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Investigating pesticide exposure and oxidative stress in preschool children is essential for elucidating the determinants of environmental health in early life, with human biomonitoring of urinary pesticide metabolites serving as a critical strategy for achieving this objective. This study demonstrated biomonitoring of 2 phenoxyacetic acid herbicides, 2 organophosphorus pesticide metabolites, and 4 pyrethroid pesticide metabolites in 159 preschool children and evaluated their association with oxidative stress biomarker 8-hydroxydeoxyguanosine. An enzymatic deconjugation process was used to release urinary pesticide metabolites, which were then extracted and enriched by supported liquid extraction, and quantified by ultra-high performance liquid chromatography-tandem mass spectrometry with internal standard calibration. Dichloromethane: methyl tert‑butyl ether (1:1, v/v) was optimized as the solvent for supported liquid extraction, and we validated the method for linear range, recovery, matrix effect and method detection limit. Method detection limit of the pesticide metabolites ranged from 0.01 μg/L to 0.04 μg/L, with satisfactory recoveries ranging from 70.5 % to 95.5 %. 2,4,5-Trichlorophenoxyacetic acid was not detected, whereas the other seven pesticide metabolites were detected with frequencies ranging from 10.1 % to 100 %. The concentration of urinary pesticide metabolites did not significantly differ between boys and girls, with the median concentrations being 9.39 μg/L for boys and 4.90 μg/L for girls, respectively. Spearman correlation analysis indicated that significant positive correlations among urinary metabolites. Bayesian kernel machine regression revealed a significant positive association between urinary pesticide metabolites and 8-hydroxydeoxyguanosine. Para-nitrophenol was the pesticide metabolite that contributed significantly to the elevated level of oxidative stress., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Previous studies have indicated adverse health effects of exposure to polycyclic aromatic hydrocarbons (PAHs), but evidence on the association between PAH exposure and immunity is scarce and its underlying mechanism is largely unknown. This study assessed human exposure to PAHs by determining the concentrations of PAHs in serum and their metabolites in paired urine. The oxidative stress and inflammation levels were evaluated by urinary DNA damage biomarker 8-hydroxydeoxyguanosine, white blood cell counts and C-reaction protein. We investigated the relationship between PAH exposure and seven immunological components, and explored the indirect roles of oxidative stress and inflammation by mediation and moderation analysis. Multivariate regression analysis revealed that 1-hydroxynaphthalene and 2-hydroxyfluorene were negatively associated with immunoglobulin A, and 3-hydroxyphenanthrene was negatively correlated with complement component 3. Restricted cubic spline analysis demonstrated nonlinear relationships between some individual PAHs or their metabolites with immunological components. Bayesian kernel machine regression and quantile g-computation revealed significant associations of higher PAH exposure with decreased immunoglobulin G and kappa light chain levels. Phenanthrene was the compound that contributed the most to reduced immunoglobulin G. Mediation analysis demonstrated significant indirect effects of 8-hydroxydeoxyguanosine and white blood cell counts on the association between higher PAH exposure and decreased immunological components. Moderation analysis revealed that PAH exposure and decreased immunological components are significantly associated with higher levels of C-reaction protein and white blood cell counts. The results demonstrated significant immunosuppression of PAH exposure and highlighted the indirect roles of oxidative stress and inflammation. Interventions to reduce systemic inflammation may mitigate the adverse immune effects of PAH exposure. [Display omitted] • Elevated polycyclic aromatic hydrocarbon (PAH) exposure correlates with reduced immunological components. • Phenanthrene is a key contributor to reduced immunoglobulin G levels. • Nonlinear associations exist between PAHs and immunological components. • Inflammation moderates PAH exposure induced immunosuppression. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbon (PAH) exposure has been associated with adverse health effects, and accumulating evidence suggests that PAH exposure may impair liver function. However, the underlying mechanisms linking PAH exposure and liver function impairment remain unclear. This study aimed to explore the association between PAH exposure and liver function biomarkers, and the mediating effects of inflammation and oxidative stress. The cross-sectional study included 155 adults and their urinary PAH metabolites (OH-PAHs) were determined, and eight liver function biomarkers were measured in paired serum samples. A comprehensive statistical analysis investigated the linear, non-linear, individual, and joint effects of the association between urinary OH-PAHs and liver function biomarkers. The results indicated significant positive associations between urinary OH-PAH concentrations and liver function biomarker levels, suggesting that PAH exposure may adversely affect liver function. 2-hydroxyfluorene was identified as the individual metabolite contributing significantly to elevated gamma-glutamyl transferase levels. Further stratification by gender revealed that this association is more pronounced in males. Moreover, we observed significant mediation effects of the oxidative stress biomarker 8-hydroxy-2′-deoxyguanosine and the inflammatory biomarkers C-reactive protein and white blood cell count on this association. The physiological responses triggered by PAH exposure are mediated by inflammation, which serves as a link between oxidative stress, cellular injury, and elevated liver enzyme levels. The results demonstrated that increased inflammation and oxidative stress mediated the association between increased urinary OH-PAHs and elevated liver function biomarkers. The results contribute to a better understanding of the potential mechanisms underlying PAH exposure's hepatotoxic effects. [Display omitted] • Urinary polycyclic aromatic hydrocarbon metabolites were significantly associated with liver function biomarkers. • 2-hydroxyfluorene contributed significantly to elevated gamma-glutamyltransferase levels. • Oxidative stress and inflammation may mediate the physiological response pathway. [ABSTRACT FROM AUTHOR]