Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230032, China.
BMC Public Health. 2024 Oct 11;24(1):2778. doi: 10.1186/s12889-024-20267-5.
The impact of polycyclic aromatic hydrocarbons (PAHs) on lung function has garnered attention, but studies mostly focus on individual effect. This study investigates urinary PAH metabolites as biomarkers of exposure and assesses the relationships between single and combined exposures to nine urinary PAH metabolites and lung function in adults.
Data from 4040 adults in the 2007-2012 National Health and Nutrition Examination Survey (NHANES) were analyzed. Weighted generalized linear models estimated the effects of individual PAH metabolites on lung function. Additionally, weighted quantile sum (WQS) regression, quantile g-computation (qgcomp), and Bayesian kernel machine regression (BKMR) were employed to evaluate the combined impacts of multiple PAH metabolites.
Analyses of individual PAH metabolites revealed negative associations with lung function, excluding forced vital capacity (FVC). The WQS, qgcomp, and BKMR models consistently showed that exposure to multiple PAH metabolites was associated with lung function decrease. WQS indicated that 2-hydroxynaphthalene (2-NAP) was the largest contributor to the reductions in forced expiratory volume in 1 s (FEV1), FVC, peak expiratory flow (PEF), and forced expiratory flow from 25 to 75% of FVC (PEF25-75%). Additionally, 1-hydroxypyrene (1-PYR) was the primary PAH metabolite contributing to the decreases in FEV1/FVC and fractional exhaled nitric oxide (FeNO). The combined effect of urinary PAH metabolites did not affect FVC in the current smokers or FeNO in nonsmokers, but decreased FEV1/FVC in current smokers.
This study strengthens the negative relationships between multiple PAH metabolites exposure and lung function in adults. Given the limitations of this study, including the lack of knowledge of other exposure pathways and the uncertainty of urinary metabolites, further research is necessary to explore the mechanisms underlying these associations and to address the limitations in exposure assessment.
多环芳烃（PAHs）对肺功能的影响引起了关注，但研究主要集中在单一效应上。本研究调查了尿中多环芳烃代谢物作为暴露标志物，并评估了 9 种尿中多环芳烃代谢物单一和联合暴露与成年人肺功能之间的关系。
分析了 2007-2012 年国家健康和营养检查调查（NHANES）中 4040 名成年人的数据。加权广义线性模型估计了单个 PAH 代谢物对肺功能的影响。此外，还采用加权分位数总和（WQS）回归、分位数 g 计算（qgcomp）和贝叶斯核机器回归（BKMR）评估了多种 PAH 代谢物的联合影响。
对个体 PAH 代谢物的分析表明，除了用力肺活量（FVC）外，它们与肺功能呈负相关。WQS、qgcomp 和 BKMR 模型一致表明，暴露于多种 PAH 代谢物与肺功能下降有关。WQS 表明，2-羟基萘（2-NAP）是用力呼气量 1 秒（FEV1）、FVC、呼气峰流速（PEF）和 FVC 25%至 75%之间的强制呼气流量（PEF25-75%）降低的最大贡献者。此外，1-羟基芘（1-PYR）是导致 FEV1/FVC 和呼出气一氧化氮分数（FeNO）降低的主要 PAH 代谢物。尿中多环芳烃代谢物的联合作用对当前吸烟者的 FVC 或非吸烟者的 FeNO 没有影响，但降低了当前吸烟者的 FEV1/FVC。
本研究加强了多环芳烃代谢物暴露与成年人肺功能之间的负相关关系。鉴于本研究的局限性，包括缺乏对其他暴露途径的了解和对尿代谢物的不确定性，需要进一步研究以探讨这些关联的机制，并解决暴露评估中的局限性。
