Lancaster Environment Centre, Lancaster University, Lancaster LA1 4YQ, United Kingdom.
School of Medicine, Stanford University, Stanford, California 94305, United States.
J Hazard Mater. 2024 Dec 5;480:136090. doi: 10.1016/j.jhazmat.2024.136090. Epub 2024 Oct 9.
Unhealthy biological aging is related to higher incidence of varied age-related diseases, even higher all-cause mortality. Previous small sample size study suggested that Per- and poly-fluoroalkyl substances (PFAS) was associated with biological aging, but the evidence of exposure-response relationships, potential effect modifiers, and potential mediators were not investigated. Therefore, we conducted a cross-sectional analysis of national study including 14, 865 adults in the US from 8 survey cycles of NHANES from 2003 to 2018, to investigate the associations of PFAS compounds in body serum, including perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorononanoic acid (PFNA), and perfluorohexane sulfonic acid (PFHxS), with biological aging. Generalized linear models showed that higher human exposure to PFAS was associated with accelerated biological aging. Importantly, human exposure to PFOA, PFOS, PFNA, and PFHxS with detected level (above 0.10 ng/mL) was associated with an average of 3.3 year (95 %CI: 2.7, 3.9, P < 0.001), 14.9 year (95 %CI: 7.2, 22.7, P < 0.001), 10.9 years (95 %CI: 3.9, 17.7, P < 0.001), and 8.8 years (95 %CI: 4.8, 12.9, P < 0.001) of biological aging acceleration. Cubic spline models indicated exposure-response relationships where there was no safe threshold of PFAS level regarding harms to human healthy aging. The weighted sum regression model found the significant associations of PFAS compound mixture with biological aging acceleration, and PFOA was the dominant contributor among 4 PFAS compounds. Mediation analysis suggested that C-reactive protein, one of the inflammation biomarkers, might play as mediator in PFAS-induced accelerated biological aging, but not Triglyceride-glucose index. In summary, our study suggests that the effects of PFAS on biological aging acceleration should be of concern and more action plans to address their negative impact on human health should be launched.
不健康的生物衰老与多种与年龄相关的疾病的发病率较高有关，甚至与全因死亡率较高有关。之前的小样本量研究表明，全氟和多氟烷基物质（PFAS）与生物衰老有关，但没有研究暴露-反应关系、潜在的效应修饰剂和潜在的介质。因此，我们对美国 8 个 NHANES 调查周期中来自 14865 名成年人的全国性研究进行了横断面分析，以研究血清中 PFAS 化合物（包括全氟辛酸（PFOA）、全氟辛烷磺酸（PFOS）、全氟壬酸（PFNA）和全氟己烷磺酸（PFHxS））与生物衰老之间的关系。广义线性模型显示，人类对 PFAS 的暴露程度越高，生物衰老的速度就越快。重要的是，人类对可检测水平（高于 0.10ng/ml）的 PFOA、PFOS、PFNA 和 PFHxS 的暴露与平均 3.3 年（95%CI：2.7，3.9，P<0.001）、14.9 年（95%CI：7.2，22.7，P<0.001）、10.9 年（95%CI：3.9，17.7，P<0.001）和 8.8 年（95%CI：4.8，12.9，P<0.001）的生物衰老加速有关。三次样条模型表明，在 PFAS 对人类健康衰老的危害方面，没有安全的 PFAS 水平阈值。加权和回归模型发现，PFAS 化合物混合物与生物衰老加速之间存在显著关联，而在这 4 种 PFAS 化合物中，PFOA 是主要贡献者。中介分析表明，C 反应蛋白（一种炎症生物标志物）可能在 PFAS 诱导的生物衰老加速中发挥中介作用，但不是甘油三酯-葡萄糖指数。总之，我们的研究表明，PFAS 对生物衰老加速的影响应该引起关注，并应启动更多的行动计划来解决其对人类健康的负面影响。
