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Persistent organic pollutants (POPs) have been associated with adverse health effects in marine mammals. However, the complex mixtures to which free-ranging populations are exposed constrain the elucidation of cause-and-effect relationships between specific POPs and the observed health risks. In this study, we 1) assembled data from studies showing polychlorinated biphenyl (PCB)-associated effects on the health of free-ranging harbor seals in the northeastern Pacific Ocean, 2) carried out additional POP analyses on seal samples to broaden the available data on contaminant residues, and 3) derived estimates of individual POPs and their toxic risks. Taken together, these components were used to generate a new toxicity reference value (TRV) for the protection of marine mammal health. In this case study of seals in British Columbia, Canada, and Washington State, USA, PCBs were the single most abundant POP and were correlated with several adverse health effects. PCB exposures consistently exceeded regulatory toxicity thresholds for fish-eating wildlife. Nursing seal pups were at particular risk, reflecting their greatly increased dietary intake of PCBs and their sensitivity to developmental toxicity. Based on the collective evidence obtained, we propose TRVs (consisting of 5% tissue residue concentration and dose) of 1.3 mg/kg lipid weight tissue residue in blubber and 0.05 mg/kg lipid weight tolerable daily intake in prey. Insofar as the TRVs are lower than previously established TRVs and regulatory guidelines, our study highlights the current underestimation of risks associated with PCBs in high-trophic-level wildlife.

Diesel is a complex mixture containing polycyclic aromatic hydrocarbons, which persist after a spill, pass readily from water into tissues, and are toxic to early life stages of fish. The bioavailability and chronic toxicity of hydrocarbons dissolved into water from floating diesel (water-accommodated fraction) and chemically dispersed diesel (chemically enhanced water-accommodated fraction) were measured by the extent of ethoxyresorufin-O-deethylase (EROD) induction in juvenile rainbow trout (Oncorhynchus mykiss) and by the severity of blue sac disease in embryos. The water-accommodated fraction of floating diesel was virtually nontoxic to embryos at nominal concentrations up to 1,000 mg/L, causing only small weight changes. Liver EROD induction in juvenile trout was only observed at the highest nominal water-accommodated fraction concentration (10,000 mg/L). Chemical dispersion increased the bioavailability and toxicity of diesel to trout by 100-fold. Diesel chemically enhanced water-accommodated fraction induced EROD activity, caused blue sac disease, and impaired development and growth of embryonic trout at nominal concentrations as low as 10 mg/L; 88% mortality occurred at 100 mg/L. However, when total hydrocarbon concentrations were measured, differences between dispersed and undispersed diesel disappeared, with a median lethal concentration of 8 mg/L of total hydrocarbons and sublethal median effective concentrations ranging from 1.3 to 6.1 mg/L. Dispersion of diesel by high-energy mechanical mixing was recently reported to cause acute lethality to juvenile trout between 40 and 200 mg/L. Therefore, dispersion of oil by any means increases the bioavailability and apparent toxicity of diesel to fish embryos without changing the toxicity of its components. Nevertheless, in an actual spill, dispersion of diesel increases the effects of oil on fish populations.

Polychlorinated biphenyls and other persistent organic pollutants have been associated with immunotoxicity and outbreaks of (infectious) disease in marine mammals by rendering them vulnerable to infection by pathogens such as viruses and bacteria. In an immunotoxicological study of free-ranging harbor seals (Phoca vitulina), we obtained samples of blood and blubber from seal pups that were live-captured from two remote and two near-urban sites in British Columbia, Canada, and Washington state, USA. Using these samples, we quantified hematology, innate immune function, adaptive immune function, and polychlorinated biphenyl accumulation. While controlling for confounding factors (age, sex, and condition), univariate correlations between phagocytosis (r2 = 0.30, p = 0.002), respiratory burst (r2 =0.45, p= 0.000), T-lymphocyte function (r2 = 0.16, p = 0.028), lymphocyte signaling (r2 = 0.17, p = 0.025), and lymphocyte counts (r2 = 0.29, p = 0.002), and polychlorinated biphenyl concentrations suggested chemical-associated immunotoxicity. Principal component analysis of immunological endpoints provided additional evidence of immunotoxic effects in seals. However, principal component analysis also identified a noncontaminant-related factor by distinguishing between seals inhabiting urban versus remote sites, with results being consistent with increased pathogen exposure. Elevated fecal coliform concentrations in water, and observations of terrestrial spill-over pathogens in local seals, further support the notion of biological pollution at these sites. Although our study highlights the role that environmental contaminants might play in rendering marine mammal populations vulnerable to disease through immunotoxicity, it also suggests that biological pollution represents an emerging conservation concern.

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Diesel spills are all too frequent disturbances of freshwater ecosystems, largely as a result of the quantities transported and consumed. Assessing the risk that such events may pose to aquatic life remains a difficult process, because of the complexity of this hydrocarbon mixture and our limited knowledge of its toxicity. A diesel spike experiment with rainbow trout (Oncorhynchus mykiss) fry was carried out to fill this knowledge gap. Survival, growth, and gene expression changes were assessed and toxicity thresholds were determined. Whereas the biological end points were consistent in the determination of (sub)lethal doses, microarrays supplied additional information on the mechanism of toxicity (oxygen deprivation) and potential long-term effects (feminization, immune system alterations) of diesel exposure on salmonids. Hemoglobins, prostaglandins, cytochromes, and gluthathion-S-transferases were among the molecular biomarkers proposed for use in future risk assessments based on microarray results. By bridging traditional toxicity testing with recent microarray technologies, this study shows the potential of genomics tools in ecotoxicity studies as well as industrial applications, including risk assessment, in the near future.

Vitamin A is a nutrient essential to all mammals for growth and development, as well as for the maintenance of reproductive, endocrine, and immune systems. Environmental contaminant-related disruption of vitamin A has been observed in many wildlife species and can therefore be used as a biomarker of toxic effects. However, the natural processes regulating vitamin A uptake, storage, and distribution among compartments are poorly understood in marine mammals. In this study, 20 young healthy harbour seals (Phoca vitulina) were captured to establish a compartmentbased model providing a foundation for a mechanistic understanding of vitamin A physiology and disruption. Vitamin A (retinol, retinyl palmitate, and (or) retinoic acid) was quantified in blood plasma and in biopsy samples of liver, blubber, and skin. Although the highest concentrations of vitamin A were found in liver, blubber represents a more important storage depot, with an estimated 66% of the total retinoid content of the compartments measured. We suggest that vitamin A physiology in the precocious harbour seal has evolved to deal with high vitamin A availability during a short nursing period and to sustain growth during the postweaning fast. Positive correlations in vitamin A concentrations among liver, blubber, and skin support the use of less invasive biopsy sampling of just blubber or skin, which can provide physiologically relevant information in biomarker studies of free-ranging marine mammals.Résumé : La vitamine A est un élément nutritif essentiel à la croissance et au développement de tous les mammifères, mais aussi au maintien de leurs systèmes endocrinien et immunitaire. Une perturbation dans l'homéostasie de la vitamine A reliée à la présence de contaminants dans le milieu a été observée chez plusieurs espèces en nature et peut donc servir de biomarqueur des effets toxiques. Cependant, les processus naturels qui régissent l'absorption de la vitamine A, sa mise en réserve et sa répartition dans les différents compartiments sont mal connus chez les mammifè-res marins. Nous avons capturé 20 jeunes phoques communs (Phoca vitulina) en santé dans le but de créer un modèle à compartiments qui serve de base à notre compréhension mécaniste de la physiologie et de la perturbation de l'homéostasie de la vitamine A. La vitamine A (rétinol, palmitate de rétinyle et (ou) acide rétinoïque) a été dosée dans le plasma sanguin et dans des échantillons du foie, du lard et de la peau prélevés chez des phoques. Les concentrations les plus élevées de vitamine A ont été trouvées dans le foie, mais le lard représente un site de réserve encore plus important avec une proportion estimée de 66 % des rétinoïdes contenus dans l'ensemble des compartiments. Nous croyons que la physiologie de la vitamine A a évolué chez le phoque précoce de façon à ce que celui-ci puisse tirer profit de la disponibilité importante de cette vitamine durant l'allaitement et de façon à favoriiser sa croissance après le jeûne qui suit le sevrage. Des corrélations positives entre les concentrat...

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