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Purpose The primitive recycling of electronic waste (ewaste) in developing countries is causing serious environmental pollution. The objective of this study was to determine the contamination and toxicity of surface sediment of Nanguan River, which runs through the ewaste recycling area of Taizhou, East China. Materials and methods Surface sediments were collected from Nanguan River, including one from the control site, four near the household workshops, and two near the industrial parks. Levels of polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs), and heavy metals/metalloid (Ni, Pb, Cd, Cr, Zn, Cu, Hg, and As), which are most widely detected in e-waste contaminated surroundings, were determined. Acute toxicity and genetic toxicity were evaluated by luminescence inhibition assay in luminescent bacterium Vibrio qingaiensis sp. nov. (Q67) and Vicia faba roots tip micronucleus assay, respectively. Results and discussion The surface sediment has been seriously contaminated by PCBs, PAHs, and heavy metals/ metalloid due to the e-waste disassembly process. Significant acute and genetic toxicity of the sediments presented a big threat to the aquatic life and human health through food chain, as the river is an extent water source for local residents.Conclusions The environmental issue of e-waste recycling is emergent and measures should be taken to mitigate the adverse impacts of e-waste disassembly.

Background This study aimed to explore the effect of long non-coding RNA (LncRNA) H19 on the proliferation and invasion of lung carcinoma cells A549, and to determine its molecular targets. Methods A549 cells were with either LncRNA H19 or LncRNA H19 shRNA, and the expression levels of LncRNA H19 were evaluated by quantitative real-time PCR (RT-PCR). We measured cell proliferation using the CCK-8 assay, cell counting assays, and colony formation assay in response to shLncRNA H19-2. Cell migration and invasion were assessed by wound healing assay and Transwell assay, respectively. The mRNA and protein expression levels of E-cadherin, N-cadherin, and vimentin were determined by RT-PCR and western blot, respectively. Results The three LncRNA H19 shRNAs used in our study significantly reduced the expression levels of LncRNA H19 in A549 cells ( P <0.05). Moreover, LncRNA H19 shRNA 2 (shLncRNA-2) was the most potent inhibitor of LncRNA H19 expression, and was selected for further experimentation. Transfection with shLncRNA H19-2 significantly decreased the proliferation, migration, and invasion of A549 cells, while overexpression of LncRNA H19 had the opposite effect in these cells ( P <0.05). In response to shLncRNA H19-2, the expression levels of E-cadherin were notably elevated ( P <0.05), while the expression levels of N-cadherin and vimentin were decreased ( P <0.05). In contrast, overexpression of LncRNA H19 induced the expression of E-cadherin, and blocked the expression of N-cadherin, and vimentin ( P <0.05). Conclusion Our results suggest that LncRNA H19 mediates the proliferation and invasion of lung cancer cells via upregulation of N-cadherin and vimentin, and downregulation of E-cadherin.