Mining causes extensive damage to aquatic ecosystems via acidification, heavy metal pollution, sediment loading, and Ca decline. Yet little is known about the effects of mining on freshwater systems in the Southern Hemisphere. A case in point is the region of western Tasmania, Australia, an area extensively mined in the 19th century, resulting in severe environmental contamination. In order to assess the impacts of mining on aquatic ecosystems in this region, we present a multiproxy investigation of the lacustrine sediments from Owen Tarn, Tasmania. This study includes a combination of radiometric dating (¹⁴C and ²¹⁰Pb), sediment geochemistry (XRF and ICP-MS), pollen, charcoal and diatoms. Generalised additive mixed models were used to test if changes in the aquatic ecosystem can be explained by other covariates. Results from this record found four key impact phases: (1) Pre-mining, (2) Early mining, (3) Intense mining, and (4) Post-mining. Before mining, low heavy metal concentrations, slow sedimentation, low fire activity, and high biomass indicate pre-impact conditions. The aquatic environment at this time was oligotrophic and dystrophic with sufficient light availability, typical of western Tasmanian lakes during the Holocene. Prosperous mining resulted in increased burning, a decrease in landscape biomass and an increase in sedimentation resulting in decreased light availability of the aquatic environment. Extensive mining at Mount Lyell in the 1930s resulted in peak heavy metal pollutants (Pb, Cu and Co) and a further increase in inorganic inputs resulted in a disturbed low light lake environment (dominated by Hantzschia amphioxys and Pinnularia divergentissima). Following the closure of the Mount Lyell Co. in 1994 CE, Ca declined to below pre-mining levels resulting in a new diatom assemblage and deformed diatom valves. Therefore, the Owen Tarn record demonstrates severe sediment pollution and continued impacts of mining long after mining has stopped at Mt. Lyell Mining Co.

Hydroponic experiments were conducted to study the effects of microplastic particles of polystyrene (PS) and polytetrafluoroethylene (PTFE) on arsenic (As) content in leaves and roots of rice seedlings, and the changes in root vigor and physiological and biochemical indicators under single or combined PS and PTFE with As(III) treatment. Rice biomass decreased with increasing concentrations of PS, PTFE, and As(III) in the growth medium. The highest root (leaf) biomass decreases were 21.4% (10.2%), 25.4% (11.8%), and 26.2% (16.2%) with the addition of 0.2 g L⁻¹ PS, 0.2 g L⁻¹ PTFE, and 4 mg L⁻¹ As(III), respectively. Microplastic particles and As(III) inhibited biomass accumulation by inhibiting root activity and RuBisCO activity, respectively. The addition of As(III) and microplastic particles (PS or PTFE) inhibited photosynthesis through non-stomatal and stomatal factors, respectively; furthermore, net photosynthetic rate, chlorophyll fluorescence, and the Chl a content of rice were reduced with the addition of As(III) and microplastic particles (PS or PTFE). Microplastic particles and As(III) induced an oxidative burst in rice tissues through mechanical damage and destruction of the tertiary structure of antioxidant enzymes, respectively, thereby increasing O₂⁻ and H₂O₂ in roots and leaves, inducing lipid peroxidation, and destroying cell membranes. When PS and PTFE were added at 0.04 and 0.1 g L⁻¹, respectively, the negative effects of As(III) on rice were reduced. Treatment with 0.2 g L⁻¹ PS or PTFE, combined with As(III), had a higher impact on rice than the application of As(III) alone. PS and PTFE reduced As(III) uptake, and absorbed As decreased with the increasing concentration of microparticles. The underlying mechanisms for these effects may involve direct adsorption of As, competition between As and microplastic particles for adsorption sites on the root surface, and inhibition of root activity by microplastic particles.

Chromium (Cr) is an internationally recognized carcinogenic hazard that causes serious pulmonary toxicity. However, Cr-induced pulmonary toxicity lacks effective treatment to date. Sulforaphane (SFN), a well-known organosulfur compound, has gained increasing attention because of its unique biological function. This study investigates if SFN could decrease K₂Cr₂O₇-induced pulmonary toxicity and a potential mechanism involved using a rat 35-day Cr-induced pulmonary toxicity model and the mouse alveolar type II epithelial cell line (MLE-12). The results showed that SFN prevented Cr-induced oxidative stress, histopathological lesions, inflammation, apoptosis, and changes in protein kinase B (Akt) and glycogen synthase kinase 3 beta (GSK-3β) levels in vivo and in vitro. However, SFN can not play the protective effect against K₂Cr₂O₇-induced cell injury after treating by an Akt-specific inhibitor (MK-2206 2HCl) in MLE-12 cells. Furthermore, SFN increased the expression of nuclear factor-E2-related factor-2 (Nrf2) phase II detoxification enzymes. Collectively, this study demonstrates that SFN prevents K₂Cr₂O₇-induced lung toxicity in rats through enhancing Nrf2-mediated exogenous antioxidant defenses via activation of the Akt/GSK-3β/Fyn signaling pathway. SFN may be a novel natural substance to cure Cr-induced lung toxicity.

Microplastics are plastic fragments of particle sizes less than 5 mm, which are widely distributed in marine and terrestrial environments. In this study, earthworms Eisenia fetida were exposed to 100 and 1000 μg of 100 nm and 1300 nm fluorescent polystyrene microplastics (PS-MPs) per kg of artificial soil for 14 days. Uptake or accumulation of PS-MPs in earthworm intestines, histopathological changes, oxidative stress, and DNA damage were assessed to determine the toxicological effects of PS-MPs on E. fetida. The results showed that the average accumulated concentrations in the earthworm intestines were higher for 1300 nm PS-MPs (0.084 ± 0.005 and 0.094 ± 0.003 μg/mg for 100 and 1000 μg/kg, respectively) than for 100 nm PS-MPs (0.015 ± 0.001 and 0.033 ± 0.002 μg/mg for 100 and 1000 μg/kg, respectively). In addition, histopathological analysis indicated that the intestinal cells were damaged after exposure to PS-MPs. Furthermore, PS-MPs significantly changed glutathione (GSH) level and superoxide dismutase (SOD) activity. The GSH levels were 86.991 ± 7.723, 165.436 ± 4.256–167.767 ± 18.642, and 93.590 ± 4.279–173.980 ± 15.523 μmol/L in the control, 100 nm, and 1300 nm PS-MPs treatment groups. In addition, the SOD activities were 10.566 ± 0.621, 9.039 ± 0.787–9.408 ± 0.493, and 7.959 ± 0.422–9.195 ± 0.327 U/mg protein for the control, 100 nm, and 1300 nm PS-MPs treatment groups, respectively, indicating that oxidative stress was induced after PS-MPs exposure. Furthermore, the comet assay suggested that exposure to PS-MPs induced DNA damage in earthworms. Overall, 1300 nm PS-MPs showed more toxic effect than 100 nm PS-MPs on earthworms. These findings provide new insights regarding the toxicological effects of low concentrations of microplastics on earthworms, and on the ecological risks of microplastics to soil animals.

Knowledge of arsenic (As) levels in gold (Au) mining areas in the Amazon is critical for determining environmental risks and the health of the local population, mainly because this region has the largest mineral potential in Brazil and one of the largest in the world. The objective of this study was to assess the environmental and human health risks of As in tailings from Au exploration in the eastern Amazon. Samples were collected from soils and tailings from different exploration forms from 25 points, and the total concentration, pollution indexes and human health risk were determined. Concentrations of As were very high in all exploration areas, especially in tailings, whose maximum value reached 10,000 mg kg⁻¹, far above the investigation value established by the Brazilian National Council of the Environment, characterizing a polluted area with high environmental risk. Exposure based on the daily intake of As demonstrated a high health risk for children and adults, whose non-carcinogenic risk indexes of 17.8, extremely above the acceptable limit (1.0) established by the United States Environmental Protection Agency. High levels of As in reactive fractions in underground, cyanidation, and colluvium mining areas, as well as extremely high gastric and intestinal bioaccessibility were found, suggesting that high levels may be absorbed by the local population. The results show that the study area is highly polluted through Au mining activities, putting the environment and population health at risk, and that there is an urgent need for intervention by the environmental control agencies for remediation.

The widespread presence of microplastics in global aquatic ecosystems has aroused growing concern about the potential impacts of microplastics on aquatic biota. In marine and freshwater environments, microplastics are distributed pervasively within water bodies from the upper water column to the bottom layer, making them available to a large variety of aquatic organisms that inhabit different locations. The ingestion of microplastic particles may cause harm to aquatic organisms. Although China’s aquatic environments have been seriously polluted by microplastics, the impacts of microplastics on aquatic biota remain to be elucidated. This review summarizes the current state of knowledge about microplastic pollution in aquatic biota in China; specifically, the concentration and characteristics of microplastic particles in aquatic organisms from both seawater and freshwater environments are discussed. The results showed that various aquatic organisms in China have been found to consume microplastics. The average number of microplastic pieces discovered in biota ranged from 0.07 particles to 164 particles per individual in different organisms. The most frequently observed colors of microplastics detected in biota were blue and transparent, and the detected microplastics mainly consisted of fibers. In addition, the impacts of microplastics on aquatic organisms, including physical impacts, chemical impacts, the trophic transfer of microplastics and the potential risks to humans, were discussed. Finally, knowledge gaps were identified in order to guide future studies.

Di(2-ethylhexyl) phthalate (DEHP), the most extensively used plasticizer in plastic formulations, is categorized as a priority environmental contaminant with carcinogenic, teratogenic, and mutagenic toxicities. Many isolated microorganisms exhibit outstanding performance as pure cultures in the laboratory but are unable to cope with harsh environmental conditions in the field. In the present study, a microbial consortium (CM9) with efficient functionality was isolated from contaminated farmland soil. CM9 could consistently degrade 94.85% and 100.00% of DEHP (1000 mg/L) within 24 h and 72 h, respectively, a higher efficiency than those of other reported pure and mixed microorganism cultures. The degradation efficiencies of DEHP and di-n-butyl phthalate were significantly higher than those of dimethyl phthalate and diethyl phthalate (p < 0.05). The primary members of the CM9 consortium were identified as Rhodococcus, Niabella, Sphingopyxis, Achromobacter, Tahibacter, and Xenophilus. The degradation pathway was hypothesized to include both de-esterification and β-oxidation. In contaminated soil, bioaugmentation with CM9 and biochar markedly enhanced the DEHP removal rate to 87.53% within 42 d, compared to that observed by the indigenous microbes (49.31%) (p < 0.05). During simulated bioaugmentation, the dominant genera in the CM9 consortium changed significantly over time, indicating their high adaptability to soil conditions and contribution to DEHP degradation. Rhodococcus, Pigmentiphaga and Sphingopyxis sharply decreased, whereas Tahibacter, Terrimonas, Niabella, Unclassified_f_Caulobacteraceae, and Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium showed considerable increases. These results provide a theoretical framework for the development of in situ bioremediation of phthalate (PAE)-contaminated soil by composite microbial inocula.

The m-aminophenol (m-AP) is a widely used industrial chemical, which enters water, soils, and sediments with waste emissions. A common soil metal oxide, birnessite (δ-MnO2), was found to mediate the transformation of m-AP with fast rates under acidic conditions. Because of the highly complexity of the m-AP transformation, mechanism-based models were taken to fit the transformation kinetic process of m-AP. The results indicated that the transformation of m-AP with δ-MnO2 could be described by precursor complex formation rate-limiting model. The oxidative transformation of m-AP on the surface of δ-MnO2 was highly dependent on reactant concentrations, pH, temperature, and other co-solutes. The UV-VIS absorbance and mass spectra analysis indicated that the pathway leading to m-AP transformation may be the polymerization through the coupling reaction. The m-AP radicals were likely to be coupled by the covalent bonding between unsubstituted C2, C4 or C6 atoms in the m-AP aromatic rings to form oligomers as revealed by the results of activation energy and mass spectra. Furthermore, the toxicity assessment of the transformation productions indicated that the toxicity of m-AP to the E. coli K-12 could be reduced by MnO2 mediated transformation. The results are helpful for understanding the environmental behavior and potential risk of m-AP in natural environment.

The industrial and agricultural activities based on phosphorous can increase the F content in the surrounding area, causing a widespread adverse effect on the organisms. However, the current information on the superposed health risk posed by the multi-exposure to the F contamination in an area jointly affected by agricultural and industrial activities (DA) is limited. Herein, the F distribution in multi-environmental media and the exposure risk to humans by ingestion, inhalation, and dermal contact pathways are studied in an DA. The content of soil water-soluble fluorine (WF) was higher in the DA than in the area individually affected by agricultural activities (SA). This indicated a superposed contribution of the industrial and agricultural activities to increase the F toxicity in the soil. The correlation of the soil pH and the organic matter content with the soil WF concentration in DA suggested an inter-relationship between the soil physicochemical properties and the toxicity of F in the soil by industrial and agricultural activities. Irrigation water was not a major anthropogenic source of the cropland soil F. The large variation in F concentration in the crops (101.8–195.6%) might have originated from the discrepancies in the soil F content and air F concentration. The air F pollution (0.6–1.6 μg dm⁻² d⁻¹) in the area particularly influenced by intensive industrial activities should be important. The exposure of residents to F was mainly from the ingestion of F-enriched crops. The higher exposure of adults to F than that of children could be attributed to more industrial and agricultural outdoor activities, larger exposure area of the skin, and more daily ingestion of F-enriched food by adults. Overall, present insights into the distribution of and the multi-exposure to F may be beneficial for decreasing the adverse F effects on the residents in DAs worldwide.

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.