Hearings - Testimony
EPA’s Spill Prevention Control and Countermeasure Program
Wednesday, December 14, 2005
Riki Ott, PhD
Author, Marine Toxicologist

Thank you for inviting me to testify on oil spill prevention standards.


My name is Riki Ott. I have a masters and doctorate in marine toxicology with a focus in oil pollution. I was on the scene before, during, and after the infamous Exxon Valdez oil spill. I am a 20-year resident of Cordova, Alaska. At the time of the oil spill, I was a commercial salmon fisherm’am in Prince William Sound. After the pink salmon and herring populations collapsed, unexpectedly, in 1992 and 1993—along with Cordova’s economy, I retired from fishing to focus on helping rebuild my community.

I have since co-founded three nonprofit organizations to deal with lingering social, economic, and environmental harm from this spill (www.alaskaforum.org, www.copperriver.org, www.orafoundation). I’ve also written a book on the legacy of the Exxon Valdez oil spill (Ott 2005).

The lessons from our tragedy apply to spills of any size––as well as public health and the environment. I would like to share three lessons with this committee and explain how each relates to the SPCC proposed rule. These lessons are:

-- Oil is far more toxic than we thought.
-- Prevention is critical.
-- Better, safer cleanup products need to be used.

1. Oil is far more toxic than we thought.

A paradigm shift in the scientific understanding of oil toxicity has occurred since passage of the Clean Water Act (CWA) and the Oil Pollution Act of 1990 (OPA 90). It is important to realize the limitations of the 1970s science. This science is based on standard laboratory bioassays, using single species, exposed for 96 hours to only the Water Soluble Fraction of crude oil. Based on these studies, scientists thought toxic components of oil evaporated quickly and sub-lethal effects were limited to invertebrates, and occurred at exposure levels of parts per million. This 1970s science underpins the risk assessment assumptions used by the EPA in its proposed rule change.

The collapse of pink salmon and Pacific herring stocks in Prince William Sound was a tipping point for science, because the reality of what was occurring in the Sound––that is, long-term harm from the 1989 spill––did not match the 1970s understanding that oil only caused short-term harm.

To determine what was going on in Prince William Sound, interdisciplinary teams of scientists conducted four ecosystem studies from 1993 to 2001. These complex studies were conducted in the field, using lab tests to interpret and/or validate field findings. The ecosystem studies used multiple species over multiple generations and focused on a particularly toxic fraction of crude oil called polycyclic aromatic hydrocarbons or PAHs. PAHs were largely ignored by the 1970s science.

As a result of the ecosystems studies, scientists now realize that crude oil is 1,000 times more toxic than previously thought. In many of the birds, fish, and mammals studied, 1–20 parts per billion PAHs were found to impair reproduction, disrupt immune system function, and generally decrease overall fitness (health) of individuals, resulting in declines of localized populations (Bodkin et al. 2002; Carls et al. 1999, 2002; Esler et al. 2000, 2002; Golet et al. 2002; Matkin et al. 1999; Thomas and Thorne 2003; Trust et al. 2000).

Further, these effects are still happening in areas once heavily oiled. Only 7 of 28 species are listed as fully recovered by the Exxon Valdez Oil Spill Trustee Council (EVOSTC 2002). After 16 years, there is relatively fresh, toxic oil still on the beaches, and it is still bioavailable (Carls et al. 2001; Short et al. 2004), much to the amazement of scientists and disappointment of residents. I have a sample collected this past summer that I’ll pass around when I’m done. The emerging paradigm is summarized in an article in Science in December 2003 (Attachment 1: Peterson et al. 2003)

Findings in medical science support the new paradigm and show that low levels of PAHs also harm public health. For example, medical doctors link low levels of PAH exposure with asthma, depression, and chemical sensitivities (Ashford and Miller 1998). In 1999 the EPA added 22 PAHs in crude oil to its list of persistent, bioaccumulative, toxic pollutants. This list includes lead, dioxin, mercury, PCBs, and DDT––and now PAHs (U.S. EPA 2000).

This relates to today’s hearing because the 1990s science on oil toxicity supplants the 1970s science and changes the risk assessment equation. Oil is more toxic than we thought. Since oil exposure causes greater known risk to the public and the environment, we need to increase, not decrease, spill prevention standards to reduce the likelihood of spilling it.

2. Prevention is critical.

Another reason to maintain strong standards for spill prevention is industry’s general inability to contain and clean up spilled oil. The public has witnessed, time and again, industry’s inept fumbling ever since England’s Torrey Canyon spill (in 1968). Even one of the most technologically sophisticated companies in the world only managed to recover a small fraction of what was spilled in Prince William Sound (Ott 2005; Spies et al. 1996).

The size of the spill doesn’t matter. The 1,000-gallon spill in Puget Sound, Washington, (2004) oiled hundreds of miles of coastline, while the massive Exxon Valdez oiled thousands.

This relates to today’s hearing because the EPA’s proposal to lower the threshold for spill planning and prevention essentially guarantees the small facilities will have more spills. Why? Because less liability equates to more spilled oil.

The National Research Council found that for tankers, oil spillage dropped off significantly after 1991, following passage of OPA 90 (2002). Industry watchers attribute the reduced spillage to preventative measures and increased industry concerns over escalating financial liability (de Bettencourt et al. 2001). As one senior U.S. Coast Guard officer put it, the “requirement for some ships to assume a higher level of financial liability for spilling oil has likely had a greater impact on reducing the amount spilled than the plethora of ‘command and control ’regulations that (preceded or) followed OPA 90” (Elliott 2001, 31).

Reducing oil spills and oil pollution is a matter of making the polluter pay. Oil companies are experts at externalizing costs to society and the environment. Spill cleanup involves high costs to society––because taxpayers foot the bill and because cleanup workers risk their health to deal with hazardous waste cleanups, including oil spills. Facility owners should be held responsible for spill prevention––not exempted from it.

3. Better, safer cleanup products need to be used.

The third reason for maintaining strong oil spill prevention standards is that, when oil does spill, industry’s preferred method of cleanup is chemical products. This often creates more problems than is solves, because cleanup products often contain industrial solvents to dissolve oil and grease and, thus, are environmental hazards.

One dispersant that was used during the Exxon Valdez cleanup is Exxon’s Corexit 9527, which contains an OSHA human health hazard called 2-butoxyethanol. Exxon’s Material Safety Data Sheet for Corexit 9527 states: “Prevent liquid from entering sewers, watercourses, or low areas. Contain spilled liquid . . .” (Exxon 1992). This product was sprayed on water and beaches during Exxon’s cleanup. It is currently stockpiled in Alaska, California, Washington, Hawaii, Texas, Florida, New York, and Puerto Rico––and likely other places.

How is this allowed? The EPA maintains a schedule of chemical products for use in the National Oil and Hazardous Substances Pollution Contingency Plan. The EPA only screens products for effects on animals and the environment–-not humans. Yet, it’s not just the environment that’s at risk when chemical products are used––it’s spill responders and the public in places where drinking water or land may become contaminated. Evidence of sick workers from the Exxon Valdez cleanup suggests it’s time to include effects on humans in product assessment (Ott 2005).

There are no guarantees that the products are safe for the environment either (Attachment 2: Nichols 2001). Products are designed for specific purposes; however, the EPA admits its system is rife with abuse: “misuse . . . may cause further harm to the environment than the oil alone” (ibid., 1481).

For example, during the Exxon Valdez cleanup, dispersants designed for open water use were applied directly on beaches, despite voluntary guidelines adopted by the Alaska Regional Response Team (1989) through a consensus process with stakeholders that dispersant use was not recommended on beaches and in nearshore areas.

Other problems with the Product Schedule that should concern this committee are:
–– A loophole in subpart J, which allows South Louisiana crude to be mixed 50:50 with Prudhoe Bay crude so dispersants will meet the EPA’s minimum 45 percent effectiveness threshold for product listing (Nichols 2001). This creates an illusion that dispersants work and eliminates industry incentive to develop ones that actually do.

–– No formal de-listing process in Schedule C, requiring the manufacturer to notify the EPA when products are no longer manufactured, and to provide a written explanation for the de-listing. This is like discovering a product is dangerous, but never publicly announcing its recall, or the reasons for the recall, so the public is unaware of any health risk from use or exposure.

–– No requirement to test stockpiled product periodically to ensure effectiveness.

This relates to today’s hearing because it is cheaper for industry to throw chemical products at spilled oil than to prevent the spill from happening in the first place. Reducing spill prevention standards is another example of externalizing costs to the public because it virtually ensures more cleanup products will be used.

To summarize, I’ve addressed three reasons for maintaining strong oil spill prevention standards, based on direct experience in dealing with an oil spill. First, oil is more toxic than we thought; second, oil is nearly impossible to contain and cleanup once it does spill; and third, the chemical cleanup products introduce more risk for spill responders, the public, and the environment. All of what I’ve discussed is covered in my book (Ott 2005), which I would like to leave with this committee.

I urge this committee to reject the EPA’s proposed rulemaking to lower standards for spill prevention for small facilities.

Thank you for the opportunity to testify.




Rice, S. D., R. B. Spies, D. A. Wolfe, B. A. Wright, eds. 1996. Proceedings of the EVOS Symposium. American Fisheries Society Symposium 18. Bethesda, MD: American Fisheries Society.


IOSC International Oil Spill Conference Proceedings. American Petroleum Institute: Washington,DC.


Attachment 1: Peterson, C. H., S. D. Rice, J. W. Short, D. Esler, J. L. Bodkin, B. E. Ballachey, and D. B. Irons. 2003. Long-term ecosystem response to the EVOS. Science 302:2082–2086.

Attachment 2: Nichols, W. J. 2001. The U.S. EPA: National oil and hazardous substances pollution contingency plan, subpart J product schedule (40 CFR 300.900). IOSC 2001,1479–1483.


Alaska Regional Response Team. 1989. RRT Oil Dispersant Guidelines for Alaska. www.pwsrcac.org/projects/EnvMonitor/dispers.html

Ashford, N. and C. Miller. 1998. Chemical Exposures: Low Levels and High Stakes. 2d. ed. NewYork: John Wiley & Sons.

Bodkin, J., B. E. Ballachey, T. A. Dean, A. K. Fukuyama, S. C.Jewett, L. McDonald, D. H. Monson, C. E. O’Clair, and G. R. VanBlaricom. 2002.Sea otter population status and the process of recovery from the 1989 EVOS. Marine Ecology Progress Series 241: 237–253.

Carls, M. G., Babcock, M. M., P. M. Harris, G. V. Irvine, J. A. Cusick, and S. D. Rice. 2001. Persistence of oiling in mussel beds after the EVOS. Marine Environmental Research 51: 167–190.

Carls, M. G., G. D. Marty, and J. E. Hose. 2002. Synthesis of the toxicological and epidemiological impacts of the EVOS on Pacific herring in PWS, AK. Canadian Journal of Fisheries and Aquatic Sciences 59: 153–172.

Carls, M., S. D. Rice, and J. E. Hose. 1999. Sensitivity of fish embryos to weathered crude oil: Part I. Low-level exposure during incubation causes malformations, genetic damage, and mortality in larval Pacific herring (Clupea Pallasi). Environmental Toxicology and Chemistry 18(3): 481–493, 1999.

de Bettencourt, M., G. Merrick, T. Deal, and B. Travis. 2001. Safeguarding the public interest: A look at government policies that affect the OPA 90 oil spill liability trust fund and oil spill costs. IOSC 2001, 725–729.

Elliott, J. E. 2001. Preventing oil spills in the twenty-first century: An ecological economics perspective. IOSC 2001, 27–33.

Esler, D., T. D. Bowman, K. A. Trust, B. E. Ballachey, T. A. Dean, S. C. Jewett, and C. E. O’Clair. 2002. Harlequin duck population recovery following the EVOS: Progress, process and constraints. Marine Ecology Progressive Series 241: 271–286.

Esler, D., J. A. Schmutz, R. L. Jarvis, and D. M. Mulcahy. 2000. Winter survival of adult female harlequin ducks in relation to history of contamination by the EVOS. Journal of Wildlife Management 64(3): 839–847.

EVOS TC. 2002. Exxon Valdez Oil Spill Trustee Council 2002 Status Report. ADFG, Anchorage, AK.

Exxon Company, USA. 1992. MSDS for Corexit 9527. Houston, TX, 14 June.

Golet, G. H., P. E. Seiser, A. D. McGuire, D. D. Roby, J. B. Fischer, K. J. Kuletz, D. B. Irons, T. A. Dean, S. C. Jewett, and S. H. Newman. 2002. Long-term direct and indirect effects of the EVOS on pigeon guillemots in PWS, AK. Marine Ecology Progress Series 241: 287–304.

National Research Council. 2002. Oil in the Sea III: Inputs, Fates, and Effects. Washington, DC: National Academies Press.

Matkin, C. O., G. Ellis, P. Olesiuk, and E.Saulitis. 1999. Association patterns and inferred genealogies of resident killer whales, Orcinus orca, in PWS, AK. Fisheries Bulletin 97: 900–919.

Ott, R. 2005. Sound Truth and Corporate Myth$: The Legacy of the Exxon Valdez Oil Spill (Dragonfly Sisters Press: Cordova, AK).

Peterson, C. H., S. D. Rice, J. W. Short, D. Esler, J. L. Bodkin, B. E. Ballachey, and D. B. Irons. 2003. Long-term ecosystem response to the EVOS. Science 302: 2082–2086.

Short, J. W., M. R. Lindeberg, P. M. Harris, J. M. Maselko, J. J. Pella, and S. D. Rice. 2004. Estimate of oil persisting on the beaches of PWS 12 years after the EVOS. Environmental Science and Technology 38(1): 19–25.

Spies, R. B., S. D. Rice, D. A. Wolfe, and B. A. Wright. 1996. The effect of the EVOS on the Alaskan coastal environment. AFSS 18: 1–16.

Thomas, G. L., and R. E. Thorne. 2003. Acoustical-optical assessment of Pacific herring and their predator assemblage in Prince William Sound, Alaska. Aquatic Living Resources 16: 247–253.

Trust, K., D. Esler, B. R. Woodin, and J. J. Stegeman. 2000. Cytochrome P450-1A induction in sea ducks inhabiting nearshore areas of PWS, AK. Marine Pollution Bulletin 40(5): 397–403.

U.S. EPA. 2000. 1999 Persistent, Bioaccumulative, and Toxic Pollutants Initiative (PBTI) Report. Pollution Prevention Information Clearinghouse, Washington, DC. www.epa.gov/pbt/accomp99.htm.


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