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Steven J. Bursian

Publications and source records attributed to Steven J. Bursian.

5 recordsLinked to original sources

Overview of avian toxicity studies for the Deepwater Horizon Natural Resource Damage Assessment

The Oil Pollution Act of 1990 establishes liability for injuries to natural resources because of the release or threat of release of oil. Assessment of injury to natural resources resulting from an oil spill and development and implementation of a plan for the restoration, rehabilitation, replacement or acquisition of natural resources to compensate for those injuries is accomplished through the Natural Resource Damage Assessment (NRDA) process. The NRDA process began within a week of the Deepwater Horizon oil spill, which occurred on April 20, 2010. During the spill, more than 8500 dead and impaired birds representing at least 93 avian species were collected. In addition, there were more than 3500 birds observed to be visibly oiled. While information in the literature at the time helped to identify some of the effects of oil on birds, it was not sufficient to fully characterize the nature and extent of the injuries to the thousands of live oiled birds, or to quantify those injuries in terms of effects on bird viability. As a result, the US Fish and Wildlife Service proposed various assessment activities to inform NRDA injury determination and quantification analyses associated with the Deepwater Horizon oil spill, including avian toxicity studies. The goal of these studies was to evaluate the effects of oral exposure to 1–20 ml of artificially weathered Mississippi Canyon 252 oil kg bw -1 day -1 from one to 28 days or one to five applications of oil to 20% of the bird's surface area. It was thought that these exposure levels would not result in immediate or short-term mortality but might result in physiological effects that ultimately could affect avian survival, reproduction and health. These studies included oral dosing studies, an external dosing study, metabolic and flight performance studies and field-based flight studies. Results of these studies indicated changes in hematologic endpoints including formation of Heinz bodies and changes in cell counts. There were also effects on multiple organ systems, cardiac function and oxidative status. External oiling affected flight patterns and time spent during flight tasks indicating that migration may be affected by short-term repeated exposure to oil. Feather damage also resulted in increased heat loss and energetic demands. The papers in this special issue indicate that the combined effects of oil toxicity and feather effects in avian species, even in the case of relatively light oiling, can significantly affect the overall health of birds.

Ecotoxicology and Environmental Safety

Dietary exposure of mink (Mustela vison) to fish from the Housatonic River, Berkshire County, Massachusetts, USA: Effects on organ weights and histology and hepatic concentrations of polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalence

The effects of feeding ranch mink ( Mustela vison ) diets containing polychlorinated biphenyl (PCB)-contaminated fish (88 gold fish [ Carassius auratus ] weighing a total of 70.3 kg and 16 carp [ Cyprinus carpio ] weighing a total of 77.3 kg) collected from the Housatonic River (HR; Berkshire County, MA, USA) in October 1999 on organ weights and histology and hepatic concentrations of total PCBs (ΣPCBs) and 2,3,7,8-tetrachlorodibenzo- p -dioxin toxic equivalence (TEQ) were evaluated. Diets contained 0.22 to 3.54% HR fish, which provided 0.34 to 3.7 μg ΣPCBs/g feed (3.5-69 pg TEQ/g feed). Female mink were fed the diets eight weeks before breeding through weaning of kits at six weeks of age. Offspring were maintained on their respective diets for an additional 180 d. The dietary concentration of PCBs that caused a decrease in kit survival (3.7 μg ΣPCBs/g feed [69 pg TEQ/g]) resulted in a maternal hepatic concentration of 3.1 μg ΣPCBs/g wet weight (218 pg TEQ/g). Organ weights were not consistently affected. Mandibular and maxillary squamous cell proliferation was apparent in 31-week-old juveniles exposed to as low as 0.96 (xg ΣPCBs/g feed (9.2 pg TEQ/g). Juveniles in this treatment group had a liver concentration of 1.7 μg ΣPCBs/g wet weight (40 pg TEQ/g). Because inclusion of PCB-contaminated fish, which comprised approximately 1% of the diet, resulted in mandibular and maxillary squamous cell proliferation, it is possible that consumption of up to 30-fold that quantity of HR fish, as could be expected for wild mink, would result in more severe lesions characterized by loss of teeth, thus impacting survivability.

Environmental Toxicology and Chemistry

Effects of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), or an extract derived from field-collected cormorant eggs injected into double-crested cormorant (Phalacrocorax auritus) eggs

Double-crested cormorant ( Phalacrocorax auritus ) eggs were injected with either 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126), 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), or an extract derived from field-collected double-crested cormorant eggs. These compounds were injected into the yolks of cormorant eggs from an isolated colony on Lake Winnipegosis, Manitoba, Canada. Upon hatching, chicks were necropsied. The brain, bursa, heart, liver, and spleen were removed and weighed. An approximate median lethal dose (LD50) of 158 μg/kg egg was determined for PCB 126, which is 69 times greater than the LD50 determined for the chicken ( Gallus domesticus ) in a previous study. A significantly greater mortality occurred at the highest dose of TCDD (4.0 μg/kg egg) when compared to the vehicle control. However, the mortality data did not provide sufficient information for the determination of an LD50. The cormorant egg extract did not adversely affect hatchability. No significant increases were observed in the incidence of developmental abnormalities, including pronounced edema, in any of the treatment groups, nor were there any relevant effects on body and organ weights. Based on the results from this study, the cormorant appears to be considerably less sensitive to polyhalogenated diaromatic hydrocarbons than the chicken, which has been the typical species used for egg injection studies.

Manitoba

Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification

Mink are known to be very sensitive to the toxic effects of planar polychlorinated biphenyls (pPCBs), polychlorinated dibenzo- p -dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs), collectively known as planar halogenated hydrocarbons (PHHs). Previously, we reported the reproductive effects in mink fed a diet containing 10, 20, or 40% fish taken from Saginaw Bay, Lake Huron. The present study reports the chemical characterization of the diets and the adult mink livers, along with a comparison of an additive model of toxicity with the results of the H4IIE bioassay on these samples. The assessment of dietary or tissue-based exposure of the mink to 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) and related compounds revealed that TCDD equivalents of the PHH mixtures largely followed an additive model of toxicity as compared with the H4IIE bioassay. Consistent dietary and liver tissue-based threshold concentrations for reproductive toxicity in mink were determined regardless of whether PHHs were quantified as TEQs (additive toxicity) or TCDD-EQs (H4IIE bioassay). Significant reproductive effects were observed in the lowest treatment group (10% fish or 19.4 pg of H4IIE bioassay-derived TCDD-EQs/g). Consumption-normalized mink liver biomagnification factors (BMFs) were 6.4−74.2 for PCDDs, <1−75.8 for PCDFs, <1−15.9 for PCBs, and in general, increased with degree of chlorination within each class. Based on TEQs or TCDD-EQ, this study confirms that mink are among the most, if not the most, sensitive mammalian species to the reproductive toxicity of TCDD and related compounds.

Environmental Science & Technology

A comparison of water quality criteria for the Great Lakes based on human and wildlife health

Water quality criteria (WQC) can be derived in several ways. The usual techniques involve hazard and risk assessment procedures. For non-persistent, non-biomagnified compounds and elements, WQC are experimentally derived from their acute and chronic toxicity to aquatic organisms. For those persistent chlorinated hydrocarbons (PCHs) that are bioaccumulated and biomagnified, these traditional techniques have not been effective, partly because effects higher in the food web were not considered. Polychlorinated biphenyls (PCBs) are the bioaccumulative synthetic chemicals of primary toxicological significance to the Great Lakes biota which have caused widespread injury to wildlife. In the Laurentian Great Lakes, the primary emphasis of hazard assessments has been on the potential for adverse effects in humans who eat fish. The primary regulatory endpoint of traditional hazard and risk assessments underlying current WQC are the probabilities of additional cancers occurring in the human population. The analysis presented here indicates that this is not adequate to restore sensitive wildlife species that are highly exposed to PCBs, especially those that have suffered serious population declines. Because WQC are legal instruments, the methods of deriving WQC have large implications for remediation, litigation, and damage assessments. Here WQC are derived for six species based on the responses of wildlife in the field or produced by feeding fish to surrogate species, rather than projecting a potential of increased cancer rates in humans. If the most sensitive wildlife species are restored and protected for very sensitive reproductive endpoints, then all components of the ecosystem, including human health, should be more adequately protected. The management of Great Lakes wildlife requires an understanding of the injury and causal relationships to persistent toxic substances.

Journal of Great Lakes Research