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Airborne particulate matter (PM) is a recognized risk factor for human populations. Here we assessed the toxic potential of the organic constituents from PM collected in urban and rural sites during warm and cold periods of 2012/2013, and fractionated into 6 size fractions. The finest PM fraction (<0.5 μm) showed the highest biological activity (dioxin-like activity and fish embryotoxicity) in all samples, and the maximal activity was observed in rural samples from the cold period. Zebrafish embryo transcriptome analysis showed a strong induction of the AhR signaling pathway correlated to PAH concentrations. Oxidative stress-related genes and pancreatic and eye-lens gene markers appeared de-regulated in embryos exposed to urban extracts, whereas exposure to rural extracts affected genes implicated in basic cellular functions. The observed effects can be directly related to air pollution-related human disorders, suggesting different potential adverse outcomes for human populations exposed to air pollution from specific sources.

Atmospheric polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants that represent a risk not only to humans, but to all living organisms. High-molecular weight PAHs are more toxic than lighter relatives, and also have a higher tendency to bind onto air particles (i.e., particle matter, PM). PM is a major constituent of air pollution. Adequate assessment of the biological impact of PM requires the analysis, not only of the effects on human health, but also on the environment. Since the aquatic systems work as a natural sink to these air pollutants, assessing the effects of particle-bound PAHs on aquatic organisms may further characterize its potential aquatic toxicity, also providing simple and low-cost alternative assays to investigate PM biological effects in vivo. We review the current scientific literature, addressing the atmospheric PAHs fate, transformation and deposition, pertinent particle-bound PAHs toxicity data, and the potential aquatic toxic burden. Conceptual and experimental procedures that could improve future investigations and risk assessments are also considered.

Atmospheric particulate matter (PM) is a recognized risk factor contributing to a number of diseases in human populations and wildlife globally. Organic matter is a major component of PM, but its contribution to overall toxicity of PM has not been thoroughly evaluated yet. In the present work, the biological activity of organic extracts from PM1 (particles with less than 1 μm of aerodynamic diameter) collected from an urban road site in the centre of Barcelona (NE Spain) was evaluated using a yeast-based assay (AhR-RYA) and different gene expression markers in zebrafish embryos. Dioxin-like activity of the extracts correlated to primary emissions from local traffic exhausts, reflecting weekday/weekend alternance. Expression levels of cyp1a and of gene markers for key cellular processes and development (ier2, fos) also correlated to vehicle emissions, whereas expression of gene markers related to antioxidant defence and endocrine effects (gstal, hao1, ttr) was strongly reduced in samples with strong contribution from regional air masses with aged secondary organic species or with strong influence of biomass burning emissions. Our data suggest that the toxic potential of PM1 organic chemical constituents strongly depends on the emission sources and on the process of ageing from primary to secondary organic aerosols.

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Cadmium is a priority hazardous substance, persistent in the aquatic environment, with the capacity to interfere with crustacean moulting. Moulting is a vital process dictating crustacean growth, reproduction and metamorphosis. However, for many organisms, moult disruption is difficult to evaluate in the short term, what limits its inclusion in monitoring programmes. N-acetyl-β-D-glucosaminidase (NAGase) is an enzyme acting in the final steps of the endocrine-regulated moulting cascade, allowing for the cast off of the old exoskeleton, with potential interest as a biomarker of moult disruption. This study investigated responses to waterborne cadmium of NAGase activity of Carcinus maenas originating from estuaries with different histories of anthropogenic contamination: a low impacted and a moderately polluted one. Crabs from both sites were individually exposed for seven days to cadmium concentrations ranging from 1.3 to 2000 μg/L. At the end of the assays, NAGase activity was assessed in the epidermis and digestive gland. Detoxification, antioxidant, energy production, and oxidative stress biomarkers implicated in cadmium metabolism and tolerance were also assessed to better understand differential NAGase responses: activity of glutathione S-transferases (GST), glutathione peroxidase (GPx) glutathione reductase (GR), levels of total glutathiones (TG), lipid peroxidation (LPO), lactate dehydrogenase (LDH), and NADP(+)-dependent isocitrate dehydrogenase (IDH). Animals from the moderately polluted estuary had lower NAGase activity both in the epidermis and digestive gland than in the low impacted site. NAGase activity in the epidermis and digestive gland of C. maenas from both estuaries was sensitive to cadmium exposure suggesting its usefulness for inclusion in monitoring programmes. However, in the digestive gland NAGase inhibition was found in crabs from the less impacted site but not in those from the moderately contaminated one. Altered glutathione levels were observed in cadmium-treated crabs from the contaminated site possibly conferring enhanced tolerance to these animals through its chelator action. Investigation of enhanced tolerance should thus be accounted for in monitoring programmes employing NAGase as biomarker to avoid data misinterpretation.