Polybrominated diphenyl ethers (PBDEs) are still present in sewage sludge and sludge-amended soil, even though commercial PBDEs were prohibited or voluntarily phased out several years ago. In this study, levels and compositional profiles of seven major PBDE congeners in sludge are assessed in relation to their usage patterns in commercial products, and years of being banned and phased out in North America, Europe, and Asia. Annual accumulations and future long-term changes of PBDE in sludge-amended soil are estimated. BDE-209 has the highest concentration, followed by BDE-99 and BDE-47. The highest concentrations, up to 23,500 ng g−1, of PBDEs in sludge were found in North America until 2004–2007, whereas since then sludge PBDE concentrations, up to 6600 ng g−1 have been higher in Asia than on the other two continents. The amount of sludge applied and the soil organic matter content play important roles in determining PBDE concentrations in sludge-amended soil. The estimated concentrations of BDE-47, -99, and -209 in soils receiving sludge applications during the past 15 years are 40–300 times higher than in soils after the initial sludge application. The accumulated concentrations of BDE-47 and BDE-99 are expected to decrease by 99% between 2016 and 2100, whereas the decrease in the BDE-209 concentration is predicted to be approximately 87%.

Hexachlorobenzene (HCB) and pentachlorobenzene (PeCBz) have been listed as unintentional POPs in the annex of the Stockholm Convention and thus, attracted attention by government and researchers. Since the intentional production and use has ceased in most countries, the unintentional releases to the environment have increased. This study gathered 206 and 78 emission factors (EFs) of unintentional HCB and PeCBz from scientific publications and governmental reports, respectively. Most of the EFs referred to the release vector “air” (EFAir) and to a less extent to “product” (EFProduct). EFs were proposed for different source categories/classes used in the Toolkit according to the technologies that released the HCB or PeCBz. Overall, lowest and highest EFAir for HCB were found in the metallurgical industry range from 1 μg/t in well controlled plants (coke, iron and steel) up to 40,000 μg/t (secondary zinc). EFs for PeCBz were in similar order of magnitude. Due to lack of data, EFs to water, land or residue cannot be proposed. Using linear regression and statistical analysis such as Pearson correlation, we found strongest correlation of EFAir between HCB and PeCBz (R2 = 0.79, P < 0.01) and weaker, but still significant, correlations for EFAir between PCDD/PCDFTEQ and HCB (R2 = 0.56; P < 0.01) or PeCBz (R2 = 0.31 P < 0.01) for various thermal processes.

The recent discovery of pyrethroid-resistant Hyalella azteca populations in California, USA suggests there has been significant exposure of aquatic organisms to these terrestrially-applied insecticides. Since resistant organisms are able to survive in relatively contaminated habitats they may experience greater pyrethroid bioaccumulation, subsequently increasing the risk of those compounds transferring to predators. These issues were evaluated in the current study following toxicity tests in water with permethrin which showed the 96-h LC50 of resistant H. azteca (1670 ng L⁻¹) was 53 times higher than that of non-resistant H. azteca (31.2 ng L⁻¹). Bioaccumulation was compared between resistant and non-resistant H. azteca by exposing both populations to permethrin in water and then measuring the tissue concentrations attained. Our results indicate that resistant and non-resistant H. azteca have similar potential to bioaccumulate pyrethroids at the same exposure concentration. However, significantly greater bioaccumulation occurs in resistant H. azteca at exposure concentrations non-resistant organisms cannot survive. To assess the risk of pyrethroid trophic transfer, permethrin-dosed resistant H. azteca were fed to fathead minnows (Pimephales promelas) for four days, after which bioaccumulation of permethrin and its biotransformation products in fish tissues were measured. There were detectable concentrations of permethrin in fish tissues after they consumed dosed resistant H. azteca. These results show that bioaccumulation potential is greater in organisms with pyrethroid resistance and this increases the risk of trophic transfer when consumed by a predator. The implications of this study extend to individual fitness, populations and food webs.

The prevalence of antibiotic resistance genes (ARGs) in modern environment raises an emerging global health concern. In this study, soil samples were collected from three sites in petrochemical plant that represented different pollution levels of polycyclic aromatic hydrocarbons (PAHs). Metagenomic profiling of these soils demonstrated that ARGs in the PAHs-contaminated soils were approximately 15 times more abundant than those in the less-contaminated ones, with Proteobacterial being the preponderant phylum. Resistance profile of ARGs in the PAHs-polluted soils was characterized by the dominance of efflux pump-encoding ARGs associated with aromatic antibiotics (e.g., fluoroquinolones and acriflavine) that accounted for more than 70% of the total ARGs, which was significantly different from representative sources of ARG pollution due to wide use of antibiotics. Most of ARGs enriched in the PAHs-contaminated soils were not carried by plasmids, indicating the low possibilities of them being transferred between bacteria. Significant correlation was observed between the total abundance of ARGs and that of Proteobacteria in the soils. Proteobacteria selected by PAHs led to simultaneously enriching of ARGs carried by them in the soils. Our results suggested that PAHs could serve as one of selective stresses for greatly enriching of ARGs in the human-impacted environment.

Antibiotics and antibiotic resistance genes (ARGs) in soil can affect human health via the food chain. Biochar is a soil amendment but its impacts on ARGs and the microbial communities associated with soil and vegetables are unclear. Therefore, we established three lettuce pot culture experiments, i.e., O300: 300 mg/kg oxytetracycline (OTC), BO300: 300 mg/kg OTC + 2% biochar, and a control without OTC or biochar. We found that under BO300, the relative abundances of ARGs were reduced by 51.8%, 43.4%, and 44.1% in lettuce leaves, roots, and soil, respectively, compared with O300. intI1 was highly abundant in soil and lettuce, and it co-occurred with some ARGs (tetW, ermF, and sul1). Redundancy analysis and network analysis indicated that the bacterial community succession was the main mechanism that affected the variations in ARGs and intI1. The reduction of Firmicutes due to the biochar treatment of soil and lettuce was the main factor responsible for the removal of tetracycline resistance genes in leaves. Biochar application led to the disappearance of human pathogenic bacteria (HPB), which was significantly correlated with the abundances of ermF and ermX. In summary, biochar is an effective farmland amendment for reducing the abundances of antibiotics, ARGs, and HPB in order to ensure the safety of vegetables and protect human health.

Quantitative identification of nitrate (NO3−-N) sources is critical to the control of nonpoint source nitrogen pollution in an agricultural watershed. Combined with water quality monitoring, we adopted the environmental isotope (δD-H2O, δ18O-H2O, δ15N-NO3−, and δ18O-NO3−) analysis and the Markov Chain Monte Carlo (MCMC) mixing model to determine the proportions of riverine NO3−-N inputs from four potential NO3−-N sources, namely, atmospheric deposition (AD), chemical nitrogen fertilizer (NF), soil nitrogen (SN), and manure and sewage (M&S), in the ChangLe River watershed of eastern China. Results showed that NO3−-N was the main form of nitrogen in this watershed, accounting for approximately 74% of the total nitrogen concentration. A strong hydraulic interaction existed between the surface and groundwater for NO3−-N pollution. The variations of the isotopic composition in NO3−-N suggested that microbial nitrification was the dominant nitrogen transformation process in surface water, whereas significant denitrification was observed in groundwater. MCMC mixing model outputs revealed that M&S was the predominant contributor to riverine NO3−-N pollution (contributing 41.8% on average), followed by SN (34.0%), NF (21.9%), and AD (2.3%) sources. Finally, we constructed an uncertainty index, UI90, to quantitatively characterize the uncertainties inherent in NO3−-N source apportionment and discussed the reasons behind the uncertainties.

In this study, we aimed to identify the toxic effects of chlorpyrifos exposure on the tissues of common carp. For this purpose, we evaluated histopathological changes in the brain, gills, liver, kidney, testis, and ovaries after 21 days of chlorpyrifos exposure. Activation of 8-OHdG, cleaved caspase-3, and iNOS were assesed by immunofluorescence assay in chlorpyrifos-exposed brain and liver tissue. Additionally, we measured the expression levels of caspase-3, caspase-8, iNOS, MT1, CYP1A, and CYP3A genes in chlorpyrifos-exposed brain tissue, as well as the expression levels of FSH and LH genes in chlorpyrifos-exposed ovaries, using qRT-PCR. We observed severe histopathological lesions, including inflammation, degeneration, necrosis, and hemorrhage, in the evaluated tissues of common carp after both high and low levels of exposure to chlorpyrifos. We detected strong and diffuse signs of immunofluorescence reaction for 8-OHdG, iNOS, and cleaved caspase-3 in the chlorpyrifos-exposed brain and liver tissues. Furthermore, we found that chlorpyrifos exposure significantly upregulated the expressions of caspase-3, caspase-8, iNOS, and MT1, and also moderately upregulated CYP1A and CYP3A in the brain tissue of exposed carp. We also noted downregulation of FSH and LH gene expressions in chlorpyrifos-exposed ovary tissues. Based on our results, chlorpyrifos toxication caused crucial histopathological lesions in vital organs, induced oxidative stress, inflammation, and apoptosis in liver and brain tissues, and triggered reproductive sterility in common carp. Therefore, we can propose that chlorpyrifos toxication is highly dangerous to the health of common carp. Moreover, chlorpyrifos pollution in the water could threaten the common carp population. Use of chlorpyrifos should be restricted, and aquatic systems should be monitored for chlorpyrifos pollution.

The antagonistic effect of selenium (Se) on mercury (Hg) toxicity has been known for decades. Earlier studies mainly focused on Hg-Se interaction based on biokinetics and bioaccumulation, but the influences of Se on in vivo biotransformation of methylmercury (MeHg) have not been well understood. We conducted a 42-day exposure study to investigate the dynamic changes of MeHg and its primary degradation product - inorganic mercury (IHg) - in different organs of black seabream (Acanthopagrus schlegeli) exposed to different dietary Se levels. A physiologically based pharmacokinetic (PBPK) model was then developed to describe the biotransformation and disposition of MeHg under the influence of Se. Our results demonstrated that Se significantly increased the transformation from MeHg into IHg, thereby decreasing the accumulation of MeHg. The simulation further showed that the intestine was the major site for demethylation, with an estimated rate 1.5-fold higher in high Se treatment than in low Se treatment. However, the hepatic demethylation rate was extremely low and comparable between the two treatments (0.012–0.015 d−1). These results strongly suggested that the intestine instead of the commonly assumed liver was the major site for Hg-Se interaction. Furthermore, Se did not show significant influences on the distribution and elimination of MeHg, but promoted the uptake and elimination of the generated IHg from demethylation. Therefore, Se-induced demethylation especially in the intestine played an important role in mitigating the MeHg accumulation. This study provided new sight to elucidate the Hg-Se interaction in fish.

Per- and polyfluoroalkyl substances (PFASs) are a family of compounds that includes numerous compound classes. To date, only a subset of these PFASs have been studied thoroughly in the general population. In this study, pooled serum samples from Australia collected in 2002–2013 were analyzed for PFASs according to gender and age (age categories of 0–4 years, 5–15 years, 16–30 years, 31–45 years, 46–60 years, and >60 years), in total 54 pooled samples and 4920 individuals. Compound classes included were perfluorocarboxylic acids (PFCAs), perfluorosulfonic acids (PFSAs), and two groups of PFCA precursor compounds; polyfluoroalkyl phosphate diesters (diPAPs), and fluorotelomer sulfonic acids (FTSAs). Several PFASs that were not reported in previous studies of Australian serum samples were found in this sample set including; diPAPs, FTSAs, perfluoropentane sulfonic acid (PFPeS), perfluoroheptane sulfonic acid (PFHpS), perfluoroheptane carboxylic acid (PFHpA), perfluoroundecanoic acid (PFUnDA), perfluorododecanoic acid (PFDoDA), and perfluorotridecanoic acid (PFTrDA). Various temporal trends were observed with a significant reduction (p < 0.05) between 2002 and 2013 for 8:2 FTSA, perflurohexane sulfonic acid (PFHxS), PFHpS, PFOS, and perflurooctanoic acid (PFOA). Levels of longer-chained PFDA and PFUnDA started to decrease more recently, between 2006 and 2013, while PFDoDA increased during the same time period. Higher levels in younger age groups (0–4 and 5–15 years) compared to adults (>15 years) were found for 8:2 FTSA and PFHpA, while levels of PFHpS, PFOS, PFUnDA, PFDoDA and PFTrDA were higher in adult age groups compared to younger age groups. Gender-specific patterns were seen for PFOA, PFHxS, PFHpS and PFOS, where levels were lower in women. Changes in manufacturing processes were reflected in the temporal time trends, and differences in bioaccumulation potential between homologues could be associated with age trends. Our results emphasize the importance of including emerging classes of PFASs in biomonitoring studies.

The chemical composition of PM2.5 and cellular effects from exposure to fine aerosol extracts were studied for samples collected in Beijing, Tianjin, Shijiazhuang, and Hengshui, China in winter 2015. Effects of priority polycyclic aromatic hydrocarbons (PAHs) and their oxygenated derivatives (OPAHs) in PM2.5 on cell cultures were a major focus of the study. Total quantified PAHs and OPAHs at Shijiazhuang and Hengshui were higher than at Beijing and Tianjin, and benz(a)anthracene, chrysene and 1,8-naphthalic anhydride were the most abundant species. Exposure to PM2.5 extracts caused a concentration-dependent decline in cell viability and a dose-dependent increase in nitric oxide production. Two cytokines, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), also increased when A549 test cells were exposed to PM2.5 extracts. PAHs and OPAHs in PM2.5 can potentially cause cell damage and induce cytotoxicity and pro-inflammatory responses: benzo(a)anthracene-7,12-dione was highly correlated with NO production, dibenz(a,h)anthracene and 1,4-chrysenequinone were correlated with TNF-α production, and 1-naphthaldehyde was significantly correlated with IL-6 production. The study provides a new approach for evaluating relationships between air-quality and cell toxicity with respect to specific chemicals.