Inflammatory and oxidative stress biomarkers induced by silica exposure in crystal craftsmen

Abstract

Background Identification of biomarkers associated with the diagnosis and prognosis of silicosis would be highly advantageous in the clinical setting. The aim of this study is to evaluate inflammatory and oxidative stress biomarkers in subjects exposed to silica. Methods A cross‐sectional study of crystal craftsmen currently (n = 34) or formerly (n = 35) exposed and a group of nonexposed subjects (n = 12) was performed. Personal respirable dust samples were collected. Plasma inflammatory mediators (bone morphogenetic protein‐ BMP2 and chemokines CXCL16, and CCL5), oxidative stress enzymes (thiobarbituric acid reactive substances [TBARs] and superoxide dismutase [SOD]), and nitrite (NO2−) were analyzed in parallel with nitric oxide in exhaled breath (FeNO). Results Being currently or formerly exposed to silica was related to increased levels of CXCL16 and TBARs. Currently, exposed subjects showed decreased levels of SOD. Thirty‐seven craftsmen with silicosis (26 formerly and 11 currently exposed) showed higher levels of CXCL16, which was positively associated with the radiological severity of silicosis. Compared with the nonexposed, subjects with silicosis had higher levels of TBARs and those with complicated silicosis had lower levels of SOD. In multivariate analysis, higher levels of CXCL16 were associated with exposure status and radiological severity of silicosis. Smoking was not a confounder. FeNO did not distinguish between the exposure status and the presence of silicosis. Conclusion CXCL16 emerged as a potential biomarker that could distinguish both silica exposure and silicosis. TBARs were elevated in exposed individuals. However, their clinical applications demand further investigation in follow‐up studies of representative samples.

Serum levels of inflammatory mediators as prognostic biomarker in silica exposed workers

“…Previous research has described increased levels of inflammatory serum markers in silica exposed subjects 8 , 15 . It has been observed that the presence of different polymorphisms, alongside with TNF, IL-1RA and TGF-β1 16 – 18 confer a higher risk of disease, and that levels of TNF-α show an increase before the development of a clinically recognised silicosis 19 and that are associated with disease severity.…”

“…Once the disease is contracted, silicosis can evolve to cause important morbidity and mortality, even after exposure is ceased. To date, different potential biomarkers have been suggested 8 but the lack of definitive results precludes use in clinical practice.…”

Volume-based tomography for the diagnosis of incipient silicosis in former gold miners

“…This study showed that, even in individuals with relevant exposure and ILO category 0 radiographs, CT classification of nodules was able to capture the presence of silicosis, which was supported by a dose–response gradient. Likewise, improved understanding of the basic pathophysiology of silicosis and the role of many cytokines, chemokines and other mediators involved in pulmonary fibrotic response,27 35 along with modern imaging techniques, may improve the recognition of early signs of the disease.…”

Nanopartículas: Efectos en La Salud Humana Y El Medio Ambiente

“…Las NPs de muy baja biosolubilidad como SiO2, CeO2, ZrO2, y asbestos pueden destruir a estas células liberando enzimas y ROS. Esto genera citoquinas inflamatorias y fibróticas, causando daños en el tejido [28]. En resumen, se han identificado varios procesos de daño toxicológico, sin embargo, los mecanismos completos que subyacen a ciertos hallazgos toxicológicos aún no se comprenden del todo y siguen siendo objeto de intensa investigación.…”