Soils provide the service of attenuating and detoxifying pollutants. Such ability, natural attenuation capacity (NAC), is one of the most important ecosystem services for urban soils. We improved the ecosystem-service performance index (EPX) model by integrating with entropy weight determination method to evaluate the NAC of residential soils in Beijing. Eleven parameters related to the soil process of pollutants fate and transport were selected and 115 residential soil samples were collected. The results showed that bulk density, microbial functional diversity and soil organic matter had high weights in the NAC evaluation. Urban socio-economic indicators of residential communities such as construction age, population density and property & management fee could be employed in kinetic fittings of NAC. It could be concluded urbanization had significant impacts on NAC in residential soils. The improved method revealed reasonable and practical results, and it could be served as a potential measure for application to other quantitative assessment.

A substantial amount of sulfate is often supplied in paddy fields with concomitant applications of chemical fertilizers and manure for rice growth. It is unclear how solubility and speciation of arsenic (As) are affected by the levels of soil sulfate and their relationship to soil redox status and sulfur (S) and iron (Fe) speciation in a short cycle of soil reducing (flooding) and oxidizing (drying) periods. The objective of this study was to investigate the solubility of As in relation to chemical speciation of As and S in different levels of soil sulfate through a time series of measurements during a 40-day reduction period (Eh < −130 mV) followed by a 32-day reoxidation period (Eh > 400 mV) using X-ray absorption fine structure (XAFS) spectroscopy. An excess of sulfate decreased extractable and dissolved As in the soil reducing period due to retardation of soil reduction process that decreased soluble As(III) in the soil solid phase. The As species at the end of soil reducing period were 38–41% As(V), 46–51% As(III), and 11–13% As2S3-like species, regardless of initial S treatments. In the following soil reoxidation, As2S3-like species were sensitive to oxidation and disappeared completely in the first 2 days when the Eh value increased rapidly above 160 mV. The addition of extra sulfate to the soil did not result in the formation of neither reduced S species nor As2S3-like species. About 50% of As(III) to the total As persisted over 32 days of soil reoxidation period (Eh > 400 mV), suggesting some mechanisms against oxidation of As(III) such as physical sequestration in soil microsites. This study demonstrates that the extra SO4 in paddy soils can help mitigate the dissolution of As in reduction and reoxidation periods.

Concentrations of nine organophosphate flame retardants (OPFRs) and eight polybrominated diphenyl ethers (PBDEs) were measured in samples of indoor dust (n = 85) and air (n = 45) from Australian houses, offices, hotels, and transportation (buses, trains, and aircraft). All target compounds were detected in indoor dust and air samples. Median ∑₉OPFRs concentrations were 40 μg/g in dust and 44 ng/m³ in indoor air, while median ∑₈PBDEs concentrations were 2.1 μg/g and 0.049 ng/m³. Concentrations of FRs were higher in rooms that contained carpet, air conditioners, and various electronic items. Estimated daily intakes in adults are 14000 pg/kg body weight/day and 330 pg/kg body weight/day for ∑₉OPFRs and ∑₈PBDEs, respectively. Our results suggest that for the volatile FRs such as tris(2-chloroethyl) phosphate (TCEP) and TCIPP, inhalation is expected to be the more important intake pathway compared to dust ingestion and dermal contact.

Although several air pollution studies have examined the relationship between people living close to roadways and human health, we are unaware of studies that have examined the distance-decay of this effect based on a snapshot of congestion and focused on a micro-level traffic emission inventory. In this paper we estimate the distance-decay of premature mortality risk related to PM₂.₅ emitted by traffic congestion in Hamilton, Canada, in 2011 We employ the Stochastic User Equilibrium (SUE) traffic assignment algorithm to estimate congested travel times for each road link in our study area. Next, we used EPA's MOVES model to estimate mass of PM₂.₅, and then R-line dispersion model to predict concentration of PM₂.₅. Finally, we apply Integrated Exposure Response Function (IERF) to estimate PM₂.₅-related premature mortality at 100 m × 100 m grid resolution. We estimated total premature mortality over Hamilton to be 73.10 (95%CI: 39.05; 82.11) deaths per year. We observed that the proximity to a roadway increases the risk of premature mortality and the strength of this risk decreases as buffer sizes are increased. For example, we estimated that the premature mortality risk within buffer 0–100 m is 29.5% higher than for the buffer 101–200 m, 179.3% higher than for the buffer 201–300 m, and 566% higher than for the buffer 301–400 m. Our study provides a new perspective on exposure increments from traffic congestion. In particular, our findings show health effects gradients across neighborhoods, capturing microscale near-road exposure up to 2000 m of the roadway. Results from this research can be useful for policymakers to develop new strategies for the challenges of regulating transportation, land use, and air pollution.

A full-factorial test design was applied to systematically investigate the contribution and significance of water chemistry parameters (pH, divalent cations and dissolved organic carbon (DOC) concentration) and their interactions on the behavior and fate of copper nanoparticles (CuNPs). The total amount of Cu remaining in the water column after 48 h of incubation was mostly influenced by divalent cation content, DOC concentration and the interaction of divalent cations and DOC. DOC concentration was the predominant factor influencing the dissolution of CuNPs, which was far more important than the effect of pH in the range from 6 to 9 on the dissolution of the CuNPs. The addition of DOC at concentrations ranging from 5 to 50 mg C/L resulted in a 3–5 fold reduction of dissolution of CuNPs after 48 h of incubation, as compared to the case without addition of DOC. Divalent cation content was found to be the most influential factor regarding aggregation behavior of the particles, followed by DOC concentration and the interaction of divalent cations and DOC. In addition, the aggregation behavior of CuNPs rather than particulate dissolution explained most of the variance in the sedimentation profiles of CuNPs. These results are meaningful for improved understanding and prediction of the behavior and fate of metallic NPs in aqueous environments.

The associations of air pollution with chronic kidney disease (CKD) have not yet been fully studied. We enrolled 8,497 Taipei City residents older than 65 years and calculated the estimated glomerular filtration rate (eGFR) using the Taiwanese Chronic Kidney Disease Epidemiology Collaboration equation. Proteinuria was assessed via dipstick on voided urine. CKD prevalence and risk of progression were defined according to the KDIGO 2012 guidelines. Land-use regression models were used to estimate the participants’ one-year exposures to PM of different sizes and traffic-related exhaust, PM₂.₅ absorbance, nitrogen dioxide (NO₂), and NOₓ. Generalized linear regressions and logistic regressions were used to examine the associations of one-year air pollution exposures with eGFR, proteinuria, CKD prevalence and risk of progression. The results showed that the interquartile range (IQR) increments of PM₂.₅ absorbance (0.4 × 10⁻⁵/m) and NO₂ (7.0 μg/m³) were associated with a 1.07% [95% confidence interval (CI): 0.54–1.57] and 0.84% (95% CI: 0.37–1.32) lower eGFR, respectively; such relationships were magnified in subjects who had an eGFR >60 ml/min/1.73 m² or who were non-diabetic. Similar associations were also observed for PM₁₀ and PM₂.₅₋₁₀. Two-pollutant models showed that PM₁₀ and PM₂.₅ absorbance were associated with a lower eGFR. The odd ratios (ORs) of CKD prevalence and risk of progression also increased with exposures to PM₂.₅ absorbance and NO₂. In summary, one-year exposures to traffic-related air pollution were associated with lower eGFR, higher CKD prevalence, and increased risk of CKD progression among the elderly population. Air pollution-related impaired renal function was stronger in non-CKD and non-diabetic subjects.

Cyanobacterial blooms have become a common phenomenon in eutrophic freshwater ecosystems worldwide. Microcystis is an important bloom-forming and toxin-producing genus in continental aquatic ecosystems, which poses a potential risk to Human populations as well as on aquatic organisms. Microcystis is known to produce along with various bioactive peptides, the microcystins (MCs) that have attracted more attention notably due to their high hepatotoxicity.To better understand the effects of cyanobacterial blooms on fish, medaka fish (Oryzias latipes) were sub-chronically exposed to either non-MC-producing or MC-producing living strains and, for this latter, to its subsequent MC-extract of Microcystis aeruginosa. Toxicological effects on liver have been evaluated through the combined approach of histopathology and ‘omics’ (i.e. proteomics and metabolomics). All treatments induce sex-dependent effects at both cellular and molecular levels. Moreover, the modalities of exposure appear to induce differential responses as the direct exposure to the cyanobacterial strains induce more acute effects than the MC-extract treatment. Our histopathological observations indicate that both non-MC-producing and MC-producing strains induce cellular impairments. Both proteomic and metabolomic analyses exhibit various biological disruptions in the liver of females and males exposed to strain and extract treatments. These results support the hypothesis that M. aeruginosa is able to produce bioactive peptides, other than MCs, which can induce toxicological effects in fish liver. Moreover, they highlight the importance of considering cyanobacterial cells as a whole to assess the realistic environmental risk of cyanobacteria on fish.

Environmental chemicals originating from human activities, such as persistent organic pollutants (POPs), may interfere with the endocrine system of aquatic organisms. The effect of these chemicals on biota and human populations is of high public concern but remains poorly understood, especially in aquatic environments of South America. The aim of this study was to investigate the bioavailability of POPs and the related effects in caged male tilapia (Oreochromis niloticus) in four cascading reservoirs of the Iguaçu River, Southern Brazil. POPs including organochlorine pesticides (OCPs), polychlorinated biphenyl (PCBs), and polybrominated diphenyl ethers (PBDEs) were determined in the reservoir water and tissue samples of tilapia after two months of exposure. The PCB levels in water (14.7 ng L−1) were 14 times higher than the limits permitted by the Brazilian legislation in the Salto Santiago (SS) reservoir. Similarly, concentrations of aldrin and its metabolites (6.05 ng L−1) detected in the water sample of the Salto Osório (SO) reservoir were also above the permitted limits. RT-qPCR analysis revealed different transcript levels of cytochrome P450 enzymes (CYP1A and CYP3A) in the liver among the four groups, with induced activity in tilapia from the SS reservoir. Quantification of the CYP3A mRNA expression and catalytic activity showed higher values for fish caged at the SS reservoir. The fish from this site also had a higher number of eosinophils observed in the testes. Although overt measurements of endocrine disruption were not observed in caged fish, alteration of CYP enzymes with co-occurrence of organochlorine contaminants in water may suggest bioavailability of contaminants from agricultural sources to biota. Additional studies with feral or caged animals for a longer duration may be necessary to evaluate the risks of the waterways to humans and wildlife.

Household cookstove emissions are an important source of carbonaceous aerosols globally. The light-absorbing organic carbon (OC), also termed brown carbon (BrC), from cookstove emissions can impact the Earth's radiative balance, but is rarely investigated. In this work, PM2.5 filter samples were collected during combustion experiments with red oak wood, charcoal, and kerosene in a variety of cookstoves mainly at two water boiling test phases (cold start CS, hot start HS). Samples were extracted in methanol and extracts were examined using spectrophotometry. The mass absorption coefficients (MACλ, m2 g−1) at five wavelengths (365, 400, 450, 500, and 550 nm) were mostly inter-correlated and were used as a measurement proxy for BrC. The MAC365 for red oak combustion during the CS phase correlated strongly to the elemental carbon (EC)/OC mass ratio, indicating a dependency of BrC absorption on burn conditions. The emissions from cookstoves burning red oak have an average MACλ 2–6 times greater than those burning charcoal and kerosene, and around 3–4 times greater than that from biomass burning measured in previous studies. These results suggest that residential cookstove emissions could contribute largely to ambient BrC, and the simulation of BrC radiative forcing in climate models for biofuel combustion in cookstoves should be treated specifically and separated from open biomass burning.

The primary objective of the present study was to review the impact of Cd exposure on gut microbiota and intestinal physiology, as well as to estimate whether gut may be considered as the target for Cd toxicity. The review is based on literature search in available databases. The existing data demonstrate that the impact of Cd on gut physiology is two-sided. First, Cd exposure induces a significant alteration of bacterial populations and their relative abundance in gut (increased Bacteroidetes-to-Firmicutes ratio), accompanied by increased lipopolysaccharide (LPS) production, reflecting changed metabolic activity of the intestinal microbiome. Second, in intestinal wall Cd exposure induces inflammatory response and cell damage including disruption of tight junctions, ultimately leading to increased gut permeability. Together with increased LPS production, impaired barrier function causes endotoxinemia and systemic inflammation. Hypothetically, Cd-induced increase gut permeability may also result in increased bacterial translocation. On the one hand, bacteriolysis may be associated with aggravation of endotoxemia. At the same time, together with Cd-induced impairment of macrophage inflammatory response, increased bacterial translocation may result in increased susceptibility to infections. Such a supposition is generally in agreement with the finding of higher susceptibility of Cd-exposed mice to infections. The changed microbiome metabolic activity and LPS-induced systemic inflammation may have a significant impact on target organs. The efficiency of probiotics in at least partial prevention of the local (intestinal) and systemic toxic effects of cadmium confirms the role of altered gut physiology in Cd toxicity. Therefore, probiotic treatment may be considered as the one of the strategies for prevention of Cd toxicity in parallel with chelation, antioxidant, and anti-inflammatory therapy.