to stage. All patients had stopped exposure to SA
for years.

Results: We studied 109 patients (66 SS, 43 CS) and 23 controls. We present 3 markers, ACE
(angiotensin-converting enzyme), LDH (lactate dehydrogenase) and monocytes together with
ratios such as SIRI (systemic inflammatory response index), AISI (aggregate systemic
inflammatory index) and LMR (lymphocyte-to-monocyte inflammation ratio) with statistically
significant differences between SS and CS: ACE: 69.55 vs 86.21 (p = 0.003), LDH: 208.16 vs
256.41 (p = 0.001), AISI: 335.37 vs 442.34 (p = 0.03). SIRI 1.35 vs 1.79 (p = 0.012), LMR: 3.06 vs
2.67 (p = 0.034) and monocytes: 0.56 vs 0.63 (p = 0.035). Controls and SS: ACE: 41.28 vs 69.55
(p = 0.001), Lymphocytes: 2.09 vs 1.66 (p = 0.001), neutrophil-lymphocyte ratio (NLR): 1.82 vs
2.49 (p = 0.001), SII (systemic immunoinflammation index): 404.19 vs 595.21 (p = 0.001 ), LMR:
4.07 vs 3.06 (p = 0.001), PLR (platelet-lymphocyte ratio): 112.83 vs 159.50 (p = 0.001), AISI:
237.37 vs 335.37 (p = 0.001). Differences between controls and CS cases were more marked
than controls and SS.

Conclusions: Our findings show that an inflammatory state exists. The biomarkers studied can
help predict the evolution of the disease, requiring longitudinal studies.