Bioavailability and Ecotoxicity of Lead in Soil: Implications for Setting Ecological Soil Quality Standards.

Ecological soil quality standards for lead (Pb) that account for soil Pb bioavailability have not yet been derived. We derived such standards based on specific studies of the long-term bioavailability and toxicity of Pb to soil organisms and a compilation of field data on the bioaccumulation of Pb in earthworms. Toxicity thresholds of Pb to plants, invertebrates, or microorganisms vary over more than 2 orders of magnitude, and the lowest values overlap with the range in natural Pb background concentrations in soil. Soils freshly spiked with Pb2+ salts exhibit higher Pb bioavailability and lower toxic thresholds than long-term aged and leached equivalents. Comparative toxicity tests on leaching and aging effects suggest using a soil Pb threshold that is 4.0 higher, to correct thresholds of freshly spiked soils. Toxicity to plants and earthworms, and microbial N-transformation and bioaccumulation of Pb in earthworms increase with decreasing effective cation exchange capacity (eCEC) of the soil, and models were derived to normalize data for variation of the eCEC among soils. Suggested ecological quality standards for soil expressed as total soil Pb concentration are lower for Pb toxicity to wildlife via secondary poisoning compared with direct Pb toxicity to soil organisms. Standards for both types of receptors vary by factors of approximately 4 depending on soil eCEC. The data and models we have collated can be used for setting ecological soil quality criteria for Pb in different regulatory frameworks. Environ Toxicol Chem 2021;40:1950-1963. © 2021 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Metal Bioavailability Models: Current Status, Lessons Learned, Considerations for Regulatory Use, and the Path Forward.

Since the early 2000s, biotic ligand models and related constructs have been a dominant paradigm for risk assessment of aqueous metals in the environment. We critically review 1) the evidence for the mechanistic approach underlying metal bioavailability models; 2) considerations for the use and refinement of bioavailability-based toxicity models; 3) considerations for the incorporation of metal bioavailability models into environmental quality standards; and 4) some consensus recommendations for developing or applying metal bioavailability models. We note that models developed to date have been particularly challenged to accurately incorporate pH effects because they are unique with multiple possible mechanisms. As such, we doubt it is ever appropriate to lump algae/plant and animal bioavailability models; however, it is often reasonable to lump bioavailability models for animals, although aquatic insects may be an exception. Other recommendations include that data generated for model development should consider equilibrium conditions in exposure designs, including food items in combined waterborne-dietary matched chronic exposures. Some potentially important toxicity-modifying factors are currently not represented in bioavailability models and have received insufficient attention in toxicity testing. Temperature is probably of foremost importance; phosphate is likely important in plant and algae models. Acclimation may result in predictions that err on the side of protection. Striking a balance between comprehensive, mechanistically sound models and simplified approaches is a challenge. If empirical bioavailability tools such as multiple-linear regression models and look-up tables are employed in criteria, they should always be informed qualitatively and quantitatively by mechanistic models. If bioavailability models are to be used in environmental regulation, ongoing support and availability for use of the models in the public domain are essential. Environ Toxicol Chem 2019;39:60-84. © 2019 SETAC.

Effects of Soil Properties on the Toxicity and Bioaccumulation of Lead in Soil Invertebrates.

The present study examined the effects of soil physical and chemical properties on the toxicity of lead (Pb) to earthworms (Eisenia fetida) and collembolans (Folsomia candida), and on bioaccumulation of Pb by earthworms, in soils amended with Pb salts. Toxicity tests were conducted in 7 soils varying in soil properties (pH 4.7-7.4, effective cation exchange capacity [eCEC] 4-42 cmolc /kg, organic carbon 10-50 g C/kg) that were leached and pH corrected after spiking with PbCl2 . The median effect concentrations (EC50s) based on total soil Pb concentrations ranged from 35 to 5080 mg Pb/kg for earthworms and 389 to >7190 mg/kg for Collembola. Significant positive correlations were observed between log (EC50) for earthworm reproduction and log (eCEC, total C, exchangeable Ca and Mg, or clay content), but no significant correlations were observed between Pb toxicity to Collembola and soil properties. Expressing Pb dose as either the free ion (Pb2+ ) activity in porewater or as the measured dissolved porewater concentration of Pb did not explain differences in toxicity among soils. The bioaccumulation factors (BAFs) for Pb in earthworms ranged up to >10-fold across 6 soil treatments, with a median of 0.16, and the BAF was significantly correlated with eCEC (p = 0.038, r = -0.84), but not with any other soil properties. Soil properties related to eCEC (total C, exchangeable Ca and Mg, clay content) had a significant effect on Pb toxicity and bioaccumulation in earthworms, but no relationship was found for Collembola. As a major soil property affecting the bioavailability of Pb, CEC should be incorporated into any soil hazard assessment of Pb as a modifying factor of toxicity and bioaccumulation for earthworms. Environ Toxicol Chem 2019;38:1486-1494. © 2019 SETAC.

Chronic effects of lead exposure on topsmelt fish (Atherinops affinis): Influence of salinity, organism age, and relative sensitivity to other marine species.

The aim of the present study was to determine the influence of salinity and organism age on the chronic toxicity of waterborne lead (Pb) to Atherinops affinis and to compare the relative Pb sensitivity of A. affinis with other marine species. Chronic Pb exposure experiments were conducted in a water flow-through testing system. Survival, standard length, dry weight, and tissue Pb concentration were measured and lethal concentrations (LCs), effect concentrations (ECs), and bioconcentration factors (BCFs) were calculated. In general, increasing salinity and organism age decreased Pb toxicity. The LC50s for larval fish at 14 and 28 ppt salinity were 15.1 and 79.8 µg/L dissolved Pb, respectively; whereas, the LC50 for juvenile fish was 167.6 µg/L dissolved Pb at 28 ppt salinity. Using standard length data, the EC10 values for larval fish were 16.4 and 82.4 µg/L dissolved Pb at 14 and 28 ppt salinity, respectively. The dry weight EC25s for low and high salinity were 15.6 and 61.84 µg/L dissolved Pb, respectively. The BCFs were higher with the lower salinity study (1703) in comparison to the higher salinity study (654). Results of Pb speciation calculation showed higher fraction of Pb2+ in water with lower salinity, explaining the higher observed toxicity of Pb in lower salinity water than higher salinity water. Atherinops affinis is more sensitive to Pb than several other marine species. Evidence of abnormal swimming and skeletal deformities were observed in Pb exposure treatments. Results of the present study are useful for marine biotic ligand modeling and support ecological risk assessment and deriving Pb environmental quality criteria for marine environments. Environ Toxicol Chem 2018;37:2705-2713. © 2018 SETAC.

Are Lead Exposures a Risk in European Fresh Waters? A Regulatory Assessment Accounting for Bioavailability.

An indicative compliance assessment of the Europe-wide bioavailable lead Environmental Quality Standard of 1.2 µg L-1 (EQS) was undertaken against regulatory freshwater monitoring data from six European member states and FOREGS database. Bio-met, a user-friendly tool based upon Biotic Ligand Models (BLMs) was used to account for bioavailability, along with the current European Water Framework Directive lead dissolved organic carbon correction approach. The outputs from both approaches were compared to the BLM. Of the 9054 freshwater samples assessed only 0.6% exceeded the EQS of 1.2 µg L-1 after accounting for bioavailability. The data showed that ambient background concentrations of lead across Europe are unlikely to influence general compliance with the EQS, although there may be isolated local issues. The waters showing the greatest sensitivity to potential lead exposures are characterized by relatively low DOC (< 0.5 mg L-1), regardless of the pH and calcium concentrations.

Experimentally derived acute and chronic copper Biotic Ligand Models for rainbow trout.

We evaluated the effects of varying water chemistry ([Ca2+]=0.2-3mM, [Mg2+]=0.05-3mM, dissolved organic matter (DOM, natural, from maple leaves)=0.3-10mg of CL-1, pH=5.0-8.5) on the acute (96-h, unfed fish) and chronic (30-d, fed fish) toxicity of waterborne Cu to juvenile rainbow trout (Oncorhynchus mykiss) exposed in flow-through conditions. Acute and chronic Biotic Ligand Models (BLMs) were developed from the obtained toxicity data-sets, using the Visual MINTEQ software. Our results indicate that Cu is predominantly an acute toxicant to rainbow trout, as there were no observable growth effects and the 96-h and 30-d LC50 values were similar, with mortality mostly occurring within the first few days of exposure. Calcium and DOM were greatly protective against both acute and chronic Cu toxicity, but Mg seemed to only protect against chronic toxicity. Additional protection by pH 5.0 in acute exposure and by pH 8.5 in chronic exposure occurred. In the range of conditions tested, the observed 96-h LC50 and 30-d LC20 values varied by a factor of 39 and 27 respectively. The newly developed acute and chronic BLMs explained these variations reasonably well (i.e. within a 2-fold error), except at pH≥8 where the high observed acute toxicity could not be explained, even by considering an equal contribution of CuOH+ and Cu2+ to the overall Cu toxicity. The 96-h LC50 values of 59% of 90 toxicity tests from 19 independent studies in the literature were reasonably well predicted by the new acute BLM. The LC20 predictions from the new chronic BLM were reasonable for 7 out of 14 toxicity tests from 6 independent chronic studies (with variable exposure durations). The observed deviations from BLM predictions may be due to uncertainties in the water chemistry in these literature studies and/or to differences in fish sensitivity. A residual pH effect was also observed for both the acute and the chronic data-sets, as the ratio of predicted vs. observed LC values generally increased with the pH. Additional mechanistic studies are required to understand the influence of pH, Na, and Mg on Cu toxicity to trout. The present study presents the first experimentally developed chronic Cu BLM for the rainbow trout. To the best of our knowledge, it also presents the first acute Cu BLM that is based on a published data-set for trout. These newly developed BLMs should contribute to improving the risk assessment of Cu to fish in freshwater.

Development of biotic ligand model-based freshwater aquatic life criteria for lead following us environmental protection agency guidelines.

The US Environmental Protection Agency's (USEPA's) current ambient water quality criteria (AWQC) for lead (Pb) in freshwater were developed in 1984. The criteria are adjusted for hardness, but more recent studies have demonstrated that other parameters, especially dissolved organic carbon (DOC) and pH, have a much stronger influence on Pb bioavailability. These recent studies have been used to support development of a biotic ligand model (BLM) for Pb in freshwater, such that acute and chronic Pb toxicity can be predicted over a wide range of water chemistry conditions. Following USEPA guidelines for AWQC development and using a methodology consistent with that used by the USEPA in developing its recommended BLM-based criteria for copper in 2007, we propose acute and chronic BLM-based AWQC for Pb in freshwater. In addition to the application of the BLM approach that can better account for site-specific Pb bioavailability, the toxicity data sets presented are much more robust than in 1984, and there are now sufficient chronic Pb toxicity data available that use of an acute-to-chronic ratio is no longer necessary. Over a range of North American surface waters with representative water chemistry conditions, proposed acute BLM-based Pb criteria ranged from approximately 20 to 1000 µg/L and chronic BLM-based Pb criteria ranged from approximately 0.3 to 40 µg/L. The lowest criteria were for water with low DOC (1.2 mg/L), pH (6.7), and hardness (4.3 mg/L as CaCO3), whereas the highest criteria were for water with high DOC (9.8 mg/L), pH (8.2), and hardness (288 mg/L as CaCO3 ). Environ Toxicol Chem 2017;36:2965-2973. © 2017 SETAC.

Updated species sensitivity distribution evaluations for acute and chronic lead toxicity to saltwater aquatic life.

The US Environmental Protection Agency's (USEPA's) ambient water quality criteria (AWQC) for lead (Pb) in salt water were developed in 1984. The acute and chronic criteria are 210 and 8.1 µg/L dissolved Pb, respectively. Because data were limited in 1984, the chronic criterion was derived using an acute-to-chronic ratio, but there are now sufficient toxicity data such that an acute-to-chronic ratio is no longer needed. Based on the data now available, the proposed updated acute and chronic salt water Pb AWQC (following USEPA methods) are 100 and 10 µg/L, respectively. In the European Union, a chronic salt water predicted no-effect concentration based on the median 5th percentile hazardous concentration (HC5-50) was developed in 2008 for the Registration, Evaluation, Authorisation, and Restriction of Chemicals program, which forms the basis for deriving chronic environmental quality standards for Pb in European marine waters. The salt water HC5-50 previously derived for Pb was 6.1 µg/L, whereas the proposed, updated chronic salt water HC5-50 derived following European Union methods is 11.0 µg/L. Thus, despite differences in derivation methodologies, the proposed AWQC and HC5-50 values are very consistent. Studies evaluating the effect of water quality factors on bioavailability and toxicity of Pb in salt water are limited; the effect of water quality on Pb toxicity in salt water should be considered in future studies. Environ Toxicol Chem 2017;36:2974-2980. © 2017 SETAC.

Interactions of waterborne and dietborne Pb in rainbow trout, Oncorhynchus mykiss: Bioaccumulation, physiological responses, and chronic toxicity.

In Pb-contaminated environments, simultaneous exposure to both waterborne and dietborne Pb is likely to occur. This study examined the potential interactive effects of these two pathways in juvenile rainbow trout that were exposed to Pb in the water alone, in the diet alone, and in combination for 7 weeks. The highest waterborne Pb concentration tested (110µgL(-1)) was approximately equivalent to the 7-week LC20 (97µgL(-1)) measured in a separate trial, while the lowest was a concentration often measured in contaminated environments (8.5µgL(-1)). The live diet (10% daily ration on a wet mass basis) consisted of oligochaete worms (Lumbriculus variegatus) pre-exposed for 28days to the same waterborne Pb concentration, and the highest dietary dosing rate to the trout was 12.6µg Pb g fish(-1)day(-1). With waterborne exposure, whole body Pb burden increased to a greater extent in the worms than in the fish. Nonetheless, in trout waterborne exposure still resulted in 20-60-fold greater Pb accumulation compared to dietborne Pb exposure. However, combined exposure to both waterborne and dietborne Pb reduced the whole body accumulation extensively at waterborne Pb>50µgL(-1), with similar antagonistic interaction in liver and carcass (but not gill or gut) at a lower threshold of 20µgL(-1). Growth effects in trout were minimal with marginal reductions in the dietborne and combined exposures seen only at 110µgL(-1). Chronic Pb exposure reduced lipid and carbohydrates level in the worms by 50% and 80% respectively, while protein was unchanged, so growth effects in trout may have been of indirect origin. After 7 weeks, Ca(2+) homeostasis in the trout was unaffected, but there were impacts on Na(+). Blood Na(+) was reduced in waterborne and dietborne exposures, while gut Na(+)/K(+) ATPase activities were reduced in waterborne and combined exposures. This study is the first, to our knowledge to examine the interaction of waterborne and dietborne Pb exposure in fish. While physiological impacts of Pb were observed in both worms and fish, higher concentrations of dietborne Pb actually protected fish from waterborne Pb bioaccumulation and these effects. The impacts of metals on diet quality should not be neglected in future dietborne toxicity studies using live prey.

Revisiting the mechanisms of copper toxicity to rainbow trout: Time course, influence of calcium, unidirectional Na(+) fluxes, and branchial Na(+), K(+) ATPase and V-type H(+) ATPase activities.

In order to resolve uncertainties as to the mechanisms of toxic action of Cu and the protective effects of water [Ca], juvenile rainbow trout were acclimated to baseline soft water (SW, [Na(+)]=0.07, [Ca(2+)]=0.15, [Mg(2+)]=0.05mmolL(-1)) and then exposed to Cu with or without elevated [Ca] but at constant titratable alkalinity (0.27mmolL(-1)). The 96-h LC50 was 7-fold higher (63.8 versus 9.2µgCuL(-1); 1.00 versus 0.14µmolCuL(-1)) at [Ca]=3.0 versus 0.15mmolL(-1). Gill Cu burden increased with exposure concentration, and higher [Ca] attenuated this accumulation. At 24h, the gill Cu load (LA50≈0.58µgCug(-1); 9.13nmolCug(-1)) predictive of 50% mortality by 96h was independent of [Ca], in accord with Biotic Ligand Model (BLM) theory. Cu exposure induced net Na(+) losses (J(Na)net) by increasing unidirectional Na(+) efflux rates (J(Na)out) and inhibiting unidirectional Na(+) uptake rates (J(Na)in). The effect on J(Na)out was virtually immediate, whereas the effect on J(Na)in developed progressively over 24h and was associated with an inhibition of branchial Na(+), K(+) ATPase activity. The J(Na)in inhibition was eventually significant at a lower Cu threshold concentration (15µgCuL(-1)) than the J(Na)out stimulation (100µg Cu L(-1)). Elevated Ca protected against both effects, as well as against the inhibition of Na(+), K(+) ATPase activity. Branchial V-type H(+) ATPase activity was also inhibited by Cu exposure (100µgCuL(-1)), but only after 24h at high [Ca] (3.0mmolL(-1)). These novel results therefore reinforce the applicability of BLM theory to Cu, clarify that whether Na(+) influx or efflux is more sensitive depends on the duration of Cu exposure, show that elevated water [Ca], independent of alkalinity, is protective against both mechanisms of Cu toxicity, and identify V-type H(+)ATPase as a new Cu target for future investigation.

Can the biotic ligand model predict Cu toxicity across a range of pHs in softwater-acclimated rainbow trout?

This study examined the effects of pH (5.0-8.5) on the toxicity of waterborne Cu to juvenile rainbow trout (Oncorhynchus mykiss) in soft water under flow-through conditions. Relationships between 96 h or 30 day Cu toxicity and 24 h lethal Cu accumulation on the gills (24 h LA(50-Acute) or 24 h LA(50-Chronic)) were examined in the context of predictions made using the biotic ligand model (BLM). Acute toxicity was relatively constant across pHs except for a 2- to 3-fold higher LC(50) at pH 5.0. In the chronic exposure, the fish had similar tolerance to Cu from pH 5.0 to 8.0, but were 3- to 4-fold more tolerant at pH 8.5. This pattern was not captured by the current BLM which predicts that acute and chronic LC(50) values should increase progressively from pH 5.0 to 8.5, with much greater values than those observed at the higher pH range. BLM-based water quality criteria would not be protective for trout at pH 8.0 or 8.5 in acute exposure to Cu in soft water. The measured 24 h LA(50-Acute) and LA(50-chronic) at pH 8.5 were higher, and 24 h LA(50-Chronic) at pH 5.0 was lower than those at the other pHs. This study indicates that gill Cu bioaccumulation does not explain toxicity at high or low pH, and the BLM needs revision to adequately predict Cu toxicity to trout in soft water.

Modes of metal toxicity and impaired branchial ionoregulation in rainbow trout exposed to mixtures of Pb and Cd in soft water.

Models such as the Biotic Ligand Model (BLM) predict how natural organic matter (NOM) and competing ions (e.g., Ca(2+), H(+) and Na(+)) affect metal bioavailability and toxicity in aquatic organisms. However, such models focus upon individual metals, not metal mixtures. This study determined whether Pb and Cd interact at the gill of rainbow trout (Oncorhynchus mykiss) when trout were exposed to environmentally relevant concentrations of these metals (Cd<100 nmol L(-1); Pb<500 nmol L(-1)) in soft (<100 micromol Ca(2+)L(-1)), moderately acidic (pH 6.0) water. The 96-h LC50 for Pb was 482 nmol L(-1), indicating that Pb was one-order of magnitude more toxic in soft, acidic water than in harder, circumneutral pH waters. The LC50 for Cd alone was also low, 6.7 nmol L(-1). Surprisingly, fish acclimated to soft water had multiple populations of Pb-gill and Cd-gill binding sites. A low capacity, high affinity population of Pb-gill binding sites had a B(max) of 18.2 nmol g(-1) wet weight (ww) and apparent K(Pb-gill)=7.05, but a second low affinity population could not be saturated up to free Pb concentrations approaching 4000 nmol L(-1). Two populations of Cd-gill binding sites were characterized: a high affinity, low capacity population with an apparent K(Cd-gill)=7.33 and B(max)=1.73 nmol g(-1) ww, and a low affinity, high capacity population with an apparent K(Cd-gill)=5.86, and B(max)=13.7 nmol g(-1) ww. At low concentrations, Cd plus Pb accumulation was less than additive because Cd out-competed Pb for gill binding sites, which were likely apical Ca(2+)-channels. While disturbances to Ca(2+) influx were caused by Cd alone, Pb alone had no effect. However, Pb exacerbated Cd-induced disturbances to Ca(2+) influx demonstrating that, although Pb- plus Cd-gill binding was less than additive due to competition, the effects (ionic disturbances) were more than additive (synergistic). Pb was also likely binding to intracellular targets, such as branchial carbonic anhydrase, which led to inhibited Na(+) influx. This ionic disturbance was exacerbated by Cd. We conclude that exposure to environmentally relevant concentrations of Pb plus Cd results in less than additive metal-gill binding in soft, moderately acidic waters. However, ionic disturbances caused by Cd plus Pb are greater than additive, and this may ultimately increase the toxicity of Cd-Pb mixtures to fishes. Our findings suggest that it may be necessary to re-evaluate water quality criteria and assumptions of the BLM for fish exposed to mixtures of Pb and Cd in the acidic, soft waters found in the Canadian Shield, Scandinavia and other sensitive regions.

Pre-exposure to waterborne nickel downregulates gastrointestinal nickel uptake in rainbow trout: indirect evidence for nickel essentiality.

Nickel (Ni) may be both a toxicant and a micronutrient, but its essentiality to aquatic animals is not established. Interactions between branchial and gastrointestinal routes of metal uptake are important for understanding metal regulation and essentiality in aquatic animals. Adult rainbowtrout (Oncorhynchus mykiss) were pre-exposed to a sublethal concentration of waterborne Ni (7.43 micromol L(-1)) or a control water (0.12 micromol L(-1)) for 45 days, and subsequently, a gastrointestinal dose of radiolabeled Ni (1.08 micromol kg(-1) wet wt) was infused into the stomach of both non-pre-exposed and Ni pre-exposed trout to test whether pre-exposure to waterborne Ni would affect gastrointestinal uptake. The fish pre-exposed to waterborne Ni exhibited a markedly greater level of total Ni in the blood plasma (approximately 10-fold) but not in red blood cells (RBC). Pre-exposure downregulated the gastrointestinal uptake of radiolabeled Ni (new Ni) in the plasma and RBCs, providing evidence for the first time of homeostatic interaction between the two routes of Ni uptake. The plasma and RBC concentrations of new Ni in the non-pre-exposed and Ni pre-exposed groups were linear in the first 2 h and then approached a plateau. Only a small fraction of the infused dose (1.6-3.7%) was found in the internal organs of both groups at 24 h. Waterborne Ni, but not the infused Ni, greatly increased total Ni levels in the gills (6.1 fold), kidney (5.6 fold), scales (4.2 fold), and gut tissues (1.5-4.2 fold). It appears that gut, kidney and scales play important roles for Ni homeostasis by providing uptake, clearance and storage sites. Overall, our results suggest that Ni is subject to homeostatic regulation in the rainbow trout, a property that is characteristic of essential metals.

Renal function in the freshwater rainbow trout after dietary cadmium acclimation and waterborne cadmium challenge.

Renal function was examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 52 d and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Dietary Cd had no major effects on UFR (urine flow rate) and GFR (glomerular filtration rate) but caused increased renal excretion of glucose, protein, and major ions (Mg(2+), Zn(2+), K(+), Na(+), Cl(-) but Ca(2+)). However, dietary Cd did not affect any plasma ions except Na(+) which was significantly elevated in the Cd-acclimated trout. Plasma glucose and ammonia levels fell by 25% and 36% respectively, but neither plasma nor urine urea was affected in Cd-acclimated fish. Dietary Cd exposure resulted in a remarkable increase of Cd load in the plasma (48-fold, approximately 22 ng/mL) and urine (60-fold, 8.9 ng/mL), but Cd excretion via the kidney was negligible on a mass-balance basis. Clearance ratio analysis indicates that all ions, Cd, and metabolites were reabsorbed strongly (58-100%) in both naïve and dietary Cd exposed fish, except ammonia which was secreted in both groups. Mg(2+), Na(+), Cl(-) and K(+) reabsorption decreased significantly (3-15%) in the Cd-exposed fish relative to the control. Following waterborne Cd challenge, GFR and UFR were affected transiently, and only Mg(2+) and protein excretion remained elevated with no recovery with time in Cd-acclimated trout. Urinary Ca(2+) and Zn(2+) excretion rates dropped with an indication of renal compensation towards plasma declines of both ions. Cadmium challenge did not cause any notable effects on urinary excretion rates of metabolites. However, a significant decrease in Mg(2+) reabsorption but an increase in total ammonia secretion was observed in the Cd-acclimated fish. The study suggests that dietary Cd acclimation involves physiological costs in terms of renal dysfunction and elevated urinary losses.

Plasma clearance of cadmium and zinc in non-acclimated and metal-acclimated trout.

Adult rainbow trout were pre-exposed to a sublethal concentration of waterborne cadmium (Cd, 26.7 nmol/l) or waterborne zinc (Zn, 2294 nmol/l) for 30 days to induce acclimation. A single dose of radiolabeled Cd (64.4 nmol/kg) or Zn (183.8 nmol/kg) was injected into the vascular system of non-acclimated and Cd- or Zn-acclimated trout through indwelling arterial catheters. Subsequently, repetitive blood samples over 10 h and terminal tissue samples (liver, heart, bile, stomach, intestine, kidney, gills, muscle, and spleen) were taken to characterize the effect of metal acclimation on clearance kinetics in vivo. Plasma clearance of Cd in Cd-acclimated fish (0.726+/-0.015 and 0.477+/-0.012 ml/min per kg for total and newly accumulated Cd, respectively), was faster than that in non-acclimated trout (0.493+/-0.013 and 0.394+/-0.009 ml/min per kg). Unlike plasma Cd, the levels of Cd in red blood cells (RBCs) were 1.2-2.2 times higher in Cd-acclimated fish than in non-acclimated fish. At 10 h post-injection, the liver accumulated the highest proportion ( approximately 22%) of the injected Cd dose in both non-acclimated and Cd-acclimated fish but did not account for the difference in plasma levels of Cd between two groups. Plasma clearance of Zn ( approximately 0.23 ml/min per kg for new Zn) was substantially lower than Cd clearance. Pre-acclimation to waterborne Zn reduced the new Zn levels in RBCs, but did not affect the clearance of Zn from blood plasma or tissue burdens of Zn in fish. Bile concentrations of both Cd and Zn were elevated in acclimated fish, but total bile burden accounted for <1% of the injected metal dose. The results suggest that the detoxification process of injected plasma Cd is stimulated by pre-acclimation to waterborne Cd, and that Zn levels are homeostatically controlled in both non-acclimated and acclimated trout.