Detection of genotoxicity and toxicity of wastewater treatment plant (WTP) effluents after pretreatment with ferrate (VI)

Abstracts / Toxicology Letters 229S (2014) S40–S252

P-2.74 Risk assessment of indoor exposure to formaldehyde: A potential threat José L. Domingo ∗ , Joaquim Rovira, Neus Roig, Marta Schuhmacher, Martí Nadal Universitat Rovira i Virgili, Reus, Spain Formaldehyde is a carcinogenic substance to humans, being included in the Group 1 by the IARC. In addition, the acute exposure to formaldehyde may cause eye and respiratory tract irritation as well as skin sensitization. The main indoor sources of formaldehyde are, among others, wood-pressed products, insulation materials, paints, household cleaning products, and cigarettes. Although this chemical is a well-known indoor pollutant, data on indoor concentrations of formaldehyde are scarce in some countries, such as Spain. In February 2014, samples of indoor air were collected by using personal air sampling pumps in three locations (bedroom, living room, and outdoor) of 10 randomly selected homes in Catalonia, Spain. Ten more samples were taken in different workplaces (e.g., offices, shops, classrooms, etc.). Mean levels of formaldehyde in air of bedrooms and living rooms were similar (27.3 and 22.5 ␮g/m3 , respectively), being also significantly correlated (p < 0.05). Airborne levels of formaldehyde in workplaces were also similar to those found indoors (mean: 22.5 ␮g/m3 ). On the other hand, air samples collected outdoors showed significantly lower concentrations, ranging from 0.96 to 3.37 ␮g/m3 . The mean 24-h inhalation to formaldehyde for a Catalan adult was estimated in 3.94 ␮g/kg day. The results of the human health risk assessment indicated that both non-carcinogenic (Hazard Quotient >1) and cancer (>10−4 ) risks were above the recommended guidelines. Despite these results are in agreement with those found in other European countries, especial attention should be paid on the indoor exposure to formaldehyde and the occurrence of other volatile organic compounds. http://dx.doi.org/10.1016/j.toxlet.2014.06.420 P-2.75 Ecotoxicity of PAHs in Mediterranean soils: The role of photodegradation under different climate change scenarios José L. Domingo 1,∗ , Montse Marquès 1 , Montse Mari 1 , Marta Schuhmacher 1 , Jordi Sierra 1,2 , Martí Nadal 1 Universitat Rovira i Virgili, Reus, Spain, 2 Universitat de Barcelona, Barcelona, Spain

1

Climate change is estimated to induce important changes in some environmental factors. In turn, polycyclic aromatic hydrocarbons (PAHs) are important airborne pollutants which are deposited in soils. This study was aimed at determining the ecotoxicological effects of temperature and solar radiation in PAH-polluted soils. The A horizon of two typical Mediterranean soils was contaminated by using a mixture of the US EPA priority 16 PAHs, including benzo(a)pyrene. Samples were incubated in a climate chamber and subjected to two different climate change scenarios, according to temperature (T) and solar radiation (rad): (a) base scenario, by applying current Mediterranean average climate conditions (T: 20 ◦ C, rad: 36,000 lux); (b) A2 IPCC climate change scenario (T = +4 ◦ C, radiation: 90,000 lux). In addition, soils covered by aluminum foil and subjected to the same conditions, were used as control samples. Soils were removed from the climate chamber daily during the first week, and 2, 4 and 8 weeks after the begin-

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ning of the irradiation test. Microtox® was used to measure any potential changes in the activity of the bioluminescent bacterium Vibrio fischeri in aqueous and organic phases. Moreover, 3-day germination tests were carried out by using Graminae, Raphanus and Lactuca seeds. Microtox® in aqueous phase and germination tests showed a low sensitivity to the PAH toxicity in soils. In turn, the Microtox® organic phase was tested to be a quick and effective method to assess the toxicity of PAHs in soils, being consistent with the physico-chemical properties (low solubility in water and high Kow ) of these chemicals. http://dx.doi.org/10.1016/j.toxlet.2014.06.421 P-2.76 Effects of prometryne on early life stages of common carp Josef Velisek ∗ , Jaroslava Lidová, Alzbeta Stara, Dalibor Koutnik, Jana Machova University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, South Bohemian Research Center of Aquaculture and Biodiversity of Hydrocenoses, Vodnany, Czech Republic The aquatic environment continues to be under threat by the use of pesticides resulting in high risk to non-target organisms. Such pesticides are carried into aquatic environments by surface runoff from sites of application and can negatively affect the health of aquatic organisms. Toxicity of prometryne on early life stages of common carp (Cyprinus carpio) was assessed. The developmental stages of carp were exposed to prometryne at four concentrations, 0.51 ␮g/L (reported concentration in Czech rivers), 0.08, 1.2, and 4.0 mg/L for 35 days. Lethal concentrations of prometryne at 35 days were estimated as 2.31 mg/L (LC50); lowest observed-effect concentration (LOEC) was 1.10 mg/L; and no observed-effect concentration (NOEC) was 0.85 mg/L. Fulton’s condition factor was significantly lower in fish exposed to 4.0 mg/L after 7, 14, and 21 days. By day 14, fish exposed to 4.0 mg/L prometryne showed lower mass and total length compared to controls. Fish exposed the 1.2 and 4.0 mg/L showed delay in development and severe hyperaemia in gill, liver, caudal and cranial kidney. Liver showed diffused steatosis associated with the loss of cellular shape and the presence of lipid inclusions in hepatic cells. Our data suggest that prometryne in the recorded environmental concentration 0.51 ␮g/L had no effect on early-life stages of carp. Supported by the project CENAQUA No. CZ.1.05/2.1.00/01.0024; CENAQUA II No. LO1205 NPU I program; by the Strengthening of excellence scientific teams in USB FFPW No. CZ.1.07/2.3.00/20.0024 and by the GAJU No. 018/2014/Z. http://dx.doi.org/10.1016/j.toxlet.2014.06.422 P-2.77 Detection of genotoxicity and toxicity of wastewater treatment plant (WTP) effluents after pretreatment with ferrate (VI) Katerina Malachova 1,∗ , Hana Sezimova 1 , Radovan Rozinek 2 1 Faculty of Science, University of Ostrava, Chittussiho 10, 700 10 Ostrava, Czech Republic, 2 Bochemie a.s., Lidická 326, 735 95 Nov´ y Bohumín, Czech Republic

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Abstracts / Toxicology Letters 229S (2014) S40–S252

Efficiency of the oxidative technology using ferrate (VI) [Fe(VI)] to accelerate remediation of effluents from WTP treating either municipal or municipal/industrial wastewaters was investigated. Fe(VI) accelerates degradation of many micropollutants and its application is very promising as it is able to oxidize a number of organic compounds, i.e. nitrogen-, sulfur- and chloroderivatives, tensides, aniline, cetylpyridium chloride, residues of many pharmaceuticals and hormonal preparations, and some inorganic compounds. Genotoxicity was evaluated by Ames test with and without the liver S9 activation. Aquatic toxicity was measured by Vibrio fischeri bioluminiscence test and Lemna minor inhibition test. The toxicity for higher organisms was detected by Sinapis alba growth inhibition test. The mutagenicity tests showed that the effectivity of oxidative degradation was proportionate to the amount of Fe(VI) applied. At concentrations below 10 mg l−1 the oxidation of pollutants was incomplete which lead to an increase of mutagenicity. The use of higher Fe(VI) concentrations resulted in a significant decrease of mutagenicity. The toxicity tests showed that Fe(VI) represented ecological friendly oxidants exhibiting an inhibitory effect when used at concentrations of ≥40 mg l−1 . The study was supported by the EU and CR projects CZ.1.05/2.1.00/03.0100, LO1208 and FR TI4/363. http://dx.doi.org/10.1016/j.toxlet.2014.06.423 P-2.78 Of mice and men: Mechanistic studies on the developmental neurotoxicity of polybrominated diphenyl ethers (PBDES) in a 3D in vitro model Katharina Dach 1,∗ , Henrik Alm 1,2 , Susanne Giersiefer 1 , Ellen Fritsche 1 1

IUF – Leibniz Institute for Environmental Medicine, Duesseldorf, NRW, Germany, 2 Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden Polybrominated diphenyl ethers (PBDEs) are brominated flame retardants causing neurodevelopmental deficits in rodents. Epidemiological studies also suggest an impact on human brain development. The molecular mechanisms of their developmental neurotoxicity (DNT) are inscrutable, but they might interfere with thyroid hormone (TH) signaling due to their endocrine disrupting properties. Since THs play a crucial role in brain development, the interaction of PBDEs with cellular TH signaling as a possible mechanism for DNT is investigated. PBDE effects are studied using two 3D in vitro models, based on human (h) and murine (m) neural progenitor cells (NPCs), which mimic basic processes of brain development: proliferation, migration, differentiation and apoptosis, and also allow to compare sensitivity between species. BDE-99, one of the main PBDEs found in human tissues, did not reduce migration and viability of mNPCs and hNPCs, but inhibited human and murine neuro- and oligodendrogenesis. Human oligodendrogenesis was the most sensitive endpoint being 10× more sensitive than human neurogenesis as least sensitive endpoint (IC50 : 2 ␮M and 23 ␮M). Sensitivity of murine neurogenesis and oligodendrogenesis differs only slightly (IC50 : 10 ␮M and 14 ␮M). Furthermore, BDE-99 reduced thyroid hormone triiodothyronine (T3 )-induced transcription of hairless, a gene directly regulated by TH receptor ␣ (THR␣), in hNPCs but not in mNPCs. Involvement of TH disruption in BDE-99-induced disturbances of NPC differentiation is the scope of ongoing experiments.

These results reveal that BDE-99 inhibits neuro- and oligodendrogenesis in a species-specific manner while human NPCs have a greater sensitivity towards BDE-99 than their murine counterparts. http://dx.doi.org/10.1016/j.toxlet.2014.06.424 P-2.79 The effect of saxitoxin on the differentiation of D3 embryonic stem cells into a neural lineage Katie O’Neill ∗ , Ian Musgrave The University of Adelaide, Adelaide, South Australia, Australia The neurotoxin saxitoxin (STX) is produced in both marine and freshwater environments. Its production by cyanobacteria in Australian freshwater makes STX a potential hazard to drinking water supplies and a concern to public health. STX blocks voltage-gated sodium channels, halting the inflow of sodium ions and subsequently the generation of action potentials. Acute exposure leads to paralysis and death by respiratory depression. Guidelines for acute exposure through drinking water exist, derived from guidelines established for acute exposure through shellfish ingestion; yet chronic low dose exposure, which is the likely pattern of exposure through drinking water, has not been investigated. Due to the involvement of voltage-gated sodium channels in neurite outgrowth and development we hypothesise that chronic exposure to STX could affect developing neurons. We therefore used murine embryonic stem cells to determine if STX inhibits their differentiation into a neural lineage. D3 cells were differentiated into a neural lineage using retinoic acid in the presence or absence of STX at the acute guideline level (3 ␮g/L) in accordance with the 4−/4+ principle. Cells were assessed by examination of morphological development of neuronal features and expression of 3 gene markers (oct4, mixL1 and nestin). Preliminary morphology results showed a statistically significant decrease in neuronal scores, suggesting STX at the guideline level reduced the neural progression of cells compared to controls. If results from the gene analysis confirm that differentiation is inhibited then further investigation into this pattern of exposure would be warranted, as this has implications for the safety of drinking water. http://dx.doi.org/10.1016/j.toxlet.2014.06.425 P-2.80 Route to route extrapolation factors for regulatory risk assessment—A probabilistic approach Katrin Schroeder 1,∗ , Simone Hoffmann-Doerr 2 , Inge Mangelsdorf 1 , Sylvia Escher 1 1

Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany, 2 Henkel AG & Co. KGaA, Duesseldorf, Germany In human risk assessment any relevant exposure route has to be addressed. Consequently, for numerous chemicals no-adverseeffect-levels have to be determined for all three routes (dermal, oral and inhalation), leading to testing that demands a large number of animals. On the other hand, the 3R principles (reduction, refinement and replacement of animal testing) shall be implemented in risk assessment according to several regulations, e.g. REACh. A reduction of animal numbers could be achieved by using route-to-route (R2R) extrapolation factors (EF) to derive the relevant route-specific no-adverse-effect-level. One prerequisite for