In this study, the interactions between microplastics, chosen among the most widely used in industry such as polypropylene (PP) and high-density polyethylene (HDPE), and a model freshwater microalgae, Chlamydomas reinhardtii, were investigated. It was shown that the presence of high concentrations of microplastics with size >400 μm did not directly impact the growth of microalgae in the first days of contact and that the expression of three genes involved in the stress response was not modified after 78 days. In parallel, a similar colonization was observed for the two polymers. However, after 20 days of contact, in the case of PP only, hetero-aggregates constituted of microalgae, microplastics and exopolysaccharides were formed. An estimation of the hetero-aggregates composition was approximately 50% of PP fragments and 50% of microalgae, which led to a final density close to 1.2. Such hetero-aggregates appear as an important pathway for the vertical transport of PP microplastics from the water surface to sediment. Moreover, after more than 70 days of contact with microplastics, the microalgae genes involved in the sugar biosynthesis pathways were strongly over-expressed compared to control conditions. The levels of over-expression were higher in the case of HDPE than in PP condition. This work presents the first evidence that depending on their chemical nature, microplastics will follow different fates in the environment.

Mining activities have introduced various pollutants to surrounding aquatic and terrestrial environments, causing adverse impacts to the environment. Indigenous microbial communities are responsible for the biogeochemical cycling of pollutants in diverse environments, indicating the potential for bioremediation of such pollutants. Antimony (Sb) has been extensively mined in China and Sb contamination in mining areas has been frequently encountered. To date, however, the microbial composition and structure in response to Sb contamination has remained overlooked. Sb and As frequently co-occur in sulfide-rich ores, and co-contamination of Sb and As is observed in some mining areas. We characterized, for the first time, the microbial community profiles and their responses to Sb and As pollution from a watershed heavily contaminated by Sb tailing pond in Southwest China. The indigenous microbial communities were profiled by high-throughput sequencing from 16 sediment samples (535,390 valid reads). The comprehensive geochemical data (specifically, physical-chemical properties and different Sb and As extraction fractions) were obtained from river water and sediments at different depths as well. Canonical correspondence analysis (CCA) demonstrated that a suite of in situ geochemical and physical factors significantly structured the overall microbial community compositions. Further, we found significant correlations between individual phylotypes (bacterial genera) and the geochemical fractions of Sb and As by Spearman rank correlation. A number of taxonomic groups were positively correlated with the Sb and As extractable fractions and various Sb and As species in sediment, suggesting potential roles of these phylotypes in Sb biogeochemical cycling.

Mercury (Hg) is recognized as a dangerous contaminant due to its bioaccumulation and biomagnification within trophic levels, leading to serious health risks to aquatic biota. Therefore, there is an urgent need to unravel the mechanisms underlying the toxicity of Hg. To this aim, a metabolomics approach based on protonic nuclear magnetic resonance (1H NMR), coupled with chemometrics, was performed on the gills of wild golden grey mullets L. aurata living in an Hg-polluted area in Ria de Aveiro (Portugal). Gills were selected as target organ due to their direct and continuous interaction with the surrounding environment. As a consequence of accumulated inorganic Hg and methylmercury, severe changes in the gill metabolome were observed, indicating a compromised health status of mullets. Numerous metabolites, i.e. amino acids, osmolytes, carbohydrates, and nucleotides, were identified as potential biomarkers of Hg toxicity in fish gills. Specifically, decrease of taurine and glycerophosphocholine, along with increased creatine level, suggested Hg interference with the ion-osmoregulatory processes. The rise of lactate indicated anaerobic metabolism enhancement. Moreover, the increased levels of amino acids suggested the occurrence of protein catabolism, further supported by the augmented alanine, involved in nitrogenous waste excretion. Increased level of isobutyrate, a marker of anoxia, was suggestive of onset of hypoxic stress at the Hg contaminated site. Moreover, the concomitant reduction in glycerophosphocholine and phosphocholine reflected the occurrence of membrane repair processes. Finally, perturbation in antioxidant defence system was revealed by the depletion in glutathione and its constituent amino acids. All these data were also compared to the differential Hg-induced metabolic responses previously observed in liver of the same mullets (Brandão et al., 2015). Overall, the environmental metabolomics approach demonstrated its effectiveness in the evaluation of Hg toxicity mechanisms in wild fish under realistic environmental conditions, uncovering tissue-specificities regarding Hg toxic effects namely in gills and liver.

To increase understanding on the mechanisms of cultivar difference in contaminant accumulation in crops, this study was designed to compare the physiological responses to di-n-butyl phthalate (DBP) exposure between low (Lvbao70) and high (Huaguan) DBP cultivars of Chinese flowering cabbage (Brassica parachinensis L.). Under high DBP exposure, significant differences in various physiological responses were observed between the two cultivars, which might account for the variation in DBP accumulation. Ultrastructure observation also showed different alterations or damages in the mesophyll cell structures between both cultivars, especially for the chloroplast disintegration, starch grain quantity, and plastoglobuli accumulation. Compared with Huaguan, Lvbao70 suffered greater decreases in biomass, chlorophyll content, carbon assimilation, gas exchange parameters, photosynthetic electron transport capacity, and antioxidase activities, which would have resulted in a great reduction of photosynthetic capacity. Although Lvbao70 enhanced energy dissipation and activities of some antioxidant enzymes, they did not provide sufficient protection against oxidative damage caused by DBP. The result suggested that the lower DBP tolerance of Lvbao70 might be associated with its poor physiological performances, which was responsible for its lower DBP accumulation to protect itself from toxicity. Additionally, Lvbao70 had a significantly lower transpiration rate and stomatal conductance than Huaguan, which might be the factors regulating DBP-accumulation variation.

Our previous research showed that endosulfan triggers the extrinsic coagulation pathway by damaging endothelial cells and causes hypercoagulation of blood. To identify the mechanism of endosulfan-impaired endothelial cells, we treated human umbilical vein endothelial cells (HUVECs) with different concentrations of endosulfan, with and without an inhibitor for Notch, N-[N-(3, 5-difluorophenacetyl)-1-alanyl]S-Phenylglycinet-butylester (DAPT, 20 μM), or a reactive oxygen species (ROS) scavenger, N-Acetyl-l-cysteine (NAC, 3 mM), for 24 h. The results showed that endosulfan could inhibit cell viability/proliferation by increasing the release of lactate dehydrogenase (LDH), arresting the cell cycle in both S and G2/M phases, and inducing apoptosis in HUVECs. We also found that endosulfan can damage microfilaments, microtubules, and nuclei; arrest mitosis; remarkably increase the expressions of Dll4, Notch1, Cleaved-Notch1, Jagged1, Notch4, Hes1, and p21; and significantly induce ROS and malondialdehyde production in HUVECs. The presence of DAPT antagonized the above changes of cycle arrest, proliferation inhibition, and expressions of Dll4, Notch1, Cleaved-Notch1, Hes1, and p21 caused by endosulfan; however, NAC could attenuate LDH release; ROS and malondialdehyde production; apoptosis; and the expression levels of Dll4, Notch1, Cleaved-Notch1, Notch4, and Hes1 induced by endosulfan. These results demonstrated that endosulfan inhibited proliferation through the Notch signaling pathway as a result of oxidative stress. In addition, endosulfan can damage the cytoskeleton and block mitosis, which may add another layer of toxic effects on endothelial cells.

This study evaluated concentrations of main air pollutants in a Portuguese preschool (indoors/outdoors) environment, with emphasis on elemental characterization of different PM fractions, and estimated risks for the pupils (aged 3–5 years). With exception to total volatile organic compounds, levels of PM10, PM2.5, CO, CO2, and formaldehyde were below legislative guidelines. Calcium, sodium, aluminium, and potassium were the most abundant elements in indoor PM (82–84% of the analysed content) resulting mainly from crustal sources. Carcinogenic elements (1–2% of the indoor analysed content) were mostly PM2.5-bound (83–91%). Indoor-to-outdoor ratios of individual elements indicated contributions of indoor origin and from penetration of outdoor emissions indoors; trace metals were associated with ambient anthropogenic emissions (namely traffic). Non-carcinogenic and carcinogenic risks from overall preschool exposure were acceptable for children; for adults carcinogenic risks exceeded (4–11 times) the USEPA recommend value of 10−6, being 8–40 times higher than for children.

Mercury (Hg) accumulation records spanning the last 16,000 years before present (yr BP, relative to AD 1950) were derived from a peat core collected from Dajiuhu mire, central China. The natural Hg concentration and accumulation rate (free from anthropogenic influence) were 135.5 ± 53.9 ng g−1 and 6.5 ± 4.5 μg m−2 yr−1, respectively. The increase in Hg flux that started from a core depth of 96.5 cm (3358 cal yr BP) is independent of soil erosion and organic matter content. We attribute this to an increase in atmospheric Hg deposition derived from regional anthropogenic activities. Anthropogenic Hg accumulation rates (Hg-ARA) in the pre-industrial period peaked during the Ming and the early Qing dynasties (582–100 cal yr BP), with Hg-ARA of 9.9–24.6 and 10.7–24.4 μg m−2 yr−1, respectively. In the industrial interval (post∼1850 AD), Hg-ARA increased progressively and reached 32.7 μg m−2 yr−1 at the top of the core. Our results indicate the existence of regional atmospheric Hg pollution spanning the past ∼3400 years, and place recent Hg enrichment in central China in a broader historical context.

It is well-known that the health effects of PM increase as particle size decreases: particularly, great concern has risen on the role of UltraFine Particles (UFPs). Starting from the knowledge that the main fraction of atmospheric aerosol in Rome is characterized by significant levels of PM2.5 (almost 75% of PM10 fraction is PM2.5), the paper is focused on submicron particles in such great urban area. The daytime/nighttime, work-/weekdays and cold/hot seasonal trends of submicron particles will be investigated and discussed along with NOx and total PAH drifts demonstrating the primary origin of UFPs from combustion processes. Furthermore, moving from these data, the total dose of submicron particles deposited in the respiratory system (i.e., head, tracheobronchial and alveolar regions in different lung lobes) has been estimated. Dosimeter estimates were performed with the Multiple-Path Particle Dosimetry model (MPPD v.2.1). The paper discusses the aerosol doses deposited in the respiratory system of individuals exposed in proximity of traffic. During traffic peak hours, about 6.6 × 1010 particles are deposited into the respiratory system. Such dose is almost entirely made of UFPs. According to the greater dose estimated, right lung lobes are expected to be more susceptible to respiratory pathologies than left lobes.