8 research outputs found

    Variations in the concentration, source and flux of polycyclic aromatic hydrocarbons in sediments of the Pearl River Estuary: Implications for anthropogenic impacts

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    Variations in the distribution, source composition, mass inventory and burial flux of polycyclic aromatic hydrocarbons (PAHs) in surface sediments from the Pearl River Estuary (PRE) collected in 2011 and 2019 were analyzed to investigate the influence of the anthropogenic activities. Total concentrations of 16 priority PAHs in 2019 (200.40 ± 188.86 ng g−1 dry weight on average) were at the medium level among global bays/estuaries/coastal areas. In 2019, PAH concentrations have decreased by about 50% compared to 2011 and the dominant composition has changed from low- to high-molecular-weight PAHs. The qualitative and quantitative source apportionment analysis indicates that the dominant source of PAHs has shifted from petroleum (40.33%) in 2011 to traffic emission (44.17%) in 2019. The source variation in the PRE can be attributed to the transformation of the energy source structure from petrogenic to pyrogenic in the Pearl River Delta. The estimated PAH mass inventory of the top 5-cm sediment was 38.70 metric tons in 2019, which was about 41 metric tons lower than that in 2011. The average deposition fluxes have dropped from 418.91 ± 261.02 ng cm−2 yr−1 in 2011 to 215.52 ± 246.63 ng cm−2 yr−1 in 2019. The decreasing PAH concentration is related to the sediment coarsening and decline of total organic carbon. These findings in the PRE can be applied to other estuarine environments influenced by anthropogenic activities

    The Role of Metal Components in the Cardiovascular Effects of PM<sub>2.5</sub>

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    <div><p>Exposure to ambient fine particulate matter (PM<sub>2.5</sub>) increases risks for cardiovascular disorders (CVD). However, the mechanisms and components responsible for the effects are poorly understood. Based on our previous murine exposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, to test the hypothesis that specific chemical component of PM<sub>2.5</sub> is responsible for PM<sub>2.5</sub> associated CVD. Daily ambient and personal exposures to PM<sub>2.5</sub> and 35 elements were measured in the two cities. A total of 60 healthy nonsmoking adult women residents were recruited for measurements of inflammation biomarkers. In addition, circulating endothelial progenitor cells (CEPCs) were also measured in 20 subjects. The ambient levels of PM<sub>2.5</sub> were comparable between Jinchang and Zhangye (47.4 and 54.5”g/m<sup>3</sup>, respectively). However, the levels of nickel, copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levels of C-reactive protein (3.44±3.46 vs. 1.55±1.13), interleukin-6 (1.65±1.17 vs. 1.09±0.60), and vascular endothelial growth factor (117.6±217.0 vs. 22.7±21.3) were significantly higher in Jinchang. Furthermore, all phenotypes of CEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggest that specific metals may be important components responsible for PM<sub>2.5</sub>-induced cardiovascular effects and that the reduced capacity of endothelial repair may play a critical role.</p> </div

    Percent excess risk from the mean values of biomarkers per inter-quartile-range increase in

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    <p>: 1) risk factors and air pollution in univariate regression model. “Jinchang” is an indicator (Jinchang=1; Zhangye=0). Metal concentrations are log-transformed (Panel A); 2) PM2.5 and selected metals, adjusting for age, cotinine level, BMI, blood sugar, LDL, HDL, triglycerides, systolic and diastolic blood pressure. Metal concentrations are log-transformed (Panel B). </p
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