Raleigh Ecological Services Field Office
Conserving the Nature of America

Publications

The following materials document investigations of the Raleigh Field Office's Environmental Contaminants Program or those of our partners. Complete references and abstracts are available here; please contact the office directly for copies of publications, reports, or presentations.

2008 Publications

Augspurger, T.P., D.E. Tillitt, S.J. Bursian, S.D. Fitzgerald, D.E. Hinton and R.T. Di Giulio. 2008. Embryo toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin to the wood duck (Aix sponsa). Archives of Environmental Contamination and Toxicology. In press. http://dx.doi.org/10.1007/s00244-008-9198-2

  • We examined the sensitivity of the wood duck (Aix sponsa) embryo to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by injecting the toxicant into their eggs. Six groups of wood duck eggs (n = 35 to 211 per trial) were injected with 0 to 4600 pg TCDD/g egg between 2003 and 2005. Injections were made into yolk prior to incubation, and eggs were subsequently incubated and assessed weekly for mortality. Significant TCDD-induced mortality was not observed through day 25 (90% of incubation). Liver, heart, eye, and brain histology were generally unremarkable. Hepatic ethoxyresorufin-O-deethylase activity, a biomarker of dioxin-like compound exposure, was induced by 12-fold in the 4600 pg/g treatment relative to controls. The median lethal dose for chicken (Gallus domesticus) eggs we dosed identically to wood duck eggs was about 100 pg/g, similar to other assessments of chickens. Among dioxin-like compound embryo lethality data for 15 avian genera, the wood duck 4600 pg/g no-observed-effect level ranks near the middle. Because no higher doses were tested, wood ducks may be like other waterfowl (order Anseriformes), which are comparatively tolerant to embryo mortality from polychlorinated dibenzo-p-dioxins and dibenzofurans when exposed by egg injection.

Augspurger, T.P., K.R. Echols, P.H. Peterman, T.W. May, C.E. Orazio, D.E. Tillitt and R.T. Di Giulio. 2008. Accumulation of environmental contaminants in wood duck (Aix sponsa) eggs with emphasis on polychlorinated dibenzo-p-dioxins and dibenzofurans. Archives of Environmental Contamination and Toxicology. In press. http://dx.doi.org/10.1007/s00244-008-9199-1

  • We measured polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), organochlorine pesticides, and mercury in wood duck (Aix sponsa) eggs collected near a North Carolina (USA) bleached kraft paper mill. Samples were taken a decade after the mill stopped using molecular chlorine. Using avian toxic equivalency factors, 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity equivalent (TEQ) concentrations were 1–30 pg/g fresh wet weight in eggs (n = 48) collected near the mill in 2002–2005 and were significantly higher than those from a reference site (‹1 pg/g) 25 km away. Geometric mean wood duck egg TEQs (6 pg/g) were one-fifth those measured at this site prior to the cessation of molecular chlorine bleaching. Concentrations of mercury in wood duck eggs from nests of the Roanoke River sites ranged from 0.01 to 0.14 ug/g (geometric mean, 0.04 ug/g) and were significantly higher than those from the reference site, where concentrations did not exceed 0.04 ug/g (geometric mean, 0.02 ug/g). All concentrations were lower than those associated with adverse effects in birds. The congener profiles, lack of contamination in reference site eggs, and decline in contaminant concentrations after process changes at the mill provide strong evidence that mill discharges influenced contamination of local wood duck eggs. Collectively, the results indicate that the wood duck is an effective sentinel of the spatial and temporal extent of PCDD, PCDF, and mercury contamination.

Wang, N., R.J. Erickson, C.G. Ingersoll, C.D. Ivey, E.L. Brunson, T. Augspurger and M.C. Barnhart. 2008. Influence of pH on the acute toxicity of ammonia to juvenile freshwater mussels (Fatmucket, Lampsilis siliquoidea) Environmental Toxicology and Chemistry 27: 1141-1146. Seatac Journals

  • The objective of the present study was to evaluate the influence of pH on the toxicity of ammonia to juvenile freshwater mussels. Acute 96-h ammonia toxicity tests were conducted with 10-d-old juvenile mussels (fatmucket, Lampsilis siliquoidea) at five pH levels ranging from 6.5 to 9.0 in flow-through diluter systems at 20°C. Acute 48-h tests with amphipods (Hyalella azteca) and 96-h tests with oligochaetes (Lumbriculus variegatus) were conducted concurrently under the same test conditions to determine the sensitivity of mussels relative to these two commonly tested benthic invertebrate species. During the exposure, pH levels were maintained within 0.1 of a pH unit and ammonia concentrations were relatively constant through time (coefficient of variation for ammonia concentrations ranged from 2 to 30% with a median value of 7.9%). The median effective concentrations (EC50s) of total ammonia nitrogen (N) for mussels were at least two to six times lower than the EC50s for amphipods and oligochaetes, and the EC50s for mussels decreased with increasing pH and ranged from 88 mg N/L at pH 6.6 to 0.96 mg N/L at pH 9.0. The EC50s for mussels were at or below the final acute values used to derive the U.S. Environmental Protection Agency's acute water quality criterion (WQC). However, the quantitative relationship between pH and ammonia toxicity to juvenile mussels was similar to the average relationship for other taxa reported in the WQC. These results indicate that including mussel toxicity data in a revision to the WQC would lower the acute criterion but not change the WQC mathematical representation of the relative effect of pH on ammonia toxicity.

Cope W.G., R.B. Bringolf, D.B. Buchwalter, T.J. Newton, C.G. Ingersoll, N. Wang , T. Augspurger, F.J. Dwyer, M.C. Barnhart, R.J. Neves and E. Hammer. 2008. Differential exposure, duration, and sensitivity of Unionoidean bivalve life stages to environmental contaminants. Journal of the North American Benthological Society 27: 451-462.

  • Freshwater mussels (superfamily Unionoidea) are in serious global decline and in urgent need of protection and conservation. The declines have been attributed to a wide array of human activities resulting in pollution and water-quality degradation, and habitat destruction and alteration. Linkages among poor water quality, pollutant sources, and mussel decline in rivers and streams have been associated with results of laboratory-based tests of specific pollutants. However, uncertainties remain about the relationship of laboratory data to actual contaminant exposure routes for various mussel species, life stages, and in the habitats occupied during these exposures.We evaluated the pathways of exposure to environmental pollutants for all 4 life stages (free glochidia, encysted glochidia, juveniles, adults) of unionoidean mussels and found that each life stage has both common and unique characteristics that contribute to observed differences in exposure and sensitivity. Free glochidia typically are exposed only briefly (e.g., seconds to days) through surface water, whereas adults sustain exposure over years to decades through surface water, pore water, sediment, and diet. Juveniles live largely burrowed in the sediment for the first 0 to 4 y of life. Thus, sediment, pore water, and diet are the predominant exposure routes for this life stage, but surface water also might contribute to exposure during certain periods and environmental conditions. The obligate parasitic stage (encysted glochidia stage) on a host fish might be exposed from surface water while partially encysted or from toxicants in host-fish tissue while fully encysted. Laboratory methods for testing for acute and chronic exposures in water have advanced, and toxicant-specific information has increased in recent years. However, additional research is needed to understand interactions of life history, habitat, and long-term exposure to contaminants through water, pore water, sediment, and diet so that the risks of environmental exposures can be properly assessed and managed.

2007 Publications

Augspurger, T., F.J. Dwyer, C.G. Ingersoll and C.M. Kane. 2007. Editorial: Advances and opportunities in assessing the contaminant sensitivity of freshwater mussel early life stages. Environmental Toxicology and Chemistry 26: 2025-2028.

  • No abstract available

Wang, N., T. Augspurger, M.C. Barnhart, J.R. Bidwell, W.G. Cope, F.J. Dwyer, S. Geis, I.E. Greer, C.G. Ingersoll, C.M. Kane, T.W. May, R.J. Neves, T.J. Newton, A.D. Roberts and D.W. Whites. 2007. Intra- and inter-laboratory variability in acute toxicity tests with glochidia and juvenile mussels. Environmental Toxicology and Chemistry 26: 2029-2035.

  • The present study evaluated the performance and variability in acute toxicity tests with glochidia and newly transformed juvenile mussels using the standard methods outlined in American Society for Testing and Materials (ASTM). Multiple 48-h toxicity tests with glochidia and 96-h tests with juvenile mussels were conducted within a single laboratory and among five laboratories. All tests met the test acceptability requirements (e.g., =90% control survival). Intralaboratory tests were conducted over two consecutive mussel-spawning seasons with mucket (Actinonaias ligamentina) or fatmucket (Lampsilis siliquoidea) using copper, ammonia, or chlorine as a toxicant. For the glochidia of both species, the variability of intralaboratory median effective concentrations (EC50s) for the three toxicants, expressed as the coefficient of variation (CV), ranged from 14 to 27% in 24-h exposures and from 13 to 36% in 48-h exposures. The intralaboratory CV of copper EC50s for juvenile fatmucket was 24% in 48-h exposures and 13% in 96-h exposures. Interlaboratory tests were conducted with fatmucket glochidia and juveniles by five laboratories using copper as a toxicant. The interlaboratory CV of copper EC50s for glochidia was 13% in 24-h exposures and 24% in 48-h exposures, and the interlaboratory CV for juveniles was 22% in 48-h exposures and 42% in 96-h exposures. The high completion success and the overall low variability in test results indicate that the test methods have acceptable precision and can be performed routinely.

Wang, N., C.G. Ingersoll, D.K. Hardesty, C.D. Ivey, J.L. Kunz, T.W. May, F.J. Dwyer, A.D. Roberts, T. Augspurger, C.M. Kane, R.J. Neves and M.C. Barnhart. 2007. Acute toxicity of copper, ammonia, and chlorine to glochidia and juveniles of freshwater mussels (Unionidae). Environmental Toxicology and Chemistry 26: 2036-2047.

  • The objective of the present study was to determine acute toxicity of copper, ammonia, or chlorine to larval (glochidia) and juvenile mussels using the recently published American Society for Testing and Materials (ASTM) Standard guide for conducting laboratory toxicity tests with freshwater mussels. Toxicity tests were conducted with glochidia (24- to 48-h exposures) and juveniles (96-h exposures) of up to 11 mussel species in reconstituted ASTM hard water using copper, ammonia, or chlorine as a toxicant. Copper and ammonia tests also were conducted with five commonly tested species, including cladocerans (Daphnia magna and Ceriodaphnia dubia; 48-h exposures), amphipod (Hyalella azteca; 48-h exposures), rainbow trout (Oncorhynchus mykiss; 96-h exposures), and fathead minnow (Pimephales promelas; 96-h exposures). Median effective concentrations (EC50s) for commonly tested species were >58 µg Cu/L (except 15 µg Cu/L for C. dubia) and >13 mg total ammonia N/L, whereas the EC50s for mussels in most cases were ‹45 µg Cu/L or ‹12 mg N/L and were often at or below the final acute values (FAVs) used to derive the U.S. Environmental Protection Agency 1996 acute water quality criterion (WQC) for copper and 1999 acute WQC for ammonia. However, the chlorine EC50s for mussels generally were >40 µg/L and above the FAV in the WQC for chlorine. The results indicate that the early life stages of mussels generally were more sensitive to copper and ammonia than other organisms and that, including mussel toxicity data in a revision to the WQC, would lower the WQC for copper or ammonia. Furthermore, including additional mussel data in 2007 WQC for copper based on biotic ligand model would further lower the WQC.

Wang, N., C.G. Ingersoll, I.E. Greer, D.K. Hardesty, C.D. Ivey, J.L. Kunz, W.G. Brumbaugh, F.J. Dwyer, A.D. Roberts, T. Augspurger, C.M. Kane, R.J. Neves and M.C. Barnhart. 2007. Chronic toxicity testing of juvenile mussels with copper and ammonia. Environmental Toxicology and Chemistry 26: 2048-2056.

  • The objectives of the present study were to develop methods for conducting chronic toxicity tests with juvenile mussels under flow-through conditions and to determine the chronic toxicity of copper and ammonia to juvenile mussels using these methods. In two feeding tests, two-month-old fatmucket (Lampsilis siliquoidea) and rainbow mussel (Villosa iris) were fed various live algae or nonviable algal mixture for 28 d. The algal mixture was the best food resulting in high survival (=90%) and growth. Multiple copper and ammonia toxicity tests were conducted for 28 d starting with two-month-old mussels. Six toxicity tests using the algal mixture were successfully completed with a control survival of 88 to 100%. Among copper tests with rainbow mussel, fatmucket, and oyster mussel (Epioblasma capsaeformis), chronic value ([ChV], geometric mean of the no-observed-effect concentration and the lowest-observed-effect concentration) ranged from 8.5 to 9.8 µg Cu/L for survival and from 4.6 to 8.5 µg Cu/L for growth. Among ammonia tests with rainbow mussel, fatmucket, and wavy-rayed lampmussel (L. fasciola), the ChV ranged from 0.37 to 1.2 mg total ammonia N/L for survival and from 0.37 to 0.67 mg N/L for growth. These ChVs were below the U.S. Environmental Protection Agency 1996 chronic water quality criterion (WQC) for copper (15 µg/L; hardness 170 mg/L) and 1999 WQC for total ammonia (1.26 mg N/L; pH 8.2 and 20°C). Results indicate that toxicity tests with two-month-old mussels can be conducted for 28 d with >80% control survival; growth was frequently a more sensitive endpoint compared to survival; and the 1996 chronic WQC for copper and the 1999 chronic WQC for total ammonia might not be adequately protective of the mussel species tested. However, a recently revised 2007 chronic WQC for copper based on the biotic ligand model may be more protective in the water tested.

March, F.A., F.J. Dwyer, T. Augspurger, C.G. Ingersoll, N. Wang and C.A. Mebane 2007. An evaluation of freshwater mussel toxicity data in the derivation of water quality guidance and standards for copper. Environmental Toxicology and Chemistry 26: 2066-2074.

  • The state of Oklahoma has designated several areas as freshwater mussel sanctuaries in an attempt to provide freshwater mussel species a degree of protection and to facilitate their reproduction. We evaluated the protection afforded freshwater mussels by the U.S. Environmental Protection Agency (U.S. EPA) hardness-based 1996 ambient copper water quality criteria, the 2007 U.S. EPA water quality criteria based on the biotic ligand model and the 2005 state of Oklahoma copper water quality standards. Both the criterion maximum concentration and criterion continuous concentration were evaluated. Published acute and chronic copper toxicity data that met American Society for Testing and Materials guidance for test acceptability were obtained for exposures conducted with glochidia or juvenile freshwater mussels. We tabulated toxicity data for glochidia and juveniles to calculate 20 species mean acute values for freshwater mussels. Generally, freshwater mussel species mean acute values were similar to those of the more sensitive species included in the U.S. EPA water quality derivation database. When added to the database of genus mean acute values used in deriving 1996 copper water quality criteria, 14 freshwater mussel genus mean acute values included 10 of the lowest 15 genus mean acute values, with three mussel species having the lowest values. Chronic exposure and sublethal effects freshwater mussel data available for four species and acute to chronic ratios were used to evaluate the criterion continuous concentration. On the basis of the freshwater mussel toxicity data used in this assessment, the hardness-based 1996 U.S. EPA water quality criteria, the 2005 Oklahoma water quality standards, and the 2007 U.S. EPA water quality criteria based on the biotic ligand model might need to be revised to afford protection to freshwater mussels.

Ward, S.E., T. Augspurger, F.J. Dwyer, C.M. Kane and C.G. Ingersoll. 2007. Risk assessment of water quality in three North Carolina streams supporting federally-endangered freshwater mussels. Environmental Toxicology and Chemistry 26: 2075-2085.

  • Water quality data were collected from three drainages supporting the endangered Carolina heelsplitter (Lasmigona decorata) and dwarf wedgemussel (Alasmidonta heterodon) to determine the potential for impaired water quality to limit the recovery of these freshwater mussels in North Carolina, USA. Total recoverable copper, total residual chlorine, and total ammonia nitrogen were measured every two months for approximately a year at sites bracketing wastewater sources and mussel habitat. These data and state monitoring datasets were compared with ecological screening values, including estimates of chemical concentrations likely to be protective of mussels, and federal ambient water quality criteria to assess site risks following a hazard quotient approach. In one drainage, the site-specific ammonia ecological screening value for acute exposures was exceeded in 6% of the samples, and 15% of samples exceeded the chronic ecological screening value; however, ammonia concentrations were generally below levels of concern in other drainages. In all drainages, copper concentrations were higher than ecological screening values most frequently (exceeding the ecological screening values for acute exposures in 65–94% of the samples). Chlorine concentrations exceeding the acute water quality criterion were observed in 14 and 35% of samples in two of three drainages. The ecological screening values were exceeded most frequently in Goose Creek and the Upper Tar River drainages; concentrations rarely exceeded ecological screening values in the Swift Creek drainage except for copper. The site-specific risk assessment approach provides valuable information (including site-specific risk estimates and ecological screening values for protection) that can be applied through regulatory and nonregulatory means to improve water quality for mussels where risks are indicated and pollutant threats persist.

2006 Publications

Hewitt, A.H., W.G. Cope, T.J. Kwak, T. Augspurger, P.R. Lazaro and D. Shea. 2006. Influence of water quality and associated contaminants on survival and growth of the endangered Cape Fear shiner. Environmental Toxicology and Chemistry 25: 2288-2298.

  • Abstract: The Cape Fear shiner (Notropis mekistocholas) is a recently described cyprinid species endemic to the Cape Fear River Basin of North Carolina, USA. Only five populations of the fish remain; thus, it is listed as endangered by the U.S. Government. Determining habitat requirements of the Cape Fear shiner, including water quality and physical habitat, is critical to the survival and future restoration of the species. To assess water quality in the best remaining and in the historical habitats, we conducted a 28-d in situ bioassay with captively propagated Cape Fear shiners. Fish were deployed at 10 sites in three rivers, with three cages per site and 20 fish per cage. Water and sediment samples were collected and analyzed for selected metals and organic contaminants. Passive sampling devices also were deployed at each site and analyzed for organic contaminants at test termination. Fish survival, growth (as measured by an increase in total length), and contaminant accumulation were measured on completion of the bioassay. Survival of caged fish averaged 76% (range, 53–100%) and varied significantly among sites and rivers. Caged fish accumulated quantities of cadmium, mercury, polychlorinated biphenyls, and other persistent contaminants over the test duration and grew significantly at only four sites. No apparent relations were observed between exposure to or accumulation of a specific contaminant and reduced growth or survival of fish among all the sites. However, a generalized hazard assessment showed that certain sites exhibited trends in cumulative contaminant presence with reduced fish survival and growth, thereby enabling the identification of the existing riverine habitat most suitable for reintroduction or population augmentation of this endangered fish.

2005 Publications

Winger, P.V., P.J. Lasier and T. Augspurger. 2005. Potential impact of Dare County landfills on Alligator River National Wildlife Refuge. Integrated Environmental Assessment and Management 1: 267-282.

  • Abstract: Runoff of leachate from East Lake and Dare County Construction and Demolition Debris landfills has the potential to impact wildlife resources at Alligator River National Wildlife Refuge, Dare and Hyde Counties, North Carolina. Sediment quality of samples collected in August 2000 at 14 locations down-gradient from the landfills was assessed by measuring metal and organic contaminants in the sediments, chronic toxicity of solid-phase sediment (28-d static-renewal exposures; survival and growth as test endpoints) and acute toxicity of sediment porewater (96-h static exposures) to Hyalella azteca (Crustacea: Amphipoda). In addition, contaminant bioaccumulation from 4 sediments was determined using 28-d exposures of Lumbriculus variegatus (freshwater oligochaete). Although survival was not impaired, length of H. azteca was significantly reduced in sediments from 5 locations. Pore water from 4 locations was acutely toxic to H. azteca. Metals and a few polycyclic aromatic hydrocarbons (PAHs) were bioaccumulated by L. variegatus from the sediments. Several metals and PAHs exceeded sediment quality guidelines, and metals in porewater from several sites exceeded water quality criteria for the protection of aquatic wildlife. Runoff of leachate from the landfills has reduced sediment quality and has the potential to adversely affect wildlife resources at Alligator River National Wildlife Refuge.

Keller, A.E. and T. Augspurger. 2005. Toxicity of fluoride to the endangered unionid mussel, Alasmidonta raveneliana, and surrogate species. Bulletin of Environmental Contamination and Toxicology 74: 242-249.

Dwyer, F.J., F.L. Mayer, L.C. Sappington, D.R. Buckler, C.M. Bridges, I.E. Greer, D.K. Hardesty, C.E. Henke, C.G. Ingersoll, J.L. Kunz, D.W. Whites, T. Augspurger, D.R. Mount, K. Hattala and G.N. Neuderfer. 2005. Assessing contaminant sensitivity of endangered and threatened aquatic species: Part 1. Acute toxicity of five chemicals. Archives of Environmental Contamination and Toxicology 48: 143-154.

  • Abstract: Assessment of contaminant impacts to federally identified endangered, threatened and candidate, and state-identified endangered species (collectively referred to as "listed" species) requires understanding of a species' sensitivities to particular chemicals. The most direct approach would be to determine the sensitivity of a listed species to a particular contaminant or perturbation. An indirect approach for aquatic species would be application of toxicity data obtained from standard test procedures and species commonly used in laboratory toxicity tests. Common test species (fathead minnow, Pimephales promelas; sheepshead minnow, Cyprinodon variegatus; and rainbow trout, Oncorhynchus mykiss) and 17 listed or closely related species were tested in acute 96-hour water exposures with five chemicals (carbaryl, copper, 4-nonylphenol, pentachlorophenol, and permethrin) representing a broad range of toxic modes of action. No single species was the most sensitive to all chemicals. For the three standard test species evaluated, the rainbow trout was more sensitive than either the fathead minnow or sheepshead minnow and was equal to or more sensitive than listed and related species 81% of the time. To estimate an LC50 for a listed species, a factor of 0.63 can be applied to the geometric mean LC50 of rainbow trout toxicity data, and more conservative factors can be determined using variance estimates (0.46 based on 1 SD of the mean and 0.33 based on 2 SD of the mean). Additionally, a low- or no-acute effect concentration can be estimated by multiplying the respective LC50 by a factor of approximately 0.56, which supports the United States Environmental Protection Agency approach of multiplying the final acute value by 0.5 (division by 2). When captive or locally abundant populations of listed fish are available, consideration should be given to direct testing. When direct toxicity testing cannot be performed, approaches for developing protective measures using common test species toxicity data are available.
  • pdf version of this paper (192kb). The original publication is available at www.springerlink.com.

Dwyer, F.J., D.K. Hardesty, C.E. Henke, C.G. Ingersoll, D.W. Whites, T. Augspurger, T.J. Canfield, D.R. Mount and F.L. Mayer. 2005. Assessing contaminant sensitivity of endangered and threatened aquatic species: Part III. Effluent toxicity tests. Archives of Environmental Contamination and Toxicology 48: 174-183.

  • Abstract: Toxicity tests using standard effluent test procedures described by the U.S. Environmental Protection Agency were conducted with Ceriodaphnia dubia, fathead minnows (Pimephales promelas), and seven threatened and endangered (listed) fish species from four families: (1) Acipenseridae: shortnose sturgeon (Acipenser brevirostrum); (2) Catostomidae; razorback sucker (Xyrauchen texanus); (3) Cyprinidae: bonytail chub (Gila elegans), Cape Fear shiner (Notropis mekistocholas) Colorado pikeminnow (Ptychocheilus lucius), and spotfin chub (Cyprinella monacha); and (4) Poecillidae: Gila topminnow (Poeciliopsis occidentalis). We conducted 7- day survival and growth studies with embryo-larval fathead minnows and analogous exposures using the listed species. Survival and reproduction were also determined with C. dubia. Tests were conducted with carbaryl, ammonia—or a simulated effluent complex mixture of carbaryl, copper, 4-nonylphenol, pentachlorophenol and permethrin at equitoxic proportions. In addition, Cape Fear shiners and spotfin chub were tested using diazinon, copper, and chlorine. Toxicity tests were also conducted with field-collected effluents from domestic or industrial facilities. Bonytail chub and razorback suckers were tested with effluents collected in Arizona whereas effluent samples collected from North Carolina were tested with Cape Fear shiner, spotfin chub, and shortnose sturgeon. The fathead minnow 7-day effluent test was often a reliable estimator of toxic effects to the listed fishes. However, in 21 % of the tests, a listed species was more sensitive than fathead minnows. More sensitive species results varied by test so that usually no species was always more or less sensitive than fathead minnows. Only the Gila topminnow was consistently less sensitive than the fathead minnow. Listed fish species were protected 96% of the time when results for both fathead minnows and C. dubia were considered, thus reinforcing the value of standard whole-effluent toxicity tests using those two species. If the responses of specific listed species are important for management decisions, our study supports the value in developing culture and testing procedures for those species.
  • pdf version of this paper (128kb). The original publication is available at www.springerlink.com.

Rocke T.E., N.J. Thomas, C.U. Meteyer, C.F. Quist, J.R. Fischer, T. Augspurger and S.E. Ward. 2005. Attempts to identify the source of avian vacuolar myelinopathy for waterbirds. Journal of Wildlife Diseases 41: 163-170.

  • Abstract: Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots (Fulica americana), mallard ducks and ducklings (Anas platyrhynchos), quail (Coturnix japonica), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels (Falco sparverius), and American crows (Corvus brachyrhynchos). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla, or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.
  • pdf version of this paper (86kb)

2003 Publications

Augspurger, T., J.R. Fischer, N.J. Thomas, L. Sileo, R.E. Brannian, K.J.G. Miller and T.E. Rocke. 2003. Vacuolar myelinopathy in waterfowl from a North Carolina impoundment. Journal of Wildlife Diseases 39: 412-417.

  • Abstract: Vacuolar myelinopathy was confirmed by light and electron microscopic examination of mallards (Anas platyrhynchos), ring-necked ducks (Aythya collaris), and buffleheads (Bucephala albeola) collected during an epizootic at Lake Surf in central North Carolina (USA) between November 1998 and February 1999. Clinical signs of affected birds were consistent with central nervous system impairment of motor function (incoordination, abnormal movement and posture, weakness, paralysis). This is the first report of this disease in wild waterfowl.
  • pdf version of this paper (2MB)

Augspurger, T., A.E. Keller, M.C. Black, W.G. Cope and F.J. Dwyer. 2003. Water quality guidance for protection of freshwater mussels (Unionidae) from ammonia exposure. Environmental Toxicology and Chemistry 22(11): 209-215.

  • Abstract: Ammonia toxicity data for freshwater mussels (Unionidae), a significantly imperiled taxa, were used to derive estimates of concentrations that would not likely be harmful in acute and chronic exposures and to assess the protectiveness of current U.S. Environmental Protection Agency (U.S. EPA) water quality criteria to this family of organisms. Thirty acute (24–96-h) median lethal concentrations (LC50s), covering 10 species in eight unionid genera, were used to calculate genus mean acute values (GMAVs) ranging from 2.56 to 8.97 mg/L total ammonia as N at pH 8. Freshwater mussels are at the sensitive end of the range when added to the GMAVs from the database used to derive the U.S. EPA criteria maximum concentration (CMC). We derived two estimates of acute exposure water quality guidance for the protection of freshwater mussels (CMCFM) by a recalculation of the CMC after adding freshwater mussel GMAVs to the U.S. EPA data set. The CMCFMs of 1.75 and 2.50 mg/L total ammonia as N at pH 8 average 60% less than the U.S. EPA CMC of 5.62 mg/L total ammonia as N at pH 8 for application when salmonids are present. These values average about 75% less than the CMC for application when salmonids are absent. No chronic ammonia exposure data existed for unionids. Thus, we applied a range of estimated acute:chronic ratios to the acute toxicity data set, expanded with the freshwater mussel GMAVs, to estimate continuous ammonia concentrations that may be protective of freshwater mussels (CCCFM). These estimates ranged from 0.3 to 1.0 mg/L total ammonia as N at pH 8, about 20 to 75% less than the U.S. EPA criteria continuous concentration (CCC) of 1.24 mg/L total ammonia as N at pH 8 and 25oC. The current numeric criteria for ammonia may not be protective of mussels, more than half of whose nearly 300 species are in decline in North America. While the CMCFM and CCCFM are not equivalent to revised U.S. EPA criteria, they are offered as interim guidance for the protection of freshwater mussels.

Dodder, N.G., B. Strandberg, T. Augspurger and R.A. Hites. 2003. Lipophilic organic compounds in lake sediment and American coot (Fulica americana) tissues, both affected and unaffected by avian vacuolar myelinopathy. Science of the Total Environment 311: 81-89.

  • Abstract: Avian vacuolar myelinopathy (AVM) is a disease of unknown etiology, which has been diagnosed in a variety of birds from surface water reservoirs in the southeastern United States. Pathology suggests a natural or anthropogenic compound may be the cause of this disease. With the goal of identifying the toxicant that causes AVM, we qualitatively analyzed sediments and American coot (Fulica americana) tissues from reservoirs that were affected and unaffected by AVM using high-resolution gas chromatographic low-resolution mass spectrometry. Polychlorinated biphenyls (PCBs), octachlorodibenzo-p-dioxin, and biogenic and anthropogenic polycyclic aromatic hydrocarbons (such as retene) were the most abundant compounds in the sediment. Penta- and hexachlorobenzene, oxychlordane, p,p’-DDE, dieldrin, and polychlorinated biphenyls were the most abundant compounds in the avian tissues. None of these compounds were more abundant in the AVM affected sediments and tissues than in the unaffected media. Therefore, it is unlikely that any of these compounds are the cause of this avian disease.
  • pdf version of this paper (135 KB)

Larsen, R.S., F.B. Nutter, T. Augspurger, T.E. Rocke, N.J. Thomas and M.K. Stoskopf. 2003. Failure to transmit avian vacuolar myelinopathy to mallard ducks. Journal of Wildlife Diseases 39: 707-711.

  • Abstract not available in electronic format

Fischer, J.R., L.A. Lewis, T. Augspurger and T.E. Rocke. 2002. Avian vacuolar myelinopathy: A newly recognized fatal neurologic disease of eagles, waterfowl, and other birds. Transactions of the 67th North American Wildlife and Natural Resources Conference 67: 51-61.

  • Abstract not available in electronic format

2002 Publications

Rocke, T.E., N.J. Thomas, T. Augspurger and K. Miller. 2002. Epizootiologic studies of avian vacuolar myelinopathy in waterbirds. Journal of Wildlife Diseases 38: 678-684.

  • Abstract: Epizootic avian vacuolar myelinopathy (AVM) was first recognized as a neurologic disease in bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana) in Arkansas, USA in 1994 and 1996, respectively, but attempts to identify the etiology of the disease have been unsuccessful to date. Between 1998 and 2001, wing clipped sentinel birds (wild American coots and game farm mallards [Anas platyrhynchos]) were released at Lake Surf, North Carolina, a lake with recurrent outbreaks of AVM, in order to gain a better understanding of the epizootiology of the disease. As early as 5–7 days post-release, sentinel coots and mallards showed neurologic signs of disease and were confirmed with AVM upon histologic examination of their brains. Serial releases of sentinel mallards during the summer, fall, and winter of 2000–01 demonstrated that exposure to the causative agent at a threshold sufficient to manifest disease was seasonal and occurred over about a 2 mo period, during November and December. Our findings that disease onset can be very rapid (5–7 days) and that exposure to the causative agent of AVM is site-specific, seasonal (late fall to early winter), and occurs over a relatively short duration (several months) supports the hypothesis that the disease is caused by a chemical substance, most likely of natural origin.
  • pdf version of this paper (50 KB)

Larsen, R.S., F.B. Nutter, T. Augspurger, T.E. Rocke, L. Tomlinson, N.J. Thomas and M.K. Stoskopf. 2002. Clinical features of avian vacuolar myelinopathy in American coots. Journal of the American Veterinary Medical Association 221: 80-85.

1998 Publications

Augspurger, T. and A. Boynton. 1998. Organochlorines and mercury in peregrine falcon eggs from western North Carolina. Journal of Raptor Research 32: 251-254.

  • Abstract: Concentrations of organochlorine pesticides and mercury were determined in five Peregrine Falcon (Falco peregrinus) eggs collected from a re-established population in western North Carolina. Geometric mean concentrations of p,p'DDE (3.37 ppm fresh wet weight), total metabolites of DDT (3.73 ppm), total chlordane components and metabolites (1.11 ppm), dieldrin (0.27 ppm), lindane (0.02 ppm), and mercury (0.10 ppm) were generally below levels associated with reproductive impairment. The 0.334 mm arithmetic mean eggshell thickness was approximately 7% thinner than normal, pre-DDT era Peregrine Falcon eggshells from the original United States eastern population.

Augspurger, T., J.C. Franson, K.A. Converse, P.R. Spitzer and E.A. Miller. 1998. An epizootic of common loons in coastal waters of North Carolina: Concentrations of elemental contaminants and results of necropsies. Environmental Toxicology and Chemistry 17:205-209.

  • Abstract. A 1993 die-off of common loons (Gavia immer) in the coastal waters of North Carolina was investigated with emphasis on comparing mercury, selenium, arsenic and lead between birds from the epizootic and reference specimens. Die-off specimens were emaciated with no ingested foreign bodies, and no lesions suggestive of infectious disease. Results of bacteriology, virology, parasitology, and botulism testing were unremarkable. The geometric mean concentrations (wet weight) of liver mercury (10.9 ppm), selenium (10.4 ppm), and arsenic (0.96 ppm) did not differ between specimens from the die-off and a sample of "reference" loons from the same area which died of other causes. Liver lead concentrations were ‹0.20 ppm in all but one sample (5.83 ppm). The geometric mean mercury concentration in the primary remiges of die-off specimens (5.44 ppm-dry weight) was significantly lower than in reference birds. Liver mercury significantly correlated with liver selenium on a molar concentration basis. We interpret the range of liver mercury concentrations in birds from the epizootic, similar liver mercury concentrations in reference loons, and higher mercury in reference loon feathers as evidence that factors other than mercury were primarily responsible for the emaciation diagnosed as the cause of mortality.

1996 Publications

Augspurger, T., M.R. Smith, C.U. Meteyer and K.A. Converse. 1996. Mortality of passerines adjacent to a North Carolina corn field treated with granular carbofuran. Journal of Wildlife Diseases 32:113-116.

  • Abstract. Red-winged blackbirds (Agelaius phoeniceus) were collected during an epizootic in southeastern North Carolina (USA). Activity of brain cholinesterase (ChE) was inhibited by 14 to 48% in three of five specimens, and returned to normal levels after incubation. Gastrointestinal tracts were analyzed for 30 anti-ChE agents. Carbofuran, the only compound detected, was present in all specimens at levels from 5.44 to 72.7 µg/g wet weight. Application of granular carbofuran in an adjacent corn field, results of necropsy examinations, and chemical analyses are consistent with a diagnosis of carbofuran poisoning in these specimens.

1995 Publications

Facemire, C., T. Augspurger, D. Bateman, M. Brim, P. Conzelman, S. Delchamps, E. Douglas, L. Inmon, K. Looney, F. Lopez, G. Masson, D. Morrison, N. Morse and A. Robison. 1995. Impacts of mercury contamination in the southeastern United States. Water, Air, and Soil Pollution 80: 923-926.

  • Abstract not available in electronic format

Fleming, W.J., T.P. Augspurger and J.A. Alderman. 1995. Freshwater mussel die-off attributed to anticholinesterase poisoning. Environmental Toxicology and Chemistry 14: 877-879.

  • In 1990, we investigated a die-off of freshwater mussels in north-central North Carolina. An estimated 1,000 mussels of several species were found dead or moribund, including about 111 Tar spinymussels (Elliptio steinstansana), a federally listed endangered species. The die-off occurred during a period of low flow and high water temperature in a stream reach dominated by forestry and agriculture. Pathological examinations did not show any abnormalities and indicated that the die-off was an acute event. Chemical analyses of mussels, sediments, and water revealed no organophosphorus or carbamate pesticides. Cholinesterase activity in adductor muscle from Eastern elliptios (Elliptio complanata) collected at the kill site and downstream was depressed 73 and 65%, respectively, compared with upstream reference samples. The depression is consistent with a diagnosis of anticholinesterase poisoning. This is the first documented case in which cholinesterase-inhibiting compounds have been implicated in a die-off of freshwater mussels.

1990 Publications

Benkert, K. 1990. Assessment of organic and metal contaminants in Lower Back Bay and Upper Currituck Sound. In H.G. Marshall and M.D. Norman (eds). Proceedings of the Back Bay Symposium. Virginia Beach, VA November 2-3, 1990. Biological Sciences Section, Old Dominion University.

  • Abstract not available in electronic format

Program Contacts

Tom Augspurger, Ecologist, 919-856-4520 ext. 21

Sara Ward, Ecologist, 919-856-4520 ext. 30
Last Updated: January 6, 2009