Inorganic arsenic (iAs) is a naturally occurring metalloid present in drinking water and polluted air exposing millions of people globally. Epidemiological studies have linked iAs exposure to the development of numerous diseases including cognitive impairment, cardiovascular failure and cancer. Despite intense research, an effective therapy for chronic arsenicosis has yet to be developed. Laboratory studies have been of great benefit in establishing the pathways involved in iAs toxicity and providing insights into its mechanism of action. However, the in vivo analysis of arsenic toxicity mechanisms has been difficult by the lack of reliable in vivo biomarkers of iAs’s effects. To address this issue we have applied the use of our recently developed stress reporter models to study iAs toxicity. The reporter mice Hmox1 (oxidative stress/inflammation; HOTT) and p21 (DNA damage) were exposed to iAs at acute and chronic, environmentally relevant, doses. We observed induction of the oxidative stress reporters in several cell types and tissues, which was largely dependent on the activation of transcription factor NRF2. We propose that our HOTT reporter model can be used as a surrogate biomarker of iAs-induced oxidative stress, and it constitutes a first-in-class platform to develop treatments aimed to counteract the role of oxidative stress in arsenicosis. Indeed, in a proof of concept experiment, the HOTT reporter mice were able to predict the therapeutic utility of the antioxidant N-acetyl cysteine in the prevention of iAs associated toxicity.

Cadmium (Cd) is a toxic heavy metal that can be discharged into water environment through industrial activities, threatening the health of aquatic organisms and humans. MicroRNA (miRNA) plays an important role in the process of autophagy. The purpose of this experiment was to study the mechanism of Cd-induced autophagy in common carp hepatopancreas. We established a Cd poisoning model of common carp and explored ultrastructure, two oxidation indicators, three antioxidant indicators, miR-25-3p, two heat shock proteins (Hsps), and nine autophagy-related genes. The results confirmed that deleterious effect of Cd caused the injury of hepatopancreas and the appearance of hepatopancreas autophagic cells in common carp. At the same time, Cd exposure increased the contents of hydrogen peroxide (H₂O₂) and malonaldehyde (MDA), and decreased the activities of catalase (CAT), superoxide dismutase (SOD), and total antioxidative capacity (T-AOC), meaning that Cd caused oxidative stress via the imbalance between peroxide level and antioxidant capacity. Moreover, exposure to Cd increased mRNA expression of microtubule associated protein-1 light chain 3 beta (LC3-II), Dynein, Beclin 1, autophagy-related gene 5 (Atg5), and autophagy-related gene 12 (Atg12); and decreased mRNA expression of mechanistic target of rapamycin kinase (mTOR), indicating that excess Cd caused autophagy, and AMPK/mTOR/ULK1 signaling pathway took part in autophagy induced by Cd in common carp hepatopancreas. Furthermore, Cd down-regulated miR-25-3p and up-regulated its three target genes (AMPK, ULK1 as well as PTEN), suggesting that miR-25-3p mediated autophagy induced by Cd. In addition, we found that Hsps were activated via the up-regulation of Hsp70 and Hsp90. Moreover, oxidative stress mediated autophagy via Hsps in Cd-treated common carp hepatopancreas and Cd-induced autophagy was time dependent. In summary, miR-25-3p, oxidative stress, and Hsps participated in autophagy caused by Cd in common carp hepatopancreas. This study provided a new idea for the mechanism of Cd-induced autophagy in hepatopancreas.

Indoor air quality ((IAQ) in classrooms was associated with the daily exposure of school-age children who are particularly vulnerable to air pollutants exposure, while few data exist to evaluate classroom indoor air quality nationwide in China. The subsample of the CIEHS 2018 study was performed in 66 classrooms of 22 primary schools nationwide in China. Temperature, relative humidity, PM₂.₅, PM₁₀, CO₂, CO, formaldehyde concentrations, bacteria and fungi were detected in all classrooms by using the instruments that meet the specified accuracy. The ratios of indoor to outdoor (I/O) of PM₂.₅ were calculated in each classroom to identify whether the indoor environment the pollutants comes from outdoors. The indoor PM₂.₅, PM₁₀, CO, HCHO, bacteria and fungi GM concentration are 47.40 μg/m³, 72.91 μg/m³, 0.37 mg/m³, 0.02 mg/m³, 347.51 CFU/m³ and 362.76 CFU/m³, respectively. We observed that there were 66.5%, 52.6%, 22.4%, 1.8%, and 9.6% of the classrooms that exceeded the guideline values of PM₂.₅, PM₁₀, CO₂, HCHO, and bacteria, respectively. It should be attention that all of the classroom's PM₂.₅ concentrations in Shijiazhuang and Nanning, PM₁₀ concentrations in Nanning, CO₂ concentration in Lanzhou were exceeded the suggested values. Bacteria contamination in Shijiazhuang's classrooms is also serious. All classroom CO concentrations meet the requirement. The results indicated that classroom indoor PM₂.₅ was significantly positively correlated with indoor PM₁₀ and CO₂, while was negative correlated with temperature, CO, and fungi. Our results suggest that indoor air pollution in classrooms was a severe problem in Chinese primary schools. It is necessary to strengthen ventilation in the classroom to improve indoor air quality. What's more, a healthy learning environment should be created for primary school students.

Antibiotics are emerging pollutants in our environment. These treatments have been widely used for their low cost, convenient use, and prominent effects. However, the prolonged or excessive use of such drugs can cause toxicity in aquatic organisms. These effects include genotoxicity, metabolic alteration, delayed development and decreased immunity, which carry further risks for ecological systems. In the present study, juvenile common carp (Cyprinus carpio) were exposed to norfloxacin (NOR) for 42 days, with NOR concentrations ranging from 100 ng/L to 1 mg/L, to assess the effects of environmental concentrations of antibiotics, to investigate the effects of NOR on intestinal morphology, enzymatic activity, and transcriptomic levels of RNA in fish, as well as a risk assessment on human health was carried out. The results demonstrated that oxidative stress was induced, the barrier function of the intestine was damaged, and changes occurred in the expression of immune-related genes in fish chronically exposed to antibiotics. Moreover, NOR could affect the regulation of the NF-κB signaling pathway. Thus, environmental concentrations of antibiotics can influence the intestinal health of fish and potentially posing health risks to humans.

Twenty-five years after the first look at polycyclic aromatic compounds (PACs) in Canada, this article presents current knowledge on Canadian PAC emission sources. The analysis is based on national inventories (the National Pollutant Release Inventory (NPRI) and the Air Pollutant Emissions Inventory (APEI)), an analysis of Canadian forest fires, and several air quality model-ready emissions inventories. Nationally, forest fires continue to dominate PAC emissions in Canada, however there is uncertainty in these estimates. Though forest fire data show a steady average in the total annual area burned historically, an upward trend has developed recently. Non-industrial sources (home firewood burning, mobile sources) are estimated to be the second largest contributor (∼6-8 times lower than forest fires) and show moderate decreases (25%–65%) in the last decades. Industrial point sources (aluminum production, iron/steel manufacturing) are yet a smaller contributor and have seen considerable reductions (90% +) in recent decades. Fugitive emissions from other industrial sources (e.g. disposals by the non-conventional oil extraction and wastewater sectors, respectively) remain a gap in our understanding of total PAC emissions in Canada. Emerging concerns about previously unrecognized sources such as coal tar-sealed pavement run-off, climate change are discussed elsewhere in this special issue. Results affirm that observations at the annual/national scale are not always reflective of regional/local or finer temporal scales. When determining which sources contribute most to human and ecosystem exposure in various contexts, examination at regional and local scales is needed. There is uncertainty overall in emissions data stemming in part from various accuracy issues, limitations in the scope of the various inventories, and inventory gaps, among others.

In toxicology, standard sigmoidal concentration-response curves are used to predict effects concentrations and set chemical regulations. However, current literature also establishes the existence of complex, bimodal concentration-response curves, as is the case for arsenic toxicity. This bimodal response has been observed at the molecular level, but not characterized at the whole organism level. This study investigated the effect of arsenic (sodium arsenite) on post-gastrulated zebrafish embryos and elucidated effects of bimodal concentration-responses on different phenotypic perturbations.Six hour post fertilized (hpf) zebrafish embryos were exposed to arsenic to 96 hpf. Hatching success, mortality, and morphometric endpoints were evaluated both in embryos with chorions and dechorionated embryos. Zebrafish embryos exhibited a bimodal response to arsenic exposure. Concentration-response curves for exposed embryos with intact chorions had an initial peak in mortality (88%) at 1.33 mM arsenic, followed by a decrease in toxicity (~20% mortality) at 1.75 mM, and subsequently peaked to 100% mortality at higher concentrations. To account for the bimodal response, two distinct concentration-response curves were generated with estimated LC10 values (and 95% CI) of 0.462 (0.415, 0.508) mM and 1.69 (1.58, 1.78) mM for the ‘low concentration’ and ‘high concentration’ peaks, respectively. Other phenotypic analyses, including embryo length, yolk and pericardial edema all produced similar concentration-response patterns. Tests with dechorionated embryos also resulted in a bimodal toxicity response but with lower LC10 values of 0.170 (0.120, 0.220) mM and 0.800 (0.60, 0842) mM, respectively. Similarities in bimodal concentration-responses between with-chorion and dechorionated embryos indicate that the observed effect was not caused by the chorion limiting arsenic availability, thus lending support to other studies such as those that hypothesized a conserved bimodal mechanism of arsenic interference with nuclear receptor activation.

The mass, chemical composition and toxicological properties of fine particulates (PM₂.₅) emitted from cooking activities in three Hong Kong based restaurants and two simulated cooking experiments were characterized. Extracts from the PM₂.₅ samples elicited significant biological activities [cell viability, generation of reactive oxygen species (ROS), DNA damage and inflammation effect (TNF-α)] in a dose-dependent manner. The composition of PAHs, oxygenated PAHs (OPAHs) and azaarenes (AZAs) mixtures differed between samples. The concentration ranges of the Σ30PAHs, Σ17OPAHs and Σ4AZAs and Σ7Carbonyls in the samples were 9627–23,452 pg m⁻³, 503–3700 pg m⁻³, 33–263 pg m⁻³ and 158 – 5328 ng m⁻³, respectively. Cell viability caused by extracts from the samples was positively correlated to the concentration of benzo[a]anthracene, indeno[1,2,3-cd]pyrene and 1,4-naphthoquinone in the PM₂.₅ extracts. Cellular ROS production (upon exposure to extracts) was positively correlated with the concentrations of PM₂.₅, decaldehyde, acridine, Σ17OPAHs and 7 individual OPAHs. TNF-α showed significant positive correlations with the concentrations of most chemical species (elemental carbon, 16 individual PAHs including benzo[a]pyrene, Σ30PAHs, SO₄²⁻, Ca²⁺, Ca, Na, K, Ti, Cr, Mn, Fe, Cu and Zn). The concentrations of Al, Ti, Mn, Σ30PAHs and 8 individual PAHs including benzo[a]pyrene in the samples were positively correlated with DNA damage caused by extracts from the samples. This study demonstrates that inhalation of PM₂.₅ emitted from cooking could result in adverse human health effects.

Recent studies have shown that sub-lethal doses of herbicides may affect plant flowering, however, no study has established a direct relationship between the concentrations of deposited herbicide and plant flowering. Here the aim was to investigate the relationship between herbicide spray drift deposited on non-target plants and plant flowering in a realistic agro-ecosystem setting. The concentrations of the herbicide glyphosate deposited on plants were estimated by measuring the concentration of a dye tracer applied together with the herbicide. The estimated maximal and average deposition of glyphosate within the experimental area corresponded to 30 g glyphosate/ha (2.08% of the label rate of 1440 g a.i./ha) and 2.4 g glyphosate/ha (0.15% label rate), respectively, and the concentrations decreased rapidly with increasing distance from the spraying track. However, there were not a unique relation between distance and deposition, which indicate that heterogeneities of turbulence, wind speed and/or direction can strongly influence the deposition from 1 min to another during spraying. The effects of glyphosate on cumulative flower numbers and flowering time were modelled using Gompertz growth models on four non-target species. Glyphosate had a significantly negative effect on the cumulative number of flowers on Trifolium pratense and Lotus corniculatus, whereas there were no significant effects on Trifolium repens, and a positive, but non-significant, effect on number of flowers on Cichorium intybus. Glyphosate did not affect the flowering time of any of the four species significantly. Lack of floral resources is known to be of major importance for pollinator declines. The implications of the presented results for pesticide risk assessment are discussed.

To explore the performance of Streptomyces pactum (Act12) alone (A) and jointly with sulfur (SA) in the phytoextraction practice of potentially toxic elements (PTEs) (Cd and Zn), as well as their effects on soil chemical properties and microbial community composition, this paper selected potherb mustard (Brassica juncea, Coss.) as the test plant to assess the feedback of soil-plant ecosystems. Metal uptake values in lone Act12 treatments were higher than that of Act12 + sulfur treatments, and showed dose dependent with Act12 due to the higher biomass production. According to the biochemical analyses of rhizosphere soils, Act12 inoculation significantly increased urease (20.4%) and dehydrogenase (58.5%) while reducing alkaline phosphatase (68.0%) activity. The production of soil organic acids was, in descending order, formic acid > oxalic acid > malic acid > propionic acid and indicated a stimulated variation under treatments (SA > A > control). High-throughput sequencing revealed that bacterial community compositions were consistent in both phylum and genus taxonomies, while the final overall proportions were modified. The populations of the predominant phyla Proteobacteria and Bacteroidetes increased after sulfur application. The contribution of Act12 to the relative abundance of microbiota was minor compared to sulfur. Based on a redundancy analysis, soil chemical properties are the drivers of microbial activities and the main contributor to plant growth. Our results suggested Act12 inoculation may be part of an effective strategy enhancing phytoremediation of PTE-contaminated soils through chemical and biotic processes, and provided important implications for sustainable land utilization and crop production.