Risk of weathered residual Exxon Valdez oil to pink salmon embryos in Prince William Sound



It has been hypothesized that pink salmon eggs incubating in intertidal streams transecting Prince William Sound (PWS) beaches oiled by the Exxon Valdez oil spill were exposed to lethal doses of dissolved hydrocarbons. Since polycyclic aromatic hydrocarbon (PAH) levels in the incubation gravel were too low to cause mortality, the allegation is that dissolved high-molecular-weight hydrocarbons (HPAH) leaching from oil deposits on the beach adjacent to the streams were the source of toxicity. To evaluate this hypothesis, we placed pink salmon eggs in PWS beach sediments containing residual oil from the Exxon Valdez oil spill and in control areas without oil. We quantified the hydrocarbon concentrations in the eggs after three weeks of incubation. Tissue PAH concentrations of eggs in oiled sediments were generally <100 ppb and similar to background levels on nonoiled beaches. Even eggs in direct contact with oil in the sediment resulted in tissue PAH loads well below the lethal threshold concentrations established in laboratory bioassays, and very low concentrations of HPAH compounds were present. These results indicate that petroleum hydrocarbons dissolved from oil deposits on intertidal beaches are not at concentrations that pose toxic risk to incubating pink salmon eggs. The evidence does not support the hypothesis that interstitial pore water in previously oiled beaches is highly toxic.


A recurring issue over the 17 years since the Exxon Valdez oil spill in Prince William Sound (PWS) is the potential toxicity of residual oil buried on the PWS beaches [1]. Although oil-induced mortality was alleged to have occurred in pink salmon (Oncorhynchus gorbuscha) eggs by Bue et al. [2,3] in oil-impacted streams from 1989 through 1993 and again in 1997, there was insufficient oil in stream sediments, measured as total polycyclic aromatic hydrocarbons (mean TPAH of 0.5–267 ppb, 1989), to cause any risk of mortality to pink salmon [4]. Mortality was later shown to have been caused by mechanical shock from sampling unrelated to oil [5,6], and it has since been recognized by Alaska Department of Fish and Game (Juneau, AK, USA) that sampling problems may have prevented assessment of the oil effects on pink salmon eggs ([7]; http://www.arlis.org/).

National Oceanic and Atmospheric Administration researchers at Auke Bay Laboratory (Juneau, AK, USA) had a different view and attributed egg mortality to interstitial toxic water infiltrating from oil deposits on the adjacent beaches [8,9]. The suggestion is that oil leaches from buried deposits into adjacent stream sediments containing incubating pink salmon eggs and that extremely low aqueous TPAH concentrations of very weathered oil, based on a laboratory study [10], are lethal to those embryos. The leaching of oil deposits is presented as long-term population-level risks to pink salmon by high-molecular-weight PAH (HPAH) compounds under a new concept of oil toxicity [1,11] and is referred to as the interstitial toxic water hypothesis [8,10].

The interstitial toxic water hypothesis is based on two premises. The first is that over time petroleum hydrocarbons, particularly HPAH, in buried deposits of weathered Exxon Valdez oil on the shore dissolve into pore water at increasingly more toxic levels. The second is that dissolved HPAH concentrations from the weathered oil are carried via pore water into adjacent intertidal salmon streams at concentrations high enough to cause mortality of developing salmon embryos. In the present study we tested these assumptions in PWS by exposing eggs to residual Exxon Valdez oil in beach environments away from flushing stream flows and by placing eggs in direct contact with deposits of weathered oil on beaches.


Field studies were conducted in the fall of 2003. Beach sites were selected that were heavily oiled in 1989 by the Exxon Valdez oil spill and were considered the most representative of conditions that could leach dissolved PAH into adjacent salmon stream sediments. Reference sites were selected from nonoiled beaches.

Study sites

The five study locations on shores that were heavily oiled in 1989 included Snug Harbor on the southeast side of Knight Island, at a site 20 m west of the stream; Sleepy Bay on the northeast end of Latouche Island, at a site 100 m north of the stream; North Evans Bay on the northeast end of Evans Island, at a site 140 m north of the stream; Bay of Isles at the junction of the west and north arms of the inlet on the northeast side of Knight Island, on the mudflat protected by a small peninsula; and east Herring Bay on the north side of Knight Island, at a site 50 m west of the drain from a small lake entering the bay (Fig. 1).

Figure Fig. 1..

Map of the Prince William Sound (PWS) oiled and control beach study sites.

North Evans Bay and Sleepy Bay were in direct line of the oil drift from the spill site at Bligh Reef and received oiling as severe as any area in PWS [12]. The site selected at Sleepy Bay was an oil deposit appearing either as black viscous mass or as a dense surface sheen on the water in pits dug in the intertidal zone. The Bay of Isles site was also in direct line with Bligh Reef, and the protection of the small peninsula caused oil to accumulate in the large peat bog/marsh or mudflat behind the peninsula. Although there is no pink salmon stream at the Bay of Isles site, it is well known as an example of a persisting oil deposit. The test site was in the middle of the mudflat where oil sheen was present on the undisturbed sediment surface at low tide. No evidence of oil in intertidal sediments at the Snug Harbor site was visible. At North Evans, oil appeared as a light sheen in some locations when the substrate was disturbed, and at east Herring Bay, a site where pink salmon spawned naturally on the beach area during August-September, buried oil was detected when excavating below the natural redd sites.

The five nonoiled reference beach site locations included Ewan Bay, an inlet on the mainland northwest of Chenega Island, 150 m west of the stream mouth; Drier Bay on the west side of Knight Island, on the east side of and immediately adjacent to the stream mouth; Bainbridge Creek, on a deep inlet at the northwest side of Bainbridge Island, on the north side of the steam delta; Horseshoe Bay, on the west side of Latouche Island, on the broad stream delta 30 m east of the stream; and Culross Passage, on a rocky beach at the southeast entrance of the passage (Fig. 1).

Pink salmon egg treatment

To assess the impact of the oil deposits, pink salmon eggs were placed on oiled beaches and later retrieved for PAH analysis, or eggs naturally spawned were excavated from their redds for analysis. On August 15–17, eggs were spawned from fish in streams near the study sites, fertilized, water hardened, and held in glass jars to provide an experimental pool for each site (except east Herring Bay). Four artificial redds were prepared at each site, and each redd was supplied with 200 to 400 eggs placed in Nytex® (Wildlife Supply Company, Buffalo, NY, USA) 1-mm-mesh bags measuring 15 by 20 cm. The bags were filled using plastic spoons that were discarded after preparing each site. The bags containing the eggs were placed in their respective redds measuring approximately 30 cm wide and 30 cm deep, with the top of the bag approximately 15 cm below the surface at each site. Redds were separated by 3 to 4 m along a line running approximately perpendicular to the shoreline, beginning at the high-tide level. The egg bags were covered with the excavated gravel, and rocks were placed on top to protect the eggs from wave action. The sites were mapped and marked with small floats for later recovery.

Egg samples were recovered from the beaches on September 7 after an incubation period of approximately three weeks. The bags were excavated and eggs removed directly into precleaned 100-ml glass jars using plastic implements and gloves. At east Herring Bay, the naturally spawned eggs were excavated from the stretch of the spawning beach over the oil deposits. Redds were located and eggs were sampled by making random excavations 20 to 30 cm deep and collecting them with a small nylon dip net. The eggs were placed in the glass jars and frozen until laboratory analysis.

Sediment samples were also collected from the gravel removed from the oiled and nonoiled study sites where the eggs were buried to determine sediment PAH concentrations at those sites. Sediment samples were collected with plastic spoons and placed in clean, labeled glass jars and frozen. At Bay of Isles and Sleepy Bay, sediment samples were taken from the excavation at the time of egg recovery. At all other sites, sediment samples were taken when eggs were buried. The oiled sediments from natural redd sites at east Herring Bay were sampled by excavating into the oil layer approximately 15 cm deeper beneath the redd sites from which eggs had been sampled.

Chemical analysis methods

All egg and sediment samples were shipped frozen to Battelle Laboratory (Duxbury, MA, USA) for analysis of PAH. All egg samples were analyzed for PAH concentrations. Tissue PAH concentrations represented a separate homogenized sub-sample of eggs from each sample bag analyzed. Sediment samples from three oiled beaches showing evidence of persisting deposits were analyzed for PAH concentrations. Only two sediment samples were analyzed from nonoiled beaches for comparison since most tissue TPAH levels in the embryos were at low background concentrations (geometric mean <50 ppb).

The chemical analyses methodology used in the present study was the same as that used for PAH analyses in the laboratory studies on oil toxicity to pink salmon embryos [10,11]. Extraction of sediment samples used a modification of the ambient temperature solvent agitation method described by Brown et al. [13] and modified by Peven and Uhler ([14]; http://www.lib.noaa.gov/). Sediment extracts were reduced in volume to 1 ml, spiked with PAH, and analyzed by gas chromatography/mass spectrometry (GC/MS) for PAH. Following the procedures described by Peven and Uhler [14], salmon eggs were extracted by maceration in solvent at ambient temperature. Salmon egg extracts were processed through an alumina cleanup column to isolate a combined saturated and aromatic hydrocarbon fraction [15]. Further fractionation of the resulting extracts was by high-performance liquid chromatography gel permeation chromatography [14]. The eluate PAH fraction was collected, concentrated under a stream of nitrogen, and spiked with PAH internal standards prior to PAH analysis by GC/MS. Sediment extract aliquots were analyzed for total petroleum hydrocarbons and saturated hydrocarbon target analytes by capillary column GC/flame ionization detector (U.S. Environmental Protection Agency [U.S. EPA] Method 8015 Modified) ([16]; www.epa.gov/epaoswer/hazwaste/test/sw846.htm) after procedures by Douglas et al. [17] and Boehm et al. [15]. Sample extracts were analyzed for PAH and alkyl PAH target analytes by capillary column GC/MS (U.S. EPA Method 8270 Modified) ([16]; www.epa.gov/epaoswer/hazwaste/test/sw846.htm) operated in the selective ion monitoring mode using the techniques described in Boehm et al. [15] and Page et al. [12], which were also used in specific data quality objectives and procedures. Target PAH analytes in both sediment and tissue samples included the low-molecular-weight PAH (LPAH), naphthalene, acenaphthylene, acenaphthene, biphenyl, fluorene, anthracene, phenanthrene, dibenzothiophene, the HPAH, fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[e]pyrene, benzo[a]pyrene, perylene, indeno[1,2,3-cd]pyrene, dibenz[a,h]anthracene, benzo[ghi]perylene, and the C1- through C3- or C4-alkyl homologues of naphthalene, fluorene, phenanthrene/anthracene, dibenzothiophene, and fluoranthene/pyrene.

Most analytical results are reported as total PAH which is the sum of all PAH analytes. However, naphthalene was present in some laboratory blank quality control samples for salmon eggs. It also represented more than half the TPAH in egg samples containing the lowest TPAH concentrations. Because much of the naphthalene in egg samples probably was a laboratory artifact and not representative of the concentration in eggs in the field, TPAH is expressed in this paper as total PAH minus parent naphthalene. The same adjustment was made for sediment samples, so concentration comparisons could be made within this beach study.

Statistical analysis

The objective of statistical analyses on sediment and tissue TPAH concentrations was to test for positive correlations between the two. Pearson correlation analyses [18] were run on combined oiled and nonoiled categories. Data were log-transformed prior to analyses in order to normalize residuals. Tests were at α = 0.05 and one tailed (for a positive correlation).


All the eggs were recovered from the beach sites except for Drier Bay, where one of the four artificial redds could not be located. The eggs recovered were generally in good condition, with some live eggs present showing eyes through the egg capsule, suggesting that groundwater may have infiltrated the beaches in sufficient quantities to help maintain the embryos up to the time of recovery. Dead eggs with coagulated yolks were also present in all the bags and in some cases eggs were crushed or had ruptured capsules. Sand had infiltrated some bags, indicating encroachment of surrounding sediments. In addition, the rocks marking the excavation sites at Sleepy Bay were displaced, suggesting strong current/wave action.

Table Table 1.. Sediment-total polycyclic aromatic hydrocarbons (TPAH) concentrations from five Prince William Sound (PWS) beaches and tissue TPAH concentrations of eggs buried in 10 PWS beaches from mid-August to September in the fall of 2003. At Sleepy Bay, Bay of Isles, and Herring Bay, incubation sites were selected within oil deposits as black mousse or dense sheen. At other oiled beaches, eggs were placed in sites without mousse but where oil had concentrated in 1989. Control beaches were sites where no oil washed ashore. Tissue TPAH of fertilized eggs before incubation was 6 ppb
 Sediment TPAH (ppb)
Sample no.Sleepy Baya OiledBay of Islesa OiledHerring Baya OiledBainbridge Bay ControlCulross Passage Control
  1. a Black mousse or heavy sheen.

 Tissue TPAH (ppb)
Sample no.Sleepy Baya OiledBay of Islesa OiledHerring Baya OiledBainbridge Bay ControlCulross Passage Control
31824 76
4625287 139
Sample no.Evans Island OiledSnug Harbor OiledHorseshoe Bay ControlEwan Bay ControlDrier Bay Control

Sediment TPAH

Concentrations of TPAH in sediments from the 11 artificial redds ranged over three orders of magnitude, from 24 to 23,149 ng/g dry weight (ppb) (Table 1). The reference beach sites at Bainbridge and Culcross were analyzed to establish background levels, which confirmed that the range (<40 ppb) was characteristic of nonoiled beaches in 1989 [11], the year of the spill. The background concentrations of TPAH in sediments on other beaches were not analyzed because the tissue concentrations were essentially no different than nonoiled reference sites, and thus sediment concentrations were assumed to be similar. Since the objective was to locate and analyze the effect of oil deposits on TPAH absorption by pink salmon eggs, the emphasis was on those few sites where known oil deposits existed.

The sediment samples taken at Sleepy Bay showed TPAH concentrations ranging between 171 and 23,149 ppb (Table 1). This included the highest sediment concentration observed, and oil was visible in the artificial redds in the form of black mousse at the time of recovery. The moderately weathered oil recovered from Sleepy Bay sediments was enriched in HPAH and depleted in LPAH compared to lightly weathered oil removed from the beaches shortly after the spill in 1989 (Fig. 2a). (See the Appendix for identification of chemical abbreviations.) Of the TPAH composition, naphthalenes, phenanthrenes/anthracenes, dibenzothiophenes, and chrysenes, for example, were 12.5, 27.9, 25.0, and 10.4%, respectively, in the 2003 Sleepy Bay sample, whereas those components in the lightly weathered oil removed from the beach in 1989 were 43.7, 17.5, 17.0, and 2.9%, respectively.

Figure Fig. 2..

Polycyclic aromatic hydrocarbon (PAH) composition of the (a) Sleepy Bay, northeast Latouche Island, naturally weathered crude oil deposit in sediments from 2003, excluding naphthalene (N0) 2.7 ng/g, and (b) tissue PAH composition of eggs removed from contact with the Sleepy Bay oil deposit excluding naphthalene (N0) 16.3 ng/g. See Appendix 1 for total polycyclic aromatic hydrocarbons symbols.

At Bay of Isles the sediment TPAH concentrations ranged from 170 to 6,608 ppb over the four samples. Persistent heavy deposits of oil have been documented several times in the peat bog/marsh sediments at the site, and, as mentioned in Materials and Methods, we observed extensive oil sheen at this location.

The sediment taken from beneath the naturally spawned eggs at east Herring Bay also showed a relatively high sediment TPAH concentration (17,673 ppb; Table 1). When the east Herring Bay sites were excavated beneath the eggs, oil sheen rose to the surface, and a brown flocculate material was mixed with the gravel, indicative of well-weathered oil residue.

As demonstrated in Table 1, the sites selected to assess effects of high oil concentrations varied in sediment TPAH concentrations in part by our selection process to locate the most extreme concentrations. Understandably, the TPAH levels on the oiled beaches were lower than mean midintertidal concentrations on oiled beaches in 1989 [14], and, also to be expected, the composition of the petroleum hydrocarbons after 14 years of weathering showed a higher percentage of HPAH relative to LPAH concentrations than in the 1989 samples.

Embryo tissue TPAH

Most egg samples from the oiled and nonoiled study sites contained TPAH concentrations below 30 ppb (Table 1) with a median of 11 ppb. The correlation between sediment and egg TPAH concentrations was low and not statistically significant (R2 = 0.045, p = 0.266). Concentrations of TPAH in eggs ranged from 6 to 625 ppb at the oil deposit sites and from 6 to 38 ppb at the nonoiled sites (Table 1). Three samples from sites with high sediment TPAH concentrations, including two samples from Bay of Isles (287 and 515 ppb) and one from Sleepy Bay (625 ppb), had TPAH concentrations over an order of magnitude greater than the median tissue TPAH of 11 ppb but well below levels shown to be toxic under laboratory conditions (∼6,000 ppb [10]; >7,100 ppb [11]). The highest Sleepy Bay egg sample (625 ppb) was associated with the highest sediment TPAH concentration (23,149 ppb). All other egg samples from Bay of Isles and Sleepy Bay had TPAH concentrations within the range observed for nonoiled sites, even though sediment samples from these two locations showed relatively high TPAH concentrations (Table 1), with the presence of oil evident as mousse, sheen, or a brown residual flocculent in the excavations.

Most noteworthy was the TPAH composition of the embryo tissue samples that had been placed in artificial redds contaminated with the black mass of the oil deposit at Sleepy Bay. The TPAH composition of eggs with the highest concentrations was dominated by alkyl naphthalenes (Fig. 2b; see also the Appendix), representing 45% of the total PAH. The phenanthrenes/anthracenes and dibenzothiophenes were 15 and 19% of the composition, respectively, and chrysenes represented 3.2% in the tissue-TPAH of 625 ppb. This was comparable to laboratory observations of embryos exposed for three weeks to naturally weathered oil previously removed from PWS beaches in 1989. The tissue-TPAH composition at the maximum concentration in which no mortality occurred, Brannon et al. [11] showed naphthalene compounds representing 47.6% of the total, with the phenanthrenes/anthracenes and dibenzothiophenes at 14.1 and 16.3%, respectively, and chrysenes at 0.5% in the tissue TPAH of 7,800 ppb. With the exception of the slightly higher chrysene percentage in the eggs at Sleepy Bay (but lower in total chrysene composition at 20 ppb compared to laboratory-exposed eggs at 33 ppb), the TPAH percentage composition of the tissue was remarkably similar to the laboratory samples exposed to the relatively fresh naturally weathered oil stored since 1989.

All egg samples buried on oiled beaches at North Evans and Snug Harbor but not in contact with visible oil deposits showed only low tissue TPAH concentrations (<18 ppb). Eggs in natural redds overlying oil deposits on the eastern Herring Bay beach also contained only background concentrations of TPAH (∼13 ppb). Excluding the samples that were in direct contact with oil at Sleepy Bay and Bay of Isles, the geometric mean TPAH concentration for oiled sites (10.3 ppb) did not exceed that for the nonoiled reference sites (11.2 ppb). Tissue concentrations in oiled and nonoiled sites in 2003 were comparable to concentrations found in eggs and alevins from nonoiled locations in 1989 to 1991, where mean tissue TPAH levels were <40 ppb [4].


The objective of the present study was to assess the assumptions requisite for the interstitial toxic water hypothesis, that water leaching from oil deposits on the beaches adjacent to pink salmon streams was lethal to incubating embryos. We assessed the requisite assumptions by placing eggs in artificial redds in beaches known to harbor oil deposits and also by placing eggs in direct contact with those deposits. If eggs incubating in streams could be threatened by leachate from the adjacent oiled beach, as suggested in the interstitial toxic water hypothesis, then eggs placed on those beaches and away from the flushing freshwater stream flow should absorb TPAH concentrations that clearly represent toxic levels to incubating embryos. Moreover, if the oil deposits become effectively more toxic to embryos as HPAH increase in concentration over time from weathering, then the concentrations of HPAH in the developing eggs should be greater than they were when the oil deposits were less weathered. Thus, placing the eggs directly in oil deposits exposed on the oiled beaches is a worst-case test of the effects of weathered crude oil on pink salmon embryos.

Bioavailability and tissue TPAH concentrations

Concentrations of TPAH in eggs at most oiled sites were <40 ppb, well below those known to be lethal (6,000 ppb [10]; >7,100 ppb [11]). Excluding oil deposits at Sleepy Bay and Bay of Isles, there was no relationship between tissue and sediment TPAH concentrations. Mean tissue TPAH concentrations were not significantly higher at oiled over nonoiled beaches, there was no significant correlation between tissue and sediment TPAH, and there was no evidence of increased tissue loads in oiled over nonoiled beaches. Unless the eggs were in direct contact with the oil deposit, the effect of dissolution of the deposit on embryos even in close proximity to the source (15 cm-1.5 m) was not apparent in embryo tissue TPAH concentrations. Consequently, there was no evidence of high TPAH concentrations in interstitial waters surrounding the oil deposit and thus no evidence supporting the concept that oil deposits were a threat to eggs associated with oiled beaches. These data suggest that HPAH compounds are relatively insoluble and that the large volume of marine water flushing the beach sediments during daily tidal cycles dilute any aqueous TPAH emanating from such deposits.

Tissue TPAH did increase when directly in contact with oil deposits but did not elevate to lethal concentrations. At Sleepy Bay, tissue TPAH levels did not exceed 625 ppb even though the eggs were in contact with sediment TPAH concentrations of 23,149 ppb. Similar results were observed for eggs placed on other beaches with high sediment TPAH concentrations. At Bay of Isles, tissue TPAH levels did not exceed 515 ppb, despite eggs having been placed in the mudflats within an oil/sediment sheen, where sediment TPAH concentrations reached 6,608 ppb. East Herring Bay was also revealing because the pink salmon spawned naturally over buried oil deposits. Despite 17,673 ppb TPAH in the buried oil beneath the redds, only low TPAH levels of 11.7 and 13.8 ppb were present in eggs resting in redds less than 15 cm above the deposit and under the influence of vertical cyclic tidal infiltration.

Composition analysis and the interstitial toxic water hypothesis

Contrary to previous understanding of oil toxicity, Auke Bay Laboratory investigators have suggested that it is not the LPAH components of oil that pose the greatest long-term risk to pink salmon and the aqueous environment but rather the exposure to the HPAH compounds [9]. Rice et al. [9] refer to this as the oil toxicity paradigm shift from short-term LC50 (lethal concentrations to 50%) determinations and from acute effects to long-term effects and from parts-per-million to parts-per-billion toxicity. Their hypothesis is based on interpretation of laboratory results of Heintz et al. [10], where toxicity was thought to have occurred at very low concentrations of HPAH, and the theory was promoted that toxic levels of HPAH leaching into the interstitial water account for embryo mortality years after the spill [9,10,19] as an explanation of the egg mortality reported by Bue et al. [2].

The interstitial toxic water hypothesis relies on the two premises: First, HPAH homologues become more bioavailable (and thus more toxic) over time as the crude oil weathers, and, second, the dissolved HPAH are carried with pore water into adjacent intertidal salmon streams at concentrations high enough to harm the developing salmon embryos. Both of these two premises must occur or the hypothesis is invalid.

Our results are not consistent with the first premise regarding bioavailability of toxic dissolved TPAH concentrations. In the laboratory studies by Brannon et al. [11], the sediment TPAH approaching the lethal threshold of laboratory-weathered oil was 8,300 ppb, in which naphthalenes were 2,890 ppb, making up 35% of the total. In contrast, HPAH (all PAH compounds from fluoranthenes to benzoperylenes) were 747 ppb, or 9% of the total, representing a ratio of 4:1 between naphthalenes and HPAH. In the corresponding laboratory embryo tissue TPAH of 7,100 ppb, naphthalenes were 2,631 ppb, 37% of the TPAH, and HPAH at 251 ppb, 3.5% of the total, or a ratio of 10:1, respectively.

However, in the Sleepy Bay oil deposit, the sediment TPAH was 23,149 ppb, and because of LPAH losses due to greater solubility during weathering, the naphthalenes had diminished to 2,882 ppb, 12% of the TPAH, much lower than concentrations of HPAH at 5,183 ppb, 22% of the total, and a ratio of approximately 1:2, respectively. The HPAH compounds were accumulating in the oil deposit because of their much lower solubility.

The most compelling evidence of low HPAH solubility was apparent in the embryo tissue. Naphthalenes (280 ppb) made up 45% of the tissue TPAH (625 ppb), while HPAH (46 ppb) were only 7% of the total. This was the circumstance even though the HPAH concentration in the sediment was nearly twice that of naphthalenes.

Bioavailability of petroleum hydrocarbons of well-weathered oil is low because the remaining oil mass is dominated by HPAH homologues that are relatively insoluble. Consequently, the HPAH were less in eggs (46 ppb) in contact with the well-weathered oil deposit (TPAH 23,149 ppb) than HPAH in eggs (251 ppb) exposed to lower laboratory concentrations (TPAH 8,300 ppb) of less weathered oil [11]. Because of their relative insolubility, HPAH compounds are mostly what remain in the asphalt debris on the beaches, and that material will persist for a long time integrated within the other beach substrates.

These were noteworthy results because in the presence of much higher concentrations of naturally weathered oil the total tissue TPAH was much reduced compared with laboratory exposures of much lower oil concentrations [11], and the tissue HPAH concentrations were nominal because of the limited availability of HPAH. The pertinent point of this discussion is that the sediment TPAH, composed largely of HPAH, did not transfer to the embryo tissue as the new oil toxicity paradigm predicts [9]. Therefore, the first premise on the increased bioavailability of HPAH is unsupported by evidence from the present study. The evidence shows that weathered oil deposits in beaches are not a source of readily available toxic compounds.

Our results also refute the second premise, that HPAH concentrations in weathered oil deposits are transferred in pore water through the beach substrate at toxic levels to incubating embryos in adjacent streams. It is noted that the tissue load of embryos in the laboratory study by Brannon et al. [11] was at a level close to or higher in relative concentration than that initially in the sediment TPAH. For example, in the laboratory, the tissue TPAH of 7,100 ppb was approximately 85% of the gravel TPAH of 8,300 ppb in the 1,500-ppm oil-on-gravel test lots, and in most other test concentrations, the ratio of tissue to sediment TPAH is even higher. However, the tissue load in eggs on Sleepy Bay beach, but not immersed in the oil deposit (<19 ppb), was at a level <0.1% of the adjacent highest sediment TPAH (23,149 ppb) and <0.3% of the lethal toxic threshold (>7,100 ppb) of weathered oil measured in the laboratory [11].

Similarly, mean tissue TPAH concentrations in eggs buried or naturally spawned in close proximity to oil-contaminated sediments at Bay of Isles (6,608 ppb sediment TPAH) and east Herring Bay (17,673 ppb sediment TPAH) were approximately 216 and 13 ppb, respectively, <4% and <0.1% of the respective sediment TPAH and well below the toxic dose. Therefore, while the dissolved TPAH available for absorption by embryos in the field was only a fraction of what is available under laboratory conditions, no interstitial transport of TPAH levels above background control concentrations was apparent even on beaches away from diluting freshwater flows. Consequently, there is no evidence supporting the second premise that transport of pore water from weathered oil deposits poses a toxic risk to incubating pink salmon embryos.

A critical point exposed by these field data is that in order for the interstitial toxic water hypothesis to be viable, the pore water must have extreme toxicity of bioavailable HPAH homologues in order to overcome the diluting and flushing effects of stream flow and tidal cycles. However, the enrichment of HPAH in oil-contaminated sediments, with their corresponding much reduced presence in the embryo tissue TPAH, demonstrates that the high molecular weight and putatively the most toxic analytes [1,9] remain undissolved and unavailable to eggs except for a little more than trace amounts. At all three oiled sites, Sleepy Bay, Bay of Isles, and Herring Bay, the tissue TPAH compositions were dominated by naphthalenes (Fig. 2b). Since naphthalenes were the primary components partitioned in the embryo tissues, even when they were very low in the contaminated sediments, it indicates that naphthalenes dominate uptake over the more prevalent HPAH compounds in weathered oil deposits because of limited solubility of HPAH analytes.

We emphasize that these field studies were conducted on the oiled beaches with only tidal flushing and without freshwater flow over the artificial redds, which was the most extreme exposure of eggs to interstitial toxic water emanating from the known oil deposits at those sites. Moreover, the weathered oil deposits were high in HPAH composition, which should have increased the dissolved HPAH availability, if they were soluble [9]. However, not only did the eggs show low tissue TPAH levels, but the HPAH homologues were minor contributors. We suggest, therefore, that with the major dilution of soluble analytes around oil deposits by marine tidal cycles, as well as the freshwater flushing of the incubation substrate, the risk to incubating pink salmon embryos in streams adjacent to weathered oil deposits on the beach is extremely low.


The interstitial toxic water hypothesis proposed by Auke Bay researchers on the Exxon Valdez oil spill effects was based on the premises that, first, HPAH homologues dissolved from buried deposits are present at toxic levels to pink salmon embryos and, second, that highly toxic pore water is transported into the incubation environment of adjacent intertidal salmon streams. The low hydrocarbon uptake of eggs in direct contact with weathered oil deposits dominated by HPAH homologues and the preponderance of LPAH compounds in tissues of embryos exposed to those conditions render dissolved HPAH concentrations from buried oil deposits too low to be of risk to pink salmon embryos in adjacent intertidal streams. This conclusion is corroborated by the field studies using the tissue TPAH criteria recommended by Auke Bay investigators [10]. Mean tissue PAH levels of embryos in oiled streams in 1989–1991 were <100 ppb [4], demonstrating that weathered oil deposits on beaches did not pose a risk to incubating pink salmon embryos in streams adjacent to those deposits. The interstitial toxic water hypothesis and the alleged lingering risk from the Exxon Valdez oil spill in the proposed new oil toxicity paradigm [9] are without foundation.


The authors acknowledge the support of ExxonMobil Corporation that made the present study possible. We thank Battelle Laboratory (Duxbury, MA, USA), for the chemical analyses of sediment and tissue samples. We appreciate the reviews by A.E. Bence, A.W Maki, and J.M. Neff. This research was independent of the Aquaculture Research Institute, University of Idaho, and does not represent the opinion of the Institute.



Table  . APPENDIX. Polycyclic aromatic hydrocarbons and symbols