The Treatment of Aquaculture Wastewater with Biological Aerated Filters: From the Treatment Process to the Microbial Mechanism.

Algal cell proliferation has posed significant problems for traditional water treatment facilities; these problems are attributed to surface hydrophilicity and electrostatic repulsion. Biological aerated filters (BAFs) have been extensively used in wastewater treatment to remove pollutants such as algal cells by utilizing the adsorption and separation capabilities of the filter media. In this study, a BAF was supplemented with biological filter medium (Marchantia polymorpha) to assess its effectiveness of pretreating aquaculture wastewater. In terms of process performance, steady and consistent treatment was achieved by the BAF with M. polymorpha (BAF2) under an algal cell density as high as 1.65 × 108 cell/L, with average removal rates for NH4+-N and algae cells of 74.4% and 81.9%, respectively. The photosynthetic activity parameters (rETRmax, α, Fv/Fm, and Ik) of the influent and effluent were quantitatively assessed, and M. polymorpha was found to remove algae by disrupting the photosynthetic system of the algal cells. Furthermore, the addition of the M. polymorpha filter medium enhanced the community structure of the functional microbes in the BAF system. The highest microbial community richness and diversity were observed in the BAF2. Meanwhile, M. polymorpha promoted an increase in the abundance of denitrifying bacteria, including Bdellovibrio and Pseudomonas. Overall, this work offers a unique perspective on the aquaculture wastewater pretreatment process and BAF design.

Surfactant recovery and efficient separation of PAHs from surfactant solutions by low-cost waste activated sludge and two-stage design optimization.

The treatment and surfactant recovery of soil washing/flushing effluent containing high levels of surfactants and organic pollutants are critical for the surfactant-assisted remediation of soils and waste management due to their complexity and high-potential risks. Combination of waste activated sludge material (WASM) and a kinetic-based two-stage system design was introduced in this study as a novel strategy for the separation of phenanthrene and pyrene from Tween 80 solutions. The results showed that WASM can effectively sorb phenanthrene and pyrene with high affinities (Kd) of 2325.5 L·kg-1 and 9911.2 L·kg-1, respectively. This allowed a high-level recovery of Tween 80 of 90.47 ± 1.86%, with selectivity of up to 69.7. In addition, a two-stage design was constructed, and the results showed an improved reaction time (approximately 5% of equilibrium time in conventional single-stage process) and increased the separation levels of phenanthrene or pyrene from Tween 80 solutions. For instance, the minimal total operating time for the sorption of 99% pyrene from 1.0 g·L-1 Tween 80 was only 23.0 min in the two-stage process compared to that of 480 min with a 71.9% removal level in the single-stage system. Results indicated that the combination of low-cost waste WASH and two-stage design was a high-efficiency and time-saving way to recover surfactants from soil washing effluents.

Selected dechlorination of triclosan by high-performance g-C3N4/Bi2MoO6 composites: Mechanisms and pathways.

Environmental-friendly and efficient strategies for triclosan (TCS) removal have received more attention. Influenced by COVID-19, a large amount of TCS contaminants were accumulated in medical and domestic wastewater discharges. In this study, a unique g-C3N4/Bi2MoO6 heterostructure was fabricated and optimized by a novel and simple method for superb photocatalytic dechlorination of TCS into 2-phenoxyphenol (2-PP) under visible light irradiation. The as-prepared samples were characterized and analyzed by XRD, BET, SEM, XPS, etc. The rationally designed g-C3N4/Bi2MoO6 (4:6) catalyst exhibited notably photocatalytic activity in that more than 95.5% of TCS was transformed at 180 min, which was 3.6 times higher than that of pure g-C3N4 powder. This catalyst promotes efficient photocatalytic electron-hole separation for efficient dechlorination by photocatalytic reduction. The samples exhibited high recyclable ability and the dechlorination pathway was clear. The results of Density Functional Theory calculations displayed the TCS dechlorination selectivity has different mechanisms and hydrogen substitution may be more favorable than hydrogen abstraction in the TCS dechlorination hydrogen transfer process. This work will provide an experimental and theoretical basis for designing high-performance photocatalysts to construct the systems of efficient and safe visible photocatalytic reduction of aromatic chlorinated pollutants, such as TCS in dechlorinated waters.

Perfluorooctanoic acid and perfluorooctanesulfonic acid induce immunotoxicity through the NF-κB pathway in black-spotted frog (Rana nigromaculata).

Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are widely detected in the environment and wild animals, thus posing a threat to wildlife and public health; however, knowledge about their immunotoxicity and the underlying mechanism remains limited. In the present study, male black-spotted frogs (Rana nigromaculata) were exposed to environmentally relevant concentrations (0, 1, and 10 µg/L) of PFOA or PFOS for 21 days; subsequently, biochemical analysis, molecular docking, and gene expression determination were conducted. The results indicated that exposure to 10 µg/L PFOA decreased the serum levels of immunoglobulin A. PFOS exposure significantly increased the hepatic levels of interleukin-1ß, interleukin-6, tumor necrosis factor-α, interferon-γ, and nitric oxide; but PFOA significantly increased the levels of only tumor necrosis factor-α. Furthermore, PFOA and PFOS exposure significantly decreased the activity of inducible nitric oxide synthase and total nitric oxide synthase. IBRv2 analysis indicated that PFOA and PFOS had a similar effect on these immune indicators, but PFOS was more toxic than PFOA. Molecular docking revealed that PFOA and PFOS can bind to nuclear factor-κB (NF-κB) by forming stable hydrogen bonds. PFOA and PFOS exposure upregulated the gene expression of NF-κB and its downstream genes. Significant correlations between the expression of genes involved in the NF-κB pathway and immune-related indicators suggests that PFOA- and PFOS-induced immunotoxicity was associated with the activation of NF-κB. Our findings provide novel insights into the potential role of NF-κB in immunotoxicity induced by PFOA and PFOS in frogs.

Selective production of singlet oxygen for harmful cyanobacteria inactivation and cyanotoxins degradation: Efficiency and mechanisms.

Knowledge about the impact of singlet oxygen (1O2) on the characteristics and inactivation of harmful cyanobacterial organic matter is limited. In this study, the feasibility of using an improved single-iron doped graphite-like phase carbon nitride catalyst (FeCN) to activate peroxymonosulfate (PMS) catalytic production of 1O2 to inactivate four harmful cyanobacteria was investigated. The inactivation efficiencies at 30 min were 92.77%, 66.84%, 91.06%, and 93.45% for Microcystis aeruginosa (M. aeruginosa), Nodularia harveyana, Oscillatoria sp., and Nostoc sp., respectively. This was associated with adjusting experimental parameters, such as the FeCN and PMS doses and initial pH, to obtain the maximum 1O2 yield. The quenching experiment results and electron paramagnetic resonance spectra showed that 1O2 generated via the non-radical pathway might play a dominant role in inactivating harmful cyanobacteria and degrading harmful algal toxins (Microcystin-LR and Nodularin). In addition, the FeCN-PMS system not only effectively destroyed the integrity of harmful cyanobacterial cells but also effectively degraded cyanobacterial toxins, thereby preventing severe secondary contamination by cell rupture. A possible removal mechanism was proposed. This reveals the potential of 1O2 to simultaneously inactivate harmful cyanobacteria and degrade harmful cyanobacterial toxins.

Efficient Microcystis aeruginosa coagulation and removal by palladium clusters doped g-C3N4 with no light irradiation.

Efficient treatment of cyanobacterial blooms in eutrophication waters by safe and reliable nanomaterials is a big challenge for reducing environmental health risks. Herein, a novel strategy combining palladium clusters (Pdn) with g-C3N4 nanocomposite was presented to achieve high-efficient removal of Microcystis aeruginosa cells through coagulation and breakage. Interestingly, 95.17% of algal cells (initial concentration of 5.6 × 106 cells mL-1) were promptly removed in the Pd/g-C3N4 (5%) system within only 10 min and without visible light irradiation and persulfate activation. Both the release of potassium ion and microcystin during the removal process and the transmission electron microscope observations of Microcystis aeruginosa cells proved that the integrity of the algal cell membrane was destroyed. The removal of Microcystin-LR (MC-LR) were further confirmed in the next process. Pd metal interaction and breakage against algal cells may cause disruption of algal cells. This study describes a novel technology for the superfast removal of harmful algae and may provide a new insight into the control of cyanobacterial blooms in practical applications.

Assessing the hepatotoxicity of PFOA, PFOS, and 6:2 Cl-PFESA in black-spotted frogs (Rana nigromaculata) and elucidating potential association with gut microbiota.

Pollution caused by per- and polyfluoroalkyl substances (PFASs) has become a major global concern. The association between PFAS-induced hepatotoxicity and gut microbiota in amphibians, particularly at environmentally relevant concentrations, remains elusive. Herein we exposed male black-spotted frogs (Rana nigromaculata) to 1 and 10 µg/L waterborne perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), and 6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA) for 21 days; subsequently, liver histopathological, oxidative stress, molecular docking, gene/protein expression, and gut microbiome analyses were conducted. PFOS and 6:2 Cl-PFESA exposure enhanced serum alanine aminotransferase and aspartate aminotransferase activities, and markedly increased hepatic area of vacuoles and inflammatory cell infiltration, while PFOA exposure increased serum alanine aminotransferase but not aspartate aminotransferase activities and affected hepatic area of vacuoles and inflammatory cell infiltration to a lesser extent. All three PFASs elevated catalase, glutathione S-transferase, and glutathione peroxidase activities and glutathione and malondialdehyde contents in the liver, suggesting the induction of oxidative stress. Further, PFASs could bind to mitogen-activated protein kinases (p38, ERK, and JNK), upregulating not only their expression but also the expression of downstream oxidative stress-related genes and that of P-p38, P-ERK, and Nrf2 proteins. In addition, PFAS exposure significantly increased the relative abundance of Proteobacteria and Delftia and decreased that of Firmicutes and Dietzia, Mycoplasma, and Methylobacterium-Methylorubrum in the order of PFOS ≈ 6:2 Cl-PFESA > PFOA. Altogether, it appears that PFOS and 6:2 Cl-PFESA are more toxic than PFOA. Finally, microbiota function prediction, microbiota co-occurrence network, and correlation analysis between gut microbiota and liver indices suggested that PFAS-induced hepatotoxicity was associated with gut microbiota dysbiosis. Our data provide new insights into the role of gut microbiota in PFAS-induced hepatotoxicity in frogs.

Per- and Polyfluoroalkyl Substances (PFASs) Impair Lipid Metabolism in Rana nigromaculata: A Field Investigation and Laboratory Study.

Per- and polyfluoroalkyl substances (PFASs) are ubiquitous environmental pollutants, causing environmental threats and public health concerns, but information regarding PFAS hepatotoxicity remains elusive. We investigated the effects of PFASs on lipid metabolism in black-spotted frogs through a combined field and laboratory study. In a fluorochemical industrial area, PFASs seriously accumulate in frog tissues. PFAS levels in frog liver tissues are positively related to the hepatosomatic index along with triglyceride (TG) and cholesterol (TC) contents. In the laboratory, frogs were exposed to 1 and 10 µg/L PFASs, respectively (including PFOA, PFOS, and 6:2 Cl-PFESA). At 10 µg/L, PFASs change the hepatic fatty acid composition and significantly increase the hepatic TG content by 1.33 to 1.87 times. PFASs induce cross-talk accumulation of TG, TC, and their metabolites between the liver and serum. PFASs can bind to LXRα and PPARα proteins, further upregulate downstream lipogenesis-related gene expression, and downregulate lipolysis-related gene expression. Furthermore, lipid accumulation induced by PFASs is alleviated by PPARα and LXRα antagonists, suggesting the vital role of PPARα and LXRα in PFAS-induced lipid metabolism disorders. This work first reveals the disruption of PFASs on hepatic lipid homeostasis and provides novel insights into the occurrence and environmental risk of PFASs in amphibians.

Functionalizing biochar by Co-pyrolysis shaddock peel with red mud for removing acid orange 7 from water.

Biochar modification by metal/metal oxide is promising for improving its adsorption capability for contaminants, especially the anions. However, conventional chemical modifications are complicated and costly. In this study, novel Fe/Fe oxide loaded biochars (RMBCs) were synthesized from a one-step co-pyrolysis of red mud (RM) and shaddock peel (SP), and their potential application for removing anionic azo dye (acid orange 7, AO7) from the aqueous environment was evaluated. Fe from red mud was successfully loaded onto biochars pyrolyzed at 300-800 °C, which presented from oxidation form (Fe2O3) to the reduction forms (FeO and Fe0) with increasing pyrolysis temperature. The RMBC produced at 800 °C with RM:SP mass ratio of 1:1 (RMBC8001:1) exhibited the best capability for AO7 removal (∼32 mg/g), attributed to both adsorption and degradation. The higher surface area of RMBC8001:1 and its greater affinity for AO7 led to the higher adsorption. In addition, RMBC8001:1-induced degradation of AO7 was another key mechanism for AO7 removal. The reduction forms of Fe (FeO or Fe0) in RMBC8001:1 may provide electrons for breaking down the azo bond in AO7 molecules and result in degradation, which is further enhanced in acid conditions due to the participation of readily release of Fe2+ and the available H+ in AO7 degradation. Furthermore, RMBC8001:1 can be easily separated from the treated water by using magnetic field, which significantly benefits its separation in wastewater treatment.

Novel strategies for 2,8-dichlorodibenzo-p-dioxin degradation using ternary Au-modified iron doped TiO2 catalysts under UV-vis light illumination.

Polychlorinated dibenzo-p-dioxins (PCDDs), characterized by their extreme toxicity, high persistency and bioaccumulation, regard as one of the most concerned environmental pollutants on the priority list. In this study, microwave-hydrothermal and photoreduction methods were adopted for fabrication of ternary Au@Fe/TiO2 composites for removal of 2,8-dichlorodibenzo-p-dioxin (2,8-DCDD) under UV-Vis light irradiation. The acquired materials were characterized and analyzed by XRD, TEM, XPS, UV-Vis DRS, PL, etc. As a result, the 1%Au@1%Fe/TiO2 exhibited much higher photocatalytic activity that 96.3% of 2,8-DCDD was removed within 160 min with respect to that of Fe/TiO2 (3.0 times) and TiO2 (5.5 times). It revealed the active substances might be produced, which were verified by ESR analysis. In a comparison, the 1%Au@1%Fe/TiO2 also exhibited high activity in that 97.2% of 2,8-DCDD was removed within 240 min under an anoxic atmosphere. The 1%Au@1%Fe/TiO2 systems were all pH-dependent that 2,8-DCDD could be fully degraded in neutral conditions. The results of repeatability on 1%Au@1%Fe/TiO2 showed that the sample was high stability. Fe doping improved the charge separation of TiO2 and Au modification improved the activity via SPR effect and Mott-Schottky barrier. The degradation mechanisms and pathways were proposed and discussed in detail. The current work develops a new approach on photocatalytic oxidation and reductive dechlorination of dioxins and may open a new opportunity to extend the application range of TiO2 catalysts.

Perfluorooctanoic acid-induced immunotoxicity via NF-kappa B pathway in zebrafish (Danio rerio) kidney.

Perfluorooctanoic acid (PFOA) is widely used in industrial production due to its stable chemical structure and hydrophobic and oleophobic characteristics. PFOA has been frequently detected in environmental media and organisms, leading to increased health risks. There is a lack of information about the immunotoxicity of aquatic organisms induced by PFOA, and the molecular mechanisms remain unclear. In this study, LC-MS analysis proved that PFOA can accumulate in the kidney of zebrafish. In the 0.05 mg/L PFOA treatment group, the accumulation of PFOA in the kidney after 21 days of exposure significantly increased by 79.89%, compared to 14 days of exposure. And a hydropic endoplasmic reticulum, swelling of mitochondria and vacuolization were observed in kidney immune cells of zebrafish. The Toll-like receptor 2 (TLR2)/myeloid differentiation factor 88 (myd88)/NF-κB (P65) pathway was activated when PFOA exerted its effects, which led to regulation of antibody expression; RT-PCR results showed that the mRNA expression level of interleukin-4 (IL-4) decreased in a dose-dependent manner, decreasing to 29.6% of the control level in the 1 mg/L PFOA group after 21 d of exposure. According to triangle plot analysis, immunoglobulin exhibited a notable stress response to PFOA at an early phase; a high concentration of PFOA may disrupt the immune system of zebrafish. Third-order polynomial fitting analysis showed that the high-mRNA-expression regions of IL-4 and antibodies were partially consistent. The results indicated that PFOA could affect antibodies by increasing the concentrations of proinflammatory cytokines. Changes in antibody levels further influenced the expression of other cytokines, which eventually caused disorders in the zebrafish immune system. This study expands the understanding of PFOA-induced immunosuppression and suggests that toxicity mechanisms should be considered for further health risk assessment of emerging pollutants.

The effects of autophagy in rat tracheal epithelial cells induced by silver nanoparticles.

The massive use of silver nanoparticles (AgNPs) is potentially harmful to exposed humans. Although previous studies have found that AgNPs can induce cell autophagy, few studies have focused on the toxic pathways and mechanisms of autophagy induced by AgNPs in rat respiratory epithelial (RTE) cells. In this study, RTE cells were exposed to two kinds of AgNPs in vitro to ascertain the influence of mTOR-autophagy pathway-associated protein expression, including Beclin1, LC3B, Atg5, and Atg7. After exposure to different sizes and concentrations of AgNPs for 12 h, the uptake of silver in RTE cells reached 0.45 µg/L to 1.11 µg/L, indicating that AgNPs can enter RTE cells, leading to toxic effects. Our study found that this toxic effect was related to autophagy caused by ROS accumulation that was mediated by the mTOR pathway. With increasing AgNP exposure concentrations, the expression of p-mTOR was significantly downregulated, and expression of the autophagy-related proteins Beclin1, LC3B, Atg5, and Atg7 was significantly increased in RTE cells in all exposed groups. At a concentration of 1000 µg/L, the expression of LC3BII/LC3BI in all exposed groups was 24.49 times and 12.71 times that of the control, and the expression of Atg7 in all exposed groups was 23.21 times and 13.21 times that of the control. The upregulation of autophagy-related proteins in the AgNP-10 nm exposure groups was greater than that of the AgNP-100 nm exposure group. In summary, the mTOR pathway mediates AgNP-induced autophagy in RTE cells, which leads to damage to the respiratory system barrier and human health risks. This study can facilitate the development of prevention and intervention policies against adverse consequences induced by AgNPs.

More serious autophagy can be induced by ZnO nanoparticles than single-walled carbon nanotubes in rat tracheal epithelial cells.

Metal oxide nanoparticles and carbon nanoparticles, as common nanoparticles (NPs), can cause autophagy in certain cells, which will lead to biohealth risk issues. This study determined the difference in autophagy induced by zinc oxide nanoparticles (ZnO NPs) and single-walled carbon nanotubes (SWCNTs) in respiratory epithelial cells. ICP-OES results showed that NPs uptake as well as the intercellular contents of particles affected cytotoxicity in a dose-dependent manner. ZnO NPs-30 nm had a distinct green dot structure representing autophagy, the SWCNTs exposure group had a few green light spots at a concentration of 10 µg/L. The ROS content of the ZnO NP-30 nm exposure group had the greatest increase at a concentration of 1000 µg/L, which was 2.5 times higher than that of the control, the SWCNTs exposure group showed a 2.2-fold increase. A slight downregulation of p-mTOR was detected, and the ZnO NPs-30 nm treatment group had the significant downregulation rate. The gene and protein expression levels of Beclin-1 and LC3B were upregulated as the exposure concentration increased. The protein expression of Beclin-1 and LC3B in the 1000 µg/L ZnO NPs-30 nm exposure group were 5.21 times and 4.12 times that of the control, respectively. The mRNA expression of Beclin-1 and LC3B in the 1000 µg/L ZnO NPs-30 nm exposure group were 5.04 times and 3.61 times that of the control, respectively. At any concentration, the effect of ZnO NPs-30 nm was greater than that of the SWCNTs. Interaction and crosstalk analysis showed that exposure to ZnO NPs-30 nm caused autophagy through the aggregation of undegraded autophagosomes, whereas SWCNTs exposure induced diminished intercellular oxidative stress to inhibit autophagy. Therefore, this study demonstrated that the effects of autophagy induced by ZnO NPs-30 nm and SWCNTs were different. The health risks of ZnO-30 nm NPs are higher than those of SWCNTs.

Effects of aging and weathering on immobilization of trace metals/metalloids in soils amended with biochar.

Biochar is an effective amendment for trace metal/metalloid (TMs) immobilization in soils. The capacity of biochar to immobilize TMs in soil can be positively or negatively altered due to the changes in the surface and structural chemistry of biochar after soil application. Biochar surfaces are oxidized in soils and induce structural changes through physical and biochemical weathering processes. These changes in the biochar surface and structural chemistry generally increase its ability to immobilize TMs, although the generation of dissolved black carbon during weathering may increase TM mobility. Moreover, biochar modification can improve its capacity to immobilize TMs in soils. Over the short-term, engineered/modified biochar exhibited increased TM immobilization capacity compared with unmodified biochar. In the long-term, no large distinctions in such capacities were seen between modified and unmodified biochars due to weathering. In addition, artificial weathering at laboratories also revealed increased TM immobilization in soils. Continued collection of mechanistic evidence will help evaluate the effect of natural and artificial weathering, and biochar modification on the long-term TM immobilization capacity of biochar with respect to feedstock and synthesis conditions in contaminated soils.

Neurotoxic Anatoxin-a Can Also Exert Immunotoxicity by the Induction of Apoptosis on Carassius auratus Lymphocytes in vitro When Exposed to Environmentally Relevant Concentrations.

Hazardous anatoxin-a (ANTX-a) is produced by freshwater algal blooms worldwide, which greatly increases the risk of consumer exposure. Although ANTX-a shows widespread neurotoxicity in aquatic animals, little is known about its mechanism of action and biotransformation in biological systems, especially in immunobiological models. In this study, transmission electron microscopy results showed that ANTX-a can destroy lymphocytes of Carassius auratus in vitro by inducing cytoplasmic concentration, vacuolation, and swollen mitochondria. DNA fragmentations clearly showed a ladder pattern in agarose gel electrophoresis, which demonstrated that the apoptosis of fish lymphocytes was caused by exposure to ANTX-a. Flow cytometry results showed that the apoptotic percentage of fish lymphocytes exposed to 0.01, 0.1, 1, and 10 mg/L of ANTX-a for 12 h reached 18.89, 22.89, 39.23, and 35.58%, respectively. ANTX-a exposure induced a significant increase in reactive oxygen species (ROS) and malonaldehyde (MDA) in lymphocytes. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and the glutathione (GSH) content of the 0.01 mg/L ANTX-a-treated group decreased significantly by about 41, 46, 67, and 54% compared with that of the control group (p < 0.01), respectively. Although these observations were dose-dependent, these results suggested that ANTX-a can induce lymphocyte apoptosis via intracellular oxidative stress and destroy the antioxidant system after a short exposure time of only 12 h. Besides neurotoxicity, ANTX-a may also be toxic to the immune system of fish, even when the fish are exposed to environmentally relevant concentrations, which clearly demonstrated that the potential health risks induced by ANTX-a in aquatic organisms requires attention.

Mechanism of immunosuppression in zebrafish (Danio rerio) spleen induced by environmentally relevant concentrations of perfluorooctanoic acid.

Perfluorooctanoic acid (PFOA) has been identified as a new persistent organic pollutant. This pollutant is ubiquitous in water and environments. Although PFOA is toxic to fishes, the precise immunotoxicological mechanism remains unclear. In this study, HPLC-MS analysis proved that PFOA can accumulate in the spleen of zebrafish. As comparison of 7-day and 14-day data, the cumulative content in the spleen significantly increased by 26% even in the 0.1 mg/L PFOA-treated group. Morphological observations revealed that PFOA can damage immune cells in zebrafish spleen by inducing vacuolization, lipofuscin granule production, and mitochondrial swelling. The Toll-like receptor 2 (TLR2)/myeloid differentiation factor 88 (myd88)/NF-κB (P65) pathway can mediate the mRNA expression levels of interferon (IFN) and B cell-activating factor (BAFF); immunoglobulin (Ig) secretion is further regulated. RT-PCR results indicated that the expression levels of P65 and IFN in the 1 mg/L group after PFOA exposure for 7 d increased by 4.03- and 3.28-fold, respectively, in a dose-dependent manner compared with those of the control group. The linear correlation coefficient (r2) was analyzed, and the results indicated that the Ig-mediated pathway can be affected by PFOA. For example, the r2 between IgD and P65 decreased from 0.641 (7 d) to 0.295 (14 d) after the cells were exposed to PFOA for a prolonged time; the r2 between IgD and IFN increased from 0.562 (7 d) to 0.808 (14 d). The triangle plot method strongly demonstrated that increased PFOA concentration and prolonged exposure to PFOA can inhibit Ig secretion. Therefore, immune organs, particularly the spleen, of zebrafish are vulnerable to PFOA. These results can help to improve the understanding of the possible noncarcinogenic risk mechanisms induced by PFOA.

Distribution, input pathway and soil-air exchange of polycyclic aromatic hydrocarbons in Banshan Industry Park, China.

Given the steel industry park-city paired structure commonly found across China and it associated environmental pollution, the objective of this study was to examine the spatial-temporal distributions of polycyclic aromatic hydrocarbons (PAHs) as well as the relative contributions of the main influx pathways in Banshan steel industry park, China. We analyzed the concentrations of 16 PAHs in soil, air, water and dry/wet deposition samples using gas chromatography-mass spectrometry (GC-MS). The concentrations of ∑(16)-PAHs ranged from 572 to 4,654 µg/kg in April 2010; and the average concentration is 12.7% and 26.1% higher than that of April 2009 and April 2008, respectively, mainly due to the rapid increase of highly toxic high molecular weight (MW) PAHs. The principal input pathway for high and low MW PAHs was determined to be dry deposition (e.g., 69.73% for Benzo[a]pyrene) and wet deposition (e.g., 78.87% for Naphthalene), respectively. Together, 54.79% of total PAHs found in this region are via dry deposition, whereas wet deposition and river water irrigation contribute to 25.46% and 19.76% (corrected with toxic equivalency factors). The approach to the soil-air equilibrium was assessed by calculating fugacity quotients between soil and air samples, and the results indicate that the soil acted as a secondary source for light MW atmospheric PAHs and a sink for higher MW PAHs. It was also determined that the soil acted as a source for median MW PAHs, particularly PY.