Nontargeted Analysis of the Chemical Exposome in Preterm Birth: A Pilot Study of Placenta and Maternal Serum
Abstract
Preterm birth is a leading cause of neonatal morbidity and mortality, yet the role of chemical exposures in its etiology remains poorly understood. We hypothesized that untargeted chemical profiling of paired maternal serum and placenta would reveal distinct exposure signatures and metabolic disruptions associated with preterm birth. We analyzed paired maternal serum and placenta samples from 83 pregnant women in New York City, USA, including 30 who delivered preterm (<37 weeks), by non-targeted analysis (NTA) using ultrahigh-performance liquid chromatography coupled to Orbitrap high-resolution mass spectrometry (UHPLC-Orbitrap HRMS). We confirmed 29 chemicals (Level 1), 28 of them exogenous, tentatively identified 1012 peak features (Level 2), and annotated 1180 peak features via in silico simulation (Level 3). Five Level 1 confirmed exogenous chemicals (i.e., dodecyltrimethylammonium, N,N-dimethyldecylamine oxide, rimsulfuron, triphenylphosphine oxide, and 2,6-dichlorobenzamide) and 208 tentatively identified Level 2 chemicals detected in this study appear not to have been previously detected in human blood samples. We identified 119 and 170 significantly differentially enriched features in serum and placenta, respectively (BH-corrected p < 0.05). Serum samples showed changes in glutathione, tryptophan, pyruvate, arachidonic acid, and phospholipid pathways in preterm birth. Our data suggest that chemical exposures might collectively amplify metabolic vulnerabilities in oxidative stress, lipid metabolism, and amino acid catabolism relevant to preterm birth.
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BibTeX
@article{ji2026nontargeted,
title = {{Nontargeted Analysis of the Chemical Exposome in Preterm Birth: A Pilot Study of Placenta and Maternal Serum}},
author = {Xiaowen Ji and Mathusa Lakuleswaran and Wenjie Lyu and Marina Sirota and Arthur David and Xianchuan Xie and Julian Edwards and Miaomiao Wang and June-Soo Park and Dimitri Abrahamsson},
journal = {Environment \& Health},
year = {2026},
month = sep,
doi = {10.1021/envhealth.6c00264},
url = {https://ehesp.hal.science/hal-05761399v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Nontargeted Analysis of the Chemical Exposome in Preterm Birth: A Pilot Study of Placenta and Maternal Serum
AU - Xiaowen Ji
AU - Mathusa Lakuleswaran
AU - Wenjie Lyu
AU - Marina Sirota
AU - Arthur David
AU - Xianchuan Xie
AU - Julian Edwards
AU - Miaomiao Wang
AU - June-Soo Park
AU - Dimitri Abrahamsson
PY - 2026
DA - 2026/09/15
JO - Environment & Health
DO - 10.1021/envhealth.6c00264
UR - https://ehesp.hal.science/hal-05761399v1
AB - Preterm birth is a leading cause of neonatal morbidity and mortality, yet the role of chemical exposures in its etiology remains poorly understood. We hypothesized that untargeted chemical profiling of paired maternal serum and placenta would reveal distinct exposure signatures and metabolic disruptions associated with preterm birth. We analyzed paired maternal serum and placenta samples from 83 pregnant women in New York City, USA, including 30 who delivered preterm (<37 weeks), by non-targeted analysis (NTA) using ultrahigh-performance liquid chromatography coupled to Orbitrap high-resolution mass spectrometry (UHPLC-Orbitrap HRMS). We confirmed 29 chemicals (Level 1), 28 of them exogenous, tentatively identified 1012 peak features (Level 2), and annotated 1180 peak features via in silico simulation (Level 3). Five Level 1 confirmed exogenous chemicals (i.e., dodecyltrimethylammonium, N,N-dimethyldecylamine oxide, rimsulfuron, triphenylphosphine oxide, and 2,6-dichlorobenzamide) and 208 tentatively identified Level 2 chemicals detected in this study appear not to have been previously detected in human blood samples. We identified 119 and 170 significantly differentially enriched features in serum and placenta, respectively (BH-corrected p < 0.05). Serum samples showed changes in glutathione, tryptophan, pyruvate, arachidonic acid, and phospholipid pathways in preterm birth. Our data suggest that chemical exposures might collectively amplify metabolic vulnerabilities in oxidative stress, lipid metabolism, and amino acid catabolism relevant to preterm birth.
SN - 2833-8278
ER -