Rigorous studies on long-term changes of heavy metal distribution in forest soils since the implementation of emission controls are rare. Hence, we resampled 97 old-growth beech stands in the Vienna Woods. This study exploits an extensive data set of soil (infiltration zone of stemflow and between trees area) and foliar chemistry from three decades ago. It was hypothesized that declining deposition of heavy metals is reflected in soil and foliar total contents of Pb, Cu, Zn, Ni, Mn and Fe. Mean soil contents of Pb in the stemflow area declined at the highest rate from 223 to 50 mg kg−1 within the last three decades. Soil contents of Pb and Ni decreased significantly both in the stemflow area and the between trees area down to 80–90 cm soil depth from 1984 to 2012. Top soil (0–5 cm) accumulation and simultaneous loss in the lower soil over time for the plant micro nutrients Cu and Zn are suggested to be caused by plant uptake from deep horizons. Reduced soil leaching, due to a mean soil pH (H2O) increase from 4.3 to 4.9, and increased plant cycling are put forward to explain the significant increase of total Mn contents in the infiltration zone of beech stemflow. Top soil Pb contents in the stemflow area presently exceed the critical value at which toxicity symptoms may occur at numerous sites. Mean foliar contents of all six studied heavy metals decreased within the last three decades, but plant supply with the micro nutrients Cu, Zn, Mn and Fe is still in the optimum range for beech trees. It is concluded that heavy metal pollution is not critical for the studied beech stands any longer. Microsites, affected by beech stemflow, are very useful for studying the legacy of high atmospheric heavy metal deposition.

The use of Ni and Cu isotopes for tracing contamination sources in the environment remains a challenging task due to the limited information about the influence of various biogeochemical processes influencing stable isotope fractionation. This work focuses on a relatively simple system in north-east Norway with two possible endmembers (smelter-bedrock) and various environmental samples (snow, soil, lichens, PM10). In general, the whole area is enriched in heavy Ni and Cu isotopes highlighting the impact of the smelting activity. However, the environmental samples exhibit a large range of δ⁶⁰Ni (−0.01 ± 0.03‰ to 1.71 ± 0.02‰) and δ⁶⁵Cu (−0.06 ± 0.06‰ to −3.94 ± 0.3‰) values which exceeds the range of δ⁶⁰Ni and δ⁶⁵Cu values determined in the smelter, i.e. in feeding material and slag (δ⁶⁰Ni from 0.56 ± 0.06‰ to 1.00 ± 0.06‰ and δ⁶⁵Cu from −1.67 ± 0.04‰ to −1.68 ± 0.15‰). The shift toward heavier Ni and Cu δ values was the most significant in organic rich topsoil samples in the case of Ni (δ⁶⁰Ni up to 1.71 ± 0.02‰) and in lichens and snow in the case of Cu (δ⁶⁵Cu up to −0.06 ± 0.06‰ and −0.24 ± 0.04‰, respectively). These data suggest an important biological and biochemical fractionation (microorganisms and/or metal uptake by higher plants, organo-complexation etc.) of Ni and Cu isotopes, which should be quantified separately for each process and taken into account when using the stable isotopes for tracing contamination in the environment.

Information on naturally occurring thyroid disease in wild animals in general and in small mammals specifically is extremely limited. In the present field-based work, we investigated the structure and function of thyroid glands of deer mice (Peromyscus maniculata) studied as sentinels of ecosystem sustainability on reclaimed areas post-mining on the oil sands of northeastern Alberta, because of their greater sensitivity to contaminants relative to meadow voles (Microtus pennsylvanicus) on the same sites. Extraction of bitumen in the oil sands of northeastern Alberta, results in the release of contaminants including polycyclic aromatic compounds (PACs), metals, and metalloids to the environment that have a measurable biological cost to wildlife living in the affected areas. In previous investigations, deer mice exposed to pollution at reclaimed areas showed compromised ability to regenerate glutathione indicating oxidative stress, together with decreased testicular mass and body condition during the breeding season. In the present study, thyroid glands from those deer mice from the reclaimed site had markedly increased follicular cell proliferation and decreased colloid compared to animals from the reference site. This pathology was positively associated with the greater oxidative stress in the deer mice. Thyroid hormones, both thyroxine and triiodothyronine, were also higher in animals with greater oxidative stress indicating increased metabolic demands from contaminant related subclinical toxicity. This work emphasizes the value of using a combination of endocrinological, histological and oxidative stress biomarkers to provide sensitive measures of contaminant exposure in small mammals on the oil sands.

Even though clinical, epidemiological and toxicological studies have progressively provided a better knowledge of the underlying mechanisms by which air pollution-derived particulate matter (PM) exerts its harmful health effects, further in vitro studies on relevant cell systems are still needed. Hence, aiming of getting closer to the human in vivo conditions, primary human bronchial epithelial cells derived from normal subjects (NHBE) or sensitive chronic obstructive pulmonary disease (COPD)-diseased patients (DHBE) were differentiated at the air-liquid interface. Thereafter, they were repeatedly exposed to air pollution-derived PM2.5 to study the occurrence of some relevant genetic and/or epigenetic endpoints. Concentration-, exposure- and season-dependent increases of OH-B[a]P metabolites in NHBE, and to a lesser extent, COPD-DHBE cells were reported; however, there were more tetra-OH-B[a]P and 8-OHdG DNA adducts in COPD-DHBE cells. No increase in primary DNA strand break nor chromosomal aberration was observed in repeatedly exposed cells. Telomere length and telomerase activity were modified in a concentration- and exposure-dependent manner in NHBE and particularly COPD-DHBE cells. There were a global DNA hypomethylation, a P16 gene promoter hypermethylation, and a decreasing DNA methyltransferase activity in NHBE and notably COPD-DHBE cells repeatedly exposed. Changes in site-specific methylation, acetylation, and phosphorylation of histone H3 (i.e., H3K4me3, H3K9ac, H3K27ac, and H3S10ph) and related enzyme activities occurred in a concentration- and exposure-dependent manner in all the repeatedly exposed cells. Collectively, these results highlighted the key role played by genetic and even epigenetic events in NHBE and particularly sensitive COPD-DHBE cells repeatedly exposed to air pollution-derived PM2.5 and their different responsiveness. While these specific epigenetic changes have been already described in COPD and even lung cancer phenotypes, our findings supported that, together with genetic events, these epigenetic events could dramatically contribute to the shift from healthy to diseased phenotypes following repeated exposure to relatively low doses of air pollution-derived PM2.5.

Although pharmaceuticals and personal care products have been used and introduced into the environment in large quantities, little information on potential ecological risks is currently available considering their effects on living organisms. We verified the feasibility of using synchrotron-based mid-infrared (SR-FTIR) spectromicroscopy to explore in vivo toxic effects on single living Chlorococcum sp. cells. The study provided important information to achieve a better understanding of the toxic mechanism of triclosan and carbamazepine on living algae Chlorococcum sp. Triclosan and carbamazepine had distinctive toxic effects on unicellular living algae. Most strikingly, triclosan had more dramatic toxic effects on biochemical components than carbamazepine. Triclosan can affect algae primarily by inhibiting fatty acid synthesis and causing protein aggregation. The toxicity response was irreversible at higher concentrations (100.000 μM), but attenuated at lower concentrations (0.391 μM) as time passes. Carbamazepine can produce hydrophobic interactions to affect the phospholipid bilayer and work on specific proteins to disfunction the cell membrane. Carbamazepine-exposed cells developed a resistance while extending exposure time. This is the first demonstration from an ecological standpoint that SR-FTIR can provide an innovative approach to reveal the toxicity of emerging pollutants in aquatic environments.

In this study, we investigate the convenience of quantile regression to predict extreme concentrations of NO2. Contrarily to the usual point-forecasting, where a single value is forecast for each horizon, probabilistic forecasting through quantile regression allows for the prediction of the full probability distribution, which in turn allows to build models specifically fit for the tails of this distribution.Using data from the city of Madrid, including NO2 concentrations as well as meteorological measures, we build models that predict extreme NO2 concentrations, outperforming point-forecasting alternatives, and we prove that the predictions are accurate, reliable and sharp. Besides, we study the relative importance of the independent variables involved, and show how the important variables for the median quantile are different than those important for the upper quantiles. Furthermore, we present a method to compute the probability of exceedance of thresholds, which is a simple and comprehensible manner to present probabilistic forecasts maximizing their usefulness.

Benzotriazole (BT) and its associated derivatives are used ubiquitously in industrial processes, and can be detected in indoor temperature coolants and in chemicals designed to inhibit corrosion. This chemical has been widely detected in aquatic environments and shows some degree of environmental persistence. Evidence has shown that BT exposure can negatively affect endocrine systems and can result in neurotoxicity in fish. However, no study has examined whether this chemical exhibits hepatotoxicity in fish, and if so, what are the underlying mechanism associated with the damage. To address this knowledge gap, we measured the liver proteome of adult male Chinese rare minnow (Gobiocypris rarus) exposed to either 0.05, 0.5, or 5 mg/L BT for 28 days. Overall, 17 proteins were induced and 9 were reduced in abundance following BT treatment (ratio > 1.5, p < 0.05). Pathway analysis revealed that cellular processes affected by BT included xenobiotic clearance, oxidative stress response, apoptosis, and translation. Moreover, transcripts related to these toxic pathways were also significantly affected by BT. In addition, rare minnows exposed to BT showed signs of hypertrophy of hepatocytes, nuclei pyknosis, and higher levels of cellular vacuolization compared to the controls, thus these early proteomic responses in the liver may be related to pathology (i.e. adverse outcome pathway). Our data demonstrate that BT dysregulates molecular responses in the liver and tissue pathology indicative of damage. This study provides new insight into BT hepatotoxicity in Chinese rare minnow.

Extensive dose response studies have assessed the potential of toxic chemical agents to induce aneuploidy in the yeast model. An assessment of such findings revealed that hormetic-like biphasic dose responses were commonly observed. A preliminary estimate of the frequency of the hormetic responses using a priori entry and evaluative criteria was approximately 65–80%. These findings suggest the possibility of hormetic effects being extended to genotoxic endpoints.

Recently, several bioavailability-based models have been shown to predict acute metal mixture toxicity with reasonable accuracy. However, the application of such models to chronic mixture toxicity is less well established. Therefore, we developed in the present study a chronic metal mixture bioavailability model (MMBM) by combining the existing chronic daphnid bioavailability models for Ni, Zn, and Pb with the independent action (IA) model, assuming strict non-interaction between the metals for binding at the metal-specific biotic ligand sites. To evaluate the predictive capacity of the MMBM, chronic (7d) reproductive toxicity of Ni-Zn-Pb mixtures to Ceriodaphnia dubia was investigated in four different natural waters (pH range: 7–8; Ca range: 1–2 mM; Dissolved Organic Carbon range: 5–12 mg/L). In each water, mixture toxicity was investigated at equitoxic metal concentration ratios as well as at environmental (i.e. realistic) metal concentration ratios. Statistical analysis of mixture effects revealed that observed interactive effects depended on the metal concentration ratio investigated when evaluated relative to the concentration addition (CA) model, but not when evaluated relative to the IA model. This indicates that interactive effects observed in an equitoxic experimental design cannot always be simply extrapolated to environmentally realistic exposure situations. Generally, the IA model predicted Ni-Zn-Pb mixture toxicity more accurately than the CA model. Overall, the MMBM predicted Ni-Zn-Pb mixture toxicity (expressed as % reproductive inhibition relative to a control) in 85% of the treatments with less than 20% error. Moreover, the MMBM predicted chronic toxicity of the ternary Ni-Zn-Pb mixture at least equally accurately as the toxicity of the individual metal treatments (RMSEMix = 16; RMSEZn only = 18; RMSENi only = 17; RMSEPb only = 23). Based on the present study, we believe MMBMs can be a promising tool to account for the effects of water chemistry on metal mixture toxicity during chronic exposure and could be used in metal risk assessment frameworks.

Vehicle emissions have become one of the key factors affecting the urban air quality and climate change in the Pearl River Delta (PRD) region, so it is important to design policies of emission reduction based on quantitative Co-benefits for air pollutants and greenhouse gas (GHG). Emissions of air pollutants and GHG by 2020 was predicted firstly based on the no-control scenario, and five vehicle emissions reduction scenarios were designed in view of the economy, technology and policy, whose emissions reduction were calculated. Then Co-benefits between air pollutants and GHG were quantitatively analyzed by the methods of coordinate system and cross-elasticity. Results show that the emissions reduction effects and the Co-benefits of different measures vary greatly in 2015–2020. If no control scheme was applied, most air pollutants and GHG would increase substantially by 20–64% by 2020, with the exception of CO, VOC and PM2.5. Different control measures had different reduction effects for single air pollutant and GHG. The worst reduction measure was Eliminating Motorcycles with average reducing rate 0.09% for air pollutants and GHG, while the rate from Updated Emission Standard was 41.74%. Eliminating Yellow-label Vehicle scenario had an obvious reduction effect for every single pollutant in the earlier years, but Co-benefits would descent to zero in later by 2020. From the perspective of emission reductions and co-control effect, Updated Emission Standard scenario was best for reducing air pollutants and GHG substantially (tanα=1.43 and Els=1.77).