Effective and economically viable method to remove elevated metal(loid)s from farm and industrial lands remains a major challenge. In this study, magnetic biochar-based adsorbents with Fe₃O₄ particles embedded in a porous biochar matrix was synthesized via iron (Fe) treated biochar or thermal pyrolysis of Fe treated cedar sawdust. Application and separation of the adsorbent to a multi-contaminated soil slurry simultaneously removed 20–30% of arsenic, cadmium and lead within 24 h. Fast removal of multi-metal(loid)s result from the decrease in all operationally defined fractions of metal(loid)s, not limited to the exchangeable fraction. The direct removal of arsenic-enriched soil particles was observed via micro X-ray fluorescence maps. Furthermore, through comparison of biochars with different production methods, it has been found that magnetization after pyrolysis treatment leads to stronger metals/metalloids adsorption with a higher qₑ (bound sorbate) than other treatments but pyrolysis after magnetization stabilized Fe oxides on the biochar surface, indicating a higher biochar recovery rate (∼65%), and thus a higher metal(loid)s removal efficiency. The stability of Fe oxides on the surface of biochar is the determining factor for the removal efficiency of metal(loid)s from soil.

Soil anthropogenic contaminants can limit enzymatic nutrient mineralization, either by direct regulation or via impacts on the microbial community, thus affecting plant growth in agricultural and non-agricultural soils. The impact on phosphatase activity of mixing two contaminated, post-industrial rail yard soils was investigated; one was vegetated and had high phosphatase function, the other was barren and had low enzymatic function. The two soils had different abiotic properties, including contaminant load, vegetation cover, soil aggregate size distribution, and phosphatase potential. An experimental gradient was established between the two soils to systematically vary the abiotic properties and microbial community composition of the two soils, creating a gradient of novel ecosystems. The time dependence of extracellular phosphatase activity, soil moisture, and organic matter content was assessed along this gradient in the presence and absence of plants. Initially, mixtures with higher percentages of functional, vegetated soil had higher phosphatase activities. Phosphatase activity remained unchanged through time (65 days) in all soil mixtures in unplanted pots, but it increased in planted pots. For example, in the presence of plants, phosphatase activity increased from 0.6 ± 0.1 to 2.4 ± 0.3 μmol•h⁻¹•gdᵣy ₛₒᵢₗ⁻¹ from day one to day 65 in the 1:1 functional:barren soil mixture. The presence of plants also promoted moisture retention. Inoculation of poorly functioning soil with 10% of the functional soil with its microbial community did not, over 65 days, revitalize the poorly functioning soil. The findings showed that abiotic limitations to enzymatic activity in barren brownfield soils could be mitigated by establishing primary production but not by the addition of enzymatically active microbial communities alone.

Lead (Pb) is one of the predominant heavy metals in e-waste recycling arears and recognized as a notorious environmental neurotoxic substance. However, whether Pb at environmentally relevant concentrations could cause neurobehavioral alteration and even what kind of signaling pathway Pb exposure would disrupt in zebrafish were not fully uncovered. In the present study, 6 h postfertilization (hpf) zebrafish embryos were exposed to Pb at the concentrations of 0, 5, 10, and 20 μg/L until 144 hpf. Then the neurobehavioral indicators including locomotor, turnings and social behaviors, and the expressions of selected genes concerning brain-derived neurotrophic factor (BDNF) signaling were investigated. The results showed that significant changes were obtained under 20 μg/L Pb exposure. The hypoactivity of zebrafish larvae in locomotor and turning behaviors was induced during the dark period, while hyperactivity was observed in a two-fish social assay during the light period. The significantly downregulation of genes encoding BDNF, its receptor TrkB, and N-methyl-D-aspartate glutamate receptor (NMDAR) suggested the involvement of NMDAR-dependent BDNF signaling pathway. Overall, our study demonstrated that developmental exposure to Pb at environmentally relevant concentrations caused obvious neurobehavioral impairment of zebrafish larvae by disrupting the NMDAR-dependent BDNF signaling, which could exert profound ecological consequences in the real environment.

Microbiome community structure is intimately involved in key biological functions in the gastrointestinal (GI) system including nutrient absorption and lipid metabolism. Recent evidence suggests that disruption of the GI microbiome is a contributing factor to metabolic disorders and obesity. Poor diet and chemical exposure have been independently shown to cause disruption of the GI microbiome community structure and function. We hypothesized that the addition a chemical exposure to overfeeding exacerbates adverse effects on the GI microbiome community structure and function. To test this hypothesis, adult zebrafish were fed a normal feeding regime (Control), an overfeeding regime (OF), or an overfeeding regime contaminated with diethylhexyl phthalate (OF + DEHP), a suspected obesogen-inducing chemical. After 60 days, fecal matter was collected for sequencing, identification, and quantification of the GI microbiome using the 16s rRNA hypervariable region. Analysis of beta diversity indicated distinct microbial profiles between treatments with the largest divergence between Control and OF + DEHP groups. Based upon functional predictions, OF + DEHP treatment altered carbohydrate metabolism, while both OF and OF + DEHP affected biosynthesis of fatty acids and lipid metabolism. Co-occurrence network analysis revealed decreases in cluster size and a fracturing of the microbial community network into unconnected components and a loss of keystone species in the OF + DEHP treatment when compared to Control and OF treatments. Data suggest that the addition of DEHP in the diet may exacerbate microbial dysbiosis, a consequence that may explain in part its role as an obesogenic chemical.

Long-term trends (2004–2017) in the chemical composition and sources of PM₂.₅ (particulate matter smaller than 2.5 μm in diameter) in a metropolitan area were investigated using daily integrated PM₂.₅ chemical speciation data and continuous air pollution measurements. Eleven source factors were identified: coal combustion characterized by secondary sulphate, secondary nitrate, summertime organic carbon (OC), regional elemental carbon (EC), biomass burning, oil combustion, primary tailpipe emissions, non-tailpipe emissions related to road dust, non-tailpipe emissions related to brake wear, metal production, and road salt. Overall, coal combustion, secondary nitrate, regional EC, and oil combustion underwent marked decreases in concentrations with large reduction rates ranging from −8% yr⁻¹ to −18% yr⁻¹, contributing to an overall 34% decrease in annual PM₂.₅ over the past 14 years. Decreases in local tailpipe emissions (−3% yr⁻¹) were consistent with the reduction of traffic-related air pollutants. In contrast, non-tailpipe emissions remained constant until 2010–2011 and then increased with a range of rates of 21% yr⁻¹ to 27% yr⁻¹ from 2011 to 2016. The contribution of summertime OC increased to approximately 27% in the summer of 2013–2016, rising to become the largest PM₂.₅ source driven by the reduction of regional sources. The chemical composition of PM₂.₅ in the urban area drastically changed from inorganic-rich to organic- and metal-rich particles during 2013–2016. The depletion of ascorbic acid was measured using filter samples collected over one year to identify PM₂.₅ components and sources contributing to the oxidative potential (OP) of PM₂.₅. The OP was clearly associated with trace elements (e.g., Ba, Cu, Fe). Non-tailpipe emissions related to road dust and brake wear presented high redox activity per mass of PM₂.₅. This work suggests that summertime OC and non-tailpipe emissions in recent years have become increasingly important. As such, policies targeting traffic-related PM₂.₅ should focus on these sources for maximum impact.

Ground-level ozone (O₃) pollution and its impact on crop growth and yield have become one of the serious environmental problems in recent years, especially in economically active and densely populated areas. In this study, rice yield and the associated economic losses due to O₃ were estimated by using observational O₃ concentration ([O₃]) data during growing seasons in Southern China. O₃-induced yield losses were calculated by using O₃ exposure metrics of AOT40 and M7. The spatial distribution of these two metrics is relatively consistent, the highest areas located in the Yangtze River Basin. Under the current O₃ level, during double-early rice, double-late rice and single rice growing seasons, the relative yield losses estimated with AOT40 (M7) were 6.8% (1.2%), 10.2% (1.9%) and 10.4% (2.0%), respectively. O₃-induced rice production loss for double-early rice, double-late rice and single rice totaled 2.4 million metric tons (0.4 million metric tons), 4.3 million metric tons (0.7 million metric tons) and 11.0 million metric tons (1.9 million metric tons) and associated economic losses were 108.1 million USD (18.3 million USD), 190.2 million USD (32.4 million USD) and 486.4 million USD (82.9 million USD) based on AOT40 (M7) metric. This study indicates that regional risks to rice from O₃ exposure and provide quantitative evidence of O₃-induced impacts on rice yields and economic losses across Southern China. Therefore, the establishment of scientific O₃ risk assessment method is of great significance to prevent yield production and economic losses caused by O₃ exposure. Policymakers should strengthen supervision of emissions of O₃ precursors to mitigate the rise of O₃ concentration, thereby reducing O₃ damage to agricultural production.

Particles emitted from five typical types of vehicles (including light-duty gasoline vehicles, LDG; heavy-duty gasoline vehicles, HDG; diesel buses, BUS; light-duty diesel vehicles, LDD and heavy-duty diesel vehicles, HDD) were collected with a dilution sampling system and an electrical low-pressure impactor (ELPI+, with particle sizes covering fourteen stages from 6 nm to 10 μm) on dynamometer benches. The mass concentrations and emission factors (EF) for organic carbon (OC) and elemental carbon (EC) were obtained with a DRI Model 2001 thermal/optical carbon analyzer. A respiratory deposition model was used to calculate the deposition fluxes of size-segregated carbonaceous aerosols in human respiratory system. Results indicated that the OC produced from LDG mainly existed in the size range of 2.5–10 μm, while EC from HDG enriched in 0.94–2.5 μm. For diesel vehicles, both OC and EC concentrations peaked at 0.094–0.25 μm. The OC/EC ratios for PM₂.₅ varied from different types of vehicles, from 0.61 to 8.35. The primary emissions from LDD and HDD exhibited high OC/EC ratios (>3), suggesting that using OC/EC higher than 2 to indicate the formation of secondary organic aerosol (SOA) was not universal. The emission factors for OC and EC of LDG (HDG) in PM₁₀ were 1.78 (3.14) mg km⁻¹ and 0.88 (4.32) mg km⁻¹, respectively. The OC2 and OC3 were the main section (over 60%) of OC emitted from all the five types of vehicles. EC1 was the most abundant EC fraction of LDG (76.9%), while EC2 dominated for other types of vehicles (more than 62%). About 60% of the OC in ultrafine particles could be deposited in the alveoli. Diesel EC mainly could be deposited in the alveolar region. It is necessary to control the emission of ultrafine particles and diesel EC.

Fluoride mediated disruption of sex steroid hormones has been demonstrated in animals. However, evidence from humans was limited and contradictory, especially for children and adolescents. Based on data of the National Health and Nutrition Survey (NHANES) 2013–2016, a total of 3392 subjects aged 6–19 years were analyzed in this cross-sectional study. Both plasma and water fluoride levels were quantified electrometrically using the ion-specific electrode. Sex steroid hormones of total testosterone, estradiol and sex hormone-binding globulin (SHBG) were tested in serum. Percent changes and 95% confidence intervals (CIs) in sex steroid hormones associated with tertiles of fluoride levels (setting the first as reference) were estimated using adjusted linear regression models by stratification of gender and age. Compared with subjects at the first tertile of plasma fluoride, percent changes (95% CIs) in testosterone were −8.08% (−17.36%, 2.25%) and −21.65% (−30.44%, −11.75%) for the second and third tertiles, respectively (P ₜᵣₑₙd <0.001). Male adolescents at the third tertile of plasma fluoride had decreased levels of testosterone (percent change = −21.09%, 95% CIs = −36.61% to −1.77%). Similar inverse associations were also found when investigating the relationships between plasma fluoride and estradiol. Besides, the data indicated decreased levels of SHBG associated with water and plasma fluoride among the male adolescents (percent change of the third tertile = −9.39%, 95% CIs = −17.25% to −0.78%) and female children (percent change of the second tertile = −10.78%, 95% CIs = −17.55% to −3.45%), respectively. The data indicated gender- and age-specific inverse associations of fluoride in plasma and water with sex steroid hormones of total testosterone, estradiol and SHBG in U.S. children and adolescents. Prospective cohort studies are warranted to confirm the causality.

The microbial characteristics and bacterial communities of sediment sludge upon different concentrations of exposure to uranium were investigated by high solution transmission electron microscopy (HRTEM), energy dispersive X-ray spectroscopy (EDS), X-ray photoelectron spectroscopy (XPS) and high-throughput sequencing. After exposure to initial uranium concentrations of 10–50 μM for 24 h in synthetic wastewater, the removal efficiencies of uranium reached 80.7%–96.5%. The spherical and short rod bacteria were dominant in the sludge exposed to uranium. HRTEM-EDS and XPS analyses indicated that reduction and adsorption were the main mechanisms for uranium removal. Short-term exposure to low concentrations of uranium resulted in a decrease in bacterial richness but an increase in diversity. A dramatic change in the composition and abundances of the bacterial community were present in the sediment sludge exposed to uranium. The highest removal efficiency was identified in the sediment sludge exposed to 30 μM uranium, and the dominant bacteria included Acinetobacter (44.9%), Klebsiella (20.0%), Proteiniclasticum (6.7%), Enterobacteriaceae (6.6%), Desulfovibrio (4.4%), Porphyromonadaceae (4.1%), Comamonas (2.4%) and Sedimentibacter (2.3%). By comparison to the inoculum sediment sludge, exposure to uranium caused a substantial difference in the majority of bacterial abundance.

Hypoxia is a major stressor in aquatic environments and it is frequently linked with excess nutrients resulting from sewage effluent discharges and agricultural runoff, which often also contain complex mixtures of chemicals. Despite this, interactions between hypoxia and chemical toxicity are poorly understood. We exposed male three-spined stickleback during the onset of sexual maturation to a model anti-androgen (flutamide; 250 μg/L) and a pesticide with anti-androgenic activity (linuron; 250 μg/L), under either 97% or 56% air saturation (AS). We assessed the effects of each chemical, alone and in combination with reduced oxygen concentration, by measuring the transcription of spiggin in the kidney, as a marker of androgen signalling, and 11 genes in the liver involved in some of the molecular pathways hypothesised to be affected by the exposures. Spiggin transcription was strongly inhibited by flutamide under both AS conditions. In contrast, for linuron, a strong inhibition of spiggin was observed under 97% AS, but this effect was supressed under reduced air saturation, likely due to interactions between the hypoxia inducible factor and the aryl hydrocarbon receptor (AhR) pathways. In the liver, hypoxia inducible factor 1α was induced following exposure to both flutamide and linuron, however this was independent of the level of air saturation. This work illustrates the potential for interactions between hypoxia and pollutants with endocrine or AhR agonist activity to occur, with implications for risk assessment and management.