In current study, we investigated the changes of proteome profiles of Pycnoporus sanguineus after a single exposure of Cr(VI), TBBPA and a combined exposure of TBBPA and Cr(VI), with the goal of illuminating the cellular mechanisms involved in the interactions of co-existed TBBPA and Cr(VI) with the cells of P. sanguineus at the protein level. The results revealed that some ATP-binding cassette (ABC) transporters were obviously induced by these pollutants to accelerate the transportation, transformation and detoxification of TBBPA and Cr(VI). Cr(VI) could inhibit the bioremoval of its organic co-pollutants TBBPA through suppressing the expression of several key proteins related to the metabolism of TBBPA by P. sanguineus, including two cytochrome P450s, pentachlorophenol 4-monooxygenase and glutathione S-transferases. Furthermore, Cr(VI) possibly reduced the cell vitality and growth of P. sanguineus by enhancing the expression of imidazole glycerol phosphate synthase as well as by decreasing the abundances of proteins associated with the intracellular metabolic processes, such as the tricarboxylic acid cycle, purine metabolism and glutathione biosynthesis, thereby adversely affecting the biotransformation of TBBPA. Cr(VI) also inhibited the expression of peptidyl prolyl cis/trans isomerases, thus causing the damage of cell membrane integrity. In addition, some important proteins participated in the resistance to Cr(VI) toxicity were observed to up-regulate, including heat shock proteins, 26S proteasome, peroxiredoxins and three critical proteins implicated in S-adenosyl methionine synthesis, which contributed to reducing the hazard of Cr(VI) to P. sanguineus. The results of this study provide novel insights into the physiological responses and molecular mechanism of white rot fungi P. sanguineus to the stress of concomitant TBBPA and Cr(VI).

The potential leakage from marine CO2 storage sites is of increasing concern, but few studies have evaluated the probable adverse effects on marine organisms. Fish, one of the top predators in marine environments, should be an essential representative species used for water column toxicity testing in response to waterborne CO2 exposure. In the present study, we conducted fish life cycle toxicity tests to fully elucidate CO2 toxicity mechanism effects. We tested sub-lethal and lethal toxicities of elevated CO2 concentrations on marine medaka (Oryzias melastigma) at different developmental stages. At each developmental stage, the test species was exposed to varying concentrations of gaseous CO2 (control air, 5%, 10%, 20%, and 30%), with 96 h of exposure at 0–4 d (early stage), 4–8 d (middle stage), and 8–12 d (late stage). Sub-lethal and lethal effects, including early developmental delays, cardiac edema, tail abnormalities, abnormal pigmentation, and mortality were monitored daily during the 14 d exposure period. At the embryonic stage, significant sub-lethal and lethal effects were observed at pH < 6.30. Hypercapnia can cause long-term and/or delayed developmental embryonic problems, even after transfer back to clean seawater. At fish juvenile and adult stages, significant mortality was observed at pH < 5.70, indicating elevated CO2 exposure might cause various adverse effects, even during short-term exposure periods. It should be noted the early embryonic stage was found more sensitive to CO2 exposure than other developmental stages of the fish life cycle. Overall, the present study provided baseline information for potential adverse effects of high CO2 concentration exposure on fish developmental processes at different life cycle stages in marine ecosystems.

Urban water pollution poses risks of waterborne infectious diseases. Therefore, in order to improve urban liveability, effective pollution mitigation strategies are required underpinned by predictions generated using water quality models. However, the lack of reliability in current modelling practices detrimentally impacts planning and management decision making. This research study adopted a novel approach in the form of Bayesian Networks to model urban water quality to better investigate the factors that influence risks to human health. The application of Bayesian Networks was found to enhance the integration of quantitative and qualitative spatially distributed data for analysing the influence of environmental and anthropogenic factors using three surrogate indicators of human health risk, namely, turbidity, total nitrogen and fats/oils. Expert knowledge was found to be of critical importance in assessing the interdependent relationships between health risk indicators and influential factors. The spatial variability maps of health risk indicators developed enabled the initial identification of high risk areas in which flooding was found to be the most significant influential factor in relation to human health risk. Surprisingly, population density was found to be less significant in influencing health risk indicators. These high risk areas in turn can be subjected to more in-depth investigations instead of the entire region, saving time and resources. It was evident that decision making in relation to the design of pollution mitigation strategies needs to account for the impact of landscape characteristics on water quality, which can be related to risk to human health.

Ionizing radiation causes a variety of effects, including DNA damage associated to cancers. However, the effects in progeny from irradiated parents is not well documented. Using zebrafish as a model, we previously found that parental exposure to ionizing radiation is associated with effects in offspring, such as increased hatching rates, deformities, increased DNA damage and reactive oxygen species. Here, we assessed short (one month) and long term effects (one year) on gene expression in embryonic offspring (5.5 h post fertilization) from zebrafish exposed during gametogenesis to gamma radiation (8.7 or 53 mGy/h for 27 days, total dose 5.2 or 31 Gy) using mRNA sequencing. One month after exposure, a global change in gene expression was observed in offspring from the 53 mGy/h group, followed by embryonic death at late gastrula, whereas offspring from the 8.7 mGy/h group was unaffected. Interestingly, one year after exposure newly derived embryos from the 8.7 mGy/h group exhibited 2390 (67.7% downregulated) differentially expressed genes. Overlaps in differentially expressed genes and enriched biological pathways were evident between the 53 mGy/h group one month and 8.7 mGy/h one year after exposure, but were oppositely regulated. Pathways could be linked to effects in adults and offspring, such as DNA damage (via Atm signaling) and reproduction (via Gnrh signaling). Comparison with gene expression analysis in directly exposed embryos indicate transferrin a and cytochrome P450 2x6 as possible biomarkers for radiation response in zebrafish. Our results indicate latent effects following ionizing radiation exposure from the lower dose in parents that can be transmitted to offspring and warrants monitoring effects over subsequent generations.

Following the Deepwater Horizon (DWH) event in 2010, hydrocarbons were deposited on the continental slope in the northeastern Gulf of Mexico through marine oil snow sedimentation and flocculent accumulation (MOSSFA). The objective of this study was to test the hypothesis that benthic foraminiferal δ13C would record this depositional event. From December 2010 to August 2014, a time-series of sediment cores was collected at two impacted sites and one control site in the northeastern Gulf of Mexico. Short-lived radioisotopes (210Pb and 234Th) were employed to establish the pre-DWH, DWH, and post-DWH intervals. Benthic foraminifera (Cibicidoides spp. and Uvigerina spp.) were isolated from these intervals for δ13C measurement. A modest (0.2–0.4‰), but persistent δ13C depletion in the DWH intervals of impacted sites was observed over a two-year period. This difference was significantly beyond the pre-DWH (background) variability and demonstrated that benthic foraminiferal calcite recorded the depositional event. The longevity of the depletion in the δ13C record suggested that benthic foraminifera may have recorded the change in organic matter caused by MOSSFA from 2010 to 2012. These findings have implications for assessing the subsurface spatial distribution of the DWH MOSSFA event.

The occurrence of algae bloom would lead to the release of algae-derived organic matter (AOM) and then alter the abundance and behavior of dissolved organic matter (DOM) in aquatic ecosystems. In this study, the characteristics and photodegradation of AOM, naturally occurring organic matter (NOM) derived from soil and plants and their mixtures were explored to reveal the potential interactions between AOM and NOM in water. Results indicated that the protein-like components from AOM and the humic-like components from SRNOM took place inter-component interactions in the AOM-NOM mixtures. Meanwhile, application of two-dimensional Fourier transform infrared correlation spectroscopic (2D-FTIR-COS) analysis revealed that carboxylic C=O had a high priority to bind with other functional groups (e.g., phenolic-OH, polysaccharides C-O, amideⅡC-N/N-H and celluloses C-H). More crucially, it was found that the AOM-NOM mixtures subjected to a very different photodegradation behavior to their end-members (i.e., AOM and NOM), likely because of the occurrence of AOM-NOM interactions as well as their roles in mediating the yield of reactive oxygen species. For instance, the presence of AOM led to increased photodegradation degrees of the chromophoric fraction in NOM. In contrast, the NOM did not exhibit any photosensitization role in the photodegradation of the proteins from AOM. This study has potential implications for our understanding of the carbon cycling in anthropogenically impacted aquatic systems such as inland rivers and lakes.

Aluminum dialkyl phosphinates (ADPs) are a promising class of chemicals offering superior flame retardance. However, knowledge on their behavior in vivo is scarce. Hydrolysis has been suggested as one of the major routes of environmental degradation of ADPs. Herein, aluminum methylcyclohexyl phosphinic (AMHP), a kind of ADPs with industrial production in China, and its hydrolysate methyl cyclohexyl phosphinic acid (MHPA) were continuously exposed to Sprague Dawley (SD) rats for 28 days in this study. The same ratio of MHPA in organs to serum and the same daily excretion of MHPA were observed for AMHP exposure group and MHPA exposure group, suggesting the hydrolysis of AMHP in vivo. The hydrolysis of AMHP to MHPA was further confirmed by in vitro simulated human gastric intestinal juice. Therefore, both AMHP and MHPA distributed in liver, kidney and even brain in the form of MHPA. More than 80% of AMHP and MHPA could be excreted by feces and urine. Feces are the main route of excretion of AMHP and MHPA. The denseness of the inflammatory cell in the hepatic portal area and biochemical indexes showed the obvious dose-effect relationship. However, the toxicity of AMHP and MHPA was quite low even with exposure level up to 100 mg/kg dw/day. The low cumulative ability and mild toxicity indicated AMHP as a promising substitute for brominated flame retardant.

Soil aggregates are often considered the basic structural elements of soils. Aggregates of different size vary in their ability to retain or transfer heavy metals in the environment. Here, after incubation of a sieved (<2 mm) topsoil with copper, bulk soil was separated into four aggregate-size fractions and their adsorption characteristics for Cu were determined. By combining nano-scale secondary ion mass spectrometry and C-1s Near Edge X-ray Absorption Fine Structure Spectroscopy, we found that copper tends to bind onto organic matter in the <2 μm and 20–63 μm aggregates. Surprisingly, Cu correlated with carboxyl-C in the <2 μm aggregates but with alkyl-C in the 20–63 μm aggregates. This is the first attempt to visualize the spatial distribution of copper in aggregate size fractions. These direct observations can help improve the understanding of interactions between heavy metals and various soil components.

Orofacial clefts (OFCs) have multifactorial etiologies. Prenatal exposure to heavy metals can induce OFCs in animal models, but evidence from studies of human subjects is scarce. We examined whether concentrations of mercury (Hg), cadmium (Cd), lead (Pb), and arsenic (As) in placental tissues are associated with risk for OFCs in offspring. This population-based case-control study included 103 newborns affected by OFCs with available placental tissues and 206 controls randomly selected from 509 non-malformed newborns with available placenta samples, recruited in five rural counties in northern China. Sociodemographic information was collected using a structured questionnaire in face-to-face interviews. The concentrations of Hg, Cd, Pb, and As in placental tissues were analyzed using an inductively coupled plasma-mass spectrometry in helium mode. The median concentrations of Hg (7.4 ng/g), Cd (57.1 ng/g), and Pb (96.1 ng/g) were all statistically significantly higher in OFC cases than in controls (Hg 5.5 ng/g, Cd 38.6 ng/g, and Pb 67.9 ng/g, respectively); no differences were observed between the two groups in median concentrations of As. Concentrations above the median for all subjects were associated with a 2.33-fold (95% confidence interval [CI] 1.33–2.09) increased OFC risk for Cd and a 3.08-fold (95% CI 1.74–5.47) increased risk for Pb. The risk for OFCs increased with concentration tertiles, with an adjusted odds ratio of 3.06 (95% CI 1.36–6.88) for the second tertile and 8.18 (95% CI 6.64–18.37) for the highest tertile of Cd, and 3.88 (95% CI 1.78–8.42) for the second tertile and 5.17 (95% CI 2.37–11.29) for the highest tertile of Pb. The association between Hg concentration and OFC risk was borderline nonsignificant after adjusting for confounding factors. Prenatal exposure to Cd and Pb, as reflected by their concentrations in placental tissues, is associated with an increased risk for neonatal OFCs.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants in soil and are considered priority pollutants due to their carcinogenicity. Bioremediation of PAH-contaminated soils is often limited by the low solubility and strong sorption of PAHs in soil. Synthetic surfactants and biosurfactants have been used to enhance the bioavailability of PAHs and to accelerate microbial degradation. However, few studies have compared synthetic and biosurfactants in their efficiency in promoting PAH biodegradation in either native or bioaugmented soils. In this study, we evaluated mineralization of ¹⁴C-pyrene in soils with or without the augmentation of Mycobacterium vanbaalenii PYR-1, and characterized the effect of Brij-35 (synthetic) and rhamnolipid biosurfactant at different amendment rates. Treatment of rhamnolipid biosurfactant at 140 or 1400 μg surfactant g-dry soil⁻¹ rates resulted in a significantly longer lag period in ¹⁴C-pyrene mineralization in both native and bioaugmented soils. In contrast, amendment of Brij-35 generally increased ¹⁴C-pyrene degradation, and the greatest enhancement occurred at 21.6 or 216 μg surfactant g-dry soil⁻¹ rates, which may be attributed to increased bioavailability. Brij-35 and rhamnolipid biosurfactant were found to be non-toxic to M. vanbaalenii PYR-1 at 10X CMC, thus indicating rhamnolipid biosurfactant likely served as a preferential carbon source to the degrading bacteria in place of ¹⁴C-pyrene, leading to delayed and inhibited ¹⁴C-pyrene degradation. Mineralization of ¹⁴C-pyrene by M. vanbaalenii PYR-1 was rapid in the unamended soils, and up to 60% of pyrene was mineralized to ¹⁴CO₂ after 10 d in the unamended or Brij-35 surfactant-amended soils. Findings of this study suggest that application of surfactants may not always lead to enhanced PAH biodegradation or removal. If the surfactant is preferentially used as an easier carbon substrate than PAHs for soil microorganisms, it may actually inhibit PAH biodegradation. Selection of surfactant types is therefore crucial for the effectiveness of surfactant-aided bioremediation of PAH-contaminated soils.