Toxicity of Oil and Dispersed Oil on Juvenile Mud Crabs,Rhithropanopeus harrisii

In order to simulate an offshore oil spill event, we assessed the acute toxicity of the non-dispersed and the chemically dispersed water-accommodated fraction (WAF) of crude oil using Louisiana sweet crude and Corexit^® 9500A with juvenile Harris mud crabs (Rhithropanopeus harrisii), an important Gulf of Mexico benthic crustacean. The chemical dispersion of crude oil significantly increased acute toxicity of the WAF in juvenile mud crabs compared to naturally dispersed oil. The majority of the mortality in the chemically dispersed treatments occurred within 24 h. While higher concentrations of chemically dispersed WAF had no survivors, at lower concentrations surviving juvenile crabs displayed no long-term effects. These results suggest that if the juvenile crabs survive initial exposure, acute exposure to dispersed or non-dispersed crude oil may not induce long-term effects.     

Comparative toxicity of four chemically dispersed and undispersed crude oils to rainbow trout embryos

The chronic toxicity of crude oil to fish embryos depends on the chemical constituents of the test oil and on factors that control the exposure of embryos to those constituents. The partitioning of chemicals from oil to water depends on the surface area of oil exposed to water and thus on the susceptibility of oil to be dispersed into droplets. The chronic toxicity of four different crude oils to embryos of rainbow trout (Oncorhynchus mykiss) was measured by exposure to the water-accommodated fraction (WAF; no droplet formation) and to the chemically enhanced WAF (CEWAF) of each oil. When effects were compared with the amount of WAF or CEWAF added to test solutions, chemical dispersion increased toxicity dramatically, by >35 to >300-fold, with the smallest difference measured for the lightest and least viscous oil. When effects were compared with measured concentrations of oil in test solutions, there were no differences in toxicity between WAF and CEWAF treatments, indicating that chemical dispersion promoted droplet formation and the partitioning of hydrocarbons from oil to water. On a dilution basis, the differences in toxicity among the four oils were correlated with the concentrations in oil of polynuclear aromatic hydrocarbons (PAH), particularly those with three to five rings, and with their viscosity, an index of dispersibility. However, when PAH concentrations were measured in solution, toxicity did not vary substantially among the four oils, suggesting that the PAH of each oil had equivalent toxicities and that differences in toxicity represented differences in dispersability.     

Acute toxicity of hydrogen cyanide to freshwater fishes.

Acute toxicity of hydrogen cyanide was determined at various temperatures from 4 degrees to 30 degrees C and oxygen concentrations of 3.36 to 9.26 mg/L on different life history stages of five species of fish: fathead minnow, Pimephales promelas Refinesque; bluegill, Lepomis macrochirus Rafinesque; yellow perch, Perca flavescens (Mitchill); brook trout, Salvelinus fontinalis (Mitchill); and rainbow trout, Salmo gairdneri Richardson. Median lethal threshold concentrations and 96-hr LC50's were established by flow-through type biassays. Acute toxicity varied from 57 microgram/L for juvenile rainbow trout to 191 microgram/L for field stocks of juvenile fathead minnows. Juvenile fish were more sensitive at lower temperatures and at oxygen levels below 5 mg/L. For most species juveniles were most sensitive and eggs more resistant.     

Effect of dispersant on the composition of the water-accommodated fraction of crude oil and its toxicity to larval marine fish

Newly hatched mummichog (Fundulus heteroclitus) were exposed in a 96-h static renewal assay to water-accommodated fractions of dispersed crude oil (DWAF) or crude oil (WAF) to evaluate if the dispersant-induced changes in aqueous concentrations of polycyclic aromatic hydrocarbons (PAH) affected larval survival, body length, or ethoxyresorufin-O-deethylase (EROD) activity. Weathered Mesa light crude oil (0.05-1 g/L) and filtered seawater with or without the addition of Corexit 9500 were used to prepare DWAF and WAE At 0.2 g/L, the addition of dispersant caused a two- and fivefold increase in the concentrations of total PAH (sigmaPAH) and high-molecular-weight PAH (HMWPAH) with three or more benzene rings. Highest mortality rates (89%) were observed in larvae exposed to DWAF (0.5 g/L; sigmaPAH, 479 ng/ml). A reduction in body length was correlated with increased levels of sigmaPAH (r2 = 0.65, p = 0.02) and not with HMWPAH. The EROD activity increased linearly with HMWPAH (r2 = 0.99, p = 0.001) and not with sigmaPAH. Thus, chemical dispersion increased both the sigmaPAH concentrations and the proportion of HMWPAH in WAF. Dispersed HMWPAH were bioavailable, as indicated by a significantly increased EROD activity in exposed mummichog larvae, and this may represent a significant hazard for larval fish.     

Assessment of the bioactivity of creosote-contaminated sediment by liver biotransformation system of rainbow trout

A sediment site in the Lake J?ms?nvesi (municipality of Pet?j?vesi, Finland) contaminated by creosote was investigated to assess the possible ecotoxicological risks it may cause to benthic animals, including ones which may arise due to physical measures in remediating the site. It is suggested that polycyclic aromatic hydrocarbons (PAHs) are bioavailable to fish and other aquatic animals during exposure to contaminated water, sediment, and food. In order to assess toxicological risks of sediment contents to fish, juvenile rainbow trout (Onchorhynchus mykiss) were intraperitoneally dosed with extracts of the creosote-contaminated sediments and their elutriates. This was compared to pristine lake sediment spiked with creosote. Activity of CYP1A1 in trout liver was measured as ethoxyresorufin O-deethylase (EROD). When compared to vehicle controls and the pristine reference sediment (0.9-1.3 pmol/min/mg PMS protein), the extract of creosote-contaminated sediment of Lake J?ms?nvesi induced EROD activity up 20-30 times with a dose of 100 mg/kg [total PAHs (mg)/(kg) in fish]. The rise of EROD was associated with increasing levels of PAH metabolites in bile, analyzed as 1-OH pyrene equivalents.     

Oil dispersant increases PAH uptake by fish exposed to crude oil

The use of oil dispersants is a controversial countermeasure in the effort to minimize the impact of oil spills. The risk of ecological effects will depend on whether oil dispersion increases or decreases the exposure of aquatic species to the toxic components of oil. To evaluate whether fish would be exposed to more polycyclic aromatic hydrocarbon (PAH) in dispersed oil relative to equivalent amounts of the water-accommodated fraction (WAF), measurements were made of CYP1A induction in trout exposed to the dispersant (Corexit 9500), WAFs, and the chemically enhanced WAF (dispersant; CEWAF) of three crude oils. The crude oils comprised the higher viscosity Mesa and Terra Nova and the less viscous Scotian Light. Total petroleum hydrocarbon and PAH concentrations in the test media were determined to relate the observed CYP1A induction in trout to dissolved fractions of the crude oil. CYP1A induction was 6- to 1100-fold higher in CEWAF treatments than in WAF treatments, with Terra Nova having the greatest increase, followed by Mesa and Scotian Light. Mesa had the highest induction potential with the lowest EC50 values for both WAF and CEWAF. The dispersant Corexit was not an inducer and it did not appear to affect the permeability of the gill surface to known inducers such as beta-napthoflavone. These experiments suggest that the use of oil dispersants will increase the exposure of fish to hydrocarbons in crude oil.     

Toxicity testing of crude oil and related compounds using early life stages of the crimson-spotted rainbowfish (Melanotaenia fluviatilis)

The toxicity of petroleum hydrocarbons to marine aquatic organisms has been widely investigated; however, the effects on freshwater environments have largely been ignored. In the Australian freshwater environment, the potential impacts of petroleum hydrocarbons are virtually unknown. The toxicity of crude oil and related compounds were measured in the sensitive early life stages of the crimson-spotted rainbowfish (Melanotaenia fluviatilis). Waterborne petroleum hydrocarbons crossed the chorion of embryonic rainbowfish, reducing survival and hatchability. Acute exposures resulted in developmental abnormalities at and above 0.5 mg/L total petroleum hydrocarbons (TPH). Deformities included pericardial edema, disturbed axis formation, and abnormal jaw development. When assessing the acute toxicities of the water-accommodated fraction (WAF) of crude oil, dispersants, dispersant-oil mixtures, and naphthalene to larval rainbowfish, the lowest to highest 96-h median lethal concentrations for day of hatch larvae were naphthalene (0.51 mg/L), dispersed crude oil WAF (DCWAF)-9527 (0.74 mg/L TPH), WAF (1.28 mg/L TPH), DCWAF-9500 (1.37 mg/L TPH), Corexit 9500 (14.5 mg/L TPH), and Corexit 9527 (20.1 mg/L). Using naphthalene as a reference toxicant, no differences were found between the sensitivities of larval rainbowfish collected from adults exposed to petroleum hydrocarbons during embryonic development and those collected from unexposed adults.     

Influence of a dispersant on the bioaccumulation of phenanthrene by topsmelt (Atherinops affinis)

Chemical dispersants enhance oil spill dispersion by forming water-accommodated micelles with oil droplets. However, how dispersants alter bioavailability and subsequent bioaccumulation of hydrocarbons is not well understood. Thus, the goal was to investigate the influence of a chemical dispersant on the disposition (uptake, biotransformation, and depuration) of a model hydrocarbon, [14C]-phenanthrene ([14C]PHN), by larval topsmelt (Atherinops affinis). Exposure was via aqueous-only or combined dietary and aqueous routes from a water-accommodated fraction (WAF) of Prudhoe Bay Crude Oil (PBCO) or a WAF of Corexit 9527-dispersed PBCO (DO). Trophic transfer was measured by incorporating into exposure media both a rotifer (Brachionus plicatilis) as food for the fish and a phytoplankton (Isochrysis galbana) as food for the rotifers. Short-term (4 h) bioconcentration of PHN was significantly decreased in topsmelt when oil was treated with dispersant (P < 0.05), but differences diminished after 12 h. When trophic transfer was incorporated, PHN accumulation was initially delayed but after 12 h attained similar levels. Dispersant use also significantly decreased the proportion of biotransformed PHN (as 9-phenanthrylsulfate) produced by topsmelt (P < 0.05). However, overall PHN depuration was not affected by dispersant use. Thus, chemical dispersant use in oil spill response may reduce short-term uptake but not long-term accumulation of hydrocarbons such as PHN in pelagic fish.     

The influence of water temperature on induced liver EROD activity in Atlantic cod (Gadus morhua) exposed to crude oil and oil dispersants

Juvenile Atlantic cod were exposed to either the water-accommodated fraction (WAF) or the chemically enhanced water-accommodated fraction (CEWAF) of Mediterranean South American (MESA), a medium grade crude oil at three different temperatures. Two concentrations of each mixture were tested, 0.2% and 1.0% (v/v) at 2, 7 and 10 °C. Corexit 9500 was the chemical dispersant tested. The liver enzyme ethoxyresorufin-O-deethylase (EROD) was measured during a 72-h exposure. The WAF of oil had significant (P<0.05) effect on enzyme activity compared to controls at only one sampling time: 48 h at 10 °C. Exposure of CEWAF of oil resulted in significantly (P<0.05) elevated EROD activity compared to controls. The level of EROD induction was temperature related with higher induction being observed in cod exposed to CEWAF at higher temperatures. Total polycyclic aromatic hydrocarbon (PAH) concentrations in exposure water were significantly higher in chemically dispersed mixtures. While PAH concentrations were lower in the 2 °C water compared to 7 or 10 °C (8.7 vs 11.9 μg mL⁻¹), the level of EROD induction was approximately 9 and 12 times lower at 2 °C compared to 7 or 10 °C, respectively, suggesting the metabolic rate of the cod plays a role in the enzyme response. These data suggest the risk of negative impacts associated with exposure to chemically dispersed oil may be affected by water temperature and that risk assessment of potential effects of WAF or CEWAF should consider the effects of water temperature on the physiology of the fish as well as the effectiveness of dispersants.     

The Effect of Different Oil Spill Remediation Techniques on Petroleum Hydrocarbon Elimination in Australian Bass (Macquaria novemaculeata)

Petroleum hydrocarbons were investigated in juvenile Australian bass, Macquaria novemaculeata, following exposure to the water accommodated fraction (WAF) of Bass Strait crude oil, chemically dispersed crude oil, and burnt crude oil. Each treatment was administered for 16 days either through the water column or through the diet (amphipod, Allorchestes compressa). Polycyclic aromatic hydrocarbon (PAH) elimination was determined by measuring biliary benzo(a)pyrene (B(a)P) and naphthalene-type metabolites. Biliary PAH-type metabolite concentrations varied with the type of oil spill remediation technique, route of exposure (food versus water), and exposure concentration. Fish exposed to chemically dispersed crude oil via the water exhibited the highest PAH-type biliary metabolite concentrations, relative to fish exposed to other treatments. In fish exposed via the diet, the highest concentration of both types of biliary metabolites also appeared in the dispersed oil–exposed individuals. The results suggest that chemically dispersing oil may have the greatest effect on bioavailability of hydrocarbons, both through waterborne and food chain exposures. Received: 22 January 2000/Accepted: 22 July 2000     

Chronic effects of silver exposure on ion levels, survival, and silver distribution within developing rainbow trout (Oncorhynchus mykiss) embryos

Rainbow trout embryos were chronically exposed to silver (as AgNO3) in moderately hard water (120 mg CaCO3/L, 0.70 mM Cl-, 1.3 mg/L dissolved organic matter. 12.3+/-0.1 degrees C) at nominal concentrations of 0.1, 1, and 10 microg/L (measured = 0.117+/-0.008, 1.22+/-0.16, and 13.51+/-1.58 microg/L, respectively) to investigate the effects on mortality, ionoregulation, and silver uptake and distribution of the embryo. Mortalities in the low concentrations (0.1 and 1.2 microg/L) were not significantly different from controls throughout embryonic development (days 1-32 postfertilization). Mortalities of embryos in the 13.5-microg/L treatment reached 56% by day 32 postfertilization (33% when accounting for control mortality), by which time more than 50% of surviving embryos had hatched. Accumulation of silver in whole embryos of 1.2- and 13.5-microg/L treatments reached the highest concentrations of 0.13 and 0.24 microg/g total silver, respectively, by day 32, but whole embryo silver burden was not correlated with mortality. Silver concentrations in different compartments of the whole embryo (chorion, dissected embryo, and yolk) were greatest just before hatch and were higher in the chorion for all experimental treatments. Up to 85% of total whole embryo silver content was bound to the chorion, which acts as a protective barrier during silver exposure. Whole embryo Na+ concentration in the 13.5-microg/L treatment was significantly reduced relative to controls from days 23 to 32 postfertilization, and levels in the embryo were reduced by 40% at day 32 postfertilization, indicating that silver toxicity in the whole embryo is associated with an ion regulatory disturbance that is similar to the acute effect of AgNO3 in juvenile and adult trout.     

Influence of exposure duration on the toxicity of triclopyr ester to fish and aquatic insects

Flow-through toxicity tests were conducted to determine the effects of exposure time on the toxicity of triclopyr butoxyethyl ester (Garlon^® 4) to fish (rainbow trout and chinook salmon) and stream insects (Hydropsyche sp. and Isonychia sp.). The toxicity of triclopyr ester to fish increased with exposure time, but the rate of increase in toxicity declined with increasing exposure duration. Median lethal concentrations for rainbow trout exposed for 1, 6, or 24 h were 22.5, 1.95, and 0.79 mg/L triclopyr ester (expressed as acid equivalent, nominal concentrations), respectively. Comparable values for chinook salmon were 34.6, 4.7, and 1.76 mg/L. The toxicity of triclopyr ester to aquatic insects also increased with increasing exposure time, but was considerably less than the toxicity to fish. There was no significant mortality (chi-square p>0.05) of insects following 3-h exposures to the maximum test concentration of approximately 110 mg/L. Median lethal concentrations following 9- and 24-h exposures were 14.9 and 4.0 ml/L for Hydropsyche sp., and 37.0 and 8.8 mg/L for Isonychia sp., respectively. At each exposure time in the toxicity tests, there was a sharp increase in mortality over relatively small increases in concentration, resulting in extremely steep slopes of the probit lines (6.3–33.8), and indicating an apparent response threshold. The herbicide exhibited delayed lethal effects, particularly in fish, but only at short term exposures to higher concentrations. The risk of adverse effects on fish and aquatic insects from triclopyr ester contamination, based on the results of these time-toxicity tests, is discussed.     

Acute and chronic toxicity of nitrate to early life stages of lake trout (Salvelinus namaycush) and lake whitefish (Coregonus clupeaformis)

The acute and chronic toxicity of the nitrate ion (NO3-) to the embryos, alevins, and swim-up fry of lake trout (Salvelinus namaycush) and lake whitefish (Coregonus clupeaformis) were tested in laboratory aquaria. The acute (96-h) median lethal concentration (LC50) for swim-up fry was 1,121 mg NO3-N/L for lake trout and 1,903 mg NO3-N/L for lake whitefish. The chronic (approximately 130-150-d) LC50s for embryos to swim-up fry were 190 and 64 mg NO3-N/L, respectively. Sublethal effects on developmental timing and fry body size were observed at concentrations of 6.25 and 25 mg NO3-N/L, respectively, in the chronic tests. These results confirm that the Canadian nitrate water-quality guideline of 2.9 mg NO3-N/L, which was derived from chronic tests on a temperate-zone amphibian, is applicable to the early life stages of two species of Arctic fish. However, it does not support use of the guideline for acute exposures during early life stages of salmonid fish or for acute or chronic exposures to adult fish, which are relatively insensitive to nitrate.     

Acute toxicity of hydrogen cyanide to freshwater fishes

Acute toxicity of hydrogen cyanide was determined at various temperatures from 4° to 30°C and oxygen concentrations of 3.36 to 9.26 mg/L on different life history stages of five species of fish: fathead minnow,Pimephales promelas Refinesque; bluegill,Lepomis macrochirus Rafinesque yellow perch,Perca flavescens (Mitchill); brook trout,Salvelinus fontinalis (Mitchill); and rainbow trout,Salmo gairdneri Richardson. Median lethal threshold concentrations and 96-hr LC50's were established by flow-through type bioassays. Acute toxicity varied from 57μg/L for juvenile rainbow trout to 191μg/L for field stocks of juvenile fathead minnows. Juvenile fish were more sensitive at lower temperatures and at oxygen levels below 5 mg/L. For most species juveniles were most sensitive and eggs more resistant. Paper No. 9954, Scientific Journal Series,Minnesota Agricultural Experiment Station, St. Paul, Minnesota. Research supported by theU.S. Environmental Protection Agency, Environmental Research Laboratory, Duluth, Minnesota, under Grant No. R802914.     

阿特拉津对斑马鱼影响的研究

目的研究农药阿特拉津是否具有雌激素效应。方法选择斑马鱼为受试动物，随机分为对照组和阿特拉津暴露组。观察不同浓度的阿特拉津（0．1、0．5、1．0、5．0、10．0mg／L）对斑马鱼的生长、体内卵黄蛋白原（Vtg）含量及肝脏7-乙氧基-3-异吩口恶唑酮-脱乙基酶（EROD）酶活力的影响。结果经14d暴露后，阿特拉津浓度低于1．0mg/kg时雄性斑马鱼体重增长分别为对照组的1．57、1．81和2．07倍；当阿特拉津浓度高于1．0mg／kg时，实验组斑马鱼体重出现负增长现象。当阿特拉津浓度为1．0、5．0和10．0mg／kg时，实验组雌性斑马鱼体重分别为对照组的-0．42、-2．18和-1．32倍。阿特拉津可诱导雄性斑马鱼体内Vtg表达，具有雌激素效应并抑制肝脏中EROD酶活力，与对照组相比，差异均有统计学意义（P〈0．01）。结论阿特拉津对水生动物有明确的生长和生殖毒性。     

Effect of Maintaining Rainbow Trout in Creosote Microcosms on Lens Optical Properties and Liver 7-Ethoxyresorufin-O-Deethylase (EROD) Activity

Previously, exposure of fish to polycyclic aromatic hydrocarbons (PAHs) in both field and laboratory settings has been associated with eye damage, but this has only been expressed qualitatively. In this study, an automated scanning laser system has been employed to quantitatively evaluate changes in lens optical quality in rainbow trout (Oncorhynchus mykiss) following their in vivo exposure to creosote, which is a complex mixture with many PAHs. Rainbow trout were placed in 12,000-L outdoor microcosms dosed with 0, 3, or 10 μl/L liquid creosote for a 28-day period. Collected fish were examined for changes in focal length variability (FLV), lens size, and weight. These measurements were compared with induction of hepatic ethoxyresorufin-O-deethylase (EROD) activity and hepatic and water concentrations of priority pollutant PAHs. The optical quality of rainbow trout lenses was significantly reduced following creosote exposure, as indicated by increased FLV. Lens damage was significantly related to hepatic EROD activity, and both effects rose with creosote dose. Analytical measurements of microcosm water indicated elevated concentrations of PAHs in creosote-dosed ponds, including compounds capable of inducing rainbow trout EROD activity in vitro. Hepatic concentrations of PAHs were low and not related to creosote dose, likely due to rapid metabolism and elimination. This study demonstrates for the first time employment of a highly sensitive and quantitative technique to measure lens damage in fish exposed to contaminants in situ. The relationship between this effect and hepatic CYP1A activity may suggest a mechanistic linkage, which could lead to the use of EROD activity as an indicator of toxic effect rather than just chemical exposure. Received: 17 May 1999/Accepted: 24 September 1999     

Vitellogenin as a biomarker for estrogenic effects in brown trout, Salmo trutta: laboratory and field investigations

The sensitivity of juvenile brown trout towards estrogenic chemicals (17beta-estradiol [E2], estrone [E1], 17alpha-ethinylestradiol [EE2], 4-tert-octylphenol [OP], and n-butylparaben [BP]) was tested in laboratory experiments with plasma and liver vitellogenin concentrations as endpoints. Vitellogenin concentrations were also assessed in juvenile brown trout collected in streams affected by agricultural runoff and discharges from scattered houses in the open land. In the laboratory, juvenile brown trout were exposed to the chemicals in flow-through tanks for 7 to 12 d and concentration-response relationships for the induction of vitellogenin synthesis were obtained. The actual exposure concentrations were determined by liquid chromatography-mass spectrometry. The median plasma vitellogenin concentration in first year control brown trout reared in recirculated groundwater was 165 ng/ml with 783 ng/ml as the highest value. The median effective concentration (EC50) values for vitellogenin induction (based on plasma concentrations) were 3.7 ng EE2/L, 15 ng E2/L, 88 ng E1/L, 68 microg BP/L, and 7 microg OP/L. Median effective concentrations derived from liver vitellogenin concentrations were similar. The 166 brown trout caught in the field were mainly first and second year fish and a few third year fish. Plasma vitellogenin concentrations were below 1000 ng/L in 146 of the fish, between 1000 ng/L and 4234 ng/L in 19 fish and 5.3 x 10(6) ng/L in one male fish. Vitellogenin concentrations did not differ between first and second year fish, but were elevated in third year fish. The data may indicate that juvenile (<2 years) trout with plasma vitellogenin concentrations above 1000 ng/ml have had their vitellogenin synthesis induced by exposure to estrogens in the environment. Plasma and liver vitellogenin concentrations were closely correlated in brown trout with elevated vitellogenin concentrations. It is noteworthy, however, that exposure to synthetic estrogens (EE2, BP, and OP) resulted in higher liver concentrations (for the same plasma concentration) than exposure to the natural estrogens E1 and E2.     

An Ecological Risk Assessment of the Acute and Chronic Effects of the Herbicide Clopyralid to Rainbow Trout (<Emphasis Type="Italic">Oncorhynchus mykiss</Emphasis>)

Clopyralid (3,6-dichloro-2-pyridinecarboxylic acid) is a pyridine herbicide frequently used to control invasive, noxious weeds in the northwestern United States. Clopyralid exhibits low acute toxicity to fish, including the rainbow trout (Oncorhynchus mykiss) and the threatened bull trout (Salvelinus confluentus). However, there are no published chronic toxicity data for clopyralid and fish that can be used in ecological risk assessments. We conducted 30-day chronic toxicity studies with juvenile rainbow trout exposed to the acid form of clopyralid. The 30-day maximum acceptable toxicant concentration (MATC) for growth, calculated as the geometric mean of the no observable effect concentration (68 mg/L) and the lowest observable effect concentration (136 mg/L), was 96 mg/L. No mortality was measured at the highest chronic concentration tested (273 mg/L). The acute:chronic ratio, calculated by dividing the previously published 96-h acutely lethal concentration (96-h ALC₅₀; 700 mg/L) by the MATC was 7.3. Toxicity values were compared to a four-tiered exposure assessment profile assuming an application rate of 1.12 kg/ha. The Tier 1 exposure estimation, based on direct overspray of a 2-m deep pond, was 0.055 mg/L. The Tier 2 maximum exposure estimate, based on the Generic Exposure Estimate Concentration model (GEENEC), was 0.057 mg/L. The Tier 3 maximum exposure estimate, based on previously published results of the Groundwater Loading Effects of Agricultural Management Systems model (GLEAMS), was 0.073 mg/L. The Tier 4 exposure estimate, based on published edge-of-field monitoring data, was estimated at 0.008 mg/L. Comparison of toxicity data to estimated environmental concentrations of clopyralid indicates that the safety factor for rainbow trout exposed to clopyralid at labeled use rates exceeds 1000. Therefore, the herbicide presents little to no risk to rainbow trout or other salmonids such as the threatened bull trout.     

Validation of the narcosis target lipid model for petroleum products: gasoline as a case study

The narcosis target lipid model (NTLM) was used to predict the toxicity of water-accommodated fractions (WAFs) of six gasoline blending streams to algae (Pseudokirchnereilla subcapitata, formerly Selenastrum capricornutum), juvenile rainbow trout (Oncorhynchus mykiss), and water flea (Daphnia magna). Gasolines are comprised of hydrocarbons that on dissolution into the aqueous phase are expected to act via narcosis. Aquatic toxicity data were obtained using a lethal-loading test in which WAFs were prepared using different gasoline loadings. The compositions of the gasolines were determined by analysis of C3 to C13 hydrocarbons grouped in classes of n-alkanes, iso-alkanes, aromatics, cyclic alkanes, and olefins. A model was developed to compute the concentrations of hydrocarbon blocks in WAFs based on gasoline composition and loading. The model accounts for the volume change of the gasoline, which varies depending on loading and volatilization loss. The predicted aqueous composition of WAFs compared favorably to measurements, and the predicted aqueous concentrations of WAFs were used in the NTLM to predict the aquatic toxicity of the gasolines. For each gasoline loading and species, total toxic units (TUs) were computed with an assumption of additivity. The acute toxicity of gasolines was predicted to within a factor of two for algae and daphnids. Predicted TUs overestimated toxicity to trout because of experimental factors that were not considered in the model. This analysis demonstrates the importance of aliphatic hydrocarbon loss to headspace during WAF preparation and the contribution of both aromatic and aliphatic hydrocarbons test to the toxicity of gasolines in closed systems and loss of aliphatics to headspace during WAF preparation. Model calculations indicate that satisfactory toxicity predictions can be achieved by describing gasoline composition using a limited number of aromatic and aliphatic hydrocarbon blocks with different octanol-water partition coefficients.     

Chronic toxicity of diethylenetriamine pentaacetic acid to crimson-spotted rainbowfish (Melanotaenia fluviatilis): effects on reproduction, condition, and ethoxyresorufin O-deethylase activity.

The chronic effects of the chelating agent diethylenetriamine pentaacetic acid (DTPA) on reproduction, condition factor, liver somatic index (LSI), gonad somatic index (GSI), and ethoxyresorufin O-deethylase (EROD) activity of adult Australian crimson-spotted rainbowfish (Melanotaenia fluviatilis) were assessed. Breeding groups of three females and two males were exposed to 0, 1, 10, or 100 mg/liter DTPA (nominal) in a 28-day "static-renewal" experiment. Overall, the toxicity of DTPA to adult crimson-spotted rainbowfish was relatively low. Reproduction was not affected at concentrations up to 100 mg/liter DTPA, although an early effect on hatchability was potentially attributed to direct toxicity to rainbowfish eggs. DTPA also had little effect on the condition of adult rainbowfish, with condition factor and GSI being unaffected at concentrations up to 100 mg/liter, the latter finding supporting the reproduction results. However, LSI in male rainbowfish exposed to 100 mg/liter was significantly lower than in those exposed to 1 mg/liter DTPA (P相似文献