D.G. Dixon

Changes in hepatic mixed-function oxygenase (MFO) activity, plasma steroid levels and age at maturity of a white sucker (Catostomus commersoni) population exposed to bleached kraft pulp mill effluent

Abstract The impacts of bleached kraft mill effluent (BKME) on a white sucker (Catostomus commersoni) population were examined during May, July and August 1989, and compared with two reference sites. At the time of this study, the effluent received only primary treatment. BKME-exposed white sucker exhibited increased liversomatic indices and elevated mixed-function oxygenase (MFO) activity in both July and August. They also showed lower gonadosomatic indices and an increased age to maturity. The females contained fewer eggs at maturity, while the males had reduced development of secondary sexual characteristics. These fish also had severe reductions in plasma steroid levels throughout the year, including testosterone, and 17α,20β-dihydroxyprogesterone in both sexes, as well as 11-ketotestosterone in males and 17β-estradiol in females. BKME-exposed white sucker were shorter, older and had decreased growth rates compared to those at the reference sites. These fish also exhibited an increased condition factor, yet showed decreased visceral lipid stores. Relative to those at the reference sites, the stomach contents of the BKME-exposed fish revealed reduced numbers of organisms per gut, reduced taxa per gut and an increased number of empty stomachs. The decreased energetic commitment to reproduction, along with the increased condition factor, suggested a disruption in metabolic capability and altered energy allocation in fish exposed to BKME.

The use of fish cell cultures as an indication of contaminant toxicity to fish

Abstract The cytotoxicity of 12 chemicals to rainbow trout cells (RTG-2) was determined in culture. The indicator of cytotoxicity was the inability of cells to attach to a growth surface after chemical exposure. From most toxic to least toxic, these chemicals were pentachlorophenol, p-methylaminophenol, 2,4-dichlorophenol, p-chlorophenol, p-cyanophenol, p-nitrophenol, benzene, p-methylphenol, aniline, phenol, p-methoxyphenol and 1,2,4-trichlorobenzene. The cytotoxicity of these compounds was found to be significantly correlated to their water-borne toxicity to rainbow trout.

Modelling Bioaccumulation and Toxicity of Metal Mixtures

ABSTRACT Bioaccumulation of metals in mixtures may demonstrate competitive, anticompetitive, or non-competitive inhibition, as well as various combinations of these and/or enhancement of metal uptake. These can be distinguished by plotting (metal in water)/(metal in tissue) against metal in water and comparison to equivalent plots for single-metal exposure. For the special case of pure competitive inhibition where only one site of uptake is involved, inhibition of metal accumulation in any metal mixture can be predicted from bioaccumulation of the metals when present singly. This is consistent with the commonly used Biotic Ligand Model (BLM) but does not explain bioaccumulation of metals in Hyalella azteca. Options for modelling toxicity of metal mixtures include concentration or response addition based on metal concentrations in either water or tissues. If the site of toxic action is on the surface of the organism, if this is the same as the site of metal interaction for bioaccumulation, if there is only one such type of site, and if metal bioaccumulation interactions are purely competitive (as in the BLM), then metal toxicity should be concentration additive and predictable from metal concentrations in either water or tissues. This is the simplest toxicity interaction to model but represents only one of many possibilities. The BLM should, therefore, be used with caution when attempting to model metal interactions, and other possibilities must also be considered.

Effect of total body lipid on the toxicity and toxicokinetics of pentachlorophenol in rainbow trout (Oncorhynchus mykiss)

Abstract Juvenile rainbow trout were fed high fat (21%) or low fat (13%) practical diets for 11 wk in order to establish a significant difference in total body lipid; a difference of 3% was obtained. An acute lethality test (144 h) was performed on the two diet groups using pentachlorophenol (PCP). Elimination rate constants (k2) and acute lethality thresholds were estimated by fitting a one-compartment, first-order bioconcentration model to both the LC50/time data, and the time-to-death/water-concentration data. Estimates using these two methods were, respectively, 2.32 and 2.29 d−1 for the high fat treatment, and 2.84 and 2.66 d−1 for the low fat treatment. There was no significant difference in the resistance of fish to PCP due to lipid or weight as determined by a regression of time-to-death on these variables. Whole-body PCP levels, were measured in individual fish that died during the bioassay. Mean lethal body residues were found to range from 0.08 to 0.15 mmol PCP kg−1 and significant differences were found between both diet treatments and exposure concentrations. Analysis of covariance on the lethal residue data showed that lipid levels interacted significantly with exposure concentration, suggesting that the fish do not act as an ideal single compartment. Correction of PCP residues for fish lipid content showed that some of the variation in lethal body burdens could be accounted for by lipid content. In fish which survived the lethality bioassay at 91 μg 1−1, lipid levels were significantly decreased compared to initial levels. At the 91 1−1 μg exposure concentration PCP residues were not correlated with the body lipid content.

Characterizing the immunotoxicity of creosote to rainbow trout (Oncorhynchus mykiss): a microcosm study

Abstract Several immune parameters were evaluated in rainbow trout (Oncorhynchus mykiss) after they had been exposed for 28 days in microcosms dosed initially with liquid creosote concentrations of 0, 5, 9, 17, 31, 56 and 100 μl/l. The most noticeable changes were concentration-dependent reductions in pronephros leukocyte oxidative burst and the number of sIg+ peripheral blood leukocytes. Plasma lysozyme levels were reduced, while pronephros leukocyte phagocytic activity was enhanced marginally across creosote concentrations. Blastogenesis in response to lipopolysaccharide (LPS) was slightly impaired in head kidney leukocyte cultures prepared from creosote-exposed fish, whereas blastogenesis in response to phytohaemagglutinin (PHA) and concanavalin-A (ConA) was unaffected. Overall the results suggest that creosote has the potential to alter some innate immune functions in rainbow trout. Polycyclic aromatic hydrocarbons (PAHs), a major constituent of liquid creosote, are the suspected immune altering agents. The LOEC of the immune responses measured in this study was 17 μl/l using nominal creosote concentrations, representing a total PAH concentration of 611.63 ng/l in the water.

Induction of cytochrome P4501A by binary mixtures of polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in liver cell lines from rat and trout

Abstract The induction of ethoxyresorufin- o -deethylase (EROD) activity by binary combinations of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) and seven polychlorinated biphenyls (PCBs) was examined in liver cell lines from rat (H4IIE) and rainbow trout (RTL-W1). The non-ortho PCBs were 77, 81, 126, and 169; the mono-ortho PCBs were 105, 118, and 156. Binary combinations yielded less-than-additive interactions more commonly with RTL-W1 than with H4IIE. In RTL-W1, less-than-additive behaviour was observed at mono-ortho PCB/TCDD ratios of greater than 10u2008000 to 1 and at non-ortho PCB/TCDD ratios of greater than 80 to 1. In H4IIE, less-than-additive interactions were observed at mono-ortho PCB/TCDD ratios of greater than 20u2008000 to 1, but only additive interactions were seen between TCDD and non-ortho PCBs. With both cell lines, greater-than-additive interactions were not found. These results imply that bioassays with these cell lines could lead to lower TCDD-equivalent concentrations than would be determined by chemical analysis.

Acute toxicity of pulse-dosed methoxychlor to juvenile American flagfish (Jordanella floridae goode and bean) as modified by age and food availability

Abstract A factorial design was used to determine the effects of age (2, 4 and 8 day) and ration (fed and starved) on the acute toxicity of pulse-dosed methoxychlor to juvenile American flagfish ( Jordanella floridae Goode and Bean). The relative tolerance of the fish to methoxychlor was assessed by determining the 2 h pulse-exposure concentration causing 50% mortality (LC 50 ) over the subsequent 96 h. There was a statistically significant impact of age on the pulse-exposure LC 50 for fed juveniles: respective mean values for 2, 4 and 8 day fish were 3.2, 13.5 and 38.6 mg·l −1 . Conversely, for starved juveniles, there was no impact of age on LC 50 : mean values ranged from 1.6 to 3.8 mg·l −1 . At both 4 and 8 days starved fish were significantly less tolerant of methoxychlor than fed fish. Respective mean LC 50 values for starved and fed juveniles were 1.6 and 13.5 mg·l −1 at 4 days and 3.8 and 38.6 at 8 days. Ration level had no significant impact on LC 50 for 2 day juveniles. The median lethal time (LT 50 ) 96 h after pulse-exposure of 8 day juveniles also varied with ration level. Exposure to 1.29 mg·l −1 methoxychlor resulted in a LT 50 of 57 min for starved fish, significantly reduced relative to the 144 min LT 50 shown by fed fish. The 96-h LC 50 for continuously exposed adult flagfish was 0.29 mg·l −1 , 10 to 20 times lower than the pulse-exposure LC 50 values obtained with juveniles.

The comparative chronic toxicity of thiocyanate and cyanide to rainbow trout

Abstract Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to thiocyanate (SCN−, as KSCN (SD, n)) concentrations of 720 (98, 12) or 89 (12, 12) μmol 1−1 or cyanide concentrations of (CN−, as KCN) 0.98 (0.38, 14) or 0.32 (0.10, 14) μmol 1−1 for 16 weeks in a flow-through system. No mortality was evident, but significant bioconcentration of SCN− in plasma occurred in all trout exposed to SCN− or CN−. Mild chronic SCN− toxicity, as characterized by diffuse colloid goitre, slightly reduced growth, decreased hepatosomatic and splenosomatic indices and hematocrit, was observed in trout exposed to 720 μmol SCN− 1−1. The only changes observed in fish exposed to 89 μmol SCN− 1−1 or to CN− were increases in plasma SCN− and scattered areas of colloid goitre, with no evidence of toxicity. Exposure of rainbow trout to CN− at concentrations up to 0.98 μmol 1−1 for 16 weeks does not result in toxicity, either owing to the direct effects of CN− or owing to the indirect effects of endogenously produced SCN−.

Kinetics of uranium uptake in soft water and the effect of body size, bioaccumulation and toxicity to Hyalella azteca.

The kinetics of uptake and the effect of body size on uranium (U) bioaccumulation and toxicity to Hyalella azteca exposed to water-only U concentrations in soft water were evaluated. The effect of body size on U bioaccumulation was significant with a slope of -0.35 between log body concentration and log body mass. A saturation kinetic model was satisfactory to describe the uptake rate, elimination rate and the effect of gut-clearance on size-corrected U bioaccumulation in H. azteca. The one-week lethal water concentrations causing 50% mortality for juvenile and adult H. azteca were 1100 and 4000 nmol U/L, respectively. The one-week lethal body concentration causing 50% mortality was 140 nmol U/g for juvenile H. azteca and 220 nmol U/g for adult H. azteca. One-week bioaccumulation studies that properly account for body-size and gut-clearance times can provide valuable data on U bioavailability and toxicity in the environment.

Models of Cadmium Accumulation and Toxicity to Hyalella azteca during 7- and 28-Day Exposures

ABSTRACT The inhibition of Cd accumulation by Ca in the amphipod Hyalella azteca in short-term (7-d) exposures appears to follow anti-competitive, rather than competitive, inhibition. Increasing Ca reduces Cd accumulation more at high than at low Cd concentrations. Cadmium accumulation and toxicity in chronic exposures can be predicted using the 7-d model to which the effects of acclimation, Cd inhibition of acclimation, and growth dilution are added. The resultant model is complex and species-specific, making it unwieldy for direct application in water quality guideline or criteria development. However, it does demonstrate that a mechanistic explanation of the relationship between short- and long-term accumulation and toxicity is possible, as well as suggest why the acute-to-chronic ratio changes with water chemistry. It is not, therefore, appropriate to estimate chronic Cd toxicity to H. azteca from acute toxicity assuming a constant acute-to-chronic ratio. The standard Biotic Ligand Model (BLM) can also be fit to the chronic bioaccumulation and toxicity data. This may be a more practical approach to guideline or criteria development, provided it is understood that this is an empirical fit of the model and that the underlying mechanisms are far more complex than those invoked in the standard BLM.