背景:没有研究检查过多氟烷基物质(PFAS)暴露与慢性阻塞性肺疾病(COPD)风险之间的关系。本研究旨在探讨这种关系。
方法:这项研究纳入了4541名具有PFAS数据的个体,COPD,和协变量来自NHANES2007-2018。血清PFAS包括全氟己烷磺酸盐(PFHxS),全氟壬酸(PFNA),全氟辛酸(PFOA),全氟辛烷磺酸(PFOS)进行了分析,因为侦探率很高。考虑到PFAS水平的偏斜分布,使用自然对数变换的PFAS(Ln-PFAS)。Logistic回归分析,限制三次样条(RCS),并进行加权分位数和(WQS)回归,非线性,和混合效果。使用中介分析来评估白蛋白的介导作用。
结果:COPD患者的PFHxS水平较高,PFNA,PFOA,和全氟辛烷磺酸与没有COPD的人相比。Ln-PFNA(男性OR:1.92,95%CI:1.31至2.80,P:<0.001;女性OR:1.07,95%CI:0.81至1.40,P:0.636)和ln-PFOA(男性OR:2.17,95%CI:1.38至3.41,P:<0.001;女性OR:1.49,95%CI:1.08至2.05,P:0.016)与PFNA暴露与性别对COPD风险的交互作用显著(P交互作用:<0.001)。RCS曲线表明了ln-PFOA之间的非线性关系(P非线性:0.001),ln-PFNA(P非线性:0.045),和男性的COPD风险。WQS分析显示,男性混合PFAS暴露与COPD风险相关(OR:1.44,95%CI:1.18至1.75,P:<0.001)。白蛋白介导PFOA与COPD的关系(介导比例:-17.94%)。
结论:这项研究得出结论,PFOA和PFNA与男性较高的COPD风险有关,血清白蛋白在PFOA与COPD的关系中起中介作用。这些发现有助于COPD的预防。需要进一步的研究来探索潜在的机制。
BACKGROUND: No study has examined the association between per- and polyfluoroalkyl substances (PFAS) exposure and chronic obstructive pulmonary disease (COPD) risk. This study aims to explore this relationship.
METHODS: This study enrolled 4541 individuals who had available data on PFAS, COPD, and covariates from NHANES 2007-2018. Serum PFAS including perfluorohexane sulfonate (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) were analyzed, because of high detective rates. Considering the skew distribution of PFAS levels, the natural logarithm-transformed PFAS (Ln-PFAS) was used. Logistic regression analysis, restricted cubic spline (RCS), and weighted quantile sum (WQS) regression were performed to explore the single, nonlinear, and mixed effects. A mediating analysis was used to evaluate the mediated effects of albumin.
RESULTS: Individuals with COPD had higher levels of PFHxS, PFNA, PFOA, and PFOS compared to those without COPD. Ln-PFNA (OR males: 1.92, 95 % CI:1.31 to 2.80, P: <0.001; OR females: 1.07, 95 % CI: 0.81 to 1.40, P: 0.636) and ln-PFOA (OR males: 2.17, 95 % CI:1.38 to 3.41, P: <0.001; OR females: 1.49, 95 % CI: 1.08 to 2.05, P: 0.016) were associated with COPD risk especially in males. The interaction between PFNA exposure and sex on COPD risk was significant (P interaction: <0.001). The RCS curve demonstrated the nonlinear relationship between the ln-PFOA (P nonlinear:0.001), ln-PFNA (P nonlinear:0.045), and COPD risk in males. WQS analysis showed mixed PFAS exposure was correlated with COPD risk in males (OR: 1.44, 95 % CI:1.18 to 1.75, P: <0.001). Albumin mediated the relationship between PFOA and COPD (mediated proportion: -17.94 %).
CONCLUSIONS: This study concludes PFOA and PFNA are linked to a higher COPD risk in males, and serum albumin plays a mediating role in the relationship between PFOA and COPD. Thess findings are beneficial for the prevention of COPD. Further studies are required to explore potential mechanisms.