Xing Wei-Yi, Liu Fang-Hua, Wang Dong-Dong, Liu Jia-Ming, Zheng Wen-Rui, Liu Jia-Xin, Wu Lang, Zhao Yue-Yang, Xu He-Li, Li Yi-Zi, Wei Yi-Fan, Huang Dong-Hui, Li Xiao-Ying, Gao Song, Ma Qi-Peng, Gong Ting-Ting, Wu Qi-Jun
Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China; Clinical Research Center, Shengjing Hospital of China Medical University, Shenyang, China; Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University, Shenyang, China.
Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China; Clinical Research Center, Shengjing Hospital of China Medical University, Shenyang, China; Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University, Shenyang, China; Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Ecotoxicol Environ Saf. 2025 Feb;291:117825. doi: 10.1016/j.ecoenv.2025.117825. Epub 2025 Jan 30.
Although evidence suggests that perfluoroalkyl and polyfluoroalkyl substances (PFASs) are positively correlated to several disease risks, no studies have proven if plasma PFASs are related to ovarian cancer survival.
To explore the association between plasma PFASs and high-grade serous ovarian cancer (HGSOC) overall survival (OS) in the population who did not smoke.
We conducted a nested case-control study within the Ovarian Cancer Follow-Up Study, matching 159 dead patients and 159 survival ones based on body mass index, sample date, and age at diagnosis. Nine plasma PFASs were extracted by solid phase extraction and measured using a liquid chromatography system coupled with tandem mass spectrometry. Baseline plasma concentrations of perfluorinated carboxylic acids (PFCAs) [perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroheptanoic acid (PFHpA)] and perfluorinated sulfonic acids (PFSAs) [perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS)] were calculated. Odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) were calculated via conditional logistic regression models. To elucidate the combined effects, Bayesian kernel machine (BKMR), and regression quantile g-computation (QGC) models were utilized.
In full-adjusted model, significant differences were observed between HGSOC survival and perfluorobutane sulfonic acid, PFHpA, PFHxS, PFOS, PFCA, and PFSA. ORs and 95 %CIs were 2.74 (1.41-5.31), 1.97 (1.03-3.76), 2.13 (1.15-3.95), 2.28 (1.16-4.47), 3.74 (1.78-7.85), and 2.56 (1.31-5.01), respectively for the highest tertile compared with the lowest tertile. The QGC and BKMR models indicated that elevated concentrations of PFAS mixtures were associated with poor OS in HGSOC.
Both individual and mixed plasma PFASs may relate to poor OS of HGSOC. Further research is necessary to establish causality, and it is recommended to reinforce environmental risk mitigation strategies to minimize PFAS exposure.
尽管有证据表明全氟烷基和多氟烷基物质(PFASs)与多种疾病风险呈正相关,但尚无研究证实血浆中的PFASs是否与卵巢癌生存率相关。
探讨在不吸烟人群中血浆PFASs与高级别浆液性卵巢癌(HGSOC)总生存期(OS)之间的关联。
我们在卵巢癌随访研究中进行了一项巢式病例对照研究,根据体重指数、采样日期和诊断时年龄,将159例死亡患者与159例存活患者进行匹配。通过固相萃取法提取9种血浆PFASs,并使用液相色谱系统串联质谱进行测量。计算全氟羧酸(PFCAs)[全氟辛酸(PFOA)、全氟壬酸(PFNA)、全氟癸酸(PFDA)和全氟庚酸(PFHpA)]和全氟磺酸(PFSAs)[全氟辛烷磺酸(PFOS)和全氟己烷磺酸(PFHxS)]的基线血浆浓度。通过条件逻辑回归模型计算比值比(ORs)和相应的95%置信区间(CIs)。为阐明联合效应,采用了贝叶斯核机器(BKMR)和回归分位数g计算(QGC)模型。
在完全调整模型中,观察到HGSOC生存率与全氟丁烷磺酸、PFHpA、PFHxS、PFOS、PFCA和PFSA之间存在显著差异。与最低三分位数相比,最高三分位数的ORs和95% CIs分别为2.74(1.41 - 5.31)、1.97(1.03 - 3.76)、2.13(1.15 - 3.95)、2.28(1.16 - 4.47)、3.74(1.78 - 7.85)和2.56(1.31 - 5.01)。QGC和BKMR模型表明,PFAS混合物浓度升高与HGSOC的OS较差有关。
个体和混合血浆PFASs均可能与HGSOC的OS较差有关。有必要进一步研究以确定因果关系,建议加强环境风险缓解策略以尽量减少PFAS暴露。