Testing of an oral dosing technique for double-crested cormorants, Phalacocorax auritus, laughing gulls, Leucophaeus atricilla, homing pigeons, Columba livia, and western sandpipers, Calidris mauri, with artificially weather MC252 oil.

Scoping studies were designed to determine if double-crested cormorants (Phalacocorax auritus), laughing gulls (Leucophaues atricilla), homing pigeons (Columba livia) and western sandpipers (Calidris mauri) that were gavaged with a mixture of artificially weathered MC252 oil and food for either a single day or 4-5 consecutive days showed signs of oil toxicity. Where volume allowed, samples were collected for hematology, plasma protein electrophoresis, clinical chemistry and electrolytes, oxidative stress and organ weigh changes. Double-crested cormorants, laughing gulls and western sandpipers all excreted oil within 30min of dose, while pigeons regurgitated within less than one hour of dosing. There were species differences in the effectiveness of the dosing technique, with double-crested cormorants having the greatest number of responsive endpoints at the completion of the trial. Statistically significant changes in packed cell volume, white cell counts, alkaline phosphatase, alanine aminotransferase, creatine phosphokinase, gamma glutamyl transferase, uric acid, chloride, sodium, potassium, calcium, total glutathione, glutathione disulfide, reduced glutathione, spleen and liver weights were measured in double-crested cormorants. Homing pigeons had statistically significant changes in creatine phosphokinase, total glutathione, glutathione disulfide, reduced glutathione and Trolox equivalents. Laughing gulls exhibited statistically significant decreases in spleen and kidney weight, and no changes were observed in any measurement endpoints tested in western sandpipers.

Toxic effects of orally ingested oil from the Deepwater Horizon spill on laughing gulls.

The explosion of the Deepwater Horizon oil rig released, millions of gallons of oil into the environment, subsequently exposing wildlife, including numerous bird species. To determine the effects of MC252 oil to species relevant to the Gulf of Mexico, studies were done examining multiple exposure scenarios and doses. In this study, laughing gulls (Leucophaeus atricilla, LAGU) were offered fish injected with MC252 oil at target doses of 5 or 10mL/kg bw per day. Dosing continued for 27 days. Of the adult, mixed-sex LAGUs used in the present study, ten of 20 oil exposed LAGUs survived to the end of the study; a total of 10 of the oil exposed LAGUs died or were euthanized within 20 days of initiation of the study. Endpoints associated with oxidative stress, hepatic total glutathione (tGSH), oxidized glutathione (GSSG) and reduced glutathione (rGSH) significantly increased as mean dose of oil increased, while the rGSH:GSSG ratio showed a non-significant negative trend with oil dose. A significant increase in 3-methyl histidine was found in oil exposed birds when compared to controls indicative of muscle wastage and may have been associated with the gross observation of diminished structural integrity in cardiac tissue. Consistent with previous oil dosing studies in birds, significant changes in liver, spleen, and kidney weight when normalized to body weight were observed. These studies indicate that mortality in response to oil dosing is relatively common and the mortality exhibited by the gulls is consistent with previous studies examining oil toxicity. Whether survival effects in the gull study were associated with weight loss, physiologic effects of oil toxicity, or a behavioral response that led the birds to reject the dosed fish is unknown.

Dermal exposure to weathered MC252 crude oil results in echocardiographically identifiable systolic myocardial dysfunction in double-crested cormorants (Phalacrocorax auritus).

During the Deepwater Horizon Natural Resource Damage Assessment, gross morphologic cardiac abnormalities, including softer, more distensible musculature, were noted upon gross necropsy in hearts from laughing gulls and double-crested cormorants exposed to weathered MC252 crude oil. A species specific, echocardiographic technique was developed for antemortem evaluation of function that was used to evaluate and better characterize cardiac dysfunction. Control (n=12) and treated (n=13) cormorant groups of similar sex-ratio and ages were dermally treated with approximately 13ml of water or weathered MC252 crude oil, respectively, every 3 days for 6 dosages. This resulted in a low to moderate external exposure. Upon visualization and clinical assessment of the hearts of all test subjects, comprehensive diagnostic cardiographic measurements were taken twice, prior to oil application and after a 21day dermal oil exposure. Oil-treated birds showed a decrease in cardiac systolic function, as characterized by an increased left ventricular internal dimension-systole and left ventricular stroke volume as well as concurrent decreased left ventricular ejection fraction and left ventricular fractional shortening when compared to both control birds' and the treated birds' time zero values. These changes are indicative of a possible dilative cardiomyopathy induced by oil exposure, although further elucidation of possible collagen damage is recommended. Arrhythmias including tachycardia in two treated birds and bradycardia in all treated birds were documented, indicating further clinically significant abnormalities induced by MC252 oil that warrant further investigation. A statistically significant increase in free calcium concentration, important to muscular and neurologic function in treated birds was also noted. This study documents that weathered MC252 oil caused clinically significant cardiac dysfunction that could result in mortality and decrease recruitment.

Reprint of: Overview of avian toxicity studies for the Deepwater Horizon Natural Resource Damage Assessment.

The Oil Pollution Act of 1990 establishes liability for injuries to natural resources because of the release or threat of release of oil. Assessment of injury to natural resources resulting from an oil spill and development and implementation of a plan for the restoration, rehabilitation, replacement or acquisition of natural resources to compensate for those injuries is accomplished through the Natural Resource Damage Assessment (NRDA) process. The NRDA process began within a week of the Deepwater Horizon oil spill, which occurred on April 20, 2010. During the spill, more than 8500 dead and impaired birds representing at least 93 avian species were collected. In addition, there were more than 3500 birds observed to be visibly oiled. While information in the literature at the time helped to identify some of the effects of oil on birds, it was not sufficient to fully characterize the nature and extent of the injuries to the thousands of live oiled birds, or to quantify those injuries in terms of effects on bird viability. As a result, the US Fish and Wildlife Service proposed various assessment activities to inform NRDA injury determination and quantification analyses associated with the Deepwater Horizon oil spill, including avian toxicity studies. The goal of these studies was to evaluate the effects of oral exposure to 1-20ml of artificially weathered Mississippi Canyon 252 oil kg bw-1 day-1 from one to 28 days or one to five applications of oil to 20% of the bird's surface area. It was thought that these exposure levels would not result in immediate or short-term mortality but might result in physiological effects that ultimately could affect avian survival, reproduction and health. These studies included oral dosing studies, an external dosing study, metabolic and flight performance studies and field-based flight studies. Results of these studies indicated changes in hematologic endpoints including formation of Heinz bodies and changes in cell counts. There were also effects on multiple organ systems, cardiac function and oxidative status. External oiling affected flight patterns and time spent during flight tasks indicating that migration may be affected by short-term repeated exposure to oil. Feather damage also resulted in increased heat loss and energetic demands. The papers in this special issue indicate that the combined effects of oil toxicity and feather effects in avian species, even in the case of relatively light oiling, can significantly affect the overall health of birds.

Overview of avian toxicity studies for the Deepwater Horizon Natural Resource Damage Assessment.

The Oil Pollution Act of 1990 establishes liability for injuries to natural resources because of the release or threat of release of oil. Assessment of injury to natural resources resulting from an oil spill and development and implementation of a plan for the restoration, rehabilitation, replacement or acquisition of natural resources to compensate for those injuries is accomplished through the Natural Resource Damage Assessment (NRDA) process. The NRDA process began within a week of the Deepwater Horizon oil spill, which occurred on April 20, 2010. During the spill, more than 8500 dead and impaired birds representing at least 93 avian species were collected. In addition, there were more than 3500 birds observed to be visibly oiled. While information in the literature at the time helped to identify some of the effects of oil on birds, it was not sufficient to fully characterize the nature and extent of the injuries to the thousands of live oiled birds, or to quantify those injuries in terms of effects on bird viability. As a result, the US Fish and Wildlife Service proposed various assessment activities to inform NRDA injury determination and quantification analyses associated with the Deepwater Horizon oil spill, including avian toxicity studies. The goal of these studies was to evaluate the effects of oral exposure to 1-20ml of artificially weathered Mississippi Canyon 252 oil kg bw-1 day-1 from one to 28 days or one to five applications of oil to 20% of the bird's surface area. It was thought that these exposure levels would not result in immediate or short-term mortality but might result in physiological effects that ultimately could affect avian survival, reproduction and health. These studies included oral dosing studies, an external dosing study, metabolic and flight performance studies and field-based flight studies. Results of these studies indicated changes in hematologic endpoints including formation of Heinz bodies and changes in cell counts. There were also effects on multiple organ systems, cardiac function and oxidative status. External oiling affected flight patterns and time spent during flight tasks indicating that migration may be affected by short-term repeated exposure to oil. Feather damage also resulted in increased heat loss and energetic demands. The papers in this special issue indicate that the combined effects of oil toxicity and feather effects in avian species, even in the case of relatively light oiling, can significantly affect the overall health of birds.

Embryo toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin to the wood duck (Aix sponsa).

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.

The effects of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) on mink (Mustela vison) reproduction and kit survivability and growth.

This study was conducted to determine if dietary exposure to 3,3'4,4',5-pentachlorobiphenyl (PCB 126) would have an adverse effect on the reproductive performance of female mink (Mustela vison) and survivability and growth of their kits. Standard dark, female mink were fed diets containing PCB 126 at concentrations of 0, 0.24, 2.4, and 24 microg PCB 126/kg feed (0, 24, 240 and 2,400 ng 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD] toxic equivalents [TEQs]/kg, respectively) from 21 days prior to breeding until weaning of their kits at six weeks of age. There were no significant differences in the number of females that whelped or the average litter size between the control group and the 0.24 microg PCB 126/kg feed group. In addition, kit body weights at birth and at three, six and 28 weeks of age as well as kit survivability through weaning were similar between the two groups. In contrast, female mink fed diets containing 2.4 and 24 microg PCB 126/kg feed that had confirmed matings, failed to whelp. Histological examination of their uterine horns verified fetal implantation sites or placental scars, which indicated partial fetal development. Based on the impaired reproductive performance reported in this study, a no observable adverse effect level (NOAEL) of 0.24 microg PCB 126/kg feed (24 ng TEQs/kg) and a lowest observable adverse effect level (LOAEL) of 2.4 microg PCB 126/kg feed (240 ng TEQs /kg) were determined.

Assessment of effects in mink caused by consumption of carp collected from the Saginaw River, Michigan, USA.

Polychlorinated hydrocarbons, including polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs), are ubiquitous environmental contaminants that bioconcentrate in the food chain. Numerous studies have demonstrated mink (Mustela vison) to be one of the most sensitive species to this group of compounds. In recent studies, a lesion characterized by osteoinvasion of epithelial cells into the mandible and maxilla of young mink fed diets containing 3,3',4,4',5-pentachlorobiphenyl (PCB 126) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was observed. The objective of the present study was to determine if proliferation of maxillary and mandibular squamous epithelia could be induced in ranch mink exposed to environmentally-derived polychlorinated hydrocarbons (PCBs, PCDDs, and PCDFs) in utero, during lactation, and throughout the growth period. Adult female mink were fed diets containing 0, 10, 20, or 30% carp (Cyprinus carpio) collected from the Saginaw River, Bay City, Michigan, USA, that provided 0.03, 0.83, 1.1, and 1.7 mg total PCBs (tPCBs)/kg feed and 2.5, 28, 47, and 73 ng TCDD toxic equivalents (TEQs)/kg feed, respectively, three weeks prior to breeding through weaning of the resulting offspring. Mink kits were maintained on their respective diets for up to 27 weeks of age. At 6 and 27 weeks of age, six to eight mink in each treatment group were necropsied and their jaws examined for evidence of maxillary and mandibular squamous epithelial proliferation. Results indicated that inclusion of up to 30% carp in the diet (1.7 mg tPCBs/kg feed, 73 ng TEQs/kg feed) had no effect on mink reproduction and kit survivability. However, maxillary and mandibular squamous epithelial proliferation was evident in four of the seven 27-week-old juveniles in the 20% carp group (1.1 mg tPCBs/kg feed, 47 ng TEQs/kg feed) and six of the eight juveniles in the 30% carp group (1.7 mg tPCBs/kg feed group, 73 ng TEQs/kg feed). Hepatic concentrations of tPCBs and TEQs increased in both the 6-week-old kits and the 27-week-old juveniles as the percentage of dietary carp increased. The livers of 6-week-old kits were also assessed for the presence of polybrominated diphenyl ethers, which increased as the percentage of Saginaw River carp in the diet increased.

Efficacy of a commercial mycotoxin binder in alleviating effects of ochratoxin A, fumonisin B1, moniliformin and zearalenone in adult mink.

The addition of nutritionally inert adsorbents to mycotoxin-contaminated animal feed has been a popular approach to decreasing toxicity in animals and carryover of mycotoxins from contaminated feed to animal by-products. Some studies suggest that esterified glucomannan derived from the cell wall of Saccharomyces cerevisiae is effective in reducing the bioavailability of at least some of the mycotoxins occurring in contaminated feed. Because cereal grains are important components of ranch mink diets, mycotoxicoses in mink is a potential problem faced by mink ranchers. We conducted a series of studies to determine if inclusion of a commercially available esterified glucomannan in ranch mink feed was effective in alleviating clinical signs indicative of exposure to ochratoxin A, fumonisin B1, moniliformin or zearalenone in adult mink. In 4 separate trials, mink were fed diets that contained 2.5, 5 or 10 mg ochratoxin A/kg feed, 200 mg fumonisin B1/kg feed, 20 mg moniliformin/kg feed, or 30 mg zearalenone/kg feed with or without 2 g esterified glucomannan/kg feed. Male mink fed diets containing ochratoxin A had significantly decreased feed intake as well as renal lesions characteristic of exposure to that mycotoxin. Inclusion of the esterified glucomannan did not ameliorate these effects. Male mink exposed to fumonisin B1 had increased urinary sphinganine concentration, which was not significantly reduced by the mycotoxin adsorbent. Male mink that consumed monilformin-contaminated diets had characteristic ultrastructural changes in the heart that were not reduced in severity by the esterified glucomannan. Female mink exposed to zearalenone had increased uterine weight, which was not reversed by inclusion of commercial mycotoxin binder in the contaminated feed. The results of this study suggest that a commercial esterified glucomannan was generally ineffective in alleviating effects indicative of exposure to ochratoxin A, fumonisin B1, monilformin and zearalenone in mink.

Mechanisms of TCDD-induced abnormalities and embryo lethality in white leghorn chickens.

The toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds in birds has been well-established in laboratory and field studies. Observed effects of TCDD and related chemicals in birds include developmental deformities, reproductive failure, liver damage, wasting syndrome and death. The mechanism of action of TCDD at the cellular level is primarily mediated through the aryl hydrocarbon receptor (AhR). However, the mechanism of toxic action at the organism level is poorly understood. In this study, the role of radical oxygen species and mixed function oxidize (MFO; cytochrome P4501A) in the mechanism of TCDD-induced abnormalities and lethality were examined by co-injecting radical scavengers and an MFO inhibitor (piperonyl butoxide). Egg injection studies were conducted to determine if in ovo TCDD exposure can cause oxidative stress in white leghorn chicken eggs. Test agents were injected into the yolk prior to incubation. Treatments included TCDD (150 ng/kg), triolein (vehicle control), and various co-treatments including MnTBAP (a mimetic of superoxide dismutase), piperonyl butoxide, piroxicam, vitamin A acetate, and vitamin E succinate. Phenytoin, which is known to cause teratogenesis through oxidative stress was used as a positive control. Eggs were incubated until hatch and then the following parameters were assessed: mortality, hatching success, abnormalities, weights for whole body, liver, heart and brain, and biochemical endpoints for oxidative stress. As a measure of exposure, concentrations of TCDD and ethoxyresorufin-O-deethylase (EROD) activities were measured in tissues of hatchlings. While greater mortality and abnormalities were observed in the TCDD treatment groups, the number of the replicates were not great enough to detect statistically significant differences in abnormality rates for the co-treatments. Some of the observed developmental abnormalities included edema, liver necrosis and bill, eye and limb deformities with TCDD treatments, bill and brain deformities with phenytoin treatments, eye abnormalities with Vitamin E treatments, and abnormal feather pigmentation with piperonyl butoxide treatments.

Reproductive toxicity of ergot alkaloids in mink.

Ergot alkaloids are-synthesized by fungi of the Claviceps family that infect rye as well as other cereals and grains. Since a portion of the ranch mink diet is cereal, mink are at a risk of being exposed to ergot alkaloids. This study was performed to determine the reproductive toxicity of ergot alkaloids derived from ergot-contaminated oats in mink. Four groups of 12 female mink each were fed diets containing 0, 3, 6 or 12 ppm ergot alkaloids from 2w prior to the breeding season until the kits were approximately 33-d old (133 d). Females were mated with untreated males. Ergo talkaloids caused a transient decrease in feed consumption, but body weights were unaffected. The gestation period of the mink in the 6 ppm group was longer compared to controls. The number of mink whelping varied significantly with 9 mink whelping each in the control and 3 ppm groups compared to 4 mink in the 6 ppm group and 1 in the 12 ppm group. Ergot alkaloids had a significant effect on kit survivabilitywith no kits surviving in the 12 ppm group. Serum prolactin was significantly depressed in the 3 ergot alkaloid groups compared to the control group. This study indicated that ingestion of ergot alkaloids at 3 ppm or higher resulted in reproductive toxicity in mink.

Health effects following chronic dosing with tungsten-iron and tungsten-polymer shot in adult game-farm mallards.

Permanent approval of shot composed of tungsten-iron and tungsten-polymer for waterfowl hunting by the U.S. Fish and Wildlife Service was pending the results of the present study that examined the health and reproductive effects of the two shot types on mallards (Anas platyrhynchos) over a 150-day period. We collected data pertaining to the effects of tungsten-iron and tungsten-polymer shot on mortality, body weight, organ weight, tissue pathology, and shot erosion. Thirty-two bird groups (sexes equal) of adult mallards were dosed orally with eight #4 steel shot (control), eight #4 tungsten-iron shot, or eight #4 tungsten-polymer shot on days 0, 30, 60, 90, and 120 of a 150-day trial (26 January 1998 to 25 June 1998). An additional 12 mallards (sexes equal) were dosed orally with eight #4 lead shot (positive control) on day 0 of the study. All lead-dosed ducks died by day 25, whereas no ducks died in the other treatment groups. Significant liver hemosiderosis was present in all control and tungsten-iron-dosed males, in five of eight control and three of eight tungsten-iron-dosed females, and in one tungsten-polymer-dosed male examined. The rate of shot erosion was highest for tungsten-polymer shot (99%), followed by tungsten-iron (72%), and steel (55%) shot. Tungsten-iron or tungsten-polymer shot repeatedly administered to adult mallards did not have deleterious health effects during the 150-day trial based on mortality, body weights, organ weights, and histology of the liver and kidneys.

Hematological effects and metal residue concentrations following chronic dosing with tungsten-iron and tungsten-polymer shot in adult game-farm mallards.

The U.S. Fish and Wildlife Service required a chronic dosing study that assessed the health and reproductive effects of tungsten-iron and tungsten-polymer shot in adult game-farm mallards (Anas platyrhynchos) prior to granting permanent approval of the shot for waterfowl hunting. Herein, we present the effects of tungsten-iron and tungsten-polymer shot on various hematologic parameters and metal residue concentrations in the femur, liver, kidneys, and gonads. Thirty-two-bird groups (sexes equal) of adult mallards were dosed orally with eight #4 steel shot (control), eight #4 tungsten-iron shot, or eight #4 tungsten-polymer shot on days 0, 30, 60, 90, and 120 of a 150 day trial (26 January 1998 to 25 June 1998). An additional 12 mallards (sexes equal) received eight #4 lead shot (positive control) on day 0 of the study. Lead-dosed mallards had significantly decreased hematocrit, hemoglobin concentration, and whole-blood delta aminolevulinic acid dehydratase activity on day 7, as well as significant changes in a number of plasma chemistry parameters compared to ducks in the control, tungsten-iron, or tungsten-polymer groups. Mallards dosed with tungsten-iron or tungsten-polymer shot had occasional significant differences in hematocrit and plasma chemistry values when compared to control mallards over the 150 day period, but these changes were not considered to be indicative of deleterious effects. Low concentrations of tungsten were detected in gonad and kidney samples from males and females and in liver samples from females dosed with tungsten-polymer shot. Tungsten was also detected in femur samples from tungsten-polymer-dosed mallards. Higher concentrations of tungsten were detected in femur, liver, kidney, and gonad samples from tungsten-iron-dosed ducks. Tungsten-iron or tungsten-polymer shot repeatedly administered to adult mallards did not cause adverse hematological effects during the 150 day trial. Concentrations of tungsten in the femur, liver, kidneys, and gonads were generally higher in tungsten-iron-dosed ducks when compared to tungsten-polymer-dosed ducks.

Chronic toxicity of dietary 2,3,7,8-tetrachlorodibenzo-p-dioxin to mink.

Mature female natural dark mink (Mustela vison) were fed 0.0006 (control), 0.016, 0.053, 0.180, or 1.40 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 131-132 d to ascertain the chronic toxic effects of TCDD in mink, including reproduction. Consumption of the 1.4 ppb TCDD diet resulted in lethargy, bloody stools, and 16.7% mortality. Final mink body weights were inversely proportional to the dietary TCDD concentrations. Due to subnormal mink breeding, definitive effects of TCDD on mink reproductive performance were not ascertained; however, there were significant dose-dependent decreases in kit (young mink) birth weight and survival from birth to 3 w of age in the groups that had reproduction. There were also significant differences in adult minkwhite blood cell counts, plasma total solids, serum iron, phosphorus, albumin, total protein, total CO2, cholesterol, osmolality, and anion gap concentrations, and alanine aminotransaminase activity between the various dietary groups. During the latter stages alopecia and thickened, deformed, and elongated toenails were observed in the adult mink fed 1.4 ppb TCDD. At termination the mink fed 1.4 ppb TCDD had ascites, gastric ulcers, intestinal hemorrhages, depletion of adipose tissue, and mottled and/or discolored livers, spleens, and kidneys. Focal lymphocytic meningitis in region of the olfactory bulb was present in 42% of the mink fed 1.4 ppb TCDD. These results confirmed the high sensitivity of mink to TCDD and revealed a toenail abnormality not previously reported for mink fed TCDD.

Dietary exposure to 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2,3,7,8-tetrachlorodibenzo-p-dixon (TCDD) does not induce proliferation of squamous epithelium or osteolysis in the jaws of weanling rats.

Previous studies demonstrated that dietary exposure to 24 ppb 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2.4 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced maxillary and mandibular proliferation of periodontal squamous epithelium, osteolysis of alveolar bone, and loose and displaced teeth in juvenile mink (Mustela vison). This study determined if such effects could be induced in laboratory rats. Feeding weanling male Long Evans rats 20 or 100 ppb PCB 126 or 1 or 10 ppb TCDD for up to 101 days caused a dose-dependent decrease in body weight gains but did not produce the jaw lesion observed in PCB 126- or TCDD-treated mink.

Persistent fetal intraocular vasculature in the European ferret (Mustela putorius): clinical and histological aspects.

OBJECTIVE: To describe the clinical and histological appearance of persistent fetal intraocular vasculature in a colony of ferrets. Design Prospective study. ANIMALS STUDIED: Eighty-six European ferrets (Mustela putorius). Procedure Both eyes of 76 genetically related progeny and 10 breeding, adult, colony-raised ferrets were studied using a slit lamp biomicroscope and an indirect ophthalmoscope. Ferret progeny were examined after eyelid opening at 5-6 weeks of age, and at 12 months of age. After euthanasia, globes were enucleated and examined histologically. RESULTS: Persistent fetal intraocular vasculature was evident in 21 progeny ferrets at 5-6 weeks of age and in three mature progenitor ferrets. Clinical appearance of diminutive vasculature was characterized by focal remnants of the posterior tunica vasculosa lentis, muscae volitantes, and an occluded hyaloid artery extending from the optic papilla and terminating in the anterior vitreous body. Extensive persistent vasculature was characterized by a perfused hyaloid artery, vasa hyaloidea propria and posterior tunica vasculosa lentis, posterior cortical and capsular cataract, and proliferation of fibrovascular tissue along the posterior lens capsule. Fetal vasculature persisted in 7 of 21 progeny ferrets at one year of age and in three progenitor ferrets. Results of histologic examination showed persistence of the hyaloid vasculature, proliferation of retrolental fibrovascular tissue with osseous metaplasia, posterior capsular and cortical cataract, and occasional retinal detachment. CONCLUSIONS: Persistent fetal intraocular vasculature in ferrets appears similar clinically and histologically to persistent fetal intraocular vasculature reported in humans and dogs. The ferret may be a suitable animal model for vasculogenic mechanisms of persistent fetal intraocular vasculature and for evaluating vasoinhibitory growth factors and angiostatic test compounds.

Squamous epithelial proliferation in the jaws of mink fed diets containing 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2,3,7,8-tetrachlorodibenzo-P-dioxin (TCDD).

Previous research has shown that ingestion of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) by juvenile mink (kits) caused a lesion in the mandible and maxilla that consisted of proliferation of sQuamous epithelium in the periodontal ligament, osteolysis of adjacent alveolar bone, and loose and displaced teeth. Similar, but less severe changes, developed in adult mink fed 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The present study was conducted to compare similarities and differences of the lesion within the jaws of mink fed these 2 polyhalogenated hydrocarbons. Diets containing 24 ppb PCB 126 or 2.4 ppb TCDD were fed to 6-w-old kits for 36 d. Similar diets were fed to 12-w-old kits for 35 d. Some of these mink were then fed untreated feed for an additional 50 d. All mink treated with PCB 126 or TCDD had reductions in body weight gains which were more severe in the 6-w-old kits than the 12-week-old kits. By 28 days of exposure, many of the 6- and 12-week-old mink treated with PCB 126 or TCDD had loose and displaced incisor teeth. Canine teeth were grossly more prominant. Radiographs showed maxillary and mandibular osteolysis with lysis of the lamina dura in treated mink. Withdrawal of the toxicants from the diets of the 12-w-old mink failed to alleviate the lesions, which continued to be progressively more severe.

Proliferation of maxillary and mandibular periodontal squamous cells in mink fed 3,3',4,4',5-pentachlorobiphenyl (PCB 126).

This report characterizes squamous cell proliferation in young farm mink (Mustela vison) fed a diet supplemented with 0.024 ppm 3,3',4,4',5-pentachlorobiphenyl (polychlorinated biphenyl [PCB] congener 126). One to 2 months of dietary exposure to PCB 126 resulted in gross lesions of the upper and lower jaws consisting of mandibular and maxillary nodular proliferation of the gingiva and loose teeth. The maxilla and mandible of the PCB-treated mink were markedly porous because of loss of alveolar bone. Histologically, this osteoporosis was caused by proliferation of squamous cells that formed infiltrating cords. This report clearly documents the fact that the environmental contaminant PCB 126 can cause osteoinvasive squamous proliferation in young mink, although the dose used in the present study was 7 and 36 times higher than what is typically encountered in contaminated bird eggs and fish, respectively.