Wei Jiajun, Wu Jinyu, Kong Hongyue, Jiang Liuquan, Wang Yong, Guo Ying, Feng Quan, Nie Jisheng, Shi Yiwei, Zhang Xinri, Kong Xiaomei, Yu Xiao, Liu Gaisheng, Yang Fan, Dong Jun, Yang Jin
MOE 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.
Xishan Coal Electricity Corporation Occupational Disease Prevention and Control Institute.
Environ Health Prev Med. 2025;30:26. doi: 10.1265/ehpm.24-00335.
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/m-years. RCS models revealed a rapid decline in forced vital capacity (FVC), forced expiratory volume in the first second (FEV), and their percentages of predicted values when CDE exceeded 25 mg/m-years. The dust exposure level (<5 mg/m-years) causing significant changes in CC16 was much lower than the level (25 mg/m-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.
通过工作年限来反映粉尘接触水平并不准确。此外，确定肺功能下降的预测指标对煤矿工人具有重要意义。本研究旨在探讨克拉拉细胞分泌蛋白（CC16）水平是否能反映早期肺功能变化。
通过构建工作暴露矩阵来替代工作年限，对1461名煤矿工人的累积呼吸性粉尘暴露（CDE）水平进行回顾性评估。通过建立随机森林模型选择影响肺功能和CC16的重要因素。随后，从多个角度探讨CC16反映肺损伤的潜力。首先，使用受限立方样条（RCS）模型比较粉尘暴露后肺功能指标和血浆CC16水平的变化趋势。然后进行中介分析，以研究CC16在粉尘暴露与肺功能下降之间的关联中的作用。最后，探讨基线CC16水平与随访肺功能之间的关联。
CDE的中位数为35.13mg/m-年。RCS模型显示，当CDE超过25mg/m-年时，用力肺活量（FVC）、第1秒用力呼气量（FEV）及其预测值百分比迅速下降。导致CC16发生显著变化的粉尘暴露水平（<5mg/m-年）远低于导致肺功能指标发生变化的水平（25mg/m-年）。CC16介导了11.1%至26.0%的与粉尘相关的肺功能下降。此外，基线CC16水平较低的工人未来肺功能下降幅度更大。
CC16水平在反映早期肺功能损伤方面比肺指标更敏感，并在粉尘暴露引起的肺功能下降中起中介作用。低基线CC16水平预示着未来肺功能不佳。
