Development of a sediment bioassay to determine bioavailability of PAHs to fish

Abstract

Recent work has shown that MFO induction and loss of control of steroid hormone production occurs in fish after exposure to pulp mill effluents, PCBs, PAHs, and some pesticides. We had recently developed laboratory assays to evaluate the effluents on these responses, but were lacking a protocol for a sediment assay. This paper describes the development of a sediment test capable of demonstrating MFO induction in fish. MFO responses were evident in rainbow trout within 4 days of exposure to contaminated sediments. Further testing showed that fish were responding to chemicals from the sediments, but not from bottom water, and a survey of sediment from thirteen contaminated areas showed that MFO induction more closely paralleled PAH levels in the sediments than the observed PCB concentrations. The sites showing MFO induction were also the sites where sediment toxicity was demonstrated with laboratory bioassays using Daphnia magna and Hyalella azteca. The protocol has been further refined to describe the quantity of sediment required and duration of testing. This test will enable us to study the biochemical effects of exposure to contaminated sediments. The protocol could also be used to prioritize areas of contamination and to evaluate dredging impacts and remediation success.

Evaluation of an Exposure Assay to Measure Uptake of Sediment Pah by Fish

“…By eight days, induction approached control levels, likely because the fish had taken up and metabolized PAH that readily desorb from sediments. A similar pattern of response to HH sediments was observed by Munkittrick et al (1995), but over a longer time period. This suggests exposure to relatively labile compounds such as PAH, which are rapidly metabolized and excreted by fish (Niimi and Palazzo, 1986;Fragoso et al, 1998Fragoso et al, , 1999, in contrast to persistent compounds such as chlorinated dioxins or PCBs.…”

“…Hence, the sediments contain a wide range of PAH and metal concentrations ( Table I). The most contaminated sample was taken from Randle's Reef, in the same area as sediments sampled by Munkittrick et al (1995).…”

“…Munkittrick et al (1995) were among the first to demonstrate that laboratory bioassays of EROD activity of fish exposed to contaminated sediments provided a practical and sensitive index of bioavailability, with strong correlations among sites in PAH content and CYP1A response. However, only a few methodological variables that might affect test results have been evaluated.…”

Single and combined effects of selected pharmaceuticals at sublethal concentrations on multiple biomarkers in Carassius auratus

“…With regard to time response, EROD, GST and SOD activities reached maximum after 2 days of exposure, then fold induction decreased after longer exposure periods. Waterborne or sediment exposure of fish to PAHs has been reported to result in a rapid initial rise of EROD activity and after having reached a maximum, induction starts to decline after some time (Munkittrick et al 1995;Whyte et al 2000). Possibly this response pattern indicates that once the metabolic activity has been established, enzyme activities decline again to a steady state (Munkittrick et al 1995).…”

Variation of antioxidant/detoxification enzyme activities in response to benzo[a]pyrene in the gazami crab Portunus trituberculatus

“…Finally, EROD and GST activities were inhibited. Such reaction is universal among mammals, birds, and fishes (Munkittrick et al 1995). At the end of the release period, EROD and GST activities in the gill and liver of both test groups, except for the liver GST activity of the 0.45 μg L −1 test group, could recover to the level of the control group and remain stable (P > 0.05).…”