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The potential health risk caused by long-term exposure to heavy metals in household dust is not only depended on their total content, but also bioaccessibility. In this study, twenty-one dust samples were collected from residential buildings, schools, and laboratories in 14 provincial-capital/industrial cities of China, aiming to evaluate the total contents, fractionation, bioaccessibility and health risks of nine heavy metals (As, Cd, Cr, Ni, Pb, Mn, Zn, Fe, and Cu). Results showed that the highest levels of Cd, Cr, Ni and Zn were found in laboratory dust, As, Pb and Mn in school dust, and Fe and Cu in residential dust, indicating different source profiles of the heavy metals. The mean bioaccessibility of the heavy metals across all samples as evaluated using SBRC (Solubility Bioavailability Research Consortium), IVG (In Vitro Gastrointestinal), and PBET (Physiologically Based Extraction Test) assays was 58.4%, 32.4% and 17.2% in gastric phase (GP), and 24.9%, 21.9% and 9.39% in intestinal phase (IP), respectively. Cadmium had the highest content in the fractions of E1+C2 (43.7%), as determined by sequential extraction, and Pb, Mn, and Zn had a higher content in E1+C2+F3 (64.2%, 67.2%, 78.8%), resulting in a higher bioaccessibility of these heavy metals than others. Moreover, the bioaccessibility of most heavy metals was inversely related to dust pH (R = −0.18 in GP; −0.18 in IP; P < 0.01) and particle size, while a positive correlation was observed with total organic carbon (R = 0.40 in GP; 0.38 in IP; P < 0.01). The exposure risk calculated by the highest bioaccessibility was generally lower than that calculated by the total content. However, Pb in one school dust sample had an unacceptable carcinogenic risk (adult risk = 1.19 × 10−4; child risk = 1.08 × 10−4). This study suggests that bioaccessibility of heavy metals in household dust is likely related to geochemical fractions and physical/chemical properties. Further research is needed to explore the sources of bioaccessible heavy metals in household dust. [Display omitted] • Bioaccessibility of nine metals in 21 household dusts from 14 cities were studied. • Bioaccessibility showed a trend of SBRC > IVG > PBET. • Metal bioaccessibility was positively correlated with dust TOC and E1+C2 fractions. • Metal bioaccessibility was inversely related to dust pH and particle size. • Bioaccessibility-based health risks of heavy metal were assessed and more accurate. [ABSTRACT FROM AUTHOR]

Imidacloprid is a neonicotinoid that targets sucking pests, such as aphids and the green leaf bug and has been widely applied in wheat fields to control wheat aphids in China. To investigate the involvement of miRNAs in imidacloprid resistance, we sequenced small RNA libraries of Sitobion miscanthi Fabricius, across two different treatments using Illumina short-read sequencing technology. As a result, 265 microRNAs (miRNAs), of which 242 were known and 23 were novel, were identified. Quantitative analysis of miRNA levels showed that 23 miRNAs were significantly up-regulated, and 54 miRNAs were significantly down-regulated in the nymphs of S. miscanthi treated with imidacloprid in comparison with those of the control. Modulation of the abundances of differentially expressed miRNAs, smi-miR-316, smi-miR-1000, and smi-miR-iab-4 by the addition of the corresponding antagomir/inhibitor to the artificial diet significantly changed the susceptibility of S. miscanthi to imidacloprid. Subsequently, the post-transcriptional regulatory mechanism was conducted, smi-miR-278 and smi-miR-316 were confirmed to be participated in the post-transcriptional regulation of nAChRα1A and CYP4CJ6, respectively. The results suggested that miRNAs differentially expressed in response to imidacloprid could play a critical regulatory role in the metabolism of S. miscanthi to imidacloprid. [Display omitted] • 77 differentially expressed miRNAs identified under imidacloprid exposure using Illumina short-read sequencing technology. • Modulation abundances of smi-miR-316, smi-miR-1000 and smi-miR-iab-4 significantly changed the susceptibility to imidacloprid. • CYP4CJ6 and nAChRα1A could be regulated by smi-miR-316 and smi-miR-278, respectively. [ABSTRACT FROM AUTHOR]