Ana Paula Scalia Carneiro1, Eduardo Algranti2, Nathalie Chérot-Kornobis3, Frank Silva Bezerra4, Ana Maria Tibiriça Bon5, Nayara Felicidade Tomaz Braz6, Débora Maria Soares Souza7, Guilherme de Paula Costa7, Marco Antônio Bussacos8, Olívia Maria de Paula Alves Bezerra9, André Talvani7. 1. Workers' Health Division of the Clinics Hospital of Federal University of Minas Gerais, Belo Horizonte, Brazil. 2. Division of Medicine, Fundacentro, São Paulo, Brazil. 3. CHU Lille, Occupational Medicine Department, University of Lille, Lille, France. 4. Laboratory of Experimental Pathophysiology/DECBI, Federal University of Ouro Preto, Ouro Preto, Minas Gerais, Brazil. 5. Division of Chemical Risks, Fundacentro, São Paulo, Brazil. 6. Interdisciplinary Laboratory for Medical Research, Department of Neuroscience, School of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil. 7. Laboratory of Immunobiology of Inflammation/DECBI, Federal University of Ouro Preto, Ouro Preto, Brazil. 8. Division of Epidemiology and Statistics, Fundacentro, São Paulo, Brazil. 9. School of Medicine, Department of Family Medicine, Mental and Collective Health, Federal University of Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
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.
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.
Authors: José Jesús Blanco-Pérez; Sara Blanco-Dorado; Javier Rodríguez-García; Mª Elena Gonzalez-Bello; Ángel Salgado-Barreira; Adriana Carolina Caldera-Díaz; Abel Pallarés-Sanmartín; Alberto Fernandez-Villar; Francisco Javier González-Barcala Journal: Sci Rep Date: 2021-06-25 Impact factor: 4.379