Environmental exposure to arsenic is a major public health challenge worldwide. In detailing the hallmark signs of chronic arsenic exposure, previous studies have shown that epigenetic and immune dysfunction are associated with arsenic-induced skin lesions; however, knowledge regarding interactions between the mechanisms listed above is limited. In this study, a total of 106 skin samples were collected over the past 20 years. Based on the presence or absence of high arsenic exposure, the participants were divided into arsenic exposure (72) and reference (34) groups. Additionally, the arsenic exposure group was further divided into the non-cancer group (31, including skin hyperpigmentation and hyperkeratosis) and the skin cancer group (41, including Bowen’s disease, basal cell carcinoma and squamous cell carcinoma) according to a skin histopathological examination. First, the associations among miR-155, NF-AT1 with immunological dysfunction and arsenic-induced skin lesions and carcinogenesis were confirmed using these skin samples. In the arsenic-exposed group, miR-155–5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-γ (IFN-γ) were significantly decreased (p < 0.05). Clear correlations were observed among these factors (p < 0.05). In immortalized human keratinocytes, silencing and overexpression of NF-AT1 could alter the expression and secretion of immunological dysfunction indicators (IL-2 and IFN-γ) that are induced by arsenic exposure (p < 0.05); however, miR-155–5p levels did not change significantly (p > 0.05). The miR-155–5p mimic and inhibitor could regulate the NF-AT1-mediated immunological dysfunction caused by arsenic (p < 0.05). Our study provides some limited evidence that miR-155–5p regulates the NF-AT1-mediated immunological dysfunction that is involved in the pathogenesis and carcinogenesis of arsenic. The second major finding was that Krt1 and Krt10 are markers of hyperkeratosis caused by arsenic, and Krt6c is a potential biomarker that can reflect arsenic carcinogenesis.

In the general population, chronic exposure to low-dose persistent organic pollutants (POPs), particularly organochlorine pesticides (OCPs), has been recently linked to many chronic diseases. Widespread contamination of the food chain and human adipose tissue has made avoiding exposure to these chemicals impossible; thus, alternative strategies for decreasing the chemical burden must be investigated. Recently, macronutrient intake was found to significantly modify the toxicokinetics of POPs in animal experimental studies. Thus, we evaluated whether macronutrient intake was related to serum concentrations of OCPs in healthy adults without cardio-metabolic diseases. Subjects included 1,764 adults, aged 20 years or above, who participated in the National Health and Nutrition Examination Survey 1999–2004. Macronutrient intake was assessed based on a 24-h dietary recall interview. Six individual OCPs commonly detected among the general population were evaluated as markers of OCPs and other coexisting lipophilic chemicals stored in adipose tissue and released into circulation. High fat intake was associated with lower concentrations of OCPs, while high carbohydrate intake showed the opposite result. When three types of fats were individually evaluated, both saturated fatty acids and monounsaturated fatty acids, but not polyunsaturated fatty acids, were inversely associated with serum concentrations of OCPs. Adjustment for possible confounders did not change the results. When stratified by age, gender, body mass index, and physical activity, these associations were similar in most subgroups. Thus, similar to the findings observed in animal experimental studies, a moderate-fat diet with low carbohydrate intake was related to low serum concentrations of OCPs in humans. Although these findings need to be replicated, changing dietary macronutrient intake can be investigated as a practical strategy for dealing with unavoidable lipophilic chemical mixtures such as OCPs in modern society.

Little is known about how forests adjust their gas-exchange mode while atmospheric CO₂ rises globally and air quality changes regionally. The present study aims at addressing this research gap for boreal spruce trees growing in three different regions of Canada, submitted to distinct levels of atmospheric emissions, by examining the amount of carbon gained per unit of water lost in trees, i.e., the intrinsic water use efficiency (iWUE).Under pristine air quality conditions, middle-to long-term trends passed from no-reaction mode to passive strategies due to atmospheric CO₂, and short-term iWUE variations mostly ensue from year-to-year climatic conditions. In contrast, in trees exposed to pollutants from a copper smelter and an oil-sands mining region, air quality deterioration generated swift, long-term iWUE rises immediately at the onset of operations. In this case, the very active foliar strategy sharply reduced the intra-foliar CO₂ (Ci) pressure. Statistical modeling allowed identifying emissions as the main trigger for the iWUE swift shifts; subsequent combined effects of emissions and rising CO₂ led to passive foliar modes in the recent decades, and short-term variations due to climatic conditions appeared all along the series.Overall, boreal trees under different regional conditions modified their foliar strategies mostly without changing their stem growth. These findings underline the potential of acidifying emissions for prompting major iWUE increases due to lowering the stomatal apertures in leaves, and the combined influence of rising CO₂ in modulating other foliar responses. A fallout of this research is that degrading air quality may create true divergences in the relationship between tree-ring isotopes and climatic conditions, an impact to consider prior to using isotopic series for paleo-climatic modeling.

Antibiotic resistance surveillance data is lacking in many parts of the world, limiting effective therapy and management of resistance development. Analysis of urban wastewater, which contains bacteria from thousands of individuals, opens up possibilities to generate informative surveillance data in a standardized and resource-efficient way. Here, we evaluate the relationship between antibiotic resistance prevalence in E. coli from wastewater and clinical samples by studying countries with different resistance situations as assessed by traditional clinical surveillance. Composite, influent wastewater samples were collected over 24 h from treatment plants serving major cities in ten European countries. Using a broth screening method, resistance to six antibiotic classes was analyzed for 2507 E. coli isolates (n = 247–252 per country). Resistance prevalence in wastewater E. coli was compared to that in clinical E. coli reported by the European Antibiotic Resistance Surveillance Network. Resistance prevalence was lower in wastewater than clinical E. coli but followed similar geographic trends. Significant relationships were found for resistance to aminopenicillins (R² = 0.72, p = 0.0019) and fluoroquinolones (R² = 0.62, p = 0.0072), but not for aminoglycosides (R² = 0.13, p = 0.31) and third-generation cephalosporins (R² = 0.00, p = 0.99) where regression analyses were based on considerably fewer resistant isolates. When all four antibiotic classes were taken into account, the relationship was strong (R² = 0.85, p < 0.0001). Carbapenem resistance was rare in both wastewater and clinical isolates. Wastewater monitoring shows promise as method for generating surveillance data reflecting the clinical prevalence of antibiotic resistant bacteria. Such data may become especially valuable in regions where clinical surveillance is currently limited.

Maternal nicotine exposure during lactation induces liver damage in adult male rats. However, the mechanism in males is unknown and females have not been tested. Here, we determined the liver lipid composition and lipogenic enzymes in male and female offspring at two ages in a model of postnatal nicotine exposure. Osmotic minipumps were implanted in lactating Wistar rat dams at postnatal day (PND) 2 to release 6 mg/kg/day of nicotine (NIC group) or saline (CON group) for 14 days. Offspring received a standard diet from weaning until euthanasia at PND120 (1 pup/litter/sex) or PND180 (2 pups/litter/sex). At PND120, NIC males showed lower plasma triglycerides (TG), steatosis degree 1, higher hepatic cholesterol (CHOL) ester, free fatty acids, monoacylglycerol content as well as acetyl-coa carboxylase-1 (ACC-1) and fatty acid synthase (FAS) protein expression in the liver compared to CON males. At this age, NIC females had preserved hepatocytes architecture, higher plasma CHOL, higher CHOL ester and lower total CHOL content in the liver compared to CON females. At PND180, NIC males showed steatosis degrees 1 and 2, higher TG, lower free fatty acids and total CHOL content in the liver and an increase in ACC-1 hepatic protein expression. NIC females had higher plasma TG and CHOL levels, no change in hepatic morphology, lower CHOL ester and free fatty acids in the liver, which also showed higher total ACC-1 and FAS protein expression. Maternal nicotine exposure induces long-term liver dysfunction, with an alteration in hepatic cytoarchitecture that was aggravated with age in males. Concerning females, despite unchanged hepatic cytoarchitecture, lipid metabolism was compromised, which deserves further attention.

Perfluorooctane sulfonate (PFOS) has been widely used as a surface coating for household products. It still exists in living environments despite being restricted, due to its bioaccumulation and long half-life. Studies have shown that PFOS has the ability to induce adipogenic differentiation of human cells. Human mesenchymal stem cells (hMSCs) distributed within the adipose tissue might be a potential target of accumulated PFOS. However, traditional end-point toxicity assays failed to examine the subtle changes of cellular function exposed to low-dose persistent organic pollutants in real time. In the present work, highly sensitive and long-retained (more than 30 days) fluorescence based polymeric nanosensors were developed and employed for real-time assessment of cellular functions. hMSCs were engineered with sensor molecules encapsulated poly (lactic-co-glycolic acid) (PLGA) particles. Once internalized by hMSCs, PLGA particles continuously release and replenish sensor molecules to cytoplasm, resulting in prolonged fluorescence signal against photo bleaching and dilution by exocytosis. With this method, the dynamic changes of viability, ROS induction, and adipogenic differentiation related mRNA expression of hMSCs were monitored. PFOS with the concentration as low as 0.1 μM can induce cellular ROS and enhance the PPARγ and ap2 mRNA expression, suggesting the effect on promoting adipogenic differentiation of hMSCs.

In recent years, antibiotic pollution has become worse, especially in China. In this study, the ecotoxicological effects of four frequently used antibiotics with different lipophilic degrees (log Kow) (sulfadiazine (SD), sulfamethazine (SM2), enrofloxacin (ENR), and norfloxacin (NOR)) at four concentrations of 1, 5, 20, and 50 mg L⁻¹ were examined using batch cultures of green alga Chlorella vulgaris and cyanobacterium Chrysosporum ovalisporum for 16 days based on changes in chlorophyll fluorescence parameters (chl a, Fv/Fm, and ΦPSII) and responses of the antioxidant system. Besides, the antibiotics removal efficiencies of the two microalgae were investigated. Sulfonamides (SD and SM2) had no significant inhibitory effect on the growth of C. ovalisporum, but had an inhibitory effect on C. vulgaris, whereas fluoroquinolones (ENR and NOR) significantly inhibited C. ovalisporum. The activities of superoxide dismutase, catalase, and glutathione reductase suggested that C. vulgaris was more tolerant to these antibiotics than C. ovalisporum. The increased malondialdehyde level in both algae indicated their tolerance against antibiotics. When compared with C. ovalisporum, C. vulgaris presented better capacity to remove antibiotics. In summary, the four antibiotics exerted time- or concentration-dependent ecotoxicological effects on the microalgae examined, whereas the microalgae could remove the antibiotics based on the log Kow of the antibiotics. The findings of this study contribute to effective understanding of the ecotoxicological effects of antibiotics and their removal by microalgae.

Biochar has a wide range of feedstocks, and different feedstocks often resulted in different properties, such as element distribution and heavy metal immobilization performance. In this work, batch experiments were conducted to assess the effectiveness of biochar pyrolyzed from kitchen waste (KWB), corn straw (CSB), and peanut hulls (PHB) on immobilization of Cd and Pb in contaminated soil by planting swamp cabbage (Ipomoea aquatica Forsk.) with a combination of toxicological and physiological tests. The results showed that biochar could all enhance the soil pH, and reduce extractable Pb and Cd in soil by 22.61%–71.01% (KWB), 18.54%–64.35% (CSB), and 3.28%–60.25% (PHB), respectively. The biochar led to a drop in Cd and Pb accumulation in roots, stems, and leaves by 45.43%–97.68%, 59.13%–96.64%, and 63.90%–99.28% at the dosage of 60.00 mg/kg, respectively. The root length and fresh weight of swamp cabbage were promoted, while superoxide dismutase (SOD) and peroxidase (POD) decreased after biochar treatment. The distribution of heavy metal fractions before and after biochar treatment indicated that biochar could transform Cd and Pb into a state of lower bioavailability, thus inhibiting Cd and Pb uptake by swamp cabbage. Biochar with different feedstocks could be ranked by the following order according to immobilization performance: KWB > CSB > PHB.

Co-presence of organic pollutants and heavy metals in soil is causing increasing concerns, but the lack of knowledge of relation between soil ecology and pollutant fate is limiting the developing of specific control strategy. This study investigated soil change under pyrene stress and its interaction with cadmium (Cd). Soil physicochemical properties were not seriously influenced. However, pollutants’ presence easily varied soil microbial activity, quantity, and diversity. Under high-level pyrene, Cd presence contributed to soil indigenous microorganisms’ adaption and soil microbial community structure stability. Soils with both pyrene and Cd presented 7.11–12.0% higher pyrene degradation compared with single pyrene treatment. High-throughput sequencing analysis indicated the proportion of Mycobacterium sp., a commonly known PAHs degrader, increased to 25.2–48.5% in treatments from 0.52% in control. This phenomenon was consistent with the increase of PAHs probable degraders (the ratio increased to 2.86–6.57% from 0.24% in control). Higher Cd bioavailability was also observed in soils with both pollutants than that with Cd alone. And Cd existence caused the elevation of Cd resistant bacterium Limnobacter sp. (increased to 12.2% in CdCK from 2.06% in control). Functional gene prediction also indicated that abundance of genes related to nutrient metabolism decreased dramatically with pollutants, while the abundances of energy metabolism, lipid metabolism, secondary metabolites biosynthesis-related genes increased (especially for aromatic compound degradation related genes). These results indicated the mutual effect and internal-interaction existed between pollutants and soils resulted in pollutants’ fate and soil microbial changes, providing further information regarding pollutants dissipation and transformation under soil microbial response.

Evidence for effects of PM₂.₅ on systemic oxidative stress in pregnant women is limited, especially in early pregnancy. To estimate the associations between ambient PM₂.₅ exposures and biomarkers of lipid peroxidation and total antioxidant capacity (T-AOC) in women with normal early pregnancy (NEP) and women with clinically recognized early pregnancy loss (CREPL), 206 early pregnant women who had measurements of serum malondialdehyde (MDA) and T-AOC were recruited from a larger case-control study in Tianjin, China from December 2017 to July 2018. Ambient PM₂.₅ concentrations of eight single-day lags exposure time windows before blood collection at the women’s residential addresses were estimated using temporally-adjusted land use regression models. Effects of PM₂.₅ exposures on percentage change in the biomarkers were estimated using multivariable linear regression models adjusted for month, temperature, relative humidity, gestational age and other covariates. Unconstrained distributed lag models were used to estimate net cumulative effects. Increased serum MDA and T-AOC were significantly associated with increases in PM₂.₅ at several lag exposure time windows in both groups. The net effects of each interquartile range increase in PM₂.₅ over the preceding 8 days on MDA were significantly higher (p < 0.001) in CREPL [52% (95% CI: 41%, 62%)] than NEP [22% (95% CI: 9%, 36%)] women. Net effects of each interquartile range increase in PM₂.₅ over the preceding 5 days on T-AOC were significantly lower (p = 0.010) in CREPL [14% (95% CI: 9%, 19%)] than NEP [24% (95% CI: 18%, 29%)] women. Exposure to ambient PM₂.₅ may induce systemic lipid peroxidation and antioxidant response in early pregnant women. More severe lipid peroxidation and insufficient antioxidant capacity associated with PM₂.₅ was found in CREPL women than NEP women. Future studies should focus on mechanisms of individual susceptibility and interventions to reduce PM₂.₅-related oxidative stress in the first trimester.