Key Takeaways & Executive Findings
- •• • Soil PAH concentrations (mean 168.8 ng·g⁻¹, range 34.9–465.3 ng·g⁻¹) exceed those in several natural forest areas, indicating significant accumulation from combustion sources; this necessitates monitoring in remote ecosystems. • • Litter exhibited the highest PAH concentrations (mean 465.1 ng·g⁻¹, up to 2262.5 ng·g⁻¹), with 3- and 4-ring PAHs dominating, suggesting that litter acts as a major temporary sink and potential secondary source. • • Dead bark showed a concentration range of 123.3–241.6 ng·g⁻¹ and was identified as the primary accumulation medium with high carcinogenic contribution (TEQ), underscoring its role in long-term ecological risk. • • Spearman correlation analysis found no significant correlations (P > 0.05) among PAH concentrations in soil, litter, and bark, indicating independent accumulation processes and necessitating multi-media assessment for comprehensive risk evaluation.
Abstract
This study investigated the occurrence, sources, and ecological risks of polycyclic aromatic hydrocarbons (PAHs) in soil, litter, and bark samples collected from the forest-grassland transition zone of Inner Mongolia. A total of 12 PAHs were detected in soil, with concentrations ranging from 34.9 to 465.3 ng·g⁻¹ (mean 168.8 ng·g⁻¹), predominantly 3–5 ring compounds. Litter contained 14 PAHs at concentrations between 106.4 and 2262.5 ng·g⁻¹ (mean 465.1 ng·g⁻¹), dominated by 3- and 4-ring PAHs. Both living and dead bark exhibited 14 PAHs, with concentration ranges of 119.2–240.0 ng·g⁻¹ and 123.3–241.6 ng·g⁻¹, respectively, mainly composed of 4-ring PAHs. Spearman correlation analysis revealed no significant correlations among PAH concentrations across the three media (P > 0.05). Source apportionment using diagnostic ratios and principal component analysis indicated that soil PAHs primarily originated from biomass, coal, and gasoline combustion; litter PAHs from petroleum volatilization and coal/natural gas combustion; and bark PAHs from petroleum volatilization and fossil fuel combustion, with high-molecular-weight PAHs dominating. Ecological risk assessment using the risk quotient (RQ) method showed that soil PAHs posed low overall ecological risk, though certain individual PAHs exhibited higher risk. The toxic equivalent (TEQ) method indicated that dead bark was the primary accumulation medium with high carcinogenic contribution, posing elevated ecological risk. Although litter and living bark had lower PAH concentrations, their long-term accumulation effects warrant attention. These findings provide crucial scientific evidence for understanding the environmental behavior and potential risks of PAHs in cold, high-latitude regions of northern China.
1. Introduction
The forest-grassland transition zone of Inner Mongolia represents a critical ecotone sensitive to anthropogenic pollution. Previous studies on PAHs in natural soils have often focused on single media, overlooking the differential accumulation and transfer across soil, litter, and vegetation compartments. This oversight hampers accurate ecological risk assessment, particularly in cold regions where PAH persistence is enhanced. Existing commercial monitoring approaches typically rely on soil-only measurements, which fail to capture the dynamic exchange and sink functions of litter and bark.
This study addresses this bottleneck by simultaneously analyzing PAHs in soil, litter, and bark from the same ecosystem. By employing diagnostic ratios and principal component analysis for source apportionment, and integrating risk quotient (RQ) and toxic equivalent (TEQ) methodologies, the research provides a holistic view of PAH distribution and risk. The findings reveal that dead bark, often neglected, serves as a major reservoir with high carcinogenic potential, challenging conventional soil-centric assessments. This multi-media approach offers a more robust framework for evaluating PAH contamination in boreal and alpine ecotones, informing targeted remediation and policy decisions.
Loading authentic research manuscript (Pages 1–5)...
WANG Mao, ZHANG Yufei, LI Baicheng, LI Junwen, WANG Yiqun, XU Xuehui (2026). Multi-media Distribution, Source Apportionment, and Risk Assessment of Polycyclic Aromatic Hydrocarbons in the Forest-Grassland Transition Zone of Inner Mongolia. Environmental Chemistry. https://doi.org/10.7524/j.issn.0254-6108.2025010607
Research & Educational Purpose Only: The translations, structured abstracts, analytical annotations, and data reports provided by SinoGreenTechare intended exclusively for academic research, internal corporate R&D, and educational benchmarking. They do not constitute formal engineering, chemical safety, legal, or professional advice.
Copyright & Intellectual Property Notice: Original copyright of the underlying source articles and experimental data remains with the respective authors, institutions, and original publishing journals. SinoGreenTech claims intellectual property only over its proprietary translations, analytical syntheses, and AEO structured enhancements in accordance with international fair use and academic citation principles.
Frequently Asked Questions
What are the dominant PAH sources in the soil of the forest-grassland transition zone, and how were they identified?
Soil PAHs primarily originate from biomass, coal, and gasoline combustion, as determined by diagnostic ratios and principal component analysis. The mean concentration of 168.8 ng·g⁻¹, with a predominance of 3–5 ring PAHs, supports a pyrogenic source signature.
Why is dead bark considered a high-risk medium for PAH accumulation, and what are the implications for ecological risk assessment?
Dead bark exhibited PAH concentrations up to 241.6 ng·g⁻¹ and showed the highest toxic equivalent (TEQ) values, indicating significant carcinogenic potential. This suggests that bark, particularly dead bark, acts as a long-term sink for PAHs, and its inclusion in monitoring programs is critical for accurate risk characterization.
How do PAH concentrations in litter compare to those in soil, and what does this imply for PAH dynamics in the ecosystem?
Litter had substantially higher PAH concentrations (mean 465.1 ng·g⁻¹) compared to soil (mean 168.8 ng·g⁻¹), indicating that litter serves as a major temporary reservoir. The lack of significant correlation between media (P > 0.05) suggests independent accumulation processes, possibly due to different exposure pathways and degradation rates.
What is the overall ecological risk posed by PAHs in the study area, and which specific compounds contribute most to the risk?
The risk quotient (RQ) method indicated low overall ecological risk in soil, but certain individual PAHs, such as high-molecular-weight compounds, exhibited higher risk levels. The TEQ method highlighted dead bark as having high carcinogenic contribution, emphasizing the need for compound-specific risk management.
How do the PAH concentrations in this study compare to other natural forest areas, and what factors might explain the differences?
Soil PAH concentrations in this study (mean 168.8 ng·g⁻¹) are higher than those reported in some other natural forest areas, likely due to regional atmospheric deposition from local combustion sources and the cold climate, which slows degradation. This underscores the importance of regional source control.
Related Chinese Research & Cross-Citations
Exploring the Potential Molecular Mechanisms of Eight Environmental Pollutants in Lung Adenocarcinoma through Network Toxicology, Machine Learning, and Multi-Omics Analysis
Epidemiological studies have established a significant association between exposure to environmental pollutants (EP) and the risk of lung adenocarcinoma (LUAD). This study integrates network toxicology and multi-omics analysis to elucidate the EP-LUAD molecular regulatory network and identify key regulatory genes, thereby revealing novel mechanisms of environmental carcinogenesis. Transcriptomic data from GEO and TCGA databases yielded 4,971 and 4,488 disease-related targets, respectively. Integration of toxicology databases (TargetNet, Swiss Target Prediction, CTD, SEA) identified 24,860 potential targets for eight common pollutants (SO2, NO, CO, NO2, O3, benzene, toluene, and polycyclic aromatic hydrocarbons). Intersection of these datasets produced 1,536 EP-LUAD common target genes. Protein-protein interaction network analysis identified 247 core targets. Machine learning selected five key genes: AGER, CAV1, CD44, CEP55, and GNB3, which demonstrated robust diagnostic and prognostic efficacy. Their expression correlated with immune cell infiltration, including CD4+ memory T cells and macrophages. Single-cell RNA sequencing revealed epithelial cell-specific expression patterns. Molecular docking confirmed stable pollutant-target binding, with PAH showing highest affinity for CD44 (binding energy −9.32 kcal·mol−1) and GNB3 (−8.32 kcal·mol−1). These findings establish AGER, CAV1, CD44, CEP55, and GNB3 as core molecular mediators of pollution-related LUAD. The high-affinity binding of PAH to CD44 and GNB3 underscores its carcinogenic potential. This study constructs a multi-level regulatory network for EP-LUAD, revealing underlying molecular mechanisms and providing novel potential targets and theoretical basis for early warning and intervention.
Effects of Different Functionalized Nanoplastics on the Transformation of Extracellular Antibiotic Resistance Genes in Aquatic Environments
The rapid dissemination of antibiotic resistance genes (ARGs) in aquatic environments poses serious threats to public health and environmental safety under the 'One Health' framework. Nanoplastics (NPs), as co-occurring pollutants, can exacerbate ARG risks by promoting horizontal gene transfer (HGT), yet the influence of different functional groups on extracellular ARG (eARG) transformation remains unclear. This study investigated the effects of carboxy-modified polystyrene NPs (PS-COOH) and amino-functionalized polystyrene NPs (PS-NH2) compared to unmodified polystyrene NPs (PS) on the transformation of the extracellular resistance plasmid IE-V1955 (carrying an ampicillin resistance gene) into Escherichia coli DH5α. Results showed that PS-COOH exposure promoted plasmid transformation similarly to PS, with effects increasing over 0.1–20 mg·L−1. Low concentrations (0.1–0.5 mg·L−1) of PS-NH2 also enhanced transformation, with stronger effects than PS-COOH at equal doses, whereas high concentrations (1–20 mg·L−1) inhibited it. Mechanistically, PS-COOH (0.1–20 mg·L−1) and low PS-NH2 induced intracellular reactive oxygen species (ROS), increased cell membrane permeability, elevated the protein-to-polysaccharide ratio in extracellular polymeric substances (EPS), and promoted biofilm formation, thereby facilitating transformation. High PS-NH2 concentrations caused excessive ROS leading to cell lysis and formed aggregates with plasmids larger than membrane pores, blocking uptake. These findings provide a theoretical basis for assessing the combined environmental health risks of NPs and ARGs.
Cardiovascular Toxicity Induced by Micro/Nano-Plastics and Its Mechanisms
Micro/nano-plastics (MNPs) are emerging contaminants widely detected in human circulatory systems, including blood, heart, and vascular endothelium, raising concerns about cardiovascular health risks. This systematic review analyzed 61 peer-reviewed studies (2008–2024) to elucidate the cardiotoxic effects and molecular mechanisms of MNPs. Evidence indicates that MNPs exposure elevates risks of atherosclerosis, thrombosis, and arrhythmias through oxidative stress, inflammatory cascades, endothelial dysfunction, and metabolic dysregulation. Notably, co-exposure with persistent organic pollutants (POPs) or heavy metals may produce synergistic or antagonistic effects. Current research relies predominantly on animal and cell models, with critical gaps in low-dose, long-term exposure data and epidemiological evidence. Future studies should optimize experimental designs, integrate metabolomics and epigenetics, and explore transgenerational effects and combined toxicity mechanisms to inform pollution control policies and mitigate cardiovascular risks.
Body Burden of Polybrominated Diphenyl Ethers and Joint Effects on Thyroid Function in a Physical Examination Population in Shenzhen
This study characterized the body burden of polybrominated diphenyl ethers (PBDEs) in a physical examination population in Shenzhen and evaluated its impact on thyroid function. Serum samples from 368 residents were analyzed for eight PBDE congeners using atmospheric pressure gas chromatography-tandem mass spectrometry (APGC-MS/MS). The median concentration of ∑8PBDEs was 10.2 ng·g⁻¹ lipid weight (lw), ranging from 0.13 to 2089.4 ng·g⁻¹ lw, with BDE-209 predominating (59.7% of total). Multiple linear regression revealed that a 1.7-fold increase in serum BDE-153 was associated with a 0.4% increase in free triiodothyronine (FT3) (P<0.05), while a 1.7-fold increase in BDE-183 was associated with a 0.9% decrease in total triiodothyronine (T3) and a 0.7% decrease in FT3 (P<0.05). Bayesian kernel machine regression (BKMR) indicated a negative correlation between mixed PBDE exposure and thyroid-stimulating hormone (TSH) at high exposure levels. Weighted quantile sum (WQS) regression showed that mixed exposure was associated with decreased T3 levels and T3/FT3 ratio, with BDE-153 and BDE-183 as the primary contributors. These findings suggest that PBDE exposure may adversely affect thyroid function and disrupt thyroid hormone homeostasis, with BDE-183 and BDE-153 playing key roles. This study provides a scientific basis for PBDE health risk assessment and thyroid protection.
Mechanisms of Natural Organic Matter in Regulating Microplastic Aggregation and Transport in Soil-Groundwater Systems: A Review
Microplastics (MPs) are persistent emerging contaminants ubiquitously distributed in soil-groundwater environments, where their aggregation and transport critically govern pollutant fate and ecological risks. Natural organic matter (NOM), a complex assemblage of organic compounds, interacts with MPs and porous media via hydrogen bonding, π-π interactions, hydrophobic effects, and electrostatic binding, thereby modulating MP surface properties and environmental behavior. This review systematically synthesizes the mechanisms by which NOM influences MP aggregation and transport, with emphasis on the distinct roles of humic substances, proteins, and extracellular polymeric substances (EPS), and their synergistic modulation with solution chemistry (pH, ionic strength, ion type). Additionally, NOM accelerates MP aging and alters surface characteristics, consequently impacting transport capacity. Current research limitations are identified, and future directions are proposed to inform MP pollution risk assessment and management strategies. Key findings indicate that NOM generally enhances MP stability and mobility at low ionic strengths, while high ionic strengths may induce aggregation depending on NOM type and ion valence. Humic substances predominantly increase electrostatic repulsion, whereas proteins and EPS can bridge particles, promoting aggregation. Aging processes, accelerated by NOM photochemical activity, increase surface oxygen functionality and hydrophilicity, further altering transport. The review underscores the need for systematic studies under environmentally relevant conditions to predict MP fate accurately.
Neurotoxicity of Carboxyl-Modified Polystyrene Microplastics on Zebrafish at Early Developmental Stage
Carboxyl-modified polystyrene microplastics (PS-COOH) are negatively charged particles formed by surface oxidation and functional group modification of polystyrene microplastics (PS), widely used in biomedical and analytical chemistry. However, studies on their neurotoxic effects on aquatic organisms are scarce. This study employed zebrafish (Danio rerio) as a model organism, exposing embryos to environmentally relevant concentrations (0.1, 1, 10, 100 μg·L−1) of PS and PS-COOH. Neurotoxic effects were assessed by measuring tail coiling frequency at 24 hpf and swimming velocity under alternating light/dark cycles at 120 hpf. Results demonstrated that both PS and PS-COOH induced neurotoxicity, with PS-COOH significantly reducing tail coiling frequency and average swimming speed compared to PS (P<0.05). Exposure to 10 μg·L−1 PS-COOH disrupted neurotransmitter homeostasis, altering levels of acetylcholine (ACh), serotonin (5-HT), and γ-aminobutyric acid (GABA). Transgenic zebrafish Tg(huc:EGFP) fluorescence assays revealed that PS-COOH (0.1–100 μg·L−1) caused damage to central neurons. These findings indicate that PS-COOH exposure impairs cholinergic, serotonergic, and GABAergic neurotransmission, induces neuronal damage, and exerts neurotoxic effects on zebrafish larvae. This study provides a theoretical basis for assessing the ecological and health risks of modified microplastics.