The complex QDs-Indolicidin (QDs-Ind) has been previously shown to be a good antimicrobial system with a low acute toxicity on Daphnia magna (D. magna). However, multigenerational effects caused by exposure to QDs-Ind and after subsequent recovery are still unknown. In this study, we performed multigenerational exposure tests and we evaluated individual fitness, population growth, DNA alteration, expression of Dhb (haemoglobin), Vtg (vitellogenin), CYP4 (cytochrome P450s CYP4 family), and CYP314 (cytochrome P450s mitochondrial family 314) genes on three generation of D. magna. Results showed that the total amount of eggs produced per female and total number of brood per female and body lengths were significantly decreased, Dhb, CYP4 were upregulated while Vtg was down-regulated except at reproduction days when it was slightly up-regulated under QDs-Ind exposure. Random Amplification of Polymorphic DNA (RAPD) method has proven to be useful to qualitative assess of DNA damage during generation and to underline modification in somatic or germinal cells. The results of the study suggest that effects of chronic exposure cannot be ignored.

Reactive nitrogen (Nr) is an important driver of global change, causing alterations in ecosystem biodiversity and functionality. Environmental assessments require monitoring the emission and deposition of both the amount and types of Nr. This is especially important in heterogeneous landscapes, as different land-cover types emit particular forms of Nr to the atmosphere, which can impact ecosystems distinctively. Such assessments require high spatial resolution maps that also integrate temporal variations, and can only be feasibly achieved by using ecological indicators. Our aim was to rank land-cover types according to the amount and form of emitted atmospheric Nr in a complex landscape with multiple sources of N. To do so, we measured and mapped nitrogen concentration and isotopic composition in lichen thalli, which we then related to land-cover data. Results suggested that, at the landscape scale, intensive agriculture and urban areas were the most important sources of Nr to the atmosphere. Additionally, the ocean greatly influences Nr in land, by providing air with low Nr concentration and a unique isotopic composition. These results have important consequences for managing air pollution at the regional level, as they provide critical information for modeling Nr emission and deposition across regional as well as continental scales.

Exposure to lead(Pb) or cadmium(Cd) has been related to decreasing thyroxine in many previous studies. The underlying mechanisms have not been clarified. Heavy metal-induced thyroid autoimmunity in pregnant women has been found, despite having been rarely explored in the general population.We aimed to determine whether the blood levels of lead(BPb) or cadmium(BCd) related to the levels of sera antibodies to thyroid proteins and thyroid dysfunction in the general population.Our study included 5628 Chinese adults and was based on the 2014 SPECT-China study. Thyroid dysfunction and subclinical thyroid dysfunction were defined by total triiodothyronine (TT3), total thyroxine(TT4) and thyroid stimulating hormone (TSH).Thyroid peroxidase antibody (TPOAb), thyroglobulin antibodies (TGAb), TT3, TT4, and TSH were measured by immunochemiluminometric assays. BPb and BCd levels were tested by atomic absorption spectrometry. Linear and logistic regression models were used to analyze the associations.After adjustment for age, body mass index, smoking status (men only) and drinking status, the natural log(ln) BPb was positively related to the lnTPOAb (B = 0.062, P < 0.05) and to the lnTSH (B = 0.047, P < 0.01) in women. The lnBCd in women was positively related to the lnTGAb (B = 0.046, P < 0.05). In the adjusted logistic regression models, the BCd of women was positively related to their hypothyroid status and TGAb tertiles. The ORs of women in the middle and higher TPOAb tertiles were 1.38 (P < 0.001) and 1.35 (P < 0.001) times greater for every ln-unit increase in BPb, respectively. In men, no continuous correlation was found among variables.In women, BPb and BCd levels were related to higher TSH and hypothyroid status, respectively, suggesting a Pb and Cd induction of sex-biased thyroid autoimmunity.

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.

Eighteen polycyclic aromatic hydrocarbons (PAHs) were measured in surficial sediments along a marine transect from the North Pacific into the Arctic Ocean. The highest average Σ18PAHs concentrations were observed along the continental slope of the Canada Basin in the Arctic (68.3 ± 8.5 ng g−1 dw), followed by sediments in the Chukchi Sea shelf (49.7 ± 21.2 ng g−1 dw) and Bering Sea (39.5 ± 11.3 ng g−1 dw), while the Bering Strait (16.8 ± 7.1 ng g−1 dw) and Central Arctic Ocean sediments (13.1 ± 9.6 ng g−1 dw) had relatively lower average concentrations. The use of principal components analysis with multiple linear regression (PCA/MLR) indicated that on average oil related or petrogenic sources contributed ∼42% of the measured PAHs in the sediments and marked by higher concentrations of two methylnaphthalenes over the non-alkylated parent PAH, naphthalene. Wood and coal combustion contributed ∼32%, and high temperature pyrogenic sources contributing ∼26%. Petrogenic sources, such as oil seeps, allochthonous coal and coastally eroded material such as terrigenous sediments particularly affected the Chukchi Sea shelf and slope of the Canada Basin, while biomass and coal combustion sources appeared to have greater influence in the central Arctic Ocean, possibly due to the effects of episodic summertime forest fires.

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.

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.

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.

Plants and their associated bacteria have been suggested to play a role in air pollution mitigation, especially in urban areas. Particularly, epiphytic bacteria might be able to degrade atmospheric hydrocarbons. However, phyllospheric bacterial communities are highly variable depending on several factors, e.g. tree species, leaf age and physiology, environmental conditions. In this work, bacterial communities hosted by urban Platanus x acerifolia leaves were taxonomically characterized using high throughput sequencing of 16S rRNA gene, and their temporal and spatial variability was assessed by comparing samples collected from different locations in the city of Milan (Italy) and in different months. The diversity of alkane hydroxylase (alkB) phylotypes harboured by phyllospheric bacteria associated to urban Platanus trees was also evaluated. Results revealed that temporal changes, which are related to seasonality, acted as a stronger driver both on Platanus phyllospheric community structure and on alkB phylotype diversity than sampling location. Biodiversity of bacterial communities decreased along the growing season, leading to a strong dominance by the genus Stenotrophomonas. On the contrary, diversity of hydrocarbon-degrading populations increased over the months, although it resulted lower than that reported for other habitats. It was therefore hypothesized that atmospheric hydrocarbons might play a key role in the selection of phyllospheric populations in urban areas.

The role of marine plastic debris and microplastics as a carrier of hazardous chemicals in the marine environment is an emerging issue. This study investigated expanded polystyrene (EPS, commonly known as styrofoam) debris, which is a common marine debris item worldwide, and its additive chemical, hexabromocyclododecane (HBCD). To obtain a better understanding of chemical dispersion via EPS pollution in the marine environment, intensive monitoring of HBCD levels in EPS debris and microplastics was conducted in South Korea, where EPS is the predominant marine debris originate mainly from fishing and aquaculture buoys. At the same time, EPS debris were collected from 12 other countries in the Asia-Pacific region, and HBCD concentrations were measured. HBCD was detected extensively in EPS buoy debris and EPS microplastics stranded along the Korean coasts, which might be related to the detection of a quantity of HBCD in non-flame-retardant EPS bead (raw material). The wide detection of the flame retardant in sea-floating buoys, and the recycling of high-HBCD-containing EPS waste inside large buoys highlight the need for proper guidelines for the production and use of EPS raw materials, and the recycling of EPS waste. HBCD was also abundantly detected in EPS debris collected from the Asia-Pacific coastal region, indicating that HBCD contamination via EPS debris is a common environmental issue worldwide. Suspected tsunami debris from Alaskan beaches indicated that EPS debris has the potential for long-range transport in the ocean, accompanying the movement of hazardous chemicals. The results of this study indicate that EPS debris can be a source of HBCD in marine environments and marine food web.