Although runoff from trafficked urban areas is recognized as a potentially significant pathway of micropollutants, runoff pollution remains poorly documented, except for relatively few historical pollutants such as some metals and hydrocarbons. Therefore, in this work, road and parking lot runoff from four sites with contrasting traffic levels were analyzed for a very broad spectrum of molecules and elements. A total of 128 pollutants and micropollutants were monitored, including inorganic (n = 41) and organic (n = 87) pollutants. Both the dissolved and particulate phases were considered. For a reduced number of samples, non-targeted screening by high-resolution mass spectrometry (HRMS) was carried out. For targeted screening, the contamination profiles were quite homogeneous, but the concentrations significantly differed between the different sites. Sites with the highest traffic density exhibited the highest concentrations for polycyclic aromatic hydrocarbons (PAHs), some traffic-related metals, alkylphenols and phthalates. Overall, for most micropollutants, the parking lot runoff exhibited the lowest concentrations, and the specificity of this site was confirmed by its HRMS fingerprint. Non-target screening allowed the sites to be discriminated based on the occurrence of specific compounds. Unlike the results of targeted screening, the HRMS intra-site variability was lower than its inter-site variability. Unknown substances were tentatively identified, either characteristic of each site or ubiquitous of all samples.
The occurrence of nanoplastics (NPs) and microplastics (MPs) in aquatic ecosystems and their capacity to sorb hydrophobic pollutants is nowadays an issue of great concern. This study aimed to assess the potential bioavailability and acute toxicity of polystyrene (PS) NPs (50 and 500 nm) and of MPs (4.5 µm), alone and with sorbed benzo(a)pyrene (B(a)P), in the embryo/larval stages of brine shrimps and zebrafish. Exposure to pristine plastics up to 50.1 mg PS/L did not cause significant impact on brine shrimp survival, while some treatments of plastics-B(a)P and all concentrations of B(a)P (0.1–10 mg/L) resulted acutely toxic. In zebrafish, only the highest concentrations of MPs-B(a)P and B(a)P caused a significant increase of malformation prevalence. Ingestion of NPs was observed by 24–48 h of exposure in the two organisms (from 0.069 to 6.87 mg PS/L). In brine shrimps, NPs were observed over the body surface and within the digestive tract, associated with feces. In zebrafish, NPs were localized in the eyes, yolk sac, and tail at 72 h, showing their capacity to translocate and spread into the embryo. MP ingestion was only demonstrated for brine shrimps. In zebrafish embryos exposed to plastics-B(a)P, B(a)P appeared in the yolk sac of the embryos. The presence of B(a)P was also noticeable in brine shrimps exposed to 500 nm NPs-B(a)P. In conclusion, NPs entered and spread into the zebrafish embryo and PS NPs, and MPs were successful vectors of B(a)P to brine shrimp and zebrafish embryos. Particle size played a significant role in explaining the toxicity of plastics–B(a)P. Our study provides support for the idea that plastics may pose a risk to aquatic organisms when combined with persistent organic pollutants such as B(a)P.
The role of polychlorinated biphenyls (PCBs) on exposure-related endocrine effects has been poorly investigated in wild birds. This is the case for stress hormones including corticosterone (CORT). Some studies have suggested that environmental exposure to PCBs and altered CORT secretion might be associated. Here we investigated the relationships between blood PCB concentrations and circulating CORT levels in seven free-ranging polar seabird species occupying different trophic positions, and hence covering a wide range of PCB exposure. Blood ∑₇PCB concentrations (range: 61-115,632 ng/g lw) were positively associated to baseline or stress-induced CORT levels in three species and negatively associated to stress-induced CORT levels in one species. Global analysis suggests that in males, baseline CORT levels generally increase with increasing blood ∑₇PCB concentrations, whereas stress-induced CORT levels decrease when reaching high blood ∑₇PCB concentrations. This study suggests that the nature of the PCB-CORT relationships may depend on the level of PCB exposure.