Potential Hazards of Polycyclic Aromatic Hydrocarbons in Great Lakes Tributaries Using Water Column and Porewater Passive Samplers and Sediment Equilibrium Partitioning.

The potential for polycyclic aromatic hydrocarbon (PAH)-related effects in benthic organisms is commonly estimated from organic carbon-normalized sediment concentrations based on equilibrium partitioning (EqP). Although this approach is useful for screening purposes, it may overestimate PAH bioavailability by orders of magnitude in some sediments, leading to inflated exposure estimates and potentially unnecessary remediation costs. Recently, passive samplers have been shown to provide an accurate assessment of the freely dissolved concentrations of PAHs, and thus their bioavailability and possible biological effects, in sediment porewater and overlying surface water. We used polyethylene passive sampling devices (PEDs) to measure freely dissolved porewater and water column PAH concentrations at 55 Great Lakes (USA/Canada) tributary locations. The potential for PAH-related biological effects using PED concentrations were estimated with multiple approaches by applying EqP, water quality guidelines, and pathway-based biological activity based on in vitro bioassay results from ToxCast. Results based on the PED-based exposure estimates were compared with EqP-derived exposure estimates for concurrently collected sediment samples. The results indicate a potential overestimation of bioavailable PAH concentrations by up to 960-fold using the EqP-based method compared with measurements using PEDs. Even so, PED-based exposure estimates indicate a high potential for PAH-related biological effects at 14 locations. Our findings provide an updated, weight-of-evidence-based site prioritization to help guide possible future monitoring and mitigation efforts. Environ Toxicol Chem 2024;43:1509-1523. © 2024 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Structure-based modeling to assess binding and endocrine disrupting potential of polycyclic aromatic hydrocarbons in Daniorerio.

Environmental contaminants, such as polycyclic aromatic hydrocarbons (PAHs), have raised concerns regarding their potential endocrine-disrupting effects on aquatic organisms, including fish. In this study, molecular docking and molecular dynamics techniques were employed to evaluate the endocrine-disrupting potential of PAHs in zebrafish, as a model organism. A virtual screening with 72 PAHs revealed a correlation between the number of PAH aromatic rings and their binding affinity to proteins involved in endocrine regulation. Furthermore, PAHs with the highest binding affinities for each protein were identified: cyclopenta[cd]pyrene for AR (-9.7 kcal/mol), benzo(g)chrysene for ERα (-11.5 kcal/mol), dibenzo(a,e)pyrene for SHBG (-8.7 kcal/mol), dibenz(a,h)anthracene for StAR (-11.2 kcal/mol), and 2,3-benzofluorene for TRα (-9.8 kcal/mol). Molecular dynamics simulations confirmed the stability of the protein-ligand complexes formed by the PAHs with the highest binding affinities throughout the simulations. Additionally, the effectiveness of the protocol used in this study was demonstrated by the receiver operating characteristic curve (ROC) analysis, which effectively distinguished decoys from true ligands. Therefore, this research provides valuable insights into the endocrine-disrupting potential of PAHs in fish, highlighting the importance of assessing their impact on aquatic ecosystems.

Combined influence of the nanoplastics and polycyclic aromatic hydrocarbons exposure on microbial community in seawater environment.

Nanoplastics (NPs) and polycyclic aromatic hydrocarbons (PAHs) are recognized as persistent organic pollutant (POPs) with demonstrated physiological toxicity. When present in aquatic environments, the two pollutants could combine with each other, resulting in cumulative toxicity to organisms. However, the combined impact of NPs and PAHs on microorganisms in seawater is not well understood. In this study, we conducted an exposure experiment to investigate the individual and synergistic effects of NPs and PAHs on the composition, biodiversity, co-occurrence networks of microbial communities in seawater. Exposure of individuals to PAHs led to a reduction in microbial community richness, but an increase in the relative abundance of species linked to PAHs degradation. These PAHs-degradation bacteria acting as keystone species, maintained a microbial network complexity similar to that of the control treatment. Exposure to individual NPs resulted in a reduction in the complexity of microbial networks. Furthermore, when PAHs and NPs were simultaneously present, the toxic effect of NPs hindered the presence of keystone species involved in PAHs degradation, subsequently limiting the degradation of PAHs by marine microorganisms, resulting in a decrease in community diversity and symbiotic network complexity. This situation potentially poses a heightened threat to the ecological stability of marine ecosystems. Our work strengthened the understanding of the combined impact of NPs and PAHs on microorganisms in seawater.

Changes in the Non-targeted Metabolomic Profile of Three-year-old Toddlers with Elevated Exposure to Polycyclic Aromatic Hydrocarbons.

Objective: To investigate changes in the urinary metabolite profiles of children exposed to polycyclic aromatic hydrocarbons (PAHs) during critical brain development and explore their potential link with the intestinal microbiota. Methods: Liquid chromatography-tandem mass spectrometry was used to determine ten hydroxyl metabolites of PAHs (OH-PAHs) in 36-month-old children. Subsequently, 37 children were categorized into low- and high-exposure groups based on the sum of the ten OH-PAHs. Ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry was used to identify non-targeted metabolites in the urine samples. Furthermore, fecal flora abundance was assessed by 16S rRNA gene sequencing using Illumina MiSeq. Results: The concentrations of 21 metabolites were significantly higher in the high exposure group than in the low exposure group (variable importance for projection > 1, P < 0.05). Most of these metabolites were positively correlated with the hydroxyl metabolites of naphthalene, fluorine, and phenanthrene ( r = 0.336-0.531). The identified differential metabolites primarily belonged to pathways associated with inflammation or proinflammatory states, including amino acid, lipid, and nucleotide metabolism. Additionally, these distinct metabolites were significantly associated with specific intestinal flora abundances ( r = 0.34-0.55), which were mainly involved in neurodevelopment. Conclusion: Higher PAH exposure in young children affected metabolic homeostasis, particularly that of certain gut microbiota-derived metabolites. Further investigation is needed to explore the potential influence of PAHs on the gut microbiota and their possible association with neurodevelopmental outcomes.

Effects of polycyclic aromatic hydrocarbons on the gut-testis axis.

Polycyclic aromatic hydrocarbons (PAHs) are a large group of organic compounds which are comprised of two or more fused benzene rings. As a typical environmental pollutant, PAHs are widely distributed in water, soil, atmosphere and food. Despite extensive researches on the mechanisms of health damage caused by PAHs, especially their carcinogenic and mutagenic toxicity, there is still a lack of comprehensive summarization and synthesis regarding the mechanisms of PAHs on the gut-testis axis, which represents an intricate interplay between the gastrointestinal and reproductive systems. Thus, this review primarily focuses on the potential forms of interaction between PAHs and the gut microbiota and summarizes their adverse outcomes that may lead to gut microbiota dysbiosis, then compiles the possible mechanistic pathways on dysbiosis of the gut microbiota impairing the male reproductive function, in order to provide valuable insights for future research and guide further exploration into the intricate mechanisms underlying the impact of gut microbiota dysbiosis caused by PAHs on male reproductive function.

Ecotoxicological risk of asphalt pavements to aquatic animals associated with pollutant leaching.

Contaminants such as heavy metals and polycyclic aromatic hydrocarbons (PAHs) can be released from asphalt pavement and transported through stormwater runoff to nearby water bodies, leading to water pollution and potential harm to living aquatic animals. This study characterizes the heavy metal and PAH leaching from various asphalt paving materials and their potential ecotoxicological effects on zebrafish Danio rerio. Artificial runoffs were prepared in the laboratory concerning the effects of water, temperature, and traffic. The concentrations of heavy metals and PAHs in the leachates were quantified, while the toxicity assessment encompassed mortality, metal stress, PAH toxicity, inflammation, carcinogenicity, and oxidative damage. Gene expressions of related proteins or transcription factors were assessed, including metallothionines, aryl hydrocarbon receptors, interleukin-1ß, interleukin-10, nuclear factor-κB, tumor necrosis factor-α, tumor suppressor p53, heat shock protein 70, and reactive oxygen species (ROS). The findings demonstrate that leachates from asphalt pavements containing waste bottom ash, crumb rubber, or specific chemicals could induce notable stress and inflammation responses in zebrafish. In addition, potential carcinogenic effects and the elevation of ROS were identified within certain treatment groups. This study represents the first attempt to assess the ecotoxicity of pavement leachates employing a live fish model, thereby improving the current understanding of the environmental impact of asphalt pavements.

Co-pyrolysis of chicken manure with tree bark for reduced biochar toxicity and enhanced plant growth in Arabidopsis thaliana.

Co-pyrolysis of chicken manure with tree bark was investigated to mitigate salinity and potentially toxic element (PTE) concentrations of chicken manure-derived biochar. The effect of tree bark addition (0, 25, 50, 75 and 100 wt%) on the biochar composition, surface functional groups, PTEs and polycyclic aromatic hydrocarbons (PAH) concentration in the biochar was evaluated. Biochar-induced toxicity was assessed using an in-house plant growth assay with Arabidopsis thaliana. This study shows that PTE concentrations can be controlled through co-pyrolysis. More than 50 wt% of tree bark must be added to chicken manure to reduce the concentrations below the European Biochar Certificate-AGRO (EBC-AGRO) threshold. However, the amount of PAH does not show a trend with tree bark addition. Furthermore, co-pyrolysis biochar promotes plant growth at different application concentrations, whereas pure application of 100 wt% tree bark or chicken manure biochar results in decreased growth compared to the reference. In addition, increased plant stress was observed for 100 wt% chicken manure biochar. These data indicate that co-pyrolysis of chicken manure and tree bark produces EBC-AGRO-compliant biochar with the potential to stimulate plant growth. Further studies need to assess the effect of these biochars in long-term growth experiments.

Structured expert judgement approach of the health impact of various chemicals and classes of chemicals.

INTRODUCTION: Chemical contamination and pollution are an ongoing threat to human health and the environment. The concern over the consequences of chemical exposures at the global level continues to grow. Because resources are constrained, there is a need to prioritize interventions focused on the greatest health impact. Data, especially related to chemical exposures, are rarely available for most substances of concern, and alternate methods to evaluate their impact are needed. STRUCTURED EXPERT JUDGMENT (SEJ) PROCESS: A Structured Expert Judgment (Research Outreach, 2021) process was performed to provide plausible estimates of health impacts for 16 commonly found pollutants: asbestos, arsenic, benzene, chromium, cadmium, dioxins, fluoride, highly hazardous pesticides (HHPs), lead, mercury, polycyclic-aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), Per- and Polyfluorinated Substances (PFAs), phthalates, endocrine disrupting chemicals (EDCs), and brominated flame retardants (BRFs). This process, undertaken by sector experts, weighed individual estimations of the probable global health scale health impacts of each pollutant using objective estimates of the expert opinions' statistical accuracy and informativeness. MAIN FINDINGS: The foremost substances, in terms of mean projected annual total deaths, were lead, asbestos, arsenic, and HHPs. Lead surpasses the others by a large margin, with an estimated median value of 1.7 million deaths annually. The three other substances averaged between 136,000 and 274,000 deaths per year. Of the 12 other chemicals evaluated, none reached an estimated annual death count exceeding 100,000. These findings underscore the importance of prioritizing available resources on reducing and remediating the impacts of these key pollutants. RANGE OF HEALTH IMPACTS: Based on the evidence available, experts concluded some of the more notorious chemical pollutants, such as PCBs and dioxin, do not result in high levels of human health impact from a global scale perspective. However, the chemical toxicity of some compounds released in recent decades, such as Endocrine Disrupters and PFAs, cannot be ignored, even if current impacts are limited. Moreover, the impact of some chemicals may be disproportionately large in some geographic areas. Continued research and monitoring are essential; and a preventative approach is needed for chemicals. FUTURE DIRECTIONS: These results, and potential similar analyses of other chemicals, are provided as inputs to ongoing discussions about priority setting for global chemicals and pollution management. Furthermore, we suggest that this SEJ process be repeated periodically as new information becomes available.

Air pollution and skin diseases: A comprehensive evaluation of the associated mechanism.

Air pollutants deteriorate the survival environment and endanger human health around the world. A large number of studies have confirmed that air pollution jeopardizes multiple organs, such as the cardiovascular, respiratory, and central nervous systems. Skin is the largest organ and the first barrier that protects us from the outside world. Air pollutants such as particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) will affect the structure and function of the skin and bring about the development of inflammatory skin diseases (atopic dermatitis (AD), psoriasis), skin accessory diseases (acne, alopecia), auto-immune skin diseases (cutaneous lupus erythematosus(CLE) scleroderma), and even skin tumors (melanoma, basal cell carcinoma (BCC), squamous-cell carcinoma (SCC)). Oxidative stress, skin barrier damage, microbiome dysbiosis, and skin inflammation are the pathogenesis of air pollution stimulation. In this review, we summarize the current evidence on the effects of air pollution on skin diseases and possible mechanisms to provide strategies for future research.

Elevated plasma solMER concentrations link ambient PM2.5 and PAHs to myocardial injury and reduced left ventricular systolic function in children.

Exposure to fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) is known to be associated with the polarization of pro-inflammatory macrophages and the development of various cardiovascular diseases. The pro-inflammatory polarization of resident cardiac macrophages (cMacs) enhances the cleavage of membrane-bound myeloid-epithelial-reproductive receptor tyrosine kinase (MerTK) and promotes the formation of soluble MerTK (solMER). This process influences the involvement of cMacs in cardiac repair, thus leading to an imbalance in cardiac homeostasis, myocardial injury, and reduced cardiac function. However, the relative impacts of PM2.5 and PAHs on human cMacs have yet to be elucidated. In this study, we aimed to investigate the effects of PM2.5 and PAH exposure on solMER in terms of myocardial injury and left ventricular (LV) systolic function in healthy children. A total of 258 children (aged three to six years) were recruited from Guiyu (an area exposed to e-waste) and Haojiang (a reference area). Mean daily PM2.5 concentration data were collected to calculate the individual chronic daily intake (CDI) of PM2.5. We determined concentrations of solMER and creatine kinase MB (CKMB) in plasma, and hydroxylated PAHs (OH-PAHs) in urine. LV systolic function was evaluated by stroke volume (SV). Higher CDI values and OH-PAH concentrations were detected in the exposed group. Plasma solMER and CKMB were higher in the exposed group and were associated with a reduced SV. Elevated CDI and 1-hydroxynaphthalene (1-OHNa) were associated with a higher solMER. Furthermore, increased solMER concentrations were associated with a lower SV and higher CKMB. CDI and 1-OHNa were positively associated with CKMB and mediated by solMER. In conclusion, exposure to PM2.5 and PAHs may lead to the pro-inflammatory polarization of cMacs and increase the risk of myocardial injury and systolic function impairment in children. Furthermore, the pro-inflammatory polarization of cMacs may mediate cardiotoxicity caused by PM2.5 and PAHs.

Mechanism of cytochrome P450s mediated interference with glutathione and amino acid metabolisms from halogenated PAHs exposure.

Epidemiological evidence indicates that exposure to halogenated polycyclic aromatic hydrocarbons (HPAHs) is associated with many adverse effects. However, the mechanisms of metabolic disorder of HPAHs remains limited. Herein, effects of pyrene (Pyr), and its halogenated derivatives (1-chloropyrene (1-Cl-Pyr), 1-bromopyrene (1-Br-Pyr)) on endogenous metabolic pathways were investigated, in human hepatoma (HepG2) and HepG2-derived cell lines expressing various human cytochrome P450s (CYPs). Non-targeted metabolomics results suggested that 1-Br-Pyr and Pyr exposure (625 nM) induced disruption in glutathione and riboflavin metabolism which associated with redox imbalance, through abnormal accumulation of oxidized glutathione, mediated by bioactivation of CYP2E1. Conversely, CYP2C9-mediated 1-Cl-Pyr significantly interfered with glutathione metabolism intermediates, including glycine, L-glutamic acid and pyroglutamic acid. Notably, CYP1A1-mediated Pyr-induced perturbation of amino acid metabolism which associated with nutrition and glycolipid metabolism, resulting in significant upregulation of most amino acids, whereas halogenated derivatives mediated by CYP1A2 substantially downregulated amino acids. In conclusion, this study suggested that Pyr and its halogenated derivatives exert potent effects on endogenous metabolism disruption under the action of various exogenous metabolic enzymes (CYPs). Thus, new evidence was provided to toxicological mechanisms of HPAHs, and reveals potential health risks of HPAHs in inducing diseases caused by redox and amino acid imbalances.

Bioaccumulation of polycyclic aromatic hydrocarbons and their human health risks depend on the characteristics of microplastics in marine organisms of Sanggou Bay, China.

Microplastics pose a threat to marine environments through their physical presence and as vectors of chemical pollutants. However, the impact of microplastics on the accumulation and human health risk of chemical pollutants in marine organisms remains largely unknown. In this study, we investigated the microplastics and polycyclic aromatic hydrocarbons (PAHs) pollution in marine organisms from Sanggou Bay and analyzed their correlations. Results showed that microplastic and PAHs concentration ranged from 1.23 ± 0.23 to 5.77 ± 1.10 items/g, from 6.98 ± 0.45 to 15.07 ± 1.25 µg/kg, respectively. The microplastic abundance, particularly of fibers, transparent and color plastic debris, correlates strongly with PAH contents, indicating that microplastics increase the bioaccumulation of PAHs and microplastics with these characteristics have a significant vector effect on PAHs. Although consuming seafood from Sanggou Bay induce no carcinogenic risk from PAHs, the presence of microplastics in organisms can significantly increases incremental lifetime cancer risk of PAHs. Thus, microplastics can serve as transport vectors for PAHs with implications for the potential health risks to human through consumption. This study provides new insight into the risks of microplastics in marine environments.

Ryegrass uptake behavior and forage risk assessment after exposing to soil with combined polycyclic aromatic hydrocarbons and cadmium.

Internalization of chemicals and the forage risks of ryegrass under the combined exposure to PAHs and Cd at environmental concentrations were studied here. The effect of soil pH was also concerned due to the widely occurred soil acidification and general alkali remediation for acidification soil. Unexpectedly, as same as the acid-treated group (pH 6.77), the alkali-treatment (pH 8.83) increased Cd uptake compared with original soil pH group (pH 7.92) for the reason of CdOH+ and CdHCO3+ formed in alkali-treated group. Co-exposure to PAHs induced more oxidative stress than Cd exposure alone due to PAHs aggregated in young root regions, such as root tips, and consequently, affecting the expression of Cd-transporters, destroying the basic structure of plant cells, inhibiting the energy supply for the transporters, even triggering programmed cell death, and finally resulting in decreased Cd uptake. Even under environmental concentrations, combined exposure caused potential risks derived from both PAHs and Cd. Especially, ryegrass grown in alkali-treated soil experienced an increased forage risks despite the soil meeting the national standards for Cd at safe levels. These comprehensive results reveal the mechanism of PAHs inhibiting Cd uptake, improve the understanding of bioavailability of Cd based on different forms, provide a theoretical basis to formulate the safety criteria, and guide the application of actual soil management.

A novel approach to assess the health risk of aryl hydrocarbon receptor-bound contaminants via inhalation exposure using CYP1A1 expression as a biomarker.

Polycyclic aromatic hydrocarbons (PAHs) and dioxins are potential causes of multiple diseases by activating the aryl hydrocarbon receptor (AhR) pathway. Health risk assessment of chemicals primarily relies on the relative potency factor (RPF), although its accuracy may be limited when solely using EC50 values. The induction of cytochrome P4501A1 (CYP1A1) serves as a biomarker for AhR activation and is an integrator of dioxin-like toxicity. Here, we present a method for evaluating the risks associated with AhR activation using mathematical models of dose-CYP1A1 induction. The dose-effect curves for certain PAHs and dioxins, including Ant, BghiP, 1,2,3,4,7,8-HxCDD, and others, exhibited a non-classical S-shaped form. The toxic equivalent factor (TEF) profiles revealed a broad range of toxic equivalent factor values. The TEFs for PAHs ranged from approximately 0.01 to 6, with higher values being observed when the concentration was less than 10-10 M, with the exceptions of Ace, Phe, and BghiP. Most congeners of dioxins got the lowest TEF value at around 10-10 M, ranging from 0.04 to 1.00. The binding affinity of AhR to ligands did not display a strong correlation with the EC50 of CYP1A1 expression, suggesting that the AhR-mediated effects of PAHs and dioxins are not fixed but instead fluctuate with the dose. Air samples acquired from a parking area were used to compare the proficiency of RPF and our current approach. In the current method, naphthalene and chrysene were the primary contributors of PAHs to AhR-mediated risks in parking lots air samples, respectively. However, the contributions of naphthalene and chrysene could be disregarded in the RPF approach.

Polycyclic aromatic hydrocarbons exposure and arterial stiffness-related plasma miRNAs: A panel study.

The underlying mechanisms between polycyclic aromatic hydrocarbons (PAHs) exposure and arterial stiffness are poorly understood. We carried out a panel study involving three repeated surveys to examine the associations of individual and mixture of PAHs exposure with arterial stiffness-related miRNAs among 123 community adults. In linear mixed-effect (LME) models, we found that urinary 9-hydroxyfluorene (9-OHFlu), 2-hydroxyphenanthrene (2-OHPh), 9-hydroxyphenanthrene (9-OHPh) at lag 0 day were positively linked to miR-146a and/or miR-222. The Bayesian kernel machine regression (BKMR) analyses revealed positive overall associations of PAHs mixture at lag 0 day with miR-146a and miR-222, and urinary 9-OHFlu contributed the most. In addition, an inter-quartile range (IQR) increase in urinary 9-OHFlu at lag 0 day was associated with elevated miR-146a and miR-222 by 0.16 (95% CI: 0.02, 0.30) to 0.34 (95% CI: 0.13, 0.54). Accordingly, exposure to PAHs, especially 9-OHFlu at lag 0 day, was related to elevated arterial stiffness-related plasma miRNAs.

Salmonid smolt caudal fin and liver transcriptome responses to low sulfur marine diesel and high sulfur fuel oil water accommodated fractions for assessing oil spill effects in marine environments.

The environmental impact of oil spills is a critical concern, particularly pertaining to low sulfur marine diesel (LSMD) and high sulfur fuel oil (HSFO) that are commonly involved in coastal spills. Although transcriptomic biomonitoring of sentinel animals can be a powerful tool for assessing biological effects, conventional methods utilize lethal sampling to examine the liver. As a non-lethal alternative, we have previously shown salmonid caudal fin cyp1a1 is significantly responsive to LSMD-derived toxicants. The present study further investigated the transcriptomic biomonitoring potential of coho salmon smolt caudal fin in comparison to liver tissue in the context of LSMD and HSFO seawater accommodated fraction (seaWAF) exposure in cold-water marine environments. Assessing the toxicity of these seaWAFs involved quantifying polycyclic aromatic hydrocarbon (tPAH50) concentrations and generating gene expression profiles. Initial qPCR analyses revealed significant cyp1a1 response in both liver and caudal fin tissues of both genetic sexes to all seaWAF exposures. RNA-Seq analysis, focusing on the highest LSMD and HSFO seaWAF concentrations (28.4±1.8 and 645.08±146.3 µg/L tPAH50, respectively), revealed distinct tissue-specific and genetic sex-independent transcriptomic responses with an overall enrichment of oxidative stress, cell adhesion, and morphogenesis-related pathways. Remarkably, the caudal fin tissue exhibited transcriptomic response patterns comparable to liver tissue, particularly consistent differential expression of 33 gene transcripts in the liver (independent of sex and oil type) and 44 in the caudal fin. The present work underscores the viability of using the caudal fin as a non-lethal alternative to liver sampling for assessing and tracking oil spill exposure in marine environments.

Bioconcentration and lethal effects of gas-condensate and crude oil on nearshore copepod assemblages.

The progressive establishment of gas platforms and increasing petroleum accidents pose a threat to zooplankton communities and thus to pelagic ecosystems. This study is the first to compare the impacts of gas-condensate and crude oil on copepod assemblages. We conducted microcosm experiments simulating slick scenarios at five different concentrations of gas-condensate and crude oil to determine and compare their lethal effects and the bioconcentration of low molecular weight polycyclic aromatic hydrocarbons (LMW-PAHs) in eastern Mediterranean coastal copepod assemblages. We found that gas-condensate had a two-times higher toxic effect than crude oil, significantly reducing copepod survival with increased exposure levels. The LMW-PAHs bioconcentration factor was 1-2 orders of magnitude higher in copepods exposed to gas-condensate than in those exposed to crude oil. The median lethal concentration (LC50) was significantly lower in calanoids vs. cyclopoid copepods, suggesting that calanoids are more susceptible to gas-condensate and crude oil pollution, with potential trophic implications.

Large-scale soil application of hydrochar: Reducing its polycyclic aromatic hydrocarbon content and toxicity by heating.

The beneficial roles of hydrochar in carbon sequestration and soil improvement are widely accepted. Despite few available reports regarding polycyclic aromatic hydrocarbons (PAHs) generated during preparation, their potential negative impacts on ecosystems remain a concern. A heating treatment method was employed in this study for rapidly removing PAHs and reducing the toxicity of corn stover-based hydrochar (CHC). The result showed total PAHs content (∑PAH) decreased and then sharply increased within the temperature range from 150 °C to 400 °C. The ∑PAH and related toxicity in CHC decreased by more than 80% under 200 °C heating temperature, compared with those in the untreated sample, representing the lowest microbial toxicity. Benzo(a)pyrene produced a significant influence on the ecological toxicity of the hydrochar among the 16 types of PAHs. The impact of thermal treatment on the composition, content, and toxicity of PAHs was significantly influenced by the adsorption, migration, and desorption of PAHs within hydrochar pores, as well as the disintegration and aggregation of large molecular polymers. The combination of hydrochar with carbonized waste heat and exhaust gas collection could be a promising method to efficiently and affordably reduce hydrochar ecological toxicity.

Assessment of parent and alkyl -PAHs in surface sediments of Iranian mangroves on the northern coast of the Persian Gulf: Spatial accumulation distribution, influence factors, and ecotoxicological risks.

Spatial patterns, potential origins, and ecotoxicological risk of alkylated (APAH) -and parent -(PPAH) polycyclic aromatic hydrocarbons (PAHs) were studied in mangrove surface sediments along the northern coasts of the Persian Gulf, Iran. The mean total concentrations (ngg-1dw) ∑32PAH, ∑PPAHs and ∑APAHs in sediments were 3482 (1689-61228), 2642 (1109-4849), and 840 (478-1273), respectively. The spatial variability was similar among these PAH groups, with the highest levels occurring in Nayband National Marine Park (NNMP). Physicochemical environmental factors, such as sediment grain size, and total organic carbon (TOC) contents, are significant factors of PAH distribution. These findings suggest that PAH pollution level is moderate-to-high, supporting the current view that mangrove ecosystems are under intensive anthropogenic impacts, such as petrochemical, oil and gas loads, port activities, and urbanization. Non-parametric multidimensional scaling (NPMDS) ordination demonstrated that NNMP mangrove is the critical site exhibiting high loading of PAH pollutants. Here, for the first time in this region, Soil quality guidelines (SQGs), Toxic equivalency quotient (TEQ), Mutagenic equivalency quotient (MEQ), and composition indices comprising Mean maximum permissible concentration quotient (m-MPC-Q), and Mean effect range median quotient (m-ERM-Q) methods were used to have a comprehensive risk assessment for PAH compounds and confirmed medium-to-high ecological risks of PAHs in the study area, particularly in the western part of the Gulf, highlighting the industrial impacts on the environment.

A multigenerational study can detect the evolutionary response to BaP exposure in the non-biting freshwater midge Chironomus riparius.

The release of polycyclic aromatic hydrocarbons (PAHs) into the environment is posing a threat to ecosystems and human health. Benzo(a)pyrene (BaP) is considered a biomarker of PAH exposure and is classified as a Group 1 carcinogen. However, it was not known whether BaP is mutagenic, i.e. induces inherited germline mutations. In this study, we used a recently established method, which combines short-term mutation accumulation lines (MAL) with whole genome sequencing (WGS) to assess mutagenicity in the non-biting midge Chironomus riparius. The mutagenicity analysis was supplemented by an evaluation of the development of population fitness in three successive generations in the case of chronic exposure to BaP at a high concentration (100 µg/L). In addition, the level of ROS-induced oxidative stress was examined in vivo. Exposure to the higher BaP concentration led to an increase in germline mutations relative to the control, while the lower concentration showed no mentionable effect. Against expectations, BaP exposure decreased ROS-level compared to the control and is thus probably not responsible for the increased mutation rate. Likewise, the higher BaP concentration decreased fitness measured as population growth rate per day (PGR) significantly over all generations, without signs of rapid evolutionary adaptations. Our results thus highlighted that high BaP exposure may influence the evolutionary trajectory of organisms.