Perfluoroalkyl acids (PFAAs) are persistent in the environment, highly bio-accumulative in the body, and likely hepatotoxic in humans. There is evidence of sex-specific physiological responses to PFAA exposure. However, epidemiological studies seldom stratify the analyses by sex. Given the high prevalence of liver disease in general population adolescents, this study was designed to determine whether or not there is association between exposure to PFAAs and biomarkers of liver function in adolescent participants of the 2013–2016 National Health and Nutrition Examination Survey, and whether or not such association is sex-specific. Multivariate linear regressions were performed to examine the association between single PFAAs [perfluorooctane sulfonic acid (PFOS); linear form of perfluorooctanoic acid (PFOA); perfluorohexane sulfonic acid (PFHxS); perfluorononanoic acid (PFNA)], and biomarkers of liver function — gamma glutamyltransferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin. Multivariate logistic regressions were performed to estimate adjusted odd ratios (aOR) of elevated ALT, AST and GGT. The study results show that, in females, there was a positive association of the highest PFOA quartile with increased ALT, AST and GGT, and the highest PFNA quartile with increased ALT and AST. Conversely, in male adolescents there was an association of the highest linear PFOA quartile with decreased ALT, and the highest PFNA quartile with ALT and AST. Females had higher odds of clinically-defined elevated ALT with increased PFOA (aOR = 1.79; 95% CI: 1.05, 3.04) or PFNA (aOR = 2.28; 95% CI: 1.08, 2.28), whereas males had decreased odds of clinically-defined elevated ALT with increased n-PFOA (aOR = 0.43; 95% CI: 0.20, 0.93) or PFNA (aOR = 0.5; 95% CI: 0.28, 0.89). In conclusion, there were sex differences in the association between serum PFAA levels and biomarkers of liver function. These results may provide support for analyzing sex-based adverse effects of PFAAs.

Copper (Cu) induced phytotoxicity has become a serious environmental problem as a consequence of significant metal release through anthropogenic activity. Understanding the spatial distribution of Cu in plants such as willow is essential to elucidate the mechanisms of metal accumulation and transport in woody plants, particularly as affected by variable environment conditions such as soil flooding. Using synchrotron-based X-ray fluorescence (μ-XRF) techniques, the spatial distribution of Cu and other nutrient elements were investigated in roots and stems of Salix (S.) integra exposed to 450 mg kg⁻¹ Cu under non-flooded (NF)/flooding (F) conditions for 90 d. S. integra grown in the F condition exhibited significant higher tolerance index (TI, determined by the ratio of total biomass in Cu treatments to control) (p < 0.05) than that in the NF condition, indicating soil flooding alleviated Cu toxicity to willow plants. The μ-XRF revealed that Cu was preferentially located in the root cap and meristematic zone of the root tips. Under the NF condition, the Cu intensity in the root epidermis was more highly concentrated than that of the F condition, suggesting the soil flooding significantly inhibited Cu uptake by S. integra. The pattern of the Cu spatial distribution in the S. integra stem indicated that the F condition severely reduced Cu transport via the xylem vessels as a consequence of decreasing the transpiration rate of leaves. To our knowledge, this is the first study to report the in vivo Cu distribution in S. integra in a scenario of co-exposure to the Cu and the soil flooding over a long period. The finding that Cu uptake varies significantly with flooding condition is relevant to the development of strategies for plants to detoxify the metals and to maintain the nutrient homeostasis.

Di-(2-ethylhexyl) phthalate (DEHP) is a prevalent environmental contaminant that severely impacts the health of human and animals. Taxifolin (TAX), a plant flavonoid isolated from yew, exerts protective effects on cardiac diseases. Nevertheless, whether DEHP could induce cardiomyocyte hypertrophy and its mechanism remains unclear. This study aimed to highlight the specific molecular mechanisms of DEHP-induced cardiomyocyte hypertrophy and the protective potential of TAX against it. Chicken primary cardiomyocytes were treated with DEHP (500 μM) and/or TAX (0.5 μM) for 24 h. The levels of glucose and adenosine triphosphate (ATP) were detected, and cardiac hypertrophy-related genes were validated by real-time quantitative PCR (qRT-PCR) and Western blot (WB) in vitro. The results showed that DEHP-induced cardiac hypertrophy was ameliorated by TAX, as indicated by the increased cardiomyocyte area and expression of atrial natriuretic peptide (ANP), natriuretic peptides A-like (BNP) and β-myosin heavy cardiac muscle (β-MHC). Furthermore, DEHP induced cardiac hypertrophy via the interleukin 6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway in vitro. In addition, DEHP disrupted mitochondrial function and glycometabolism by activating the insulin-like growth factor 1 (IGF1)/phosphatidylinositol 3-kinase (PI3K) pathway and the peroxisome proliferator activated receptors (PPARs)/PPARG coactivator 1 alpha (PGC-1α) pathway to induce cardiac hypertrophy in vitro. Intriguingly, those DEHP-induced changes were obviously alleviated by TAX treatment. Taken together, cardiac hypertrophy was induced by DEHP via activating the IL-6/JAK/STAT3 signaling pathway, triggering glycometabolism disorder and mitochondrial dysfunction in vitro, can be ameliorated by TAX. Our findings may provide a feasible molecular mechanism for the treatment of cardiomyocyte hypertrophy induced by DEHP.

Nitrogen (N) deposition has rapidly increased and is influencing forest ecosystem processes and functions on a global scale. Understanding process-specific N transformations, i.e., gross N transformations, in forest soils in response to N deposition is of great significance to gain mechanistic insights on the linkages between global N deposition and N availability or loss in forest soils. In this paper, we review factors controlling N mineralization, nitrification and N immobilization, particularly in relation to N deposition, discuss the limitations of net N transformation studies, and synthesize the literature on the effect of N deposition on gross N transformations in forest ecosystems. We found that more than 97% of published papers evaluating the effect of N deposition (including N addition experiments that simulate N deposition) on soil N cycle determined net rates of mineralization and nitrification, showing that N deposition significantly increased those rates by 24.9 and 153.9%, respectively. However, studies on net N transformation do not provide a mechanistic understanding of the effect of N deposition on N cycling. To date, a small number of studies (<20 published papers) have directly quantified the effect of N deposition on gross N transformation rates, limiting our understanding of the response of soil N cycling to N deposition. The responses to N deposition of specific N transformation processes such as autotrophic nitrification, heterotrophic nitrification, dissimilatory nitrate reduction to ammonium, N mineralization, and N immobilization are poorly studied. Future research needs to use more holistic approaches to study the impact of N deposition on gross N transformation rates, N loss and retention, and their microbial-driven mechanisms to provide a better understanding of the processes involved in N transformations, and to understand the differential responses between forest and other ecosystems.

The increased bioeconomy targets for the biomass share of renewable energy production across Europe should be met using land unsuitable for food production. Miscanthus breeding programs targeted the production of plants with a diverse range of traits allowing a wider utilization of land resources for biofuel production without competing with arable crops. These traits include increasing tolerances to drought, chilling, and to metal(loid)s excess. Two novel Miscanthus hybrids, GNT41 and GNT34, were compared against Miscanthus x giganteus (Mxg) on metal-contaminated arable land in Poland. This study aimed at evaluating their yield, biomass quality and quantifying seasonal differences in photosynthetic and transpiration parameters. A secondary objective was to identify key physiological mechanisms underlying differences in metal accumulation between the investigated plants. The new hybrids produced a similar yield to Mxg (13–15 t ha−1 yr−1), had shorter shoots, higher Leaf Area Index and stem number. Based on gas exchange measurements, GNT34 exhibited isohydric (water-conserving) behavior. The stomatal response to light of the new hybrids was at least twice as fast as that of Mxg, a trait that is often associated with increased seasonal water use efficiency. This contributed to the almost 40% reduction in shoot Pb and Cd concentrations for the new hybrids as compared to Mxg. This suggested that promoting stomatal regulation in conjunction with improved water conservation may be a target for improving plants for wider use on metals contaminated land.

In this work PM₂.₅ was collected during winter and summer in a Sardinian village (Gonnostramatza, Italy) highly affected by biomass burning emissions. A multi-technique approach was adopted for the complete PM chemical characterization. The bulk characterization was performed by IC (Ion Chromatography), HPAEC (High-Performance Anion-Exchange Chromatography), TOT (Thermal Optical Transmittance) and ED-XRF (Energy-Dispersive X-Ray Fluorescence) while XPS (X-ray Photoelectron Spectroscopy) was used for the surface characterization. Using levoglucosan as specific tracer of biomass burning emissions, the assessment of the impact of this source was carried out and it represent the major PM source at the investigate site during winter. In winter the average levoglucosan concentration is 2096 ± 324 ng/m³ while during summer its concentration is negligible (18 ± 7 ng/m³). Levoglucosan content in PM₂.₅ during winter is on average 13.7%; it is estimated that 65% of PM₂.₅ is due to wood burning. XPS has been exploited in this work aiming at highlighting possible differences between surface and bulk composition of PM₂.₅. The surface of the particulate matter resulted enriched in carbon compared to the bulk. Among the components of XPS C1s signals recorded on the samples collected during winter, it was found that the signal at 286.5 eV, which is due to the presence of COH, reflects the bulk composition of levoglucosan.

Despite high production and usage of parabens and bisphenols, little is known about their spatiotemporal distribution in the marine environment. In this study, we determined the concentrations of several parabens and their metabolites as well as bisphenol analogues in sediment collected from coastal areas of northern China. All sediment samples, including surface sediment and sediment cores, contained at least one of the parabens analyzed, and the total concentrations of parabens (ΣPBs; sum of six parabens) ranged from 1.37 to 24.2 ng/g dw (geometric mean: 3.30–6.09 g/g dw), which was comparable to or slightly higher than those found for the total concentrations of five detectable bisphenols (ΣBPAs; geometric mean: 2.18–4.61 ng/g dw). 4-hydroxybenzoic acid, a common metabolite of parabens, was found in all samples at concentrations in the range of 6.85–437 ng/g dw, which was one order of magnitude lower than those found for benzoic acid. Methyl-, ethyl-, and propyl-parabens were the predominant paraben analogues, collectively accounting for >88% of ΣPBs. Bisphenol A and bisphenol F were the two major bisphenols, collectively accounting for >86% of ΣBPAs. We also examined vertical profiles in concentrations of target analytes in sediment cores. The sediment core from the Shandong Peninsula showed a gradual increase in the concentrations of several parent and metabolic parabens as well as bisphenols during the past decade. Relatively higher concentrations of parabens and bisphenols were found in sediment cores collected from industrialized areas. Significant positive correlations were found among the concentrations of parabens in sediment, which suggested the existence of similar sources for these compounds. Overall, our findings suggest that the Bohai Sea coast is moderately contaminated with parabens and bisphenols in comparison to other coastal areas in China or elsewhere.

The gut microbiota is important for maintaining homeostasis of the host. Gut microbes represent the initial site for toxicant processing following dietary exposures to environmental contaminants. The diet is the primary route of exposure to polychlorinated biphenyls (PCBs), which are absorbed via the gut, and subsequently interfere with neurodevelopment and behavior. Developmental exposures to PCBs have been linked to increased risk of neurodevelopmental disorders (NDD), including autism spectrum disorder (ASD), which are also associated with a high prevalence of gastrointestinal (GI) distress and intestinal dysbiosis. We hypothesized that developmental PCB exposure impacts colonization of the gut microbiota, resulting in GI pathophysiology, in a genetically susceptible host. Mouse dams expressing two heritable human mutations (double mutants [DM]) that result in abnormal Ca²⁺ dynamics and produce behavioral deficits (gain of function mutation in the ryanodine receptor 1 [T4826I-RYR1] and a human CGG repeat expansion [170–200 CGG repeats] in the fragile X mental retardation gene 1 [FMR1 premutation]). DM and congenic wild type (WT) controls were exposed to PCBs (0–6 mg/kg/d) in the diet starting 2 weeks before gestation and continuing through postnatal day 21 (P21). Intestinal physiology (Ussing chambers), inflammation (qPCR) and gut microbiome (16S sequencing) studies were performed in offspring mice (P28–P30). Developmental exposure to PCBs in the maternal diet caused significant mucosal barrier defects in ileum and colon (increased secretory state and tight junction permeability) of juvenile DM mice. Furthermore, PCB exposure increased the intestinal inflammatory profile (Il6, Il1β, and Il22), and resulted in dysbiosis of the gut microbiota, including altered β-diversity, in juvenile DM mice developmentally exposed to 1 mg/kg/d PCBs when compared to WT controls. Collectively, these findings demonstrate a novel interaction between PCB exposure and the gut microbiota in a genetically susceptible host that provide novel insight into environmental risk factors for neurodevelopmental disorders.

The application of biochar in remediation and recovery of heavy metals and/or organic contaminants in water and soil is increasing. However, the adverse effect of biochar to aquatic organisms has not received enough attention. In this study, we conducted a study on the biotoxicity of biochar pyrolyzed from pine needle under oxygen-limited conditions. The toxicity of biochar was expressed with the following endpoints: cell growth, chlorophyll-a (Chl-a), reactive oxygen species (ROS), superoxide dismutase (SOD) content of Scenedesmus obliquus (S. obliquus) and the luminescence of Photobacterium phosphoreum (P. phosphoreum). Here, the effect of free radicals (FRs) contained in biochar was stressed. Our results show that the toxicity of biochar is significantly correlated with the concentration of FRs in biochar particles. Meanwhile, we found the FRs-containing biochar could induce the production of acellular ROS (such as ·OH) in water, which would also induce the production of interior cellular ROS in aquatic organisms. Our findings provide a new insight into the mechanism of toxicity aroused by biochar applications and aid in understanding its potential ecological risk.

The growing production and extensive use of organophosphate flame retardants (OPFRs) have led to an increase in their environmental distribution and human exposure. Developmental toxicity is a major concern of OPFRs' adverse health effects. However, the impact of OPFRs exposure on vascular development and the toxicity pathway for developmental defects are poorly understood. In this study, we investigated the effects of exposure to tris(1,3-dichloro-2-propyl) phosphate (TDCPP), a frequently detected OPFR, on early vascular development, and the possible role of nuclear factor erythroid 2-related factor (Nrf2)-dependent angiogenic pathway in TDCPP's vascular toxicity. TDCPP exposure at 300 and 500 μg/L impeded the growth of intersegmental vessels (ISV), a type of microvessels, as early as 30 hpf. Consistently, a similar pattern of decreased extension and remodeling of common cardinal vein (CCV), a typical macrovessel, was observed in zebrafish at 48 hpf and 72 hpf. Developing vasculature in zebrafish was more sensitive than general developmental parameters to TDCPP exposure. The expression of genes related to VEGF signaling pathway dose-dependently decreased in TDCPP-treated larvae. In in vitro experiments using human umbilical vein endothelial cells (HUVECs), the increased cell proliferation induced by VEGF was suppressed by TDCPP exposure in a dose-dependent fashion. In addition, we found a repression of Nrf2 expression and activity in TDCPP-treated larvae and HUVECs. Strikingly, the application of CDDO-Im, a potent Nrf2 activator, enhanced VEGF and protected against defective vascular development in zebrafish. Our results reveal that vascular impairment is a sensitive index for early exposure to TDCPP, which could be considered in the environmental risk assessment of OPFRs. The identification of Nrf2-mediating VEGF pathway provides new insight into the adverse outcome pathway (AOP) of OPFRs.