Current air quality models usually underestimate the concentration of ambient air sulfate, but the cause of this underestimation remains unclear. One reason for the underestimation is that the sulfate formation mechanism in the models is incomplete, and does not adequately consider the impact of the synergistic effects of high concentrations of multiple pollutants on sulfate formation. In this work, the roles of gaseous NO₂, NH₃ and solution ionic strength in the formation of sulfate in the aqueous phase were quantitatively investigated using a glass reactor and a 30 m³ smog chamber, separately. The results showed that sulfate formation was enhanced to different degrees in the presence of gas-phase NO₂, NH₃ and their coexistence as solutes in both liquid solution and aerosol water. NH₃ enhances the aqueous oxidation of SO₂ by NO₂ mainly by accelerating the uptake of SO₂ through increased solubility. More importantly, we found that high ionic strength in aerosol water could significantly accelerate the aqueous oxidation of SO₂, resulting in unexpectedly high S(VI) formation rates. We estimate that under severe haze conditions, heterogeneous oxidation of SO₂ by NO₂ on aerosols may be much shorter than that through gas phase oxidation by OH, aided by high ionic strengths in aerosols. Considering the existence of complex air pollution conditions with high concentrations of NO₂, NH₃ and aerosol water, as expected in typical urban and suburban settings, the sulfate formation mechanisms revealed in the present work should be incorporated into air quality models to improve the prediction of sulfate concentrations.

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.

Anthropogenic activity-mediated nutrient pollution, especially nitrogen enrichment, poses one of the major threats to river ecosystems. However, it remains unclear how and to which extent it affects aquatic microbial communities, especially in heavily polluted rivers. In this study, a significant environmental gradient, particularly nitrogen gradient, was observed along a wastewater receiving river, the North Canal River (NCR). The pollution level was highest, moderate, and lowest in the up-, middle, and down-streams, respectively. The community composition of bacterioplankton transitioned from being Betaproteobacteria-dominated upstream to Gammaproteobacteria-dominated downstream. Copiotrophic groups, such as Polynucleobacter (Betaproteobacteria) and Hydrogenophaga (Betaproteobacteria), were dominant in the upstream. Multiple statistical analyses indicated that total nitrogen (TN) was the most important factor driving the adaptive shifts of community structure. Analyses of co-occurrence networks showed that the complexity of networks was disrupted in the up- and middle streams, while enhanced in the downstream. Our findings here suggested that microbial interactions were reduced in response to the aggravation of nutrient pollution. Similar to these changes, we observed significant dissimilarity of composition of functional groups, with highest abundance of nitrogen metabolism members under the highest level of nitrogen enrichment. Further analyses indicated that most of these functional groups belonged to Betaproteobacteria, suggesting the potential coupling of community composition and function diversity. In summary, adaptive shifts of bacterioplankton community composition, as well as species interactions, occurred in response to nutrient pollution in highly polluted water bodies.

The ultra-high Cd polluted environment is a special habitat in nature. Analysis of the biological adaptation and resistance mechanism of Auxenochlorella protothecoides UTEX234 to ultra-high Cd stress would offer some inspiring understanding on Cd detoxification mechanism and help discovering highly active bioremediation agents. In this study, integrated analyses of the transcriptome, multi-physiological and biochemical data and fatty acid profilings of UTEX2341 were performed for the first time. It was found that exogenous Ca ions could alleviate Cd stress. Manganese-dependent superoxide dismutase and peroxidase also participated in intracellular detoxification. And non-enzymatic antioxidants rather than one specific enzymatic antioxidant were suggested to be used as “core antioxidants”, which witnessed better performance in Cd detoxification. In addition, Cd stress improved sixteen alkane value and biofuel yield and quality.

Breast milk, especially colostrum, is not just a source of nutrients and immune factors for the newborn, but also accumulates environmental persistent pollutants and its diverse microbes affect the early colonization of the newborn's gut. Little is known about associations between environmental pollutants and the microbial composition of human colostrum. We assessed the influence of hexachlorocyclohexane (HCH), a persistent organic pollutant (POP), in colostrums on the microbial composition of human colostrum samples. HCH concentrations in 89 colostrum samples collected from a population living on the easternmost island of China were measured via gas chromatography equipped with mass spectrometer (GC-MS), HCH exposure risks for infants via dietary intake of breast milk were assessed, and for 29 colostrum samples the microbiota were profiled using 16S rRNA gene pyrosequencing to assess the association with HCH exposure levels. Our study confirmed high colostrum exposure levels of total HCHs (12.19 ± 13.68 μg L⁻¹) in this Chinese population. We predominantly identified Proteobacteria (67.6%) and Firmicutes (25.1%) in colostrum and microbial diversity at the genus level differed between samples with different HCH levels; e.g., Pseudomonas which contains several HCH degrading strains was found in significantly higher abundance in γ-HCH rich samples. Also, microbes that were statistically significantly associated with HCH levels were also highly correlated with each other (false discovery rate (FDR)＜0.01) and clustered in network analysis. Microbial diversity is associated with HCH levels in human colostrum and these associations might be attributable to their HCH degrading ability. These finding provide first insights into the role that environmental persistent pollutants may play in the microbial composition of human colostrum and the colonization of the infant gut.

Carbonaceous aerosols are linked to severe haze and health effects, while its origins remain still unclear over China. PM2.5 samples covering four seasons from Jan. 2016 to Jan. 2017 were collected at six sites in Chifeng, a representative agro-pastoral transitional zone of North China focusing on the characteristics and sources of organic carbon (OC) and elemental carbon (EC). The annual averages of OC, EC were 9.00 ± 7.24 μg m−3, 1.06 ± 0.79 μg m−3 with site Songshan in coal mining region exhibited significantly enhanced levels. The residential heating emissions, air stagnation, and secondary organic formation all contributed the higher OC, EC levels in winter. Meanwhile, the impacts from open biomass burning were most intensive in spring. The retroplumes via Lagrangian model highlighted a strong seasonality of regional sources which had more impacts on EC increases. The Positive Matrix Factorization (PMF) model resolved six primary sources, namely, coal combustion, biomass burning, industrial processes, oil combustion, fugitive dust, and fireworks. Coal combustion and biomass burning comprised large fractions of OC (30.57%, 30.40%) and EC (23.26%, 38.47%) across the sites, while contributions of industrial processes and oil combustion clearly increased in the sites near industrial sources as smelters. PMF and EC tracer method gave well correlated (r=0.65) estimates of Secondary OC (SOC). The proportion of coal combustion and SOC were more enhanced along with PM2.5 elevation compared to other sources, suggesting their importances during the pollution events.

High-density polyethylene (HDPE) is a known sorbent for non-ionic organic compounds in technical applications. Nevertheless, there is little information available describing sorption to industrial HDPE for a broad range of compounds. With a better understanding of the sorption properties of synthetic polymers, environmental risk assessment would achieve a higher degree of accuracy, especially for microplastic interactions with organic substances. Therefore, a robust methodology for the determination of sorbent properties for non-ionic organic compounds by HDPE is relevant for the understanding of molecular interactions for both technical use and environmental risk assessment.In this work, sorption properties of HDPE material used for water pipes were characterized using a poly-parameter linear free-energy relationship (ppLFER) approach. Sorption batch experiments with selected probe sorbates were carried out in a three-phase system (air/HDPE/water) covering an aqueous concentration range of at least three orders of magnitude. Sorption in the concentration range below 10⁻² of the aqueous solubility was found to be non-linear and the Freundlich model was used to account for this non-linearity. Multiple regression analysis (MRA) using the determined distribution coefficients and literature-tabulated sorbate descriptors was performed to obtain the ppLFER phase descriptors for HDPE. Sorption properties of HDPE were then derived from the ppLFER model and statistical analysis of its robustness was conducted. The derived ppLFER model described sorption more accurately than commonly used single-parameter predictions, based i.e., on log Kₒ/w. The ppLFER predicted distribution data with an error 0.5 log units smaller than the spLFERs. The ppLFER was used for a priori prediction of sorption by the characterized sorbent material. The prediction was then compared to experimental data from literature and this work and demonstrated the strength of the ppLFER, based on the training set over several orders of magnitude.

Endocrine-disrupting chemicals (EDCs) are widely used in various consumer goods. Consequently, humans are constantly exposed to EDCs, which is associated with a variety of endocrine-related diseases. In this study, we demonstrated the effects of bisphenol A (BPA), benzyl butyl phthalate (BBP), and di(2-ethylhexyl) phthalate (DEHP) on estrogen receptor alpha (ERα) expression under normoxia and hypoxia. First, we confirmed the effects of EDCs on ER activity using OECD Test Guideline 455. Compared to the 100% activity induced by 1 nM 17-β-estradiol (positive control), BPA and BBP exhibited 50% ERα activation at concentrations of 1.31 μM and 4.8 μM, respectively. In contrast, and consistent with previous reports, DEHP did not activate ERα. ERα is activated and degraded by hypoxia in breast cancer cells. BPA, BBP, and DEHP enhanced ERα-mediated transcriptional activity under hypoxia. All three EDCs decreased ERα protein levels under hypoxia in MCF-7 cells. The transcriptional activity of hypoxia-inducible factor-1 was decreased and secretion of vascular endothelial growth factor (VEGF) was increased by BPA and BBP under hypoxia in MCF-7 cells, but not by DEHP. All three EDCs decreased the ERα protein expression level in Ishikawa human endometrial adenocarcinoma cells, and DEHP caused a weak decrease in VEGF secretion under hypoxia. These results demonstrate down-regulation of ERα by EDCs may influence the pathological state associated with hypoxia.

Spirocyclic tetramic acids are widely used in controlling phytophagous mite species throughout the world. the data set is incomplete and provides insufficient evidence for drawing the same conclusion for fish. To fill the gap whether these acaricides alter lipid metabolism on vertebrates, zebrafish embryos exposed to a series concentration of pesticides, the developmental effects, enzyme activities and levels of gene expression were assessed, battery of biomarker utilized by the integrated biomarker response (IBRv2) model. The 96 h-LC₅₀ of spirodiclofen, spiromesifen and spirotetramat were 0.14, 0.12 and 5.94 mg/L, respectively. Yolk sac deformity, pericardial edema, spinal curvature and tail malformation were observed. Three spirocyclic acids were unfavouring the lipid accumulation of by inhibited the acetyl-CoA carboxylase (ACC), fatty acid synthesis (FAS), fatty acid binding proteins (FABP2) and lipoprotein lipase (LPL) activity. The total cholesterol (TCHO) level significantly decreased in the 0.072 mg/L spirodiclofen group and 0.015 and 0.030 mg/L in the spiromesifen groups. No expected change in spirotetramat group on the TCHO and triglycerides (TGs) levels for any of the treatments. The mRNA levels of the genes related to lipid metabolism also significantly altered. In both spirodiclofen and spiromesifen, ACC achieved the highest scores among a battery of biomarkers using integrated biomarker response (IBRv2). The results suggest that spiromesifen was the most toxic for embryos development and spirodiclofen was the most toxic for lipid metabolism in embryos. The 0.07 mg/L of spirodiclofen, 0.05 mg/L of spiromesifen and 2.00 mg/L would cause malformation on zebrafish embryos. This study will provide new insight that fatty acid metabolism may be a suitable biomarker for the spirocyclic tetramic acids in fish species.

Unplanned oil spills during offshore oil production are a serious problem for the industry and the marine environment. Here we assess the biodegradation potential of marine microorganisms from three water depths in the Campos Basin (South Atlantic Ocean): (i) 5 m (surface), (ii) ∼80 m (chlorophyll maximum layer), and (iii) ∼1200 m (near the bottom). After incubating seawater samples with or without crude oil for 52 days, we used metagenomics and classic microbiology techniques to analyze microbial abundance and diversity, and measured physical-chemical parameters to better understand biodegradation processes. We observed increased microbial abundance and concomitant decreases in dissolved oxygen and hydrocarbon concentrations, indicating oil biodegradation in the three water depths treatments within approximately 27 days. An increase in metagenomic sequences of oil-degrading archaea, fungi, and bacteria (Alcanivorax, Alteromonas, Colwellia, Marinobacter, and Pseudomonas) accompanied by a significant increase in metagenomic sequences involved in the degradation of aromatic compounds indicate that crude oil promotes the growth of microorganisms with oil degradation potential. The abundance of genes involved in biodegrading benzene, toluene, ethylbenzene, xylene, alkanes, and poly-aromatic hydrocarbons peaked approximately 3 days after oil addition. All 12 novel metagenome-assembled genomes contained genes involved in hydrocarbon degradation, indicating the oil-degrading potential of planktonic microbes in the Campos Basin.