Evidence map›Paper›PMID 40240158›Full record

ArticleEnvironmental health and preventive medicine2025

Plasma club cell secretory protein reflects early lung injury: comprehensive epidemiological evidence.

Jiajun Wei, Jinyu Wu, Hongyue Kong, Liuquan Jiang, Yong Wang, Ying Guo, Quan Feng, Jisheng Nie, Yiwei Shi, Xinri Zhang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Environmental health and preventive medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Jiajun WeiMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Jinyu WuMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Hongyue KongMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Liuquan JiangXishan Coal Electricity Corporation Occupational Disease Prevention and Control Institute.
Yong WangMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Ying GuoMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Quan FengMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Jisheng NieMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.
Yiwei ShiNHC Key Laboratory of Pneumoconiosis, Shanxi Key Laboratory of Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Shanxi Medical University.
Xinri ZhangNHC Key Laboratory of Pneumoconiosis, Shanxi Key Laboratory of Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Shanxi Medical University.
Xiaomei KongNHC Key Laboratory of Pneumoconiosis, Shanxi Key Laboratory of Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Shanxi Medical University.
Xiao YuNHC Key Laboratory of Pneumoconiosis, Shanxi Key Laboratory of Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Shanxi Medical University.
Gaisheng LiuXishan Coal Electricity Corporation Occupational Disease Prevention and Control Institute.
Fan YangXishan Coal Electricity Corporation Occupational Disease Prevention and Control Institute.
Jun DongXishan Coal Electricity Corporation Occupational Disease Prevention and Control Institute.
Jin YangMOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is inaccurate to reflect the level of dust exposure through working years. Furthermore, identifying a predictive indicator for lung function decline is significant for coal miners. The study aimed to explored whether club cell secretory protein (CC16) levels can reflect early lung function changes.

methodsThe cumulative respiratory dust exposure (CDE) levels of 1,461 coal miners were retrospectively assessed by constructed a job-exposure matrix to replace working years. Important factors affecting lung function and CC16 were selected by establishing random forest models. Subsequently, the potential of CC16 to reflect lung injury was explored from multiple perspectives. First, restricted cubic spline (RCS) models were used to compare the trends of changes in lung function indicators and plasma CC16 levels after dust exposure. Then mediating analysis was performed to investigate the role of CC16 in the association between dust exposure and lung function decline. Finally, the association between baseline CC16 levels and follow-up lung function was explored.

resultsThe median CDE were 35.13 mg/m

conclusionsCC16 levels are more sensitive than lung indicators in reflecting early lung function injury and plays mediating role in lung function decline induced by dust exposure. Low baseline CC16 levels predict poor future lung function.

Indexed as

Air Pollutants, OccupationalDustLung InjuryOccupational ExposureUteroglobinAdultBiomarkersChinaCoal MiningFemaleHumansMaleMiddle AgedRetrospective StudiesAir Pollutants, OccupationalBiomarkersDustSCGB1A1 protein, humanUteroglobinClub cell secretory proteinCoal workers’ pneumoconiosisCumulative respiratory dust exposureLung function

Identifiers

PMID40240158
PMCPMC12006028

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.