This study was conducted to assess the merits and limitations of various high-pressure membranes, tight nanofiltration (NF) membranes in particular, for the removal of trace organic compounds (TrOCs). The performance of a low-pressure reverse osmosis (LPRO) membrane (ESPA1), a tight NF membrane (NF90) and two loose NF membranes (HL and NF270) was compared for the rejection of 23 different pharmaceuticals (PhACs). Efforts were also devoted to understand the effect of adsorption on the rejection performance of each membrane. Difference in hydrogen bond formation potential (HFP) was taken into consideration. Results showed that NF90 performed similarly to ESPA1 with mean rejection higher than 95%. NF270 outperformed HL in terms of both water permeability and PhAC rejection higher than 90%. Electrostatic effects were more significant in PhAC rejection by loose NF membranes than tight NF and LPRO membranes. The adverse effect of adsorption on rejection by HL and ESPA1 was more substantial than NF270 and NF90, which could not be simply explained by the difference in membrane surface hydrophobicity, selective layer thickness or pore size. The HL membrane had a lower rejection of PhACs of higher hydrophobicity (log D>0) and higher HFP (>0.02). Nevertheless, the effects of PhAC hydrophobicity and HFP on rejection by ESPA1 could not be discerned. Poor rejection of certain PhACs could generally be explained by aspects of steric hindrance, electrostatic interactions and adsorption. High-pressure membranes like NF90 and NF270 have a high promise in TrOC removal from contaminated water.
Observed effects of metal mixtures on animals and plants often differ from the estimates, which are commonly calculated by adding up the biological responses of individual metals. This difference from additivity is commonly referred to as being a consequence of specific interactions between metals. The science of how to quantify metal interactions and whether to include them in risk assessment models is in its infancy. This review summarizes the existing predictive tools for evaluating the combined toxicity of metals present in mixtures and indicates the advantages and disadvantages of each method. We intend to provide eco-toxicologists with background information on how to make good use of the tools and how to advance the methods for assessing toxicity of metal mixtures. It is concluded that statistically significant deviations from additivity are not necessarily biologically relevant. Incorporation of interactions between metals in a model does not on forehand mean that the model is more accurate than a model developed based on additivity only. It is recommended to first use a relatively simple method for effect prediction of uninvestigated metal mixtures. To improve the reliability of toxicity modeling for metal mixtures, further efforts should focus on balancing the relationship between the significance of statistics and the biological meaning, and unraveling the toxicity mechanisms of metals and their mixtures.
Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas. 相似文献
