Secondary prevention of silicosis and silico‐tuberculosis by periodic screening of silica dust exposed workers using serum club cell protein 16 as a proxy marker

AbstractSilicosis is an irreversible, incurable and progressive occupational disease caused by prolonged exposure to crystalline-silica dust while working in the relevant industries. Conventionally diagnosis is done by chest radiology, often in an advanced stage as early symptoms often go unnoticed. Early detection and necessary intervention (secondary prevention) could be a realistic possible control strategy for controlling silicosis as no effective treatment is available to stop and/or reverse the pathological process. Additionally, these patients are also vulnerable to pulmonary tuberculosis, which often becomes difficult to treat and with uncertain treatment outcome. Considering India has a huge burden of silicosis and silico-tuberculosis, a rapid and inexpensive screening method was realized to be an urgent need for early detection of silicosis among silica dust exposed workers. Serum club cell protein 16 (CC16) is evidenced to be a useful proxy screening marker for early detection of silicosis as evidenced from the recent research work of ICMR-National Institute of Occupational Health (ICMR-NIOH), India. In this study a lateral-flow assay for semi-quantitative estimation of serum CC16 level was developed. The detection was performed using gold nanoparticles conjugated anti-CC16 monoclonal antibodies. A sum of 106 serum samples was tested to do the performance evaluation of the assay. A concentration of 6 ng/ml or less produced one band, 6.1–9 ng/ml produced two bands, while more than 9 ng/ml produced all the three bands at the test zone. The sensitivity of the assay was 100% while the specificity was 95%. This assay may be used as a sensitive tool for periodic screening of silica dust exposed vulnerable workers for early detection of silicosis in them.

Download Full-text

Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD

Molecular Medicine Reports ◽

10.3892/mmr.2018.9216 ◽

2018 ◽

Cited By ~ 3

Author(s):

Min Pang ◽

Hong‑Yan Liu ◽

Ting Li ◽

Dan Wang ◽

Xiao‑Yun Hu ◽

...

Keyword(s):

Cigarette Smoke ◽

Lung Inflammation ◽

Disease Model ◽

Cell Protein ◽

Club Cell

Download Full-text

Club cell protein 16 and cytokeratin fragment 21-1 as early predictors of pulmonary complications in polytraumatized patients with severe chest trauma

PLoS ONE ◽

10.1371/journal.pone.0175303 ◽

2017 ◽

Vol 12 (4) ◽

pp. e0175303 ◽

Cited By ~ 10

Author(s):

Lukas L. Negrin ◽

Gabriel Halat ◽

Stephan Kettner ◽

Markus Gregori ◽

Robin Ristl ◽

...

Keyword(s):

Chest Trauma ◽

Pulmonary Complications ◽

Cell Protein ◽

Club Cell ◽

Early Predictors

Download Full-text

Emphysema and extrapulmonary tissue loss in COPD: a multi-organ loss of tissue phenotype

European Respiratory Journal ◽

10.1183/13993003.02146-2017 ◽

2018 ◽

Vol 51 (2) ◽

pp. 1702146 ◽

Cited By ~ 18

Author(s):

Bartolome R. Celli ◽

Nicholas Locantore ◽

Ruth Tal-Singer ◽

John Riley ◽

Bruce Miller ◽

...

Keyword(s):

Surfactant Protein ◽

Forced Expiratory Volume ◽

Fat Free Mass ◽

Tissue Loss ◽

Cell Protein ◽

Surfactant Protein D ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Club Cell ◽

Body Compartments

We tested whether emphysema progression accompanies enhanced tissue loss in other body compartments in 1817 patients from the ECLIPSE chronic obstructive pulmonary disease (COPD) cohort.Clinical and selected systemic biomarker measurements were compared in subjects grouped by quantitative tomography scan emphysema quartiles using the percentage of low attenuation area (LAA%). Lowest and highest quartile patients had amino-acid metabolomic profiles. We related LAA% to 3 years decline in lung function (forced expiratory volume in 1 s (FEV1)), body mass index (BMI), fat-free mass index (FFMI) and exacerbations, hospitalisations and mortality rates.Participants with more baseline emphysema had lower FEV1, BMI and FFMI, worse functional capacity, and less cardiovascular disease but more osteoporosis. Systemic C-reactive protein and interleukin-6 levels were similar among groups, but club cell protein 16 was higher and interleukin-8, surfactant protein D and soluble receptor for advanced glycation end product were lower with more emphysema. Metabolomics differed between extreme emphysema quartiles. Patients with more emphysema had accelerated FEV1, BMI and FFMI decline and more exacerbations, hospitalisations and mortality.COPD patients with more emphysema undergo excessive loss of pulmonary and extrapulmonary tissue, which is probably related to abnormal tissue maintenance. Because of worse clinical outcomes, we propose this subgroup be named the multi-organ loss of tissue (MOLT) COPD phenotype.

Download Full-text

Pneumoproteins in Offshore Drill Floor Workers

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph16030300 ◽

2019 ◽

Vol 16 (3) ◽

pp. 300 ◽

Cited By ~ 3

Author(s):

Niels E. Kirkhus ◽

Bente Ulvestad ◽

Lars Barregard ◽

Øivind Skare ◽

Raymond Olsen ◽

...

Keyword(s):

Strong Association ◽

Surfactant Protein ◽

Cell Protein ◽

Surfactant Protein D ◽

Drilling Mud ◽

Air Concentration ◽

Work Period ◽

Club Cell ◽

Before And After ◽

Oil Mist

The aim was to assess pneumoproteins and a certain biomarker of systemic inflammation in drill floor workers exposed to airborne contaminants generated during drilling offshore, taking into consideration serum biomarkers of smoking, such as nicotine (S-Nico) and cotinine. Blood samples of club cell protein 16 (CC-16), surfactant protein D (SP-D) and C-reactive protein (CRP) were collected before and after a 14-day work period from 65 drill floor workers and 65 referents. Air samples of oil mist, drilling mud components and elemental carbon were collected in person. The drill floor workers were exposed to a median air concentration of 0.18 mg/m3 of oil mist and 0.14 mg/m3 of airborne mud particles. There were no differences in the concentrations of CC-16 and SP-D across the 14-day work period and no difference between drill floor workers and referents at baseline after adjusting for differences in sampling time and smoking. CRP decreased across the work period. There was a strong association between the CC-16 concentrations and the time of sampling. Current smokers with S-Nico > detection limit (DL) had a statistically significantly lower CC-16 concentration, while smokers with S-Nico <DL had CC-16 concentrations similar to that of the non-smokers. Fourteen days of work offshore had no effect on serum pneumoprotein and CRP concentrations. However, the time of blood sampling was observed to have a strong effect on the measured concentrations of CC-16. The effect of current smoking on the CC-16 concentrations appears to be dependent on the S-Nico concentrations.

Download Full-text

Short halt in vaping modifies cardiorespiratory parameters and urine metabolome: a randomized trial

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00268.2019 ◽

2020 ◽

Vol 318 (2) ◽

pp. L331-L344 ◽

Cited By ~ 2

Author(s):

Martin Chaumont ◽

Vanessa Tagliatti ◽

El Mehdi Channan ◽

Jean-Marie Colet ◽

Alfred Bernard ◽

...

Keyword(s):

Oxygen Tension ◽

Lung Function Test ◽

Cell Protein ◽

Lung Epithelium ◽

Short Term ◽

Baseline Serum ◽

Transcutaneous Oxygen ◽

Gas Exchanges ◽

Club Cell ◽

Urine Metabolome

Propylene glycol and glycerol are e-cigarette constituents that facilitate liquid vaporization and nicotine transport. As these small hydrophilic molecules quickly cross the lung epithelium, we hypothesized that short-term cessation of vaping in regular users would completely clear aerosol deposit from the lungs and reverse vaping-induced cardiorespiratory toxicity. We aimed to assess the acute effects of vaping and their reversibility on biological/clinical cardiorespiratory parameters [serum/urine pneumoproteins, hemodynamic parameters, lung-function test and diffusing capacities, transcutaneous gas tensions (primary outcome), and skin microcirculatory blood flow]. Regular e-cigarette users were enrolled in this randomized, investigator-blinded, three-period crossover study. The periods consisted of nicotine-vaping (nicotine-session), nicotine-free vaping (nicotine-free-session), and complete cessation of vaping (stop-session), all maintained for 5 days before the session began. Multiparametric metabolomic analyses were used to verify subjects’ protocol compliance. Biological/clinical cardiorespiratory parameters were assessed at the beginning of each session (baseline) and after acute vaping exposure. Compared with the nicotine- and nicotine-free-sessions, a specific metabolomic signature characterized the stop-session. Baseline serum club cell protein-16 was higher during the stop-session than the other sessions ( P < 0.01), and heart rate was higher in the nicotine-session ( P < 0.001). Compared with acute sham-vaping in the stop-session, acute nicotine-vaping (nicotine-session) and acute nicotine-free vaping (nicotine-free-session) slightly decreased skin oxygen tension ( P < 0.05). In regular e-cigarette-users, short-term vaping cessation seemed to shift baseline urine metabolome and increased serum club cell protein-16 concentration, suggesting a decrease in lung inflammation. Additionally, acute vaping with and without nicotine decreased slightly transcutaneous oxygen tension, likely as a result of lung gas exchanges disturbances.

Download Full-text