The present study aims at phytoremediation of Lemna gibba L. in aqueous solutions with different concentrations of TC and Degradation Products (DPs). It also tries to determine whether there are differences in TC, ETC, EATC, and ATC levels, accumulated by Lemna gibba L. Exposure concentrations of 50, 100, and 300 ppb have been selected for TC and DPs, showing that the highest TC50, TC100, and TC300 concentrations in the plant have been 23.5+1.1, 80.1+3.9, and 274+13 ppb, respectively, while the highest ETC50, ETC100, and ETC300 have proven to be 39.5+1.9, 47.8+2.4, and 168+8.4 ppb, respectively. The highest EATC50, EATC100, and EATC300 concentrations in the plant have been 45.3+2.3; 65+3.0 and 173+9.0 ppb, respectively, whereas the highest ATC50, ATC100, and ATC300 concentrations in Lemna gibba L. have been 34.7+1.7, 39.6+0.2, and 114+5.6 ppb, respectively. TC, ETC, EATC, and ATC concentrations in Lemna gibba L. have increased with the increase of initial TC, ETC, EATC, and ATC concentration.

Telomere length (TL) is an index of cellular aging and can predict the incidences of many age-related diseases. Change of TL might be affected by environmental pollution and individual's genetic background. In this cohort study, we aimed to evaluate the associations between polycyclic aromatic hydrocarbons (PAHs) exposure and longitudinal TL shortening, and investigate whether genetic variations in TERT-CLPTM1L can modify these associations. We measured the baseline concentrations of twelve urinary PAH metabolites and genotyped six variants at TERT-CLPTM1L among 1243 coke-oven workers. The relative leukocyte TL was detected in both baseline and follow-up (4 years later) visits. The TL shortening were estimated by TL decline and TL ratio. We found that the urinary level of 1-hydroxypyrene (1-OHP) had significant dose-response relationships with increased TL decline [β(95%CI) = 0.078(0.023, 0.133), P = 0.005] and TL ratio [β(95%CI) = 0.096(0.037, 0.155), P = 0.002]. Besides, urinary 1-hydroxynaphthalene (1-OHNa) was marginally dose-related with elevated TL decline [β(95%CI) = 0.053(-0.001, 0.107), P = 0.055] and TL ratio [β(95%CI) = 0.057(-0.002, 0.116), P = 0.058]. Analyses of TERT-CLPTM1L variants showed that the rs401681 and rs465498 could modify the effect of 1-OHP on increasing TL decline (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.012 and 0.035, respectively) and TL ratio (Pᵢₙₜₑᵣₐcₜᵢₒₙ = 0.014 and 0.067, respectively), which were pronounced among rs401681TT and rs465498CC carriers, but not seen among rs401681TC + CC and rs465498CT + TT carriers. In conclusion, elevated exposure to PAHs can accelerate the TL shortening and this effect can be modified by TERT-CLPTM1L variants. These results may add potential evidence for gene-environment interactions on dynamic changes of telomere length. Further studies are warranted to validate these findings and uncover the underlying mechanisms.

Tools to predict environmental fate processes during remediation of persistent organic pollutants (POPs) in soil are desperately needed since they can elucidate the overall behavior of the chemical and help to improve the remediation process. A dynamic multimedia fate model (SoilPlusVeg) was further developed and improved to account for rhizoremediation processes. The resulting model was used to predict Polychlorinated Biphenyl (PCB) fate in a highly contaminated agricultural field (1089 ng/g d.w.) treated with tall fescue (Festuca arundinacea), a promising plant species for the remediation of contaminated soils. The model simulations allowed to calculate the rhizoremediation time (about 90 years), given the available rhizoremediation half-lives and the levels and fingerprints of the PCB congeners, to reach the legal threshold, to show the relevance of the loss processes from soil (in order of importance: degradation, infiltration, volatilization, etc.) and their dependence on meteorological and environmental dynamics (temperature, rainfall, DOC concentrations). The simulations showed that the effective persistence of PCBs in soil is deeply influenced by the seasonal variability. The model also allowed to evaluate the role of DOC as a possible enhancer of PCB degradation as a microorganism “spoon feeder” of PCBs in the soil solution. Additionally, we preliminary predicted how the contribution of PCB metabolites could modify the PCB fingerprint and their final total concentrations. This shows that the SoilPlusVeg model could be used in selecting the best choices for a sustainable rhizoremediation of a POP contaminated site.

The mechanisms contributing to toxic effects of airborne lower-chlorinated PCB congeners (LC-PCBs) remain poorly characterized. We evaluated in vitro toxicities of environmental LC-PCBs found in both indoor and outdoor air (PCB 4, 8, 11, 18, 28 and 31), and selected hydroxylated metabolites of PCB 8, 11 and 18, using reporter gene assays, as well as other functional cellular bioassays. We focused on processes linked with endocrine disruption, tumor promotion and/or regulation of transcription factors controlling metabolism of both endogenous compounds and xenobiotics. The tested LC-PCBs were found to be mostly efficient anti-androgenic (within nanomolar – micromolar range) and estrogenic (at micromolar concentrations) compounds, as well as inhibitors of gap junctional intercellular communication (GJIC) at micromolar concentrations. PCB 8, 28 and 31 were found to partially inhibit the aryl hydrocarbon receptor (AhR)-mediated activity. The tested LC-PCBs were also partial constitutive androstane receptor (CAR) and pregnane X receptor (PXR) agonists, with PCB 4, 8 and 18 being the most active compounds. They were inactive towards other nuclear receptors, such as vitamin D receptor, thyroid receptor α, glucocorticoid receptor or peroxisome proliferator-activated receptor γ. We found that only PCB 8 contributed to generation of oxidative stress, while all tested LC-PCBs induced arachidonic acid release (albeit without further modulations of arachidonic acid metabolism) in human lung epithelial cells. Importantly, estrogenic effects of hydroxylated (OH-PCB) metabolites of LC-PCBs (4-OH-PCB 8, 4-OH-PCB 11 and 4′-OH-PCB 18) were higher than those of the parent PCBs, while their other toxic effects were only slightly altered or suppressed. This suggested that metabolism may alter toxicity profiles of LC-PCBs in a receptor-specific manner. In summary, anti-androgenic and estrogenic activities, acute inhibition of GJIC and suppression of the AhR-mediated activity were found to be the most relevant modes of action of airborne LC-PCBs, although they partially affected also additional cellular targets.

Recently, concerns have been raised that residues of glyphosate-based herbicides may interfere with the homeostasis of the intestinal bacterial community and thereby affect the health of humans or animals. The biochemical pathway for aromatic amino acid synthesis (Shikimate pathway), which is specifically inhibited by glyphosate, is shared by plants and numerous bacterial species. Several in vitro studies have shown that various groups of intestinal bacteria may be differently affected by glyphosate. Here, we present results from an animal exposure trial combining deep 16S rRNA gene sequencing of the bacterial community with liquid chromatography mass spectrometry (LC-MS) based metabolic profiling of aromatic amino acids and their downstream metabolites. We found that glyphosate as well as the commercial formulation Glyfonova®450 PLUS administered at up to fifty times the established European Acceptable Daily Intake (ADI = 0.5 mg/kg body weight) had very limited effects on bacterial community composition in Sprague Dawley rats during a two-week exposure trial. The effect of glyphosate on prototrophic bacterial growth was highly dependent on the availability of aromatic amino acids, suggesting that the observed limited effect on bacterial composition was due to the presence of sufficient amounts of aromatic amino acids in the intestinal environment. A strong correlation was observed between intestinal concentrations of glyphosate and intestinal pH, which may partly be explained by an observed reduction in acetic acid produced by the gut bacteria. We conclude that sufficient intestinal levels of aromatic amino acids provided by the diet alleviates the need for bacterial synthesis of aromatic amino acids and thus prevents an antimicrobial effect of glyphosate in vivo. It is however possible that the situation is different in cases of human malnutrition or in production animals.

Organophosphate esters (OPEs) are widely used in household products as flame retardants or plasticizers and have become ubiquitous pollutants in environmental media. However, little is known about OPE metabolites in humans, especially in children. In this study, eight OPE metabolites were measured in 411 urine samples collected from 6 to 14-year-old children in South China. Bis(2-chloroethyl) phosphate (BCEP), bis(1-chloro-2-propyl) phosphate (BCIPP) and diphenyl phosphate (DPHP) were the dominant OPE metabolites, and their median concentrations were 1.04, 0.15 and 0.28 μg/L, respectively. The levels of urinary OPE metabolites in the present study were much lower than those in participants from other countries, with the exception of BCEP, suggesting widespread exposure to tris(2-chlorethyl) phosphate (TCEP, the parent chemical of BCEP) in South China. No significant difference in the concentrations of any of the OPE metabolites was observed between males and females (p > .05). Significant negative correlations were observed between age and BCEP, BCIPP, bis(1,3-dichloro-2-propyl) phosphate (BDCIPP), di-o-cresyl phosphate (DoCP) and di-p-cresyl phosphate (DpCP) (DCP), or DPHP (p < .05). Pearson correlation coefficients between urinary OPE metabolites indicated multiple sources and OPE exposure pathways in children. The estimated daily intake suggested that children in South China have a relatively high exposure level to TCEP. To the best of our knowledge, this is the first study to report the urinary levels of OPE metabolites in Chinese children.

N-ethyl perfluorooctane sulfonamide (N-EtFOSA) is commonly known as the active ingredient of sulfluramid. It can be degraded to perfluorooctane sulfonic acid (PFOS) in biota and environment. Earthworms (Eisenia fetida) were exposed with N-EtFOSA to examine the bioaccumulation, elimination and metabolism of N-EtFOSA by the earthworms after in vivo and in vitro exposure. N-EtFOSA could be biodegraded in quartz sands to perfluorooctane sulfonamide (FOSA) and PFOS. In the in vivo tests, in addition to parent N-EtFOSA, three metabolites, including perfluorooctane sulfonamide acetate (FOSAA), FOSA and PFOS also accumulated in earthworms as a result of N-EtFOSA biotransformation, with FOSA as the predominant metabolite. The bioaccumulation factor (BAF) and uptake rate coefficient (ku) of N-EtFOSA from sand were 20.4 and 2.41·d−1, respectively. The elimination rate constants (ke) decreased in the order FOSAA (0.130·d−1) > N-EtFOSA (0.118·d−1) > FOSA (0.073·d−1) > PFOS (0.051·d−1). The biotransformation of N-EtFOSA in earthworm was further confirmed by the in vitro test involving incubation of earthworm homogenates with N-EtFOSA. This work provides evidence on the accumulation and transformation of N-EtFOSA in terrestrial invertebrates and will be helpful to explore the indirect sources of FOSA and PFOS in environmental biota.

Benzene is widely employed in the field of production, and its toxicity on biological systems has received increasing attention. Cell proliferation is a major life characteristic of living organisms. KLF15 and NOTCH1 are mature and classical genes in cell proliferation studies, particularly in the area of tumor investigation. The aim of this study was to investigate the effect and mechanism of VNN3 on cell proliferation induced by 1,4-benzoquinone (1,4-BQ), an important metabolite of benzene, and obtain a sensitive biomarker for the hazard screening and health care of benzene exposure. Normally growing AHH-1 cells were cultured in vitro and were incubated with different concentrations of 1,4-BQ (0, 10, 20, and 40 μM) for 24 h. A CCK-8 assay was used to assess the cell viability, whereas EdU was used to detect the cell proliferation of AHH-1 cells. The expression of VNN3, KLF15 and NOTCH1 was detected by real-time PCR. Moreover, a lentiviral model was constructed in AHH-1 cells to interfere with VNN3 expression. The results showed that 1,4-BQ clearly increased the expression of VNN3. Moreover, 1,4-BQ dose-dependently inhibited cell proliferation and caused increased KLF15 expression; in contrast, the NOTCH1 expression decreased in AHH-1 cells. Furthermore, following interference with the VNN3 expression, the cell proliferation inhibition and the expression of KLF15 and NOTCH1 were rescued. To further investigate the action of VNN3 in benzene hematotoxicity, we assessed it in benzene-exposed workers. The results showed that there was a remarkable correlation between the VNN3 expression and hemogram, which included RBC, NEUT and HGB. In addition, analysis of the KLF15 and NOTCH1 expression showed that the VNN3 expression was related to cell proliferation, which was consistent with the in vitro results. In conclusion, VNN3 influences cell proliferation induced by 1,4-BQ by regulating the expression of KLF15 and NOTCH1. VNN3 may represent a potential biomarker of benzene toxicity.

Ibuprofen (IBU), as a commonly used non-steroidal anti-inflammatory drug (NSAID) and pharmaceutical and personal care product (PPCP), is frequently prescribed by doctors to relieve pain. It is widely released into environmental water and soil in the form of chiral enantiomers by the urination and defecation of humans or animals and by sewage discharge from wastewater treatment plants. This study focused on the alteration of metabolism in the adult zebrafish (Danio rerio) brain after exposure to R-(-)-/S-(+)-/rac-IBU at 5 μg L−1 for 28 days. A total of 45 potential biomarkers and related pathways, including amino acids and their derivatives, purine and its derivatives, nucleotides and other metabolites, were observed with untargeted metabolomics. To validate the metabolic disorders induced by IBU, 22 amino acids and 3 antioxidant enzymes were selected to be quantitated and determined using targeted metabolomics and enzyme assay. Stereoselective changes were observed in the 45 identified biomarkers from the untargeted metabolomics analysis. The 22 amino acids quantitated in targeted metabolomics and 3 antioxidant enzymes determined in enzyme assay also showed stereoselective changes after R-(-)-/S-(+)-/rac-IBU exposure. Results showed that even at a low concentration of R-(-)-/S-(+)-/rac-IBU, disorders in metabolism and antioxidant defense systems were still induced with stereoselectivity. Our study may enable a better understanding of the risks of chiral PPCPs in aquatic organisms in the environment.

Mercury is a globally distributed toxicant to aquatic animals and mammals. However, the potential risks of environmental relevant mercury in terrestrial systems remain largely unclear. The metabolic profiles of the earthworm Eisenia fetida after exposure to soil contaminated with mercury at 0.77 ± 0.09 mg/kg for 2 weeks were investigated using a two-dimensional nuclear magnetic resonance-based (¹H-¹³C NMR) metabolomics approach. The results revealed that traditional endpoints (e.g., mortality and weight loss) did not differ significantly after exposure. Although histological examination showed sub-lethal toxicity in the intestine as a result of soil ingestion, the underlying mechanisms were unclear. Metabolite profiles revealed significant decreases in glutamine and 2-hexyl-5-ethyl-3-furansulfonate in the exposed group and remarkable increases in glycine, alanine, glutamate, scyllo-inositol, t-methylhistidine and myo-inositol. More importantly, metabolic network analysis revealed that low mercury in the soil disrupted osmoregulation, amino acid and energy metabolisms in earthworms. A metabolic net link and schematic diagram of mercury-induced responses were proposed to predict earthworm responses after exposure to mercury at environmental relevant concentrations. These results improved the current understanding of the potential toxicity of low mercury in terrestrial systems.