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USGS1991

Potencies of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners, relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin, for producing early life stage mortality in rainbow trout (Oncorhynchus mykiss)

The presence of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) in feral lake trout eggs ( Salvelinus namaycush ) may increase the risk of lake trout early life stage mortality in the Great Lakes. To assess the combined toxicity of PCDDs, PCDFs, and PCBs to lake trout early development, toxic potencies, relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), were determined for individual PCDD, PCDF, and PCB congeners, based on rainbow trout ( Oncorhynchus mykiss ) early life stage mortality. Newly fertilized rainbow trout eggs were injected with graded doses of 2,3,7,8-TCDD, or a PCDD, PCDF, or PCB congener. LD 50 values were determined based on the egg dose that caused mortality from hatching onset to swim-up. Toxic equivalency factors (TEFs) were calculated as 2,3,7,8-TCDD LD 50 /congener LD 50 . TEFs were for PCDDs: 2,3,7,8-TCDD = 1.0; 1,2,3,7,8-PeCDD = 0.730;and 1,2,3,4,7,8-HxCDD = 0.319; for PCDFs: 2,3,4,7,8-PeCDF = 0.359; 1,2,3,4,7,8-HxCDF = 0.280; 1,2,3,7,8-PeCDF = 0.034; and 2,3,7,8-TCDF = 0.028; and for PCBs: 3,3',4,4',5-PeCB = 0.005; 3,3',4,4'-TCB = 0.00016; 2,3,3',4,4'-PeCB and 2,3',4,4',5-PeCB < 0.00007. For PCDDs, fish-specific TEFs were 10- to 100-fold higher than TEFs determined in H4IIE rat hepatoma cells, but were similar to TEFs proposed for risk assessment. For PCDFs, fish specific TEFs were similar to TEFs determined in H4IIE cells and TEFs proposed for risk assessment. However, the most significant finding was that for the coplanar PCBs and mono- ortho -chlorinated analogues of the coplanar PCBs fish-specific TEFs were 1/14 to 1/80 less than both those determined in H4IIE cells and proposed for risk assessment. Using these fish-specific TEFs, the risk associated with exposure of early life stages of Sake trout to complex mixtures of PCDDs, PCDFs, and PCBs in the Great Lakes can be estimated.

Aquatic Toxicology↗

USGS1992

An egg injection method for assessing early life stage mortality of polychlorinated dibenzo- p -dioxins, dibenzofurans, and biphenyls in rainbow trout, (Oncorhynchus mykiss)

To characterize the risk that polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) pose to salmonid early life stage survival, we developed a method to expose rainbow trout (Oncorhynchus mykiss) eggs to graded doses of PCDD, PCDF, and PCB congeners, using 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a prototype. Rainbow trout eggs were injected 24–50 h post-fertilization with 0.2 μl of 50 mM phosphatidylcholine (PC) liposomes (control) or 0.2 μl of 5–7 graded doses of TCDD incorporated into 50 mM PC liposomes. Injection volume never exceeded 0.6% egg volume. Immediately following injection, the injection site was sealed with Super glue®, resulting in 92–97% of TCDD dose retained by the egg. Following both egg injection and waterborne egg exposure. TCDD toxicity in rainbow trout was manifested by half-hatching mortality but predominantly by sac fry mortality associated with hemorrhages, pericardial edema, and yolk sac edema. TCDD LD 50 s, following injection and waterborne exposure of rainbow trout eggs, were 421 (331–489) and 439 (346–519) pg TCDD/g egg (LD 50 , 95% fiducial limits), respectively. As in rainbow trout, TCDD toxicity in lake trout (Salvelinus namaycush) following the same two routes of exposure was manifested by half-hatching mortality but predominantly by sac fry mortality preceded by hemorrhages and yolk sac edema. LD 50 s, based on the dose of TCDD in lake trout eggs, were 47 (21–65) and 65 (60–71) pg/g following injection and waterborne exposure, respectively. The egg injection method is ideal for assessing the relationship between early life stage mortality in rainbow trout and graded egg doses of individual PCDD, PCDF, or PCB congeners.

Aquatic Toxicology↗

USGS1992

Effects of chronic exposure to soft, acidic water on gill development and chloride cell numbers in embryo-larval brook trout, Salvelinus fontinalis

Recruitment failure is considered to be a major factor contributing to the decline of fish populations in soft, acidic waters; direct mortality of embryo-larval fishes has been postulated as a major cause of the decline. Little is understood of the physiological consequences to embryo-larval fishes of prolonged exposure to soft, acidic waters; however, dysfunction of respiratory and ionoregulatory processes is suspected. In order to evaluate the effects of acid exposure on the respiratory and ionoregulatory systems of developing brook trout, Salvelinus fontinalis, differences in gill morphology and numbers of chloride cells were compared between groups cf developing embryo-larval fish continuously exposed to moderately hard well water (130.0 mg.l -1 as CaCO 3 , pH 7.94) or to reconstituted soft, acidic water (4.4 mg.l -1 as CaCO 3 , pH 5.25) designed to mimic acidic waters of northern Wisconsin acidified lakes. Exposures were maintained for up to 48 days (82 days after fertilization) during critical periods of growth and differentiation of branchial structures. The second right gill arch of each fish was examined for changes in the development of filaments and lamellae and for differences in numbers of chloride cells. Gills of fish that developed in soft, acidic water contained greater numbers of normal and degenerating chloride cells, exhibited hyperplasia of primary epithelium and multiple fusions of adjacent filaments and lamellar epithelium than the gills of control fish. Filament and lamellar lengths and numbers of lamellae per filament were significantly less ( P < 0.05) in fish that developed in soft, acidic water than in fish exposed to well water.

Wisconsin↗

USGS1993

Assimilation efficiency for sediment-sorbed benzo(a)pyrene by Diporeia spp.

Two methods are currently available for determining contaminant assimilation efficiencies (AE) from ingested material in benthic invertebrates. These methods were compared using the Great Lakes amphipod Diporeia spp. and [ 14 C]benzo(a)pyrene (BaP) sorbed to Florissant sediment (< 63 µ m). The first approach, the direct measurement method, uses total organic carbon as a tracer and yielded AE values ranging from 45.9~50.4%. The second approach, the dual-labeled method, uses 51 Cr as a non-assimilated tracer and did not yield AE values for our data. The inability of the dual-labeled approach to estimate AEs was due, in part, to the selective feeding by Diporeia resulting in a failure of the non-assimilated tracer ( 51 Cr) to track with the assimilated tracer ([ 14 C]BaP). The failure of the dual-labeled approach was not a result of an uneven distribution of the labels among particle size classes, but more likely resulted from differential sorption of the two isotopically labeled materials to particles of differing composition. The [ 14 C]BaP apparently sorbs to organic particles that are selectively ingested, while the 51 Cr apparently sorbs to particles which are selectively excluded by Diporeia. The dual-labeled approach would be a viable and easier experimental approach for determining AE values if the characteristics that govern selective feeding can be determined.

Aquatic Toxicology↗

USGS1993

Toxicity and bioaccumulation of waterborne and dietary selenium in juvenile bluegill ( Lepomis macrochirus )

Juvenile bluegill ( Lepomis macrochirus ) were exposed to waterborne selenium as a 6:1 mixture of selenate to selenite (as Se) for 60 d and to dietary seleno- l -methionine for 90 d. Measured concentrations of total selenium in the waterborne exposure ranged from 0.16 to 2.8 mg/l, and concentrations of seleno- l -methionine in the test diet ranged from 2.3 to 25.0 mg/kg wet weight. Mortality, body weight, condition factor, swimming and feeding behavior, aggression, and selenium tissue residues were monitored during the tests. Increased mortality at measured concentrations of 0.64 mg Se/l and greater was the primary adverse effect of waterborne selenium on the juvenile bluegill. Bluegill exposed to 2.8 mg/l of waterborne Se for 30 d exhibited a significant reduction in condition factor ( K ), whereas dietary exposure of bluegill to 25 mg Se/kg for 30 d and 13 mg Se/kg or greater for 90 d elicited significant reductions in K . Mortality and swimming activity of bluegill were not affected in the dietary exposure. Net accumulation of Se from both water and diet was directly related to exposure concentration. Bioconcentration factors ranged from 5 to 7 for bluegill exposed to waterborne Se and from 0.5 to 1.0 for fish exposed to dietary Se. Results of these laboratory tests indicate that survival of bluegill may be impaired in natural waters with elevated Se concentrations.

Aquatic Toxicology↗

USGS1994

Effects of the planar PCB 3,3′,4,4′-tetrachlorobiphenyl (TCB) on ovarian development, plasma levels of sex steroid hormones and vitellogenin, and progeny survival in the white perch (Morone americana)

Adult white perch were given three intraperitoneal injections of 3,3′,4,4′-tetrachlorobiphenyl (TCB) at one of three different doses (0.2–5.0 mg TCB/kg body weight). The TCB injections were initiated approx. 3 months prior to the spawning season and given at 3-week intervals. Fewer females matured in the group receiving the highest dose of TCB. Those fish that did mature had a gonadal somatic index approximately half that of control females. Circulating levels of the sex steroid hormones, estradiol-17β and testosterone, and of the egg yolk precursor, vitellogenin, were not significantly altered by TCB exposure. By 7 days post-hatch survival of larvac produced from females exposed to 1.0 and 5.0 mg/kg TCB was reduced as compared to controls (0, 1 and 54%, respectively). These results show that: (1) TCB impairs both maturation of adult females and survival of their offspring, and (2) decreased larval survival may occur at TCB doses less than those required to decrease ovarian growth, oocyte maturation, or circulating sex steroid hormone and vitellogenin concentrations in the adult fish.

Aquatic Toxicology↗

USGS1979

Elimination of endrin by mallard ducks

Endrin is very toxic to birds and has been implicated in the deaths of birds in nature. However, it is not known how rapidly birds eliminate endrin, a factor important in determining how much is accumulated in tissues. In this study, the loss rate of endrin was followed for 64 days in mallard (Anas platyrhynchos) drakes that had been fed 20 ppm endrin for 13 days. The loss from carcass and blood was described by the equation Y = a e b square root of x where Y = the concentration of endrin in ppm, a = the concentration at day 0, e = the base of natural logarithms, b = the first order rate constant for the elimination process, and x = the number of days after cessation of endrin treatment. Endrin was lost rapidly at first; concentrations in carcasses on a wet-weight basis decreased by 50% in the first 3 days. Thereafter, endrin was eliminated more slowly; elimination of 50% of the remainder required 8.9 days, and it took 32.9 days to lose 90% of the original amount.

Toxicology↗

USGS1985

Lethal and behavioral effects of chlordimeform in bobwhite

The 7-day LC50 of chlordimeform to bobwhite (Colinus virginianus) chicks was 2835 ppm (95% CI = 2169-3705 ppm). Bobwhite chicks fed 1000 ppm (~ LC4) chlordimeform for 7 days ate less, weighed less, travelled farther from a fright stimulus in an avoidance test, and had significantly more groups make >10 light beam interruptions in an open-field test at 8 days of age than bobwhite fed 0, 1, 10, or 100 ppm chlordimeform (P< 0.05). Groups fed 100 ppm (P <0.05) and 1000 ppm (P = 0.11) for 7 days crossed more often from the shallow to deep side of a visual cliff at 8 days of age than birds fed lesser concentrations of chlordimeform. Bobwhites were retested at 15 days of age, after being fed untreated diets for 7 days following the chlordimeform diets. The 1000 ppm group still travelled greater distances in the avoidance test (P < 0.05). But open-field and visual cliff performances were similar to controls and other treatment groups. Chlordimeform concentrations causing behavioral abberations in bobwhite were appreciably higher than environmental concentrations following field applications of chlordimeform.

Toxicology↗

USGS1980

Intestinal absorption of 5 chromium compounds in young black ducks (Anas rubripes)

An in vivo intestinal perfusion technique was used to measure the absorption rates of five Cr compounds in black ducks. Cr was absorbed from saline solutions of KCr(SO 4 ) 2 and CrO 3 at a rate about 1.5 to 2.0 times greater than from solutions of Cr, Cr(NO 3 ) 3 , and Cr(C 5 H 7 O 2 ) 3 . These results suggest the ionic form of Cr in solution may be an important factor in determining absorption of Cr compounds from the small intestine.

Toxicology Letters↗

USGS1981

Avoidance behavior of young black ducks treated with chromium

Pairs of adult black ducks (Anas rubripes) were fed a diet containing 0, 20, or 200 ppm chromium in the form of chromium potassium sulfate. Ducklings from these pairs were fed the same diets as adults and were tested for their avoidance responses to a fright stimulus. Neither level of chromium had a significant effect on avoidance behavior.

Toxicology Letters↗

USGS1981

Acute toxicities of toxaphene and endrin to larvae of seven species of amphibians

Seven species of amphibian larvae were exposed to toxaphene and endrin in a continuous-flow dosing system to determine differences in sensitivity to the two compounds, EC50 and LC50 estimates varied from those for Rana sphenocephala by no more than one order of magnitude when calculated on the basis of intended concentrations. Removal of pesticides from water by the test animals was significant and it makes interpretation of results difficult. Continuous-flow toxicity tests conflict with the adaptations of amphibian larvae for static water; use of such tests for amphibians requires further evaluation.

Toxicology Letters↗

USGS1981

Effects of industrial effluents, heavy metals, and organic solvents on mallard embryo development

Mallard eggs were externally exposed at 3 and 8 days of incubation to 7 different industrial effluents and to 7 different heavy metal, organic solvent, and petroleum solutions to screen for potential embryo-toxic effects. This route of exposure was chosen in order to simulate the transfer of pollutant from the plumage of aquatic birds to their eggs. Five of the effluents including mineral pigment, scouring effluent, sludge, and tannery effluent resulted in small but significant reductions in embryonic growth. Treatment with methyl mercury chloride solution of 50 ppm (Hg) impaired embryonic growth but much higher concentrations were required to affect survival and cause teratogenic effects. Oil used to suppress road dust was the most toxic of the pollutants tested and only 0.5 microliter/egg caused 60% mortality by 18 days of development. These findings, in combination with other studies suggest that petroleum pollutants, or effluents in combination with petroleum, may pose a hazard to birds' eggs when exposure is by this route.

Toxicology Letters↗

USGS1985

Organophosphorus insecticide induced decrease in plasma luteinizing hormone concentration in white-footed mice

Oral intubation of 50 and 100 mg/kg acephate inhibited brain acetylcholinesterase (AChE) activity by 45% and 56%, and reduced basal luteinizing hormone (LH) concentration by 29% and 25% after 4 h in white-footed mice ( Peromyscus leucopus noveboracensis ). Dietary exposure to 25, 100, and 400 ppm acephate for 5 days substantially inhibited brain AChE activity, but did not affect plasma LH concentration. These preliminary findings suggest that acute exposure to organophosphorus insecticides may affect LH secretion and possibly reproductive function.

Toxicology Letters↗

USGS1985

Effects of fluoride on screech owl reproduction: Teratological evaluation, growth, and blood chemistry in hatchlings

The effects on reproduction in screech owls ( Otus asio ) of chronic dietary sodium fluoride administration at 0, 40, and 200 ppm were examined. Fluoride at 40 ppm resulted in a significantly smaller egg volume, while 200 ppm also resulted in lower egg weights and lengths. Day-one hatchlings in the 200 ppm group weighed almost 10% less than controls and had shorter crown-rump lengths. No gross abnormalities were apparent. Skeletal clearing and staining revealed significantly shorter tibiotarsus lengths in the 40 ppm and 200 ppm groups and a shorter radius-ulna length in the 200 ppm group. By 7 days of age, body weights and lengths did not differ from controls, but the tibiotarsus in the 200 ppm group remained shorter. No significant differences were detected in hematocrit, hemoglobin, plasma calcium or alkaline phosphatase. Plasma phosphorus levels were higher in the 40 ppm group than in controls. These results, in combination with the findings of Pattee et al. [25], revealed significant impairment of overall reproduction, suggesting that sodium fluoride could cause slight to moderate reproduction disorders in owls in fluoride-polluted areas.

Toxicology Letters↗

USGS1994

A review of lead poisoning in swans

Nearly 10,000 swans of six species or subspecies from 14 countries have died from poisoning caused by lead that originated from ingestion of fishing weights, shotgun pellets (shot), or contaminated vegetation or sediments associated with mining and smelting wastes. Lead contamination in mute swans in England caused local population declines during the late 1970s and 1980s. More tundra swans died from lead poisoning than any other species. The extreme record involved an estimated 7200 tundra swans that died over five winters at one locality in North Carolina. The recent legislation to ban lead fishing weights in most of England and Wales and recent replacement of lead shot with steel shot for waterfowl hunting in the United States and a few areas of Europe, including Denmark, are expected to reduce the incidence of lead poisoning in swans.

Comparative Biochemistry and Physiology, Part C: P↗

USGS1996

Regional cholinesterase activity in white-throated sparrow brain is differentially affected by acephate (Orthene®)

Effects of a 14-day dietary exposure to an organophosphorus pesticide, acephate (acetylphosphoramidothioic acid O,S-dimethyl ester), were determined on cholinesterase activity in three regions (basal ganglia, hippocampus, and hypothalamus) of the white-throated sparrow, Zonotrichia albicollis , brain. All three regions experienced depressed cholinesterase activity between 0.5–2 ppm acephate. The regions exhibited cholinesterase recovery at 2–16 ppm acephate; however, cholinesterase activity dropped and showed no recovery at higher dietary levels (>16 ppm acephate). Evidence indicates that the recovery is initiated by the magnitude of depression, not the duration. In general, as acephate concentration increased, differences in ChE activity among brain regions decreased. Three terms are introduced to describe ChE response to acephate exposure: 1) ChE resistance threshold, 2) ChE compensation threshold, and 3) ChE depression threshold. It is hypothesized that adverse effects to birds in the field may occur at pesticide exposure levels customarily considered negligible.

Comparative Biochemistry and Physiology, Part C: P↗

USGS2004

Roles of uptake, biotransformation, and target site sensitivity in determining the differential toxicity of chlorpyrifos to second to fourth instar Chironomous riparius (Meigen)

Early life stages of aquatic organisms tend to be more sensitive to various chemical contaminants than later life stages. This research attempted to identify the key biological factors that determined sensitivity differences among life stages of the aquatic insect Chironomous riparius. Specifically, second to fourth instar larvae were exposed in vivo to both low and high waterborne concentrations of chlorpyrifos to examine differences in accumulation rates, chlorpyrifos biotransformation, and overall sensitivity among instars. In vitro acetylcholinesterase (AChE) assays were performed with chlorpyrifos and the metabolite, chlorpyrifos-oxon, to investigate potential target site sensitivity differences among instars. Earlier instars accumulated chlorpyrifos more rapidly than later instars. There were no major differences among instars in the biotransformation rates of chlorpyrifos to the more polar metabolites, chlorpyrifos-oxon, and chlorpyridinol (TCP). Homogenate AChE activities from second to fourth instar larvae were refractory to chlorpyrifos, even at high concentrations. In contrast, homogenate AChE activities were responsive in a dose-dependent manner to chlorpyrifos-oxon. In general, it appeared that chlorpyrifos sensitivity differences among second to fourth instar C. riparius were largely determined by differences in uptake rates. In terms of AChE depression, fourth instar homogenates were more sensitive to chlorpyrifos and chlorpyrifos-oxon than earlier instars. However, basal AChE activity in fourth instar larvae was significantly higher than basal AChE activity in second to third instar larvae, which could potentially offset the apparent increased sensitivity to the oxon. ?? 2003 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗

USGS2005

Aqueous exposure to Aroclor 1254 modulates the mitogenic response of Atlantic salmon anterior kidney T-cells: Indications of short- and long-term immunomodulation

Polychlorinated biphenyls (PCBs) exist as persistent organic pollutants in numerous river systems in the United States. Unfortunately, some of these rivers are sites of active Atlantic salmon restoration programs, and polychlorinated biphenyls have been implicated as ancillary factors contributing to failed salmon restoration. Here, we investigate the immediate and chronic effects of intermediate duration aqueous PCB exposure (1 or 10 ??g L-1 Aroclor 1254) on the mitogen-stimulated lymphoproliferative response of Atlantic salmon anterior kidney leukocytes (AKLs). A short-term study was designed to examine immunomodulation in Atlantic salmon smolts immediately following 21 days of aqueous exposure, while a long-term study evaluated chronic impacts in the mitogen response in parr 15 months post-exposure as larvae. The proliferative response of AKLs to the mitogens concanavalin A (CON A), phytohemaglutinnin-P (PHA-P), pokeweed mitogen (PWM), and lipopolysaccharide were used as an indice of immunomodulation. The proliferative response to the T-cell mitogens CON A and PHA-P was significantly increased in the 10 ??g L-1 group (n = 10; P = 0.043 and 0.002, respectively) immediately following exposure of smolts. Additionally, The PHA-P response was significantly increased in the 1 ??g L-1 exposure group (n = 10, P = 0.036). In fish treated as larvae and tested 15 months later, the PHA-P sensitive populations exhibited elevated proliferation in the 1 and 10 ??g L-1 groups (n = 12, P < 0.04) relative to the vehicle control while the PWM response was significantly increased (n = 12, P = 0.036) only in the 10 ??g L-1 treated groups. These results demonstrate an immunomodulatory effect of PCBs on T-cell mitogen sensitive populations of lymphocytes in Atlantic salmon as well as long-term immunomodulation in PHA-P and PWM sensitive populations. ?? 2005 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗