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

**Authors:** Jiajun Wei, Jinyu Wu, Hongyue Kong, Liuquan Jiang, Yong Wang, Ying Guo, Quan Feng, Jisheng Nie, Yiwei Shi, Xinri Zhang, Xiaomei Kong, Xiao Yu, Gaisheng Liu, Fan Yang, Jun Dong, Jin Yang

PMC · DOI: 10.1265/ehpm.24-00335 · Environmental Health and Preventive Medicine · 2025-04-15

## TL;DR

This study shows that club cell secretory protein (CC16) in the blood can detect early lung damage in coal miners more effectively than traditional measures.

## Contribution

The study demonstrates that CC16 is a sensitive and predictive biomarker for early lung injury caused by dust exposure in coal miners.

## Key findings

- CC16 levels change at much lower dust exposure levels than traditional lung function indicators.
- CC16 mediates 11.1% to 26.0% of the lung function decline caused by dust exposure.
- Low baseline CC16 levels predict greater future lung function decline.

## Abstract

It 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.

The 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.

The median CDE were 35.13 mg/m3-years. RCS models revealed a rapid decline in forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and their percentages of predicted values when CDE exceeded 25 mg/m3-years. The dust exposure level (<5 mg/m3-years) causing significant changes in CC16 was much lower than the level (25 mg/m3-years) that caused changes in lung function indicators. CC16 mediated 11.1% to 26.0% of dust-related lung function decline. Additionally, workers with low baseline CC16 levels experienced greater reductions in lung function in the future.

CC16 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.

The online version contains supplementary material available at https://doi.org/10.1265/ehpm.24-00335.

## Linked entities

- **Proteins:** SCGB1A1 (secretoglobin family 1A member 1)

## Full-text entities

- **Genes:** SCGB1A1 (secretoglobin family 1A member 1) [NCBI Gene 7356] {aka CC10, CC16, CCPBP, CCSP, UGB, UP-1}
- **Diseases:** lung function decline (MESH:D055370)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12006028/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12006028/full.md

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Source: https://tomesphere.com/paper/PMC12006028