Rubber additives and relevant oxidation products in groundwater in a central China region: Levels, influencing factors and exposure.

This study investigated the presence of rubber additives and relevant oxidation products (RAROPs) in groundwater in central China's aboveground river region. Seven RAROPs were detected, and their levels in shallow groundwater showed a mild decreasing trend from the area near the Yellow River (Avg: 8.49 ng L-1) to the area on the far bank of the Yellow River (Avg: 5.01 ng L-1). In contrast, deep groundwater's RAROPs contents showed a dramatic decrease to only 0.26 ng L-1. The dominant contaminant was found to be N-(1, 3-dimethylbutyl) -N'-phenyl -p-phenylenediamine (6PPD). The vicinity of the garages and car parks was often characterized as contamination hotspots. Correlation analyses further indicated that aquaculture was likely to be a potential pathway for shallow groundwater contaminant inputs. The amount of RAROPs intake by humans through groundwater is nearly 30 times different due to the imbalanced development between urban and rural areas. Children were the most vulnerable to RAROPs. Therefore, human activities (transportation, waste tire storage, water resource allocation and utilization patterns, diversion of Yellow River water to aquaculture ponds) may exacerbate RAROPs pollution in groundwater by leaching contaminants through the surface soil. These results are important for developing appropriate utilization and protection strategies for groundwater resources in developing countries.

P-phenylenediamines (PPDs) and 6PPD-quinone in tunnel PM2.5: From the perspective of characterization, emission factors, and health risks.

P-phenylenediamines (PPDs) and a quinone derivative (6PPD-Q), as antioxidants added to tires, can inevitably enter into the environment during tire wear emission, posing potential health and ecological risks. However, investigation on their pollution characteristics in PM2.5 is still lacking, especially for high-pollution scenarios, such as tunnels. Herein, we investigated the pollution characteristics and emission factors, as well as the correlation analysis and daily intakes of PM2.5-bound PPDs and 6PPD-Q in tunnel. The results indicated heavy PPDs and 6PPD-Q pollution were observed in tunnel PM2.5, with the concentration at the two tunnel sites being 3.83 and 8.73 times higher than those at the urban site, respectively. PPDs were negatively correlated to relative humidity and positively to temperature. Emission factors of 6PPD and 6PPD-Q were 3013.54 and 1466.67 ng·veh-1·km-1 for large vehicles. PPDs and 6PPD-Q were most harmful to children, and annual exposure dosages at the tunnel sites were 4.64 times higher than those at the urban site. This study conducted a comparison of PPDs and 6PPD-Q in urban and tunnel environments for the first time. Our findings clarified the key factors to reduce the pollution of PPDs in tunnel and supported policy-making for emission reduction of PPDs and 6PPD-Q.

Presence of N, N'-Substituted p-Phenylenediamine-Derived Quinones in Human Urine.

Human exposure to various N,N'-substituted p-phenylenediamine-derived quinones (PPDQs) has been of increasing concern. Recent studies have examined N-phenyl-N'-(1,3-dimethylbutyl)-p-phenylenediamine-derived quinone (6PPDQ) in human urine to evaluate human exposure. However, other PPDQs in human urine have not been thoroughly investigated. This study analyzed six PPDQs in urine collected from 149 healthy individuals in Taizhou, China. All target PPDQs were detected, with 6PPDQ (mean 2.4 ng/mL,

Paeoniflorin alleviates toxicity and accumulation of 6-PPD quinone by activating ACS-22 in Caenorhabditis elegans.

6-PPD quinone (6-PPDQ) is extensively existed in various environments. In Caenorhabditis elegans, exposure to 6-PPDQ could cause multiple toxic effects. In the current study, we further used C. elegans to investigate the effect of paeoniflorin (PF) treatment on 6-PPDQ toxicity and accumulation and the underlying mechanism. Treatment with PF (25-100 mg/L) inhibited 6-PPDQ toxicity on reproduction capacity and locomotion behavior and in inducing reactive oxygen species (ROS) production. Additionally, PF (25-100 mg/L) alleviated the dysregulation in expression of genes governing oxidative stress caused by 6-PPDQ exposure. Moreover, PF (25-100 mg/L) inhibited the enhancement in intestinal permeability caused by 6-PPDQ exposure and the accumulation of 6-PPDQ in the body of nematodes. In 6-PPDQ exposed nematodes, PF (25-100 mg/L) increased expression of acs-22 encoding a fatty acid transporter. RNAi of acs-22 could inhibit the beneficial effect of PF against 6-PPDQ toxicity in decreasing reproductive capacity and locomotion behavior, in inducing intestinal ROS production, and in enhancing intestinal permeability. RNAi of acs-22 could also suppress the PF beneficial effect against 6-PPDQ accumulation in the body of nematodes. Therefore, our results demonstrate the function of PF treatment against 6-PPDQ toxicity and accumulation in nematodes by activating the ACS-22.

Environmentally Relevant Concentrations of S-6PPD-Quinone Caused More Serious Hepatotoxicity Than R-Enantiomer and Racemate in Oncorhynchus mykiss.

6PPD-quinone (6PPD-Q) is frequently detected in various environmental media, and the environmentally relevant concentrations can be fatal to Oncorhynchus mykiss. Notably, 6PPD-Q has two enantiomers (S-6PPD-Q and R-6PPD-Q). In this study, O. mykiss was separately exposed to each enantiomer and racemate of 6PPD-Q for 96 h at environmentally relevant concentrations, and livers were collected. Effects on the biochemical, pathological, and ultrastructural changes were assessed, and metabolomics was conducted to elucidate the potential hepatotoxicity mechanism. Compared with the control treatment, the levels of catalase (CAT, all treatments except for 0.1 µg/L rac-6PPD-Q), and glutathione-S-transferase (GST, all treatments) significantly declined. Hepatocyte space became smaller, nuclear morphology changed, and nucleolysis occurred. Mitochondrial malformation and vesicle-like structure dilation of the endoplasmic reticulum (ER) were observed in the hepatocytes, which was most serious after S-6PPD-Q exposure. Some amino acid metabolism, folate biosynthesis, taurine and hypotaurine metabolism and purine metabolism were disturbed, consistent with mitochondrial dysfunction and ER stress. The differential metabolites were in the order of S-6PPD-Q (216) > rac-6PPD-Q (88) > R-6PPD-Q (56). Thus, 6PPD-Q-induced hepatic mitochondrial dysfunction and ER stress, causing metabolic disturbance and oxidative stress might be the toxic mechanism of 6PPD-Q in O. mykiss liver, and S-6PPD-Q effects were the most serious.

Unraveling the fate of 6PPD-Q in aquatic environment: Insights into formation, dissipation, and transformation under natural conditions.

The widespread occurrence of N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) in aquatic environments and its hazards to aquatic species underscore the necessity of comprehending its environmental fate. Here, we investigated the transformation from 6PPD to 6PPD-Q and the attenuation of 6PPD-Q in surface water under natural conditions. Contrary to prior findings, this work revealed that 6PPD-Q and its precursor 6PPD-OH/6PPD-(OH)2, were not detected through target analysis and suspect screening during 6PPD transformation in the surface water under the natural conditions. 6PPD-Q predominantly accumulated in TWPs in ambient atmosphere with 1.28 % mass yield from the 6PPD dissipation. Subsequently, 6PPD-Q was eluted from TWPs and released to the water environment. The investigation on the natural attenuation of 6PPD-Q in the surface water demonstrated that direct and indirect photolysis facilitated the rapid dissipation of 6PPD-Q with a half-life of 2.57 h. Utilizing the liquid chromatography high resolution mass spectrometry (LC-HRMS), including both time of flight (TOF) MS and Orbitrap MS, twelve novel transformation products (TPs) of 6PPD-Q were identified by using a comprehensive non-targeted screening strategy. The results from two dimensions gas chromatography (GC×GC) TOF-MS revealed additional two TPs. Based on the molecular structure of TPs, four major pathways of 6PPD-Q attenuation were proposed, including bond cleavage, hydroxylation, quinone cleavage and rearrangement. All TPs were predicted to exhibit lower toxicity, indicating the natural attenuation of 6PPD-Q reduced its toxicity and potential environmental risks. This study provides crucial insights into the environmental fate of 6PPD-Q, highlighting the significance of understanding both its formation from 6PPD and its subsequent attenuation processes under natural conditions.

Development and application of diffusive gradients in thin-films for in-situ monitoring of 6PPD-Quinone in urban waters.

The occurrence and risk of N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q), derived from the oxidation of the tire antidegradant 6PPD, has raised significant concern since it was found to cause acute mortality in coho salmon when exposed to urban runoff. Given the short half-life period and low solubility of 6PPD-Q, reliable in situ measurement techniques are required to accurately understand its occurrence and behaviour in aquatic environments. Here, using the diffusive gradients in thin-films (DGT) method with HLB as a binding agent, we developed a new methodology to measure 6PPD-Q in urban waters. 6PPD-Q was rapidly and strongly adsorbed on the HLB-binding gel and was efficiently extracted using organic solvents. The HLB-DGT accumulated 6PPD-Q linearly for >7 d and its performance was not significantly affected by pH (6.5-8.5), ionic strength (0.0001-0.5 M) or dissolved organic matter (0-20 mg L-1). Field evaluation of the DGT method demonstrated its effectiveness in urban runoff, detecting 6PPD-Q levels of 15.8-39.5 ng L-1 in rivers. In snowmelt, DGT detected 6PPD-Q levels of 210 ng L-1 which is two times higher than the value obtained by grab sampling. 6PPD-Q levels were much higher in snowmelt than those in rivers. This indicates that snowfall constitutes an important transport pathway for 6PPD-Q and that DGT effectively captured the fraction continuously released from dust particles in the snow samples. 6PPD-Q posed a substantial risk to migratory fish in urban waters, and its release from tire wear particles requires further investigation. This study is the first to develop a DGT-based method for 6PPD-Q determination in urban waters, and the method can ensure an accurate measurement of the release of 6PPD-Q to the environment, particularly in rainfall or snowmelt, important pathways for its entry into the aquatic environment.

6-PPD quinone at environmentally relevant concentrations induced damage on longevity in C. elegans: Mechanistic insight from inhibition in mitochondrial UPR response.

6-PPD quinone (6-PPDQ) exists widely in water environment media, causing acute lethality to some aquatic species. Long-term exposure to 6-PPDQ reduced the lifespan of Caenorhabditis elegans. However, the molecular basis for mitochondrial control of 6-PPDQ toxicity remains largely unclear. Using HSP-6 as marker of mitochondrial unfolded protein response (mt UPR), we observed activation of mt UPR by 0.1 and 1 µg/L 6-PPDQ and inhibition in mt UPR by 10 µg/L 6-PPDQ. Additionally, increased atfs-1, ubl-5, and dve-1 expressions were caused by 0.1 and 1 µg/L 6-PPDQ and decreased expressions of these genes were induced by 10 µg/L 6-PPDQ. Neuronal and intestinal RNA interference (RNAi) of hsp-6 caused susceptibility to 6-PPDQ toxicity on longevity, and atfs-1, ubl-5, and dve-1 acted in neurons and intestine to modulate mt UPR and 6-PPDQ toxicity on longevity. Meanwhile, 6-PPDQ (1 and 10 µg/L) increased expressions of histone methyltransferase genes met-2 and set-6, and decreased expressions of histone demethylase genes jmjd-1.2 and jmjd-3.1. Neuronal RNAi of set-6 and intestinal RNAi of met-2 accelerated hsp-6, atfs-1, ubl-5, and dve-1 expressions and extended lifespan of 6-PPDQ exposed nematodes. In contrast, neuronal RNAi of jmjd-1.2 and jmjd-3.1 and intestinal RNAi of jmjd-1.2 suppressed these 4 gene expressions and reduced lifespan of 6-PPDQ exposed nematodes o. In nematodes, RNAi of hsp-6 could also enhance mitochondrial dysfunction and mitochondrial reactive oxygen species (ROS) induced by 6-PPDQ. Therefore, 6-PPDQ caused damage on longevity was associated with suppression in mt UPR, which was under regulation of certain histone methylation related signals.

A bibliometric analysis of global research hotspots and progress on emerging environmental pollutants 6PPD and 6PPD-quinone from 2004 to 2024.

The emerging toxicants, N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q), resulting from environmental exposure to N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), have gained considerable attention owing to their ubiquitous occurrence and high toxicity. We performed a scientometric analysis on this topical area of research over the past two decades, spanning from 2004 to April 2024. The overarching aim was to reveal potential future directions in this research area, exploring several key aspects. These included publication and citation growth trends, relevant subject fields, distribution of contribution by country, influential journals in the field, keyword co-occurrence network and cluster analysis, and identification of top authors. The information was collected from the Scopus database and processed using the VOS viewer software. We observed a notable increase in the number of publications over the past four years. With a share of 46.2% of publications, "Environmental Sciences" dominated as the primary scientific category. Among all journals, "Science of the Total Environment" was the most prolific, publishing 33 documents, accounting for 15.6% of the total records. China, representing 76 publications (36%), followed by the United States, with 40 (18.9%), stood out as the leading countries. The occurrence of keywords such as "Pollution exposure", "Mass spectrometry", and "toxicity" highlighted the importance of assessing the toxicological properties, analytical methods, and environmental implications of these emerging contaminants to mitigate their adverse effects and protect environmental and human health. Cai, Zongwei from Hong Kong Baptist University was highly productive in this field, publishing 11 papers. Based on the bibliometric analysis presented, it seems that the future direction of research on 6PPD and 6PPD-Q will shift towards strategies focused on their removal and treatment.

Comparative toxic effect of tire wear particle-derived compounds 6PPD and 6PPD-quinone to Chlorella vulgaris.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), a widely used antioxidant in rubber products, and its corresponding ozone photolysis product N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q), have raised public concerns due to their environmental toxicity. However, there is an existing knowledge gap on the toxicity of 6PPD and 6PPD-Q to aquatic plants. A model aquatic plant, Chlorella vulgaris (C. vulgaris), was subjected to 6PPD and 6PPD-Q at concentrations of 50, 100, 200, and 400 µg/L to investigate their effects on plant growth, photosynthetic, antioxidant system, and metabolic behavior. The results showed that 6PPD-Q enhanced the photosynthetic efficiency of C. vulgaris, promoting growth of C. vulgaris at low concentrations (50, 100, and 200 µg/L) while inhibiting growth at high concentration (400 µg/L). 6PPD-Q induced more oxidative stress than 6PPD, disrupting cell permeability and mitochondrial membrane potential stability. C. vulgaris responded to contaminant-induced oxidative stress by altering antioxidant enzyme activities and active substance levels. Metabolomics further identified fatty acids as the most significantly altered metabolites following exposure to both contaminants. In conclusion, this study compares the toxicity of 6PPD and 6PPD-Q to C. vulgaris, with 6PPD-Q demonstrating higher toxicity. This study provides valuable insight into the risk assessment of tire wear particles (TWPs) derived chemicals in aquatic habitats and plants.

Presence of N, N'-Substituted p-Phenylenediamine Quinones in Tap Water: Implication for Human Exposure.

Monitoring studies have demonstrated the wide presence of N, N'-substituted p-phenylenediamine-derived quinones (PPDQs) in environmental matrices. The general population may be potentially exposed to PPDQs through the consumption of tap water. While, the existence of PPDQs in tap water has not been well examined. To fill this gap, in this study we collected tap water samples from Hangzhou, China, and examined seven homologues of PPDQs in collected samples. All target PPDQs were identified in the collected tap water samples, with distinct detection frequencies (38-89%). PPDQs detected in tap water was dominated by N-(1, 3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPDQ; mean 0.56 ng/L, < LOD-4.0 ng/L). The profiles of PPDQs concentrations in tap water from the four districts of Hangzhou city were slightly different. The daily intake (DI) was found highest for 6PPDQ (mean 14-22 pg/kg bw/day, median 10-15 pg/kg bw/day) through tap water intake. The relatively higher DIs of various PPDQs were displayed for infants (mean 10-22 pg/kg bw/day, median 6.5-15 pg/kg bw/day), relative to the children (8.0-18 pg/kg bw/day, 5.4-12 pg/kg bw/day) and adults (6.7-14 pg/kg bw/day, 4.5-10 pg/kg bw/day). These data are crucial for assessing the overall human exposure to PPDQs. This study first, to our knowledge, reveals the concentrations and profiles of PPDQs in tap water.

Degradation and detoxification of 6PPD-quinone in water by ultraviolet-activated peroxymonosulfate: Mechanisms, byproducts, and impact on sediment microbial community.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q) has been identified to induce acute toxicity to multifarious aquatic organisms at exceptionally low concentrations. The ubiquity and harmful effects of 6PPD-Q emphasize the critical need for its degradation from water ecosystems. Herein, we explored the transformation of 6PPD-Q by an ultraviolet-activated peroxymonosulfate (UV/PMS) system, focusing on mechanism, products and toxicity variation. Results showed that complete degradation of 6PPD-Q was achieved when the initial ratio of PMS and 6PPD-Q was 60:1. The quenching experiments and EPR tests indicated that SO4•- and •OH radicals were primarily responsible for 6PPD-Q removal. Twenty-one degradation products were determined through high-resolution orbitrap mass spectrometry, and it was postulated that hydroxylation, oxidative cleavage, quinone decomposition, ring oxidation, as well as rearrangement and deamination were the major transformation pathways of 6PPD-Q. Toxicity prediction revealed that all identified products exhibited lower acute and chronic toxicities to fish, daphnid and green algae compared to 6PPD-Q. Exposure experiments also uncovered that 6PPD-Q considerably reduced the community diversity and altered the community assembly and functional traits of the sediment microbiome. However, we discovered that the toxicity of 6PPD-Q degradation solutions was effectively decreased, suggesting the superior detoxifying capability of the UV/PMS system for 6PPD-Q. These findings highlight the underlying detrimental impacts of 6PPD-Q on aquatic ecosystems and enrich our understanding of the photochemical oxidation behavior of 6PPD-Q.

Cotransport of 6PPD-Q and pristine/aged microplastics in porous media: An insight based on transport forms and mechanisms.

The environmental fate and risks of microplastics (MPs) and their associated contaminants have attracted increasing concern in recent years. In this study, the cotransport of six kinds of pristine and aged MPs and the antiager ozonation product N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) were investigated via a series of batch and transport experiments, and characteristic analysis (e.g., SEM, FTIR and XPS). Generally, pristine MPs exhibit higher adsorption ability than aged MPs due to the hydrophobic interaction. The 6PPD-Q usually exhibited both free moving and bond-MPs moving during transport process in presence of MPs, but none free 6PPD-Q was detected in presence of pristine PP MPs. The mobility of 6PPD-Q was generally facilitated in presence of MPs by bond-MPs moving due to the hydrogen bonding, halogen bonding, π-π interaction (the maximum total mass recovery of 84.11%), which efficiency was influenced with the combined effect of adsorption ability and mobility of MPs. The pristine PVC MPs showed highest facilitation on 6PPD-Q transport. The retained 6PPD-Q in porous media also was released by various MPs with different mass recovery ranged from 15.72% to 56.26% via surface moving of MPs around porous media. Both the dissolved and retained 6PPD-Q decreased the MPs mobility with the minimum mass recovery of 34.02%. Findings from this study contribute to the prediction and assessment of the combined risks of MPs and 6PPD-Q.

Environmental concentrations of 6PPD and 6PPD-Q cause oxidative damage and alter metabolism in Eichhornia crassipes.

N-(1,3-dimethylbutyl)-N '-phenyl-p-phenylenediamine (6PPD) and N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) are ubiquitous in the environment and can cause toxicity to aquatic animals. However, research on the toxicological effects of 6PPD and 6PPD-Q on aquatic plants remains limited. The present study investigated the physiological, biochemical, and metabolic responses of the floating aquatic plant Eichhornia crassipes (E. crassipes) to environmentally relevant concentrations (0.1, 1, and 10 µg·L-1) of 6PPD and 6PPD-Q. We found that 6PPD and 6PPD-Q elicited minimal effects on plant growth, but 6PPD induced a concentration-dependent decrease in the content of photosynthetic pigments. Low doses (0.1 µg·L-1 and 1 µg·L-1) of 6PPD-Q significantly elevated Reactive Oxygen Species (ROS) content in E. crassipes roots, indicating oxidative damage. Furthermore, 6PPD-Q induced a more pronounced osmotic stress compared to 6PPD. Metabolic analyses revealed that carbohydrates were significantly altered under 6PPD and 6PPD-Q treatments. The findings of this study enhance the understanding of the environmental risks posed by 6PPD and 6PPD-Q to plants and reveal the potential mechanisms of phytotoxicity.

Detection of 6-PPD and 6-PPDQ in airborne particulates and assessment of their toxicity in lung cells.

The extensive use of synthetic antioxidants, notably N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6-PPD), in rubber-related products, particularly in tire manufacturing, has induced concerns regarding their environmental impact and potential health hazards. Despite the identification of 6-PPD and its derivative, 6-PPD quinone (6-PPDQ), in various water samples and their lethal effects on certain aquatic species (e.g., coho salmon, rainbow trout and brook trout), the levels of airborne 6-PPD/6-PPDQ and their respiratory toxicity remain relatively unexplored. In this study, we aimed to evaluate the respiratory toxicity potential of 6-PPD and its derivatives, with a specific focus on detecting these compounds in airborne particulates and assessing their toxic effects on lung cells. Characterization of four airborne fine particulate (FP) samples revealed spherical morphologies with diameters ranging from 17.7 to 225.7 nm, displaying slight agglomeration and negative surface charge. methanol/acetonitrile extraction followed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) analysis confirmed the presence of both 6-PPD and 6-PPDQ on the surfaces of FPs, with significant variations (0.26-1.05 µg g-1) in loading capacity observed among the samples. Subsequent exposure of lung cells (THP-1, BEAS-2B, and A549) to 6-PPD and 6-PPDQ revealed dose-dependent declines in mitochondrial metabolic activity induced by 6-PPD, along with severe membrane damage, ATP depletion, and pro-inflammatory cytokine release. Conversely, 6-PPDQ exhibited negligible toxicity in all tested parameters. These findings underscore the potential health risks associated with airborne 6-PPD exposure and emphasize the importance of further research into the respiratory toxicity of 6-PPD derivatives.

Neurotoxicity from long-term exposure to 6-PPDQ: Recent advances.

The recent acceleration of industrialization and urbanization has brought significant attention to N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6-PPDQ), an emerging environmental pollutant from tire wear, due to its long-term effects on the environment and organisms. Recent studies suggest that 6-PPDQ can disrupt neurotransmitter synthesis and release, impact receptor function, and alter signaling pathways, potentially causing oxidative stress, inflammation, and apoptosis. This review investigates the potential neurotoxic effects of prolonged 6-PPDQ exposure, the mechanisms underlying its cytotoxicity, and the associated health risks. We emphasize the need for future research, including precise exposure assessments, identification of individual differences, and development of risk assessments and intervention strategies. This article provides a comprehensive overview of 6-PPDQ's behavior, impact, and neurotoxicity in the environment, highlighting key areas and challenges for future research.

Exposure to 6-PPD quinone disrupts glucose metabolism associated with lifespan reduction by affecting insulin and AMPK signals in Caenorhabditis elegans.

Glucose metabolism plays an important role for formation of normal physiological state of organisms. However, association between altered glucose metabolism and toxicity of 6-PPD quinone (6-PPDQ) remains largely unknown. In 1-100 µg/L 6-PPDQ exposed Caenorhabditis elegans, we observed increased glucose content. After 6-PPDQ exposure (1-100 µg/L), expressions of F47B8.10 and fbp-1 governing gluconeogenesis were increased, and expressions of hxk-1, hxk-3, pfk-1.1, pyk-1, and pyk-2 governing glycolysis were decreased. Under 6-PPDQ exposure condition, glucose content could be changed by RNAi of F47B8.10, hxk-1, and hxk-3, key genes for gluconeogenesis and glycolysis. In 6-PPDQ exposed nematodes, RNAi of daf-16 and aak-2 elevated glucose content, increased expressions of F47B8.10 and/or fbp-1, and decreased expressions of hxk-1, hxk-3, and/or pfk-1.1. Additionally, lifespan and locomotion during aging were increased by RNAi of F47B8.10 and decreased by RNAi of hxk-1 and hxk-3 in 6-PPDQ exposed nematodes. Moreover, after 6-PPDQ exposure, RNAi of F47B8.10 decreased expressions of insulin peptide genes (ins-7 and daf-28) and insulin receptor gene daf-2 and increased expressions of daf-16 and aak-2. In 6-PPDQ exposed nematodes, RNAi of hxk-1 and hxk-3 further increased expressions of ins-7, daf-28, and daf-2 and decreased expressions of daf-16 and aak-2. Our results demonstrated important association between altered glucose metabolism and toxicity of 6-PPDQ in inducing lifespan reduction in organisms.

Potential human health risk of the emerging environmental contaminant 6-PPD quinone.

The tire antioxidant 6-PPD has been widely used to enhance tire performance and extend tire lifespan. 6-PPD quinone (6-PPDQ), a quinone derivative derived from 6-PPD in the presence of ozone, has been recognized an emerging environmental contaminant. In addition to causing acute lethality to coho salmon, 6-PPDQ exhibits toxic effects on other aquatic species and mammals. Based on the existing evidence, we provide a critical overview on the human internal exposure, potential adverse effects on health, and prediction of human health risk of 6-PPDQ. 6-PPDQ could be detected in human samples, including human urine, blood, and cerebrospinal fluid. Human exposure to 6-PPDQ in the environment is inevitable and may lead to adverse health effects, including hepatotoxicity, enterotoxicity, pulmonary toxicity, neurotoxicity, reproductive toxicity, and cardiotoxicity. Additionally, potential human health risk to 6-PPDQ through exposure routes and human samples were predicted. This review is helpful to identify the existing knowledge gaps and future research directions regarding the human health effects of 6-PPDQ.

Exposure to 6-PPD quinone enhances glycogen accumulation in Caenorhabditiselegans.

Glycogen metabolism is an important biological process for organisms. In Caenorhabditis elegans, effect of 6-PPD quinone (6-PPDQ) on glycogen accumulation and underlying mechanism were examined. Exposure to 6-PPDQ (1 and 10 µg/L) increased glycogen accumulation. Meanwhile, exposure to 6-PPDQ (1 and 10 µg/L) increased expression of gsy-1 encoding glycogen synthase and decreased expression of pygl-1 encoding glycogen phosphorylase. In 6-PPDQ exposed animals, glycogen content and glycogen accumulation were inhibited by RNAi of gsy-1 and enhanced by RNAi of pygl-1. RNAi of gsy-1 increased pygl-1 expression, and RNAi of pygl-1 increased gsy-1 expression after 6-PPDQ exposure. In 6-PPDQ exposed nematodes, daf-16 and aak-2 expressions were decreased and glycogen accumulation was suppressed by RNAi of daf-16 and aak-2, suggesting alteration in daf-16 and aak-2 expressions did not mediate glycogen accumulation. Moreover, resistance to 6-PPDQ toxicity on locomotion and brood size was observed in gsy-1(RNAi) animals, and susceptibility to 6-PPDQ toxicity was found in pygl-1(RNAi) animals. Therefore, glycogen accumulation could be enhanced by exposure to 6-PPDQ in nematodes. In addition, alteration in expressions of gsy-1 and pygl-1 governing this enhancement in glycogen accumulation mediated induction of 6-PPDQ toxicity.

The spatio-temporal accumulation of 6 PPD-Q in greenbelt soils and its effects on soil microbial communities.

6 PPD-Q (6 PPD-Quinone) is an ozone-induced byproduct derived from the degradation of N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6 PPD), commonly found in road dust resulting from tire wear. However, the extent of 6 PPD-Q pollution in urban soil remains unclear. This study investigates the spatial and temporal accumulation patterns of 6 PPD-Q in greenbelt soils in Ningbo, and explores the correlation between 6 PPD-Q accumulation and soil microbial community composition and functions. Our findings indicate that 6 PPD-Q is present (ranging from 0.85 to 12.58 µg/kg) in soil samples collected from both sides of urban traffic arteries. Soil fungi exhibit higher sensitivity to 6 PPD-Q accumulation compared to bacteria, and associated fungi (Basidiomycota) may be potential biomarkers for environmental 6 PPD-Q contamination. Co-occurrence network analysis reveals that the bacterial microbial network in summer exhibits greater stability and resilience in response to 6 PPD-Q inputs than in winter. However, 6 PPD-Q accumulation disrupts the network structure of fungal communities to some extent, leading to reduced diversity in fungal microbial communities. Long-term accumulation of 6 PPD-Q weakens the nitrogen and phosphorus cycling potential within urban soil, while the enhancement of carbon cycling may further promote 6 PPD-Q degradation in urban soil. Taken together, this study provides new insights into the ecological risks of 6 PPD-Q in urban soils.