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Updated: May 27, 2025

Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System
Published on: December 21, 2016
Personal exposure to polycyclic aromatic hydrocarbons-bound particulate matter during pregnancy and umbilical
Xuan Zhang1, Jia Wang2, Yan Wu3
1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Abstract:
Exposure to polycyclic aromatic hydrocarbons (PAHs), particularly when bound to fine particulate matter (PM2.5), is an emerging concern for adverse prenatal health outcomes. This study investigates the associations between prenatal exposure to PAHs-bound PM2.5 and markers of inflammation and oxidative stress in umbilical cord blood. We conducted a prospective study of 450 mother-infant pairs, assessing PAHs-bound PM2.5 levels during pregnancy using personal air sampling. Inflammatory and oxidative stress biomarkers, including TNF-α, IL-6, IL-8, TGF-β, and Pro-oxidant Antioxidant Balance (PAB), were measured in umbilical cord blood. Multivariable linear regression was used to examine associations between individual PAHs and these biomarkers, while mixture effects were evaluated using quantile g-computation and Bayesian Kernel Machine Regression (BKMR) to assess the combined influence of 15 PAH congeners. Our findings revealed significant associations between prenatal exposure to specific PAHs and increased levels of TNF-α, IL-6, and PAB. Mixture analysis indicated that each one-quartile increase in PAH exposure was associated with a 0.31 pg/mL (95 % CI: 0.05-0.60, p = 0.01), 1.26 pg/mL (95 % CI: 0.43-2.08, p < 0.01), and 26.02 pg/mL (95 % CI: 2.98-49.07, p = 0.02) increase in TNF-α, IL-8, and TGF-β, respectively. However, IL-6 and PAB showed no significant associations. BKMR analysis further confirmed a dose-response relationship between prenatal PAH exposure and elevated inflammatory and oxidative stress markers. These findings highlight the potential health risks associated with prenatal exposure to PAHs-bound PM2.5, emphasizing the need for further research to mitigate adverse developmental effects.
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