Restoration of oiled mussel beds in Prince William Sound, Alaska.

Natural loss of hydrocarbons was often low from mussel (Mytilus trossulus) beds (which were typically not cleaned after the Exxon Valdez oil spill), thus this habitat remained a long-term source of oil. Consequently, experimental restoration of nine contaminated beds was attempted in 1994; mussels were removed, contaminated surface sediment was replaced (33 metric tons), and original mussels were returned. Hydrocarbon concentrations and mussel populations were monitored for 5 years thereafter. Post-restoration mussel population fluctuations were indistinguishable from regional changes. Increased short-term oil loss was apparent, but long-term (5 year) improvement was equivocal and difficult to distinguish from natural losses. By 1999, oil concentrations in mussels were typically at baseline levels in restored and oiled reference beds; concentrations in replaced sediment were elevated in one third of restored beds, indicating recontamination from underlying or surrounding sediment. Our results suggest mussel relocation is feasible but suggest oil might more effectively be removed from sediment mechanically or chemically than manually.

Persistence of oiling in mussel beds after the Exxon Valdez oil spill.

Persistence and weathering of Exxon Valdez oil in intertidal mussel (Mytilus trossulus) beds in Prince William Sound (PWS) and along the Gulf of Alaska was monitored from 1992 to 1995. Beds with significant contamination included most previously oiled areas in PWS, particularly within the Knight Island group and the Kenai Peninsula. In sediments, yearly mean concentrations of total petroleum hydrocarbons ranged from < 60 micrograms/g in reference beds to 62,258 micrograms/g wet wt., or approximately 0 to 523 micrograms/g dry wt. total polynuclear aromatic hydrocarbons (TPAHs). In mussels, mean TPAH concentrations ranged up to 8.1 micrograms/g dry wt. Hydrocarbon concentrations declined significantly with time in some, but not all mussels and sediments, and should reach background levels within three decades of the spill in most beds. In 1995, mean hydrocarbon concentration was greater than twice background concentration in sediments from 27 of 34 sites, and in mussels from 18 of 31 sites.

Survival in air of Mytilus trossulus following long-term exposure to spilled Exxon Valdez crude oil in Prince William Sound.

Mussels, Mytilus trossulus, were sampled in 1996 from beaches in Prince William Sound (PWS) which contained residual oil resulting from the Exxon Valdez oil spill of March 1989, and from one beach which had been lightly oiled in 1989, but contained no residual oil in 1996. The latter mussels served as un-oiled references. Mussels were also collected from Tee Harbor, Southeast Alaska, to be used as an additional reference group. Where the size of the individuals in the resident population would permit, two size groups were sampled, 32-35 and 18-20 mm in length. Polynuclear aromatic hydrocarbon (PAH) concentrations in mussel tissue, and air survival time were determined for each group of mussels. Total PAH concentrations were significantly greater in tissue of mussels from oiled beds (0.6-2.0 micrograms g-1) than from references (0.01-0.12 microgram g-1) (P < 0.01). Oil-exposed mussels had significantly lower LT50 values (P < 0.05) for air survival than reference groups. Tolerance of small mussels to air exposure was significantly greater (P < 0.01) than large mussels in both the unoiled reference and oil exposed groups.

Lack of physiological responses to hydrocarbon accumulation by Mytilus trossulus after 3-4 years chronic exposure to spilled Exxon Valdez crude oil in Prince William Sound.

Mussels, Mytilus trossulus, were sampled in 1992 and 1993 from beaches in Prince William Sound that had been oiled by the Exxon Valdez spill of March, 1989. At some of the oiled beaches, mussels were collected from beds overlying oiled sediments, and from bedrock adjacent to these beds. Mussels were also collected from beaches within the Sound that had not been impacted by the spill. Polynuclear aromatic hydrocarbon (PAH) concentrations in mussel tissue, physiological responses (byssal thread production, condition index, clearance rate, and glycogen content), were determined for each group of mussels. Total PAH concentrations in mussel tissue ranged from 0 to 6 micrograms g-1, and were significantly greater in mussels from oiled beds than those from reference beds. No significant differences were noted in byssal thread production, condition index, clearance rate, or glycogen content between oiled sample sites and reference sites. The lack of physiological response was surprising because mussels in this study were chronically exposed to PAH for 3-4 years, and none of the physiological responses measured appeared to be affected by that exposure. The lack of a physiological response suggests that chronically exposed mussels may develop a physiological tolerance to PAH, but we recognize that these measures may not have been sensitive enough to discriminate response from background noise.

Effect of water-soluble fraction of Cook Inlet crude oil on swimming performance and plasma cortisol in juvenile coho salmon (Oncorhynchus kisutch).

Swimming performance of juvenile coho salmon decreased and plasma cortisol increased, following 48-hr exposure to the water-soluble fraction (WSF) of Cook Inlet crude oil at 75% of the LC50. Exposure to 25 and 50% of the LC50 did not significantly reduce swimming performance. Plasma cortisol concentrations were highest in fish exposed to both the combined stress of WSF exposure and of forced swimming in a stamina tunnel.

Hepatic aryl hydrocarbon hydroxylase activities in coho salmon (Oncorhynchus kisutch) exposed to petroleum hydrocarbons.

Coho salmon exposed to the water soluble fraction (WSF) of Cook Inlet crude oil for a maximum of 30 days showed a greater than three-fold increase in hepatic aryl hydrocarbon hydroxylase activity. The initial increase in enzyme activity appeared between 2 and 5 days of exposure and increased as a function of increased exposure time. Persistence of the induced enzyme activity was dependent on the length and the concentration of WSF exposure. Handling stress had no effect on the AHH activity, but starvation caused a decrease in the activity.