Ocean acidification (OA) is a global problem to marine ecosystems. Cadmium (Cd) is a typical metal pollutant, which is non-essential but extremely toxic to marine organisms. The combined effects of marine pollution and climate-driven ocean changes should be considered for the effective marine ecosystem management of coastal areas. Previous reports have separately investigated the influences of OA and Cd pollution on marine organisms. However, little is known of the potential combined effects of OA and Cd pollution on marine diatoms. We investigated the sole and combined influences of OA (1500 ppm CO₂) and Cd exposure (0.4 and 1.2 mg/L) on the coastal diatom Skeletonema costatum. Our results clearly showed that OA significantly alleviated the toxicity of Cd to S. costatum growth and mitigated the oxidant stress, although the intercellular Cd accumulation still increased. OA partially rescued S. costatum from the inhibition of photosynthesis and pyruvate metabolism caused by Cd exposure. It also upregulated genes involved in gluconeogenesis, glycolysis, the citrate cycle (TCA), Ribonucleic acid (RNA) metabolism, and especially the biosynthesis of non-protein thiol compounds. These changes might contribute to algal growth and Cd resistance. Overall, this study demonstrates that OA can alleviate Cd toxicity to S. costatum and explores the potential underlying mechanisms at both the cellular and molecular levels. These results will ultimately help us understand the impacts of combined stresses of climate change and metal pollution on marine organisms and expand the knowledge of the ecological risks of OA.

As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV₁) and FVC (FEV₁/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.

Pyrrolizidine alkaloids (PAs) are common phytotoxins. We performed the first comprehensive investigation on PA contamination in Chinese honeys. LC-MS analysis revealed that 58% of 255 honey samples purchased from 17 regions across Mainland China and Taiwan contained PAs with total content ranging over 0.2–281.1 μg/kg. Monocrotaline (from Crotalaria spp), a PA never found in honey in other regions, together with echimidine (Echium plantagineum) and lycopsamine (from Senecio spp.), were three predominant PAs in PA-contaminated Chinese honeys. Further, PAs present in honeys were found to have geographically distinct pattern, indicating possible control of such contamination in future honey production. Moreover, we proposed a new risk estimation approach, which considered both content and toxic potency of individual PAs in honeys, and found that 12% of the PA-contaminated Chinese honeys tested might pose potential health risk. This study revealed a high prevalence and potential health risk of PA contamination in Chinese honeys.

Groundwater pollution early warning has been regarded as an effective tool for regional groundwater pollution prevention, especially in China. In this study, the systemic model was established to assess the groundwater pollution early warning by integrating the present situation of groundwater quality (Q), groundwater quality trend (T) and groundwater pollution risk (R). The model integrated spatial and temporal variation of groundwater quality, and combined the state and process of the groundwater pollution. Q, T and R were assessed by the methods of fuzzy comprehensive assessment, Spearman or nonparametric Mann-Kendall trend test, and overlay index, respectively. Taking the Luoyang City as an example, the groundwater pollution early warning mapping was generated, and verified by corresponding the groundwater quality classes and the early warning degrees. The results showed that the groundwater was dominated by the levels of no warning and light warning, which accounted for 77% of the study area. The serious and tremendous warning areas were affected by the worse trend and relatively bad/bad present situations of groundwater quality with the typical contaminants of total hardness, nitrate, Hg and COD. In summary, the present situation of groundwater quality was the most important factor of groundwater pollution early warning mapping in the study area. The worse trend of groundwater quality played equally a key role in the local regions, as well as the high pollution risk, which was mainly affected by the pollution source loading. Targeted measures for groundwater pollution prevention were proposed in the corresponding degrees of groundwater pollution early warning. The QTR model was proved to be effective for assessing the regional groundwater pollution early warning. The accuracy of the model could be improved if there is further data acquisition of groundwater quality in longer time series and in larger number, and further investigation of pollution sources.The QTR model is proposed and proved to be effective for assessing regional groundwater pollution early warning.

Achieving large pore size, high catalytic performance with stable structure is critical for metal–organic frameworks (MOFs) to have more hopeful prospects in catalytic applications. Herein, we had reported a method to synthesize highly reactive yet stable defective iron-based Metal organic frameworks by using different monocarboxylic acids with varying lengths as a modulator. The physical−chemical characterization illustrating that modulators could improve the crystallinity, enlarge pore size and enhance catalytic performance and octanoic acid (OA) was screened to be the suitable choice. The catalytic performance of catalysts was detected through persulfate (PS) activation for degrading Tetrabromobisphenol A (TBBPA). The study demonstrated that the highest degradation efficiency for 0.018 mmol L−1 TBBPA was that 97.79% in the conditions of the 1.0 g L−1 Fe(BDC)(DMF,F)-OA-30 dosage and TBBPA:PS = 200:1. In addition, there was observed that no obvious change of the crystal structure, little the leachable iron concentration in the solutions and no significant loss of catalytic activities of Fe(BDC)(DMF,F)-OA-30 after 5th cycles. The iron valence state of Fe(BDC)(DMF,F)-OA-30 before and after degradation and electrochemical properties reveal that the partial substitution of organic ligands by octanoic acid, when removing OA and forming defects by heat and vacuum treatment to generate coordinatively unsaturated metal sites and accelerate the original transmission of electronic, leading to enhance the activity of persulfate activation for efficient removal TBBPA.

We apply convolutional neural network (CNN) model for estimating daily 24-h averaged ground-level PM2.5 of the conterminous United States in 2011 by incorporating aerosol optical depth (AOD) data, meteorological fields, and land-use data. Unlike some of the recent supervised learning-based approaches, which only utilized the predictors from the location of which PM2.5 value is estimated, we naturally aggregate predictors from nearby locations such that the spatial correlation among the predictors can be exploited. We carefully evaluate the performance of our method via overall, temporally-separated, and spatially-separated cross-validations (CV) and show that our CNN achieves competitive estimation accuracy compared to the recently developed baselines. Furthermore, we develop a novel predictor importance metric for our CNN based on the recent neural network interpretation method, Layerwise Relevance Propagation (LRP), and identify several informative predictors for PM2.5 estimation.

Samples of soil, air, and locally grown crops from around an old e-waste dismantling area (Fengjiang) and a new e-waste dismantling area (Binhai) in Taizhou were analyzed to investigate the behavior of polychlorinated biphenyls (PCBs) released during e-waste dismantling in the soil–crop–atmosphere system. The results indicated that PCB pollution is still widespread in the study area. The PCB concentrations were clearly higher in soil from FJ than in soil from BH, and the concentrations in the functional zones decreased strongly in the order industry park > residential area > farmland. Historical and current emissions during e-waste dismantling processes are probably the main sources of PCBs to soil because PCB production and use are banned. The long half-lives of PCBs have caused the target congener concentrations in soil not to decrease markedly over 10 years. The “halo effect” may have caused PCBs in soil in the heavily polluted FJ area to diffuse into the surrounding area. Soil–air exchange of PCBs in heavily contaminated FJ area may supply PCBs to air because the temperatures in Taizhou are often high. PCBs can accumulate in crops through various pathways. Less-chlorinated PCBs (mainly including Tri-PCBs) can enter crops by root uptake and translocated to the aerial tissues, and more-chlorinated PCBs (including Penta-PCBs and Hexa-PCBs) at high concentrations in soil can enter underground crop tissues through passive transport. More-chlorinated PCBs in underground tissues cannot be transferred to aboveground tissues of tall crops but may be transferred to aboveground tissues of short crops through the root-to-stem pathway and through soil dust being transferred to aboveground external surfaces.

Present study screened the toxicological assessment of airborne particulate matter (PM), mechanistic investigation, relationship between the physicochemical characteristics and its associated toxic response. The average concentration of both PM₁₀ and PM₂.₅ exceeded the Indian National Ambient Air Quality Standards. In present study, PM bound metals; Fe, Cu, Cr, Ni, Mn, Pb, Cd, Zn, Sr and Co have been taken into account with total metal concentration of 0.83 and 0.44 μg m⁻³ of PM₁₀ and PM₂.₅ mass concentrations, respectively. The contribution of redox active metals (Fe, Cu, Cr, Ni and Mn) in PM was more as compared to non-redox metals (Pb, Cd and Co) indicating significant risk to the exposed population as these metals possess the ability to produce reactive oxygen species (ROS) which are responsible for various diseases. The cytotoxicity profiles of PM samples determined by MTT assay on two different cell lines (A549 and PBMC) exhibited dose-dependent effects after 24 h exposure, but the consequences differ with respect to particle size and sampling periods. A significant decrease in cell viability with varying PM concentrations (20, 40, 60, 80 and 100 μg ml⁻¹) with respect to control was found in both cell lines. Incubation of RBC suspension with PM samples caused pronounced disruption of RBC and thus exhibited substantial hemolytic behavior. PM samples showed a range of potency to produce reactive oxygen species (ROS). Almost all PM samples increased the level of pro-inflammatory mediator (Nitric oxide) when compared to corresponding unexposed controls suggesting the important role of reactive nitrogen species in induction of cellular toxicity.

The adverse health effects of haze and particle-bound contaminants in China have recently caused increasing concern, and particle size plays a significant role in affecting human exposure to haze-correlated pollutants. To this background, size-segregated particulate samples (nine size fractions (<0.4, 0.4–0.7, 0.7–1.1, 1.1–2.1, 2.1–3.3, 3.3–4.7, 4.7–5.8, 5.8–9.0 and > 9.0 μm) were collected in three scale-gradient cities in northern China and analysed for a series of parent, oxygenated and chlorinated polycyclic aromatic hydrocarbons (PAHs, O-PAHs and Cl-PAHs). The total geometric mean concentrations of PAHs and O-PAHs for Beijing, Zhengzhou and Xinxiang were 98.1 and 27.2, 77.9 and 77.5, 41.0 and 30.7 ng m⁻³, respectively, which were 50–200 times higher than those for Cl-PAHs (0.5, 0.7 and 0.4 ng m⁻³). Though unimodal size-distribution patterns were found for all these contaminants for these three cities, PAHs represented distinctly higher concentration levels around the peak fraction (0.7–2.1 μm) than O-PAHs and Cl-PAHs. With 4–6 ring PAHs as dominant components in all samples, the percentage proportion of 2–3 ring PAHs (ranging from 1% to 26%) generally increased with particle size increasing, implying the sources of these compounds varied little among the 9 size fractions in all three cities. The International Commission on Radiological Protection (ICRP) model and permeability coefficient method were synchronously applied to the size-segregated data for inhalation and dermal exposure assessment to intensively estimate the human exposure doses to airborne PAHs. Further, the incremental lifetime cancer risk (ILCR) was calculated and it’s found that ILCR from inhalation was higher than that from dermal uptake for children and adults in Beijing and Zhengzhou, while the ILCR for Xinxiang presented a contrary pattern, revealing dermal uptake to be an equally significant exposure pathway to airborne PAHs compared to inhalation.

Since ambient particulate matter (APM) is closely related to cardiovascular damage with mitochondria being its potential targets, this study was designed to explore the impact of APM on mitochondrial homeostasis, especially on mitochondrial dynamics and biogenesis in human vascular endothelial cells, using a kind of standard material, PM SRM1648a. As a result, internalized particles lead to mitochondrial dysfunction in EA.hy926 human endothelial cells, including mitochondrial reactive oxygen species (mtROS) overproduction, mitochondrial membrane potential (MMP) reduction and adenosine triphosphate (ATP) inhibition, coupled with additional release of mitochondrial DNA (mtDNA) into the cytosol. Moreover, morphological and structural changes in mitochondria are observed in response to PM SRM1648a. In that aspect, according to the evidence of shorter fragmented mitochondria dispersed throughout the cytoplasm, along with aberrant upregulation of fission-related mRNAs/proteins, the mitochondria exhibit a fission phenotype shifting from intact reticular network to fragmentized punctate shapes. Mechanistically, PM SRM1648a facilitates phosphorylation of DRP1 at Ser616 in HUVECs, and triggers its dephosphorylation at Ser637 residue in both EA.hy926 and HUVECs, which are supportive events for mitochondrial fission during particle exposure. Additionally, suppression of a master energy modulator, PGC-1α, reveals that PM SRM1648a has the ability to impair mitochondrial biogenesis. Collectively, it could be well concluded that PM SRM1648a interferes with the equilibrium of mitochondrial dynamics and biogenesis, which is likely to play a pivotal role in mitochondrial dysfunction driven by particles, eventually contributing to endothelial cell damage. Of note, it is more reasonable to conduct risk assessment from both cellular level and subcellular structures, among which mitochondria-targeted toxicity supplements more comprehensive understanding of APM inducible vascular toxicity.