Effect of Moisture Condition of Brick-Concrete Recycled Coarse Aggregate on the Properties of Concrete.

The application of brick-concrete recycled aggregates can alleviate the problem of increasing construction waste and increasing scarcity of natural aggregates. The different moisture condition of coarse aggregates can significantly affect the performance of brick-concrete recycled aggregate concrete. In this paper, the additional water quantity of dry and air-dried brick-concrete recycled coarse aggregate concrete was determined. Additionally, the fluidity, rheological parameters, autogenous shrinkage, strength and chloride ion penetration resistance were tested, and compared with saturated surface dry recycled brick-concrete coarse aggregate concrete and natural aggregate concrete. The results showed that the slump of concrete was increased, whereas the plastic viscosity, static and dynamic yield stress were decreased by adding additional water or using saturated surface dry coarse aggregate. Compared with the dry and saturated surface dry state, the air-dried recycled coarse aggregate concrete has the smallest 28 days autogenous shrinkage value, higher compressive strength and splitting tensile strength, and less adverse effects on chloride permeability. It is most beneficial to the performance and economy of concrete to adopt the air-dried state when the brick-concrete recycled coarse aggregate is applied in engineering.

Nonylphenol ethoxylates biodegradation increases estrogenicity of textile wastewater in biological treatment systems.

The formation of estrogenic intermediates, i.e. nonylphenol diethoxylate (NP2EO), nonylphenol monoethoxylate (NP1EO), and nonylphenol (NP), following nonylphenol ethoxylates (NPEOs) biodegradation in textile wastewater raises concerns about its endocrine disruptive activity, but the estrogenicity changes of textile wastewater throughout biological treatment processes remain unknown. In the present study, the estrogenicity of textile wastewater sampled from 10 wastewater treatment plants (WWTPs) were investigated using the reporter gene-based T47D-KBluc bioassay. Results showed that the estrogenicity of the textile wastewater significantly increased after either anaerobic or aerobic treatment in all WWTPs, with an average fold change of 3.21, although traditional pollutants were effectively removed. The estradiol equivalents of the effluent (ranging from 1.50 to 4.12 ng-E2/L) were generally higher than published effect based trigger values, indicating an increased risk for the receiving waters. Removal efficiency was high (84.46%) for NPEOs, but was low for NP2EO and NP1EO in the biological treatment processes. Nevertheless, NP had increased concentrations after the treatment. Bioanalytical equivalent concentration of the textile wastewater and that of NP2EO, NP1EO, and NP showed a good linear correlation, of which NP alone contributed more than 70% to the observed estrogenicity. Extending hydraulic retention time was found effective in reducing the estrogenicity as it allows relatively complete degradation of NP, which was further confirmed by running lab-scale A/O reactors fed with NP10EO. The results may extend our knowledge regarding the estrogenicity of textile wastewater and its reduction technologies used in WWTPs.

Structural and functional alterations of gut microbiome in mice induced by chronic cadmium exposure.

Mammalian gut microbiome is readily affected by acute or subchronic cadmium (Cd) intoxication, but it susceptibility following chronic Cd exposure at environmentally-relevant levels remains unknown. This study comprehensively assessed the effects of Cd exposure at doses of 10 and 50 ppm in drinking water for 20 weeks on gut microbiome in mice. Results showed that the Cd exposure induced alterations in gut morphology with potentially increased gut permeability and inflammation. These changes were accompanied by marked perturbation of gut microbiota characterized by significantly decreased gut microbial richness and lowered abundance of short chain fatty acid (SCFA)-producing bacteria, resulting in reduced SCFAs production in the gut. Moreover, the Cd exposure caused substantial metabolic functional changes of the gut microbiome, with significant inhibitions on gene pathways associated with metabolism of amino acid, carbohydrate, and energy, as well as promotions on metabolic pathways such as glutathione metabolism and aminobenzoate degradation. Our findings provide new insights into the hazards assessment of environmental Cd exposure towards gut microbiome.

Effects of chronic cadmium exposure at food limitation-relevant levels on energy metabolism in mice.

Cadmium (Cd) exposure has been implicated in the perturbation of energy metabolism and the development of cardiometabolic disease, but disease predisposition from chronic low-dose Cd exposure remains unclear. This study employed a mouse model to investigate the toxic effects of chronic Cd exposure at food limitation-relevant levels on energy metabolism and the associated liver and gut microbiome functions. Results showed that the Cd exposure induced the perturbation of energy metabolism in mice, evidenced by the alteration of various metabolites associated with the phosphorogen (adenosine triphosphate-creatine phosphate) system, tricarboxylic acid cycle, and lipid metabolism, as well as the increase of the cardiometabolic risk factor, triglyceride. Moreover, both liver and gut microbiome underwent marked structural/histological and functional alterations, prone to the onset of cardiometabolic disease following the Cd exposure. Certain hepatic transcription factors and gut microbes, specifically PPARα, SREBP1c, HNF4A and the Clostridiales_vadinBB60_group, were identified to be highly correlated with altered urinary metabolites, revealing potential toxicological interactions between the liver and gut microbiome, and energy metabolism. Our findings provide new insights into the progression of metabolic diseases induced by Cd exposure. We also propose a stricter Cd limitation in future food safety standards.

Inhibition of Mitochondrial Fatty Acid Oxidation Contributes to Development of Nonalcoholic Fatty Liver Disease Induced by Environmental Cadmium Exposure.

Cadmium (Cd) is one of the most prevalent toxic metal pollutants widely distributed in water and soil environments. Epidemiological studies have shown that exposure to Cd is implicated in the prevalence of nonalcoholic fatty liver disease (NAFLD) in middle-aged human population, but biological evidence is lacking and its toxicological mechanism remains unclear for the disease predisposition from environmental Cd exposure. In this study, we established a chronic Cd-exposure mouse model mimicking the liver Cd deposition in middle-aged human population to determine whether the environmental Cd exposure can induce NAFLD. Results showed that hepatic Cd burden at levels of 0.95 and 6.04 µg/g wet weight resulting from 20-week Cd exposure at different doses induced NAFLD and nonalcoholic steatohepatitis-like phenotypes in mice, respectively. The Cd exposure caused marked hepatic mitochondrial dysfunction and fatty acid oxidation deficiency, along with significant suppression of sirtuin 1 (SIRT1) signaling pathway in the liver. In vitro study confirmed that Cd evidently inhibited the mitochondrial fatty acid oxidation in hepatocytes and that SIRT1 signaling was potentially involved in the process. Our findings suggest that exposure to environmental Cd is a tangible risk factor for NAFLD, and the induced public health risks deserve greater attention.