As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV₁) and FVC (FEV₁/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.

Sulfate radical (SO₄⁻)-based advanced oxidation processes (SR-AOPs) are promising in-situ chemical oxidation technologies widely applied for soil/groundwater remediation. The presence of non-target water constituents may interfere the abatement of contaminants by SR-AOPs as well as result in the formation of unintended byproducts. Herein, we reported the formation of toxic chloronitrophenols during thermally activated persulfate oxidation of 2-chlorophenol (2CP) in the presence of nitrite (NO₂⁻). 2-Chloro-4-nitrophenol (2C4NP) and 2-chloro-6-nitrophenol (2C6NP) were identified as nitrated byproducts of 2CP with total yield up to 90%. The formation of nitrated byproducts is a result of coupling reaction between 2CP phenoxyl radical (ClPhO) and nitrogen dioxide radical (NO₂). As a critical step, the formation of ClPhO was supported by density functional theory (DFT) computation. Both 2C4NP and 2C6NP could convert to 2-chloro-4,6-dinitrophenol (2C46DNP) upon further treatment via a denitration-renitration process. The formation rate of 2C4NP and 2C6NP was closely dependent on the concentration of NO₂⁻, solution pH, and natural water constituents. ECOSAR calculation suggests that chloronitrophenols are generally more hydrophobic and ecotoxic than 2CP. Our result therefore reveals the potential risks in the abatement of chlorophenols by SR-AOP, particularly when high level of NO₂⁻ is present in water matrix.

Although the coexistence of heavy metals and environmental hormones always occur in aquatic environment, the information of the combined impacts remains unclear. To explore the multi-generational toxicity of cadmium (Cd) and tributyltin (TBT), adult zebrafish (Danio rerio) (F0) were exposed to different treated groups (100 ng/l Cd, 100 ng/l TBT and their mixture) for 90 d, with their offspring (F1 and F2) subsequently reared in the same exposure solutions corresponding to their parents. Both developmental neurotoxicity and thyroid disturbances were examined in the three (F0, F1, and F2) generations. Our results showed that co-exposure to Cd and TBT induced the developmental neurotoxicity in F1 and F2 generations, reflected by the significant lower levels of neurotransmitters (dopamine and serotonin) and the inhibited acetylcholinesterase (AChE) activities. And the thyroid endocrine disruption were observed in the two-generations larval offspring by parental exposure to Cd and/or TBT, including the significantly decreasing levels of thyroid hormones and the down-regulated the expression of genes involved in the hypothalamus-pituitary-thyroid axis, compared to the control. Additional, the embryonic toxicity and growth inhibition were also determined in the fish larvae. Overall, this study examined the impacts of parental co-exposure to Cd and TBT, with regard to developmental inhibition, nervous system damage and endocrine disruption, which highlighted that co-exposure influences are complicated and need to be considered for accurate environmental risk assessment.

Tris (2-ethylhexyl) phosphate (TEHP) is one of the most commonly used organophosphorus flame retardant (OPFR) analogues and is commonly detected in surface water and sediments. Limited information is available about the metabolic pathway or metabolite formation related to TEHP in fish. In this study, rare minnows (Gobiocyprisrarus) were exposed to TEHP in static water for 30 d to investigate the bioaccumulation and metabolite distribution in the fish muscle, liver, kidney, gill, GI-tract, ovary and testis. Based on the estimated kᵤₚ,ₚₐᵣₑₙₜ and kd,ₚₐᵣₑₙₜ values, the bioconcentration factors (BCFₚₐᵣₑₙₜ) of TEHP in fish tissues were calculated in the order of kidney > ovary ≈ liver ≈ testis > gill ≈ GI-tract > muscle; this finding was consistent with the results of our previous study on other alkyl-substituted OPFRs. In addition, this study identified the metabolic profiles of TEHP in the liver. TEHP was oxidatively metabolized by the fish to a dealkylated metabolite (di 2-ethylhexyl phosphate; DEHP) and hydroxylated TEHP (OH-TEHP). OH-TEHP further underwent extensive phase II metabolism to yield glucuronic acid conjugates. DEHP was mainly distributed in rare minnow in the following order: liver > GI-tract > kidney ≫ other tissues. However, the metabolite showed lower accumulation potential in fish tissues than TEHP, with metabolite parent concentration factors (MPCFs) for DEHP of less than 0.1 in all the investigated tissues. The BCFₚₐᵣₑₙₜ values of TEHP in various fish tissues were only 9.0 × 10⁻³-7.2 × 10⁻⁴ times its estimated tissue-water partition coefficient (Kₜᵢₛₛᵤₑ₋wₐₜₑᵣ) values based on tissue lipid, protein and water contents, which indicated the significance of biotransformation in reducing the bioaccumulation potential of TEHP in fish. The toxicokinetic data in the present study help in understanding the tissue-specific bioaccumulation and metabolism pathways of TEHP in fish and highlight the importance of toxicology research on TEHP metabolites in aquatic organisms.

Evidence is emerging that environmental exposure to bisphenol S (BPS), a substitute for bisphenol A (BPA), to humans and wildlife is on the rise. However, research on the neurobehavioral effects of this endocrine disruptive chemical is still in its infancy. In this study, we aimed to investigate the effects of long-term exposure to environmentally relevant concentrations of BPS on recognition memory and its mechanism(s) of action, especially focusing on the glutamatergic/ERK/CREB pathway in the brain. Adult female zebrafish were exposed to the vehicle, 17β-estradiol (E2, 1 μg/L), or BPS (1, 10 and 30 μg/L) for 120 days. Fish were then tested in the object recognition (OR), object placement (OP), and social recognition tasks (SR). Chronic exposure to E2 and 1 μg/L of BPS improved fish performance in OP task. This was associated with an up-regulation in the mRNA expression of several subtypes of metabotropic and ionotropic glutamate receptors, an increase in the phosphorylation levels of ERK1/2 and CREB, and an elevated transcript abundance of several immediate early genes involved in synaptic plasticity and memory formation. In contrast, the exposure to 10 and 30 μg/L of BPS attenuated fish performance in all recognition memory tasks. The impairment of these memory functions was associated with a marked down-regulation in the expression and activity of genes and proteins involved in glutamatergic/ERK/CREB signaling cascade. Collectively, our study demonstrated that the long-term exposure to BPS elicits hermetic effects on the recognition memory in zebrafish. Furthermore, the effect of BPS on the recognition memory seems to be mediated by the glutamatergic/ERK/CREB signaling pathway.

Achieving large pore size, high catalytic performance with stable structure is critical for metal–organic frameworks (MOFs) to have more hopeful prospects in catalytic applications. Herein, we had reported a method to synthesize highly reactive yet stable defective iron-based Metal organic frameworks by using different monocarboxylic acids with varying lengths as a modulator. The physical−chemical characterization illustrating that modulators could improve the crystallinity, enlarge pore size and enhance catalytic performance and octanoic acid (OA) was screened to be the suitable choice. The catalytic performance of catalysts was detected through persulfate (PS) activation for degrading Tetrabromobisphenol A (TBBPA). The study demonstrated that the highest degradation efficiency for 0.018 mmol L−1 TBBPA was that 97.79% in the conditions of the 1.0 g L−1 Fe(BDC)(DMF,F)-OA-30 dosage and TBBPA:PS = 200:1. In addition, there was observed that no obvious change of the crystal structure, little the leachable iron concentration in the solutions and no significant loss of catalytic activities of Fe(BDC)(DMF,F)-OA-30 after 5th cycles. The iron valence state of Fe(BDC)(DMF,F)-OA-30 before and after degradation and electrochemical properties reveal that the partial substitution of organic ligands by octanoic acid, when removing OA and forming defects by heat and vacuum treatment to generate coordinatively unsaturated metal sites and accelerate the original transmission of electronic, leading to enhance the activity of persulfate activation for efficient removal TBBPA.

Microplastics (MPs) pollution in the marine environment has attracted considerable global attention. However, the colonization of microorganisms on mariculture-derived MPs and their effects on mariculture remain poorly understood. In this study, the MPs (fishing nets, foams and floats) and a natural substrate, within size ranges (1–4 mm), were then incubated for 21 days in Sungo Bay (China), and the composition and diversity of bacterial communities attached on all substrates were investigated. Results showed that bacterial communities on MPs mainly originated from their surrounding seawater and sediment, with an average contribution on total MPs adherent population of 47.91% and 37.33%, respectively. Principle coordinate analysis showed that community similarity between MPs and surrounding seawater decreased with exposure time. In addition, lower average bacterial community diversity and higher relative abundances of bacteria from the genera Vibrio, Pseudoalteromonas and Alteromonas on MPs than those in their surrounding seawater and sediments indicated that MPs might enrich potential pathogens and bacteria related with carbohydrate metabolism. They are responsible for the significant differences in KEGG Orthology pathways (infectious disease and carbohydrate metabolism) between MPs and seawater. The KO pathway (Infectious Diseases) associated with MPs was also significantly higher than those with feathers in the nearshore area. MPs might be vectors for enrichment of potentially pathogenic Vibrio, and enhance the ecological risk of MPs to mariculture industry.

This three-decade long study was conducted in the Pearl River Delta (PRD), a rapidly urbanizing region in southern China. Extensive soil samples for a diverse land uses were collected in 1989 (113), 2005 (1384), 2009 (521), and 2018 (421) for heavy metals of As, Cr, Cd, Cu, Hg, Ni, Pb and Zn. Multiple pollution indices and Structural Equation Models (SEMs) were used in attribution analysis and comprehensive assessments. Data showed that majority of the sampling sites was contaminated by one or more heavy metals, but pollutant concentrations had not reached levels of concerns for food security or human health. There was an increasing trend in heavy metal contamination over time and the variations of soil contamination were site-, time- and pollutant-dependent. Areas with high concentrations of heavy metals overlapped with highly industrialized and populated areas in western part of the study region. A dozen SEMs path analyses were used to compare the relative influences of key environmental factors on soil contamination across space and time. The high or elevated soil contaminations by As, Cr, Ni, Cu and Zn were primarily affected by soil properties during the study period, except 1989–2005, followed by land use patterns. Parent materials had a significant effect on elevated soil contamination of Cd, Cr, Ni, Pb and overall soil pollution during 1989–2005. We hypothesized that other factors not considered in the present study, such as atmospheric deposition, sewage irrigation, and agrochemical uses, may be also important to explain the variability of soil contamination. This study implied that strategies to improve soil physiochemical properties and optimize landscape structures are viable methods to mitigate soil contamination. Future studies should monitor pollutant sources identified by this study to fully understand the causes of heavy metal contamination in rapidly industrialized regions in southern China.

Cadmium (Cd) exposure poses a serious environmental problem due to the metal’s bioaccumulation and difficult to eliminate from body. Understanding the mechanisms of Cd detoxification and resistance can provide insights into methods to protect against the damaging effects of the heavy metal. In the present study, we found that heat shock (HS) pretreatment increased Cd resistance of the nematode Caenorhabditis elegans by reducing the bagging phenotype and protecting the integrity of the intestinal barrier. HS pretreatment increased the expression of heat shock protein-16.2 (HSP-16.2) prior to Cd exposure, and HS-induced Cd resistance was absent in worms with hsp-16.2 loss-of-function mutation. Worm strain with daf-2(e1370) mutation presented enhanced HS-induced Cd resistance, which was eliminated in worm strains of daf-16(mu86) and hsf-1(sy441). HS pretreatment increased DAF-16 nuclear localization and HSF-1 granule formation prior to Cd exposure. DAF-16 and HSF-1 was essential in reducing bagging formation and protecting the integrity of intestinal barrier after HS pretreatment. In conclusion, the present study demonstrated that HS-induced Cd resistance in C. elegans is regulated by the DAF-16/FOXO and HSF-1 pathways through regulation of HSP-16.2 expression.

17β-estradiol (E2) often coexists with tetracyclines (TCs) in wastewater lagoons at intensive breeding farms, threatening the quality of surrounding water bodies. Microbial degradation is vital in E2 removal, but it is unclear how TCs affect E2 biodegradation. This primary study investigated the mechanisms of E2 degradation by Novosphingobium sp. ES2-1 in the presence of TCs and assessed the removal efficiency of E2 by strain ES2-1 in natural waters containing TCs. E2 biodegradation was unaffected at TCs concentrations below 0.1 mg L⁻¹ yet significantly inhibited at TCs above 10 mg L⁻¹. As elevation of TCs, E2 biodegradation rate constant decreased, and the biodegradation kinetics equation gradually deviated from the pseudo-first-order dynamics model. Importantly, the presence of TCs, especially at high-level concentrations, significantly hindered E2 ring-opening process but promoted the condensation of some phenolic ring-opening products with NH₃, thereby increasing the abundance of pyridine derivatives, which were difficult to decompose over time. Additionally, strain ES2-1 could remove 52.1–100% of nature estrogens in TCs-contaminated natural waters within 7 d. Results revealed the mechanisms of TCs in E2 biodegradation and the performance of a functional strain in estrogen removal in realistic TCs-contaminated aqueous solution.