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Do Toxicity Identification and Evaluation Laboratory-Based Methods Reflect Causes of Field Impairment?
Citation:
HO, K. T., M. L. Gielazyn, M. C. PELLETIER, R. M. BURGESS, M. G. CANTWELL, M. PERRON, J. R. SERBST, AND R. L. JOHNSON. Do Toxicity Identification and Evaluation Laboratory-Based Methods Reflect Causes of Field Impairment? ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, 43(17):6857-6863, (2009).
Impact/Purpose:
This manuscript summarizes a series of experiments used in a weight of evidence approach to determine that the toxicant identified by Toxicity Identification Evaluation (TIE) laboratory techniques was the same toxicant that caused impairments in the field. This manuscript is of significance as the Agency recently released guidance on performing TIEs.
Description:
Sediment Toxicity Identification and Evaluation (TIE) methods have been developed for both interstitial waters and whole sediments. These relatively simple laboratory methods are designed to identify specific toxicants or classes of toxicants in sediments; however, the question of whether the same toxicant identified in the laboratory is causing effects in the field remains unanswered. In this study we used a number of different methods in a weight-of evidence approach to determine if laboratory TIE methods accurately reflect field effects. A TIE performed on sediments collected from the Elizabeth River (ER), VA, USA identified polycyclic aromatic hydrocarbons (PAHs) as the major toxicants. Several lines of evidence indicated PAHs were the major toxic agents in the field as well. Concentrations of PAHs in ER sediment were elevated relative to a nearby reference site. The comet assay, which measures DNA damage and is sensitive to PAHs, indicated adverse effects in in-situ caged Merceneria merceneria in ER relative to those from a reference site. Chemical analyses of exposed M. merceneria indicated that PAHs occurred in high concentrations in the bivalve tissue. Concentrations of PCBs, and other potential toxicants, were below detection levels in the same tissue. Our final lines of evidence were the responses of M. merceneria and the mysid shrimp, Americamysis bahia, exposed to ER sediment extracts and then exposed to ultraviolet (UV) radiation. UV radiation caused a toxic diagnostic response to PAHs, not found in PCB exposed organisms. The aggregation of these various lines of evidence supports the conclusion that PAHs were the likely cause of effects in both laboratory and field exposed organisms and that laboratory based TIE findings reflect causes of field impairment.