This study aimed to investigate the effect of mono-(2-ethylhexyl) phthalate (MEHP), one of the major phthalate metabolites that are widespread in aquatic environments, on reproductive dysfunction, particularly on endocrine activity in adult male and female zebrafish. For 21 days, the zebrafish were exposed to test concentrations of MEHP (0, 2, 10, and 50 μg/mL) that were determined based on the effective concentrations (ECx) for zebrafish embryos. Exposure to 50 μg/mL MEHP in female zebrafish significantly decreased the number of ovulated eggs as well as the hepatic VTG mRNA abundance when those of the control group. Meanwhile, in female zebrafish, the biosynthetic concentrations of 17β-estradiol (E2) and the metabolic ratio of androgen to estrogen were remarkably increased in all MEHP exposed group compared with those in the control group, along with the elevated levels of cortisol. However, no significant difference was observed between these parameters in male zebrafishes. Therefore, exposure to MEHP causes reproductive dysfunction in female zebrafishes and this phenomenon can be attributed to the alteration in endocrine activities. Moreover, the reproductive dysfunction in MEHP-exposed female zebrafishes may be closely associated with stress responses, such as elevated cortisol levels. To further understand the effect of MEHP on the reproductive activities of fish, follow-up studies are required to determine the interactions between endocrine activities and stress responses. Overall, this study provides a response biomarker for assessing reproductive toxicity of endocrine disruptors that can serve as a methodological approach for an alternative to chronic toxicity testing.

The interactive effects of elevated atmospheric CO₂ and nanoparticles (NPs) on the structure and function of soil bacterial community remain unknown. Here we compared the impacts of CeO₂ (nCeO₂) and Cr₂O₃ (nCr₂O₃) nanoparticles on the taxonomic compositions and functional attributes of bacterial communities under elevated CO₂ (eCO₂). The stimulated enzyme activities (dehydrogenase, acid phosphatase and urease), increased microbial biomass carbon (MBC), and higher bacterial alpha-diversity were observed under the combined effects of eCO₂ and NPs compared to the single NP treatment, indicating eCO₂ could mitigate the adverse effect of NPs on soil microorganisms. NPs and eCO₂ are important factors influencing the alpha- and beta-diversity (17% and 18% of variations were explained) as well as functional profile (20% and 26% of variations were explained) of bacterial communities. Rising CO₂ level promoted the resilience of NP-resistant bacterial populations, primarily the members of Alphaproteobacteria, Gammaproteobacteria and Bacteroidia, which are also characterized by the fast carbon use capability. Moreover, the significantly (P < 0.05) higher metabolic quotient (qCO₂), reduced available carbon and overrepresented carbon metabolism genes at eCO₂vs. ambient CO₂ (aCO₂) indicate the acceleration of available carbon turnover in NP-exposed soils. Correlation analysis revealed that mitigation of NPs toxicity by eCO₂ could be attributed to the remarkable decline of bioavailable metals disassociated from NPs and available carbon level, as well as promotion of the rapid carbon-metabolizing microbes. Our study pointed out the positive role of eCO₂ in alleviating the adverse effect of NPs on microbiological soil environment, and results can serve as important basis in establishing guidelines for lowering the ecotoxicity of NPs.

The emergence of organophosphorus flame retardants and the efficient removal from aquatic environments have aroused increasing concerns. The Urea functionalized Fe₃O₄@LDH (Urea-Fe₃O₄@LDH) was prepared and used to adsorb triphenyl phosphate (tphp) for the first time. The tphp adsorption capacity was up to 589 mg g⁻¹, and the adsorption rate reached 49.9 mg g⁻¹ min⁻¹. Moreover, the influences of various environmental factors (pH, ionic strength and organic matter) on the tphp adsorption on the Urea-Fe₃O₄@LDH were investigated. The initial pH of the solution significantly affected the tphp adsorption, whereas the ionic strength and HA slightly affected the adsorption. The main adsorption mechanism was attributed to electrostatic interaction and π-π interaction. We believe that urea is one of excellent functional groups for the tphp adsorption removal and the materials with urea groups as the adsorbents exhibit good prospects in the future.

2,6-Dichloro-4-nitrophenol (2,6-DCNP) is an emerging chlorinated nitroaromatic pollutant, and its fate in the environment is an important question. However, microorganisms with the ability to utilize 2,6-DCNP have not been reported. In this study, Cupriavidus sp. CNP-8 having been previously reported to degrade various halogenated nitrophenols, was verified to be also capable of degrading 2,6-DCNP. Biodegradation kinetics assay showed that it degraded 2,6-DCNP with the specific growth rate of 0.124 h⁻¹, half saturation constant of 0.038 mM and inhibition constant of 0.42 mM. Real-time quantitative PCR analyses indicated that the hnp gene cluster was involved in the catabolism of 2,6-DCNP. The hnpA and hnpB gene products were purified to homogeneity by Ni-NTA chromatography. Enzymatic assays showed that HnpAB, a FAD-dependent two-component monooxygenase, converted 2,6-DCNP to 6-chlorohydroxyquinol with a Kₘ of 3.9 ± 1.4 μM and a kcₐₜ/Kₘ of 0.12 ± 0.04 μΜ⁻¹ min⁻¹. As the oxygenase component encoding gene, hnpA is necessary for CNP-8 to grow on 2,6-DCNP by gene knockout and complementation. The phylogenetic analysis showed that the hnp cluster originated from the cluster involved in the catabolism of chlorophenols rather than nitrophenols. To our knowledge, CNP-8 is the first bacterium with the ability to utilize 2,6-DCNP, and this study fills a gap in the microbial degradation mechanism of this pollutant at the molecular, biochemical and genetic levels. Moreover, strain CNP-8 could degrade three chlorinated nitrophenols rapidly from the synthetic wastewater, indicating its potential in the bioremediation of chlorinated nitrophenols polluted environments.

The combined effects and toxicological interactions of perfluoroalkyl and polyfluoroalkyl substances (PFAS) mixtures remain largely unknown even though they occur as complex mixtures in the environment. This study investigated the toxicity of individual and combined PFAS to human liver cell line (HepG2). The Combination Index (CI)-isobologram equation method was used to determine the toxicological interactions of PFAS in binary, ternary and multi-component mixtures. The results indicated that the cytotoxicity of individual PFAS to HepG2 cells increased with increasing carbon chain lengths when separated into non-sulfonated and sulfonated groups. The respective cytotoxicity of PFAS is in the order of PFDA > PFNA > PFOA > PFHpA for perfluoroalkyl carboxylic acids and in the order of PFOS > PFHxS for perfluoroalkane sulfonic acids. The toxicological interaction of PFOS and PFOA with other PFAS clearly showed a different pattern of combined toxicity in HepG2 Cells. The binary, ternary, and multi-component combinations of PFOS with PFOA, PFNA, PFDA, PFHxS, and PFHpA displayed synergistic interactions for almost all inhibitory effect levels tested, whereas, either synergistic or antagonistic effect was observed in mixtures with PFOA. Overall, the pattern of interactions of PFAS mixtures is predominated by synergism, especially at low to medium effect levels; the exceptions to this were the antagonistic interactions found in mixture with PFOA, PFHxS, and PFHpA. These cytotoxicity results may have an implication on the health risk assessment of PFAS mixtures.

Low pH and aluminum (Al)-toxicity often coexist in acidic soils. Citrus sinensis seedlings were treated with nutrient solution at a pH of 2.5, 3.0, 3.5 or 4.0 and an Al concentration of 0 or 1 mM for 18 weeks. Thereafter, malate, citrate, isocitrate, acid-metabolizing enzymes, and nonstructural carbohydrates in roots and leaves, and release of malate and citrate from roots were measured. Al concentration in roots and leaves increased under Al-toxicity, but it declined with elevating nutrient solution pH. Al-toxicity increased the levels of glucose, fructose, sucrose and total soluble sugars in leaves and roots at each given pH except for a similar sucrose level at pH 2.5–3.0, but it reduced or did not alter the levels of starch and total nonstructural carbohydrates (TNC) in leaves and roots with the exception that Al improved TNC level in roots at pH 4.0. Levels of nonstructural carbohydrates in roots and leaves rose with reducing pH with a few exceptions with or without Al-toxicity. A potential model for the possible role of root organic acid (OA) metabolism (anions) in C. sinensis Al-tolerance was proposed. With Al-toxicity, the elevated pH upregulated the OA metabolism, and increased the flow of carbon to OA metabolism, and the accumulation of malate and citrate in roots and subsequent release of them, thus reducing root and leaf Al and hence eliminating Al-toxicity. Without Al-toxicity, low pH stimulated the exudation of malate and citrate, an adaptive response of Citrus to low pH. The interactive effects of pH and pH on OA metabolism were different between roots and leaves.

In Dhaka, Bangladesh, fine particulate matter (PM₂.₅) air pollution shows strong seasonal trends, with significantly higher mean concentrations during winter than during the monsoon (winter = 178.1 μg/m³ vs. monsoon = 30.2 μg/m³). Large-scale open burning of post-harvest agricultural waste across the Indo-Gangetic Plain is a major source of PM₂.₅ air pollution in northern India during the non-monsoon period. This study evaluates the extent to which the seasonal differences in PM₂.₅ pollution concentrations in Dhaka are accounted for by biomass-burning vs. fossil-fuel combustion sources. To assess this, an index was developed based on elemental potassium (K) as a marker for biomass particulate matter, after adjusting for soil-associated K contributions. Alternatively, particulate sulfur was employed as a tracer index for fossil-fuel combustion PM₂.₅. By simultaneously regressing total PM₂.₅ on S and adjusted K, the PM₂.₅ mass for each day was apportioned into: 1) fossil-fuels combustion associated PM₂.₅; 2) biomass-burning associated PM₂.₅; and, 3) all other PM₂.₅. The results indicated that fossil-fuel combustion contributed 21.6% (19.5 μg/m³), while biomass contributed 40.2% (36.3 μg/m³) of overall average PM₂.₅ from September 2013 to December 2017. However, the mean source contributions varied by season: PM₂.₅ in Dhaka during the monsoon season was dominated by fossil-fuels sources (44.3%), whereas PM₂.₅ mass was dominated by biomass-burning (41.4%) during the remainder of the year. The contribution to PM₂.₅ and each of its source components by transport of pollution into Dhaka during non-monsoon time was also evaluated by: 1) Conditional bivariate (CBPF) and pollution rose plots; 2) Concentration weighted trajectories (CWT), and; 3) NASA satellite photos to identify aerosol loading and fire locations on high pollution days. The collective evidence indicates that, while the air pollution in Dhaka is contributed to by both local and transboundary sources, the highest pollution days were dominated by biomass-related PM₂.₅, during periods of crop-burning in the Indo-Gangetic Plain.

Tris (1,3-dichloro-2-propyl) phosphate (TDCPP) is a type halogenated organophosphate flame retardants (OPFRs), which has been identified as contaminants of emerging concern (CECs). The use and production of OPFRs began to increase gradually when brominated flame retardants (BFRs) were banned. Halogenated OPFRs, especially TDCPP have been considered to lead to mutagenicity and carcinogenesis and major concerns have been raised regarding their toxicity. In this study, the toxicity effects and mechanisms of TDCPP were summarized and ecological risk assessment was made regarding its potential impact on freshwater organisms. TDCPP has been widely detected in ecosystems throughout the world, with observed toxicity effects on both humans and freshwater organisms. Inhalation of the dust was found to be the main exposure for humans. TDCPP could be metabolized in the human body, and medium stability was achieved in human body with the main metabolite BDCPP. Aside from mutagenicity and carcinogenesis, TDCPP was also found to have the potential for endocrine disruption and impairing the human reproductive system. Furthermore, this study reviewed the results of previous toxicity experiments, including acute toxicity, growth and development toxicity, neurotoxicity, and hepatotoxicity in freshwater organisms. Risk assessment was made using the safety threshold method by comparing the toxicity data with the exposure data in freshwater. HC₅ (hazardous concentration for 5% of organisms) derived based on traditional endpoints of acute toxicity LC₅₀ (median lethal concentration) or EC₅₀ (concentration for 50% of maximal effect) was 877 μg/L. This value was much higher than the exposure concentration levels in the surface water with EXD₉₀ (exposure data with cumulative probability 90%) of 65.22 ng/L. However, based on the growth and development toxicity data, the derived HC₅ was 33.33 ng/L and the calculated MOS (margin of safety) was below 1. Therefore, the results validated the fact that the ecological risk of TDCPP could not be neglected for its growth and development toxicity.

This work discusses the identification of the transformation products (TPs) generated during the photolytic degradation of dextromethorphan (DXM) and its metabolite dextrorphan (DXO), under simulated solar radiation in aqueous solutions (Milli-Q water and river water) in order to determinate its behavior into the aquatic environment. Tentative identification of the TPs was performed by liquid chromatography/quadrupole time-of-flight mass spectrometry (LC/QTOF-MS), following a suspect screening approach. The use of high resolution-mass spectrometry (HRMS) allowed the tentative identification of DXM and DXO photoproducts based on the structure proposed by an in silico software, the accurate mass measurement, the MS/MS fragmentation pattern and the molecular formula finding. A total of 19 TPs were found to match some of the accurate masses included in a suspect list, and they were all tentatively identified by their characteristic MS-MS fragments. Most of the TPs identified showed a minor modified molecular structure like the introduction of hydroxyl groups, or demethylation. The time-evolution of precursors and TPs were monitored throughout the experiments, and degradation kinetics were presented for each analyte. Finally, the occurrence of DXM, DXO, and their tentatively proposed photodegradation TPs was evaluated in both surface and wastewater. In all real matrices, the results showed that the highest concentration was detected for DXO, followed by TP-244 (N-desmethyldextrorphan) and DXM.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.