Facing serious air pollution problems, the Chinese government has taken numerous measures to prevent and control air pollution. Understanding the sources of pollutants is crucial to the prevention of air pollution. Using numerical simulation method, this study analysed the contributions of the total local emissions and local emissions from different sectors (such as industrial, traffic, resident, agricultural, and power plant emissions) to PM₂.₅ concentration, backward trajectory, and potential source regions in Tangshan, a typical heavy industrial city in north China. The impact of multi-scale meteorological conditions on source apportionment was investigated. From October 2016 to March 2017, total local emissions accounted for 46.0% of the near-surface PM₂.₅ concentration. In terms of emissions from different sectors, local industrial emissions which accounted for 23.1% of the near-surface PM₂.₅ concentration in Tangshan, were the most important pollutant source. Agricultural emissions were the second most important source, accounting for 10.3% of the near-surface PM₂.₅ concentration. The contributions of emissions from power plants, traffic, residential sources were 2.0%, 3.0%, and 7.2%, respectively. The contributions of total local emissions and emissions from different sectors depended on multi-scale meteorological conditions, and static weather significantly enhanced the contribution of regional transport to the near-surface PM₂.₅ concentration. Eight cluster backward trajectories were identified for Tangshan. The PM₂.₅ concentration for the 8 cluster trajectories significantly differed. The near-surface PM₂.₅ in urban Tangshan (receptor point) was mainly from the local emissions, and another important potential source region was Tianjin. The results of the source apportionment suggested the importance of joint prevention and control of air pollution in some areas where cities or industrial regions are densely distributed.

The accuracy and reliability of volatile organic compound (VOC) emission data are essential for assessing emission characteristics and their potential impact on air quality and human health. This paper describes a new method for determining VOC emission data by multipoint sampling from various process units inside a large-scale refinery. We found that the emission characteristics of various production units were related to the raw materials, products, and production processes. Saturated alkanes accounted for the largest fraction in the continuous catalytic reforming and wastewater treatment units (48.0% and 59.2%, respectively). In the propene recovery unit and catalytic cracking unit, alkenes were the most dominant compounds, and propene provided the largest contributions (57.8% and 23.0%, respectively). In addition, n-decane (12.6%), m,p-xylene (12.4%), and n-nonane (8.9%) were the main species in the normal production process of the delayed coking unit. Assessments of photochemical reactivity and carcinogenic risk were carried out, and the results indicate that VOC emissions from the propene recovery unit and catalytic cracking unit should be controlled to reduce the ozone formation potential; in addition, alkenes are precedent-controlled pollutants. The cancer risk assessments reveal that 1,2-dibromoethane, benzene, 1,2-dichloroethane, and chloroform were the dominant risk contributors, and their values were much higher than the standard threshold value of 1.0 × 10⁻⁶ but lower than the significant risk value defined by the US Supreme Court. Based on the VOC composition and a classification algorithm, the samples were classified into eight main groups that corresponded to different process units in the petroleum refinery. In conclusion, this work provides valuable data for investigating process-specific emission characteristics of VOCs and performing associated assessments of photochemical reactivity and carcinogenic risk in petrochemical refineries.

Experimental data on the contribution of a dump site in Tanzania as a point source of the 17 possible congeners of PCDD/Fs to the environment is presented. Dry and wet season samples were collected around Pugu municipal dump site followed by GCxGC-TOFMS analysis. The dominant congeners were OctaCDD, 1,2,3,4,6,7,8-HepCDF; 1,2,3,4,6,7,8-HeptaCDD and 1,2,4,7-PeCDD. The concentrations of the congeners expressed as TEQ WHO₂₀₀₅ ranged from 11.69 to 48.97 pg/g with a mean of 29.44 pg/g for the dry season and TEQ WHO₂₀₀₅ 4.13–85.82 pg/g with a mean of 41.51 pg/g for the wet season. These levels were speculated high enough to accumulate in free-range chickens and cause harmful effects to humans that consumed them especially residents around Pugu dump site. Exposure of people to PCDD/Fs through dermal absorption and soil ingestion were estimated using the VLIER-HUMAAN Mathematical model. Exposure through dermal absorption was estimated to be 1.2 × 10⁻⁴ and 9.8 × 10⁻⁶ ng TEQ/kg day for children and adults respectively while through soil ingestion via consumption of contaminated foods and other sources was 0.0045 and 0.27 ng TEQ/kg day for children and adults respectively. These values however were well below the WHO tolerable daily intake. Generally, there was no significant variation for total PCDD/Fs in the dry and wet season (α = 0.08). Strong positive correlation (r = 0.94) between total PCDD/Fs and organic matter content was observed during the wet season.

Sediments serve as both source and sink of contaminants (e.g., Cu) and biologically important materials (e.g., metals, nutrients). Bioturbation by benthic organisms is ecologically relevant as bioturbation affects the physio-chemical characteristics of sediments, thus altering nutrient and contaminant distribution and bioavailability. We examined the effects of sediment-associated Cu on T. tubifex with conventional toxicity endpoints, such as mortality and growth, and less commonly used non-destructive endpoints, such as bioturbation and feeding. An experimental approach was developed to examine the applicability of simple methods to detect effects on bioturbation and feeding. Two experiments were conducted with 7-day exposures to uncontaminated or Cu-spiked natural sediment at six Cu concentrations to examine Cu bioaccumulation and effects. Endpoints included worm mortality, feeding rate and growth (experiment A) and worm bioturbation (particle diffusion and maximum penetration depth, experiment B). A microparticle tracer was placed on the sediment surface and vertical particle transport was followed over time. Adverse effects were detected for all endpoints (bioturbation, feeding rate, growth and survival): a slight positive effect at the lowest Cu concentrations followed by adverse effects at higher concentrations indicating hormesis. These simple, non-destructive endpoints, provided valuable information and demonstrated that sediment-associated contaminants, such as Cu, can influence bioturbation activity, which in turn may affect the distribution of sediment-bound or particulate pollutants, such as the plastic microparticles studied here. Thus, we suggest to use simple endpoints, such as bioturbation and feeding rate, in ecotoxicity testing since these endpoint account for the influence of interactions between pollutants and benthos and, thus, increase ecological relevance.

Understanding how essential and toxic elements are distributed in cereal grains is a key to improving the nutritional quality of cereal-based products. The main objective of this work was to characterize the distribution of Cd and of nutrients (notably Cu, Fe, Mn, P, S and Zn) in the durum wheat grain. Laser ablation inductively coupled mass spectrometry and synchrotron micro X-ray fluorescence were used for micro-scale mapping of Cd and nutrients. A dissection approach was used to quantitatively assess the distribution of Cd and nutrients among grain tissues. Micro X-ray absorption near-edge spectroscopy was used to identify the Cd chemical environment in the crease. Cadmium distribution was characterized by strong accumulation in the crease and by non-negligible dissemination in the endosperm. Inside the crease, Cd accumulated most in the pigment strand where it was mainly associated with sulfur ligands. High-resolution maps highlighted very specific accumulation areas of some nutrients in the germ, for instance Mo in the root cortex primordia and Cu in the scutellum. Cadmium loading into the grain appears to be highly restricted. In the grain, Cd co-localized with several nutrients, notably Mn and Zn, which challenges the idea of selectively removing Cd-enriched fractions by dedicated milling process.

Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.

Maternal nicotine exposure during lactation induces liver damage in adult male rats. However, the mechanism in males is unknown and females have not been tested. Here, we determined the liver lipid composition and lipogenic enzymes in male and female offspring at two ages in a model of postnatal nicotine exposure. Osmotic minipumps were implanted in lactating Wistar rat dams at postnatal day (PND) 2 to release 6 mg/kg/day of nicotine (NIC group) or saline (CON group) for 14 days. Offspring received a standard diet from weaning until euthanasia at PND120 (1 pup/litter/sex) or PND180 (2 pups/litter/sex). At PND120, NIC males showed lower plasma triglycerides (TG), steatosis degree 1, higher hepatic cholesterol (CHOL) ester, free fatty acids, monoacylglycerol content as well as acetyl-coa carboxylase-1 (ACC-1) and fatty acid synthase (FAS) protein expression in the liver compared to CON males. At this age, NIC females had preserved hepatocytes architecture, higher plasma CHOL, higher CHOL ester and lower total CHOL content in the liver compared to CON females. At PND180, NIC males showed steatosis degrees 1 and 2, higher TG, lower free fatty acids and total CHOL content in the liver and an increase in ACC-1 hepatic protein expression. NIC females had higher plasma TG and CHOL levels, no change in hepatic morphology, lower CHOL ester and free fatty acids in the liver, which also showed higher total ACC-1 and FAS protein expression. Maternal nicotine exposure induces long-term liver dysfunction, with an alteration in hepatic cytoarchitecture that was aggravated with age in males. Concerning females, despite unchanged hepatic cytoarchitecture, lipid metabolism was compromised, which deserves further attention.

Exposure to benzo(a)pyrene (BaP) has been shown to cause mitochondrial dysfunction and injury to neural cells. Resveratrol (RSV) has been studied as an antioxidant, anti-inflammatory, anti-apoptotic, and anticancer agent and can modulate mitochondrial function in vitro and in vivo. However, the molecular mechanisms underlying RSV’s protection against mitochondrial dysfunction have not been fully elucidated. To investigate whether RSV can effectively prevent BaP-induced mitochondrial dysfunction, we tested the effects of RSV in primary neuronal models. Our results confirmed that neurons exhibited mitochondrial dysfunction and apoptosis in the mitochondrial pathway after BaP-treatment, and that pretreatment with RSV could reduce that dysfunction. Further, our results indicated that RSV pretreatment enhanced mitochondrial biogenesis via the AMPK/PGC-1α pathway and activated mitophagy via the PINK1-Parkin and AMPK/ULK1 pathways, thereby coordinating mitochondrial homeostasis. We also found that RSV could alleviate mitochondrial network fragmentation caused by BaP. This work provided insights into the role of RSV in preventing BaP-induced primary neuronal apoptosis in the mitochondrial pathway, mainly via regulation of mitochondrial biogenesis and mitophagy through AMPK pathway, thus maintaining the integrity of the mitochondrial network.

The increasing prevalence and spread of antibiotic resistance genes (ARGs) in intensive aquaculture environments are of great concern to food safety and public health. However, the level of ARGs and their potential propagation factors in an industrial recirculating aquaculture system (RAS) have not previously been comprehensive explored. In this study, the levels of 14 different ARG markers and 2 kinds of mobile genetic elements (MGEs) were investigated in a RAS (including water, fish, feces, pellet feed meal, and biofilm samples) located northern China. qnrA, qnrB, qnrS, qepA, aac(6′)-Ib, and floR were dominant ARGs, which average concentration levels were presented at 4.51–7.74 copies/L and 5.36–13.07 copies/g, respectively, suggesting that ARGs were prevalent in RAS with no recorded history of antibiotic use. Elevated level of ARGs was found in water of RAS even after the final UV treatment compared with its influent. In RAS, Proteobacteria, Verrucomicrobia, Bacteroidetes, and Planctomycetes were the predominant phyla. Notably, elevated levels of potential opportunistic pathogens were observed along with abundant ARGs suggesting an increasing risk of capturing ARGs and MGEs for human pathogens. This study has revealed for the first time that reared fish, their feces, pellet feed meal as the introduction sources and the selection roles of treatment units co-driven the ARG profile, and the co-selection of water environmental factors and their consequently induced bacterial community shifts formed by their influence are the determining drivers for the ARG propagation in RAS.

No information is available on the long-term effects on thyroid and growth hormones of children exposed to phthalate-tainted products, despite the infamous 2011 Taiwan phthalate episode. We investigated estimated daily intake levels and their long-term effects on serum thyroid and growth hormone levels in children.We recruited 166 children (2–18 years old) in three visits who provided specimens and filled out a questionnaire from the Risk Assessment of Phthalate Incident in Taiwan (RAPIT) project study from 2012 to 2016. Morning spot urine samples were analyzed for nine phthalate metabolites. Serum thyroid (triiodothyronine [T₃], thyroxine [T₄], and free T₄) and growth hormone (insulin-like growth factor-1 [IGF-1] and its binding protein 3 [IGF-BP3]) levels were measured. A generalized estimating equation model was used to evaluate associations between phthalate metabolite levels and children’s thyroid and growth hormone levels.The median metabolite levels of monomethyl phthalate (MMP), Σdibutyl phthalate (DBP), and Σdi-(2-ethylhexyl) phthalate (DEHP) at visits 1, 2, and 3 were 6.59, 10.5, and 21.0 ng/mL, 0.15, 0.24, and 0.20 nmol/mL, and 0.15, 0.17, and 0.12 nmol/mL, respectively. After adjusting for potential confounding factors, we found that levels of urinary MMP were negatively associated with T₃ (β = −0.013, p = 0.047), T₄ (β = −0.016, p = 0.006), free T₄ (β = −0.012, p = 0.002), and IGF-BP3 (β = −0.025, p = 0.003). Urinary mono-ethyl phthalate (MEP) was negatively associated with IGF-1 (β = −0.027, p = 0.029) and IGF-BP3 (β = −0.016, p = 0.018). In addition, serum free T₄ was positively associated with urinary mono-2-ethyl-5-hydroxy hexyl phthalate (MEHHP) (β = 0.016, p = 0.043), mono-2-ethyl-5-oxohexyl phthalate (MEOHP) (β = 0.015, p = 0.024), and ΣDEHPm (β = 0.019, p = 0.020).Our findings support the hypothesis that specific phthalates disturb the hemostasis of thyroid and growth hormone levels in children exposed to phthalate-tainted products.