Globally, many river sediments are seriously contaminated with persistent organic pollutants (POPs) known to accumulate in aquatic food. In the Netherlands, toxicological risks of human exposure to dioxins and dioxin-like compounds led to a ban on eel fishing in the Rhine-Meuse delta. The aim of this study is to investigate differences in serum POP levels in consumers of eel from high-polluted areas and consumers of eel from low-polluted areas or aquaculture. In total 80 Dutch men were included, aged 40–70 years, with a habitual eel consumption of at least one portion (150 g) per month. Total levels of dioxins and dioxin-like compounds were measured in serum of all participants with the DR CALUX bioassay, validated with GC-MS. For a subgroup of 38 participants extensive POP measurements were performed. We revealed that consumption of eel from polluted rivers resulted in 2.5 and up to 10 times increased levels of dioxins and polychlorinated biphenyls (PCBs) respectively compared to controls. The highest PCB levels were detected for PCB 153, with a median level of 896 ng/g lipid and a maximum level of 5000 ng/g lipid in the high-exposed group. Furthermore, hydroxylated PCB metabolites (OH-PCBs: sum of 4-OH-CB107, 4-OH-CB146, 4′-OH-CB172, and 4-OH-CB187) were 8 times higher in men who consumed eel from polluted areas, and detected at levels (median 4.5 ng/g ww) reported to cause adverse health effects. Also, the majority of the perfluoroalkyl substances (PFASs) were significantly higher in consumers of eel from pullulated areas. In conclusion, this study is the first to reveal that (past) consumption of eel from polluted rivers resulted in high body burdens of dioxins, PCBs, OH-PCBs and PFASs. We confirmed the predictions made in a former risk assessment, and the high levels of dioxins and dioxin-like compounds as well as the OH-PCBs are of health concern.

Long-term exposure to primary traffic pollutants may be harmful for health but few studies have investigated effects on mortality. We examined associations for six primary traffic pollutants with all-cause and cause-specific mortality in 2003–2010 at small-area level using linear and piecewise linear Poisson regression models. In linear models most pollutants showed negative or null association with all-cause, cardiovascular or respiratory mortality. In the piecewise models we observed positive associations in the lowest exposure range (e.g. relative risk (RR) for all-cause mortality 1.07 (95% credible interval (CI) = 1.00–1.15) per 0.15 μg/m³ increase in exhaust related primary particulate matter ≤2.5 μm (PM2.5)) whereas associations in the highest exposure range were negative (corresponding RR 0.93, 95% CI: 0.91–0.96). Overall, there was only weak evidence of positive associations with mortality. That we found the strongest positive associations in the lowest exposure group may reflect residual confounding by unmeasured confounders that varies by exposure group.

Organohalogen pollutants (OHPs) including chlorinated paraffins (CPs), polybrominated diphenyl ethers (PBDEs) and other halogenated flame retardants (OHFRs) (dechlorane plus (DP), decabromodiphenyl ethane (DBDPE), 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), hexabromobenzene (HBB), hexabromocyclododecanes (HBCDs) and tetrabromobisphenol A (TBBPA)) originating from an e-waste recycling area in Guiyu, southern China were investigated in chicken and goose eggs. As expected, OHP concentrations were higher in chicken eggs collected from the location (site 1) approaching the e-waste recycling center than from the location (site 2) far from the e-waste recycling center. Also, much higher OHP levels were observed in goose eggs foraging in residential area (site 2) than that in agricultural area (site 1), suggesting a clear habitat dependent OHP bioaccumulation pattern both concerning distance from e-waste activities and type of foraging habitat. Goose eggs exhibited higher short chain chlorinated paraffins (SCCPs) concentrations but lower PBDE and OHFR levels than chicken eggs. The proportion of high brominated PBDEs (hepta-to deca-BDEs) was lower in goose eggs than that in chicken eggs and showed a clear decrease from site 1 to site 2. DP isomeric composition fanti values (the ratio of the anti-DP to the sum of the anti- and syn-DP) in goose eggs were significantly lower than those in chicken eggs (p < 0.001). These differences are likely a reflection of factors such as the species-specific differences in habitat preference and the differing environmental behaviors of the pollutants owing to their inherent properties (such as solubility and vapor pressure). Our findings suggested a high dietary intake of OHPs via home-produced eggs. For BDE99 there is a potential health concern with respect to the current dietary exposure via eggs.

4-Nitrophenol (PNP) is a persistent organic pollutant that was proven to be an environmental endocrine disruptor. The aim of this study was to evaluate the role of the estrogen receptor-α (ER-α) and aryl hydrocarbon receptor (AhR) signaling pathway in regulating the damage response to PNP in the small intestine of rats. Wistar-Imamichi male rats (21 d) were randomly divided into two groups: the control group and PNP group. Each group had three processes that were gavaged with PNP or vehicle daily: single dose (1 d), repeated dose (3 consecutive days) (3 d), and repeated dose with recovery (3 consecutive days and 3 recovery days) (6 d). The weight of the body, the related viscera, and small intestine were examined. Histological parameters of the small intestine and the quantity of mucus proteins secreted by small goblet cells were determined using HE staining and PAS staining. The mRNA expression of AhR, ER-α, CYP1A1, and GST was measured by real-time qPCR. In addition, we also analyzed the AhR, ER-α, and CYP1A1 expression in the small intestine by immunohistochemical staining. The small intestines histologically changed in the PNP-treated rat and the expression of AhR, CYP1A1, and GST was increased. While ER-α was significantly decreased in the small intestine, simultaneously, when rats were exposed to a longer PNP treatment, the damages disappeared. Our results demonstrate that PNP has an effect on the expression of AhR signaling pathway genes, AhR, CYP1A1, and GST, and ER-α in the rat small intestine.

Airborne particulate matter (PM) was collected in Beijing between 24 February and 12 March 2014 to investigate chemical characteristics and potential industrial sources of aerosols along with health risk of haze events. Results showed secondary inorganic aerosol was the major contributor to PM2.5 during haze days. Utilizing specific elements, including Fe, La, Tl and As, as fingerprinting tracers, four emission sources, namely iron and steel manufacturing, petroleum refining, cement plant, and coal combustion were explicitly identified; their elevated contributions to PM during haze days were also estimated. The average cancer risk from exposure to inhalable PM toxic metals was 1.53 × 10⁻⁴ on haze days, which is one order of magnitude higher than in other developed cities. These findings suggested heavy industries emit large amounts of not only primary PM but also precursor gas pollutants, leading to secondary aerosol formation and harm to human health during haze days.

The comet assay was used to study the DNA damage that was induced by dimethoate in the hemocyte cells of adult Chorthippus biguttulus grasshoppers (Insecta: Orthoptera) that originated from two sites with varying levels of pollution. The primary focus of the study was to examine whether continuous exposure to environmental stress can modify the effect of pesticides on genome stability. After three days of acclimation to laboratory conditions, the level of DNA damage in the hemocytes of Bow-winged grasshoppers was within a similar range in the insects from both areas. However, the level of DNA damage following dimethoate treatment was significantly higher in the insects from the reference area (Pogoria) than in the individuals from the heavily polluted location (Szopienice). Four hours after pesticide treatment, the Tail DNA (TDNA) in the hemocytes of the male and female specimens from Pogoria was as high as 75% and 50% respectively, whereas the values in males and females from Szopienice only reached 30% and 20%, respectively. A rapid decrease in DNA damage was observed in both populations 24 h after the pesticide application. The habitat of an insect (site), the administration of the dimethoate (treatment), and the period following the application of the pesticide (time), all significantly influenced the levels of DNA damage. No interactions related to TDNA were observed between the variables ‘sex’ and ‘treatment’. Similarly, the variable ‘sex’, when analyzed alongside ‘treatment’ and ‘site’ (the area from which the insects were collected), or ‘treatment’ and ‘time’ had no influence on TL. Exposure to dimethoate undoubtedly contributed to the formation of DNA damage in the hemocytes of adult C. biguttulus. However, the level of damage was clearly dependent on the place where the insects were captured.

Perfluorooctanesulphonic acid (PFOS) is a ubiquitous contaminant in the aquatic environment and our earlier studies demonstrated that chronic PFOS exposures lead to a female-biased sex ratio and decreased sperm quality in male zebrafish. The underlying mechanism for these reproductive effects is unknown. In the present study, 8 h post-fertilization (hpf) zebrafish were exposed to PFOS at 250 μg/L for 5 months, and the levels of sex hormones, expression of sex determination related genes, and histological and ultrastructural changes of gonads were fully characterized. During the sex differentiation period, we observed elevated estradiol (E2) and decreased testosterone (T) levels in whole tissue homogenates from PFOS exposed juveniles. In fully mature adult male fish, serum E2 levels were slightly increased, however, the estrogen receptor alpha (esr1) was significantly elevated in PFOS treated male gonads. Histological and electron microscopic examinations revealed structural changes in the gonads of PFOS exposed male and female adult zebrafish. In summary, chronic PFOS exposure disrupts sex hormone level and related gene expression and impairs gonadal development, which may contribute to the previously reported PFOS reproductive toxicity.

The sulfentrazone dechlorination using bimetallic nanoparticles of Fe/Ni was studied. Different variables that could influence the sulfentrazone conversion were investigated, such as nitrogen atmosphere, pH and dosage of the nanoparticles and initial concentration of sulfentrazone. The best results were obtained using controlled pH (pH 4.0) and 1.0 g L⁻¹ of nanomaterials, resulting in 100 % conversion in only 30 min. Kinetic studies were also conducted, evaluating the influence of different nanoparticle dosages (1.0 to 4.0 g L⁻¹), system temperatures (20 to 35 °C) and nickel levels in the composition of the nanomaterials (0.025 to 0.10 gNi/gFe). The mechanism of sulfentrazone conversion has changed due a direct reduction on the catalytic activity sites and indirect reduction by atomic hydrogen. Both mechanisms have followed pseudo-first order models. The conversion rate improved when the dosage of the nanomaterials, system temperature and nickel content in the composition of the nanocomposites were increased. Finally, the conversion products were elucidated by mass spectrometry and toxicity assays were performed using Daphnia Similis. The results showed that the dechlorination product is less toxic than sulfentrazone.

The Paranaguá Estuarine Complex (PEC) is an important socioeconomic estuary of the Brazilian coast that is influenced by the input of pollutants like polycyclic aromatic hydrocarbons (PAHs). Because of the apparent lack of comparative studies involving PAHs in different estuarine compartments, the aim of this study was to determine and compare PAH concentrations in surface sediment and suspended particulate material (SPM) in the PEC to evaluate their behaviour, compositions, sources and spatial distributions. The total PAH concentrations in the sediment ranged from 0.6 to 63.8 ng g−1 (dry weight), whereas in the SPM these concentrations ranged from 391 to 4164 ng g−1. Diagnostic ratios suggest distinct sources of PAHs to sediments (i.e., pyrolytic sources) and SPM (i.e., petrogenic sources such as vessel traffic). Thus, the recent introduction of PAHs is more clearly indicated in the SPM since oil related-compounds (e.g., alkyl-PAHs) remain present in similar concentrations. Further, this matrix may better reflect the current state of the environment at the time of sampling because of the absence of significant degradation.

Adsorption of weakly basic compounds by sludge is poorly understood, although it has important implications on the distribution and fate of such micropollutants in wastewater effluent and sludge. Additionally, many of these compounds are chiral, and it is likely that their interactions with sludge is stereoselective and that the process may be further modified by surfactants that coexist in these systems. Adsorption of (R) and (S)-enantiomers of five commonly used β-blockers, i.e., acebutolol, atenolol, metoprolol, pindolol and propranolol, on sludge was characterized through batch experiments. Stereoselectivity in adsorption increased with decreases in hydrophobicity of the β-blockers. The enantiomeric fraction (EF) of the amount of acebutolol, atenolol and metoprolol sorbed on sludge were 0.27, 0.55 and 0.32, respectively. Thus, Kd values of the (S)-enantiomers of acebutolol and metoprolol were approximately twice that of the (R)-enantiomer, that is, 109 ± 11 and 57 ± 8 L/kg compared to 52 ± 13 and 22 ± 8 L/kg, respectively. There was no statistically significant difference in Kd values of the enantiomers of pindolol and propranolol, suggesting stereoselectivity in adsorption was likely driven by specific polar interactions rather than hydrophobic interactions. The EF value of atenolol decreased from 0.55 ± 0.03 to 0.44 ± 0.04 after modifying the sludge with Triton X 100. These results suggested that surfactants altered adsorption of β-blockers to sludge, likely by forming ion pair complexes that promote hydrophobic interactions with the solid surfaces.