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At least 19 recordsLinked to original sources
USGS2003

Safety of Aquaflor (florfenicol, 50% Type A Medicated Article), administered in feed to channel catfish, Ictalurus punctatus

Aquaflor, a feed premix containing the broad spectrum antibacterial agent florfenicol (50% w/w), is being developed for use to control enteric septicemia (ESC) in channel catfish Ictalurus punctatus caused by the gram-negative enterobacterium Edwardsiella ictaluri . The recommended dose of Aquaflor to control ESC is 10 mg/kg body weight (BW)/day for 10 days. The study objective was to determine the safety of Aquaflor administered in feed to channel catfish at doses of 0 (control), 10, 30, and 50 mg/kg BW/day for 20 consecutive days. Parameters evaluated included daily mortality, behavioral (appetite, distribution, flight/fright response), and water chemistry observations, initial and terminal weight measurements, and gross and microscopic pathology. Medicated feed consumption was 67—86% of target with group mean doses of 8.5 mg/kg BW/day, 24.6 mg/kg BW/day, and 34.9 mg/kg BW/day. There were no mortalities or clinically observable changes noted at any of the dose levels tested. Aquaflor-related changes were limited to the food consumption and histopathology data. Although Aquaflor-related decreased feed consumption was noted in the 30 and 50 mg/kg BW/day groups, there were no differences in fish growth among the treatment groups. Aquaflor-related histopathology findings were limited to a histomorphologically evident dose-dependent decrease in hematopoietic/lymphopoietic tissue in the anterior kidneys, posterior kidneys, and spleens of channel catfish.

Toxicologic Pathology↗
USGS2003

Safety of aquaflor (florfenicol, 50% type a medicated article), administered in feed to channel catfish, Ictalurus punctatus

Aquaflor, a feed premix containing the broad spectrum antibacterial agent florfenicol (50% w/w), is being developed for use to control enteric septicemia (ESC) in channel catfish Ictalurus punctatus caused by the gram-negative enterobacterium Edwardsiella ictaluri . The recommended dose of Aquaflor to control ESC is 10 mg/kg body weight (BW)/day for 10 days. The study objective was to determine the safety of Aquaflor administered in feed to channel catfish at doses of 0 (control), 10, 30, and 50 mg/kg BW/day for 20 consecutive days. Parameters evaluated included daily mortality, behavioral (appetite, distribution, flight/fright response), and water chemistry observations, initial and terminal weight measurements, and gross and microscopic pathology. Medicated feed consumption was 67-86% of target with group mean doses of 8.5 mg/kg BW/day, 24.6 mg/kg BW/day, and 34.9 mg/kg BW/day. There were no mortalities or clinically observable changes noted at any of the dose levels tested. Aquaflor-related changes were limited to the food consumption and histopathology data. Although Aquaflor-related decreased feed consumption was noted in the 30 and 50 mg/kg BW/day groups, there were no differences in fish growth among the treatment groups. Aquaflor-related histopathology findings were limited to a histomorphologically evident dose-dependent decrease in hematopoietic/lymphopoietic tissue in the anterior kidneys, posterior kidneys, and spleens of channel catfish.

Toxicologic Pathology↗
USGS2012

Safety of florfenicol administered in feed to tilapia (Oreochromis sp.)

The safety of Aquaflor® (50% w/w florfenicol [FFC]) incorporated in feed then administered to tilapia for 20 days (2x the recommended duration) at 0, 15, 45, or 75 mg/kg body weight/day (0, 1, 3, or 5x the recommended dose of 15 mg FFC/kg BW/d) was investigated. Mortality, behavioral change, feed consumption, body size, and gross and microscopic lesions were determined. Estimated delivered doses were >96.9% of target. Three unscheduled mortalities occurred but were considered incidental since FFC-related findings were not identified. Feed consumption was only affected during the last 10 dosing days when the 45 and 75 mg/kg groups consumed only 62.5% and 55.3% of the feed offered, respectively. There were significant, dose-dependent reductions in body size in the FFC-dose groups relative to the controls. Treatment-related histopathological findings included increased severity of lamellar epithelial hyperplasia, increased incidence of lamellar adhesions, decreased incidence of lamellar telangiectasis in the gills, increased glycogen-type and lipid-type hepatocellular vacuolation in the liver, decreased lymphocytes, increased blast cells, and increased individual cell necrosis in the anterior kidney, and tubular epithelial degeneration and mineralization in the posterior kidney. These changes are likely to be of minimal clinical relevance, given the lack of mortality or morbidity observed. This study has shown that FFC, when administered in feed to tilapia at the recommended dose (15 mg FFC/kg BW/day) for 10 days would be well tolerated.

Toxicologic Pathology↗
USGS2014

Nonlesions, misdiagnoses, missed diagnoses, and other interpretive challenges in fish histopathology studies: a guide for investigators, authors, reviewers, and readers

Differentiating salient histopathologic changes from normal anatomic features or tissue artifacts can be decidedly challenging, especially for the novice fish pathologist. As a consequence, findings of questionable accuracy may be reported inadvertently, and the potential negative impacts of publishing inaccurate histopathologic interpretations are not always fully appreciated. The objectives of this article are to illustrate a number of specific morphologic findings in commonly examined fish tissues (e.g., gills, liver, kidney, and gonads) that are frequently either misdiagnosed or underdiagnosed, and to address related issues involving the interpretation of histopathologic data. To enhance the utility of this article as a guide, photomicrographs of normal and abnormal specimens are presented. General recommendations for generating and publishing results from histopathology studies are additionally provided. It is hoped that the furnished information will be a useful resource for manuscript generation, by helping authors, reviewers, and readers to critically assess fish histopathologic data.

Toxicologic Pathology↗
USGS1994

An overview of sea otter studies

The Exxron Valdez oil spill (EVOS) on 24 March 1989 threatened extensive areas of prime sea otter ( Enhydra lutris ) habitat along the coasts of south-central Alaska. The spill occurred in northeastern Prince William Sound (PWS), and oil moved rapidly south and west through PWS into the Gulf of Alaska. Much of the coastline of western PWS was heavily oiled, and the slick eventually spread as far southwest as Kodiak Island and the Alaska Peninsula (Galt and Payton 1990; Morris and Loughlin, Chapter 1). All coastal waters affected by the spill were inhabited by sea otters. Concern for the survival of sea otters following the oil spill was immediate and well founded. Sea otters are particularly vulnerable to oil contamination because they rely on pelage rather than blubber for insulation, and oiling drastically reduces the insulative value of the fur (Costa and Kooyman 1982; Siniff et al. 1982; Geraci and Williams 1990). Within days of the spill, recovery of oiled live otters and carcasses began. During the several months following the spill, sea otters became symbolic of the mortality associated with the spilled oil, and of the hope for rescue and recovery of injured wildlife (Batten 1990). An extensive sea otter rescue and rehabilitation effort was mounted in the weeks and months following the spill. Handling and treatment of the captive sea otters posed an enormous and difficult challenge, given the large number of otters held at the facilities and minimal prior experience in caring for oiled sea otters. Rehabilitation of sea otters was a separate effort from the postspill studies designed to evaluate injury to the otter populations and is not addressed in this chapter only as it relates to evaluation of damage assessment studies. Detailed information on the rehabilitation effort is presented in Bayha and Kormendy (1990) and Williams and Davis (1990). Sea otters retained a high profile in the Natural Resource Damage Assessment (NRDA) studies largely because the initial injury to the sea otter population was readily demonstrable, but also because of concerns about long-term damages. The scope of the postspill studies to assess oil-related damages to sea otters was extensive: From 1989 through 1993, more than $3,000,000 was spent, and more than 20 scientists were involved in a comprehensive research program. The studies were predominantly directed at sea otter populations in PWS. Damages to sea otters generally can be classified as either acute, defined as spill-related deaths occurring during the spill, or chronic, defined as longer term lethal or sublethal oil-related injuries. Studies of acute damages focused on estimating the total initial loss of sea otters. Characterization of the pathologies associated with exposure to oil was a secondary goal of studies of acute effects. Chronic or longer term damages may have resulted from sublethal initial exposure or continued exposure to hydrocarbons persisting in the environment. Studies of chronic effects included evaluating abundance and distribution, survival and reproduction rates, foraging behavior, and pathological, physiological, and toxicological changes in the years following the spill. The objective of this chapter is to review the studies conducted on sea otters in response to the EVOS and to synthesize the major findings of those studies relative to injury to the sea otter population associated with exposure to oil. We also provide recommendations for research to improve our understanding of the effects of future oil spills on Sea otter populations.

Alaska↗
USGS1979

Comparison of game-farm and wild-strain mallard ducks in accumulation of methylmercury

The accumulation of mercury was compared in game-farm and wild-strain mallard ducks fed a diet containing 0.5 ppm mercury in the form of methylmercury dicyandiamide. There were no significant differences between the two strains in levels of mercury that accumulated in blood, kidney, liver, breast muscle, brain, eggs, or ducklings. Mercury levels in blood were significantly correlated with levels in other tissues and eggs, as were levels in down feathers of ducklings with levels in carcasses of ducklings. The results indicate that game-farm mallards are probably suitable substitutes for wild mallards in toxicological work, that blood samples can be used to estimate levels of mercury in other tissues of adults, and that down feathers are predictive of mercury levels in duckling carcasses.

North Dakota↗
USGS2009

Hepatic pathologies in the brackish water catfish (Chrysichthys nigrodigitatus) from contaminated locations of the Lagos lagoon complex

Several toxicological studies into the effects of aquatic pollutants on the liver of teleost fish exist in literature. The focus on the liver in these studies is predicated on its central nature in the scheme of biotransformation and excretion of xenobiotics following exposure in polluted water bodies. As a consequence of the latter primary role of the liver in these processes it is regarded as a predilective site for the sub lethal effects of xenobiotics on the organism usually detectable at histological level. Hepatic histopathology recorded in livers from feral populations of the brackish water catfish Chrysichthys nigrodigitatus from locations on the Lagos lagoon complex with significant anthropogenic inputs from denizen populations and industries are presented. Liver sections from sixty specimens from two locations on the Lagos lagoon complex (Badagry lagoon: 6°24'N, 2°56'E; and Lagos lagoon: 6°29'N, 3°22'E) were analysed. Observed pathologies included hydropic degeneration (58%), portal / sinusoidal congestion (33%), hepatic necrosis (26%), hemosiderosis (12%) and foci of cellular alterations (FCA's). No obvious oncologic features were observed; the presence of the hydropic Vacuolation lesion was taken as prelude to the development of neoplasms and discussed as such.

Badagry Lagoon, Lagos Lagoon↗
USGS2024

Perfluorohexanesulfonic acid (PFHxS) induces hepatotoxicity through the PPAR signaling pathway in larval zebrafish (Danio rerio)

In recent years, the industrial substitution of long-chain per- and polyfluoroalkyl substances (PFAS) with short-chain alternatives has become increasingly prevalent, resulting in the widespread environmental detection of perfluorohexanesulfonic acid (PFHxS), a short-chain PFAS. However, there remains limited information about the potential adverse effects of PFHxS at environmental concentrations to wildlife. Here, early life stage zebrafish ( Danio rerio ) were exposed to environmentally relevant concentrations of PFHxS to better characterize the adverse effects of PFHxS on aquatic organisms. Nontargeted, transcriptomic analysis revealed potential hepatotoxic effects in exposed larvae, including macrovesicular and microvesicular hepatic steatosis, as well as focal liver necrosis. Morphological, histological, biochemical, and targeted transcript expression profiles further confirmed significant alterations in hepatocellular lesion numbers, liver pathological structures, relative liver size, liver biochemical parameters, and liver function genes. To validate the PPAR-mediated toxicological mechanism identified as an enriched pathway through in silico bioinformatics analysis, we tested the coexposure to an antagonist and PPAR morpholino knockdown. This intervention alleviated PFHxS-induced hepatic effects, including reductions in the levels of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and total triglycerides. Our results demonstrate that environmentally relevant concentrations of PFHxS can impair liver development and function in fish, which could have potential risks to aquatic organisms.

Environmental Science & Technology↗
USGS1998

Retrospective study of the diagnostic criteria in a lead-poisoning survey of waterfowl

Between 1983 and 1986 the National Wildlife Health Center (NWHC) conducted a nationwide study of lead poisoning of waterfowl from federal and state refuges. This survey was done to assist in identifying zones with lead-poisoning problems. One thousand forty one moribund or dead waterfowl were collected and examined. The presence or absence of 13 gross lesions selected as indicators of lead poisoning and 3 lesions indicating body condition was recorded. Lead-poisoning diagnoses were based on the finding of at least 6 8 ppm (wet weight) lead in the liver and either lead shot in the gizzard content or at least one convincing gross lesion indicative of lead poisoning. Four hundred and twenty-one of these waterfowl were diagnosed as lead-poisoned. The NWHC survey provided a comprehensive basis for estimating the sensitivities, specificities, and likelihood ratios of the gross lesions of lead poisoning and the associated hepatic lead concentrations for several species of waterfowl. Some of the 13 defined gross lesions were more common than others; frequencies ranged from 3% to 80% in the 421 lead-poisoned waterfowl. The most reliable indicators of lead poisoning were impactions of the upper alimentary tract, submandibular edema, myocardial necrosis, and biliary discoloration of the liver. Each of the 13 lesions occurred more frequently in the lead-poisoned birds, but each of the lesions also occurred in waterfowl that died of other causes. The number of lead shot present in a bird?s gizzard was only weakly correlated with its hepatic lead concentration; however, this weak correlation may have been adequate to account for differences in hepatic lead concentrations among species, once the weights of the species were taken into account. Although lead-poisoned ducks tended to have higher hepatic mean lead concentrations than did lead-poisoned geese or swans, the differences were probably a result of a greater dose of shot per body weight than to kinetic differences between species. Hepatic lead concentrations were independent of age and sex. Ninety-five percent of waterfowl diagnosed as lead-poisoned had hepatic lead concentrations of at least 38 ppm, dry weight (10 ppm, wet weight). Fewer than 1% of the waterfowl that died of other causes had a concentration that high. This 5th percentile, of 38 ppm dry weight (10 ppm wet weight), is a defensible criterion for identifying lead-poisoned waterfowl when interpreting hepatic lead concentrations in the absence of pathological observations.

Archives of Environmental Contamination and Toxico↗
USGS1987

Survival of striped bass larvae and yearlings in relation to contaminants and water quality in the upper Chesapeake Bay

This study was designed to evaluate survival of striped bass yolk-sac larvae and yearlings at three locations in their natural spawning habitat in the upper Chesapeake Bay (Chesapeake and Delaware Canal) using “in-situ” chambers; correlate larval and yearling survival with the presence of 11 water quality parameters, 10 inorganic contaminants and 21 organic contaminants and assess histological effects on yearlings after exposure to habitat water. The cumulative percent survival ranged from 42–59.5% for striped bass larvae after 96 hr of exposure to habitat water during two experiments. Survival in control conditions during these two experiments was 77.5 and 80.5%. Data from previous studies have shown that mortality rates for wild yolk-sac larvae ranged from 7–19% per day. Daily mortality of larvae in the present study was 13–16%; therefore, suspected acutely harmful water quality or contaminant conditions affecting survival were not substantiated. All yearling striped bass survived 10 days of exposure to habitat water. Although habitat water was not acutely toxic, histological examination of surviving yearling striped bass indicated sublethal effects. Telangiectases (lamellar dilations) of the gills was reported for yearlings exposed to habitat water. This pathological change was not found in the controls.

Delaware, Maryland↗
USGS2009

Effects of chronic ingestion of No. 2 fuel oil on mallard ducklings

No. 2 fuel oil was fed to mallard (Anas platyrhynchos) ducklings in concentrations of 0.5 and 5.0% of the diet from hatching to 18 wk of age to assess the effects of chronic oil ingestion during early development. Five growth parameters (body weight, wing length, ninth primary length, tarsal length, and bill length) were depressed in birds receiving a diet containing 5% fuel oil. There was no oil-related mortality. The 5% fuel oil diet impaired avoidance behavior of 9-d-old mallard ducklings compared with controls or ducklings fed 0.5% oil. Open-field activity was greatly increased in 16-wk-old ducklings fed 5.0% oil. Liver hypertrophy and splenic atrophy were gross evidences of pathological effects in birds on the 5.0% oil diet. More subtle effects included biochemical lesions that resulted in the elevation of plasma alanine aminotransferase and ornithine carbamoyltransferase activity.

Journal of Toxicology and Environmental Health↗
USGS2011

Relationship between oxidative stress, pathology, and behavioral signs of lead poisoning in mallards

Some of the adverse effects of lead (Pb) may be associated with oxidative damage of lipids, proteins, or DNA. In a previous study a linkage was observed between the susceptibilities of waterfowl species to Pb poisoning with oxidative stress . To investigate this relationship among the individuals of a single species, for 3 wk 4 groups of 72 mallards were fed diets containing high or low levels of vitamin E (20 or 220 Ul/kg) and high or low levels of Pb (0 or 2 g/kg). During the first week of Pb exposure, mallards developed hemolytic anemia, and during the second week, signs of neurological impairment. Histological findings in the Pb-exposed mallards were hemosiderosis, demyelinization of sciatic and brachial nerves, and tumefaction of renal tubular epithelium with the presence of intranuclear inclusion bodies. Lipid peroxidation increased with Pb exposure in blood, liver, bile, and brain, but decreased in nerves. Glutathione (GSH) increased with Pb exposure in liver and bile, and its oxidized/reduced ratio only increased in bile. Pb exposure inhibited GSH peroxidase activity (GPX) in plasma, liver, and brain, and decreased protein thiols (PSH) in blood and liver. Vitamin E resulted in significantly lower lipid peroxidation in nerves of control birds relative to unsupplemented controls, but did not alleviate any sign of lead posioning. Pb-induced pathological changes associated with hepatic and nervous functions were significantly correlated with lower GPX activity and PSH concentrations in these tissues rather than lipid peroxidation. Data suggest that inhibition of antioxidant enzymes and interaction with sulfhydryl groups of proteins may play a more important role in Pb poisoning of waterfowl than lipid peroxidation.

Journal of Toxicology and Environmental Health, Pa↗
USGS2015

Sensitivity of shovelnose sturgeon ( Scaphirhynchus platorynchus ) and pallid sturgeon ( S. albus ) early life stages to 3,30,4,40,5-pentachlorobiphenyl and 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure

Concern exists that polychlorinated biphenyls (PCBs) may be contributing to the current decline of shovelnose sturgeon ( Scaphirhynchus platorynchus ) and the US federally endangered pallid sturgeon ( Scaphirhynchus albus ). Waterborne exposures with newly fertilized eggs were used to assess developmental and morphological effects of 2 of the most potent aryl hydrocarbon receptor (AhR) agonists, 3,3′,4,4′,5-pentachlorobiphenyl (PCB-126) and 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), on early life stage shovelnose and pallid sturgeon. No dose-related effects of PCB-126 were observed on percent development or hatch in either species at concentrations as high as 1711 ng/g egg. Effects of TCDD on percent development were not assessed in shovelnose sturgeon. However, percent development was not affected by TCDD in pallid sturgeon, and percent hatch was unaffected by TCDD doses as high as 60 ng/g egg to 81 ng/g egg in either species. Morphological pathologies such as yolk sac edema and craniofacial deformities were typical of AhR agonist exposure and were similar in both species. Calculated PCB-126 50% lethal dose (LD50, 95% fiducial limits) values were 196 ng/g egg (188–203 ng/g) for shovelnose and 159 ng/g egg (122–199 ng/g) for pallid sturgeon. Likewise, calculated TCDD LD50 values were 13 ng/g egg (11–15 ng/g) for shovelnose and 12 ng/g egg (10–14 ng/g) for pallid sturgeon. These LD50 values are among the highest recorded in early life stage fish, suggesting that early life stage Scaphirhynchus sturgeon may be comparatively insensitive to AhR agonists.

Environmental Toxicology and Chemistry↗
USGS1997

Aromatic hydrocarbon pathology in fish following a large spill into the Nemadji River, Wisconsin, USA

On June 30, 1992, a train accident resulted in a rail car releasing 114,000 L of a complex mixture of aromatic hydrocarbons into the Nemadji River, a tributary of Lake Superior near Superior, Wisconsin (Table 1). Although the majority of the spilled material evaporated, damage to aquatic life was extensive. Several thousand fishes were killed and an inestimable number were exposed to low concentrations (< 5 mg/L) of the chemical concentrate for several weeks (Allen 1993). Fishes that survived the spill were examined within 7 days of exposure to determine the extent of injury when compared to fishes collected from the reference site. The liver, spleen, gill, and head kidney were examined for histopathology. Blood was collected to determine the severity of liver damage reflected by the presence of the serum enzymes (aspartate aminotransferase, alanine aminotransferase, and d - glutamyl transferase).

Bulletin of Environmental Contamination and Toxico↗
USGS2011

Behavioral, clinical, and pathological characterization of acid metalliferous water toxicity in mallards

From September to November 2000, United States Fish and Wildlife Service biologists investigated incidents involving 221 bird deaths at 3 mine sites located in New Mexico and Arizona. These bird deaths primarily involved passerine and waterfowl species and were assumed to be linked to consumption of acid metalliferous water (AMW). Because all of the carcasses were found in or near pregnant leach solution ponds, tailings ponds, and associated lakes or storm water retention basins, an acute-toxicity study was undertaken using a synthetic AMW (SAMW) formulation based on the contaminant profile of a representative pond believed to be responsible for avian mortalities. An acute oral-toxicity trial was performed with a mixed-sex group of mallards ( Anas platyrhynchos ). After a 24-h pretreatment food and water fast, gorge drinking was evident in both SAMW treatment and control groups, with water consumption rates greatest during the initial drinking periods. Seven of nine treated mallards were killed in extremis within 12 h after the initiation of dose. Total lethal doses of SAMW ranged from 69.8 to 270.1 mL/kg (mean &plusmn; SE 127.9 &plusmn; 27.1). Lethal doses of SAMW were consumed in as few as 20 to 40 min after first exposure. Clinical signs of SAMW toxicity included increased serum uric acid, aspartate aminotransferase, creatine kinase, potassium, and P levels. PCV values of SAMW-treated birds were also increased compared with control mallards. Histopathological lesions were observed in the esophagus, proventriculus, ventriculus, and duodenum of SAMW-treated mallards, with the most distinctive being erosion and ulceration of the kaolin of the ventriculus, ventricular hemorrhage and/or congestion, and duodenal hemorrhage. Clinical, pathological, and tissue-residue results from this study are consistent with literature documenting acute metal toxicosis, especially copper (Cu), in avian species and provide useful diagnostic profiles for AMW toxicity or mortality events. Blood and kidney Cu concentrations were 23- and 6-fold greater, respectively, in SAMW mortalities compared with controls, whereas Cu concentrations in liver were not nearly as increased, suggesting that blood and kidney concentrations may be more useful than liver concentrations for diagnosing Cu toxicosis in wild birds. Based on these findings and other reports of AMW toxicity events in wild birds, we conclude that AMW bodies pose a significant hazard to wildlife that come in contact with them.

New Mexico, Arizona↗
USGS1983

Accumulation, sublethal effects, and safe concentration of a refined oil as evaluated with cutthroat trout

Cutthroat trout ( Salmo clarki ) were exposed for 90 days in the laboratory to a refined oil collected from the North Platte River at a seepage site below the American Oil Company refinery at Casper, Wyoming. Fish were exposed to five concentrations and a control, and seven biological responses (survival, growth, gill pathology, liver pathology, caudal fin erosion, caudal fin pathology and swimming performance) were correlated with water concentration and tissue accumulation of petroleum hydrocarbons. Fish in the highest water concentration, 183 μ g/L total oil, accumulated tissue concentrations of 4.6 μ g/g total naphthalenes and responded adversely to all seven biological measurements. Cutthroat trout in the lowest water concentration, 24 μ g/L total oil, had a mean tissue concentration of 1.2 μ g/g total naphthalenes, but their response was similar to that of the control fish to all seven biological responses. Fish exposed to 39 μ g/L water concentration accumulated tissue concentrations of 2.7 μ g/g and responded negatively to 2 of the 7 biological measurements. Therefore, the maximum safe limit for this oil and cutthroat trout is between 24 and 39 μ g/L.

Archives of Environmental Contamination and Toxico↗
USGS2006

The effect of chronic chromium exposure on the health of Chinook salmon (Oncorhynchus tshawytscha)

This study was designed to determine fish health impairment of Chinook salmon ( Oncorhynchus tshawytscha ) exposed to chromium. Juvenile Chinook salmon were exposed to aqueous chromium concentrations (0–266 μg l −1 ) that have been documented in porewater from bottom sediments and in well waters near salmon spawning areas in the Columbia River in the northwestern United States. After Chinook salmon parr were exposed to 24 and 54 μg Cr l −1 for 105 days, neither growth nor survival of parr was affected. On day 105, concentrations were increased from 24 to 120 μg Cr l −1 and from 54 to 266 μg Cr l −1 until the end of the experiment on day 134. Weight of parr was decreased in the 24/120 μg Cr l −1 treatment, and survival was decreased in the 54/266 μg Cr l −1 treatment. Fish health was significantly impaired in both the 24/120 and 54/266 μg Cr l −1 treatments. The kidney is the target organ during chromium exposures through the water column. The kidneys of fish exposed to the greatest concentrations of chromium had gross and microscopic lesions (e.g. necrosis of cells lining kidney tububules) and products of lipid peroxidation were elevated. These changes were associated with elevated concentrations of chromium in the kidney, and reduced growth and survival. Also, variations in DNA in the blood were associated with pathological changes in the kidney and spleen. These changes suggest that chromium accumulates and enters the lipid peroxidation pathway where fatty acid damage and DNA damage (expressed as chromosome changes) occur to cause cell death and tissue damage. While most of the physiological malfunctions occurred following parr exposures to concentrations ≥120 μg Cr l −1 , nuclear DNA damage followed exposures to 24 μg Cr l −1 , which was the smallest concentration tested. The abnormalities measured during this study are particularly important because they are associated with impaired growth and reduced survival at concentrations ≥120 μg Cr l −1 . Therefore, these changes can be used to investigate the health of resident fish in natural waters with high chromium concentrations as well as provide insight into the mechanisms of chromium toxicity.

Aquatic Toxicology↗
USGS2014

Identifying non-point sources of endocrine active compounds and their biological impacts in freshwater lakes

Contaminants of emerging concern, particularly endocrine active compounds (EACs), have been identified as a threat to aquatic wildlife. However, little is known about the impact of EACs on lakes through groundwater from onsite wastewater treatment systems (OWTS). This study aims to identify specific contributions of OWTS to Sullivan Lake, Minnesota, USA. Lake hydrology, water chemistry, caged bluegill sunfish ( Lepomis macrochirus ), and larval fathead minnow ( Pimephales promelas ) exposures were used to assess whether EACs entered the lake through OWTS inflow and the resultant biological impact on fish. Study areas included two OWTS-influenced near-shore sites with native bluegill spawning habitats and two in-lake control sites without nearby EAC sources. Caged bluegill sunfish were analyzed for plasma vitellogenin concentrations, organosomatic indices, and histological pathologies. Surface and porewater was collected from each site and analyzed for EACs. Porewater was also collected for laboratory exposure of larval fathead minnow, before analysis of predator escape performance and gene expression profiles. Chemical analysis showed EACs present at low concentrations at each study site, whereas discrete variations were reported between sites and between summer and fall samplings. Body condition index and liver vacuolization of sunfish were found to differ among study sites as did gene expression in exposed larval fathead minnows. Interestingly, biological exposure data and water chemistry did not match. Therefore, although results highlight the potential impacts of seepage from OWTS, further investigation of mixture effects and life history factor as well as chemical fate is warranted.

Minnesota↗