Ingestion of food or cereal products contaminated by deoxynivalenol (DON) and related derivatives poses a threat to the health of humans and animals. However, the toxicity and underlying mechanisms of 3-acetyldeoxynivalenol (3-Ac-DON), an acetylated form of deoxynivalenol, have not been fully elucidated. In the present study, we showed that 3-Ac-DON caused significant oxidative damage, as shown by elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic dehydrogenase (LDH) in serum, increased lipid peroxidation products, such as hydrogen peroxide (H₂O₂) and malondialdehyde (MDA), decreased activities of antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD). In addition, 3-Ac-DON exposure led to elevated infiltrations of immune cell, increased apoptosis and autophagy in the liver. Interestingly, 3-Ac-DON-resulted apoptosis and liver injury were partially reduced by autophagy inhibitors. Further study showed that 3-Ac-DON-treated mice had altered ultrastructural changes of endoplasmic reticulum (ER), as well as enhanced protein levels of p-IRE1α, p-PERK, and downstream targets, indicating activation of unfolded protein response (UPR) in the liver. Importantly, 3-Ac-DON induced ER stress, oxidative damage, cell death, infiltration of immune cells, and increased mRNA levels of inflammatory cytokines were significantly abolished by 4-phenylbutyric acid (4-PBA), an ER stress inhibitor, indicating a critical role of UPR signaling for the cellular damage of the liver in response to 3-Ac-DON exposure. In conclusion, using mice as an animal model, we showed that 3-Ac-DON exposure impaired the function of liver, as shown by oxidative damage, cell death, and infiltration of immune cell, in which ER stress played an important role. Restoration of the ER function might be a preventive strategy to reduce the deleterious effect of 3-Ac-DON on the liver of animals.

There is growing interest in understanding the contribution of environmental toxicant exposure in early life to development of cardiometabolic diseases (CMD) in adulthood. We aimed to assess associations of early life exposure to arsenic and cadmium with biomarkers of CMD in children in rural Bangladesh. From a longitudinal mother-child cohort in Matlab, Bangladesh, we followed up 540 pairs. Exposure to arsenic (U–As) and cadmium (U–Cd) was assessed by concentrations in urine from mothers at gestational week 8 (GW8) and children at ages 4.5 and 9 years. Blood pressure and anthropometric indices were measured at 4.5 and 9 years. Metabolic markers (lipids, glucose, hemoglobin A1c, adipokines, estimated glomerular filtration rate (eGFR) were determined in plasma/blood of 9 years old children. In linear regression models, adjusted for child sex, age, height-for-age z score (HAZ), BMI-for-age z score (BAZ), socioeconomic status (SES) and maternal education, each doubling of maternal and early childhood U–Cd was associated with 0.73 and 0.82 mmHg increase in systolic blood pressure (SBP) respectively. Both early and concurrent childhood U–Cd was associated with diastolic (D)BP (β = 0.80 at 4.5 years; β = 0.75 at 9 years). Each doubling of U–Cd at 9 years was associated with decrements of 4.98 mg/dL of total cholesterol (TC), 1.75 mg/dL high-density lipoprotein (HDL), 3.85 mg/dL low-density lipoprotein (LDL), 0.43 mg/dL glucose and 4.29 units eGFR. Each doubling of maternal U–Cd was associated with a decrement of 1.23 mg/dL HDL. Both maternal and childhood U–As were associated with decrement in TC and HDL. Multiple comparisons were checked with family-wise error rate Bonferroni-type-approach. The negative associations of arsenic and cadmium with biomarkers of CMD in preadolescent children indicated influence of both metal(loid)s on fat and carbohydrate metabolism, while cadmium additionally influenced kidney function and BP. Thus, fewer outcomes were associated with U–As compared to U–Cd at preadolescence.

Hydraulic fracturing flowback and produced water (HF-FPW), which contains polyaromatic hydrocarbons (PAHs) and numerous other potential contaminants, is a complex wastewater produced during the recovery of tight hydrocarbon resources. Previous studies on HF-FPW have demonstrated various toxicological responses of aquatic organisms as consequences of combined exposure to high salinity, dissolved organic compounds and particle/suspended solids-bound pollutants. Noteworthy is the lack of studies illustrating the potentially toxic effects of the FPW suspended solids (FPW-SS). In this study, we investigated the acute and sublethal toxicity of suspended solids filtered from six authentic FPW sample collected from two fracturing wells, using a sediment contact assay based on early-life stages of zebrafish (Danio rerio). PAHs profiles and acute toxicity tests provided initial information on the toxic potency of the six samples. Upon exposure to sediment mixture at two selected doses (1.6 and 3.1 mg/mL), results showed adverse effects in larval zebrafish, as revealed by increased Ethoxyresorufin-O-deethylase (EROD) activity. Transcriptional alterations were also observed in xenobiotic biotransformation (ahr, pxr, cyp1a, cyp1b1, cyp1c1, cyp1c2, cyp3a65, udpgt1a1, udpgt5g1), antioxidant response (sod1, sod2, gpx1a, gpx1b) and hormone receptor signaling (esr1, esr2a, cyp19a1a, vtg1) genes. The results demonstrated that even separated from the complex aqueous FPW mixture, FPW-SS can induce toxicological responses in aquatic organisms' early life stages. Since FPW-SS could sediment to the bottom of natural wetland acting as a continuous source of contaminants, the current findings imply the likelihood of long-term environmental risks of polluted sediments on aquatic ecosystems due to FPW spills.

Indoor environment constitutes an important source of industrial additive chemicals to human exposure. We hypothesized that the influence of residential environment on human exposure varies among different types of additive chemicals and differs between children and mothers. This study determined a suite of additive chemicals in house dust from South China dwellings (n = 47) and urine from child-mother pairs. Concentrations of phthalates (PAEs; median 601 μg/g) were 2–3 orders of magnitude greater than those of parabens (0.82 μg/g), bisphenols (3.31 μg/g), and benzophenone-related chemicals (2.69 μg/g). Urinary concentrations differed between children and mothers, but the pattern of differences varied between chemical groups. Children exhibited greater urinary levels of mono-PAEs than mothers (510 versus 395 ng/mL, p = 0.152), while the latter population exhibited greater levels of parabens and benzophenones. Regression analyses indicate a lack of association between dust and urinary levels for most chemicals, suggesting that other exposure pathways can complicate human exposure scenarios. Indeed, we estimated that the daily intake via dust ingestion only constituted 0.002–0.81% of total daily intake estimated based on urine data for mothers and 0.04–5.61% for children. Future efforts are needed to better characterize source-specific exposure for different populations.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been linked to the development of certain diseases. However, the relationship between PAH exposure and thyroid disorders remains unknown. We measured 10 of the most common hydroxylated PAHs (OH-PAHs) in the urine of thyroid nodular goiter (NG) patients, papillary thyroid carcinoma (PTC) patients, and healthy controls by gas chromatography-triple-quadrupole mass spectrometry (GC-MS/MS). We found that the concentrations of 2-hydroxyfluorene (2-OH-FLU), 2-hydroxydibenzofuran (2-OH-DBF), and 1-hydroxyphenanthrene (1-OH-PHE) in the NG group, and of 2-hydroxynaphthalene (2-OH-NAP), 2-OH-DBF, and 1-OH-PHE in the PTC group were significantly higher than those in controls. In addition, participants in the high tertiles of 2-OH-FLU and 1-OH-PHE had higher risk of NG. Besides these two OH-PAHs, elevated risk of NG was observed in women in the high tertiles of 1-hydroxynaphthalene (1-OH-NAP), 2-OH-NAP, 2-OH-DBF, and 3-hydroxyfluorene (3-OH-FLU). Furthermore, participants in the high tertiles of seven OH-PAHs, namely, 1-OH-NAP, 2-OH-NAP, 2-OH-DBF, 2-OH-FLU, 3-OH-FLU, 3/9-hydroxyphenanthrene (3/9-OH-PHE), and 1-OH-PHE, had elevated risk of PTC, and females in these high tertiles had an even higher risk of PTC. Our findings suggest that PAH exposure may increase the risk of NG/PTC, and there may be a gender-specific effect of PAH exposure on the development of NG/PTC.

To characterize the emissions of polycyclic aromatic hydrocarbons (PAHs) from residential biomass burning and coal combustion in field environments, smoke samples were collected from the combustion of six types of biomass in heated kangs and four types of coal in traditional stoves and semi-gasifier stoves. The emission factors (EFs) of the total PAH were in the range of 84.5–344 mg/kg for biomass burning, with lower EFs for biomass with higher densities, and in the range of 38.0–206 mg/kg for coal combustion, with lower EFs for coals with higher maturity. Moreover, EFs were lower from high-density biomass fuels (wood trunk, 84.5 ± 11.3 mg/kg) than low-maturity coals (bituminous coal, 206 ± 16.5 mg/kg). Parent, oxygenated, alkylated, and nitrated PAHs accounted for 81.1%, 12.6%, 6.2%, and 0.1%, respectively, of the total-PAH EFs from biomass burning, and 84.7%, 13.8%, 1.4%, and 0.1%, respectively, of the total-PAH EFs from coal combustion. PAH source profiles differed negligibly between biomass fuels but differed significantly between bituminous coal and anthracite coal fuels. The characteristic species of sources were phenanthrene, 9-fluorenone, and 2-nitrobiphenyl for biomass burning, and were phenanthrene, benzo[ghi]perylene, 1,4-naphthoquinone, and 2-nitrobiphenyl for coal combustion. The ratios of benzo[b]fluoranthene/(benzo[b]fluoranthene + benzo[k]fluoranthene) were 0.40–0.45 for biomass burning and 0.89–0.91 for coal combustion, and these significantly different values constitute unique markers for distinguishing these fuels in source apportionment. Benzo[a]pyrene-equivalent factor emissions were 2.79–11.3 mg/kg for biomass and 7.49–41.9 mg/kg for coal, where parent PAHs contributed 92.0%–95.1% from biomass burning and 98.6%–98.8% from coal combustion. Total-PAH emissions from residential heating were 1552 t across Shaanxi province, to which wheat straw (445 t) in biomass burning and bituminous coal (438 t) in coal combustion were the highest contributors. Results from this study provide crucial knowledge for the source identification of PAHs as well as for the design of abatement strategies against pollutant emissions.

The crude e-waste recycling has been regulated in China since the late 2000s; however, information on the recent levels and the ecological risks of e-waste derived contaminants such as halogenated flame retardants (HFRs) in the e-waste sites are limited. We therefore examined the concentrations of several HFRs in wild, prey-sized mud carps collected from a typical e-waste site in 2006, 2011 and 2016, to understand the exposure dynamics and ecological risk of these chemicals. Several ecological and biological parameters including δ¹⁵N, δ¹³C, body size and lipid content of the fish were also examined, to ensure an overall uniformity of the sample set among the sampling years. Among the HFRs measured, polybrominated diphenyl ethers (PBDEs) were detected at the highest concentrations (contributing >90% to ∑HFRs), followed by Dechlorane Plus (DPs), polybrominated biphenyls (PBBs), and alternative brominated flame retardants (ABFRs). The fish concentrations of ∑PBDEs, ∑PBBs and ∑DPs significantly dropped by 65%, 57% and 53% from 2006 to 2011, and 12%, 74% and 51% from 2011 to 2016, respectively; likely reflecting the positive impact of the environmental regulations on crude e-waste recycling. The ∑ABFRs concentrations were also decreased by 80% from 2006 to 2011, but increased by 127% from 2011 to 2016; suggesting possible fresh input of these novel HFRs in recent years. In addition to the changes in the HFR concentrations, contaminant profiles in the fish were also changed, possibly due to environmental degradation of the HFRs. Despite our conservative method of risk assessment, we found that PBDEs posed an important risk both for the mud carp and for piscivorous wildlife that inhabit the e-waste site.

Based on the fact that mycotoxins and the food-borne bacteria coexist in the natural environment and pose a significant health hazard to humans and animals, it is important to investigate the immunosuppressive mechanism of ZEA (zearalenone), DON (deoxynivalenol), and their combination in bacterial infections. In this study, we established a mouse model of mycotoxin low-dose exposure combined with Listeria monocytogenes infection and investigated the effects of ZEA, DON and their combination on Th1-mediated anti-intracellular bacterial infection based on CD4⁺ T cell activation and differentiation using both in vitro and in vivo analyses. The present study showed that both ZEA and DON aggravated Listeria monocytogenes infection in mice and affected the activation of CD4⁺ T cells and Th1 differentiation, including the effects on costimulatory molecules CD28 and CD152 and on cross-linking of IL-12 and IL-12R, by inhibiting T cell receptor (TCR) signaling. When compared with ZEA, DON was found to have a greater impact on many related indicators. Surprisingly, the combined effects of ZEA and DON did not appear to enhance toxicity compared to treatment with the individual mycotoxins. Our findings more clearly revealed that exposure to low-dose ZEA and DON caused immunosuppression in the body by mechanisms including inhibition of CD4⁺ T cells activation and reduction of Th1 cell differentiation, thus exacerbating infection of animals by Listeria monocytogenes.

Microplastic (MP) has been detected ubiquitously in freshwater systems. Until now MP sampling, however, is predominantly based on short-term net or pumping and filtration systems which can only provide snapshots of MP abundance; especially in flowing water bodies. To improve representativeness in the determination of MP occurrences in these aquatic compartments, an integrative approach that covers larger water volumes for a longer period of time is required. In this regard, surface water supplied drinking water treatment plants (DWTPs) represent an opportunity. In DWTPs, suspended solids from thousands of cubic metres of raw water are continuously removed over several hours and enriched in coagulation/flocculation and filtration processes. Our hypothesis was that MP is also removed to a full extent, like suspended solids, and that an integrative approach for identification and quantification in raw water can be derived from the analysis of MP in the treatment sludge. To prove this hypothesis, treatment sludge from a riverside DWTP (Warnow river, North-Eastern Germany) was analysed for MP > 50 μm. A sample purification protocol overcoming potential matrix effects caused by coagulants and flocculants was developed and validated. MP was analysed using micro-Raman spectroscopy. MP occurrence determined for the Warnow river was compared with in situ reference sampling using an established pumping and filtration system at relatively stable flow conditions. As result, the number of MP particles derived from treatment sludge was extrapolated to 196 ± 42 m⁻³ for the Warnow river and is statistically insignificantly different from 233 ± 36 m⁻³ identified by conventional water sampling. In addition, the polymer distribution and particles shape indicated the validity of the integrative concept. Consequently, the determination of MP abundance for freshwater systems based on DWTP treatment sludge represents an adequate method to estimate MP concentrations in flowing waters in an integrative way.

Mussels are suggested as bioindicators of marine microplastic pollution. However, they are selective in regards to accumulation of microplastics. To make studies more targeted and comparable, ultimately helping to determine the suitability of the mussel as a bioindicator species for microplastic exposure, we review the published literature that has directly or indirectly demonstrated particle selection in mussels. The reported difference between microplastic levels in mussel tissues and environmental matrices provides evidence for their selective uptake characteristics. Both the organ-specific fate characteristics of microplastics, and the different movement patterns of microplastics in the same organ, show that selective translocation processes take place. The selective elimination is reflected in multiple aspects which include (1) the different characteristics of microplastics in excretion and mussel body; (2) the different retention time of various microplastics in mussels; and (3) the tissue-specific change in the numbers of microplastics during the depuration process. This selectivity is affected by the characteristics of the microplastics, the environmental, or laboratory exposure concentrations, feeding status, and other factors. There are still many research gaps and contradictory viewpoints in this field due to this complexity. The current methodology needs improvement and a breakthrough in standardization.