Nowadays, the ubiquitous distribution and increasing abundance of P⁺ᴵᴵᴵ in waterbodies have caused serious concerns regarding its bioavailability and potential toxicity. However, our knowledge on these issues is relatively limited. We addressed previously unknown effects of P⁺ᴵᴵᴵ on three dominate algae species i.e. Microcystic aeruginosa (M. aeruginosa), Chlorella pyrenoidesa (C. pyrenoidesa) and Cyclotella. sp in eutrophic waterbodies in China. Remarkable declines in biomass, specific growth rate and Chl-a of algae cells treated with 0.01–0.7 mg/L P⁺ᴵᴵᴵ as sole or an alternative P source were observed, indicating P⁺ᴵᴵᴵ had an inhibitory effect on the algal growth. Besides, the intracellular enzyme activities e.g superoxide dismutase (SOD) and malondialdehyde (MDA) were significantly increased with P⁺ᴵᴵᴵ stress. M. aeruginosa and Cyclotella. sp cells seemed to be more sensitive to P⁺ᴵᴵᴵ toxicity than C. pyrenoidesa since cell membrane suffered more serious stress and destruction. These findings combined, it confirmed P⁺ᴵᴵᴵ could not be utilized as bioavailable P, but had certain toxicity to the tested algae. It indicated that the increased P⁺ᴵᴵᴵ abundance in eutrophic waterbodies would accelerate the algal cell death, which could have a positive effect against algal blooms. Our results provide new insights into assessing the ecological risks of P⁺ᴵᴵᴵ in aquatic environments.

The adverse effects of fine atmospheric particulate matter with aerodynamic diameters of ≤2.5 μm (PM₂.₅) are closely associated with particulate chemicals. In this study, PM₂.₅ samples were collected from highway and industry sites in Hangzhou, China, during the autumn and winter, and their cytotoxicity and pulmonary toxicity and endocrine-disrupting potential (EDP) were evaluated in vitro and in vivo; the particulate polycyclic aromatic hydrocarbons (PAHs), phthalate esters (PAEs), and heavy metals were then characterized. The toxicological results suggested that the PM₂.₅ from highway site induced higher cytotoxicity (cell viability inhibition, intracellular oxidative stress, and cell membrane injury) and pulmonary toxicity (inflammatory response (IR) and oxidative stress (OS)) than the samples from industry site, while the PM₂.₅ from industry site exhibited higher EDP (estrogenic and anti-androgenic activity). The cytotoxicity and pulmonary toxicity of PM₂.₅ in the winter were higher than those in the autumn, while no seasonal difference in the endocrine-disrupting potential was observed (p > 0.05). The Pearson correlation analysis between the biological effects and particulate chemicals revealed that the PM₂.₅-induced inflammatory response and oxidative stress were closely associated with the particulate PAHs and heavy metals (Pearson correlation coefficients: rIR, PAHₛ = 0.822–0.988, rIR, ₕₑₐᵥy ₘₑₜₐₗₛ = 0.895–0.971, rOS, PAHₛ = 0.843–0.986, and rOS, ₕₑₐᵥy ₘₑₜₐₗₛ = 0.887–0.933), while particulate di (2-ethylhexyl)phthalate (DEHP) substantially contributed to the EDP of PM₂.₅ (rEDP, DEHP = 0.981). This study indicated that the toxicity and EDP of PM₂.₅ could vary with the surrounding environment and season, which was closely associated with the variations of particulate chemicals. Further studies are needed to clarify the associations between the harmful effects of PM₂.₅ and other contributing factors.

Wildfires are a complex environmental problem worldwide. The ashes produced during the fire bear metals and PAHs with high toxicity and environmental persistence. These are mobilized into downhill waterbodies, where they can impair water quality and human health. In this context, the present study aimed at assessing the toxicity of mimicked wildfire runoff to human skin cells, providing a first view on the human health hazardous potential of such matrices. Human keratinocytes (HaCaT) were exposed to aqueous extracts of ashes (AEA) prepared from ash deposited in the soil after wildfires burned a pine or a eucalypt forest stand. Cytotoxicity (MTT assay) and changes in cell cycle dynamics (flow cytometry) were assessed. Cell viability decreased with increasing concentrations of AEA, regardless of the ash source, the extracts preparation method (filtered or unfiltered to address the dissolved or the total fractions of contaminants, respectively) or the exposure period (24 and 48 h). The cells growth was also negatively affected by the tested AEA matrices, as evidenced by a deceleration of the progress through the cell cycle, namely from phase G0/G1 to G2. The cytotoxicity of AEA could be related to particulate and dissolved metal content, but the particles themselves may directly affect the cell membrane. Eucalypt ash was apparently more cytotoxic than pine ash due to differential ash metal burden and mobility to the water phase. The deceleration of the cell cycle can be explained by the attempt of cells to repair metal-induced DNA damage, while if this checkpoint and repair pathways are not well coordinated by metal interference, genomic instability may occur. Globally, our results trigger public health concerns since the burnt areas frequently stand in slopes of watershed that serve as recreation sites and sources of drinking water, thus promoting human exposure to wildfire-driven contamination.

The surface modifications of nanoparticles (NPs), are well-recognized parameters that affect the toxicity, while there has no study on toxicity of Al₂O₃ NPs with different surface modification. Therefore, for the first time, this study pays attention to evaluating the toxicity and potential mechanism of pristine Al₂O₃ NPs (p-Al₂O₃), hydrophilic (w-Al₂O₃) and lipophilic (o-Al₂O₃) modifications of Al₂O₃ NPs both in vitro and in vivo. Applied concentrations of 10, 20, 40, 80,100 and 200 μg/mL for 24 h exposure on Caenorhabditis elegans (C. elegans), while 100 μg/mL of Al₂O₃ NPs significantly decreased the survival rate. Using multiple toxicological endpoints, we found that o-Al₂O₃ NPs (100 μg/mL) could induce more severe toxicity than p-Al₂O₃ and w-Al₂O₃ NPs. After uptake by C. elegans, o-Al₂O₃ NPs increased the intestinal permeability, easily swallow and further destroy the intestinal membrane cells. Besides, cytotoxicity evaluation revealed that o-Al₂O₃ NPs (100 μg/mL) are more toxic than p-Al₂O₃ and w-Al₂O₃. Once inside the cell, o-Al₂O₃ NPs could attack mitochondria and induce the over-production of reactive oxygen species (ROS), which destroy the intracellular redox balance and lead to apoptosis. Furthermore, the transcriptome sequencing and RT-qPCR data also demonstrated that the toxicity of o-Al₂O₃ NPs is highly related to the damage of cell membrane and the imbalance of intracellular redox. Generally, our study has offered a comprehensive sight to the adverse effects of different surface modifications of Al₂O₃ NPs on environmental organisms and the possible underlying mechanisms.

Discharged carbon nanotubes (CNTs) likely interact with co-existing organic contaminants (OCs) and pose joint toxicity to environmental microbes. Herein, hydrophobic pentachlorophenol (PCP) and hydrophilic ciprofloxacin (CIP) were used as representative OCs and their joint toxicities with CNTs to Bacillus subtilis were systematically investigated at cellular, biochemical, and omics levels. The 3-h bacterial growth half inhibitory concentrations of CNTs, PCP, and CIP were 12.5 ± 2.6, 3.5 ± 0.5, and 0.46 ± 0.03 mg/L, respectively, and they all could damage cell membrane, increase intracellular oxidative stress, and alter bacterial metabolomics and transcriptomics; while CNTs-PCP and CNTs-CIP binary exposures exhibited distinct additive and synergistic toxicities, respectively. CNTs increased bacterial bioaccumulation of PCP and CIP via destabilizing and damaging cell membrane. PCP reduced the bioaccumulation of CNTs, while CIP had no significant effect; this difference could be owing to the different effects of the two OCs on cell-surface hydrophobicity and CNTs electronegativity. The additive toxicity outcome upon CNTs-PCP co-exposure could be a result of the balance between the increased toxicity from increased PCP bioaccumulation and the decreased toxicity from decreased CNTs bioaccumulation. The increased bioaccumulation of CIP contributed to the synergistic toxicity upon CNTs-CIP co-exposure, as confirmed by the increased inhibition of topoisomerase Ⅳ activity and interference in gene expressions regulating ABC transporters and lysine biosynthesis. The findings provide novel insights into environmental risks of CNTs.

Nicosulfuron is a sulfonylurea family herbicide which is commonly applied together with the triazine herbicide atrazine in agricultural practice. However, whether nicosulfuron can influence the biodegradation of atrazine is unclear. Therefore, the influence of nicosulfuron on atrazine removal as well as on cell viability and transcription of atrazine chlorohydrolase gene (trzN) in Arthrobacter sp. DNS10 was investigated in this study. Our results demonstrated that 76.0% of atrazine was degraded in the absence of nicosulfuron after 48h of culture, whereas 63.9, 49.1 and 42.6% was degraded in the presence of 1, 5, and 10 mg/L of nicosulfuron, respectively. Nicosulfuron also induced an increase in the level of intracellular reactive oxygen species (ROS), thereby damaging the cell membrane integrity and inhibiting the growth of the strain DNS10. Flow cytometry analysis revealed that the cell viability of strain DNS10 decreased with an increase in nicosulfuron concentration. The transcription of trzN in strain DNS10 exposed to the three described levels of nicosulfuron was 0.99, 0.72 and 0.52 times, respectively, that without nicosulfuron. In brief, nicosulfuron could inhibit atrazine removal efficiency by strain DNS10 by inducing the over-production of ROS which ultimately enhances the population of membrane-damaged cells, as well as reducing cell viability and trzN transcription. The outcomes of the present study provide new insights into the mechanism of nicosulfuron inhibition on atrazine biodegradation by strain DNS10.

Plastic materials are increasingly produced worldwide with a total estimated production of >8300 million tonnes to date, of which 60% was discarded. In the environment, plastics fragment into smaller particles, e.g. microplastics (size < 5 mm), and further weathering leads to the formation of functionally different contaminants – nanoplastics (size <1 μm). Nanoplastics are believed to have entirely different physical (e.g. transport), chemical (e.g. functional groups at the surface) and biological (passing the cell membrane, toxicity) properties compared to the micro- and macroplastics, yet, their measurement in the environmental samples is seldom available. Here, we present measurements of nanoplastics mass concentration and calculated the deposition at the pristine high-altitude Alpine Sonnblick observatory (3106 MASL), during the 1.5 month campaigh in late winter 2017. The average nanoplastics concentration was 46.5 ng/mL of melted surface snow. The main polymer types of nanoplastics observed for this site were polypropylene (PP) and polyethylene terephthalate (PET). We measured significantly higher concentrations in the dry sampling periods for PET (p < 0.002) but not for PP, which indicates that dry deposition may be the preferential pathway for PET leading to a gradual accumulation on the snow surfaces during dry periods. Air transport modelling indicates regional and long-range transport of nanoplastics, originating preferentially from European urban areas. The mean deposition rate was 42 (+32/-25) kg km⁻² year⁻¹. Thus more than 2 × 10¹¹ nanoplastics particles are deposited per square meter of surface snow each week of the observed period, even at this remote location, which raises significant toxicological concerns.

The present study aims to explore the bioaccumulation and biotic transformations of inorganic (iHg) and monomethyl mercury (MMHg) by natural pico-nanoplankton community from eutrophic lake Soppen, Switzerland. Pico-nanoplankton encompass mainly bacterioplankton, mycoplankton and phytoplankton groups with size between 0.2 and 20 μm. Species-specific enriched isotope mixture of ¹⁹⁹iHg and ²⁰¹MMHg was used to explore the accumulation, the subcellular distribution and transformations occurring in natural pico-nanoplankton sampled at 2 different depths (6.6 m and 8.3 m). Cyanobacteria, diatoms, cryptophyta, green algae and heterotrophic microorganisms were identified as the major groups of pico-nanoplankton with diatoms prevailing at deeper samples. Results showed that pico-nanoplankton accumulated both iHg and MMHg preferentially in the cell membrane/organelles, despite observed losses. The ratios between the iHg and MMHg concentrations measured in the membrane/organelles and cytosol were comparable for iHg and MMHg. Pico-nanoplankton demethylate added ²⁰¹MMHg (~4 and 12% per day depending on cellular compartment), although the involved pathways are to further explore. Comparison of the concentrations of ²⁰¹iHg formed from ²⁰¹MMHg demethylation in whole system, medium and whole cells showed that 82% of the demethylation was biologically mediated by pico-nanoplankton. No significant methylation of iHg by pico-nanoplankton was observed. The accumulation of iHg and MMHg and the percentage of demethylated MMHg correlated positively with the relative abundance of diatoms and heterotrophic microorganisms in the pico-nanoplankton, the concentrations of TN, Mg²⁺, NO₃⁻, NO₂⁻, NH₄⁺ and negatively with the concentrations of DOC, K⁺, Na⁺, Ca²⁺, SO₄²⁻. Taken together the results of the present field study confirm the role of pico-nanoplankton in Hg bioaccumulation and demethylation, however further research is needed to better understand the underlying mechanisms and interconnection between heterotrophic and autotrophic microorganisms.

In this study, we explored the influence of two metal oxide nanoparticles, nano CuO and nano ZnO (10, 50, 250 mg/kg), on accumulation of bifenthrin (100 μg/kg) in earthworms (Eisenia fetida) and its mechanism. The concentrations of bifenthrin in earthworms from binary exposure groups (bifenthrin + CuO and bifenthrin + ZnO) reached up to 23.2 and 28.9 μg/g, which were 2.65 and 3.32 times of that in bifenthrin exposure group without nanoparticles, respectively, indicating that nanoparticles facilitated the uptake of bifenthrin in earthworms. The contents of biomarkers (ROS, SOD, and MDA) in earthworms indicated that nanoparticles and bifenthrin caused damage to earthworms. Ex vivo test was utilized to investigate the toxic effects of the pollutants to cell membrane of earthworm coelomocytes and mechanism of increased bifenthrin accumulation. In ex vivo test, cell viability in binary exposure groups declined up to 30% and 21% compared to the control group after 24 h incubation, suggesting that coelomocyte membrane was injured by the pollutants. We conclude that nanoparticles damage the body cavity of earthworms, and thus lead to more accumulation of bifenthrin in earthworms. Our findings provide insights into the interactive accumulation and toxicity of nanoparticles and pesticides to soil organisms.

The synergistic cooperation of microbial cells and their extracellular polymeric substances (EPS) in biofilms is critical for the biofilm’s resistance to heavy metals and the migration and transformation of heavy metals. However, the effects of different components of biofilms have not been fully understood. In this study, the spatial distribution and speciation of copper in the colloidal EPS, capsular EPS, cell walls and membranes, and intracellular fraction of unsaturated Pseudomonas putida (P. putida) CZ1 biofilms were fully determined at the subcellular level. It was found that 60–67% of copper was located in the extracellular fraction of biofilms, with 44.7–42.3% in the capsular EPS. In addition, there was 15.5–20.1% and 17.2–21.2% of copper found in the cell walls and membranes or the intracellular fraction, respectively. Moreover, an X-ray absorption fine structure spectra analysis revealed that copper was primarily bound by carboxyl-, phosphate-, and hydrosulfide-like ligands within the extracellular polymeric matrix, cell walls and membranes, and intracellular fraction, respectively. In addition, macromolecule quantification, fourier-transform infrared spectroscopy spectra and sulfur K-edge x-ray absorption near edge structure analysis further showed the carboxyl-rich acidic polysaccharides in EPS, phospholipids in cell walls and cell membranes, and thiol-rich intracellular proteins were involved in binding of copper in the different components of biofilm. The full understanding of the distribution and chemical species of heavy metals in biofilms not only promotes a deep understanding of the interaction mechanisms between biofilms and heavy metals, but also contributes to the development of effective biofilm-based heavy metal pollution remediation technologies.