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.

About 11% of the global anthropogenic greenhouse gases (GHGs) emissions result from agricultural practices. Dairy manure (DM) application to soil is regarded as a best management practice due to C sequestration and improvement of soil physiochemical properties. However, GHGs emissions from the soil following the DM application could offset its advantages. Biochar (BC) is known to affect N transformation and GHGs emissions from soil. There had been considerably less focus on the BC amendment and its effects on GHGs emissions following DM application under field conditions. The objectives of this study were; i) to determine the temporal patterns and cumulative GHGs fluxes following DM and inorganic nitrogen (IN) application and, ii) to investigate BC amendment impact on DMY, GWP, direct N₂O emission factor (EFd) and the response of CH₄ emissions (RC) in DM based silage corn. To achieve these objectives a two-year field experiment was conducted with these treatments: 1) DM with high N conc. (DM₁: 0.37% N); 2) DM with low N conc. (DM₂: 0.13% N); 3) IN; 4) DM₁+BC; 5) DM₂+BC; 6) IN + BC; and 7) Control (N₀); and were laid out in randomized complete block design with four replications. BC amendment to DM₁, DM₂ and IN significantly reduced cumulative CO₂ emission by 16, 25.5 and 26.5%, CH₄ emission by 184, 200 and 293% and N₂O emission by 95, 86 and 93% respectively. It also reduced area-scaled and yield-scaled GWP, EFd, RC and enhanced DMY. Thus, BC application showed great potential to offset the negative effects of DM application i.e GHGs emissions from the silage corn cropping system. Further research is needed to evaluate soil organic carbon and nitrogen dynamics (substrates for GHG emissions) after DM and BC application on various soil types and cropping systems under field conditions.

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO₂ NPs (nTiO₂-A and nTiO₂-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO₂ stress via excess secretion and compositional variation, and nTiO₂-A induced more EPS secretion than nTiO₂-R at similar toxicity concentrations. The up-regulation of the Ca²⁺ signaling pathway might play a greater role in promoting EPS secretion under nTiO₂-R exposure compared with nTiO₂-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO₂-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO₂-A than nTiO₂-R to induce more EPS secretion. More serious membrane damage caused by nTiO₂-R than nTiO₂-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca²⁺ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO₂-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO₂ exposure and provide new insights into algal bio-responses to nTiO₂ exposure.

Though invertebrates are one of the largest groups of animal species in the sea and exhibit robust immune and neural responses that are crucial for their health and survival, the potential immunotoxicity and neurotoxicity of the most produced chemical bisphenol A (BPA), especially in conjunction with microplastics (MPs), still remain poorly understood in marine invertebrate species. Therefore, the impacts of exposure to BPA and MPs alone or in combination on a series of immune and neural biomarkers were investigated in the invertebrate bivalve species blood clam (Tegillarca granosa). Evident immunotoxicity as indicated by alterations in hematic indexes was observed after two weeks of exposure to BPA and MPs at environmentally realistic concentrations. The expression of four immune-related genes from the NFκB signaling pathway was also found to be significantly suppressed by the BPA and MP treatment. In addition, exposure to BPA and MPs led to an increase in the in vivo contents of three key neurotransmitters (GABA, DA, and ACh) but a decrease in the expression of genes encoding modulatory enzymes and receptors for these neurotransmitters, implying the evident neurotoxicity of BPA and MPs to blood clam. Furthermore, the results demonstrated that the toxic impacts exerted by BPA were significantly aggravated by the co-presence of MPs, which may be due to interactions between BPA and MPs as well as those between MPs and clam individuals.

Exposure to Aluminum oxide nanoparticles (Al₂O₃ NPs) has been associated with pulmonary inflammation in recent years; however, the underlying mechanism that causes adverse effects remains unclear. In the present study, we characterized microRNA (miRNA) expression profiling in human bronchial epithelial (HBE) cells exposed to Al₂O₃ NPs by miRNA microarray. Among the differentially expressed miRNAs, miR-297, a homologous miRNA in Homo sapiens and Mus musculus, was significantly up-regulated following exposure to Al₂O₃ NPs, compared with that in control. On combined bioinformatic analysis, proteomics analysis, and mRNA microarray, NF-κB-activating protein (NKAP) was found to be a target gene of miR-297 and it was significantly down-regulated in Al₂O₃ NPs-exposed HBE cells and murine lungs, compared with that in control. Meanwhile, inflammatory cytokines, including IL-1β and TNF-α, were significantly increased in bronchoalveolar lavage fluid (BALF) from mice exposed to Al₂O₃ NPs. Then we set up a mouse model with intranasal instillation of antagomiR-297 to further confirm that inhibition of miR-297 expression can rescue pulmonary inflammation via Notch pathway suppression. Collectively, our findings suggested that up-regulation of miR-297 expression was an upstream driver of Notch pathway activation, which might be the underlying mechanism involved in lung inflammation induced by exposure to Al₂O₃ NPs.

Microbial mercury (Hg) methylation transforms inorganic mercury to neurotoxic methylmercury (MeHg) mainly in aquatic anoxic environments. Sampling challenges in marine ecosystems, particularly in submarine canyons, leads to a lack of knowledge about the Hg methylating microbia in marine sediments. A previous study showed an enrichment of mercury species in sediments from the Capbreton Canyon where both geochemical parameters and microbial activities constrained the net MeHg production. In order to characterize Hg-methylating microbial communities from coastal to deeper sediments, we analysed the diversity of microorganisms’ (16S rDNA-based sequencing) and Hg methylators (hgcA based cloning and sequencing). Both, 16S rDNA and hgcA gene analysis demonstrated that the putative Hg-methylating prokaryotes were likely within the Deltaproteobacteria, dominated by sulfur-compounds based reducing bacteria (mainly sulfate reducers). Additionally, others clades were also identified as carrying HgcA gene, such as, Chloroflexi, Spirochaetes, Elusimicrobia, PVC superphylum (Plantomycetes, Verrucomicrobia and Chlamydiae) and Euryarchaea. Nevertheless, 61% of the hgcA sequences were not assigned to specific clade, indicating that further studies are needed to understand the implication of new microorganisms carrying hgcA in the Hg methylation in marine environments. These first results suggest that sulfur cycle drives the Hg-methylation in marine ecosystem.

The pollution of aquatic bodies by pharmaceutical compounds is an emerging environmental problem, with little explored consequences. Oxytetracycline (OTC) is an antibiotic used for treatment of infections caused by a variety of microorganisms and it is widely employed in medicine, livestock husbandry and aquaculture. This pharmaceutical compound may cause deleterious effects on non-target aquatic organisms as microalgae. The objective of this study was to evaluate the effects of OTC on growth, pigment content and morpho-physiology of the microalga Isochrysis galbana Parke. The results highlighted that OTC exposure inhibited the growth of I. galbana in cultures treated with OTC 5.0 and 10.0 mg/L after 3 days and in cultures treated with OTC 5.0, 7.5 and 10.0 mg/L after 5 days. Effects of OTC on cells ultrastructure and physiology consisted in large cytoplasmic lipid inclusions and in a decrease of photosynthetic pigments amount.

Pollutant gases and particulate matters (PM) from livestock facilities can affect the health of animals and farm workers and lead to great social environmental risks. This paper presents a comprehensive study on the characteristics of ammonia (NH₃), nitrogen oxides (NOₓ), sulfur dioxide (SO₂) and PM (including PM₂.₅ and PM₁₀) in a 100,000-bird manure-belt layer house in suburb Beijing for three typical seasons of summer, autumn and winter. Indoor air was sampled at an exhaust fan of the mechanically ventilated commercial house. The monitored indoor concentrations of NH₃, NOₓ, SO₂, PM₂.₅ and PM₁₀ were 3.7–5.0 mg m⁻³, 17–58 μg m⁻³, 0–11 μg m⁻³, 100–149 μg m⁻³ and 354–828 μg m⁻³, respectively. The indoor NH₃ concentrations were largely influenced by the manure removal frequency. The NOₓ and SO₂ were mainly sourced from the ambient air, and the NOₓ was also partly sourced from manure decomposition in summer. The indoor PM₂.₅ and PM₁₀ were largely sourced from the ambient air and the indoor manure, respectively. The abundant indoor NH₃ caused significantly higher NH₄⁺ concentration in the indoor PM₁₀ (7.98 ± 9.04 μg m⁻³) than that in the ambient PM₁₀ (3.48 ± 3.52 μg m⁻³). Secondary inorganic ions (SO₄²⁻, NO₃⁻ and NH₄⁺) totally contributed 5.7% and 14.6% to the indoor and ambient PM₂.₅, respectively; they contributed 2.8% and 8.9% to the indoor and ambient PM₁₀, respectively. Organic carbon was the main component of the PM and accounted for 26.6% and 41.5% of the indoor PM₂.₅ and PM₁₀, respectively. Heavy metal elements (Zn, Cu and Cr) were likely transported from feed to manure and finally accumulated in the PM. Given the high emission potential, the air pollutants from animal production suggested potential risks for human health.

This study presents evidence for microplastic contamination in two resident species of brachyuran crab from the Thames Estuary: the native shore crab, Carcinus maenas (Linneaus, 1758) and the invasive Chinese mitten crab, Eriocheir sinensis (H. Milne Edwards, 1853). The gills, gastric mill and intestine of 94 C. maenas and 41 E. sinensis were examined. Crabs were sampled periodically (ca. every three months) between December 2018 and October 2019. A total of 874 plastics were recovered, ranging 34 μm–34 mm in length. Overall, 71.3% and 100% of C. maenas and E. sinensis, respectively, contained at least one item (fibre, film, fragment or tangle of fibres) in the gill chamber, gastric mill or gastrointestinal tract. The most common items were fibres (78.5%) but in some cases, particularly in the gastric mill, these were aggregated into tangles (7.8%). Almost all E. sinensis contained tangles of fibres (95.1%), whereas, relatively few C. maenas contained similar tangles (10.6%).

Biodiesel is considered as a valuable and less toxic alternative to diesel. However, cellular and molecular effects of repeated exposure to biodiesel emissions from a recent engine equipped with a diesel particle filter (DPF) remain to be characterized. To gain insights about this point, the lung transcriptional signatures were analyzed for rats (n = 6 per group) exposed to filtered air, 30% rapeseed biodiesel (B30) blend or reference diesel (RF0), upstream and downstream a DPF, for 3 weeks (3 h/day, 5 days/week).Genomic analysis revealed a modest regulation of gene expression level (lower than a 2-fold) by both fuels and a higher number of genes regulated downstream the DPF than upstream, in response to either RF0 or to B30 exhaust emissions. The presence of DPF was found to notably impact the lung gene signature of rats exposed to B30. The number of genes regulated in common by both fuels was low, which is likely due to differences in concentrations of regulated pollutants in exhausts, notably for compound organic volatiles, polycyclic aromatic hydrocarbons, NO or NOx. Nevertheless, we have identified some pathways that were activated for both exhaust emissions, such as integrin-, IGF-1- and Rac-signaling pathways, likely reflecting the effects of gas phase products. By contrast, some canonical pathways relative to “oxidative phosphorylation” and “mitochondrial dysfunction” appear as specific to B30 exhaust emission; the repression of transcripts of mitochondrial respiratory chain in lung of rats exposed to B30 downstream of DPF supports the perturbation of mitochondria function.This study done with a recent diesel engine (compliant with the European IV emission standard) and commercially-available fuels reveals that the diesel blend composition and the presence of an after treatment system may modify lung gene signature of rats repeatedly exposed to exhaust emissions, however in a rather modest manner.