Jeffrey W. Short

Oil sands development contributes elements toxic at low concentrations to the Athabasca River and its tributaries

We show that the oil sands industry releases the 13 elements considered priority pollutants (PPE) under the US Environmental Protection Agencys Clean Water Act, via air and water, to the Athabasca River and its watershed. In the 2008 snowpack, all PPE except selenium were greater near oil sands developments than at more remote sites. Bitumen upgraders and local oil sands development were sources of airborne emissions. Concentrations of mercury, nickel, and thallium in winter and all 13 PPE in summer were greater in tributaries with watersheds more disturbed by development than in less disturbed watersheds. In the Athabasca River during summer, concentrations of all PPE were greater near developed areas than upstream of development. At sites downstream of development and within the Athabasca Delta, concentrations of all PPE except beryllium and selenium remained greater than upstream of development. Concentrations of some PPE at one location in Lake Athabasca near Fort Chipewyan were also greater than concentration in the Athabasca River upstream of development. Canadas or Albertas guidelines for the protection of aquatic life were exceeded for seven PPE—cadmium, copper, lead, mercury, nickel, silver, and zinc—in melted snow and/or water collected near or downstream of development.

Oil sands development contributes polycyclic aromatic compounds to the Athabasca River and its tributaries

For over a decade, the contribution of oil sands mining and processing to the pollution of the Athabasca River has been controversial. We show that the oil sands development is a greater source of contamination than previously realized. In 2008, within 50 km of oil sands upgrading facilities, the loading to the snowpack of airborne particulates was 11,400 T over 4 months and included 391 kg of polycyclic aromatic compounds (PAC), equivalent to 600 T of bitumen, while 168 kg of dissolved PAC was also deposited. Dissolved PAC concentrations in tributaries to the Athabasca increased from 0.009 μg/L upstream of oil sands development to 0.023 μg/L in winter and to 0.202 μg/L in summer downstream. In the Athabasca, dissolved PAC concentrations were mostly <0.025 μg/L in winter and 0.030 μg/L in summer, except near oil sands upgrading facilities and tailings ponds in winter (0.031–0.083 μg/L) and downstream of new development in summer (0.063–0.135 μg/L). In the Athabasca and its tributaries, development within the past 2 years was related to elevated dissolved PAC concentrations that were likely toxic to fish embryos. In melted snow, dissolved PAC concentrations were up to 4.8 μg/L, thus, spring snowmelt and washout during rain events are important unknowns. These results indicate that major changes are needed to the way that environmental impacts of oil sands development are monitored and managed.

Accumulation of butyltins in muscle tissue of chinook salmon reared in sea pens treated with tri-n-butyltin

Abstract Muscle tissue of chinook salmon, Oncorhyncus tshawytscha , reared for 3 to 19 months in sea pens treated with an antifouling biocide, tri-n-butyltin (TBT), contained organotin concentrations of 0.28–0.90 μg g −1 (as TBT). Organotins are present in some pen-reared salmon sold in the United States: eleven of 15 salmon advertised as aquaculture products and purchased from public markets contained organotin concentrations of 0.081–0.20 μg g −1 . Most common cooking practices do not effectively destroy or remove butyltins from salmon muscle tissue. We believe this is the first evidence of entry of organotins into the human diet in the United States.

Long-Term Effects of Crude Oil on Developing Fish: Lessons from the Exxon Valdez Oil Spill

Habitat damage resulting from oil contamination is underestimated by acute toxicity assays. Nearshore substrates oiled by spills may become persistent pollution sources of toxic polycyclic aromatic hydrocarbons (PAH). Recent findings resulting from research following the Exxon Valdez oil spill include: (1) PAHs are released from oil films and droplets at progressively slower rates with an increasing molecular weight, leading to greater persistence of larger PAHs; (2) eggs from demersally-spawning fish species accumulate dissolved PAHs released from oiled substrates, even when the oil is heavily weathered; and (3) PAHs accumulated by embryos from aqueous concentrations of < 1 μg/L can lead to adverse sequelae appearing at random over the lifespan of an exposed cohort, probably as a result of damage during early embryogenesis. Polycyclic Aromatic Hydrocarbons (PAH) can be a slow-acting poison, and toxic effects may not manifest until long after exposure. These considerations have important policy implications regarding protection of fish natal and rearing habitats.

Long term monitoring for oil in the Exxon Valdez spill region

In the aftermath of the 1989 Exxon Valdez oil spill, a Long Term Environmental Monitoring Program (LTEMP) has been regularly sampling mussels (and some sediments) for polycyclic aromatic and saturated hydrocarbons (PAH and SHC) at sites in Port Valdez, Prince William Sound, and the nearby Gulf of Alaska region. After 1999, a decreasing trend appears in total PAH (TPAH) in tissues at all sites with current values below 100 ng/g dry weight (many below 50 ng/g). Currently, most samples reflect a predominantly dissolved-phase signal. This new low in TPAH likely represents ambient background levels. Synchrony in TPAH time-series and similarities in the hydrocarbon signatures portray regional-scale dynamics. The five inner Prince William Sound sites show similar composition and fluctuations that are different from the three Gulf of Alaska sites. The two Port Valdez sites represent a unique third region primarily influenced by the treated ballast water discharge from the Alyeska Marine Terminal. Prince William Sound has reverted to a stable environment of extremely low level contamination in which local perturbations are easily detected.

Occurrence of tri-n-butyltin-caused imposex in the North Pacific marine snail Nucella lima in Auke Bay, Alaska

Like female dog whelks (Nucella lapillus) in the Atlantic Ocean, females of the Pacific gastropod N. lima respond to low concentrations of tri-n-butyltin (TBT) by growing a penis and vas deferens. This condition, termed imposex, was found to occur in N. lima collected from August 1987 to May 1988 along a TBT pollution gradient associated with a marina in Auke Bay, Alaska. The suite of symptoms characteristic of imposex in N. lima was slightly different than in N. lapillus. Imposex, as measured by relative penis size (RPS) of females to males, increased from 0.0 to 34.27 along this gradient and as measured by vas deferens sequenceindex (VDS) increased similarly from 0.0 to 4.29. Concentrations of TBT in N. lima increased from below detection limits (about 0.010 μg Sn g-1 dry tissue wt) to 0.065 μg Sn g-1 dry tissue wt along the gradient. The gradient was determined by measuring TBT in whole-body tissues of bay mussels (Mytilus edulis). Concentrations of TBT in mussels increased from below detection limits to 0.833 μg Sn g-1 dry tissue wt in mussels from within the marina that was the major local source of TBT. Imposex, tissue TBT burden, and position along a TBT pollution gradient are significantly correlated (P<0.01) in N. lima. TBT was tested as a causative agent for imposex by exposing snails at a distant control site to TBT paint. After 1 mo exposure, 33% of the females grew a penis ranging in size from 0.2 to 0.8 mm. Our results generally corroborate those found for N. lapillus and indicate that imposex in N. lima is caused by environmental TBT exposure. We suggest that the RPS in the genus Nucella may be useful in monitoring TBT in coastal waters worldwide.

Imposex induction in Nucella lima (Gmelin) via mode of exposure to tributyltin

Abstract Exposure of Nucella lima (Gmelin) to seawater or Mytilus trossulus (Gould) flesh containing tributyltin (TBT) for 4 months resulted in the development of imposex, the superimposition of male reproductive tract characteristics in female snails, in a time-dependent manner. Specific imposex characteristics measured in female snails included growth of a penis and vas deferens, and an increase in the magnitude of two imposex indices, relative penis size (RPS) and the vas deferens sequence (YDS) index. Imposex characteristics developed to a similar degree in snails fed TBT-contaminated mussels (0.362 μg TBT/g wet weight) or exposed to 0.064 μg TBT/1 in seawater by the 2nd month of exposure. After exposure to TBT for 4 months, intensification of imposex characteristics continued during a subsequent 10-month recovery period when snails were held in TBT-free laboratory seawater and fed TBT-free mussels. No significant differences in mortality and feeding rates occurred between control snails and those exposed to 0.064 μg TBT/1 seawater or those exposed to TBT-laden mussels; significant mortality and a decreased feeding rate occurred in snails exposed to 0.914 μg TBT/1 seawater, indicating that this concentration is close to the long-term LC50. TBT was bioaccumulated from both food and seawater in direct relationship to concentration and length of exposure. Debutylization of TBT occurred at a slow rate in all experimental groups, but a higher proportion of TBT was metabolized to DBT and MET in snails exposed to 0.914μg TBT/1 seawater. For N. lima, TBT bioaccumulation from food and resulting imposex responses are equivalent to low level exposures to TBT in seawater.

Toxicity of tri-n-butyl-tin to chinook salmon, Oncorhynchus tshawytscha, adapted to seawater

Abstract The median lethal concentrations (LC50s) of tri-n-butyl-tin oxide (TBTO) to juvenile chinook salmon, Oncorhynchus tshawytscha, adapted to seawater were determined in a static renewal bioassay. LC50s were 54, 20, and 1.5 μg TBTO/l after exposures for 6, 12, and 96 h, respectively. LC50s decreased logarithmically with time for exposures between 12 and 96 h. Also determined were the average tri-n-butyl-tin (TBT) concentrations in liver, brain, and muscle tissues of salmon that died during the bioassay: 7.0, 3.5, and 0.52 μg TBT/g wet weight tissue, respectively. TBT concentrations in liver, brain, and muscle tissues of salmon that survived until day 4 of the bioassay were 4300, 1300, and 200 times exposure concentrations, respectively. Our results implicate TBT exposure as the cause of death of chinook salmon exposed to TBT-treated marine net pens at one aquaculture facility.

Effectiveness in the Laboratory of Corexit 9527 and 9500 in Dispersing Fresh, Weathered, and Emulsion of Alaska North Slope Crude Oil under Subarctic Conditions

Abstract The effect of various states of weathering (no weathering, 20% evaporatively weathered, and emulsification) on the effectiveness of oil dispersants Corexit 9527 and 9500 in dispersing Alaska North Slope crude oil into the water column was tested under laboratory conditions at a combination of realistic subarctic salinities and temperatures. A modified version of the swirling flask effectiveness test was conducted at temperatures of 3, 10 and 22 °C with salinities of 22‰ and 32‰. Petroleum dispersed into the water column following application of dispersant was measured by gas chromatography with flame ionization detection. Based on comparison of unresolved complex mixtures, dispersants dispersed less than 40% of the fresh oil and less than 10% of the weathered oil and were most effective (25–75%) when used to disperse a stable oil/water emulsion at 10 °C. At the combinations of temperature and salinity most common in the estuaries and marine waters of Alaska, dispersants effectiveness was less than 10%, the detection limits of the tests. The results indicate that oil weathering state, seawater salinity and temperature are important factors affecting dispersant performance, however because our laboratory tests were conducted at low mixing energy, considerable caution should be used in extrapolating these laboratory studies to field conditions.

Uptake and catabolism of tributyltin by blue crabs fed TBT contaminated prey

Abstract Accumulation and catabolism of tributyltin (TBT) was measured in blue crabs ( Callinectes sapidus ) after 16-day exposures to TBT-contaminated prey. TBT and the metabolites, DBT and MBT, were separated by gas chromatography and measured by atomic absorption (GCAA) in prey and in crab tissues during the 16-day test. Crabs were fed grass shrimp Palaemonetes pugio contaminated with 1·8 μg TBT, 0·09 μg DBT and 0·03 μg MBT per gram wet weight tissue. Feeding rates for exposed and nonexposed crabs were equal during the 16-day test. In 16 days, exposed crabs consumed about 2·02 μg of TBT. TBT was sequentially debutylated in a significant manner by blue crabs, but not by the grass shrimp. TBT concentrations peaked in crabs after 4 days of feeding, at 0·12 μg g −1 . DBT peaked at 8 days at 0·39 μg g −1 , and MBT peaked at 12 days at 0·35 μg g −1 . Total butyltins reached equilibrium by 8 days, but the relative toxic burden declined from 8–16 days because the proportion of TBT continued to decline. Growth, molting success and feeding rates were not affected in the juvenile crabs during the 16-day test. Catabolism of TBT reduces tissue concentrations of TBT, thereby increasing the tolerance of blue crabs to TBT.