As a globally transported pollutant, mercury (Hg) released from human activity and methylmercury (MeHg) in the food web are global concerns due to their increasing presence in the environment. In this study, we found that Hg released from municipal sewage into the environment in China is a substantial anthropogenic source based on mass sampling throughout China. In total, 160 Mg (140-190 Mg, from the 20th percentile to the 80th percentile) of Hg (THg) and 280 kg (240-330 kg) of MeHg were released from municipal sewage in China in 2015. The quantities of released THg and MeHg were the most concentrated in the coastal regions, especially in the East, North and South China regions. However, the per capita release of THg and MeHg was the highest in the Tibetan region, which is recognized as the cleanest region in China. THg released into aquatic environments was mitigated from 2001 to 2015 in China, but the amounts released into other sinks increased. This study provides the first picture of the release of Hg from municipal sewage into various sinks in China, and policy makers should pay more attention to the diversity and complexity of the sources and transport of Hg, which can lead to Hg accumulation in the food web and can threaten human health.

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The global pollutant mercury (Hg), especially as methylmercury (MeHg), threatens human and ecosystem health. But major contributors of MeHg exposure to people in China remain highly debated. We developed the China Mercury Exposure Assessment (CMEA) model, which incorporates human exposure pathways for MeHg and total Hg (THg), the interregional, including international and interprovincial, food trading as well as human physiology to provide a comprehensive system that can evaluate the pathway of Hg forms to human consumers in China. Based on the CMEA model that employed the most comprehensive and recent data, we have found that the probable daily intake (PDI) of MeHg for the Chinese population was 0.057 (range: 0.036 – 0.091 as 60% confidence interval) μg·kg−1·day−1, while that of THg was 0.35 (range: 0.22 – 0.55) μg·kg−1·day−1. MeHg exposure was dominated by fish intake, especially by farm-raised freshwater fish due to higher consumption of these fish. In 2011, fish intake contributed to 56% to the total MeHg exposure, followed by rice (26%). Consumption of farm-raised fish reduced human exposure to MeHg by 33%. On the other hand, interregional food trading increased MeHg exposure of the Chinese population, as a whole, by 7.6%. The international and interprovincial food trades contributed to 5.1% and 22% of MeHg intake, respectively. For the whole China, fish intake related exposure to MeHg was highest for the Eastern and Northeastern populations, while Tibetans were chronically exposed to the highest MeHg from other sources. Our findings highlight the importance of farmed fish and food trade for MeHg exposure.

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Terrestrial mercury (Hg) transport, induced by water erosion and exacerbated by human activities, constitutes a major disturbance of the natural Hg cycle, but the processes are still not well understood. In this study, we modeled these processes using detailed information on erosion and Hg in soils and found that vast quantities of total Hg (THg) are being removed from land surfaces in China as a result of water erosion, which were estimated at 420 Mg/yr around 2010. This was significantly higher than the 240 Mg/yr mobilized around 1990. The erosion mechanism excavated substantial soil THg, which contributed to enhanced Hg(0) emissions to the atmosphere (4.9 Mg/yr around 2010) and its transport horizontally into streams (310 Mg/yr). Erosion-induced THg transport was driven by the extent of precipitation but was further enhanced or reduced by vegetation cover and land use changes in some regions. Surface air temperature may exacerbate the horizontal THg release into water. Our analyses quantified the processes of erosion-induced THg transport in terrestrial ecosystems, demonstrated its importance, and discussed how this transport is impacted by anthropogenic inputs and legacy THg in soils. We suggest that policy makers should pay more attention to legacy anthropogenic THg sources buried in soil.

1. Events in utero appear to have a significant role in the development of cardiovascular dysfunction in adulthood. In the present study, we evaluated the effects of prenatal exposure to zymosan, a non-infectious and non-bacterial agent capable of inducing inflammation, on mean systolic arterial pressure (MSAP) in rat offspring at 6-66 weeks of age. 2. Pregnant rats were divided into three groups: (i) a control group, administered 0.5 mL, i.p., saline on gestation Days 8, 10 and 12; (ii) a zymosan-treated group, given 2.37 mg/kg, i.p., zymosan on gestation Days 8, 10 and 12; and (iii) a pyrrolidine dithiocarbamate (PDTC) + zymosan-treated group, which was given 100 mg/kg, i.p., PDTC 1 h before zymosan. At 6, 16, 26, 36, 56 and 66 weeks of age, MSAP was determined in rat offspring from all three groups. Serum levels of tumour necrosis factor (TNF)-alpha were determined in dams, as well as in offspring at 24 and 56 weeks of age. In addition, protein levels of nuclear factor (NF)-kappaB (p65) in the myocardium and kidney of offspring were determined at 24 weeks of age. 3. The results showed that MSAP and NF-kappaB (p65) levels in the myocardium and kidney of offspring from the zymosan-treated group were increased significantly compared with control. This increase was inhibited by concomitant treatment with PDTC. Serum TNF-alpha levels in dams exposed to zymosan and in their offspring at 56 weeks of age (but not at 24 weeks of age) were significantly increased compared with levels in the control group. Following lipopolysaccharide treatment (1 mg/kg, i.p.) of adult rat offspring at 24 weeks of age, there was a further increase in serum TNF-alpha levels in offspring in the zymosan-treated group compared with the other two groups. 4. The findings of the present study suggest that non-bacterial inflammation during gestation can lead to hypertension in offspring and that NF-kappaB signalling may play a critical role in this process.

Background information. APN (adiponectin), an adipocyte-derived cytokine highly presented in serum, which exerts antidiabetic, anti-atherosclerotic and cardioprotective actions, also enhances CFB (cardiac fibroblast) proliferation and protects against cardiac fibrosis. STAT3 (signal transducer and activator of transcription 3), a major mediator in the gp130/JAK2 (Janus kinase 2)/STATs signalling pathway, plays a critical role in cardioprotective events. Almost two-thirds of total myocardial cells are CFBs; however, whether APN regulates STAT3 signalling pathway has not been clarified yet in CFBs. In the present study, we investigated the effect of recombinant globular APN on the STAT3 activity in adult mouse CFBs and explored the possible signalling transduction mechanism.Results. In cultured CFBs, APN (10 μg/ml) can significantly induce delayed STAT3 Tyr 705 phosphorylation timedependently, up to 60 min, and mediate STAT3 translocation from cytoplasm to nucleus. Transfection of siRNA (small interfering RNA) specific for AdipoR1 (APN receptor 1), but not AdipoR2, obviously inhibited APN-induced STAT3 Tyr 705 phosphorylation, indicating that AdipoR1, not AdipoR2, is required for STAT3 phosphorylation. Both inhibition of gp130 by anti-gp130 neutralizing antibody and JAK2 by AG490 (a specific inhibitor for JAK2) can inhibit APN-induced STAT3 phosphorylation and STAT3 transcription activity detected using 2×pAPRE-Luc (APRE reporter) assay. Furthermore, we found that the IL (interleukin)-6 level in culture medium was significantly increased after stimulation with APN and the IL-6 mRNA level was also markedly increased in CFBs, which can be reversed by siRNA for AdipoR1, but not for AdipoR2, and that anti-IL-6 neutralizing antibody can significantly inhibit APNinduced STAT3 Tyr 705 phosphorylation.Conclusions. APN induces IL-6 production mediated by AdipoR1, not AdipoR2, in adult mouse CFBs, which leads to the stimulation of the gp130/JAK signalling pathway, and as a result causes STAT3 activation.

Mitochondrial single nucleotide polymorphisms (mtSNPs) have been reported to associate with type-2 diabetes mellitus (T2DM), but mtSNPs appear to be considerably different among different populations and regions. To determine mtSNPs in Chinese Han patients with T2DM, the entire sequences of the mitochondrial genomes from 72 T2DM Chinese (59 ± 4 years) and 50 age-matched healthy subjects (controls) in Chongqing region of Western China were directly sequenced and mtSNPs were analyzed. We found that M8, M9, D, G, R and A haplogroups exist in Chinese Han population and the frequency of haplogroup M9 was significantly higher in patients with T2DM than in the controls ( p = 0.0006, OR 0.06 [95% CI 0.008-0.476]). MtSNPs T3394C in NADH dehydrogenase subunit 1 (ND1), G4491A in ND2, T16189C and T16519C were found with significantly higher frequency in patients with T2DM than in the controls (T16189C, p = 0.0045; T16519C, p < 0.0001; T3394C, p = 0.0015; G4491A, p = 0.0015). In contrast, the frequency of C5178A in ND2 and A10398G in ND3 was higher in the controls than in patients with T2DM (C5178A, p = 0.014; A10398G, p = 0.0011). Our results indicate that mtSNPs T3394C, G4491A, T16189C and T16519C show susceptible tendency to T2DM and mtSNPs C5178A and A10398G seem to be genetic factors for against T2DM. These mtSNPs determined in our study is useful and could be used for early diagnosis and prevention of T2DM in Chinese Han population.type-2 diabetes mellitus; mitochondrial genome; single nucleotide polymorphisms; haplogroup; Chinese.Tohoku