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30 January 2026

Histidine Metabolic Pathway Modifies the Relationships Between 6:2 Cl-PFESA Exposure and Preterm Birth

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1
Shenyang Clinical Medical Research Center for Obstetrics and Gynecology, Liaoning Province Key Laboratory of Assisted Reproduction, Department of Obstetrics and Gynecology, Shenyang Women’s and Children’s Hospital, Shenyang 110011, China
2
Department of Epidemiology, School of Public Health, China Medical University, Shenyang 110122, China
3
Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China
4
Department of Clinical Laboratory, General Hospital of Northern Theater Command, Shenyang 110016, China
This article belongs to the Special Issue Multi-Media Exposure to Emerging Contaminants and Health Effects Across Physiological Systems: Exposure Pathways, Risk Assessment and Public Health Implications

Abstract

Background: Evidence linking chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) to preterm birth (PTB) is limited, and their relationships with the metabolome remain unexplored. Aims: Our study aimed to explore the role of the metabolome in the associations between Cl-PFESAs exposure and PTB. Methods: We conducted a nested case–control study in the Shenyang birth cohort, which included 206 spontaneous preterm birth cases and 206 full-term controls, matched for maternal age and pre-pregnancy BMI. We used conditional logistic regression models to analyze the associations between Cl-PFESAs exposure in umbilical cord blood and PTB. Moreover, the metabolomics of maternal blood (44 cases) between the preterm and control groups was analyzed using the interaction analysis. Results: We observed that a higher natural log-transformed 6:2 Cl-PFESA level was associated with greater odds of PTB in conditional multivariable-adjusted logistic regression models (OR = 1.738, 95% CI: 1.320, 2.287). The results of metabolomics pathway analysis showed that histidine metabolism pathways may modify the above risk. When stratified by histidine levels, the association between cord blood 6:2 Cl-PFESA and PTB was different. Conclusions: Intrauterine exposure to 6:2 Cl-PFESA was associated with increased PTB. Also, for the first time, our study illustrates that maternal plasma metabolite profiles may modify the associations of 6:2 Cl-PFESA with PTB. More research is needed to elucidate the mechanism underlying the reproductive toxicity of 6:2 Cl-PFESA in pregnant women following exposure.

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