Proales similis evidenced a higher growth in the As treatments (0.1 and 0.2 AF) at 35 ppt compared to controls. Furthemore, the T1 and T2 treatments were the most toxic, and in most cases, they induced a synergistic effect. Antagonism effects were detected in the T3 treatment at 25 and 35 ppt. The present data highlights the importance of the examination of pollution in natural environmental conditions in which many aquatic invertebrates endure.Nanoparticulate mineral UV filters, such as titanium dioxide (TiO2) nanocomposites, are being increasingly used in sunscreens as an alternative to organic UV filters. However, there is still a lack of understanding regarding their fate and behavior in aquatic environments and potential environmental impacts after being released from a bather's skin during recreational activities. In this work, we assessed the release, fate, and transformation of two commercial nanocomposite TiO2 UV filters, one hydrophobic and one hydrophilic, in ultrapure water and simulated fresh- and seawater. The hydrophobic TiO2 nanocomposite, T-SA, was coated with a primary Al2O3 photopassivation layer and a secondary stearic acid layer, while the hydrophilic TiO2 nanocomposite, T-SiO2, was coated with a single SiO2 photopassivation layer. The influence of the sunscreen formulation was examined by dispersing the TiO2 nanocomposites in their typical continuous phase (i.e., oil for T-SA and water for T-SiO2) before introduction into the aqueous system. After 48 h of aqueous aging and 48 h of settling, 88-99% of the hydrophobic T-SA remained floating on top of the water column in all aqueous systems. On the other hand, 100% of the hydrophilic T-SiO2 settled out of the water column in the fresh- and seawaters. With respect to the photopassivation coatings, no loss of the T-SA Al2O3 layer was detected after aqueous aging, but 99-100% dissolution of the SiO2 layer on the T-SiO2 nanocomposite was observed after 48 h in the fresh- and seawaters. This dissolution left behind T-SiO2 by-products exhibiting a photocatalytic activity similar to that of bare rutile TiO2. Overall, the results demonstrated that the TiO2 surface coating and sunscreen formulation type drive environmental behavior and fate and that loss of the passivation layer can result in potentially harmful, photoactive by-products. These insights will help guide regulations and assist manufacturers in developing more environmentally safe sunscreens.It has been shown that chemical modification of chitosan with sulfur (S) functional groups could significantly enhance its chelating capability with heavy metals included Cd(II). However, a molecular level understanding has been lacking. Here, we carried out X-ray absorption fine structure (XAFS) and Fourier transformed infrared (FTIR) spectra studies to bridge this knowledge gap. The results indicate that both Cd-O/N and Cd-S bonds exist in the complex of Cd(II) with dithiocarbamate chitosan (DTC-CTS). S functional groups (dithiocarbamate) in DTC-CTS play the major role in complexation with Cd(II) and S content affects the adsorption mechanism. At low S content, Cd(II) is mainly adsorbed on DTC-CTS as an outer-sphere complex with two monodentate amino groups and two water molecules in tetrahedral configuration. At high S content, Cd adsorption dominantly occurs by formation of an inner-sphere complex with two bidentate mononuclear S ligands in tetrahedral configuration. This investigation provides information on the effectiveness and mechanisms of Cd(II) removal that is critical for evaluating modified chitosan applications for stabilization of Cd(II) in surface water, groundwater, soils and sediments.Tributyltin (TBT), a bioaccumulative and persistent environmental pollutant, has been proposed as a metabolism disruptor and obesogen through targeting peroxisome proliferator-activated receptor gamma (PPARγ) receptor pathway. However, it remains unknown whether this biological effect occurs in macrophage, a cell type which cooperates closely with hepatocytes and adipocytes to regulate lipid metabolism. This study for the first time investigated the effect of TBT on PPARγ pathway in macrophages. Our results indicated that nanomolar levels of TBT was able to strongly activate PPARγ in human macrophages. TBT treatment also markedly increased the intracellular lipid accumulation, and enhanced the expression of lipid metabolism-related genes in macrophages, while these effects were all significantly down-regulated in PPARγ-deficient macrophages, confirming the involvement of PPARγ in TBT-induced lipogenesis. Next, a mouse model that C57BL/6 mice were orally exposed to TBT with the doses (250 and 500 μg/kg body weight) lower than NOAEL (no observed adverse effect level) was used to further investigate the in vivo mechanisms. And the in vivo results were consistent with cellular assays, confirming the induction of PPARγ and the increased expression of lipogenesis-regulating and lipid metabolism-related genes by TBT in vivo. In conclusion, this study not only provided the first evidence that TBT stimulated lipogenesis, activated PPARγ and related genes in human macrophages, but also provided insight into the mechanism of TBT-induced metabolism disturbance and obesity through targeting PPARγ via both in vitro cellular assays and in vivo animal models.The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al2O3 NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al2O3 NPs (p-Al2O3), hydrophilic (w-Al2O3) and lipophilic (o-Al2O3) modifications of Al2O3 NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al2O3 NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al2O3 NPs (100 μg/mL) could induce more severe toxicity than p-Al2O3 and w-Al2O3 NPs. Degrasyn manufacturer After uptake by C. elegans, o-Al2O3 NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al2O3 NPs (100 μg/mL) are more toxic than p-Al2O3 and w-Al2O3. Once inside the cell, o-Al2O3 NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis.