Heavy metals are the most commonly encountered toxic substances that increase susceptibility to various diseases after prolonged exposure. We have previously shown that healthy volunteers living near a mining area had significant contamination with heavy metals associated with significant changes in the expression of some detoxifying genes, xenobiotic metabolizing enzymes, and DNA repair genes. However, alterations of most of the molecular target genes associated with diseases are still unknown. Thus, the aims of this study were to (a) evaluate the gene expression profile and (b) identify the toxicities and potentially relevant human disease outcomes associated with long-term human exposure to environmental heavy metals in mining area using microarray analysis. For this purpose, 40 healthy male volunteers who were residents of a heavy metal-polluted area (Mahd Al-Dhahab city, Saudi Arabia) and 20 healthy male volunteers who were residents of a non-heavy metal-polluted area were included in the study. Total RNA was isolated from whole blood using PAXgene Blood RNA tubes and then reversed transcribed and hybridized to the gene array using the Affymetrix U219 GeneChip. Microarray analysis showed about 2129 genes were identified and differentially altered, among which a shared set of 425 genes was differentially expressed in the heavy metal-exposed groups. Ingenuity pathway analysis revealed that the most altered gene-regulated diseases in heavy metal-exposed groups included hematological and developmental disorders and mostly renal and urological diseases. Quantitative real-time polymerase chain reaction closely matched the microarray data for some genes tested. Importantly, changes in gene-related diseases were attributed to alterations in the genes encoded for protein synthesis. Renal and urological diseases were the diseases that were most frequently associated with the heavy metal-exposed group. Therefore, there is a need for further studies to validate these genes, which could be used as early biomarkers to prevent renal injury.

Phytate is abundant in soils, which is stable and unavailable for plant uptake. However, it occurs in root exudates of As-hyperaccumulator Pteris vittata (PV). To elucidate its effect on As uptake and growth, P. vittata was examined on agar media (63 μM P) containing 50 μM As and/or 50 or 500 μM phytate with non As-hyperaccumulator Pteris ensiformis (PE) as a congeneric control. Phytate induced efficient As and P uptake, and enhanced growth in PV, but had little effects on PE. The As concentrations in PV fronds and roots were 157 and 31 mg kg−1 in As50+phytate50, 2.2- and 3.1-fold that of As50 treatment. Phosphorus uptake by PV was reduced by 27% in As treatment than the control (P vs. P + As) but increased by 73% comparing phytate500 to phytate500+As, indicating that PV effectively took up P from phytate. Neither As nor phytate affected Fe accumulation in PV, but phytate reduced root Fe concentration in PE (46–56%). As such, the increased As and P and the unsuppressed Fe uptake in PV probably promoted PV growth. Thus, supplying phytate to As-contaminated soils may promote As uptake and growth in PV and its phytoremediation ability.

Transport of coal by train through residential neighborhoods in Metro Vancouver, British Columbia, Canada may increase the possibility of exposure to particulate matter at different size ranges, with concomitant potential negative health impacts. This pilot study identifies and quantifies train impacts on particulate matter (PM) concentrations at a single location. Field work was conducted during August and September 2014, with the attributes of a subset of passing trains confirmed visually, and the majority of passages identified with audio data. In addition to fixed ground based monitors at distances 15 and 50 m from the train tracks, an horizontally pointing mini-micropulse lidar system was deployed on three days to make backscatter and depolarization measurements in an attempt to identify the zone of influence, and sources, of train-generated PM. Ancillary wind and dust fall data were also utilized. Trains carrying coal are associated with a 5.3 (54%), 4.1 (33%), and 2.6 (17%) μgm−3 average increase in concentration over a 14 min period compared to the average concentrations over the 10 min prior to and after a train passage (“control” or “background” conditions), for PM3, PM10, and PM20, respectively. In addition, for PM10 and PM20, concentrations during train passages of non-coal-carrying trains were not found to be significantly different from PM concentrations during control conditions. Presence of coal dust particles at the site was confirmed by dust fall measurements. Although enhancements of PM concentrations during 14 min train passages were generally modest, passing coal trains occasionally enhanced concentrations at 50 m from the tracks by ∼100 μgm-3. Results showed that not every train passage increased PM concentrations, and the effect appears to be highly dependent on wind direction, local meteorology and load related factors. LiDAR imagery suggests that re-mobilization of track-side PM by train-induced turbulence may be a significant contributor to coarse particle enhancements.

The uptake and metabolism of ibuprofen (IBU) by plants at the cellular level was investigated using a suspension culture of A. thaliana. Almost all IBU added to the medium (200 μM) was metabolized or bound to insoluble structures in 5 days. More than 300 metabolites were determined by liquid chromatography-high resolution mass spectrometry (LC-HRMS) analysis, and most of these are first reported for plants here. Although hydroxylated derivatives formed by oxidation on the isobutyl side chain were the main first-step products of IBU degradation, conjugates of these products with sugar, methyl and amino acid groups were the dominant metabolites in the culture. The main portion of total added IBU (81%) was accumulated in the extractable intracellular pool, whereas the cultivation medium fraction contained only 19%. The amount of the insoluble cell-wall-bound IBU was negligible (0.005% of total IBU).

Triafamone, a sulfamide herbicide, has been extensively utilized for weed control in rice paddies in Asia. However, its fate and transformation in the environment have not been established. Through a rice paddy microcosm-based simulation trial combined with multiple spectroscopic analyses, we isolated and identified three novel metabolites of triafamone, including hydroxyl triafamone (HTA), hydroxyl triafamone glycoside (HTAG), and oxazolidinedione triafamone (OTA). When triafamone was applied to rice paddies at a concentration of 34.2 g active ingredient/ha, this was predominantly distributed in the paddy soil and water, and then rapidly dissipated in accordance with the first-order rate model, with half-lives of 4.3–11.0 days. As the main transformation pathway, triafamone was assimilated by the rice plants and was detoxified into HTAG, whereas the rest was reduced into HTA with subsequent formation of OTA. At the senescence stage, brown rice had incurred triafamone at a concentration of 0.0016 mg/kg, but the hazard quotient was <1, suggesting that long-term consumption of the triafamone-containing brown rice is relatively safe. The findings of the present study indicate that triafamone is actively metabolized in the agricultural environment, and elucidation of the link between environmental exposure to these triazine or oxazolidinedione moieties that contain metabolites and their potential impacts is warranted.

Atmospheric ammonia (NH3), a common alkaline gas found in air, plays a significant role in atmospheric chemistry, such as in the formation of secondary particles. However, large uncertainties remain in the estimation of ammonia emissions from nonagricultural sources, such as wastewater treatment plants (WWTPs). In this study, the ammonia emission factors from a large WWTP utilizing three typical biological treatment techniques to process wastewater in South China were calculated using the US EPA's WATER9 model with three years of raw sewage measurements and information about the facility. The individual emission factors calculated were 0.15 ± 0.03, 0.24 ± 0.05, 0.29 ± 0.06, and 0.25 ± 0.05 g NH3 m−3 sewage for the adsorption-biodegradation activated sludge treatment process, the UNITANK process (an upgrade of the sequencing batch reactor activated sludge treatment process), and two slightly different anaerobic-anoxic-oxic treatment processes, respectively. The overall emission factor of the WWTP was 0.24 ± 0.06 g NH3m−3 sewage. The pH of the wastewater influent is likely an important factor affecting ammonia emissions, because higher emission factors existed at higher pH values. Based on the ammonia emission factor generated in this study, sewage treatment accounted for approximately 4% of the ammonia emissions for the urban area of South China's Pearl River Delta (PRD) in 2006, which is much less than the value of 34% estimated in previous studies. To reduce the large uncertainty in the estimation of ammonia emissions in China, more field measurements are required.

Biogenic palladium nanoparticles (bio-Pd NPs) represent a promising catalyst for organohalide remediation in water and sediments. However, the available information regarding their possible impact in case of release into the environment, particularly on the environmental microbiota, is limited. In this study the toxicity of bio-Pd NPs on the model marine bacterium V. fischeri was assessed. The impacts of different concentrations of bio-Pd NPs on the respiratory metabolisms (i.e. organohalide respiration, sulfate reduction and methanogenesis) and the structure of a PCB-dechlorinating microbial community enriched form a marine sediment were also investigated in microcosms mimicking the actual sampling site conditions. Bio-Pd NPs had no toxic effect on V. fischeri. In addition, they had no significant effects on PCB-dehalogenating activity, while showing a partial, dose-dependent inhibitory effect on sulfate reduction as well as on methanogenesis. No toxic effects by bio-Pd NPs could be also observed on the total bacterial community structure, as its biodiversity was increased compared to the not exposed community. In addition, resilience of the microbial community to bio-Pd NPs exposure was observed, being the final community organization (Gini coefficient) of samples exposed to bio-Pd NPs similar to that of the not exposed one. Considering all the factors evaluated, bio-Pd NPs could be deemed as non-toxic to the marine microbiota in the conditions tested. This is the first study in which the impact of bio-Pd NPs is extensively evaluated over a microbial community in relevant environmental conditions, providing important information for the assessment of their environmental safety.

In April of 2010, the Macondo well blowout in the northern Gulf of Mexico resulted in an unprecedented release of oil into the water column at a depth of approximately 1500 m. A time series of surface and subsurface sediment samples were collected to the northwest of the well from 2010 to 2013 for molecular biomarker and bulk carbon isotopic analyses. While no clear trend was observed in subsurface sediments, surface sediments (0–3 cm) showed a clear pattern with total concentrations of n-alkanes, unresolved complex mixture (UCM), and petroleum biomarkers (terpanes, hopanes, steranes) increasing from May to September 2010, peaking in late November 2010, and strongly decreasing in the subsequent years. The peak in hydrocarbon concentrations were corroborated by higher organic carbon contents, more depleted Δ14C values and biomarker ratios similar to those of the initial MC252 crude oil reported in the literature. These results indicate that at least part of oil discharged from the accident sedimented to the seafloor in subsequent months, resulting in an apparent accumulation of hydrocarbons on the seabed by the end of 2010. Sediment resuspension and transport or biodegradation may account for the decrease in sedimented oil quantities in the years following the Macondo well spill.

Acetylacetone (AcAc) has proven to be a potent photo-activator in the degradation of color compounds. The effects of AcAc on the photochemical conversion of five colorless pharmaceuticals were for the first time investigated in both pure and natural waters with the UV/H2O2 process as a reference. In most cases, AcAc played a similar role to H2O2. For example, AcAc accelerated the photodecomposition of carbamazepine, oxytetracycline, and tetracycline in pure water. Meanwhile, the toxicity of tetracyclines and carbamazepine were reduced to a similar extent to that in the UV/H2O2 process. However, AcAc worked in a way different from that of H2O2. Based on the degradation kinetics, solvent kinetic isotope effect, and the inhibiting effect of O2, the underlying mechanisms for the degradation of pharmaceuticals in the UV/AcAc process were believed mainly to be direct energy transfer from excited AcAc to pharmaceuticals rather than reactive oxygen species-mediated reactions. In natural waters, dissolved organic matter (DOM) played a crucial role in the photoconversion of pharmaceuticals. The role of H2O2 became negligible due to the scavenging effects of DOM and inorganic ions. Interestingly, in natural waters, AcAc first accelerated the photodecomposition of pharmaceuticals and then led to a dramatic reduction with the depletion of dissolved oxygen. Considering the natural occurrence of diketones, the results here point out a possible pathway in the fate and transport of pharmaceuticals in aquatic ecosystems.