Vehicular non-exhaust emissions account for a significant share of atmospheric particulate matter (PM) pollution, but few studies have successfully quantified the contribution of non-exhaust emissions via real-world measurements. Here, we conduct a comprehensive study combining tunnel measurements, laboratory dynamometer and resuspension experiments, and chemical mass balance modeling to obtain source profiles, real-world emission factors (EFs), and inventories of vehicular non-exhaust PM emissions in Chinese megacities. The average vehicular PM₂.₅ and PM₁₀ EFs measured in the four tunnels in four megacities (i.e., Beijing, Tianjin, Zhengzhou, and Qingdao) range from 8.8 to 16.0 mg km⁻¹ veh⁻¹ and from 37.4 to 63.9 mg km⁻¹ veh⁻¹, respectively. A two-step source apportionment is performed with the information of key tracers and localized profiles of each exhaust and non-exhaust source. Results show that the reconstructed PM₁₀ emissions embody 51–64% soil and cement dust, 26–40% tailpipe exhaust, 7–9% tire wear, and 1–3% brake wear, while PM₂.₅ emissions are mainly composed of 59–80% tailpipe exhaust, 11–31% soil and cement dust, 4–10% tire wear, and 1–5% brake wear. Fleet composition, road gradient, and pavement roughness are essential factors in determining on-road non-exhaust emissions. Based on the EFs and the results of source apportionment, we estimate that the road dust, tire wear, and brake wear emit 8.1, 2.5, and 0.8 Gg year⁻¹ PM₂.₅ in China, respectively. Our study highlights the importance of non-exhaust emissions in China, which is essential to assess their impacts on air quality, human health, and climate and formulating effective controlling measures.

Air quality management is underpinned by continuous measurements of concentrations of target air pollutants in monitoring stations. Although many approaches for optimizing the number and location of air quality monitoring stations are described in the literature, these are usually focused on dense networks. However, there are small and medium-size urban areas that only require one monitoring station but also suffer from severe air pollution. Given that target pollutants are usually measured at the same sampling points; it is necessary to develop a methodology to determine the optimal location of the single station. In this paper, such a methodology is proposed based on maximizing an objective function, that balances between different pollutants measured in the network. The methodology is applied to a set of data available for the city of Cartagena, in southeast Spain. A sensitivity analysis reveals that 2 small areas of the studied city account for 80% of the optimal potential locations, which makes them ideal candidates for setting up the monitoring station. The methodology is easy to implement, robust and supports the decision-making process regarding the siting of fixed sampling sites.

Neonicotinoids (Neonics) have become the most widely used insecticides around the world in recent years. Due to the hydrophilic character, neonics are emerging contaminants in drinking water. In this study, we aimed to characterize and quantify the fate and transport of neonics in the drinking water treatment system and their contributions to the overall dietary risks. Seven neonics in 97 surface and drinking water samples in the city of Hangzhou, China were analyzed. The relative potency factor method was adopted in order to calculate the total neonics concentrations. We then used the Monte Carlo simulation to calculate the chronic daily intake (CDI) of total neonics from water consumption. All 16 surface water samples collected from two rivers contained at least two neonics, and more than 93% of those contained 3 or more neonics. Imidacloprid was detected in all 16 surface water samples, followed by clothianidin and acetamiprid with average concentrations of 11.9, 7.6, 17.6 ng L-1, respectively. The drinking water treatment plants removed approximately 50% of neonics from surface water. However, 68 out of 71 tap water samples that we collected from the household faucets contained at least one neonic, with the highest average concentrations of 5.8 ng L-1 for acetamiprid. The maximum of CDIs of total neonics from water consumption for adult and children were 10.2 and 12.4 ng kg-1 d-1, respectively, which are significantly lower than the acceptable daily intake (ADI). The results presented here shown drinking water consumption only represented an insignificant portion of dietary risks of total neonics, mainly due to the modern drinking water treatment technologies that are capable of removing significant amount of neonics from drinking water. However, the ubiquity of neonics in the drinking water sources to kitchen faucets, should be a concern for public health.

Tropospheric ozone (O₃) is a pollutant of widespread concern in the world and especially in China for its negative effects on agricultural crops. For the first time, yield and economic losses of wheat between 2014 and 2017 were estimated for the North China Plain (NCP) using observational hourly O₃ data from 312 monitoring stations and exposure-response functions based on AOT40 index (accumulated hourly O₃ concentration above 40 ppb) from a Chinese study. AOT40 values from 2014 to 2017 during the wheat growing seasons (75-days, 44 before and 30 after mid-anthesis) ranged from 3.1 to 14.9 ppm h, 4.9–17.5 ppm h, 7.3–17.6 ppm h, and 0.5–18.6 ppm h, respectively. The highest AOT40 values were observed in the Beijing-Tianjin-Hebei region. The values of relative yield losses from 2014 to 2017 were in the ranges of 6.4–30.5%, 10.0–35.8%, 14.9–34.1%, and 21.6–38.2%, respectively. The total wheat production losses in NCP for 2014–2017 accounted for 18.5%, 22.7%, 26.2% and 30.8% in the whole production, while the economic losses amounted to 6,292 million USD, 8,524 million USD, 10,068 million USD, and 12,404 million USD, respectively. The important impact of O₃ in this area, which is of global importance, should be considered when assessing wheat yield production. Our results also show an increasing trend in AOT40, relative yield loss, total crop production loss and economic loss in the four consecutive years.

The number of children diagnosed with autism spectrum disorder (ASD) has been increasing. Previous studies suggested potential association between pregnancy air pollution exposure and ASD. This systematic review and meta-analysis is intended to summarize the association between maternal exposure to outdoor air pollution and ASD in children by trimester based on recent studies.A systematic literature search in 3 databases (Medline, Embase, and Web of Science) was performed using subject headings related to ASD and air pollution since 2007. Eligible studies were screened and evaluated based on predetermined criteria. For meta-analyses, the studies were grouped by air pollutant and exposure time (prenatal period and trimesters). Within-group studies were standardized by log odds ratio (OR) and then combined by three meta-analysis methods: frequentist fixed and random effects models, and Bayesian random effects model.Initial search identified 1564 papers, of which 25 studies remained for final analysis after duplicates and ineligible studies were removed. Of the 25 studies, 13, 14, 12, and 7 studies investigated ASD in children associated with PM2.5, PM10, NO2, and ozone, respectively. The frequentist and Bayesian random effects models resulted in different statistical significance. For prenatal period, frequentist meta-analysis returned significant pooled ORs with 95% confidence intervals, 1.06(1.01,1.11) for PM2.5 and 1.02(1.01,1.04) for NO2, whereas Bayesian meta-analysis showed similar ORs with wider 95% posterior intervals, 1.06(1.00,1.13) for PM2.5 and 1.02(1.00,1.05) for NO2. Third trimester appeared to have higher pooled ORs for PM2.5, PM10, and ozone, but patterns in the time-varying associations over the trimester were inconsistent.For positive association between maternal exposure to ambient air pollution and ASD in children, there is some evidence for PM2.5, weak evidence for NO2 and little evidence for PM10 and ozone. However, patterns in associations over trimesters were inconsistent among studies and among air pollutants.

In this study, levels of dechlorane plus (DP) in breast milk and matched adipose tissue samples were measured from 54 women living in Wenling, China. Polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) were measured simultaneously for comparison. The levels of ∑DPs/∑PBDEs varied from less than one to several dozens of ng g⁻¹ lipid weight (lw) in matrices and the levels of ∑PCBs varied between several to hundreds of ng g⁻¹ lw. In the same matrix, ∑DPs and ∑PCBs/∑PBDEs showed a significant relationship (p < 0.05), indicating that they shared common sources. Accordingly, there was a strong association of lipid-adjusted concentrations of individual compounds (BDE-209 excluded) between matrices (p < 0.001), suggesting that breast milk could be a proxy for adipose tissue in human bioburden monitoring of these compounds. The predicted lipid-adjusted milk/adipose ratios varied from 0.62 to 1.5 but showed significant differences (p<0.001) between compounds, suggesting a compound-specific transfer between milk lipids and adipose tissue lipids. Specifically, the milk/adipose ratios for syn-DP and anti-DP (−1.40 and 1.3, respectively) were significantly higher than those of CB congeners and hexa/hepta-BDE congeners (p < 0.05). In addition, unlike PCBs/PBDEs (excluding BDE-209), DP’s hydrophobicity might not be responsible for its preferable distribution in milk lipids. Instead, the interaction with nonlipid factors played a key role. The fraction of anti-DP between the two kinds of matrices was not significantly different, suggesting that the biochemical transfer processes may not be efficient enough to distinguish DP isomers. Nevertheless, the congener patterns of PCBs/PBDEs gave a clue about the compound-specific transfer between milk and adipose tissue. To our knowledge, this is the first to report the relationships of DP between adipose tissue and breast milk. These results could provide useful and in-depth information on biomonitoring of DP and facilitate the understanding of the accumulation and excretion potentials of DP and its distribution-related mechanism in humans.

Fluoride has been considered as a risk factor of cardiovascular disease due to its endothelial toxicology. However, the mechanism underlying the endothelial toxicity of fluoride has not been clearly illustrated. MiR-200c-3p was strongly linked with endothelial function and its level is increased in serum of fluorosis patients, but it is unclear the role of miR-200c-3p in the fluoride induced endothelial dysfunction. In this study, we confirmed that fluoride exposure induced the apoptosis of endothelial cells both in established rats model and cultured human umbilical vein endothelial cells (HUVECs). And miR-200c-3p was found to be upregulated in NaF treated HUVECs. Fluoride stimulation increased caspase-dependent apoptosis through miR-200c-3p upregulation, with repressing expression of its target gene Fas-associated phosphatase 1 (Fap-1), which functioned as Fas inhibitor. This resulted in activation of Fas-associated extrinsic apoptosis via interaction with increased Fas, Fadd, Cleaved Caspase-8 and Cleaved Caspase-3. The activation of Fas-associated extrinsic apoptosis was abrogated by miR-200c-3p inhibitor. Furthermore, the antiapoptotic effect of downregulated miR-200c-3p was restored by Fap-1 siRNA. These results suggested a determinant role of the miR-200c-3p/Fap-1 axis in fluoride induced endothelial apoptosis.

Fumonisins (FBs) are mycotoxins that are widely distributed in crops and feed, and ingestion of FBs -contaminated crops is harmful to animal health. Furthermore, it is unknown if Fumonisins B1 (FB1) can cause intestinal toxicity. To investigate FB1-induced intestinal toxicity, mice were treated with 0 or 5 mg/kg FB1 by gavage administration for 42 days. Histopathology indicated that FB1 exposure caused proliferation of intestinal epithelial cells, intestinal villi and epithelial layer shedding, intestinal gland atrophy, and necrosis. Notably, FB1 interfered with nuclear xenobiotic receptors (NXR) homeostasis by regulating the level of aryl hydrocarbon receptor (AHR), constitutive androstane receptor (CAR), pregnane X receptor (PXR) and downstream target genes (CYP450s). Moreover, abnormal expression of inflammatory cytokines (IL-1β, IL-2, IL-4, IL-10, and TNF-α) indicated the occurrence of inflammation. The present study provides new insights regarding the mechanism of FB1-induced intestinal toxicity through activating the NXR system and by triggering inflammatory responses in the intestinal tract in mice.

Development of new approach methodologies is urgently needed to characterize the likelihood that complex mixtures of chemicals affect water quality. Omics advances in ecotoxicology allow assessment on a broadest coverage of disrupted biological pathway by mixtures. Here the usefulness of transcriptomic analyses for evaluation of combined effects and identification of main effect components are explored. Two artificial mixtures (Mix 1 and Mix 2) were tested by a concentration-dependent reduced zebrafish transcriptome (CRZT) approach and toxicity bioassays using zebrafish embryos. Then, the toxicities and transcriptomic effects of 12 component chemicals on embryos were incorporated into additivity models to characterize the combined effects of chemicals in mixtures and to identify the main bioactive compounds. Mix 1 and Mix 2 displayed similar embryo toxicities (LD₅₀: 6.6 μM and 8.7 μM, respectively), however, Mix 2 elicited broader biological process perturbations and 5-fold higher transcriptome potency (point of departure eliciting a 20% pathway response, PODₚₐₜₕ₂₀) than Mix 1. The predicted mixture toxicities derived from additivity expectations deviated by 2-fold or less from the measured embryo toxicities except for the Jaw defect endpoint; most biological processes deviated by 3-fold or less. Finally, diclofenac (DFC) and propiconazole (PCZ) were identified as the main contributing components (≥80% explanation) to the embryo toxicity and biological process perturbations by Mix 1. While DFC and chlorophene (CLP) explained up to 80% of the embryo toxicities and biological effects of Mix 2 associated with development and Metabolism processes. The CRZT approach provides a powerful tool for assessment of biological pathways perturbed by chemicals in mixtures and for identification of main bioactive compounds.

Thermo-chemical processes for converting plastic wastes into useful materials are considered promising technologies to mitigate the environmental pollution caused by plastic wastes. In this study, polyethylene terephthalate (PET) plastic wastes were used to develop cost-effective and value-added porous carbons; the developed porous carbons were subsequently tested for capturing CF₄, a greenhouse gas with a high global-warming potential. The activation temperature was varied from 600 °C to 1000 °C and the mass ratio of KOH/carbon ranged from 1 to 3 in the preparation process and their effects on the textural properties and CF₄-capture performance of the PET plastic waste-derived porous carbons were investigated. The CF₄-adsorption uptake was dictated by the specific surface area and pore volume of narrow micropores less than 0.9 nm in diameter. PET-K(2)700, which was developed by KOH activation at 700 °C and KOH/carbon mass ratio of 2, showed the highest CF₄-adsorption uptake of 2.43 mmol g⁻¹ at 25 °C and 1 atm. Also, the CF₄-adsorption data were fitted well with the Langmuir isotherm model and pseudo second-order kinetic model. The PET plastic waste-derived porous carbons exhibited a high CF₄ uptake, good CF₄/N₂ selectivity at relatively low CF₄ pressures, easy regeneration, rapid adsorption/desorption kinetics, and excellent recyclability, which are promising for practical CF₄-capture applications.