Presence of acute phase response in coal workers' pneumoconiosis.

Rego, Gumersindo; Achaerandio, G Ocio; Cuervo, V González; Menendez, Christopher; Gonezález, C Martínez; Álvarez, Carlos

doi:10.1136/oem.48.3.193

Cited by 6 publications

(5 citation statements)

References 9 publications

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“…Unusually, a series of non-specific biomarkers such as CRP, AAT and LDH were assessed in our study on silicosis; we have not found any prior study in which ferritin has been analysed. However, several studies 33 , 34 show elevated CRP levels, a non-specific biomarker, in patients exposed to silica and increasing according to silicosis severity, as was the case in our study. Our series shows elevated levels of alpha-1-AT, in a similar fashion to Montes II et al 35 .…”

Section: Discussionsupporting

confidence: 76%

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

Blanco-Pérez

Blanco‐Dorado

Rodrı́guez-Garcı́a

et al. 2021

Sci Rep

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Silicosis is a diffuse interstitial lung disease caused by sustained inhalation of silica and silicates. Several cytokines are activated by their inhalation and can mediate the process of pulmonary fibrosis. The identification of biomarkers could allow an early diagnosis before the development of radiological alterations and help monitor the evolution of patients. The objetive of this study was to determine the clinical significance of specific biomarkers, to estimate their association with the development, severity and/or progression of silicosis, and identify determinants of this evolution. We conducted a prospective observational study in patients attending the pulmonology clinic from 2009 to 2018. Serum levels of the following inflammatory mediators were assessed: interleukin-6 (IL-6), interleukin 2 receptor subunit alpha (IL2R) interleukin 1 beta (IL1B), interleukin-8 (IL-8), tumour necrosis factor-alpha (TNF-α), transforming growth factor-beta1 (TGF-β1), alpha-1 antitrypsin (AAT), C-reactive protein (CRP), lactate dehydrogenase (LDH) and ferritin in subjects exposed to silica, with and without silicosis. Association between those inflammatory mediators with lung function measurements and radiological severity of disease and their impact on prognosis were analysed. 337 exposed to silica (278 with silicosis) and 30 subjects in the control group were included. IL-8, α1AT, ferritin, CRP and LDH levels were higher in silicosis than in those exposed to silica without silicosis. IL-8, LDH and AAT levels were associated with progression of silicosis and IL-6, IL-8, LDH, AAT, ferritin, and CRP with vital status. The results of the ROC analysis indicated the potential of IL-8 as a biomarker in the presence of silicosis and for the prediction of mortality.

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Section: Discussionsupporting

confidence: 76%

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

Blanco-Pérez

Blanco‐Dorado

Rodrı́guez-Garcı́a

et al. 2021

Sci Rep

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“…Accordingly, workers from Swedish iron foundries did not present changes in their circulating CRP blood levels 52 , and neither did patients with different stages of silicosis 28 . However, in other studies including workers exposed to silica, an increase in serum CRP was detected 45 , 53 , 54 . Our results for CRP could be explained as a consequence of the fact that the inflammatory state of the patients may have become chronic, rather than acute, due to the time elapsed between exposure to silica, diagnosis and sampling, although further research is needed to confirm this hypothesis.…”

Section: Discussionmentioning

confidence: 67%

Inflammatory indices obtained from routine blood tests show an inflammatory state associated with disease progression in engineered stone silicosis patients

García-Núñez

Jiménez-Gómez

Hidalgo-Molina

et al. 2022

Sci Rep

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Patients with silicosis caused by occupational exposure to engineered stone (ES) present a rapid progression from simple silicosis (SS) to progressive massive fibrosis (PMF). Patient classification follows international rules based on radiology and high-resolution computed tomography (HRCT), but limited studies, if any, have explored biomarkers from routine clinical tests that can be used as predictors of disease status. Our objective was thus to investigate circulating biomarker levels and systemic inflammatory indices in ES silicosis patients whose exposure to ES dust ended several years ago. Ninety-one adult men, ex-workers in the manufacturing of ES, 53 diagnosed with SS and 38 with PMF, and 22 healthy male volunteers (HC) as controls not exposed to ES dust, were recruited. The following circulating levels of biomarkers like lactate dehydrogenase (LDH), angiotensin-converting-enzyme (ACE), protein C reactive (PCR), rheumatoid factor, alkaline phosphatase and fibrinogen were obtained from clinical reports after being measured from blood samples. As biochemical markers, only LDH (HC = 262 ± 48.1; SS = 315.4 ± 65.4; PMF = 337.6 ± 79.3 U/L), ACE (HC = 43.1 ± 18.4; SS = 78.2 ± 27.2; PMF = 86.1 ± 23.7 U/L) and fibrinogen (HC = 182.3 ± 49.1; SS = 212.2 ± 43.5; PMF = 256 ± 77.3 U/L) levels showed a significant sequential increase, not been observed for the rest of biomarkers, in the HC → SS → PMF direction. Moreover, several systemic inflammation indices neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), systemic inflammation response index (SIRI), systemic immune-inflammation index (SII), aggregate index of systemic inflammation (AISI) derived from whole blood cell counts showed significant differences between the HC, SS and PMF groups. All these biomarkers were analyzed using receiver operating characteristic (ROC) curves, and the results provided moderately high sensitivity and specificity for discriminating between ES silicosis patient groups and healthy controls. Our study reveals that some inflammatory biomarkers, easily available from routine blood analysis, are present in ES silicosis patients even several years after cessation of exposure to ES silica dust and they could help to know the progression of the disease.

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“…Ambient air pollution particles effect several changes in the peripheral blood, including decreases in red cell number,71 elevations in white blood cell counts,71 and increases in C-reactive protein,71 fibrinogen,38,71,72 and blood viscosity;71,73 the last two potentially contribute to the association of ambient PM with thrombotic events 74. Other particles have comparable effects on hemorheologic indices 75,76…”

Section: Particle-related Lung Injurymentioning

confidence: 99%

Lung injury after cigarette smoking is particle related

Sangani¹,

Ghio

2011

COPD

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The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2) the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 μg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis) after smoking cessation since the particle is retained in the lung and the exposure continues.

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Presence of acute phase response in coal workers' pneumoconiosis.

Abstract: To evaluate the role of personal factors in pneumoconiosis, several acute phase proteins were studied in 62 coal miners without acute illnesses and classified as having no pneumoconiosis (n = 19), simple pneumoconiosis (n = 23), or complicated pneumoconiosis with pro-

Cited by 6 publications

References 9 publications

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

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

Inflammatory indices obtained from routine blood tests show an inflammatory state associated with disease progression in engineered stone silicosis patients

Lung injury after cigarette smoking is particle related

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