Toxicity of silver to rainbow trout (Salmo gairdneri)

The mean 96-h LC₅₀'s of silver with rainbow trout were 6.5 μg l⁻¹ and 13.0 μg l⁻¹ in soft water (approximately 26 mg l⁻¹ hardness as CaCO₃) and hard water (350 mg l⁻¹ hardness as CaCO₃), respectively. The long-term, “no effect” concentration for silver, added to the water as silver nitrate, was between 0.09 and 0.17 μg l⁻¹ after 18 months exposure in soft water. The “no effect” concentration is that concentration range which defines no observed effect. Based on mortalities different from the control, no mortalities attributable to silver occurred at 0.09 μg Ag l⁻¹, whereas 17.2% mortality occurred to fish exposed to 0.17 μg ll⁻¹. The “no effect” concentration does not reflect possible effects of silver on spawning behavior or reproduction, since female rainbow trout will not generally reach sexual maturity before 3 yr. At silver concentrations of 0.17 μg l⁻¹ or greater, silver caused premature hatching of eggs and reduced growth rate in fry. In one experiment, the eggs were completely hatched within 10 days of exposure; whereas, control eggs completed hatching after 42 days. The prematurely erupted fry were not well developed and frequently died. The growth rate of surviving fry was greatly reduced.     

The acute toxicity of vanadium and copper to eyed eggs of rainbow trout (Salmo gairdneri)

The effects of vanadium (25–595 mg l⁻¹) and of copper (0.03–4.78 mg l⁻¹) on embryonic survival and hatching of eyed eggs of rainbow trout, Salmo gairdneri, were investigated. Copper was approx. 300-fold more toxic than vanadium (96-h LC₅₀ = 0.4 and 118 mg l⁻¹, respectively) but had little effect on the timing of hatch. Vanadium induced premature hatching of eyed eggs at concentrations from 44 to 595 mg l⁻¹. Concentrations of copper required to produce lethality in eyed eggs were similar to concentrations required to produce mortality in juveniles. Vanadium concentrations approx. 15 times higher were required to produce mortality in eyed eggs than in juveniles. Therefore, acute exposure of eyed rainbow trout eggs to vanadium is not a sensitive toxicity test for use in establishing water quality criteria or maximum acceptable toxicant concentrations.     

The toxicity of various mining flotation reagents to rainbow trout (Salmo gairdneri)

Preliminary testing of eight collectors (xanthates) and four frothers in 96-h static and 28-day flow-through bioassays using rainbow trout as the test organism show a great disparity in the toxicity of the chemicals administered in these two ways.For the short-term tests, the relative toxicity of the compounds is expressed as an lc₅₀ or as a range of concentration in mg l⁻¹ in which the lc₅₀ is expected to fall. Of the collectors tested in this way sodium ethyl and potassium amyl xanthate were the most toxic, with lc₅₀'s in the range of 30–50 mg l⁻¹. Among the frothers, xylenol (cresylic acid) was found to be the most toxic (5.6 mg l⁻¹ >lc₅₀ > 3.2 mg l⁻¹) while polypropylene glycol was least toxic (lc₅₀ > 1000 mg l⁻¹).The long-term tests using potassium ethyl, sodium isopropyl, sodium ethyl, and potassium amyl xanthate indicated that in the flow-through system, the toxicity of the chemicals was in the order of 100 fold greater compared with the static bioassay results.     

Some physiological responses of rainbow trout (Salmo gairdneri) to intermittent monochloramine exposure

Rainbow trout (Salmo gairdneri) were exposed for 2.5 h to monochloramine (NH₂Cl) at an average concentration of 0.16 or 0.23 mg l⁻¹ (and with peak concentrations of 0.4 or 0.6 mg l⁻¹) three times daily. This simulates conditions in the outfall area of many electric power plants. Heart rate, opercular movement, cough frequency, arterial PO₂, lactate, hemoglobin and methemoglobin were monitored. The trout responded to chloramine pulses with slight increases in opercular movement, bradycardia, and a large increase in cough rate. These factors approached control rates between periods of exposure to a peak concentration of 0.4 mg l⁻¹, but not when the peak was 0.6 mg l⁻¹. Neither hemoglobin or lactate changed, while arterial PO₂ decreased slightly but not significantly. Methemoglobin concentration increased markedly at the end of each period of exposure with some recovery between them. In contrast to free chlorine, which causes acute hypoxemia due to gill damage, chloramine at these concentrations causes little if any hypoxemia. The elevated methemoglobin levels, not seen following exposure to free chlorine, indicate that perhaps chloramine is entering the blood stream to an extent that does not occur with free chlorine. Methemoglobinemia is probably not the proximate cause of death.     

Histopathological and physiological responses of rainbow trout (Salmo gairdneri richardson) to sublethal levels of lead

Rainbow trout (Salmo gairdneri) were exposed to sublethal levels of water-borne or dietary lead for 32 weeks. The study included a histopathological assessment of all organs, examination of red cell morphology, and a comparison of oxygen consumption in liver homogenates from exposed and control fish. No effects of lead toxicity were noted in these parameters. The most sensitive and reliable indicator of lead toxicity was the development of black tails and spinal curvature. These changes were observed in 30% of trout exposed to 120 ± 31 μg Pb 1⁻¹ of water-borne lead after 30 weeks. No other effects of lead toxicity were noted.     

Cardiovascular-respiratory responses of rainbow trout (Salmo gairdneri) during chronic exposure to sublethal concentrations of cadmium

The effects of exposure to 3.6 and 6.4 μg l⁻¹ cadmium for periods up to 178 days on cardiac and ventilatory rates, hematocrit, hemoglobin concentration and erythrocyte adenosine triphosphate concentration in adult rainbow trout, Salmo gairdneri, were investigated. Except for slight transitory responses, 3.6 μg l⁻¹ cadmium had no effect on any of the cardiovascular/respiratory parameters. Significant increases in cardiac and ventilatory rates, blood hematocrit and hemoglobin were observed in fish exposed to 6.4 μg l⁻¹ Cd over the entire exposure period while erythrocyte ATP concentration declined during the last stages of exposure. Further experiments on the responses of fish exposed to 6.4 μg l⁻¹ Cd for 30 days demonstrated an impairment of oxygen transfer across the gill. The results are discussed in terms of possible gill impairment and hyperactivity as toxic responses to cadmium.     

Biological half-lives of eight polycyclic aromatic hydrocarbons (PAHs) in rainbow trout (Salmo gairdneri)

Adult rainbow trout were exposed to a single oral dose containing a mixture of eight PAHs, and fish were sampled at intervals between 5–48 days after exposure. Regression analyses on whole fish indicate levels declined significantly in four of the compounds monitored. Their biological half-lives were estimated as 9 days for phenanthrene, 7 days for fluorene and anthracene and 6 days for fluoranthene. No reliable estimates could be derived for benzo[a]pyrene, benz[a]anthracene, chrysene or pyrene because of low or nondetectable concentrations at the first sample interval although it could be suggested that their half-lives would be less than several days. The data also suggested that these PAHs are poorly absorbed by trout.     

Avoidance response of rainbow trout (Salmo gairdneri) to single-dose chlorination in a power plant discharge canal

Rainbow trout (Salmo gairdneri) were exposed to 20 min single-dose chlorine additions designed to achieve maximum total residual chlorine (TRC) concentrations of 0.04, 0.2, 0.6, and 1.0 mg l⁻¹. First retreats from the chlorine front occurred at 0.05 mg l⁻¹ TRC. Approximately 95% of the fish had moved downstream when TRC reached 0.5 mg l⁻¹, well before cumulative time-dose exposure approached lethal limits. Percentage of fish remaining near the discharge decreased linearly as TRC concentration rose, suggesting that a rapid rise in receiving water chlorine level might be beneficial in reducing cumulative time-dose exposure. Rainbow trout demonstrated the initial sensitivity to avoid lethal chlorine exposure, but complete assessment of the utility of the avoidance response must also consider distribution throughout chlorination and the potential for repeated exposure.     

Cardiovascular and respiratory changes in rainbow trout, Salmo gairdneri, exposed intermittently to chlorine

Heart rate, ventilation frequency, coughing rate, arterial blood Po₂, pH, lactate, methemoglobin, and hematocrit were monitored serially in trout exposed to free chlorine thrice daily of 0.4 or 0.5 mg l⁻¹ peak residual concentration. A simultaneous bradycardia and hyperventilation occurred with each pulse of chlorine. Coughing rate rose 15-fold during each chlorination. All three parameters tended to return toward normal rates between pulses with recovery being noticeably better in 0.4 ppm chlorine pulses.Arterial Po₂ dropped to 40% of the control value during the peak of the first pulse and pH declined 0.25 units. Subsequent chlorine pulses caused more severe declines and progressively less interpulse recovery of these parameters. Blood lactate and hematocrit values were significantly elevated. Methemoglobin rose in concentration but not to a physiologically significant level. It is concluded that free chlorine kills fish by internal hypoxia induced by damage to the gills.     

The effect of arsenic on embrional development of rainbow trout (Salmo gairdneri, RICH.)

Studies were made on the toxic effect and accumulation of arsenic in developing eggs of rainbow trout. Fertile eggs were incubated at 6–7°C in sodium arsenate or arsenic trioxide solution at concentrations of 0.05–50.0 ppm As. The effect of arsenic on the survival of embryos and on the accumulation of the element in eggs were found to be related to the arsenic concentration and to the arsenic compound used (value of As-ion).     

Effects of copper, pH and hardness on the critical swimming performance of rainbow trout (Salmo gairdneri Richardson)

Critical swimming velocities of Salmo gairdneri at 12°C were determined in different combinations of copper; pH and hardness. Measurements were made after exposure for 0.5, 5, 10, and 30 days. When copper was not applied, hardness, pH and exposure time had no appreciable effect on critical performance. Copper had the greatest effect on swimming performance at 5 days of exposure. At pH 7.5–8.0, recovery from the initial depression was complete after 10 days of exposure, but critical swimming performance did not return to control levels in pH 6.0 treatments. For any given hardness, copper had a greater effect on critical speed at low than at high pH. A given copper treatment had a more pronounced effect at low than at high hardness.No distinction could be made among total, soluble, or extractable copper but predicted concentrations of 6 specific cupric ions varied with pH and hardness. Of these copper species, only Cu²⁺ and CuOH⁺ were found to be related significantly to critical performance.Oxygen consumption of trout was determined in different combinations of copper and pH. In the presence of copper the maximum oxygen consumption decreased and the energy expenditure for a given swimming speed increased.The above observations are discussed in relation to reported toxic actions of copper.     

The toxicity of mixtures of metals and surfactants to rainbow trout (Salmo gairdneri rich.)

The toxicity to rainbow trout of two metals (copper and mercury) and three detergents (two anionics and one non-ionic) were determined with an exposure period of 14 days. Each compound was tested separately and as a metal-detergent pair. The results show that for the mixtures of anionic detergents and metals a “more-than-additive” effect exists, while for the mixture of non-ionic detergent and metal the toxic effect is probably “less-than-additive”. These findings are compared with existing data in the literature and the underlying reasons for these effects are discussed.     

The toxicity of jet fuels to fish—II: The toxicity of JP-8 to flagfish (Jordanella floridae) and rainbow trout (Salmo gairdneri) and golden shiners (Notemigonus chysoleucas)

JP-8 is a widely-used commercial and military jet fuel which may reach the aquatic environment by several avenues. The toxicity of JP-8 to cold and warm water fish was investigated to help define the impact on fresh water species. Fish were exposed to the water soluble fraction (WSF) of JP-8 in static acute bioassays and continuous-flow bioassays of approx. 4 months duration. The goal was to determine the 96-h LC₅₀ and the long-term no effect level on the life cycle. The acute toxicity to a warm water fish was found to be unaffected by pH in the range of 7.3–9.1. The no effect level with respect to growth was lower in rainbow trout than in flagfish. Fuel accumulation and depuration from fish tissues are compared for the two species, as are the effects on egg hatching. The relative toxicity of JP-8 and JP-9 (previously reported) is discussed.     

Influence of water hardness on cadmium toxicity to Salmo gairdneri rich.

Acute toxicity of cadmium to Salmo gairdneri is increased by a reduction in water hardness. The role of the chemical species of the metal in the intoxication processes in waters of different levels of hardness, is considered as well as the reasons for explaining the observed effects by biological mechanisms.The theoretical distribution of the chemical species of cadmium in water of different level of hardness (320, 80 and 20 mg CaCO₃ 1⁻¹) at pH 7.2 was calculated. The results show that similar concentrations of the same form of cadmium (Cd²⁺) gave different levels of mortality and that similar acute toxic effects were caused by different amounts of ionic form (Cd²⁺). Fish acclimated at 320 mgCaCO₃ 1⁻¹ but tested at 20 mg CaCO₃ 1⁻¹ reacted in an intermediate way, confirming the importance of the biological hypothesis.Chloride cell proliferation in gills is a common defence response to intoxication processes. Thus the presence of a higher number of chloride cells in fish acclimated to hard water would have explained the lower sensitivity to cadmium. Fish kept in water with a wide difference in hardness and acclimated, so as to have different ionic contents in the blood, had an equal number of chloride cells in the gills. A detoxification mechanism based mainly on the increase in the number and activity of chloride cells should therefore be independent per se, of hardness and rather related to the presence of metals. On the contrary, the possibility of action by cadmium could depend upon the role of calcium in regulating gill permeability.     

Chronic toxicity of water-borne and dietary lead to rainbow trout (Salmo Gairdneri) in lake Ontario water

Rainbow trout (Salmo gairdneri) exposed to lead in Lake Ontario water demonstrated a 21-day LC₅₀ of 2.4 mg l⁻¹ lead. At lead concentrations ranging from 3 to 120 μg l⁻¹, log₁₀ of lead concentrations in most tissues of exposed fish appeared linearily related to log₁₀ of lead concentrations in water. Highest concentrations occurred in opercular bone followed by gill and kidney. Lead accumulation by brain was not clearly demonstrated. Exposure to lead in water at concentrations as low as 13 μg l⁻¹ caused significant increases in red blood cell (RBC) numbers, decreases in RBC volumes, decreases in RBC cellular iron content and decreases in RBC δ-amino levulinic acid dehydratase activity. No changes were observed in hematocrit or whole blood iron content. The changes indicated increased erythropoiesis to compensate for inhibition of hemoglobin production and increased mortality of mature red blood cells. After 32 weeks exposure to 120 μg l⁻¹ lead in water, 30% of remaining fish exhibited black tails, an early indication of spinal deformities. Lead added to food was not available for lead uptake by fish. Lead content of fish exposed to dietary lead was not elevated above control levels and the majority of lead consumed could be accounted for in the faeces. Dietary lead may have slightly inhibited uptake of dietary iron.     

The effect of sublethal concentrations of copper and zinc on ventilatory activity. Blood oxygen and pH in rainbow trout (Salmo gairdneri)

Changes in buccal and opercular pressure amplitude, as well as ventilation and coughing frequency were monitored in rainbow trout using catheterization of respiratory cavities and pressure transducers. One or more of the ventilatory parameters measured were found to change under toxicant stress at concentrations of copper or zinc at or below the LC 50. Possible synergistic effects were indicated when the two metal ions were tested together.Serial analyses of arterial P_O2 and pH in fish exposed to copper and zinc individually at concentrations approximating the LC 50 showed that environmental zinc produced a sharp decrease in both P_O2 and pH. Copper, however, caused little effect other than a transient increase in pH. The toxic action of the two metals in low concentrations thus may not be the same.     

The selection and limitations of phenol as a reference toxicant to detect differences in sensitivity among groups of rainbow trout (Salmo gairdneri)

Phenol was better than sodium azide, sodium pentachlorophenate, copper sulphate and dodecylsodium sulphate in detecting differences in sensitivity among groups of rainbow trout (Salmo gairdneri). Phenol detected differences in sensitivity among strains of trout and could discern the effects of starvation, temperature stress and pre-exposure to 0.04 mg l⁻¹ chlorine on the sensitivity of trout to phenol, but not the effects of three brands of food and high mortality during holding. The sensitivity of rainbow trout to phenol was independent of weight and loading density in the bioassays. The use of phenol as a reference toxicant for the rapid detection of differences in sensitivity among groups of fish is limited because differences can only be detected by comparing the sensitivity of an unknown group of fish to that of a known, unstressed group of fish in the same bioassay. The concept of a single reference toxicant appropriate for bioassays with a variety of chemicals is questionable because differences among groups of fish, which are detectable by a reference toxicant, may not affect the results of bioassays with other chemicals. A series of physiological and behavioural screening tests and diagnostic health checks may be more useful than reference toxicants to identify groups of fish which should not be used in bioassays.     

Lethal toxicity of permethrin (NRDC-143) to rainbow trout, salmo gairdneri, in relation to body weight and water temperature

Lethal toxicity of permethrin varied inversely with water temperature and body weight. The 96 h LC 50 (median lethal concentration) for 1 g trout increased by an order of magnitude from 0.62 to 6.43 μg 1⁻¹ between 5 and 20°C. However between 5 and 10°C the 96 h LC 50 changed little from 0.6 μg 1⁻¹. Large trout (200 g) were considerably more tolerant to permethrin than small fish. Thus, the 96 h LC 50s for 1 and 200 g trout were 3.17 and 314 μg 1⁻¹ respectively at 15°C. The size effect was most pronounced between 1 and 50 g.It is to be noted that the application of permethrin for insect control coincides with the usual period of emergence of rainbow trout fry subsequent to a spawning period of April to late June.     

Toxicological effects of dehydroabietic acid (DHAA) on the trout, Salmo gairdneri Richardson, in fresh water

Toxicological and physiological effects of dehydroabietic acid (DHAA), a major poison to fishes in pulp and paper mill effluents, were studied by two experiments with rainbow trout, Salmo gairdneri Richardson: in the first, fish were acutely exposed for 4 days to an average DHAA concentration of 1.2 mg l⁻¹ (Exp. I) and in the second for 30 days to an average of 20 μg DHAA l⁻¹ (Exp. II).Compared to the controls, fish of Exp. I displayed a decreased relative weight of liver, an increased blood haematocrit, and increased haemoglobin as well as plasma protein concentrations. The aspartate aminotransferase activity of heart muscle was significantly elevated, as was also the lactate dehydrogenase (LDH) of white muscle tissue. In the blood plasma, the proportion of muscle type LDH activity was simultaneously increased. UDP-glucuronyl-transferase activities of liver and kidney were strongly decreased. Results suggest an increased and altered use of body energy reserves, decreased plasma volume and impaired liver function.Fish of Exp. II showed an increased relative weight of spleen. In addition, liver and gill LDH shifted towards heart-type. We conclude that 20 μg l⁻¹ is close to the “minimum effective concentration” of DHAA to rainbow trout.