Silver nanoparticles (AgNPs) are known to exert adverse effects on both humans and aquatic organisms; however, the toxic mechanisms underlying these effects remain unclear. In this study, we investigated the toxic mechanisms of various AgNPs with different surface electrical properties in the freshwater algae Chlorella vulgaris using an advanced proteomics approach with Data-Independent Acquisition. Citrate-coated AgNPs (Cit-AgNPs) and polyethyleneimine-coated AgNPs (PEI-AgNPs) were selected as representatives of negatively and positively charged nanoparticles, respectively. Our results demonstrated that the AgNPs exhibited surface electrical property-dependent effects on the proteomic profile of C. vulgaris. In particular, the negatively charged Cit-AgNPs specifically regulated mitochondrial function-related proteins, resulting in the disruption of several associated metabolic pathways, such as those related to energy metabolism, oxidative phosphorylation, and amino acid synthesis. In contrast, the positively charged PEI-AgNPs primarily targeted ribosome function-related proteins and interrupted pathways of protein synthesis and DNA genetic information transmission. In addition, Ag⁺ ions released from the AgNPs had a significant influence on protein regulation and the induction of cellular stress. Collectively, our findings provide new insight into the surface electrical property-dependent proteomic effects of AgNPs on C. vulgaris and should improve our understanding of the toxic mechanisms of AgNPs in freshwater algae.

Humic-like substances (HULIS) are complex mixtures that are highly associated with brown carbon (BrC) and are important components of biomass burning (BB) emissions. In this study, we investigated the light absorption, emission factors (EFs), and amounts of HULIS emitted from the simulated burning of 27 types of regionally important rainforest biomass in Southeast Asia. We observed that HULIS had a high mass absorption efficiency at 365 nm (MAE₃₆₅), with an average value of 2.6 ± 0.83 m² g⁻¹ C. HULIS emitted from BB accounted for 65% ± 13% of the amount of water-soluble organic carbon (WSOC) and 85% ± 10% of the light absorption of WSOC at 365 nm. The EFs of HULIS from BB averaged 2.3 ± 2.1 g kg⁻¹ fuel, and the burning of the four vegetation subtypes (herbaceous plants, shrubs, evergreen trees, and deciduous trees) exhibited different characteristics. The differences in EFs among the subtypes were likely due to differences in lignin content in the vegetation, the burning conditions, or other factors. The light absorption characteristics of HULIS were strongly associated with the EFs. The annual emissions (minimum–maximum) of HULIS from BB in this region in 2016 were 200–371 Gg. Furthermore, the emissions from January to April accounted for 99% of the total annual emissions of HULIS, which is likely the result of the burning activities during this season. The most significant emission regions were Cambodia, Burma, Thailand, and Laos. This study, which evaluated emissions of HULIS by simulating open BB, contributes to a better understanding of the light-absorbing properties and regional budgets of BrC in this region.

Potassium (K⁺) is the most abundant cation in phytoplankton cells, but its impact on Microcystis aeruginosa (M. aeruginosa) has not been fully documented. This study presents evidence of how K⁺ availability affects the growth, oxidative stress and microcystin (MC) production of M. aeruginosa. The iTRAQ-based proteomic analysis revealed that during K⁺ deficiency, serious oxidative damage occurred and the photosynthesis-associated and ABC transporter-related proteins in M. aeruginosa were substantially downregulated. In the absence of K⁺, a 69.26% reduction in cell density was shown, and both the photosynthesis and iron uptake were depressed, which triggered a declined production of ATP and expression of MC synthetases genes (mcyA, B and D), and MC exporters (mcyH). Through the impairment of both the MC biosynthesis and MC transportation out of cells, K⁺ depletion caused an 85.89% reduction of extracellular MC content at the end of the study. However, with increasing in the available K⁺ concentrations, photosynthesis efficiency, the expression of ABC-transporter proteins, and the transcription of mcy genes displayed slight differences compared with those in the control group. This work represents evidence that K⁺ availability can regulate the physiological metabolic activity of M. aeruginosa and K⁺ deficiency leads to depressed growth and MC production in M. aeruginosa.

The toxicities of many environmental polycyclic aromatic hydrocarbons (PAHs), in particular those of high-molecular-weight PAHs (with MW higher than 300), remain poorly characterized. The objective of this study was to evaluate the ability of selected environmentally relevant PAHs with MW 302 (MW302 PAHs) to activate the aryl hydrocarbon receptor (AhR), since this represents a major toxic mode of action of PAHs. A large number of the evaluated compounds exhibited strong AhR-mediated activities, in particular in human models. The studied MW302 PAHs also significantly contributed to the overall calculated AhR activities of complex environmental mixtures, including both defined standard reference materials and collected diesel exhaust particles. The high AhR-mediated activities of representative MW302 PAHs, e.g. naphtho[1,2-k]fluoranthene, corresponded with the modulation of expression of relevant AhR target genes in a human lung cell model, or with the AhR-dependent suppression of cell cycle progression/proliferation in estrogen-sensitive cells. This was in a marked contrast with the limited genotoxicity of the same compound(s). Given the substantial levels of the AhR-activating MW302 PAHs in combustion particles, it seems important to continue to investigate the toxic modes of action of this large group of PAHs associated with airborne particulate matter.

Silver nanoparticles (AgNPs) are widely used in consumer products due to their antibacterial property; however, their potential toxicity and release into the environment raises concern. Based on the limited understanding of AgNPs aggregation behavior, this study aimed to investigate the toxicity of uncoated (uc-AgNP) and coated with polyvinylpyrrolidone (PVP-AgNP), at low concentrations (0.5–100 ng/mL), under dark and visible-light exposure, using a plant test system. We exposed Allium cepa seeds to both types of AgNPs for 4–5 days to evaluate several toxicity endpoints. AgNPs did not cause acute toxicity (i.e., inhibition of seed germination and root development), but caused genotoxicity and biochemical alterations in oxidative stress parameters (lipid peroxidation) and activities of antioxidant enzymes (superoxide dismutase and catalase) in light and dark conditions. However, the light exposure decreased the rate of chromosomal aberration and micronuclei up to 5.60x in uc-AgNP and 2.01x in PVP-AgNP, and 2.69x in uc-AgNP and 3.70x in PVP-AgNP, respectively. Thus, light exposure reduced the overall genotoxicity of these AgNPs. In addition, mitotic index alterations and morphoanatomical changes in meristematic cells were observed only in the dark condition at the highest concentrations, demonstrating that light also reduces AgNPs cytotoxicity. The light-dependent aggregation of AgNPs may have reduced toxicity by reducing the uptake of these NPs by the cells. Our findings demonstrate that AgNPs can be genotoxic, cytotoxic and induce morphoanatomical and biochemical changes in A. cepa roots even at low concentrations, and that visible-light alters their aggregation state, and decreases their toxicity. We suggest that visible light can be an alternative treatment to remediate AgNP residues, minimizing their toxicity and environmental risks.

A new derivatization reagent, 2,3,4,5,6-pentafluorobenzyl bromide (PFBBr), was employed to determine seven perfluoroalkyl carboxylic acids (PFCAs) simultaneously in tap water with gas chromatography-mass spectrometry (GC-MS) technique in this study. Firstly, seven PFCAs were derivatized to their corresponding esters under alkaline condition. The derivatization conditions including the amount of PFBBr and K₂CO₃, derivatization temperature and time were optimized to increase the derivatization efficiency. The 14 tap water samples collected from different places of China were enriched and purified through solid phase extraction pretreatment. The limits of detection (LODs) and the limits of quantitation (LOQs) ranged from 0.1 ng/L to 0.28 ng/L and from 0.3 ng/L to 0.84 ng/L, respectively. The new method offers a linear relationship in the range from 2 ng/L to 2000 ng/L, and the correlation coefficients ranged from 0.9938 to 0.9994. The results showed that GC-MS combined with pre-column derivatization is a reliable method for the analysis of PFCAs in the aqueous environment.

Particle-bound pollutants can pose a health risk to humans. Inhalation exposure evaluated by total contaminant concentrations significantly overestimates the potential risk. To assess the risk more accurately, bioavailability, which is the fraction that enters into the systemic circulation, should be considered. Researchers have replaced bioavailability by bioaccessibility due to the rapid and cost-efficient measurement for the latter, especially for assessment by oral ingestion. However, contaminants in particulates have different behavior when inhaled than when orally ingested. Some of the contaminants are exhaled along with exhalation, and others are deposited in the lung with the particulates. In addition, a fraction of the contaminants is released into the lung fluid and absorbed by the lung, and another fraction enters systemic circulation under the action of cell phagocytosis on particulates. Even if the release fraction, i.e., release bioaccessibility, is considered, the measurement faces many challenges. The present study highlights the factors influencing release bioaccessibility and the incorporation of inhalation bioaccessibility into the risk assessment of inhaled contaminants. Currently, there are three types of extraction techniques for simulated human lung fluids, including simple chemical solutions, sequential extraction techniques, and physiologically based techniques. The last technique generally uses three kinds of solution: Gamble’s solution, Hatch’s solution, and artificial lysosomal fluid, which are the most widely used physiologically based simulated human lung fluids. External factors such as simulated lung fluid composition, pH, extraction time, and sorption sinks can affect release bioaccessibility, whereas particle size and contaminant properties are important internal factors. Overall, release bioaccessibility is less used than bioaccessibility considering the deposition fraction when assessing the risk of contaminants in inhaled particulates. The release bioaccessibility measurement poses two main challenges: developing a unified, accurate, stable, simple, and systematic biologically based method, and validating the method through in-vivo assays.

Tricresyl phosphates (TCPs), as representative aromatic organophosphate flame retardants (OPFRs), have received much attention due to their potential neurotoxicity and endocrine-disrupting effects. However, the role of estrogen receptor α (ERα) and G protein-coupled estrogen receptor (GPER) in their estrogen disrupting effects remains poorly understood. Therefore, in this study, three TCP isomers, tri-o-cresyl phosphate (ToCP), tri-m-cresyl phosphate (TmCP) and tri-p-cresyl phosphate (TpCP), were examined for their activities on ERα by using two-hybrid yeast assay, and action on GPER by using Boyden chamber assay, cAMP production assay, calcium mobilization assay and molecular docking analysis. The results showed that three TCP isomers were found to act as ERα antagonists. Conversely, they had agonistic activity on GPER to promote GPER-mediated cell migration of MCF7 cells and SKBR3 cells. Both ToCP and TpCP activated GPER-mediated cAMP production and calcium mobilization, whereas TmCP had different mode of action, it only triggered GPER-mediated calcium mobilization, as evidenced by using the specific GPER inhibitor (G15) and GPER overexpressing experiments. Molecular docking further revealed that the way of interaction of TmCP and TpCP with GPER was different from that of ToCP with GPER, and higher activity of ToCP in activating GPER-mediated pathways might be associated with the alkyl substitution at the ortho position of the aromatic ring. Our results, for the first time, found a new target, GPER, for TCPs exerting their estrogen-disrupting effects, and demonstrated complex estrogen-disrupting effects of three TCP isomers involved their opposite activities toward ERα and GPER.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O₃, PM₂.₅, NO₂, and SO₂ exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O₃ exposures and significantly but positively associated with 2-week O₃ exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO₂ exposures, respectively. However, we did not find clear associations of PM₂.₅ and SO₂ exposure with proinflammatory cytokines and with MDA. The removal of an O₃-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O₃ for different time durations may affect systemic inflammatory responses in different ways.