Li Ling, Ouyang Feiyun, He Jun, Zhang Chengcheng, Li Yilu, Luo Dan, Xiao Shuiyuan
Clinical Epidemiology Research Office, Hunan Provincial People's Hospital, First Affiliated Hospital of Hunan Normal University, Changsha, China; Department of Social Medicine and Health Management, Xiangya School of Public Health, Central South University, Changsha, China.
School of Computer & Information Sciences, University of Massachusetts Lowell, Lowell, MA, USA.
Ecotoxicol Environ Saf. 2025 Jul 17;302:118656. doi: 10.1016/j.ecoenv.2025.118656.
This study aimed to explore the single and mixed effects of per- and polyfluoroalkyl substances (PFAS) on incident primary dyslipidaemia (PD). We further evaluated the interactions between PFAS and other environmental factors. After a 3-year follow-up of 11,843 government employees, 490 were newly diagnosed with PD, and 490 healthy controls were matched based on age, sex, and study location. Six serum PFAS were detected using ultra-high-pressure liquid chromatography-tandem mass spectrometry. Individual air-pollutant exposure, demographic characteristics, lifestyles and other clinical indicators were obtained from environmental monitoring station data, questionnaires, laboratory, or physical examinations. Logistic regression was performed to analyse the single exposure of PFAS and the interactions. The weighted quantile sum (WQS) model was employed to assess the effect of PFAS mixtures. The serum perfluorooctane sulfonate (PFOS) was higher in PD group than in controls. Serum PFOS concentrations demonstrated monotonic increasing trend with PD incidence risk (OR = 1.33, 95 %CI: 1.01-1.74), and the risk of PD increased by 52 % in the high-concentration group (≥ 29.4 ng/mL) (OR = 1.52, 95 %CI: 1.01-2.30) than the low-concentration group. The WQS model demonstrated a 27 % increment in risk per quartile increase (OR = 1.27, 95 %CI: 1.00-1.62), with PFOS dominating the weight allocation (54.43 %). An antagonistic effect between serum PFOS exposure and aquatic product intake (P = 0.009) was observed. Our findings revealed a PFAS mixture exposure on increased incident PD risks and identified PFOS > 29.4 ng/mL as a potentially hazardous substance while aquatic product intake seems to partially attenuate its risk.
本研究旨在探讨全氟和多氟烷基物质（PFAS）对原发性血脂异常（PD）发病的单一及混合效应。我们进一步评估了PFAS与其他环境因素之间的相互作用。在对11843名政府雇员进行3年随访后，490人新诊断为PD，并根据年龄、性别和研究地点匹配了490名健康对照。使用超高压液相色谱-串联质谱法检测六种血清PFAS。个体空气污染物暴露、人口统计学特征、生活方式和其他临床指标来自环境监测站数据、问卷、实验室或体格检查。采用逻辑回归分析PFAS的单一暴露及相互作用。采用加权分位数和（WQS）模型评估PFAS混合物的效应。PD组血清全氟辛烷磺酸（PFOS）高于对照组。血清PFOS浓度随PD发病风险呈单调上升趋势（OR = 1.33，95%CI：1.01-1.74），高浓度组（≥29.4 ng/mL）的PD风险比低浓度组增加了52%（OR = 1.52，95%CI：1.01-2.30）。WQS模型显示，每增加一个四分位数，风险增加27%（OR = 1.27，95%CI：1.00-1.62），PFOS在权重分配中占主导地位（54.43%）。观察到血清PFOS暴露与水产品摄入量之间存在拮抗作用（P = 0.009）。我们的研究结果揭示了PFAS混合物暴露会增加PD发病风险，并确定PFOS>29.4 ng/mL为潜在有害物质，而水产品摄入似乎部分降低了其风险。
