Sediment Spatial Distribution and Quality Assessment of Metals in Chinook Salmon and Resident Killer Whale Marine Habitat in British Columbia, Canada.

At-risk resident killer whale (Orcinus orca) populations of the northeastern Pacific, Canada, and their main prey, Chinook Salmon (Oncorhynchus tshawytscha), are exposed to a variety of contaminants including chemical elements from both natural and anthropogenic sources, which may be constraining their recovery. Concentrations of 36 chemical elements in subtidal surface sediments (1-435 m depth) collected from 98 sites along the British Columbia coast were used to characterize coast-wide patterns, and a subset of metals (mercury (Hg), cadmium (Cd), arsenic (As), nickel (Ni), copper (Cu), and lead (Pb)) were selected to assess Chinook Salmon and resident killer whale marine habitat quality. Principal component analysis (PCA) showed a dominance of Hg, antimony (Sb), Pb, Cu, and zinc (Zn) for Prince Rupert Harbour, Victoria Harbour, and Burrard Inlet, suggesting local sources. Based on the PCA, geochemical properties such as total organic carbon (TOC), acid volatile sulfide (AVS), and pH explained the spatial distribution of all elements in sediment (p < 0.001). Mercury, Cd, As, Ni, Cu, and Pb hotspots were identified along the coast of Vancouver Island, the central and north coast, in the Strait of Georgia, and Haida Gwaii. Bischof Island of Haida Gwaii and Ardmillan Bay on the central coast were most contaminated and enriched by Cd, determined by geoaccumulation index (Igeo) and enrichment factor (EF), respectively. Marine habitat quality was assessed by comparing metal concentrations to Canadian Sediment Quality Guidelines (SQGs). Chinook Salmon populations may be indirectly affected by metal toxicity (As > Cd and Cu > Ni > Hg > Pb) to lower trophic level prey species. Toxicity related impacts to benthic organisms as a result of exposure to elevated Cd and As concentrations in Northern Resident Killer Whale critical habitat and to Hg, Cd, As, Ni, Cu, and Pb concentrations in Southern Resident Killer Whale critical habitat may indirectly pose a threat to resident killer whale populations, highlighting a need for management actions to reduce risks associated with these metals.

Climate change-contaminant interactions in marine food webs: Toward a conceptual framework.

Climate change is reshaping the way in which contaminants move through the global environment, in large part by changing the chemistry of the oceans and affecting the physiology, health, and feeding ecology of marine biota. Climate change-associated impacts on structure and function of marine food webs, with consequent changes in contaminant transport, fate, and effects, are likely to have significant repercussions to those human populations that rely on fisheries resources for food, recreation, or culture. Published studies on climate change-contaminant interactions with a focus on food web bioaccumulation were systematically reviewed to explore how climate change and ocean acidification may impact contaminant levels in marine food webs. We propose here a conceptual framework to illustrate the impacts of climate change on contaminant accumulation in marine food webs, as well as the downstream consequences for ecosystem goods and services. The potential impacts on social and economic security for coastal communities that depend on fisheries for food are discussed. Climate change-contaminant interactions may alter the bioaccumulation of two priority contaminant classes: the fat-soluble persistent organic pollutants (POPs), such as polychlorinated biphenyls (PCBs), as well as the protein-binding methylmercury (MeHg). These interactions include phenomena deemed to be either climate change dominant (i.e., climate change leads to an increase in contaminant exposure) or contaminant dominant (i.e., contamination leads to an increase in climate change susceptibility). We illustrate the pathways of climate change-contaminant interactions using case studies in the Northeastern Pacific Ocean. The important role of ecological and food web modeling to inform decision-making in managing ecological and human health risks of chemical pollutants contamination under climate change is also highlighted. Finally, we identify the need to develop integrated policies that manage the ecological and socioeconomic risk of greenhouse gases and marine pollutants.

Identification of Spilled Oil from the MV Marathassa (Vancouver, Canada 2015) Using Alkyl PAH Isomer Ratios.

On the morning of April 9, 2015, citizens in Vancouver (British Columbia, Canada) awoke to the sight and smell of oil on the shores of popular downtown beaches. Because the oil also had spread over the shallow seawater intakes for the Vancouver Aquarium, a preliminary screening of samples was performed as a prompt, first response to assess the risks to the Aquarium collection and guide the emergency operational response. A subsequent, more detailed examination for the presence of spilled oil in sediment, biota and water samples from the Vancouver Harbour region was then conducted based on the analysis of a large suite of alkanes, petroleum biomarkers, parent polycyclic aromatic hydrocarbons (PAHs) and alkyl PAH isomers. Most of the commonly applied biomarker ratios exhibit similar values for the spilled oil, Alberta oil (the main petroleum source for British Columbia), and pre-spill and un-oiled sediment samples. In contrast, alkyl PAH isomer ratios showed a clear distinction between the spilled oil and pre-spill samples, with the largest differences shown by isomers of the methyl fluoranthene/pyrene alkyl PAH series. This novel use of alkyl PAH isomers for fingerprinting petroleum helped to confirm the grain carrier MV Marathassa as the source of the oil that affected beach and mussel samples to document definitively the spread of the oil and to establish which samples contained a mix of the oil and hydrocarbons linked to historical activities. Finally, an initial evaluation of the biological risks of the MV Marathassa oil spill in Vancouver Harbour showed that oiled beach sediments had priority parent PAH concentrations that are likely to harm marine life.

A Risk-Based Characterization of Sediment Contamination by Legacy and Emergent Contaminants of Concern in Coastal British Columbia, Canada.

Sediments have long been used to help describe pollution sources, contaminated sites, trends over time, and habitat quality for marine life. We collected surficial sediments from 12 sites at an average seawater depth of 25 m in three near-urban areas of the Salish Sea (British Columbia, Canada) to investigate habitat quality for marine life, including heavily contaminated killer whales. Samples were analyzed using high-resolution instrumentation for a wide variety of congeners of polychlorinated biphenyls (PCBs), polybrominated diphenylethers (PBDEs), hexabromocyclododecane (HBCDD), polybrominated biphenyls, polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans, organochlorine pesticides, and polychlorinated naphthalenes (PCNs). The top six contaminant classes detected in sediments were ∑PCB > ∑PBDE > ∑PCDD/F > DDT > ∑HBCDD > ∑PCN. Near-urban harbor sediments had up to three orders of magnitude higher concentrations of contaminants than more remote sites. With limited tools available to characterize biological risks associated with complex mixtures in the real world, we applied several available approaches to prioritize the pollutant found in our study: (1) sediment quality guidelines from the Canadian Council of Ministers of the Environment where available; (2) US NOAA effects range low and other international guidelines; (3) total TEQ for dioxin-like PCBs for the protection of mammals; and (4) the calculation of risk quotients. Our findings provide an indication of the state of contamination of coastal environments in British Columbia and guidance for chemical regulations and priority setting, as well as management actions including best-practices, dredging, disposal at sea, and source control. In this regard, the legacy PCB and the emergent PBDEs should command continued priority monitoring.

Oil Spills and Marine Mammals in British Columbia, Canada: Development and Application of a Risk-Based Conceptual Framework.

Marine mammals are inherently vulnerable to oil spills. We developed a conceptual framework to evaluate the impacts of potential oil exposure on marine mammals and applied it to 21 species inhabiting coastal British Columbia (BC), Canada. Oil spill vulnerability was determined by examining both the likelihood of species-specific (individual) oil exposure and the consequent likelihood of population-level effects. Oil exposure pathways, ecology, and physiological characteristics were first used to assign species-specific vulnerability rankings. Baleen whales were found to be highly vulnerable due to blowhole breathing, surface filter feeding, and invertebrate prey. Sea otters (Enhydra lutris) were ranked as highly vulnerable due to their time spent at the ocean surface, dense pelage, and benthic feeding techniques. Species-specific vulnerabilities were considered to estimate the likelihood of population-level effects occurring after oil exposure. Killer whale (Orcinus orca) populations were deemed at highest risk due to small population sizes, complex social structure, long lives, slow reproductive turnover, and dietary specialization. Finally, we related the species-specific and population-level vulnerabilities. In BC, vulnerability was deemed highest for Northern and Southern Resident killer whales and sea otters, followed by Bigg's killer whales and Steller sea lions (Eumetopias jubatus). Our findings challenge the typical "indicator species" approach routinely used and underscore the need to examine marine mammals at a species and population level for risk-based oil spill predictions. This conceptual framework can be combined with spill probabilities and volumes to develop more robust risk assessments and may be applied elsewhere to identify vulnerability themes for marine mammals.

Polychlorinated Biphenyl-Related Alterations of the Expression of Essential Genes in Harbour Seals (Phoca vitulina) from Coastal Sites in Canada and the United States.

As long-lived marine mammals found throughout the temperate coastal waters of the North Pacific and Atlantic Oceans, harbour seals (Phoca vitulina) have become an invaluable sentinel of food-web contamination. Their relatively high trophic position predisposes harbour seals to the accumulation of harmful levels of persistent organic pollutants (POPs). We obtained skin/blubber biopsy samples from live-captured young harbour seals from various sites in the northeastern Pacific (British Columbia, Canada, and Washington State, USA) as well as the northwestern Atlantic (Newfoundland and Quebec, Canada). We developed harbour seal-specific primers to investigate the potential impact of POP exposure on the expression of eight important genes. We found correlations between the blubber mRNA levels of three of our eight target genes and the dominant persistent organic pollutant in seals [polychlorinated biphenyls (PCBs)] including estrogen receptor alpha (Esr1: r 2 = 0.12, p = 0.038), thyroid hormone receptor alpha (Thra: r 2 = 0.16; p = 0.028), and glucocorticoid receptor (Nr3c1: r 2 = 0.12; p = 0.049). Age, sex, weight, and length were not confounding factors on the expression of genes. Although the population-level consequences are unclear, our results suggest that PCBs are associated with alterations of the expression of genes responsible for aspects of metabolism, growth and development, and immune function. Collectively, these results provide additional support for the use of harbour seals as indicators of coastal food-web contamination.

Food Web Bioaccumulation Model for Resident Killer Whales from the Northeastern Pacific Ocean as a Tool for the Derivation of PBDE-Sediment Quality Guidelines.

Resident killer whale populations in the NE Pacific Ocean are at risk due to the accumulation of pollutants, including polybrominated diphenyl ethers (PBDEs). To assess the impact of PBDEs in water and sediments in killer whale critical habitat, we developed a food web bioaccumulation model. The model was designed to estimate PBDE concentrations in killer whales based on PBDE concentrations in sediments and the water column throughout a lifetime of exposure. Calculated and observed PBDE concentrations exceeded the only toxicity reference value available for PBDEs in marine mammals (1500 µg/kg lipid) in southern resident killer whales but not in northern resident killer whales. Temporal trends (1993-2006) for PBDEs observed in southern resident killer whales showed a doubling time of ≈5 years. If current sediment quality guidelines available in Canada for polychlorinated biphenyls are applied to PBDEs, it can be expected that PBDE concentrations in killer whales will exceed available toxicity reference values by a large margin. Model calculations suggest that a PBDE concentration in sediments of approximately 1.0 µg/kg dw produces PBDE concentrations in resident killer whales that are below the current toxicity reference value for 95 % of the population, with this value serving as a precautionary benchmark for a management-based approach to reducing PBDE health risks to killer whales. The food web bioaccumulation model may be a useful risk management tool in support of regulatory protection for killer whales.

Mercury Accumulation in Harbour Seals from the Northeastern Pacific Ocean: The Role of Transplacental Transfer, Lactation, Age and Location.

Mercury (Hg) bioaccumulates in the aquatic food chain in the form of methylmercury, a compound well known for its neurotoxicity. We analyzed total mercury (THg) in hair collected from 209 harbour seals captured at 10 sites in British Columbia (Canada) and Washington State (USA) between 2003 and 2010. In addition, laser ablation inductively-coupled plasma mass spectrometry (LA-ICP-MS) allowed for a highly refined analysis of THg accumulation over time by examining nine whiskers taken from 4- to 6-week-old pups. We estimate that THg concentrations in pups increased sharply at a point corresponding to mid- to late gestation of their time in utero (4.7 ± 0.8 and 6.6 ± 1.3 µg/g dry weight (dw), respectively), and then again at the onset of nursing (8.1 ± 1.3 µg/g dw). These abrupt changes highlight the importance of both pre- and post-natal THg transfer from the mother to the growing fetus and the newborn pup. While THg levels varied among sites, hair analyses from seals collected at the same site demonstrated the influence of age in THg accumulation with pups (5.3 ± 0.3 µg/g) and juveniles (4.5 ± 0.5 µg/g) having lower levels than those in adults (8.3 ± 0.8 µg/g). Our results revealed that 33 % of the pups sampled (n = 167) had THg levels that surpassed a mammalian hair threshold for neurochemical alterations. This study suggests that Hg could represent a health concern to marine wildlife, especially as atmospheric emissions of this toxic element from human activities in the Pacific Rim and worldwide continue.

Manufacturing doubt about endocrine disrupter science--A rebuttal of industry-sponsored critical comments on the UNEP/WHO report "State of the Science of Endocrine Disrupting Chemicals 2012".

We present a detailed response to the critique of "State of the Science of Endocrine Disrupting Chemicals 2012" (UNEP/WHO, 2013) by financial stakeholders, authored by Lamb et al. (2014). Lamb et al.'s claim that UNEP/WHO (2013) does not provide a balanced perspective on endocrine disruption is based on incomplete and misleading quoting of the report through omission of qualifying statements and inaccurate description of study objectives, results and conclusions. Lamb et al. define extremely narrow standards for synthesizing evidence which are then used to dismiss the UNEP/WHO 2013 report as flawed. We show that Lamb et al. misuse conceptual frameworks for assessing causality, especially the Bradford-Hill criteria, by ignoring the fundamental problems that exist with inferring causality from empirical observations. We conclude that Lamb et al.'s attempt of deconstructing the UNEP/WHO (2013) report is not particularly erudite and that their critique is not intended to be convincing to the scientific community, but to confuse the scientific data. Consequently, it promotes misinterpretation of the UNEP/WHO (2013) report by non-specialists, bureaucrats, politicians and other decision makers not intimately familiar with the topic of endocrine disruption and therefore susceptible to false generalizations of bias and subjectivity.

Ingestion of Microplastics by Zooplankton in the Northeast Pacific Ocean.

Microplastics are increasingly recognized as being widespread in the world's oceans, but relatively little is known about ingestion by marine biota. In light of the potential for microplastic fibers and fragments to be taken up by small marine organisms, we examined plastic ingestion by two foundation species near the base of North Pacific marine food webs, the calanoid copepod Neocalanus cristatus and the euphausiid Euphausia pacifia. We developed an acid digestion method to assess plastic ingestion by individual zooplankton and detected microplastics in both species. Encounter rates resulting from ingestion were 1 particle/every 34 copepods and 1/every 17 euphausiids (euphausiids > copepods; p = 0.01). Consistent with differences in the size selection of food between these two zooplankton species, the ingested particle size was greater in euphausiids (816 ± 108 µm) than in copepods (556 ± 149 µm) (p = 0.014). The contribution of ingested microplastic fibres to total plastic decreased with distance from shore in euphausiids (r (2) = 70, p = 0.003), corresponding to patterns in our previous observations of microplastics in seawater samples from the same locations. This first evidence of microplastic ingestion by marine zooplankton indicate that species at lower trophic levels of the marine food web are mistaking plastic for food, which raises fundamental questions about potential risks to higher trophic level species. One concern is risk to salmon: We estimate that consumption of microplastic-containing zooplankton will lead to the ingestion of 2-7 microplastic particles/day by individual juvenile salmon in coastal British Columbia, and ≤91 microplastic particles/day in returning adults.

Heightened biological uptake of polybrominated diphenyl ethers relative to polychlorinated biphenyls near-source revealed by sediment and plankton profiles along a coastal transect in British Columbia.

Polychlorinated biphenyl (PCB) and polybrominated diphenyl ether (PBDE) concentrations and profiles in paired sediment-plankton samples were determined along a 500 km transect in coastal British Columbia, Canada. PCB and PBDE levels in sediment were both greater in the industrialized Strait of Georgia than in remote northern sites and exhibited parallel spatial trends. In plankton, recent-use PBDE levels were higher near-source, while levels of legacy PCBs were uniform across sites. Principal component analysis of 95 PCB congeners illustrated the influence of proximity to source (i.e., latitude) on congener patterns for both matrices (sediment, r(2) = 0.52, p = 0.012; plankton, r(2) = 0.59, p = 0.016). The PCB pattern in plankton grew lighter with latitude, but the opposite pattern in sediments suggested that temperature-related fractionation, sediment processes, and basin-wide oceanography had divergent effects on each matrix. Biota-sediment accumulation factors (BSAFs) were greater for PBDEs than PCBs, but spatial profiles were similar; PCBs and PBDEs were near equilibrium in remote atmospherically driven sites (BSAF = 1.7 and 1.3) but accumulated preferentially in sediments at source-driven sites (BSAF = 0.2 and 0.4). The influences of particle-binding and hydrophobicity on the aquatic fate of PCBs and PBDEs was evident by the strong influence of log KOW on congener-specific BSAFs (PCBs, r(2) = 0.18 p < 0.001; PBDEs, r(2) = 0.61 p < 0.001). While biotic uptake of PCBs has become spatially uniform in coastal BC because of dilution over time, biomagnification of PBDEs remains higher in industrialized waters.

PCBs are associated with altered gene transcript profiles in arctic Beluga Whales (Delphinapterus leucas).

High trophic level arctic beluga whales (Delphinapterus leucas) are exposed to persistent organic pollutants (POP) originating primarily from southern latitudes. We collected samples from 43 male beluga harvested by Inuvialuit hunters (2008-2010) in the Beaufort Sea to evaluate the effects of POPs on the levels of 13 health-related gene transcripts using quantitative real-time polymerase chain reaction. Consistent with their role in detoxification, the aryl hydrocarbon receptor (Ahr) (r(2) = 0.18, p = 0.045 for 2008 and 2009) and cytochrome P450 1A1 (Cyp1a1) (r(2) = 0.20, p < 0.001 for 2008 and 2009; r(2) = 0.43, p = 0.049 for 2010) transcripts were positively correlated with polychlorinated biphenyls (PCBs), the dominant POP in beluga. Principal Components Analysis distinguished between these two toxicology genes and 11 other genes primarily involved in growth, metabolism, and development. Factor 1 explained 56% of gene profiles, with these latter 11 gene transcripts displaying greater abundance in years coinciding with periods of low sea ice extent (2008 and 2010). δ(13)C results suggested a shift in feeding ecology and/or change in condition of these ice edge-associated beluga whales during these two years. While this provides insight into the legacy of PCBs in a remote environment, the possible impacts of a changing ice climate on the health of beluga underscores the need for long-term studies.

Grizzly bear hair reveals toxic exposure to mercury through salmon consumption.

Mercury obtained from the diet accumulates in mammalian hair as it grows thus preserving a record of mercury intake over the growth period of a given hair segment. We adapted a microanalysis approach, using laser ablation inductively coupled plasma mass spectrometry, to characterize temporal changes in mercury exposure and uptake in wild and captive grizzly bears. Captive grizzlies fed diets containing known and varied amounts of mercury provided data to allow prediction of Hg ingestion rates in wild bears. Here, we show, for the first time, that 70% of the coastal grizzly bears sampled had Hg levels exceeding the neurochemical effect level proposed for polar bears. In a context where the international community is taking global actions to reduce Hg emissions through the "Minamata Convention on Mercury", our study provides valuable information on the exposure to mercury of these grizzly bears already under many threats.

PCB related effects thresholds as derived through gene transcript profiles in locally contaminated ringed seals (Pusa hispida).

Causal evidence linking toxic injury to polychlorinated biphenyl (PCB) exposure is typically confounded by the complexity of real-world contaminant mixtures to which aquatic wildlife are exposed. A local PCB "hotspot" on the Labrador coast provided a rare opportunity to evaluate the effects of PCBs on the health of a marine mammal as this chemical dominated their persistent organic pollutant (POP) burdens. The release of approximately 260 kg of PCBs by a military radar facility over a 30 year period (1970-2000) contaminated some local marine biota, including the ringed seal (Pusa hispida). The abundance profiles of eight health-related gene transcripts were evaluated in liver samples collected from 43 ringed seals in the affected area. The mRNA transcript levels of five gene targets, including aryl hydrocarbon receptor (Ahr), interleukin-1 ß (Il1b), estrogen receptor α (Esr1), insulin like growth factor receptor 1 (Igf1), and glucocorticoid receptor α (Nr3c1) correlated with increasing levels of blubber PCBs. PCB threshold values calculated using best-fit hockey-stick regression models for these five genes averaged 1,680±206 ng/g lw, with the lowest, most conservative, being 1,370 ng/g lw for Il1b. Approximately 14% of the seals in the region exceeded this threshold. The dominance of PCBs in the seals studied enabled an assessment of the effects of this chemical on gene transcripts involved in regulating the health of a highly mobile predator, something that is rarely possible in the world of complex mixtures.

Distribution and uptake of key polychlorinated biphenyl and polybrominated diphenyl ether congeners in benthic infauna relative to sediment organic enrichment.

As part of a broader study of budgets, transport, and bioaccumulation of persistent organic contaminants in the Strait of Georgia, Canada, matching samples of sediment and bulk benthos were collected near two marine sewage outfalls, two large urban harbours, and background areas. Samples were analyzed for polychlorinated biphenyl (PCB) and polybrominated diphenyl ether (PBDE) congeners. We present data for those congeners that fell within the top six rankings by concentration (23 PCBs and 10 PBDEs) within at least one of the environmental media measured in other studies (air, water, sediments, benthos, pelagic biota). Multifactor regression analyses incorporating sediment characteristics (total organic carbon, fines) predicted uptake (r (2) = 0.74 to 0.98, p < 0.04) over the range of congeners and habitats examined. PBDEs were taken up by biota more readily than PCBs, suggesting a large, potentially available biological reservoir of PBDEs in sediments. Dominant congeners in benthos comprised PBDEs 47, 99, 209, and 100 and PCBs 138/163, 153, 101, 118, and 110. PBDE uptake was anomalously high near one wastewater outfall, likely due to selective feeding on PBDE-enriched particulates from that source. Conversely, outfalls supply food and sediments with PCB concentrations similar to ambient sediments. However, organic enrichment of sediments near outfalls clearly enhanced PCB uptake by benthos, probably due to greatly increased biomass turnover near these sources. Data suggest there to be an initial reservoir of PCBs in newly settled juvenile benthos, which is much less evident for PBDEs. This is likely a consequence of the ecosystem-wide distribution of legacy PCBs but not the more current-use PBDEs. Congener-uptake patterns were dependent on source and input dynamics, feeding methods, and contaminant metabolism or debromination, particularly of deca-BDE.

Science and policy on endocrine disrupters must not be mixed: a reply to a "common sense" intervention by toxicology journal editors.

The "common sense" intervention by toxicology journal editors regarding proposed European Union endocrine disrupter regulations ignores scientific evidence and well-established principles of chemical risk assessment. In this commentary, endocrine disrupter experts express their concerns about a recently published, and is in our considered opinion inaccurate and factually incorrect, editorial that has appeared in several journals in toxicology. Some of the shortcomings of the editorial are discussed in detail. We call for a better founded scientific debate which may help to overcome a polarisation of views detrimental to reaching a consensus about scientific foundations for endocrine disrupter regulation in the EU.

Alteration of immune function endpoints and differential expression of estrogen receptor isoforms in leukocytes from 17ß-estradiol exposed rainbow trout (Oncorhynchus mykiss).

While the endocrine system is known to modulate immune function in vertebrates, the role of 17ß-estradiol (E2) in cellular immune function of teleosts is poorly understood. The cellular and molecular responses of juvenile rainbow trout (Oncorhynchus mykiss) to E2 treatment were evaluated by exposing fish to 0.47±0.02µg/L E2 (mean±SEM) for either 2 or 7d, with a subsequent 14d recovery period. After 2 and 7d of exposure to E2, hematocrit was significantly lower than in control fish. Lipopolysaccharide-induced lymphocyte proliferation was elevated on day 2 and concanavalin A-induced lymphocyte proliferation was reduced following 7d of E2 exposure. Four estrogen receptor (ER) transcripts were identified in purified trout head kidney leukocytes (HKL) and peripheral blood leukocytes (PBL). While the mRNA abundance of ERß1 and ERß2 was unaffected by treatment, ERα1 was up-regulated in HKL and PBL following 7d of E2 exposure. ERα2 was up-regulated in HKL after 7d of E2 exposure, but down-regulated in PBL after 2 and 7d of treatment. All parameters that were altered during the E2 exposure period returned to baseline levels following the recovery period. This study reports the presence of the full repertoire of ERs in purified HKL for the first time, and demonstrates that ERα transcript abundance in leukocytes can be regulated by waterborne E2 exposure. It also demonstrated that physiologically-relevant concentrations of E2 can modulate several immune functions in salmonids, which may have widespread implications for xenoestrogen-associated immunotoxicity in feral fish populations inhabiting contaminated aquatic environments.

Declining concentrations of chlorinated paraffins in endangered St. Lawrence Estuary belugas (Delphinapterus leucas): Response to regulations or a change in diet?

Very high levels of industrial contaminants in St. Lawrence Estuary (SLE) beluga whales represent one of the major threats to this population classified as endangered under the Species at Risk Act in Canada. Elevated concentrations of short-chained chlorinated paraffins (SCCPs) were recently reported in blubber of adult male SLE belugas. Recent regulations for SCCPs in North America, combined with their replacement by medium- (MCCPs) and long-chained chlorinated paraffins (LCCPs), highlight the importance of tracking this toxic chemical class. The objectives of this study were to evaluate (1) levels and profiles of chlorinated paraffins (CPs) in samples obtained from carcasses of adult male, adult female, juvenile, newborn, and fetus beluga, and (2) trends in adult male belugas between 1997 and 2018. Factors potentially influencing CP temporal trends such as age, feeding ecology and sampling year were also explored. SCCPs dominated (64 to 100%) total CP concentrations across all age and sex classes, MCCPs accounted for the remaining proportion of total CPs, and LCCPs were not detected in any sample. The chlorinated paraffin homolog that dominated the most in beluga blubber was C12Cl8. Adult male SCCP concentrations from this study were considerably lower (> 2000-fold) than those recently reported in Simond et al. (2020), likely reflecting a previously erroneous overestimate due to the lack of a suitable analytical method for SCCPs at the time. Both SCCPs and total CPs declined over time in adult males in our study (rate of 1.67 and 1.33% per year, respectively), presumably due in part to the implementation of regulations in 2012. However, there is a need to better understand the possible contribution of a changing diet to contaminant exposure, as stable isotopic ratios of carbon also changed over time.

Immunotoxic and cytotoxic effects of atrazine, permethrin and piperonyl butoxide to rainbow trout following in vitro exposure.

For many current use pesticides, limited information exists on their cytotoxicity and immunotoxicity in non-target organisms such as fish. We examined the effects of atrazine, permethrin and piperonyl butoxide (PBO) exposure, in vitro, on rainbow trout (Oncorhynchus mykiss) lymphocyte viability and proliferation. Purified rainbow trout peripheral blood leukocytes (PBLs) were exposed in vitro to the test chemicals (0, 0.01, 0.1, 1 and 10 µM) for 96 h, with and without the mitogen lipopolysaccharide. All three chemicals caused a decrease in both lymphocyte viability and proliferation at 10 µM, while atrazine also suppressed proliferation of PBLs at 1 µM. The in vitro toxicity of these chemicals to this salmonid underscores the need for further investigation using in vivo studies and host resistance models.

Habitat-based PCB environmental quality criteria for the protection of endangered killer whales (Orcinus orca).

The development of an area-based polychlorinated biphenyl (PCB) food-web bioaccumulation model enabled a critical evaluation of the efficacy of sediment quality criteria and prey tissue residue guidelines in protecting fish-eating resident killer whales of British Columbia and adjacent waters. Model-predicted and observed PCB concentrations in resident killer whales and Chinook salmon were in good agreement, supporting the model's application for risk assessment and criteria development. Model application shows that PCB concentrations in the sediments from the resident killer whale's Critical Habitats and entire foraging range leads to PCB concentrations in most killer whales that exceed PCB toxicity threshold concentrations reported for marine mammals. Results further indicate that current PCB sediment quality and prey tissue residue criteria for fish-eating wildlife are not protective of killer whales and are not appropriate for assessing risks of PCB-contaminated sediments to high trophic level biota. We present a novel methodology for deriving sediment quality criteria and tissue residue guidelines that protect biota of high trophic levels under various PCB management scenarios. PCB concentrations in sediments and in prey that are deemed protective of resident killer whale health are much lower than current criteria values, underscoring the extreme vulnerability of high trophic level marine mammals to persistent and bioaccumulative contaminants.