Effects of tunnel wash water on biomarkers in three-spined stickleback (Gasterosteus aculeatus) and brown trout (Salmo trutta): A lab and field study
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The accumulated road pollution in tunnels is a source of contamination to the aquatic environment when tunnel wash water is released to recipient waters. Treatment facilities such as sedimentation ponds will remove most of the particle bound contaminants, but the discharge water nevertheless contains metals, PAHs and lower concentrations of a wide range of organic contaminants associated with roads and vehicles. These substances have the ability to cause harm in fish through effects such as oxidative stress, genotoxicity, compromised immunity and endocrine disruption. To determine the sub-lethal effects on fish exposed to tunnel wash water, a laboratory exposure study was set up and a field sampling campaign was conducted in a stream receving discharged tunnel wash water. The laboratory exposure study with stickleback (Gasterosteus aculeatus) and brown trout (Salmo trutta) was set up at the University of Oslo and fish were exposed for 10 and 25 days to filtered tunnel wash water from two tunnels, Granfoss and Nordby. Brown trout from the stream Årungenelva was sampled from two locations; upstream and downstream the outlet from Vassum sedimentation pond receiving effluent from the washes of three nearby tunnels. The level of PAH-metabolites in bile and EROD activity in gills was quantified in labexposed stickleback and showed that stickleback metabolised pyrene and phnenanthrene to hydroxy-metabolites, and that EROD activity in gills was significantly increased on day 5 and 10 of exposure. The transcriptional level of a selection of genes related to phase I metabolism and xenobiotic transport (CYP1A, ABCG2), heme synthesis (ALAS), phase II metabolism and oxidative stress (GST, GCS, GPx, MT), stress response (HSP70, HSP90), lipid metabolism (PPARγ) and endocrine function (VTG) was quantified in gill and liver of brown trout from both field and lab exposure. The results from the lab experiment showed that transcription of CYP1A and ALAS in gills increased following 25 days of exposure in both tunnel treatments, as did CYP1A, GST, HSP90 and VTG in liver tissue. In gill, ABCG2 was down-regulated and MT, GST, GCS and HSP90 up-regulated in brown trout exposed to either one of the tunnel treatments. GCS and HSP70 were up-regulated in liver following exposure to either one of the tunnel treatments. A more apparent effect on gene transcription was seen in the fish exposed to Nordby, reflecting the higher contaminant load in the Nordby tunnel wash water compared to Granfoss tunnel wash water. In brown trout from Årungenelva, transcription of MT and HSP90 in gills, and CYP1A and HSP70 in the liver was higher in fish from the upstream compared to the downstream location. Transcription of GPx and PPARγ in liver was higher in fish from the downstream location. Even though few differences in transcription were seen between the two field locations, the transcription level in genes that responded to tunnel wash water exposure in the lab study was as high or higher in the field samples. This could indicate that brown trout from both locations in Årungenelva is under a continuous exposure to road related contaminants. The tunnel wash water caused induction of genes related to biotransformation of xenobiotics, heme synthesis, endocrine function, mitigation of oxidative stress and stress responses in fish. Even though transcriptional effects should only be seen as a response to exposure, not necessarily higher level effects, the increased EROD activity in stickleback gill confirms that tunnel wash water has the ability to cause sub-lethal effects on an enzymatic level in fish.
Master thesis in toxicology. Department of Biosciences. Faculty of Mathematics and Natural Sciences.