Bisphenols (BPs) are common environmental pollutants that are ubiquitous in the natural environment and can affect human health. In this study, we explored the effects of perinatal exposure to BPA, BPF and BPAF on liver function involving in oxidative damage and metabolic disorders in male mouse offspring. We found that BPA exposure impairs the antioxidant defense system, increases lipid peroxidation, and causes oxidative damage in the liver. Furthermore, the levels of 13 metabolites were significantly altered following BPA exposure. We found that BPF exposure significantly increased the expression and activity of CAT, suggesting disturbances in the antioxidant defense system. Moreover, BPF exposure led to metabolic disorders in the liver due to changes in the levels of 8 key metabolites. Exposure to BPAF caused no negative effects on oxidative damage, but altered the levels of β-glucose and glycogen. In summary, perinatal exposure to BPA, BPF and BPAF differentially influence oxidative damage and metabolic disorders in the livers of male mouse offspring. The impact of early life exposure to BPs now warrants future investigations.

Emission inventories are critical to understanding the sources of air pollutants, but have high uncertainties in China due in part to insufficient on-site measurements. In this study, we developed a method of examining, screening and applying online data from the country's improving continuous emission monitoring systems (CEMS) to reevaluate a “bottom-up” emission inventory of China's coal-fired power sector. The benefits of China's current national emission standards and ultra-low emission policy for the sector were quantified assuming their full implementation. The derived national average emission factors of SO₂, NOₓ and particulate matter (PM) were 1.00, 1.00 and 0.25 kg/t-coal respectively for 2015 based on CEMS data, smaller than those of previous studies that may not fully recognize improved emission controls in recent years. The annual emissions of SO₂, NOₓ and PM from the sector were recalculated at 1321, 1430 and 334 Gg respectively, 75%, 63% and 76% smaller than our estimates based on a previous approach without the benefit of CEMS data. The results imply that online measurement with proper data screening can better track the recent progress of emission controls. The emission intensity (the ratio of emissions to economic output) of Northwest China was larger than that of other regions, attributed mainly to its less intensive economy and industry. Transmission of electricity to more-developed eastern provinces raised the energy consumption and emissions of less-developed regions. Judged by 95 percentiles of flue-gas concentrations measured by CEMS, most power plants met the current national emission standards in 2015 except for those in Northwest and Northeast China, while plants that met the ultra-low emission policy were much scarcer. National SO₂, NOₓ and PM emissions would further decline by 68%, 55% and 81% respectively if the ultra-low emission policy can be strictly implemented, implying the great potential of the policy for emission abatement.

In China, the huge amounts of energy consumption caused severe carcinogenic polycyclic aromatic hydrocarbon (PAHs) concentration in the soil and ambient air. This paper summarized that the references published in 2008–2018 and suggested that biomass, coal and vehicular emissions were categorized as major sources of PAHs in China. In 2016, the emitted PAHs in China due to the incomplete combustion of fuel was about 32720 tonnes, and the contribution of the emission sources was the sequence: biomass combustion > residential coal combustion > vehicle > coke production > refine oil > power plant > natural gas combustion. The total amount of PAHs emission in China at 2016 was significantly decreased due to the decrease of the proportion of crop resides burning (indoor and open burning).The geographical distribution of PAHs concentration demonstrated that PAHs concentration in the urban soil is 0.092–4.733 μg/g. At 2008–2012, the serious PAHs concentration in the urban soil occurred in the eastern China, which was shifted to western China after 2012.The concentration of particulate and gaseous PAHs in China is 1–151 ng/m3 and 1.08–217 ng/m3, respectively. The concentration of particle-bound PAHs in the southwest and eastern region are lower than that in north and central region of China. The incremental lifetime cancer risk (ILCR) analysis demonstrates that ILCR in the soil and ambient air in China is below the acceptable cancer risk level of 10−6 recommended by US Environmental Protection Agency (EPA), which mean that there is a low potential PAHs carcinogenic risk for the soil and ambient air in China.

Drugs are excreted from the human body as both original substances and as metabolites and enter aquatic environment through waste water. The aim of this study was to widen the current knowledge considering the effects of waterborne antidepressants with different modes of action—amitriptyline, venlafaxine, sertraline—on embryos of non-target aquatic biota—fish (represented by Danio rerio) and amphibians (represented by Xenopus tropicalis). The tested concentrations were 0.3; 3; 30; 300 and 3000 μg/L in case of amitriptyline and venlafaxine and 0.1; 1; 10; 100 and 1000 μg/L for sertraline. Test on zebrafish embryos was carried out until 144 h post fertilization, while test on Xenopus embryos was terminated after 48 h. Lethal and sublethal effects as well as swimming alterations were observed at higher tested concentrations that are not present in the environment. In contrast, mRNA expression of genes related to heart, eye, brain and bone development (nkx2.5, otx 2, bmp4 and pax 6) seems to be impacted also at environmentally relevant concentrations. In a wider context, this study reveals several indications on the ability of antidepressants to affect non target animals occupying environments which may be contaminated by such compounds.

As a country with the highest CO2 emissions and at the turning point of socio-economic transition, China's effort to reduce CO2 emissions will be crucial for climate change mitigation. Yet, due to geospatial variations of CO2 emissions in different cities, it is important to develop city-specific policies and tools to help control and reduce CO2 emissions. The key question is how to identify and quantify these variations so as to provide reference for the formulation of the corresponding mitigation policies. This paper attempts to answer this question through a case study of 26 cities in the Yangtze River Delta. The CO2 emissions pattern of each city is measured by two statistics: Gini coefficient to describe its quantitative pattern and Global Moran's I index to capture its spatial pattern. It is found that Gini coefficients in all these cities are all greater than 0.94, implying a highly polarized pattern in terms of quantity; and the maximum value for Global Moran's I index is 0.071 with a standard deviation of 0.021, indicating a weak spatial clustering trend but strong difference among these cities. So, it would be more efficient for these cities at current stage to reduce CO2 emissions by focusing on the large emission sources at certain small localities, particularly the very built-up areas rather than covering all the emission sources on every plot of the urban prefectures. And by a combination of these two metrics, the 26 cities are regrouped into nine types with most of them are subject to type HL and ML. These reclassification results then can serve as reference for customizing mitigation policies accordingly and positioning these policies in a more accurate way in each city.

Nanoplastics are widely used in modern life, for example, in cosmetics and daily use products, and are attracting concern due to their potential toxic effects on environments. In this study, the uptake of nanopolystyrene particles by Caenorhabditis elegans (C. elegans) and their toxic effects were evaluated. Nanopolystyrene particles with sizes of 50 and 200 nm were prepared, and the L4 stage of C. elegans was exposed to these particles for 24 h. Their uptake was monitored by confocal microscopy, and various phenotypic alterations of the exposed nematode such as locomotion, reproduction and oxidative stress were measured. In addition, a metabolomics study was performed to determine the significantly affected metabolites in the exposed C. elegans group. Exposure to nanopolystyrene particles caused the perturbation of metabolites related to energy metabolism, such as TCA cycle intermediates, glucose and lactic acid. Nanopolystyrene also resulted in toxic effect including induction of oxidative stress and reduction of locomotion and reproduction. Collectively, these findings provide new insights into the toxic effects of nanopolystyrene particles.

Studies on Fe uptake by phytoplankton have been often conducted using artificial culture media. However, Fe chemistry in freshwater can be influenced by riverine anthropogenic impacts and other factors causing water quality changes. In this study, therefore, Fe uptake in natural (river and reservoir) and effluent waters was investigated for the notorious bloom-forming freshwater cyanobacterium Microcystis aeruginosa. To investigate the Fe uptake mechanism, a short-term incubational assay was conducted in the presence of light, Fe(II) ligand and Fe(III) reductant, with results consistently indicating that unchelated Fe(III) is the major substrate for Fe uptake by M. aeruginosa. Further assays using various freshwater samples indicated that Fe uptake is lower in natural waters compared to that of effluent waters and, interestingly, Fe uptake was found to be limited in natural waters. These results suggest that Fe limitation can be alleviated by the inflow of effluent waters. Statistical analysis with various water quality variables indicated that Fe availability is significantly influenced by concentrations of dissolved Fe and organic matter as well as specific UV absorbance (an index of aromaticity). Overall, findings of this study highlight that watershed anthropogenic activities exert important roles in Fe uptake by freshwater cyanobacteria via alteration of Fe speciation.

This technique for setting guideline values differs from that currently used by regulatory agencies throughout the world. Data for benzene were evaluated from epidemiological studies on human populations (29 studies). Exposure durations were evaluated in terms of Long Term Exposure (LTE) and Lifetime Exposure. All data was reported as Lowest Observed Adverse Effect Levels (LOAEL) and converted into exposure doses using Average Daily Dose (ADD) and Lifetime Average Daily Dose (LADD). These values were plotted as a Toxicant Sensitivity Distribution (TSD) which was the cumulative probability of LOAEL-ADD and LOAEL-LADD. From the TSD plots, linear regression equations gave correlation coefficients (R2) ranging from 0.69 to 0.97 indicating normal distributions. Guideline Values (GVs) for LTE (8hr/day) and Lifetime (24hr/70yrs) exposure to benzene were calculated using data from human epidemiological studies as 5% level of cumulative probability (CP) of LOAEL–ADD and LOAEL–LADD from the cumulative probability distributions (CPD). The derived guideline values from the human epidemiological studies were 92 μg/kg/day for LTE and 3.4 μg/kg/day for lifetime exposure. GV for LTE is appropriate for occupational exposure and GV derived for lifetime exposure appropriate for the general population. The guideline value for occupational exposure limit was below all the guideline values developed by regulatory agencies. But the general population guideline is within the range of values formulated by European Union, ATSDR, EPAQS, USEPA and OEHHA for air quality for the general population. This is an alternative method which eliminates the application of safety factors and other sources of errors in deriving guideline values for benzene.

Based on long-term systematic sampling, information is currently limited regarding the impacts of different air pollution levels on variations of bacteria, fungi and ammonia-oxidizing microorganisms (AOMs) in fine particulate matter (PM₂.₅), especially their interactions. Here, PM₂.₅ samples were weekly collected at different air pollution levels in Beijing, China during one-year period. Microbial composition was profiled using Illumina sequencing, and their interactions were further investigated to reveal the hub genera with network analysis. Diversity of bacteria and fungi showed obvious seasonal variations, and the heavy- or severe-pollution levels mainly affected the diversity and composition of bacteria, but not fungi. While, the community structure of both bacteria and fungi was influenced by the combination of air pollution levels and seasons. The most abundant bacterial genera and some genera with highest abundance in heavy- or severe-pollution days were the hub bacteria in PM₂.₅. Whereas, only the dominant fungi in light-pollution days in winter were the hub fungi in PM₂.₅. The complex positive correlations of bacterial or fungal pathogens would aggravate the air pollution effects on human health, despite of their low relative abundances. Moreover, the strong co-occurrence and co-exclusion patterns of bacteria and fungi in PM₂.₅ were identified. Furthermore, the hub environmental factors (e.g., relative humidity and atmospheric pressure) may play central roles in the distributions of bacteria and fungi, including pathogens. Importantly, AOMs showed significant co-occurrence patterns with the main bacterial and fungal genera and potential pathogens, providing possible microbiological evidences for controlling ammonia emissions to effectively reduce PM₂.₅ pollution. These results highlighted the more obvious air pollution impacts on bacteria than fungi, and the complex bacterial-fungal interactions, as well as the important roles of AOMs in airborne microbial interactions webs, improving our understanding of bioaerosols in PM₂.₅.

Fine particulate matter (PM₂.₅) is an essential risk factor of chronic obstructive pulmonary disease (COPD). Recent studies showed weak association between PM₂.₅ and COPD incidence, but smokers who exposed to higher PM₂.₅ concentration had more opportunity to gain COPD. Cigarette smoking is the most important risk factor of COPD. Thus, we hypothesized: the role of PM₂.₅ played on cigarette-inflamed airways was more significant than normal airways. The study firstly established an animal model of C57BL/6J mice with cigarette smoke exposure and PM₂.₅ orotracheal administration. After calculating pathological scores, mean linear intercept and mean alveolar area, we found PM₂.₅ aggravated pathological injury of cigarette-inflamed lungs, but the injury on normal lungs was not significant. Meanwhile, inflammatory factors as T-bet, IFN-γ and IL-1α were tested using qRT-PCR and ELISA. The results showed PM₂.₅ aggravated inflammation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. The most important pathogenesis of COPD is abnormal apoptosis in airway epithelium, due to oxidative stress following long-term exposure to cigarette smoke. Then, apoptotic responses were detected in lungs. TUNEL analysis demonstrated that PM₂.₅ promoted DNA fragmentation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. Western-blot and immunohistochemistry showed caspase activated significantly in PM₂.₅-cigarette smoke exposed lungs and activated caspase 3 located mainly on bronchial epithelium. Next, human bronchial epithelial cells were cultured treated with cigarette smoke solution (CSS) with or without PM₂.₅. Z-VAD-FMK, a pan-caspase inhibitor, was used to suppress the activation of caspases. After analyzing cell viability, DNA fragmentation, mitochondrial activities and caspase activities, the results clarified that PM₂.₅ aggravated apoptosis in cigarette-inflamed bronchial epithelial cells and the responses could be suppressed by Z-VAD-FMK. Our results gave a new idea about the mechanism of PM₂.₅ on COPD and inferred cigarette-inflamed airways were more vulnerable to PM₂.₅ than normal airways.