Brassinosteroids (BRs), a group of steroid phytohormones, are involved in multiple aspects of plant growth, development and stress responses. Despite recent studies on BRs-promoted pesticide metabolism in plants, the underlying mechanisms remain poorly understood. Here, we showed that 24-epibrassinolide (EBR) significantly enhanced the expression of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and H2O2 accumulation in the apoplast of chlorothalonil (CHT, a broad spectrum nonsystemic fungicide)-treated tomato plants. Silencing of RBOH1 significantly decreased the efficiency of EBR-induced CHT metabolism. Moreover, the EBR-induced upregulation in the transcripts of glutaredoxin gene GRXS16 was suppressed in RBOH1-silenced plants. Further studies indicated that silencing of GRXS16 compromised EBR-induced increases in glutathione content, activity of glutathione S-transferase (GST) and transcript of GST1, leading to an increase in CHT residue. By contrast, overexpression of tomato GRXS16 enhanced the basal levels of glutathione content and GST activity that eventually decreased CHT residues in transgenic plants. Our results reveal that BR-mediated induction of a modest oxidative burst is essential for the acceleration of glutathione-dependent pesticide metabolism via redox modulators, such as GRXS16. These findings shed new light on the mechanisms of BR-induced pesticide metabolism and thus have important implication in reducing pesticide residues in agricultural products.

Adverse effects of ambient fine particles (PM₂.₅) on sperm quality and oocyte fertilization have been identified by previous research. However, insufficient human studies tested associations between PM₂.₅ and decreased fertility rates.We associated long-term exposure to PM₂.₅ and county-level fertility rates reported by 2010 census across China. Exposure assessments were based on PM₂.₅ maps (2009–2010) with a spatial resolution of 0.1° derived from satellite remote sensing data from another published study. We used a Poisson regression to examine the relationship between PM₂.₅ and fertility rates with adjustment of potential confounders including county-level socioeconomic factors (e.g. sex ratio) and a spatially smoothed trend.We found that fertility rates were significantly decreased by 2.0% (95% confidence interval: 1.8%, 2.1%) per 10 μg/m³ increment of PM₂.₅. We also found a geographical variation of the associations.The study add to epidemiological evidences on adverse effects of PM₂.₅ on fertility rates.

Particulate matter with diameters <2.5 μm (i.e., PM₂.₅) has multiple natural and anthropological sources. The association between PM₂.₅ and the exacerbation of respiratory allergy and asthma has been well studied, but the components of PM₂.₅ that are responsible for allergies have not yet been determined. Here, we elucidated the effects of aqueous and organic extract of PM₂.₅ collected during four seasons in November 2014–December 2015 in two cities (Kawasaki, an industrial area and Fukuoka, an urban area affected by transboundary pollution matter) of Japan on respiratory health. Ambient PM₂.₅ was collected by high-volume air samplers and extracted into water soluble and lipid soluble components. Human airway epithelial cells, murine bone marrow-derived antigen-presenting cells (APC) and splenocytes were exposed to PM₂.₅ extracts. We measured the cell viability and release of interleukin (IL)-6 and IL-8 from airway epithelial cells, the DEC205 and CD86 expressions on APCs and cell proliferation, and TCR and CD19 expression on splenocytes. The water-soluble or aqueous extracts, especially those from Kawasaki in fall, had a greater cytotoxic effect than the lipid-soluble or organic extracts in airway epithelial cells, but they caused almost no pro-inflammatory response. Extract of fall, especially the aqueous extract from Fukuoka, increased the DEC205 and CD86 expressions on APC. Moreover, aqueous extracts of fall, summer, and spring from Fukuoka significantly increased proliferation of splenocytes. Organic extract of spring and summer from Kawasaki significantly elevated the TCR expression, and organic extract of summer from Kawasaki decreased the CD19 expression. These results suggest that PM₂.₅ extract samples are responsible for cytotoxicity in airway epithelial cells and for activating APCs and T-cells, which can contribute to the exacerbation of respiratory diseases such as asthma. These effects can differ by PM₂.₅ components, collection areas and seasons.

Identifying contamination sources of environmental media and revealing their changing trends over time is useful for regional contamination control and environmental improvements. Four sediment cores (S1−S4) were collected from the Shima River to determine lead (Pb) concentrations, geochemical fractions and isotopic compositions, as well as the geochronology of core S3. The results show that Pb concentrations decreased from the upper and middle reach sites (means: 57.6, 95.9, and 97.6 mg kg⁻¹, respectively) to the lower reach site (43.8 mg kg⁻¹), resulting in a minimal to moderate enrichment in the sediments; enrichment increased due to anthropogenic Pb inputs at the river middle reach site since the 1990s. Sediment Pb in the geochemical fractions followed a decreasing order of reducible (47.3%) > residual (37.8%) > oxidizable (11.2%) > acid-soluble fraction (3.68%), exhibiting high mobility, further verifying the anthropogenic inputs. A descending trend in the ²⁰⁶Pb/²⁰⁷Pb ratio of the top sediments was the result of anthropogenic activities. In the present study, coal combustion, which was the major anthropogenic Pb source determined by its isotopic composition, contributed significantly (means: 18.4–60.6%) to sediment Pb based on a three end-members model. Less of a contribution (0–10.6%) was derived from vehicle exhaust. The increasing trend in the coal contribution was in accordance with that of the coal consumption in the study area. These results suggest that Pb contamination resulting from coal combustion has grown to become a major environmental issue in the study area.

Exposure to pesticides results in DNA damage and genomic instability. We previously predicted that endosulfan might be associated with leukemia, but the role of endosulfan in leukemia cells has been unexplored. The aim of this study is to elucidate molecular mechanism of endosulfan-induced DNA damage response in human leukemia cells. We performed endosulfan exposure experiments in K562 cells with varying concentrations of endosulfan for 48 h and found that endosulfan lowered cell viability in a dose-dependent manner. We observed the dramatic DNA damage using comet assay and the increase of micronucleus in 75 μM endosulfan-exposed cells. Endosulfan at 75 μM caused the expression alterations of ATM and DNA repair genes such as FANCD2, and BRCA1/2 at different exposure time points (12, 24, 48 h), which was reversed by ATM inhibitor KU-55933. Endosulfan significantly increased the mRNA expression levels of p53 and GADD45A, and decreased PCNA and XRCC2 at 48 h after exposure. Flow cytometric analysis showed that endosulfan at 50 and 75 μM induced cell cycle G1 arrest, a response attributed to down-regulation of CDK6 and up-regulation of p21. We also observed that endosulfan at 50 and 75 μM induced a considerable percentage of cells to undergo apoptosis, as detected by Annexin-V binding assays. Endosulfan resulted in the activation of caspase-3, and elevated the expression levels of PUMA and the ratio of BAX/Bcl-2. These findings suggest that endosulfan caused DNA damage response throughATM-p53 signaling pathway, implicating the potential correlation between endosulfan and leukemia.

In Part II of this work we present the results of the downscaled offline Weather Research and Forecasting/Community Multiscale Air Quality (WRF/CMAQ) model, included in the “Technology Driver Model” (TDM) approach to future U.S. air quality projections (2046–2050) compared to a current-year period (2001–2005), and the interplay between future emission and climate changes. By 2046–2050, there are widespread decreases in future concentrations of carbon monoxide (CO), nitrogen oxides (NOx = NO + NO2), volatile organic compounds (VOCs), ammonia (NH3), sulfur dioxide (SO2), and particulate matter with an aerodynamic diameter ≤ 2.5 μm (PM2.5) due mainly to decreasing on-road vehicle (ORV) emissions near urban centers as well as decreases in other transportation modes that include non-road engines (NRE). However, there are widespread increases in daily maximum 8-hr ozone (O3) across the U.S., which are due to enhanced greenhouse gases (GHG) including methane (CH4) and carbon dioxide (CO2) under the Intergovernmental Panel on Climate Change (IPCC) A1B scenario, and isolated areas of larger reduction in transportation emissions of NOx compared to that of VOCs over regions with VOC-limited O3 chemistry. Other notable future changes are reduced haze and improved visibility, increased primary organic to elemental carbon ratio, decreases in PM2.5 and its species, decreases and increases in dry deposition of SO2 and O3, respectively, and decreases in total nitrogen (TN) deposition. There is a tendency for transportation emission and CH4 changes to dominate the increases in O3, while climate change may either enhance or mitigate these increases in the west or east U.S., respectively. Climate change also decreases PM2.5 in the future. Other variable changes exhibit stronger susceptibility to either emission (e.g., CO, NOx, and TN deposition) or climate changes (e.g., VOC, NH3, SO2, and total sulfate deposition), which also have a strong dependence on season and specific U.S. regions.

Dinotefuran, as the latest generation of neonicotinoid insecticide, has broad application prospects around the world. However, dinotefuran is easily metabolized and the two main metabolites are 1-methyl-3-(tetrahydro-3-furylmethyl) urea (UF) and 1-methyl-3-(tetrahydro-3-furylmethyl) guanidium dihydrogen (DN). In the present study, the risks of UF and DN in soil on typical non-target species earthworm were investigated. In the same time, the degradation in soil and accumulation in earthworms of UF and DN were monitored. The present results showed that the toxicities of UF and DN were similar in their effect on earthworms and they were supertoxic pollutants to earthworms. The degradation trend in soil and accumulation trend in earthworms of UF and DN were consistent throughout the whole exposure period. At 1.0 mg/kg and 2.0 mg/kg, UF and DN could induce the excess production of ROS, resulting in oxidative stress effects in earthworm cells. The excess ROS induce changes in antioxidant enzyme activities, damage in biomacromolecules, and abnormal expression of function genes. The present results showed that UF and DN may have high risks for earthworms.

During the last years, declines in honey bee colonies are being registered worldwide. Cholinergic pesticides and their extensive use have been correlated to the decline of pollinators and there is evidence that pesticides act as neuroendocrine disruptors affecting the metabolism of neuropeptides. However, there is a big absence of studies with quantitative results correlating the effect of pesticide exposure with changes on neuropeptides insects, and most of them are conducted under laboratory conditions, typically with individual active ingredients. In this study, we present an analytical workflow to evaluate pesticide effects on honey bees through the analysis of (neuro)peptides. The workflow consists of a rapid extraction method and liquid chromatography with triple quadrupole for preselected neuropeptides. For non-target analysis, high resolution mass spectrometry, multivariate analysis and automatic identification of discriminated peptides using a specific software and protein sequence databases. The analytical method was applied to the analysis of target and non-target (neuro)peptides in honey bees with low and high content of a wide range of pesticides to which have been exposed in field conditions. Our findings show that the identification frequency of target neuropeptides decreases significantly in honey bees with high concentration of pesticides (pesticide concentrations ≥ 500 μg kg⁻¹) in comparison with the honey bees with low content of pesticides (pesticide concentrations ≤ 20 μg kg⁻¹). Moreover, the principal component analysis in non-target search shows a clear distinction between peptide concentration in honey bees with high level of pesticides and honey bees with low level. The use of high resolution mass spectrometry has allowed the identification of 25 non-redundant peptides responsible for discrimination between the two groups, derived from 18 precursor proteins.

This study assessed the environmental risk on coastal ecosystems posed by three phenolic compounds of special environmental and human health concern used in plastics and household products: bisphenol A (BPA), triclosan (TCS) and 4-nonylphenol (4-NP). These three chemicals are among the organic contaminants most frequently detected in wastewater. The most toxic compound tested was 4-NP, with 10% effective concentration at 11.1 μg L⁻¹ for Isochrysis galbana, 110.5 μg L⁻¹ for Mytilus galloprovincialis, 53.8 μg L⁻¹ for Paracentrotus lividus, and 29.0 μg L⁻¹ for Acartia clausi, followed by TCS (14.6 μg L⁻¹ for I. galbana, 149.8 μg L⁻¹ for M. galloprovincialis, 129.9 μg L⁻¹ for P. lividus, and 64.8 μg L⁻¹ for A. clausi). For all species tested, BPA was the less toxic chemical, with toxicity thresholds ranging between 400 and 1200 μg L⁻¹ except for A. clausi nauplii (186 μg L⁻¹). The relatively narrow range of variation in toxicity considering the broad physiological differences among the biological models used point at non-selective mechanisms of toxicity for these aromatic organics. Microalgae, the main primary producers in pelagic ecosystems, showed particularly high susceptibility to the chemicals tested. When the toxicity thresholds experimentally obtained were compared to the maximum environmental concentrations reported in coastal waters, the risk quotients obtained correspond to very low or low risk for BPA and TCS, and from low to high for 4-NP.