Polycyclic aromatic compounds in the Canadian Environment: Aquatic and terrestrial environments.

Polycyclic aromatic compounds (PACs) are ubiquitous across environmental media in Canada, including surface water, soil, sediment and snowpack. Information is presented according to pan-Canadian sources, and key geographical areas including the Great Lakes, the Alberta Oil Sands Region (AOSR) and the Canadian Arctic. Significant PAC releases result from exploitation of fossil fuels containing naturally-derived PACs, with anthropogenic sources related to production, upgrading and transport which also release alkylated PACs. Continued expansion of the oil and gas industry indicates contamination by PACs may increase. Monitoring networks should be expanded, and include petrogenic PACs in their analytical schema, particularly near fuel transportation routes. National-scale roll-ups of emission budgets may not expose important details for localized areas, and on local scales emissions can be substantial without significantly contributing to total Canadian emissions. Burning organic matter produces mainly parent or pyrogenic PACs, with forest fires and coal combustion to produce iron and steel being major sources of pyrogenic PACs in Canada. Another major source is the use of carbon electrodes at aluminum smelters in British Columbia and Quebec. Temporal trends in PAC levels across the Great Lakes basin have remained relatively consistent over the past four decades. Management actions to reduce PAC loadings have been countered by increased urbanization, vehicular emissions and areas of impervious surfaces. Major cities within the Great Lakes watershed act as diffuse sources of PACs, and result in coronas of contamination emanating from urban centres, highlighting the need for non-point source controls to reduce loadings.

The bioavailability of oil droplets trapped in river gravel by hyporheic flows.

Little is known about the fate of oil spills in rivers. Hyporheic flows of water through river sediments exchange surface and groundwater and create upwelling and downwelling zones that are important for fish spawning and embryo development. Risk assessments of oil spills to rivers do not consider the potential for hyporheic flows to carry oil droplets into sediments and the potential for prolonged exposure of fish to trapped oil. This project assessed whether oil droplets in water flowing through gravel will be trapped and whether hydrocarbons partitioning from trapped oil droplets are bioavailable to fish. Columns packed with gravel were injected with oil-in-water dispersions prepared with light crude, medium crude, diluted bitumens, and heavy fuel oil to generate a series of oil droplet loadings. The concentrations of oil trapped in the gravel increased with oil loading and viscosity. When the columns were perfused with clean water, oil concentrations in column effluents decreased to the detection limit within the first week of water flow, with sporadically higher concentrations associated with oil droplet release. Despite the low concentrations of hydrocarbons measured in column effluent, hydrocarbons were bioavailable to juvenile rainbow trout (Oncorhynchus mykiss) for more than three weeks of water flow, as indicated by strong induction of liver ethoxyresorufin-o-deethylase activity. These findings indicate that ecological risk assessments and spill response should identify and protect areas in rivers sensitive to contaminant trapping.

Effects on Trout Alevins of Chronic Exposures to Chemically Dispersed Access Western Blend and Cold Lake Blend Diluted Bitumens.

The present study assessed the chronic toxicity of 2 chemically enhanced water accommodated fractions (CEWAFs) of diluted bitumens (dilbits), Access Western Blend (AWB) and Cold Lake Blend (CLB), to rainbow trout alevins. Chemical dispersion was used to overcome the resistance to dispersion of dilbits and to generate test solutions that contained more and smaller oil droplets for increased partitioning of petroleum hydrocarbons into water. Test solutions were characterized by fluorescence spectroscopy, a rapid and inexpensive analytical tool to compare toxicity endpoints measured by fluorescence (total petroleum hydrocarbons measured by fluorescence [TPH-F]). Cumulative mortality and the prevalence and severity of malformations increased following exposure of alevins to dispersed dilbits. Toxicity curves overlapped for AWB and CLB when expressed as TPH-F and 22- to 24-d median lethal and effect concentrations ranged from 0.36 to 1.5 mg/L. Gene expression in alevins was also altered following exposure to dispersed dilbit, with relative cytochrome P450-1A mRNA levels increasing up to 170-fold for AWB and up to 240-fold for CLB. Access Western Blend and CLB caused similar toxicity to rainbow trout alevins as light to medium conventional crude oils, and rainbow trout alevins were more sensitive than yellow perch, Japanese medaka, and fathead minnow embryos exposed to dispersed AWB and CLB. The present study is the first to assess the embryotoxicity of dilbits to a Canadian freshwater salmonid species. Environ Toxicol Chem 2020;39:1620-1633. © 2020 SETAC.

Transcriptional responses in newly-hatched Japanese medaka (Oryzias latipes) associated with developmental malformations following diluted bitumen exposure.

Japanese medaka embryos were exposed to water accommodated fractions (WAF) and chemically-enhanced WAF of two types of diluted bitumen (dilbit) at concentrations bracketing the EC50s for developmental malformations. Within these treatments, fish were grouped based on the presence or absence of developmental malformations (e.g., blue sac disease (BSD)), and analyzed for novel transcriptomic responses. Microarray analyses identified novel biomarkers and gene networks in dilbit-exposed malformed embryos that were not evident in dilbit-exposed fish without BSD or in controls without dilbit. The top differentially expressed genes (DEGs) included cytochrome P450 transcripts (cyp1) in fish from all dilbit treatments (malformed and non-malformed fish), as well as: fibroblast growth factor (fgf7), AHR repressor (ahrr), and squalene monooxygenase (sqle). In dilbit-exposed fish that did not develop BSD, the only reported individual DEG was eukaryotic translation initiation factor 3 subunit D (eif3d). However, a number of other pathways were enriched, including melatonin effects on circadian clock and the antioxidant response, estrogen and androgen metabolism as well as many receptor signaling pathways. Pathways associated with hedgehog, steroid biosynthesis, and Wnt signaling were significantly altered between low and high concentrations of dilbit exposure. An effect of the dispersant control on swim bladder development was observed at concentrations 10-fold higher than those used to disperse dilbit, and a number of gene targets unique to fish in this comparison were affected. This suggests that the toxic effects of dispersant may involve alternative mechanisms to dilbit, but cause similar phenotypic responses. This study identified novel biomarkers in fish exposed to dilbit, with or without visual malformations, that can be used to assess the risks of dilbit to aquatic ecosystem health.

Temperature determines the rate at which retene affects trout embryos, not the concentration that is toxic.

The toxicity of waterborne retene (7-isopropyl-1-methyl phenanthrene) to post-hatch embryos of rainbow trout (Oncorhynchus mykiss) was assessed at 5 and 11 °C. Survival times of retene-exposed embryos were 70 % longer at 5 °C than at 11 °C, but survival times and LC50 s did not vary when time was expressed as degree-days (thermal units), i.e., at a common stage of development. The size of survivors decreased with increasing retene concentrations, but not with temperature. Retene did not bioconcentrate to any extent (bioconcentration factors < 2) at either temperature, indicating effective biotransformation by embryos. However, concentrations of retene metabolites were slightly higher at 5 °C, suggesting slower excretion rates than at 11 °C. The relative expression of cytochrome P450 proteins (CYP1A) did not vary with temperature but increased with retene concentration, as indicated by cyp1a mRNA concentrations. The induction of CYP1A protein by retene exposure was evident in the vasculature of eye, brain, heart, kidney, liver, gill, mouth, intestine, muscle, and yolk-sac. However, immunohistochemical staining was greater at 5 than at 11 °C for all tissues except liver and muscle. Overall, temperature effects on retene toxicity disappeared when the duration of embryo development and retene exposure were expressed as thermal units (degree-days). Temperature controlled the rate of embryo development and the rate of toxicity (time to a toxic endpoint), but not the concentrations that were toxic.

Oil toxicity test methods must be improved.

A review of the literature on oil toxicity tests showed a high diversity of reported test methods that may affect the composition, stability, and toxicity of oil solutions. Concentrations of oil in test solutions are dynamic because hydrocarbons evaporate, partition to test containers, bioaccumulate, biodegrade, and photo-oxidize. As a result, the composition and toxicity of test solutions may vary widely and create significant obstacles to comparing toxicity among studies and to applying existing data to new risk assessments. Some differences in toxicity can be resolved if benchmarks are based on measured concentrations of hydrocarbons in test solutions, highlighting the key role of chemical analyses. However, analyses have often been too infrequent to characterize rapid and profound changes in oil concentrations and composition during tests. The lack of practical methods to discriminate particulate from dissolved oil may also contribute to underestimating toxicity. Overall, current test protocols create uncertainty in toxicity benchmarks, with a high risk of errors in measured toxicity. Standard oil toxicity tests conducted in parallel with tests under site-specific conditions would provide an understanding of how test methods and conditions affect measured oil toxicity. Development of standard test methods could be achieved by collaborations among university, industry, and government scientists to define methods acceptable to all 3 sectors. Environ Toxicol Chem 2019;38:302-311. © 2018 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals, Inc. on behalf of SETAC.

Comparative toxicity of two diluted bitumens to developing yellow perch (Perca flavescens).

Increasing demand for diluted bitumen (dilbit) has led to the development of the oil sands industry and the expansion of transcontinental pipelines. Dilbit is an unresolved complex mixture with variable diluent and bitumen composition. Thus, it is important to understand the effects of the two most transported dilbits in Canada, Access Western Blend (AWB) and Cold Lake Blend (CLB) on a North America native and freshwater fish species, the yellow perch (Perca flavescens). Fertilized embryos were exposed to both dilbits for 16 days, from <24 h post-fertilization until hatch. The treatment regime was a static daily renewal of water accommodated fractions (WAF) and chemically-enhanced water accommodated fractions (CEWAF) at concentrations ranging from 0.01 to 21.3 µg/L of total polycyclic aromatic compounds (TPACs). Hatched embryos were assessed for malformations and changes in the expression of genes associated with phase I and II detoxification and oxidative stress. The prevalence of developmental malformations increased significantly at the highest concentrations of all treatments, with WAF treatments yielding a higher prevalence than CEWAF. The EC50s for AWB and CLB WAF and CEWAF solutions ranged from 9.8 to 24 µg/L TPACs, with the CEWAF of AWB being the least toxic. Relative mRNA levels of cyp1a showed induction by up to 18-fold in WAF and 50-fold in CEWAF treatments at similar concentrations of measured dilbit in solution. Complementary DNA methylation analysis was assessed and fish embryos exposed to AWB CEWAF and CLB WAF showed decreased DNA methylation profiles with increasing exposure to dilbit, suggesting that global gene expression is increasing in these treatments. With recent approvals of pipelines in North America, these data will support site-specific risk assessments and monitoring of Canadian ecosystems should a pipeline spill occur.

Dioxin-like contaminants are no longer a risk to the American eel (Anguilla rostrata) in Lake Ontario.

The embryotoxicity of extracts of American eels (Anguilla rostrata) was measured to determine whether maternally derived contaminants contribute to the declining recruitment of eels to Lake Ontario. Sexually maturing, large yellow and silver eels were sampled in 2007 and 2008 from 5 locations in eastern Canada, including Lake Ontario; positive controls included eels from the Hudson River, United States, and Canal Dessel-Schoten, Belgium (European eel, Anguilla anguilla). Japanese medaka eggs were injected immediately after fertilization with 1 or 10 nL of eel extract and, after 12 d, scored for signs of toxicity. Eel extracts did not cause dioxin-like embryotoxicity, reflecting the low concentrations of total dioxin equivalents measured chemically in these same extracts. Embryo mortality and reduced hatching success at high doses of eel extracts may reflect the bioaccumulation of legacy or emerging chemicals of concern. The results were consistent with long-term trends of declining concentrations of persistent organic pollutants (POPs) in tissues of eels and other fish species from Lake Ontario, trends of declining embryotoxicity of eel tissue extracts, and recent increases of recruitment of juvenile eels to Lake Ontario. If dioxin-like compounds contributed in the past to the decline of recruitment and abundance of American eels in Lake Ontario, these data suggest that recruitment should recover, following the same trends as the recovery of lake trout reproduction in Lake Ontario. Environ Toxicol Chem 2018;37:1061-1070. © 2017 SETAC.

An Embryonic Field of Study: The Aquatic Fate and Toxicity of Diluted Bitumen.

Canada has experienced a significant increase in the transport of diluted bitumen (dilbit), a predominant oil sands product that combines bitumen with diluents derived from oil-gas condensates and other proprietary compounds. The proportion of diluent and the chemical composition of dilbit vary to meet seasonal transport requirements. While the toxic effects of a variety of crude and refined oils are well-studied, the toxicity of dilbit to aquatic species is less well known. This focused review summarizes dilbit production, chemistry, and the few data on toxicity to aquatic species. These data suggest that un-weathered dilbit would cause effects on fish equivalent to those of conventional oils, but its toxicity may be lower, depending on interactions among test conditions, the behavior of dilbit added to water and the species tested.

Responses of an American eel brain endothelial-like cell line to selenium deprivation and to selenite, selenate, and selenomethionine additions in different exposure media.

The effect of selenium deprivation and addition on the American eel brain endothelial cell line (eelB) was studied in three exposure media: complete growth medium (L15/FBS), serum-free medium (L15), and minimal medium (L15/ex). L15/ex contains only galactose and pyruvate and allowed the deprivation of selenium on cells to be studied. In L15/ex, without any obvious source of selenium, eelB cells survived for at least 7 d, formed capillary-like structures (CLS) on Matrigel, and migrated to heal wounds. Three selenium compounds were added to cultures: selenite, selenate, and selenomethionine (SeMet). Adding selenite or selenate to eelB cell cultures for 24 h caused dose-dependent declines in cell viability, regardless of the exposure media. Although varying with exposure media and viability end point, selenite was approximately 70-fold more cytotoxic than selenate. By contrast, 24 h exposures to either DL- or L-SeMet in the three media caused little or no cytotoxicity. However for 7 d exposures in L15/ex, DL- and L-SeMet were very cytotoxic, even at the lowest tested concentration of 31 µM. By contrast in L15 and L15/FBS, cytotoxicity was only observed with 500 and 1000 µM L-SeMet. In L15/FBS, eelB continued to migrate and form CLS in the presence of SeMet but at 500 µM, cell migration appeared stimulated. As judged from a colony-forming assay over 14 d in L15/FBS, 500 and 1000 µM DL- and L-SeMet inhibited cell proliferation. Overall, the responses of eel cells to selenium depended on the selenium form, concentration, and exposure media, with responses to SeMet being most dependent on exposure media.

The Toxicity to Fish Embryos of PAH in Crude and Refined Oils.

Oil spills are a potential threat to the recruitment and production of fish. Polycyclic aromatic hydrocarbons (PAH), particularly 3-5-ringed alkyl PAH, are components of oil that cause chronic embryotoxicity. Toxicity is related to molecular size and octanol-water partition coefficients (Kow), indicating that water-lipid partitioning controls exposure and tissue dose. Nevertheless, more than 25% of the variation in toxicity among congeners is unexplained. Congeners with the same number of rings, alkyl carbon atoms, and Kow, but different molecular shapes, have markedly different toxicities, likely due to differences in interactions with cellular receptors. The potentiation and antagonism of metabolism and toxicity in PAH mixtures suggest that measured effect concentrations for individual PAH are conservative. Because mixture interactions are not well understood, total PAH concentrations >0.1 µg/L following oil spills should be considered hazardous.

Cold Lake Blend diluted bitumen toxicity to the early development of Japanese medaka.

Diluted bitumen (dilbit) from Alberta oil sands (Canada) is transported across major continental watersheds, yet little is known about its toxicity to fish if spilled into aquatic environments. The toxicity of Cold Lake (CLB) dilbit was assessed for medaka embryos (Oryzias latipes) exposed to water accommodated fractions (WAF) and chemically-enhanced WAF (CEWAF) using Corexit®EC9500A as dispersant. The effects of CLB toxicity were similar to conventional crude oils and Access Western Blend (AWB) dilbit. The prevalence of malformations and cyp1a mRNA synthesis in hatched fish increased monotonically with concentration during WAF and CEWAF treatments and provided a novel indicator of dilbit PAH toxicity. Apart from nfe2 (an antioxidant transcription factor), there were no statistically significant monotonic exposure-responses of ahr, arnt2, cat, sod, gpx, gst, gsr, g6pdh, p53, and hsp70 transcripts at total polycyclic aromatic hydrocarbons (TPAH) concentrations bracketing EC50s for embryotoxicity (WAF ≅ 3 µg/L; CEWAF ≅ 0.1 µg/L TPAH). Based on measured TPAH concentrations in exposure test solutions, CLB dilbit was 6-10 fold more toxic to medaka than AWB during chronic exposures. Lack of direct monotonic gene transcription responses to increasing oil concentrations during exposures that were embryotoxic suggests that the capacity of the oxidative stress response is limited in earlier lifestages or that differences exist among species in mechanisms of toxicity. This study provides a comparative framework for identifying suitable biomarkers and toxicity methods for those fish species in sensitive lifestages at highest risk of Canadian oil sands dilbit exposure following a spill in the freshwater environment.

Tracking pesticide use in the Saint Lawrence River and its ecological impacts during the World Exposition of 1967 in Montreal, Canada.

We analyzed dated sediment cores for evidence of Rhothane (dichlorodiphenyldichloroethane; DDD) applications to the Saint Lawrence River at Montreal, QC, Canada for the World Exposition of 1967 (Expo 67). More than 16,000kg of this pesticide were applied between 1965 and 1967 to abate nuisance shadflies that threatened visitor enjoyment. Concentrations of DDD and DDE in Lake Saint-François, 70km upstream of Expo 67, reached 12.2 and 11.5µg/kg dry weight (dw), respectively, with clear peaks between 1945 and 1970, consistent with historical use patterns; DDT was not detected. In Lake Saint-Pierre, ~100km downstream, DDD and DDE concentrations were 2 to 5 times higher, exceeding sediment quality guidelines, and DDT concentrations were as high as 3.8µg/kg. Once normalized for grain size and organic carbon, peaks of DDD, DDE and DDT were observed between 1945 and 1990 in the sediment record. Ratios of DDD to DDE were 1.0 or less in Lake Saint-François, consistent with their formation as degradation products of DDT. In contrast, ratios exceeded 1.0 in Lake Saint Pierre between 1965 and 1970, coinciding with Rhothane applications at Expo 67. Downstream, subfossil diatom assemblages showed little response to DDD inputs, but the abundance of some chironomid taxa increased while others decreased in tandem with elevated DDD concentrations. Overall, contamination of river sediments and impacts on insect communities by DDD applications at Expo 67 were still evident in sediment records 100km downstream of Montreal.

Environmental effects of the Deepwater Horizon oil spill: A review.

The Deepwater Horizon oil spill constituted an ecosystem-level injury in the northern Gulf of Mexico. Much oil spread at 1100-1300m depth, contaminating and affecting deepwater habitats. Factors such as oil-biodegradation, ocean currents and response measures (dispersants, burning) reduced coastal oiling. Still, >2100km of shoreline and many coastal habitats were affected. Research demonstrates that oiling caused a wide range of biological effects, although worst-case impact scenarios did not materialize. Biomarkers in individual organisms were more informative about oiling stress than population and community indices. Salt marshes and seabird populations were hard hit, but were also quite resilient to oiling effects. Monitoring demonstrated little contamination of seafood. Certain impacts are still understudied, such as effects on seagrass communities. Concerns of long-term impacts remain for large fish species, deep-sea corals, sea turtles and cetaceans. These species and their habitats should continue to receive attention (monitoring and research) for years to come.

Retene causes multifunctional transcriptomic changes in the heart of rainbow trout (Oncorhynchus mykiss) embryos.

Fish are particularly sensitive to aryl hydrocarbon receptor (AhR)-mediated developmental toxicity. The molecular mechanisms behind these adverse effects have remained largely unresolved in salmonids, and for AhR-agonistic polycyclic aromatic hydrocarbons (PAHs). This study explored the cardiac transcriptome of rainbow trout (Oncorhynchus mykiss) eleuteroembryos exposed to retene, an AhR-agonistic PAH. The embryos were exposed to retene (nominal concentration 32 µg/L) and control, their hearts were collected before, at and after the onset of the visible signs of developmental toxicity, and transcriptomic changes were studied by microarray analysis. Retene up- or down-regulated 122 genes. The largest Gene Ontology groups were signal transduction, transcription, apoptosis, cell growth, cytoskeleton, cell adhesion/mobility, cardiovascular development, xenobiotic metabolism, protein metabolism, lipid metabolism and transport, and amino acid metabolism. Together these findings suggest that retene affects multiple signaling cascades in the heart of rainbow trout embryos, and potentially disturbs processes related to cardiovascular development and function.

Development of a cell line from the American eel brain expressing endothelial cell properties.

A cell line (eelB) was developed from the outgrowth of adherent cells from brain explants of the American eel, Anguilla rostrata (Lesueur). EelB cells have been grown routinely in L-15 with 10% fetal bovine serum (FBS), undergone over 100 passages, and cryopreserved successfully. The cells from late-passage cultures (>45) were polygonal, formed capillary-like structures (CLS) on Matrigel, and stained immunocytochemically for von Willebrand factor (vWF) and for three tight junction proteins, zonula occludens-1 (ZO-1), claudin 3, and claudin 5. These results suggest that eelB is an endothelial cell line, one of the few from fish and the first from the brain. Despite this, eelB did not respond to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with the induction of CYP1A protein. The cells from early-passage cultures (<20) had more varied shapes and did not form CLS on Matrigel. Only cells from early-passage cultures formed in suspension three-dimensional aggregates that had some cells expressing alkaline phosphatase and nestin. These cells are thought to be neural stem cells and the aggregates neurospheres. The emergence of endothelial-like cells upon the continued subcultivation of cells from early-passage cultures that had neural stem cells has been described previously for mammals, but this is a first for teleosts. Remarkably, cells from all passage levels were stained strongly for senescence-associated ß-galactosidase (SA ß-Gal) activity.

Temporal variations in embryotoxicity of Lake Ontario American eel (Anguilla rostrata) extracts to developing Fundulus heteroclitus.

The recruitment of American eel (Anguilla rostrata) juveniles to Lake Ontario (LO), Canada has declined significantly since the 1980s. To investigate the possible contribution of maternally-transferred persistent organic pollutants (POPs) to this decline, this study measured temporal variations in the toxicity of complex organic mixtures extracted from LO American eels captured in 1988, 1998 and 2008 to developing Fundulus heteroclitus exposed by intravitelline (IVi) injection. The 1988 and 1998 eel extracts were most toxic, causing a pattern of sublethal embryotoxic responses similar to those previously reported in F. heteroclitus embryos exposed to single dioxin-like compounds (DLCs): stunted growth, craniofacial deformities, EROD activity induction, and reduced predatory capacities. The potency of extracts declined over time; the only significant effect of the 2008 eel extracts was EROD induction. The chemically-derived TCDD-TEQs of eel extracts, calculated using measured concentrations of some DLCs and their relative potencies for F. heteroclitus, overestimated their potency to induce EROD activity possibly due to interactions among POPs. Other POPs measured in eel extracts (non-dioxin-like PCBs, PBDEs and organochlorinated pesticides) did not appear to be important agonistic contributors to the observed toxicity. The toxicity of the complex mixtures of POPs measured in LO eels may have been underestimated as a result of several factors, including the loss of POPs during extracts preparation and a focus only on short-term effects. Based on the model species examined, our results support the hypothesis that contamination of LO with DLCs may have represented a threat to the American eel population through ecologically-relevant effects such as altered larval prey capture ability. These results prioritize the need to assess early life stage (ELS) toxicity of DLCs in Anguilla species, to investigate long-term effects of complex eel extracts to ELS of fish, and to develop biomarkers for potential effects in eel ELS sampled in the field.

Trends of persistent organic pollutants in American eel (Anguilla rostrata) from eastern Lake Ontario, Canada, and their potential effects on recruitment.

This study reports the history of contamination of American eels (Anguilla rostrata) from eastern Lake Ontario (LO) by persistent organic pollutants (POPs). Three groups of 10 large female eels captured in eastern LO in each of 1988, 1998, and 2008 were analysed for polychlorinated dibenzo-p-dioxins and furans, polychlorinated biphenyls, several organochlorine pesticides, and polybrominated diphenyl ethers. Mean concentrations were up to 3-fold lower in 2008 compared to previous years. When combined with the results of previous studies, these data show that concentrations of POPs in American eels have declined exponentially since the early 1980s by an average of 9.1±1.9% per year. Toxic equivalent (TEQ) concentrations of dioxin-like compounds (DLCs) were calculated from fish toxic equivalency factors. Assuming an efficient transfer of DLCs to their eggs, egg TEQs prior to 2000 exceeded the threshold for chronic toxicity to embryos of European eels (Anguilla anguilla) and lake trout (Salvelinus namaycush) (4-5 pg/g ww of TEQ). These results suggest that embryotoxicity of maternally-derived DLCs from LO eels, historically a major contributor to the spawning stock of American eels, could have impaired the reproductive and recruitment success of the species.

Quantitative structure-activity relationships for chronic toxicity of alkyl-chrysenes and alkyl-benz[a]anthracenes to Japanese medaka embryos (Oryzias latipes).

Alkylated polycyclic aromatic hydrocarbons (alkyl-PAHs) are a class of compounds found at significant concentrations in crude oils, and likely the main constituents responsible for the chronic toxicity of oil to fish. Alkyl substituents at different locations on the aromatic rings change the size and shape of PAH molecules, which results in different interactions with tissue receptors and different severities of toxicity. The present study is the first to report the toxicity of several alkylated derivatives of chrysene and benz[a]anthracene to the embryos of Japanese medaka (Oryzias latipes) using the partition controlled delivery (PCD) method of exposure. The PCD method maintained the desired exposure concentrations by equilibrium partitioning of hydrophobic test compounds from polydimethylsiloxane (PDMS) films. Test concentrations declined by only 13% over a period of 17 days. Based on the prevalence of signs of blue sac disease (BSD), as expressed by median effective concentrations (EC50s), benz[a]anthracene (B[a]A) was more toxic than chrysene. Alkylation generally increased toxicity, except at position 2 of B[a]A. Alkyl-PAHs substituted in the middle region had a lower EC50 than those substituted at the distal region. Except for B[a]A and 7-methylbenz[a]anthracene (7-MB), estimated EC50 values were higher than their solubility limits, which resulted in limited toxicity within the range of test concentrations. The regression between log EC50s and logKow values provided a rough estimation of structure-activity relationships for alkyl-PAHs, but Kow alone did not provide a complete explanation of the chronic toxicity of alkyl PAHs.

Mercury concentrations in amphipods and fish of the Saint Lawrence River (Canada) are unrelated to concentrations of legacy mercury in sediments.

Past industrial activity at Cornwall, Ontario, Canada has contaminated Lake Saint Francis, a fluvial lake on the Saint Lawrence River, with mercury (Hg). A spatial survey of Hg concentrations in sediments, amphipods, and yellow perch (Perca flavescens) in 2008 inferred current sources of Hg to the lake and spatial variations in risks to human consumers. Patterns of total and methyl Hg concentrations in sediment reflected upstream inputs, declining concentrations downstream, and highest concentrations at north shore sites near industrial sources; concentrations were lowest on the south shore because river currents limit north-south advective exchange. Surprisingly, concentrations of total or methyl Hg in sediments and pore water were unrelated to concentrations in amphipods and yellow perch. Concentrations in biota, and risks to consumers of fish, were highest at north shore sites near tributaries, and not at the most contaminated industrial sites. These results suggest that 'legacy' Hg in surficial sediments is not bioavailable to aquatic biota; tributaries and atmospheric deposition are possible sources of bioavailable Hg; and that sediment remediation would not resolve issues of Hg in fish. Fish consumption advisories for the entire lake based on single samples of fish could over- or under-protect consumers, depending on sampling location. To understand the actual risk to fish consumers for a large and complex lake system with multiple sources of Hg, more intensive sampling is needed to assess the spatial distribution of risk.