Background

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with lung function decline. However, the underlying mechanisms for the association remain unclear.

Objectives

To explore potential role of a lung epithelial biomarker, Club cell secretory protein (CC16), in associations between PAH exposures and lung function decline.

Methods

We investigated 3384 adults from the Wuhan-Zhuhai cohort, and followed up at three years after first examination. Linear mixed models was used to quantify dose-response relationships between urinary monohydroxylated PAH metabolites (OH-PAHs) and lung function, as well as OH-PAHs and plasma CC16. Mediation analysis was conducted to investigate role of CC16 in the association between OH-PAHs and lung function. We also estimated the relationships between OH-PAHs and lung function change in three years among participants with different levels of CC16.

Results

Each 1-unit increase of log-transformed total urinary high and low molecular weight OH-PAHs (∑ HMW OH-PAH and ∑ LMW OH-PAHs) were associated with a 22.59 and 25.25 ml reduction of FEV₁ respectively, while ∑ HMW OH-PAH was associated with a 30.38 ml reduction of FVC. Moreover, these negative associations between OH-PAHs and lung function levels were significant only among low CC16 group (< 15.83 ng/ml). CC16 concentration decreased monotonically with increased high molecular weight OH-PAHs (∑ HMW OH-PAHs) when ∑ HMW OH-PAH concentration was over 0.67 μg/mmol Cr. CC16 mediated 22.13% of the association between ∑ HMW OH-PAH and FVC among individuals with higher ∑ HMW OH-PAH. After three years of follow-up, subjects with low level of plasma CC16 had a significant decline of FVC when exposed to high level of ∑ HMW OH-PAH.

Conclusions

CC16 play an important role in the association between high molecular weight PAHs and FVC. Individuals with low plasma CC16 level might suffer a decline in lung function when exposed to high level of high molecular weight PAHs.

中文翻译：

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尿中多环芳烃代谢产物，俱乐部细胞分泌蛋白和肺功能

背景

暴露于多环芳烃（PAHs）与肺功能下降有关。但是，该关联的基本机制仍不清楚。

目标

探讨肺上皮生物标志物，俱乐部细胞分泌蛋白（CC16），在PAH暴露与肺功能下降之间的关联中的潜在作用。

方法

我们调查了武汉至珠海的3384名成年人，并在首次检查后的三年内进行了随访。线性混合模型用于量化尿单羟基化PAH代谢物（OH-PAHs）与肺功能以及OH-PAHs和血浆CC16之间的剂量反应关系。进行了中介分析，以研究CC16在OH-PAHs与肺功能之间的关联中的作用。我们还估计了CC16水平不同的参与者在三年内OH-PAHs与肺功能变化之间的关系。

结果

对数转化的尿高，低分子量总OH-PAHs（∑ HMW OH-PAH和∑ LMW OH-PAHs）每增加1个单位，FEV ₁减少22.59和25.25 ml分别将∑ HMW OH-PAH与FVC降低30.38 ml相关联。此外，仅在低CC16组（<15.83 ng / ml）中，OH-PAHs与肺功能水平之间的这些负相关性才是显着的。当∑ HMW OH-PAH浓度超过0.67μg/ mmol Cr时，CC16浓度随高分子量OH-PAHs（∑ HMW OH-PAHs）的增加而单调降低。CC16介导了ΣHMW OH-PAH较高的个体中ΣHMW OH-PAH与FVC之间的关联的22.13％。经过三年的随访，血浆CC16水平低的受试者暴露于高水平的∑ HMW OH-PAH中时FVC明显下降。

结论

CC16在高分子量PAH和FVC之间的关联中起重要作用。血浆CC16水平低的个体暴露于高水平的高分子量PAHs下可能会导致肺功能下降。