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Tiffany L. Linbo

Publications and source records attributed to Tiffany L. Linbo.

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Biological responses of Pacific herring embryos to crude oil are quantifiable at exposure levels below conventional limits of quantitation for PAHs in water and tissues

Pacific herring ( Clupea pallasii ), a cornerstone of marine food webs, generally spawn on marine macroalgae in shallow nearshore areas that are disproportionately at risk from oil spills. Herring embryos are also highly susceptible to toxicity from chemicals leaching from oil stranded in intertidal and subtidal zones. The water-soluble components of crude oil trigger an adverse outcome pathway that involves disruption of the physiological functions of cardiomyocytes in the embryonic herring heart. In previous studies, impaired ionoregulation (calcium and potassium cycling) in response to specific polycyclic aromatic hydrocarbons (PAHs) corresponds to lethal embryolarval heart failure or subtle chamber malformations at the high and low ends of the PAH exposure range, respectively. Sublethal cardiotoxicity, which involves an abnormal outgrowth (ballooning) of the cardiac ventricular chamber soon after hatching, subsequently compromises juvenile heart structure and function, leading to pathological hypertrophy of the ventricle and reduced individual fitness, measured as cardiorespiratory performance. Previous studies have not established a threshold for these sublethal and delayed-in-time effects, even with total (∑)PAH exposures as low as 29 ng/g of wet weight (tissue dose). Here, we extend these earlier findings showing that (1) cyp1a gene expression provides an oil exposure metric that is more sensitive than typical quantitation of PAHs via GC–MS and (2) heart morphometrics in herring embryos provide a similarly sensitive measure of toxic response. Early life stage injury to herring (impaired heart development) thus occurs below the quantitation limits for PAHs in both water and embryonic tissues as a conventional basis for assessing oil-induced losses to coastal marine ecosystems.

Environmental Science and Technology

Sensitivity of lake sturgeon ( Acipenser fulvescens ) early life stages to 2,3,7,8-tetrachlorodibenzo- P -dioxin and 3,3′,4,4′,5-pentachlorobiphenyl

The aquatic food web of the Great Lakes has been contaminated with polychlorinated biphenyls (PCBs) since the mid-20th century. Threats of PCB exposures to long-lived species of fish, such as lake sturgeon ( Acipenser fulvescens ), have been uncertain because of a lack of information on the relative sensitivity of the species. The objective of the present study was to evaluate the sensitivity of early–life stage lake sturgeon to 3,3′,4,4′,5-pentachlorobiphenyl (PCB-126) or 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) exposure. Mortality, growth, morphological and tissue pathologies, swimming performance, and activity levels were used as assessment endpoints. Pericardial and yolk sac edema, tubular heart, yolk sac hemorrhaging, and small size were the most commonly observed pathologies in both TCDD and PCB-126 exposures, beginning as early as 4 d postfertilization, with many of these pathologies occurring in a dose-dependent manner. Median lethal doses for PCB-126 and TCDD in lake sturgeon were 5.4 ng/g egg (95% confidence interval, 3.9–7.4 ng/g egg) and 0.61 ng/g egg (0.47–0.82 ng/g egg), respectively. The resulting relative potency factor for PCB-126 (0.11) was greater than the World Health Organization estimate for fish (toxic equivalency factor = 0.005), suggesting that current risk assessments may underestimate PCB toxicity toward lake sturgeon. Swimming activity and endurance were reduced in lake sturgeon survivors from the median lethal doses at 60 d postfertilization. Threshold and median toxicity values indicate that lake sturgeon, like other Acipenser species, are more sensitive to PCB and TCDD than the other genus of sturgeon, Scaphirhynchus , found in North America. Indeed, lake sturgeon populations in the Great Lakes and elsewhere are susceptible to PCB/TCDD-induced developmental toxicity in embryos and reductions in swimming performance.

Environmental Toxicology and Chemistry