Yafei Gao , Chenran Cai , Han Li , Lu Cheng , Hongkai Zhu , Hongwen Sun , Yang Peng , Hongzhi Zhao
{"title":"The hidden mediator between polycyclic aromatic hydrocarbon exposure and cognitive function of elder adults: FT3/FT4 ratio","authors":"Yafei Gao , Chenran Cai , Han Li , Lu Cheng , Hongkai Zhu , Hongwen Sun , Yang Peng , Hongzhi Zhao","doi":"10.1016/j.enceco.2025.11.038","DOIUrl":null,"url":null,"abstract":"<div><div>Polycyclic aromatic hydrocarbons (PAHs) are neurotoxicants that may induce cognitive deficits via thyroid dysfunction. Older adults, due to physiological decline, are more susceptible to such toxicants. This cross-sectional study involving 433 elderly adults examined the relationships between PAH exposure, cognitive decline and thyroid-mediated pathways. Urinary PAH metabolites were measured and cognitive performance was assessed using the Mini-Mental State Examination (MMSE). Participants were categorized into low-risk (n = 367) and high-risk mild cognitive impairment (MCI) groups (n = 66) based on MMSE scores. Logistic regression results indicated that the odds of MCI risk increased with each one-unit increase in log-transformed levels of 2-OHNap, 2-OHFlu, and 3-OHFlu. Linear modeling further revealed that these metabolites (OH-Nap and OH-Flu) were dose-dependently negatively associated with orientation, attention and memory. In addition, there was a nonlinear dose-response relationship between 1-OHNap and verbal ability, and ΣOH-PAHs and attention/memory. Critically, mediating effect analysis showed that the FT3/FT4 ratio mediated the association between PAH metabolites and MMSE scores with a contribution of 22.5 %–26.3 %. This study reveals the mechanism by which PAHs exposure may mediate cognitive decline in the elderly by interfering with thyroid function, providing an important scientific basis for the prevention of environmental factor-induced neurodegenerative diseases.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 418-429"},"PeriodicalIF":12.3000,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental Chemistry and Ecotoxicology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2590182625002401","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/11/27 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are neurotoxicants that may induce cognitive deficits via thyroid dysfunction. Older adults, due to physiological decline, are more susceptible to such toxicants. This cross-sectional study involving 433 elderly adults examined the relationships between PAH exposure, cognitive decline and thyroid-mediated pathways. Urinary PAH metabolites were measured and cognitive performance was assessed using the Mini-Mental State Examination (MMSE). Participants were categorized into low-risk (n = 367) and high-risk mild cognitive impairment (MCI) groups (n = 66) based on MMSE scores. Logistic regression results indicated that the odds of MCI risk increased with each one-unit increase in log-transformed levels of 2-OHNap, 2-OHFlu, and 3-OHFlu. Linear modeling further revealed that these metabolites (OH-Nap and OH-Flu) were dose-dependently negatively associated with orientation, attention and memory. In addition, there was a nonlinear dose-response relationship between 1-OHNap and verbal ability, and ΣOH-PAHs and attention/memory. Critically, mediating effect analysis showed that the FT3/FT4 ratio mediated the association between PAH metabolites and MMSE scores with a contribution of 22.5 %–26.3 %. This study reveals the mechanism by which PAHs exposure may mediate cognitive decline in the elderly by interfering with thyroid function, providing an important scientific basis for the prevention of environmental factor-induced neurodegenerative diseases.