Mercury (Hg), a potent neurotoxic element, can biomagnify through food webs once converted into methylmercury (MeHg). Some studies have found that selenium (Se) exposure may reduce MeHg bioaccumulation and toxicity, though this pattern is not universal. Se itself can also be toxic at elevated levels. We experimentally manipulated the relative concentrations of dietary MeHg and Se (as selenomethionine [SeMet]) for an aquatic grazer (the mayfly, Neocloeon triangulifer) and its food source (diatoms). Under low MeHg treatment (0.2 ng/L), diatoms exhibited a quadratic pattern, with decreasing diatom MeHg concentration up to 2.0 μg Se/L and increasing MeHg accumulation at higher SeMet concentrations. Under high MeHg treatment (2 ng/L), SeMet concentrations had no effect on diatom MeHg concentrations. Mayfly MeHg concentrations and biomagnification factors (concentration of MeHg in mayflies: concentration of MeHg in diatoms) declined with SeMet addition only in the high MeHg treatment. Mayfly MeHg biomagnification factors decreased from 5.3 to 3.3 in the high MeHg treatment, while the biomagnification factor was constant with an average of 4.9 in the low MeHg treatment. The benefit of reduced MeHg biomagnification was offset by non-lethal effects and high mortality associated with ‘protective’ levels of SeMet exposure. Mayfly larvae escape behavior (i.e., startle response) was greatly reduced at early exposure days. Larvae took nearly twice as long to metamorphose to adults at high Se concentrations. The minimum number of days to mayfly emergence did not differ by SeMet exposure, with an average of 13 days. We measured an LC50SₑMₑₜ for mayflies of 3.9 μg Se/L, with complete mortality at concentrations ≥6.0 μg Se/L. High reproductive mortality occurred at elevated SeMet exposures, with only 0–18% emergence at ≥4.12 μg Se/L. Collectively, our results suggest that while there is some evidence that Se can reduce MeHg accumulation at the base of the food web at specific exposure levels of SeMet and MeHg, Se is also toxic to mayflies and could lead to negative effects that extend across ecosystem boundaries.

Despite being effective in controlling mosquito larvae and a few other target organisms, the application of insecticides into aquatic systems may cause unintended alterations to the physiology or behavioral responses of several aquatic non-target organisms, which can ultimately lead to their death. Here, we firstly evaluated whether the susceptibility of the giant water bug, Belostoma anurum (Hemiptera: Belostomatidae), a predator of mosquito larvae, to pyriproxyfen would be similar to that of its potential prey, larvae of Aedes aegypti (Diptera: Culicidae). Secondly, we recorded the nominal concentrations of pyriproxyfen in water and evaluated whether sublethal exposures would lead to physiological or behavioral alterations on the B. anurum nymphs. We characterized the activities of three major families of detoxification enzymes (i.e., cytochrome P450 monooxygenases, glutathione-S-transferase, and general esterases) and further evaluated the abilities of pyriproxyfen sublethally-exposed B. anurum to prey upon A. aegypti larvae at different prey densities. Our findings revealed that nominal pyriproxyfen concentration significantly decreased (approximately 50%) over the first 24 h. Furthermore, when applied at the concentration of 10 μg a.i./L, pyriproxyfen was approximately four times more toxic to A. aegypti larvae (LT₅₀ = 48 h) than to B. anurum nymphs (LT₅₀ = 192 h). Interestingly, the pyriproxyfen sublethally-exposed (2.5 μg a.i./L) B. anurum nymphs exhibited reduced enzyme activities (cytochrome P450 monooxygenases) involved in detoxication processes and preyed significantly less on A. aegypti larvae when compared to unexposed predators. Collectively, our findings demonstrate that mortality-based pyriproxyfen risk assessments are not always protective of aquatic non-target organisms.

Short- and medium-chain chlorinated paraffins (SCCPs, MCCPs) are high-production volume industrial chemicals that have been previously reported to occur in food, packaging material and the environment. This study presents an assessment of dietary exposure for consumers in Southern Germany based on three different sampling approaches: (i) a classical market basket study (n = 154), (ii) the analysis of ready-made meals from restaurants (n = 10), and (iii) a total diet approach (n = 21). In 35% of the samples, CPs were below the method limit of quantification. Highest amounts of SCCPs and MCCPs were found especially in extra virgin olive oils (EVOOs) and fish. Homologue patterns indicated the partial removal of CPs during the refining of (other) edible oils. Ready-made meals contained only low amounts of CPs equal to estimations based on market basket samples. Total diet samples from the same hospital were generally comparable with each other regardless of diet, although vegetarian meal plans with high amounts of cheese and other dairy products contained up to an order of magnitude more CPs than other diets. Taking all approaches into account, calculated daily exposures for adults ranged 35–420 ng/kg bw/day for ΣSCCPs and 22–840 ng/kg bw/day for ΣMCCPs, which is between one and two orders of magnitude higher than the current dietary intake of polychlorinated biphenyls (indicator PCBs) in Europe.

The immune organs, like thymus, are one of the targets of hydrogen sulfide (H₂S). Previously we reported that H₂S induced the differential expression of mRNAs that implicating apoptosis in thymus, however, the roles of noncoding RNAs (ncRNAs) in H₂S-induced thymus injury are still unknown. Pollution gases could alter the expression of ncRNAs, which have been shown to play important roles in many physiological and pathophysiological processes, including immune activity. This study revealed that H₂S exposure induced 9 differentially expressed circRNAs and 15 differentially expressed miRNAs in chicken thymus. Furthermore, the circRNA - miRNA - mRNA network was constructed. We discovered that circR-PTPN23 - miR-15a - E2F3 was involved in the cell cycle and apoptosis. Further, an in vitro H₂S exposure model was established using HD11 cell line and demonstrated that H₂S suppressed cell proliferation and induced apoptosis. Moreover, ciR-PTPN23 and E2F3 were downregulated, but miR-15a was upregulated in both the thymus and HD11 cell line after H₂S exposure. Bioinformatics analysis revealed that ciR-PTPN23 directly bound to miR-15a and that E2F3 was the target gene of miR-15a. Knocking down ciR-PTPN23 suppressed HD11 proliferation and caused G1 arrest and apoptosis, however, this phenomenon could be partially reversed by ciR-PTPN23 overexpression or miR-15a silencing. In summary, the ciR-PTPN23 - miR-15a - E2F3 axis was involved in H₂S-induced cell proliferation suppression and apoptosis.

The long term vertical and horizontal mobility of mercury (Hg) in soils of agricultural areas of a historically contaminated Italian National Relevance Site (SIN Brescia-Caffaro) was investigated. The contamination resulted from the continuous discharge of Hg in irrigation waters by an industrial plant (Caffaro S.p.A), equipped with a mercury-cell chlor-alkali process. The contamination levels with depth ranged from about 20 mg/kg dry weight (d.w.) of soil in the top (plow) layer to less than 0.1 mg/kg d.w. at 1 m depth. The concentrations varied also spatially, up to one order of magnitude within the same field and showing a decreasing trend from the Hg source (i.e., irrigation ditches). The concentration profiles and gradients measured were explained considering Hg loading, soil properties, such as the texture, organic carbon content, pH and cation exchange capacity. A Selective Sequential Extraction (SSE) was also applied on soil samples from an ad hoc greenhouse experiment to investigate the role of different plant species in influencing Hg speciation in soils. Although most of the extracted Hg was included in scarcely mobile or immobile forms, some plant species (i.e., alfalfa) showed to importantly increase the soluble and exchangeable fractions with respect to the unplanted control soils, thus affecting mobility and potential bioavailability of Hg.

Chlordane is an organochlorine pesticide that is applied extensively. Residual concentrations that remain in soils after application are highly toxic to soil organisms, particularly affecting the earthworm gut and indigenous soil microorganisms. However, response mechanisms of the earthworm gut and indigenous soil microorganism communities to chlordane exposure are not well known. In this study, earthworms (Metaphire guillelmi) were exposed to chlordane-contaminated soils to investigate their response mechanisms over a gradient of chlordane toxicity. Results from high-throughput sequencing and network analysis showed that the bacterial composition in the earthworm gut varied more significantly than that in indigenous soil microbial communities under different concentrations of chlordane stress (2.3–60.8 mg kg⁻¹; p < 0.05). However, keystone species of Flavobacterium, Candidatus Nitrososphaera, and Acinetobacter remained stable in both the earthworm gut and bacterial communities despite varying degrees of chlordane exposure, and their relative abundance was slightly higher in the low-concentration treatment group (T1, T2) than in the high-concentration treatment group (T3, T4). Additionally, network analysis demonstrated that the average value of the mean degree of centrality, closeness centrality, and eigenvector centrality of all keystone species screened by four methods (MetagenomeSeq, LEfSe, OPLS-DA, Random Forest) were 161.3, 0.5, and 0.63, respectively, and that these were significantly higher (p < 0.05) than values for non-keystone species (84.9, 0.4, and 0.2, respectively). Keystone species had greater network connectivity and a stronger capacity to degrade pesticides and transform carbon and nitrogen than non-keystone species. The keystone species, which were closely related to the microbial community in soil indigenous flora and earthworm intestinal flora, could resist chlordane stress and undertake pesticide degradation. These results have increased understanding of the role of the earthworm gut and indigenous soil bacteria in resisting chlordane stress and sustaining microbial equilibrium in soil.

Establishment of submerged macrophyte beds and application of chemical phosphorus inactivation are common lake restoration methods for reducing internal phosphorus loading. The two methods operate via different mechanisms and may potentially supplement each other, especially when internal phosphorous loading is continuously high. However, their combined effects have so far not been elucidated. Here, we investigated the combined impact of the submerged macrophyte Vallisneria denseserrulata and a lanthanum-modified bentonite (Phoslock®) on water quality in a 12-week mesocosm experiment. The combined treatment led to stronger improvement of water quality and a more pronounced reduction of porewater soluble reactive phosphorus than each of the two measures. In the combined treatment, total porewater soluble reactive phosphorus in the top 10 cm sediment layers decreased by 78% compared with the control group without Phoslock® and submerged macrophytes. Besides, in the upper 0–1 cm sediment layer, mobile phosphorus was transformed into recalcitrant forms (e.g. the proportion of HCl–P increased to 64%), while in the deeper layers, (hydr)oxides-bound phosphorus species increased 17–28%. Phoslock®, however, reduced the clonal growth of V. denseserrulata by 35% of biomass (dry weight) and 27% of plant density. Our study indicated that Phoslock® and submerged macrophytes may complement each other in the early stage of lake restoration following external nutrient loading reduction in eutrophic lakes, potentially accelerating the restoration process, especially in those lakes where the internal phosphorus loading is high.

Microorganism-assisted phytoremediation is being developed as an efficient green approach for management of toxic metals contaminated soils and mitigating the potential human health risk. The capability of plant growth promoting Actinobacteria (Streptomyces pactum Act12 - ACT) and Firmicutes (Bacillus subtilis and Bacillus licheniformis - BC) in mono- and co-applications (consortium) to improve soil properties and enhance phytoextraction of Cd, Cu, Pb, and Zn by Brassica juncea (L.) Czern. was studied here for the first time in both incubation and pot experiments. The predominant microbial taxa were Proteobacteria, Actinobacteria and Bacteroidetes, which are important lineages for maintaining soil ecological activities. The consortium improved the levels of alkaline phosphatase, β-D glucosidase, dehydrogenase, sucrase and urease (up to 33%) as compared to the control. The bacterial inoculum also triggered increases in plant fresh weight, pigments and antioxidants. The consortium application enhanced significantly the metals bioavailability (DTPA extractable) and mobilization (acid soluble fraction), relative to those in the unamended soil; therefore, significantly improved the metals uptake by roots and shoots. The phytoextraction indices indicated that B. juncea is an efficient accumulator of Cd and Zn. Overall, co-application of ACT and BC can be an effective solution for enhancing phytoremediation potential and thus reducing the potential human health risk from smelter-contaminated soil. Field studies may further credit the understanding of consortium interactions with soil and different plant systems in remediating multi-metal contaminated environments.

The current estimations of the burden of disease (BD) of PM₂.₅ exposure is still potentially biased by two factors: ignorance of heterogeneous vulnerabilities at diverse urbanization levels and reliance on the risk estimates from existing literature, usually from different locations. Our objectives are (1) to build up a data fusion framework to estimate the burden of PM₂.₅ exposure while evaluating local risks simultaneously and (2) to quantify their spatial heterogeneity, relationship to land-use characteristics, and derived uncertainties when calculating the disease burdens. The feature of this study is applying six local databases to extract PM₂.₅ exposure risk and the BD information, including the risks of death, cardiovascular disease (CVD), and respiratory disease (RD), and their spatial heterogeneities through our data fusion framework. We applied the developed framework to Tainan City in Taiwan as a use case estimated the risks by using 2006–2016 emergency department visit data, air quality monitoring data, and land-use characteristics and further estimated the BD caused by daily PM₂.₅ exposure in 2013. Our results found that the risks of CVD and RD in highly urbanized areas and death in rural areas could reach 1.20–1.57 times higher than average. Furthermore, we performed a sensitivity analysis to assess the uncertainty of BD estimations from utilizing different data sources, and the results showed that the uncertainty of the BD estimations could be contributed by different PM₂.₅ exposure data (20–32%) and risk values (0–86%), especially for highly urbanized areas. In conclusion, our approach for estimating BD based on local databases has the potential to be generalized to the developing and overpopulated countries and to support local air quality and health management plans.

Inorganic arsenic (iAs) is a naturally occurring metalloid present in drinking water and polluted air exposing millions of people globally. Epidemiological studies have linked iAs exposure to the development of numerous diseases including cognitive impairment, cardiovascular failure and cancer. Despite intense research, an effective therapy for chronic arsenicosis has yet to be developed. Laboratory studies have been of great benefit in establishing the pathways involved in iAs toxicity and providing insights into its mechanism of action. However, the in vivo analysis of arsenic toxicity mechanisms has been difficult by the lack of reliable in vivo biomarkers of iAs’s effects. To address this issue we have applied the use of our recently developed stress reporter models to study iAs toxicity. The reporter mice Hmox1 (oxidative stress/inflammation; HOTT) and p21 (DNA damage) were exposed to iAs at acute and chronic, environmentally relevant, doses. We observed induction of the oxidative stress reporters in several cell types and tissues, which was largely dependent on the activation of transcription factor NRF2. We propose that our HOTT reporter model can be used as a surrogate biomarker of iAs-induced oxidative stress, and it constitutes a first-in-class platform to develop treatments aimed to counteract the role of oxidative stress in arsenicosis. Indeed, in a proof of concept experiment, the HOTT reporter mice were able to predict the therapeutic utility of the antioxidant N-acetyl cysteine in the prevention of iAs associated toxicity.