[Federal Register Volume 62, Number 202 (Monday, October 20, 1997)]
[Rules and Regulations]
[Pages 54508-54543]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-27261]
[[Page 54507]]
_______________________________________________________________________
Part II
Environmental Protection Agency
_______________________________________________________________________
40 CFR Part 112
Oil Pollution Prevention; Non-Transportation Related Onshore
Facilities; Rule
Federal Register / Vol. 62, No. 202 / Monday, October 20, 1997 /
Rules and Regulations
[[Page 54508]]
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 112
[FRL-5909-5]
Oil Pollution Prevention; Non-Transportation Related Onshore
Facilities
AGENCY: Environmental Protection Agency (EPA).
ACTION: Denial of petition requesting amendment of the Facility
Response Plan rule.
-----------------------------------------------------------------------
SUMMARY: EPA is denying the request submitted by various trade
associations to amend the Facility Response Plan (FRP) rule that the
Agency promulgated under section 311(j) of the Clean Water Act (CWA),
as amended by the Oil Pollution Act (OPA) of 1990. These organizations
had requested that EPA modify the FRP rule in a number of ways to treat
facilities that handle, store, or transport animal fats and vegetable
oils in a manner differently from those facilities that store
petroleum-based oils. EPA believes that the petition did not
substantiate the claimed differences between animal fats and vegetable
oils and petroleum oils so as to support a further differentiation
between these groups of oils under the FRP rule. Instead, EPA continues
to find that a worst case discharge or substantial threat of discharge
of animal fats and/or vegetable oils to navigable waters, adjoining
shorelines, or the exclusive economic zone could reasonably be expected
to cause substantial harm to the environment, including wildlife that
may be killed by the discharge of fats or vegetable oils. Moreover, EPA
believes that in setting different response strategies for petroleum
and non-petroleum oils, (with animal fat and vegetable oils in the
latter category), the FRP rule already provides for adequate
differentiation in response planning requirements for all covered
facilities.
ADDRESSES: The official record for this decision is located in the
Superfund Docket, at the U.S. Environmental Protection Agency, [Docket
Number SPCC-3]. The docket is available for inspection between 9 a.m.
and 4 p.m., Monday through Friday, excluding Federal holidays, at US
EPA Crystal Gateway 1 (CG1), 1235 Jefferson Davis Highway, Arlington,
VA 22202. Appointments to review the docket can be made by calling 703-
603-8917. The public may copy a maximum of 266 pages from any
regulatory docket at no cost. If the number of pages copied exceeds
266, however, a charge of 15 cents will be incurred for each additional
page, plus a $25.00 administrative fee.
FOR FURTHER INFORMATION CONTACT: Bobbie Lively-Diebold, Oil Pollution
Center, Office of Emergency and Remedial Response (5203G), U.S.
Environmental Protection Agency, 401 M Street, SW., Washington, DC
20460 at 703-356-8774 ([email protected]); or the RCRA/
Superfund Hotline at 800-424-9346 (in the Washington, DC metropolitan
area, 703-412-9810). The Telecommunications Device for the Deaf (TDD)
Hotline number is 800-553-7672 (in the Washington, DC metropolitan
area, 703-412-3323).
SUPPLEMENTARY INFORMATION: The contents of this Denial of Petition are
listed in the following outline:
I. Background
A. The Organizations' Petition
B. Background on the Processing and Storage of Vegetable Oils and
Animal Fats
II. Technical Evaluation of Petitioners' Claims
A. General
B. Petitioners' Claim: Animal Fats and Vegetable Oils Are Non-Toxic
1. How Animal Fats and Vegetable Oils Produce Adverse Environmental
Effects
2. Physical Properties
3. Chemical Composition
4. Environmental Effects
a. Physical Effects of Spilled Oil
b. Effects of Oil on Metabolic Requirements
c. Effects of Oil on Food and the Food Web, Communities, and
Ecosystems
d. Indirect Effects
5. Toxicity
a. Principles of Toxicology
b. Exposure From Oil Spills
c. Toxicity of Petroleum Oils
d. Toxicity of Vegetable Oils and Animal Fats
Figure 1. Toxicity and Adverse Effects of Components and
Transformation Products of Vegetable Oils and Animal Fat
6. Epidemiological Studies
a. Human Health
b. Comparison of Effects From Oil Spills With Human Consumption
of Vegetable Oils and Animal Fats
7. Other Adverse Effects from Oil Spills
a. Aesthetic Effects: Fouling and Rancidity
b. Fire Hazards
c. Effects on Water Treatment
8. FWS Comments
C. Petitioners' Claim: Animal Fats and Vegetable Oils Are Essential
Components of Human and Wildlife Diets
1. Nutritional Requirements for Dietary Fat
2. Essential Fatty Acids (EFA)
3. Adverse Effects of High Levels of EFAs
4. Adverse Effects of High Levels of Fats and Oils
5. Relevance of EFA Principles to Spills
6. FWS Comments on Essential Fatty Acids
D. Petitioners' Claim: Animal Fats and Vegetable Oils Are Readily
Biodegradable and Do Not Persist in the Environment
1. Chemical and Biological Processes Affecting Vegetable Oils and
Animal Fats in the Environment
a. Chemical Processes
b. Biological Processes
c. Rancidity
2. Environmental Fate and Effects of Spilled Vegetable Oils and
Animal Fats: Real-World Examples
3. FWS Comments on Degradation
E. Petitioners' Claim: Vegetable Oils and Animal Fats Have a High
BOD, Which Could Result in Oxygen Deprivation Where There Is a Large
Spill in a Confined Body of Water
F. Petitioners' Claim: Vegetable Oils and Animal Fats Can Coat
Aquatic Biota and Foul Wildlife
III. Petitioners' Suggested Language to Amend the July 1, 1994,
Facility Response Plan Rule
A. Background
B. Regulatory Language Changes Proposed by the Petitioners
IV. Conclusions
Acronym List
Bibliography
Appendix I: Supporting Tables
Table 1. Comparison of Physical Properties of Vegetable Oils and
Animal Fats with Petroleum Oils
Table 2. Comparison of Vegetable Oils and Animal Fats with Petroleum
Oils
Table 3. Comparison of Aqua Methods and Standard Acute Aquatic
Testing Methods
Table 4. Effects of Real-World Oil Spills
Appendix II: Edible Oil Regulatory Reform Act Differentiation
I. Background
The OPA (Pub. L. 101-380, 104 Stat. 484) was enacted to expand
prevention and preparedness activities, improve response capabilities,
ensure that shippers and oil companies pay the costs of spills that do
occur, provide an additional economic incentive to prevent spills
through increased penalties and enhanced enforcement, establish an
expanded research and development program, and establish a new Oil
Spill Liability Trust Fund administered by the U.S. Coast Guard.
Section 4202(a) of the OPA amends CWA section 311(j) to require
regulations for owners or operators of facilities to prepare and submit
``a plan for responding, to the maximum extent practicable, to a worst
case discharge, and to a substantial threat of such a discharge, of oil
or a hazardous substance.'' This requirement applies to all offshore
facilities and any onshore facility that, ``because of its location,
could reasonably be expected to cause substantial harm to the
environment by discharging into or on the navigable
[[Page 54509]]
waters, adjoining shorelines, or the exclusive economic zone''
(``substantial harm facilities'').
On July 1, 1994, EPA published its Final Rule amending the Oil
Pollution Prevention regulation (40 CFR part 112) to incorporate new
requirements to implement amended section 311(j)(5) of the CWA. (Oil
Pollution Prevention; Non-Transportation-Related Onshore Facilities;
Final Rule, 59 FR 34070, July 1, 1994). Under authority of section
311(j)(1)(C) of the CWA, the Final Rule also requires planning for a
small and medium discharge of oil, as appropriate.
In the final rule, EPA determined that for the purposes of section
311(j) planning, the OPA includes non-petroleum oils. The Agency noted
that the definition of ``oil'' in the Clean Water Act includes oil of
any kind, and that EPA uses this broad definition in 40 CFR part 110,
Discharge of Oil. Animal fats and vegetable oils fall within the CWA
definition of ``oil.''
Only a small number, no more than 1\1/4\ percent of the total SPCC
community regulated (approximately 5,400 of a total of 435,000
facilities) under 40 CFR part 112.1-112.7 meet the criteria for
substantial harm under 40 CFR 112.20. Only a small number of the 5,400
substantial harm facilities (an estimated 50 to 100) store or use
vegetable oil and animal fat and have prepared and submitted FRPs.
A. The Organizations' Petition
By a letter dated August 12, 1994, EPA received a ``Petition for
Reconsideration and Stay of Effective Date'' of the OPA-mandated FRP
final rule as that rule applies to facilities that handle, store, or
transport animal fats or vegetable oils. The petition was submitted on
behalf of seven agricultural organizations (``the Organizations'' or
``Petitioners''): the American Soybean Association, the Corn Refiners
Association, the National Corn Growers Association, the Institute of
Shortening & Edible Oils, the National Cotton Council, the National
Cottonseed Products Association, and the National Oilseed Processors
Association.
To support the Petition, the Organizations referenced an industry-
sponsored report titled ``Environmental Effects of Release of Animal
Fats and Vegetable Oils to Waterways'' (prepared by ENVIRON
Corporation, June 28, 1993), and an associated study titled ``Diesel
Fuel, Beef Tallow, RBD Soybean Oil and Crude Soybean Oil: Acute Effects
on the Fathead Minnow, Pimephales Promelas'' (prepared by Aqua Survey,
Inc., May 21, 1993). Both the report and the study had been submitted
to EPA during the facility response plan rulemaking as enclosures to a
comment filed over nine months after the close of the comment period.
Based, in part, on these studies (the ENVIRON report and Aqua Survey
study), the Petitioners asked EPA to create a regulatory regime for
response planning for non-petroleum, ``non-toxic'' oils separate from
the regime established for petroleum oils and ``toxic,'' non-petroleum
oils.
The report and the study provided information on certain physical,
toxicological, and chemical properties of animal fats and vegetable
oils compared with other types of oil. The petitioners argued that
according to the ENVIRON report, the presence of animal fats and
vegetable oils in the environment does not cause significant harm. Six
specific conclusions of the ENVIRON report regarding vegetable oils and
animal fats were that these substances are not toxic to the
environment; are essential components to human and wildlife diets;
readily biodegrade; are not persistent in the environment like
petroleum oils; do have a high Biochemical Oxygen Demand (BOD), which
could result in oxygen deprivation where there is a large spill in a
confined body of water that has low flow and dilution; and can coat
aquatic biota and foul wildlife.
The Petitioners also submitted an Appendix to their Petition that
included specific suggested language to amend the July 1, 1994, FRP
rule. The submitted language would have resulted in the following
changes regarding facilities that handle, store, or transport animal
fats and vegetable oils: Further clarified the definition of animal
fats and vegetable oil (set out in Appendix E, 1.2 of the FRP); allowed
mechanical dispersal and ``no action'' options to be considered in lieu
of the oil containment and recovery devices otherwise specified for
response for a worst case discharge; required the use of a containment
boom only for the protection of fish and wildlife and sensitive
environments; and increased required on-scene arrival time for response
resources from 12 hours (including travel time) to 24 hours plus travel
time for medium discharges and worst case Tier 1 response resources.
The Federal natural resource trustee agencies, including the Fish
and Wildlife Service (FWS), had reviewed the ENVIRON study. In an April
11, 1994, letter to the Department of Transportation's (DOT) Research
and Special Projects Administration (RSPA), the FWS stated that the
Report did not provide an accurate assessment of the dangers that non-
petroleum oils pose to fish and wildlife and environmentally sensitive
areas. The letter stated that the key facts were misrepresented,
incomplete, or omitted in the Report. FWS also observed that the
ENVIRON report failed to give appropriate significance to the fouling
potential of edible oils (USDOI/FWS, 1994).
The National Oceanic and Atmospheric Administration (NOAA) also had
evaluated the effects on the environment of spilled non-petroleum oils,
including coconut, corn, cottonseed, fish, and palm oils. (Memorandum
of Record, dated June 3, 1993, from the Department of Commerce (DOC)/
NOAA Hazardous Materials Response and Assessment Division.) The NOAA
assessment, based on literature research, addresses physical and
chemical properties and toxicity of these and other oils, and indicates
that some edible oils, when spilled, may have adverse environmental
effects. (The views of the FWS and NOAA on the adverse effects of
animal fats and vegetables are discussed in detail in the preamble to
the U.S. Coast Guard's final rule setting forth response plan
requirements for marine transportation-related facilities, [61 FR 7890,
7907-7908, Feb. 29, 1996] and are included in the docket that supports
this decision. These views also are discussed in EPA's Request for Data
and Comment on Response Strategies for Facilities That Handle, Store,
or Transport Certain Non-Petroleum Oils, 59 FR 53742-53743, October 26,
1994.)
On October 26, 1994, in view of the differing scientific
conclusions reached by the Petitioners, the FWS, and other groups and
agencies, EPA requested broader public comment on issues raised by the
Petitioners in a notice and request for data (Request for Data and
Comment on Response Strategies for Facilities That Handle, Store, or
Transport Certain Non-Petroleum Oils, 59 FR 53742, October 26, 1994).
These issues included whether to have different specific response
approaches for releases of animal fats and vegetable oils (rather than
increased flexibility), and the effects on the environment of releases
of these oils. EPA also asked commenters to recommend specific data
that relate to the comparison of petroleum and non-petroleum oils. EPA
received fourteen comments in response to its October 26, 1994, notice
and request for data.
Of these fourteen commenters, most agreed with the trade
associations' request that EPA should modify the FRP rule. Most of the
commenters asserted that, based upon the ENVIRON report, animal fats
and vegetable oils are readily biodegradable and not persistent
[[Page 54510]]
in the environment. Certain commenters also argued that vegetable oils
and animal fats are less toxic than other types of oils. Other
commenters argued that edible oils pose less risk to the environment
because they are typically stored in smaller tanks at food processing
facilities, whereas petroleum-based oils are stored in larger tanks at
petroleum facilities. One commenter, citing the unnecessary and
burdensome regulations and the excellent spill record of the animal fat
and vegetable oil industry, stated that EPA should differentiate animal
fats and vegetable oils from other types of oils. One commenter
questioned the accuracy of the ENVIRON report and stated that non-
petroleum oils can adversely affect fish and wildlife and
environmentally sensitive areas.
B. Background on the Processing and Storage of Vegetable Oils and
Animal Fats
In 1992, approximately 20.8 billion pounds of vegetable oils and
animal fats were consumed in the United States, including over 14.8
billion pounds for edible uses; and more than 5.9 billion pounds for
inedible uses, such as soap, paint or varnish, feed, resins and
plastics, lubricants, fatty acids, and other products (Hui, 1996a). The
extent of processing of vegetable oils and animal fats depends on the
ultimate use of the product. Chemical composition, which determines the
toxicity and fate of oils in the environment, changes at each step in
processing, as impurities or specific components are removed or
chemicals formed; chemical composition can also be changed by storage,
heating, or reactions in the environment (Hui, 1996d; Brekke, 1980).
Processing steps in vegetable oil facilities are generally
independent operations that are not connected by continuous flow, and
between each processing step there may be one or more storage tanks
(Hui, 1996d). Many crude vegetable oil storage tanks, which are usually
constructed of welded carbon steel, have a capacity of 1 million pounds
(approximately 140,000 gallons) (Hui, 1996d). They may be located in
the open or enclosed in a structure. Storage tanks for finished fats
and oils are generally made of iron, stainless steel, or aluminum and
typically hold between 75 and 200 tons (about 21,000 to 56,000 gallons)
of product.
In a typical integrated vegetable oil processing facility, steps
may include crude oil storage, preparation, extraction and meal
finishing, removal of gums and lecithin processing, caustic refining,
bleaching and dry removal of gums and waxes, hydrogenation,
interesterification, fractionation, deodorizing, and shortening or
margarine production (Hui, 1996d; Brekke, 1980). During these steps,
several classes of materials may be removed, such as gums,
phospholipids, pigments, free fatty acids, color bodies, pigments,
metallic prooxidants, and residual soaps. New compounds, including
oxidation products, polymers and their decomposition products, may be
formed and contaminants introduced during processing (Hui, 1996d).
Impurities are also removed and chemical structure modified during
processing of animal fats (Hui, 1996d). The major animal fats are lard
and tallow. Steps in the processing of animal fats may include
rendering, bleaching, hydrogenation, deodorizing, interesterification,
and fractionation. Rendering, the removal of fat from animal tissues
using heat or mechanical means, is often a continuous process that
results in products that require no further treatment. Further refining
removes materials, such as free fatty acids or collagen or protein, or
changes the characteristics of the fat for specialized use.
Spills of crude vegetable oils containing gums, phospholipids, free
fatty acids, and a host of other chemical components can differ greatly
from spills of processed oils in their persistence in the environment,
the environmental compartments in which they are distributed, the
breakdown products that they form, their rate of degradation, and the
exposure and environmental effects that they produce. Some minor
components of oils can affect their properties or cause adverse health
and environmental effects. Spilled oils and fats can be transformed by
physical, chemical, or biological processes to form products that are
more or less toxic than the original oil, depending on the specific oil
and the products that are formed.
The EPA has considered the Petitioners' claims in detail. EPA's
technical evaluation on the Petitioners' claims is set forth in section
II. EPA's responses to suggested changes in the FRP regulation are
provided in section III. Detailed studies and information to support
this document are provided in a Technical Document, which is located in
the Docket.
II. Technical Evaluation of Petitioners' Claims
A. General
The Petitioners claim that unlike most if not all other oils,
animal fats and vegetable oils are non-toxic, readily biodegradable,
not persistent in the environment, and in fact are essential components
of human and wildlife diets. Most of the Petitioners' arguments focus
on toxicity, although toxicity is only one of several mechanisms by
which oil spills cause environmental damage.
In making its claims, the Petitioners have disregarded fundamental
scientific principles and ignored a large body of scientific evidence
that was considered by EPA in its promulgation of rules implementing
the requirements of the CWA. The ENVIRON report submitted by the
Petitioners acknowledges that animal fats and vegetable oils can cause
oxygen deprivation and coating of animals, but the Petitioners
incorrectly minimize the importance of these mechanisms in causing
environmental damage and rely instead on limited studies in narrow
areas of toxicity, which are then improperly generalized to support the
Petitioners' claims.
Petitioners' submission emphasizes that animal fats and vegetable
oils are used by all organisms for food. The ingestion of small
quantities of edible oils by humans, however, is a completely different
situation from spills of oil into the environment. These situations
differ markedly in the extent and duration of exposure, the route of
exposure, the species exposed, the composition of the chemicals
involved, the circumstances surrounding the exposure, and the types of
effects produced--factors that determine the toxicity and severity of
the adverse effects of chemicals. Thus, even if the human consumption
of small quantities of oils in food were judged completely safe, no
inferences could be drawn about the toxicity and other effects of
vegetable oils and animal fats on environmental organisms exposed in
the very different circumstances of oil spills.
The Petitioners' arguments about toxicity do not address the
central issue: Spills of animal fats and vegetable oils kill or injure
fish, birds, mammals, and other species and produce a host of other
undesirable effects. Whether this death and destruction results from
toxicity or from other processes, spills of animal fats and vegetable
oils should be prevented and if spills occur, quickly removed to reduce
the environmental harm and other adverse effects they produce.
B. Petitioners' Claim: Animal Fats and Vegetable Oils Are Non-Toxic
The Petitioners claim that EPA's implementation of the response
plan provisions and other regulatory changes
[[Page 54511]]
under the CWA are inconsistent with established regulatory principles
and with the available scientific data related to animal fats and
vegetable oils, which, unlike other oils, are non-toxic.
EPA Response: For a number of reasons that are detailed in this
document and the Technical Document, EPA disagrees with the
Petitioners' contention that animal fats and vegetable oils are non-
toxic when spilled into the environment. First, while the Petitioners
rely on laboratory tests that measure only the acute lethal effects of
some vegetable oils and animal fats in one species of fish, these tests
say nothing about other acute toxic effects or long-term toxic effects,
or toxic effects on other species or ecosystems, or toxic effects of
oil spilled in the environment under conditions that differ from those
in the laboratory. Second, the tests submitted by the Petitioners
cannot demonstrate ``non-toxicity'' of vegetable oils and animal fats;
indeed the tests described in the study only measure the lethality of
the oils tested under a given set of experimental conditions. Third,
other information and data indicate that animal fats and vegetable
oils, their components, and degradation products are not as ``non-
toxic'' as the Petitioners assert. Fourth, while low levels of certain
animal fats and vegetable oils or their components may be essential
constituents of the diet of humans and wildlife, adverse effects occur
from exposure to high levels of these chemicals. Numerous examples in
the scientific literature demonstrate that essentiality does not confer
safety and essential elements can produce toxic effects (Klaassen et
al., 1986; NAS, 1977a; Rand and Petrocelli, 1985; Hui, 1996b).
Furthermore, EPA emphasizes that toxicity is only one of several
mechanisms by which oil spills cause environmental damage. As discussed
below, the physical effects of spilled oil--such as coating animals and
plants with oil and suffocation of aquatic organisms from oxygen
depletion--and the destruction of the food supply kill birds and
mammals, destroy fish and other aquatic species, and damage their
habitats.
By contaminating food sources, reducing breeding animals and plants
that provide future food, contaminating nesting habitats, and reducing
reproductive success through contamination and reduced hatchability of
eggs, even oils that remain in the environment for relatively short
periods of time can cause long-term deleterious effects years after the
oil was spilled.
1. How Animal Fats and Vegetable Oils Produce Adverse Environmental
Effects
The deleterious environmental effects of spills of petroleum oils
and non-petroleum oils, including animal fats and vegetable oils, are
produced through physical contact and destruction of food sources as
well as toxic contamination (USDOC/NOAA, 1996; NAS, 1985e; Crump-
Wiesner and Jennings, 1975; Frink, 1994; Frink and Miller, 1995;
Hartung, 1995; USDOI/FWS, 1994). Nearly all of the most immediate and
devastating environmental effects from oil spills--such as smothering
of fish or coating of birds and mammals and their food with oil--are
physical effects related to the physical properties of oils and their
physical interactions with living systems (Hartung, 1995).
While these immediate physical effects and effects on food sources
may not be considered the result of ``toxicity'' in the classic sense--
i.e., effects that are produced when a chemical reacts with a specific
receptor site of an organism at a high enough concentration for a
sufficient length of time (Rand and Petrocelli, 1985)-- severe
debilitation and death of fish and wildlife are caused by spills of
animal fats and vegetable oils, other non-petroleum oils, and petroleum
oils and their products. Adverse environmental effects can occur long
after the initial exposure to animal fats and vegetable oils because of
toxicity, persistence of products in the environment, or destruction of
food sources and habitat and diminished reproduction resulting from
physical effects or toxicity.
2. Physical Properties
Petroleum oils and non-petroleum oils, including vegetable oils and
animal fats, share common physical properties and produce similar
environmental effects (Crump-Wiesner and Jennings, 1975; USDOI, 1994;
Frink, 1994). When spilled in the aquatic environment, petroleum oils,
animal fats and vegetable oils and their fatty acid constituents may
float on the water's surface, become solubilized or emulsified in the
water column, or settle on the bottom as a sludge, depending on their
physical and chemical properties (Crump-Wiesner and Jennings, 1975;
DOC/NOAA, 1992, 1996). Vegetable oils and animal fats that are solid at
room temperature still serve as potent physical contaminants and are
much more difficult to remove from affected animals than petroleum oil
(Frink, 1994).
While the physical properties of vegetable oils and animal fats are
highly variable, most fall within in a range that is similar to the
physical parameters for petroleum oils. (See Appendix I, Table 1:
Comparison of Physical Properties of Vegetable Oils and Animal Fats
With Petroleum Oils and Table 2: Comparison of Vegetable Oils and
Animal Fats with Petroleum Oils). Common properties--such as
solubility, specific gravity, and viscosity--are responsible for the
similar environmental effects of petroleum and vegetable oils and
animal fats. Petroleum and vegetable oils and animal fats can enter all
parts of an aquatic system and adjacent shoreline, and similar methods
of containment, removal and cleanup are used to reduce the harm created
by spills of petroleum and vegetable oils and animal fats.
3. Chemical Composition
The chemical composition and physical properties of petroleum and
non-petroleum oils, including vegetable oils and animal fats, determine
their fate in the environment (where they go, reactions, rate of
disappearance) and the exposure and adverse effects that they produce.
The chemical composition changes at each step in processing, as
impurities or specific components are removed or chemicals formed (Hui,
1996d; Brekke, 1980). Chemical composition can also change with
storage, heating, or reactions in the environment.
The main constituents of vegetable oils and animal fats are esters
of glycerol and fatty acids (Hui, 1996b). The ester linkages can be
hydrolyzed to yield free fatty acids and glycerol. While triglycerides
(triacylglycerols) predominate, fats and oils also contain mono- and
diglycerides (mono-and diacylglycerols) and other lipids, e.g.,
phosphatides and cholesterol, free fatty acids, and small amounts of
other compounds. Fats and oils also contain other minor components,
such as polynuclear aromatic hydrocarbons (PAHs). Like vegetable oils
and animal fats, petroleum crude oils are hydrocarbon mixtures that can
be further processed to make specific products; but the hydrocarbon
constituents of petroleum oils are primarily alkanes (paraffins),
cycloalkanes, and aromatic hydrocarbons (IARC, 1989).
Fatty acids largely determine the chemical and physical properties
of triglycerides (Hui, 1996a) and influence their fate and effects in
the environment. The structure of the fatty acids can change as they
are processed, stored, heated, or transformed by physical, chemical,
and biological processes in the environment. The fatty acid composition
of vegetable oils and
[[Page 54512]]
animal fats varies with plant or animal species, season, geographical
location, feed, and other factors.
The physical and chemical properties of petroleum and non-petroleum
oils can change after they have spilled into the environment. Spilled
oil can be transformed through a wide variety of physical, chemical,
and biological processes (USDOC/NOAA, 1992a, 1996). These processes are
affected by many factors, among them temperature, oxygen, light,
ionizing radiation, and the presence of metals (Kiritsakis, 1990; Hui,
1996a, 1996d).
As the composition of the oil changes, so does its fate in the
environment and its toxicity. The products that are formed can be more
or less toxic than the original oil, depending on the specific oil and
the products that are formed. Oxidation of vegetable oils and animal
fats, which may contribute rancid off-flavors and odors, can create
products, such as cyclic monomers and oxycholesterols that are toxic at
relatively low concentrations (Hui, 1996a). Polymers of soybean oil and
sunflower oil can form concrete-like aggregates with soil or sand that
cannot be readily degraded by bacteria and remain in the environment
for many years after they are spilled (Minnesota, 1963; Mudge, 1995,
1997a, 1997b). Petroleum oils also undergo oxidation and polymerization
reactions and can form tars that persist in the environment for years
(NAS, 1985d).
4. Environmental Effects
Spills of petroleum and vegetable oils and animal fats can harm
aquatic organisms and wildlife in many ways (Crump-Wiesner and
Jennings, 1975):
Oil can coat the feathers and fur of birds and mammals and
cause drowning and hypothermia and increased vulnerability to
starvation and predators from lack of mobility.
Oils can act on the epithelial surfaces of fish,
accumulate on gills, and prevent respiration. The oil coating of
surface waters can interfere with natural processes of reaeration and
photosynthesis. Organisms and algae coated with oil may settle to the
bottom with suspended solids along with other oily substances that can
destroy benthic organisms and interfere with spawning areas.
Oils can increase BOD and deplete water of oxygen
sufficiently to kill fish.
Oils can cause starvation of fish and wildlife by coating
food and removing the food supply. Animals that ingest large amounts of
oil through contaminated food or preening themselves may die as the
result of the oil ingested. Animals can also starve because of
increased energy demands needed to maintain body temperature when they
are coated with oil.
Oils can exert a direct toxic action on fish, wildlife, or
their food supply.
Oils can taint the flavor and cause intestinal lesions
from laxative properties in fish.
Oils can foul shorelines and beaches. Oil spills can also
create rancid odors.
The environmental effects of vegetable oils and animal fats and
petroleum oils, their chemical and physical properties, and their
environmental fate are compared in Appendix I, Table 2.
a. Physical Effects of Spilled Oil. Physical effects produce nearly
all of the most immediate and devastating environmental effects from
oil spills. Even oils that remain in the environment for relatively
short periods of time can cause long-term deleterious effects years
after the oil was spilled.
Coating with Oil. Among the immediate effects of oil spills is the
coating of the feathers of birds and fur of mammals (Hartung, 1995).
Coating of animals and their food supply is produced by spills of
petroleum and non-petroleum oils alike. Birds and some mammals, such as
sea otters and river otters that depend upon entrained air for buoyancy
and insulation, are particularly vulnerable to harm from spills of non-
petroleum and petroleum oils (NAS, 1985e; Hartung, 1967, 1995). In
freshwater or tidal brackish waters, oiled birds are usually waterfowl
and wading birds, such as herons (Alexander, 1983).
Birds and mammals become coated with oil when they land in an oil
slick or surface from underneath (Hartung, 1995). Oil alters the
structure and function of the feathers and fur by disrupting their
orderly arrangement, thereby reducing entrainment of air and causing
loss of buoyancy and thermal insulation (Rozemeijer, 1992; Leighton,
1995; Frink and Miller, 1995; NAS, 1985e; Alexander, 1983; Hartung,
1967, 1995; Crump-Wiesner and Jennings, 1975). As the plumage absorbs
water, the weight and body mass of the birds increases, and the birds
sink and may drown. Birds and mammals, with feathers or fur matted down
by petroleum or non-petroleum oils, can also die from hypothermia and/
or dehydration and diarrhea or fall victim to predators.
Birds that are able to endure excess chilling while avoiding their
predators may reach shore and sit or stand in a state of shock (NAS,
1985e; Alexander, 1983). To maintain body temperature, such birds would
have to eat twice the normal amount of food; yet they are often
isolated from their food supply (Hartung, 1967, 1995; Alexander, 1983).
Fat and muscular energy reserves of these birds are rapidly exhausted
and their body temperature drops (Hartung, 1967; Croxall, 1977;
Alexander, 1983; Rozemeijer et al., 1992). As their appetite declines,
death from starvation ensues. Similarly, sea otters with fur coated
with oil require increased metabolism to compensate for major changes
in conductance and heat flow across the body surface (Hartung, 1967,
1995; Kooyman, 1977; Williams et al., 1990; NAS, 1985e).
Oiled birds tend to preen their feathers and may ingest large
amounts of oil from attempting to clean themselves and from consuming
oil-contaminated food and oil particles (Frink, 1994; Frink and Miller,
1995; Alexander, 1983; NAS, 1985e; Hartung, 1965, 1967, 1995). Bird
rescuers have described dead birds with organs filled with oil from
eating oiled food (Lyall, 1996; Frink and Miller, 1995). Oil can also
be transferred to birds through consumption of fouled prey or direct
contact with the oiled shoreline or surface water (Frink and Miller,
1995; Smith and Herunter, 1989). The coated birds that are observed
after oil spills are probably a small proportion of the total affected,
as weakened birds are likely victims of predators (Hartung, 1995;
Alexander, 1983; NAS, 1985e; Lyall, 1996; Frink and Miller, 1995;
McKelvey et al., 1980; Smith and Herunter, 1989; Minnesota, 1963).
Small spills of vegetable oil, animal fat and petroleum oils can
cause great ecological damage, depending upon the location of the spill
and other factors. Even a small spill of vegetable oil can be far more
damaging to aquatic birds than certain petroleum oils (McKelvey et al.,
1980; Smith and Herunter, 1989).
Suffocation. Suffocation and death of fish and other biota are
often the consequence of oxygen depletion of the water. Oxygen
depletion can result from reduced oxygen exchange across the air-water
surface below the spilled oil or from the high BOD produced by microor
ganisms degrading oil (Crump-Wiesner and Jennings, 1975; Mudge, 1995).
While a higher BOD is associated with greater biodegradability, it also
reflects the increased likelihood of oxygen depletion and potential
suffocation of aquatic organisms under certain environmental conditions
(Crump-Wiesner and Jennings, 1975). Oxygen depletion and suffocation
are produced by petroleum and non-petroleum oils, including animal fats
and vegetable oils. Under certain conditions, however, some vegetable
oils and animal fats
[[Page 54513]]
present a far greater risk to aquatic organisms than other oils spilled
in the environment, as indicated by their greater BOD.
According to studies designed to measure the degradation of fats in
wastewater, some food oils exhibit nearly twice the BOD of fuel oil and
several times the BOD of other petroleum-based oils (Groenewold, 1982;
Institute, 1985; Crump-Wiesner and Jennings, 1975). While the higher
BOD of food oils is associated with greater biodegradability by
microorganisms using oxygen, it also reflects the increased likelihood
of oxygen depletion and suffocation of aquatic organisms under certain
environmental conditions (Groenewold, 1982; Institute, 1985; Crump-
Wiesner and Jennings, 1975). Oil creates the greatest demand on the
dissolved oxygen concentration in smaller water bodies, depending on
the extent of mixing (Crump-Wiesner and Jennings, 1975).
Contamination of Eggs. After spills of non-petroleum and petroleum
oils, oil can be transferred from birds' plumage to the eggs they are
hatching. Petroleum and non-petroleum oils, including vegetable oils
and animal fats, can smother an avian embryo by disrupting the egg/air
interface, sealing pores, and preventing gas exchange (Albers, 1977;
Szaro and Albers, 1977; Leighton, 1995; USDOI, 1994).
In addition to the severe physical effects produced by non-
petroleum and petroleum oils, some petroleum oils can also damage
embryos apparently through mechanisms of toxicity (Albers, 1977; Szaro
and Albers, 1977; Leighton, 1995; Szaro, 1977; NAS, 1985e). Very small
quantities of petroleum or crude oil cause mortality and developmental
effects in avian embryos from a wide variety of species (Leighton,
1995; NAS, 1985c). Whether vegetable oils and animal fats can harm
embryos through toxicity as well as physical effects is unknown, for no
studies of the toxicity of vegetable oils and animal fats to avian
embryos and developing birds were located.
b. Effects of Oil on Metabolic Requirements. To survive spills of
petroleum and non-petroleum oils, animals require increased energy
(NAS, 1985e; Hartung, 1967, 1995). Birds coated with oil must eat twice
their food ration to maintain body temperature (Hartung 1967, 1995).
Yet birds are often isolated from their food sources following an oil
spill or find their food coated with oil (Hartung 1967, 1995).
Sublethal effects can increase vulnerability to disease or decrease
growth and reproductive success, although the individual may continue
to live for some time (NAS, 1985e; Frink and Miller, 1995; Smith and
Herunter, 1989).
Studies of polluted animals show that physiological stress is
manifested in higher energy demand (Sanders et. al., 1980). When
increasing environmental stress greatly elevates metabolism and reduces
assimilation, little energy remains for growth and reproduction, so
that most species disappear and only a few tolerant species survive in
chronically polluted environments. Oil pollution also forces animals to
turn from the most economical biochemical pathways to other more costly
physiological pathways.
c. Effects of Oil on Food and the Food Web, Communities, and
Ecosystems. The effects of oil on the food web and community structures
depend on the type and amount of oil spilled, the physical nature of
the area, nutritional status, oxygen concentration, and previous
exposure of the impacted area (NAS, 1985e). Geographic location appears
far more important in determining the impacts of oil spills than spill
size (Frink and Miller, 1995; McKelvey et al., 1980). The community
structure and activities of microbes that degrade petroleum oil are
affected by both catastrophic and chronic spills. The risks from oil
spills can be shifted from those associated with toxicity to those
associated with habitat, e.g., predator-prey interaction (NAS, 1985e).
The vulnerability of species and individuals to oil spills varies
greatly (NAS, 1985e), and the extent and rate of recovery depends on
many factors. In enclosed waters where recruitment of organisms from
outside becomes less important, intrinsic factors may limit the
recovery of the zooplankton community. Plant communities too can be
affected long after an oil spill, with imbalances persisting for a
decade or more, even after the floral community is reestablished
(Sanders et al., 1980). When diversity and density have increased and
stabilized many years after a spill, behavioral responses may continue
to be distorted or biochemical pathways may be shifted from efficient
to more costly pathways.
d. Indirect Effects. While not generally regarded as classic
``toxicity,'' high levels of fatty acids and triglycerides from
vegetable oils and animal fats can upset the fermentation and digestion
of ruminants, such as cattle, goats, deer, antelope, sheep, moose,
buffalos, and bighorn sheep (Van Soest, 1994). Although intake of
normal levels of lipids does not affect fermentation in ruminants,
excess unsaturated fatty acids and triglycerides can profoundly
suppress essential fermentation bacteria and alter fermentation
balance, lipid metabolism, and milk fat production. Methane suppression
is likely with a single large dose of unsaturated oil that exceeds the
threshold of tolerance by fermentation bacteria. A practical limit for
fat of about 8-10% of dietary dry matter is expected (personal
communication, D. Ullrey, 1996).
Indirect effects also occur when petroleum oil is spilled in the
environment (NAS, 1985e). After a spill of number 5 fuel oil, the
herring population was reduced because of increased fungal damage to
fish eggs, which in turn resulted from a decreased population of
amphipods which graze fungi growing on fish eggs.
5. Toxicity
Adverse effects occur through both non-toxic and toxic mechanisms.
Whether an adverse effect occurs through toxicity or other mechanisms
is often unknown (Yannai, 1980). For example, birds exposed to spilled
oil may die from non-toxic mechanisms --starvation, hypothermia,
drowning, shock, susceptibility to predators because of a food supply
that is inadequate to support increased energy requirements, and
consumption of oiled food or oil from preening that clogs their
organs-- or from the toxicity of chemicals or biotransformation
products in the oil. The deaths of the birds occur, regardless of the
mechanisms involved or knowledge about these mechanisms.
Toxicology is the study of the adverse effects of chemicals on
living organisms, including lethality; reproductive effects; effects on
development; cancer; effects on the nervous system, kidney, liver,
immune system, or other organs; and biochemical effects, such as enzyme
inhibition (Klaassen et. al., 1986; Rand and Petrocelli, 1985). To
examine the nature of toxic effects and evaluate the probability of
their occurrence, factors that affect toxicity must be known. A brief
discussion of toxicity is presented below. The supporting Technical
Document discusses toxicology in greater depth.
a. Principles of Toxicology. The toxicity of chemicals depends on
factors that are related to the organism itself, chemical composition,
external environmental factors, and the exposure situation. The
necessity of considering many factors in the evaluation of toxicity is
underscored in basic textbooks about toxicology, such as Casarett and
Doull's Toxicology that state:
``* * * Whether or not a toxic response occurs is dependent * *
* on the chemical
[[Page 54514]]
and physical properties of the agent, the exposure situation, and
the susceptibility of the biologic system or subject. Thus to
characterize fully the potential hazard of a specific chemical
agent, we need to know not only what type of effect it produces and
the dose required to produce the effect but also information about
the agent, the exposure, and the subject * * *'' (Amdur et al.,
1991).
The hazards and risks from environmental exposures to chemicals are
assessed with toxicological studies in the laboratory and with
epidemiological studies, while field studies may be used to assess the
ecological effects of chemicals on multiple species or ecosystems (NAS,
1985c; NAS, 1977a; OSTP, 1985; Rand and Petrocelli, 1985). Toxic
chemicals enter the body primarily by ingestion, inhalation, and skin
contact (Klaassen et al., 1986). The toxic effects from acute exposure
to a chemical (e.g., a single dose during a short period of time such
as 24 hours) may differ greatly from those produced by long-term
(chronic) exposures. Toxic effects can be immediate or they can be
delayed.
A substance that is harmless at low concentrations in food may be
hazardous if it comprises a large portion of the diet. Because there is
little margin of safety for many of the elements to which people are
exposed daily, the daily intake of many elements in the diet, such as
iron, could not be increased 5 or 10 times without adverse effects
(Klaassen et al., 1986).
b. Exposure From Oil Spills. Spills of petroleum and vegetable oils
and animal fats during processing, storage, and transportation can
result in acute or chronic exposures to fish and wildlife. Not only
massive spills but small quantities that are spilled repeatedly may
result in environmental harm (Alexander, 1983; McKelvey et al., 1980;
Smith and Herunter, 1989). Small volume spills can produce severe
environmental damage because of the behavior of oils in the
environment, their physical effects, and the toxicity of some oil
constituents and transformation products. Many of the immediate,
devastating effects of spilled petroleum and vegetable oils and animal
fats, such as coating, suffocation, and other physical effects, occur
during acute exposures. Long-term effects have also been reported from
spills of petroleum oil, vegetable oils and animal fat.
During an oil spill, the potential for significant exposures is
very high (Hartung, 1995). Unlike laboratory experiments using
controlled amounts of oil, large amounts of oil may be released during
spills. While the initial mortalities of birds and mammals exposed to
spilled oil are usually from drowning or hypothermia resulting from
coating, the ingestion of oil begins to contribute to effects later as
birds consume large amounts of oil through preening or ingestion of
oil-contaminated food and oil particles (Hartung, 1967, 1995). Fish and
other aquatic organisms may die from suffocation soon after an oil
spill or exhibit toxic effects, including cancer and adverse effects on
growth and reproduction, following acute or chronic exposures to
spilled oils and fats or their breakdown products.
Spilled oil can be transformed through a wide variety of physical,
chemical, and biological weathering processes that change oil
composition, behavior, exposure routes, and toxicity (USDOC/NOAA 1992,
1996). Whether the environmental fate and toxicity of the
transformation products differs from that of the parent depends upon
the specific oil and products that are formed.
c. Toxicity of Petroleum Oils. The toxic effects of petroleum oils
are summarized in Appendix I, Table 2. The effects of petroleum oils
have been investigated extensively in many species (NAS, 1985e; IARC,
1984; Albers, 1995). Commonly reported individual effects of petroleum
oils include impaired reproduction and reduced growth as well as death
in plants, fish, birds, invertebrates, reptiles and amphibians; blood,
liver, and kidney disorders in fish, birds, and mammals; malformations
in fish and birds; altered respiration or heart rate in invertebrates,
fish, reptiles, and amphibians; altered endocrine function in fish and
birds; altered behavior in many animal species; hypothermia in birds
and mammals; impaired salt gland function in birds, reptiles, and
amphibians; altered photosynthesis in plants; and increased cells in
gills and fin erosion in fish. Among the group effects of petroleum are
changes in local population and community structure in plants,
invertebrates and birds and changes in biomass of plants and
invertebrates.
Petroleum oils affect nearly all aspects of physiology and
metabolism and produce impacts on numerous organ systems of plants and
animals as well as altering local populations, community structure, and
biomass (Albers, 1995; NAS, 1985e). Impaired reproduction, reduced
growth and development, malformations, behavioral effects, blood and
liver and kidney disorders, altered endocrine function, and a host of
other effects of petroleum oils on organisms have been reported.
Certain petroleum products and crude oil fractions are associated
with increased cancer in refinery workers and laboratory animals (IARC,
1989). Many of these petroleum oils contain benzene and polynuclear
aromatic hydrocarbons (PAHs), toxic constituents that are carcinogenic
in humans and animals. Untreated and mildly treated mineral oils are
carcinogenic to humans. In experimental animals, some distillates and
cracked residues derived from the refining of crude oil and residual
(heavy) fuel oils are carcinogenic. There is limited evidence in
experimental animals for the carcinogenicity of unleaded automotive
gasoline, fuel oil number 2, crude oil, and naphtha and kerosene
produced by certain processes.
d. Toxicity of Vegetable Oils and Animal Fats. The toxicity of
vegetable oils and animal fats and the toxic effects on many systems
and organs in the body are summarized in Appendix I, Table 2 and
described briefly below. A detailed discussion of these effects is
included in the supporting Technical Document.
The acute and chronic toxicity of vegetable oils and animal fats,
types of fats, and their components and degradation products have been
evaluated in toxicology and epidemiological studies. Chemical and
physical properties of the particular animal fat or vegetable oil, the
exposure situation, the biologic systems exposed, and the environmental
conditions that are present are factors that influence the toxicity of
a chemical.
Acute lethality tests are among several measures used to evaluate
acute toxicity. They can be employed to rank chemicals or to screen
doses that may be selected for longer term toxicity testing, or they
can be an early step in tiered hazard assessment approaches. The use of
different protocols and test species in acute lethality tests makes
comparisons between tests difficult. For example, although the
Petitioners claim that the tests conducted by Aqua indicate that
smaller amounts of petroleum oils than certain vegetable oils and
animal fats kill half the population of some aquatic species; other
acute lethality studies suggest that by one measure, vegetable oils are
more toxic than petroleum-derived mineral oil. In studies comparing the
acute lethality of corn oil, cottonseed oil, and petroleum-derived
mineral oil in albino rats, no rats receiving mineral oil died, while
smaller doses of the vegetable oils administered for a shorter time
period killed rats (Boyd, 1973).
Vegetable oils and animal fats produce other types of acute
toxicity as well. Like petroleum oils, vegetable oils
[[Page 54515]]
and animal fats are laxatives that can produce diarrhea or cause lipid
pneumonia in animals. These effects can compromise the ability of
animals in the wild to escape their predators (USDOI, 1994; Frink,
1994). Clinical signs of toxicity in rats fed large amounts of corn oil
or cottonseed oil for 4 or 5 days include decreased appetite, loss of
body weight, abnormal lack of thirst, diarrhea, fur soiling,
listlessness, pale skin, incoordination, cyanosis (dark blue skin color
from deficient oxygenation of the blood), and prostration, followed by
respiratory failure and central nervous system depression, hypothermic
coma, and death. Autopsies of the rats showed violent local irritation
of the gastrointestinal tract, which allowed the absorption of oil
droplets into the bloodstream and deposition of oil in tissues,
resulting in inflammation, congestion in the blood vessels,
dehydration, degenerative changes in the kidney, loss of organ weights,
and stress reaction (Boyd, 1973).
Animals exposed to vegetable oils and animal fats can manifest a
range of chronic toxic effects. High levels of some types of fats
increase growth and obesity but cause early death in several species of
animals and may decrease their reproductive ability or the survival of
offspring (NAS/NRC, 1995). On the other hand, the growth of some fish
decreases with elevated levels of vegetable oils (Salgado, 1995; Mudge
1995, 1997a). Mortality of mussels exposed to one of four vegetable
oils began after 2 or 3 weeks of exposure. Growth inhibition, effects
on shells and shell lining, and decreases in foot extension activity
that are essential to survival were observed in mussels exposed to low
levels of sunflower oil.
Dietary fat consumption has been associated with the incidence of
some types of cancer, including mammary and colon cancer, in laboratory
animals and humans (Hui, 1996a; USDHHS, 1990; FAO/WHO, 1994). The
intake of dietary fat or certain types of fat has also been correlated
with the incidence of coronary artery disease, diabetes, and obesity in
epidemiological studies (Hui, 1996a; FAO/WHO, 1994; Nelson, 1990; Katin
at al, 1995). High dietary fat intake has also been linked to reduced
longevity and altered reproduction in laboratory animals and altered
immunity, altered steroid excretion, and effects on bone modeling and
remodeling in humans.
Some vegetable oils and animal fats contain toxic constituents,
including specific fatty acids and oxidation products formed by
processing, heating, storage, or reactions in the environment (Hui,
1996a; Berardi and Goldblatt, 1980; Yannai, 1980; Mattson, 1973). Toxic
effects on the heart, red blood cells, and immune system; effects on
metabolism; and impairment of reproduction and growth can be caused by
constituents or transformation products of vegetable oils and animal
fats. In addition, some constituents of vegetable oils and animal fats
cause cancer in rainbow trout, while lipid oxidation products may play
a role in the development of cancer and atherosclerosis (Hendricks at
al 1980a and 1980b).
Acute Toxicity: Acute Lethality Test (LC50 Test)
Submitted by Petitioners. The tests by Aqua that were submitted by the
Petitioners are acute lethality tests that measure only the death of
organisms. These tests provide no data on nonlethal acute toxicity,
including irreversible damage, or long-term effects experienced by
organisms and ecosystems. The LC50 (lethal concentration 50)
value or LD50 (lethal dose 50) value does not describe a
``safe'' level but rather a level at which 50% of test organisms are
killed under the experimental conditions of the test (Rand and
Petrocelli, 1985; Klaassen et al., 1986). (A high LC50 value
indicates low acute lethal toxicity, for a large concentration of
chemical is needed to cause 50% mortality.) If the Aqua test results
were accurate, they would indicate that diesel fuel kills half the
population of fathead minnows at lower concentrations than aerated
crude soybean oil, RBD soybean oil, and beef tallow. Spills of
petroleum oils, vegetable oils and animal fats that result in
LC50 concentrations in the environment could kill half the
organisms with sensitivity similar to fathead minnows when conditions
are identical to those in the Aqua tests.
Although the manner in which the Aqua tests were conducted
precludes accurate determination of the LC50 values, the
tests nevertheless demonstrate that petroleum oils and vegetable oils
and animal fats can injure and kill fish by toxicity or oxygen
depletion and suffocation. In the first set of the Aqua tests, all of
the minnows exposed to diesel fuel and unaerated crude soybean oil
died. The fish surfaced and gulped for air or swam spasmodically before
dying, just as they do in the environment when suffocating from oxygen
depletion following spills of petroleum and non-petroleum oils,
including vegetable oils and animal fats.
Results Questionable. However, the test procedures used by Aqua
render questionable the results suggesting that diesel fuel is more
deadly at lower concentrations than soybean oil. The procedures deviate
in important ways from standardized methodology, although the Aqua
report states that test procedures are based on accepted methodologies.
Appendix I, Table 3: Comparison of Aqua Methods and Standard Acute
Aquatic Testing Methods lists key differences between the methods used
by Aqua and the standard methods referenced in the Aqua report as well
as more recent methods published by these same organizations that were
omitted from the Aqua report. The accuracy of the LC50
estimates provided by Aqua is highly doubtful because of the following
deficiencies:
Oxygen depletion. In the first set of Aqua tests,
dissolved oxygen was below acceptable levels in the vessels with crude
soybean oil. It is impossible to determine whether oxygen depletion or
toxicity killed fish.
Short exposure period. The Aqua tests were conducted for
only 48 hours, instead of the 96 hours used in most methods. Fish that
are alive at 48 hours may not survive for 96 hours.
Unknown concentrations of test material encountered by
fish during the test: (1) Oil sheens floated on test solutions and
cloudiness was so severe that fish could not be observed for 24 hours;
(2) the Aqua report contained no data on actual chemical concentrations
of parent chemical or breakdown product, a critical determination in
static tests where concentrations change over time (Rand and
Petrocelli, 1985; NAS, 1985c). Aqua relied instead on the original
nominally designated concentrations that are highly dubious, especially
given the turbidity of the test solutions that cleared up over the
course of the test, the likely degradation of test material in the
aerated test system, and the use of vessels that were not stainless
steel or glass and may have adsorbed test material; (3) the Aqua test
did not aerate all test solutions and controls, did not maintain
dissolved oxygen concentration at 80% or more of the nominal
concentration, and did not test non-aerated and aerated oils together--
requirements of standardized methods that allow gentle aeration. If
vegetable oils degrade rapidly, as Petitioners claim elsewhere,
aeration will increase the degradation of the oils in the test system;
(4) the Aqua report provided no data on oil particle size, even when
visual inspection showed that solutions of test material were cloudy
and the NAS study referenced in the report cautioned against relying on
visual inspections of clarity (NAS, 1985c); and (5) improper data
reporting and evaluation. Results from two dissimilar tests were
combined, although the tests
[[Page 54516]]
lacked a common test substance, used different test conditions, failed
to measure actual concentrations, and included no estimates of
variability between the two sets of tests. Aqua also failed to provide
data on confidence intervals and slopes, as required by all of the
standardized methods referenced by Aqua and by the Aqua protocol.
Relevance of Acute Lethality Tests to Spills in the Environment
Challenged. Serious questions remain about the relevance of the
LC50 laboratory results to spills in the environment (NAS,
1985c, 1985e). The many test variables that influence estimates of
LC50--including the nature of the chemicals or mixtures
tested, test parameters (e.g., route and method of administration,
frequency and duration of exposure, mixing energy, temperature,
salinity, static vs. flow-through systems, duration of observations)
and biological factors (e.g., species selected for testing, sex, age or
life-stage, weight, contamination history of the organism)--rarely
reflect the conditions that occur following a spill (Rand and
Petrocelli, 1985; NAS, 1985c; Wolfe, 1986; Abel, 1996). The water-
soluble fraction used in static tests does not simulate the dynamic
process of the change in stages between aqueous and oil phases that
depends on parameters unique to each spill (NAS, 1985c). Once oil is
spilled in the environment, the composition, concentration, and
toxicity of oil and its components can be profoundly altered by
chemical and biological processes, such as evaporation and biological
oxidation.
Further, acute lethality tests by their very nature usually provide
no data on toxic effects other than death (NAS, 1985c; Rand and
Petrocelli, 1985; Klaassen et al., 1986). Indeed, a widely-used
toxicology text warns that ``defining acute toxicity based only on the
numeric value of an LD50 is dangerous'' (Hayes, 1982).
Animals that survive a toxic response nevertheless may suffer
irreversible damage (NAS, 1985e). These nonlethal, adverse effects must
be considered in assessing the risks of chemical exposure. Nor do acute
lethality tests measure long-term effects or effects on ecological
communities or changes in predator-prey relationships which occur, for
example, when animals coated with spilled oil are weakened and become
more susceptible to predators.
Acute Toxicity: Other Acute Lethality Tests (Aquatic Tests). (See
Appendix I, Table 2, for other aquatic lethality information.) Free
fatty acids are among the products formed from vegetable oils and
animal fats by processing, storage, heating, or reactions in the
environment. Static tests with juvenile fathead minnows indicate that
oleic acid, which is found in Canola, safflower, and sunflower oils, is
more acutely lethal at 96 hours than at 24 hours and is intermediate in
lethality in tests of a series of 26 organic compounds (USEPA, 1976;
Hui, 1996a).
Acute Toxicity: Other Acute Lethality Tests (Tests with Laboratory
Animals). (See Appendix I, Table 2.) Studies comparing the acute
lethality of corn oil, cottonseed oil, and mineral oil in albino rats
show that by one measure cottonseed oil and corn oil are more toxic
than petroleum-derived mineral oil, although interpretation of the
studies is complicated by differences in the experimental protocol
(Boyd, 1973). No albino rats receiving mineral oil by gavage (tube into
stomach) for 15 days died, while smaller doses of cottonseed oil and
corn oil administered for a shorter time period killed rats.
The toxic effects differed significantly in rats receiving corn oil
or cottonseed oil and those administered mineral oil (Boyd, 1973).
Clinical signs of toxicity in rats receiving corn oil or cottonseed oil
included anorexia (decreased appetite), loss of body weight, abnormal
lack of thirst, decreased urination, diarrhea, fur soiling,
listlessness, pallor (pale skin), incoordination, cyanosis (dark blue
skin color from deficient oxygenation of the blood), and prostration
(Boyd, 1973). Rats administered corn oil died after respiratory failure
and hypothermic coma, while death followed central nervous system
depression and coma in rats ingesting cottonseed oil. Autopsies showed
violent local irritation of the gastrointestinal tract that allowed the
absorption of oil droplets into the bloodstream. Oil droplets were
deposited in many body organs with resultant inflammation, vascular
congestion, degenerative changes in the kidney, and other effects. In
contrast, no deaths occurred among rats administered mineral oil for 15
days and clinical signs differed in many respects from those observed
in rats treated with corn or cottonseed oil.
Chronic Toxicity. Appendix I, Table 2 summarizes the chronic
toxicity of vegetable oils and animal fats and petroleum oils. Cancer
and adverse effects on growth, reproduction, development, and longevity
as well as other toxic effects have been observed in several species
following chronic or subchronic exposures to vegetable oils and animal
fats or their constituents. (Subchronic exposures are longer than acute
exposures, generally 1-3 months for rodents and longer than 4 days for
aquatic species.)
Dietary fat and some classes of fats that are found in vegetable
oils and animal fats have been associated with the increased incidence
of some types of cancer, including mammary and colon cancer, in
laboratory animals and humans (Hui, 1996a; USDHHS, 1990; FAO/WHO,
1994). The intake of dietary fat or of certain types of fat has also
been correlated with the incidence of coronary artery disease,
diabetes, and obesity in epidemiological studies. High dietary fat
intake has also been linked to reduced longevity and altered
reproduction in laboratory animals and altered immunity, altered
steroid excretion, and effects on bone modeling and remodeling in
humans.
In addition, some vegetable oils and animal fats contain toxic
constituents or form toxic degradation products, including specific
fatty acids and oxidation products, when they undergo processing,
heating, storage, or reactions in the environment. The toxic effects of
these chemicals are summarized briefly in Appendix I, Table 2 and
described further in section II.5.d Toxicity of Specific Fatty Acids
and Other Constituents of Vegetable Oils and Animal Fats. Among the
toxic effects observed after exposure to these chemicals are cardiac
toxicity, rupture of red blood cells, growth suppression, anemia,
impaired reproduction, and adverse effects on the immune system and
metabolism. In addition, the cyclopropene fatty acid constituents of
cottonseed oil and some other vegetable oils cause liver cancer in
rainbow trout and increase carcinogenesis of other chemicals, and some
oxidation products may play a role in the development of colon cancer
and atherosclerosis.
Cancer. Unlike petroleum oils that contain a large proportion of
PAHs, including some PAHs that are animal and/or human carcinogens,
vegetable oils and animal fats contain only small amounts of PAHs
(Kiritsakis, 1991; IARC, 1984). Dietary fat intake and consumption of
some classes of fats that are found in vegetable oils and animal fats
have been implicated in the development of certain types of cancer--
including cancer of the breast and colon and probably cancer of the
prostate and pancreas--in studies of laboratory animals and in
epidemiological studies (NAS/NRC, 1985c; Hui, 1996a; USDHHS, 1990; FAO/
WHO, 1994). An expert panel organized by two United Nations
organizations concluded that abundant data show that animals fed high-
fat diets develop tumors of the mammary gland, intestine, skin, and
pancreas more readily than animals fed low-fat diets, although caloric
restriction can override
[[Page 54517]]
the effect (WHO/FAO, 1994). Animal studies also indicate correlations
between total fat intake and liver cancer and between high-fat diets
and certain types of chemically-induced or light-induced skin tumors.
Studies describing the relationships between fat consumption and cancer
in animals and humans have been summarized recently (Hui, 1996a).
Development of some types of cancer is influenced by the type of
fat consumed. Breast cancer increased (shortened latency period for
tumor appearance, promotion of growth, and increased mammary tumor
incidence) in rodents receiving diets rich in the essential fatty acid
linoleic acid (polyunsaturated fatty acid or PUFA of the n-6 family)
compared to rodents consuming diets high in saturated fatty acids (Hui,
1996a). In contrast, fish oil containing different fatty acids (n-3
PUFA) inhibited mammary tumor development, probably by inhibiting the
effects of linoleic acid. The incidence of colon cancer is strongly
associated with diet, especially diets high in total fat and low in
fiber content in laboratory animals and epidemiological studies (Hui
1996a; USDHHS, 1990). Some types of fat, such as dietary cholesterol
and certain long-chain fatty acids, have been proposed as colon cancer
promoters, while other types of fat (n-3 PUFA) may inhibit development
of colon cancer (Hui, 1996a).
Non-Carcinogenic Toxic Effects. The non-carcinogenic toxic effects
of vegetable oils and animal fats on aquatic organisms and laboratory
animals are summarized in Appendix I, Table 2, briefly described below
and are discussed in greater detail in the Technical Document.
Non-Carcinogenic Toxic Effects on Mussels. The detrimental
environmental effects of sunflower oil have been investigated
extensively in laboratory studies and in the field at the site of the
1991 wreck of the cargo tanker M.V. Kimya, where much of its 1500-tonne
cargo of crude sunflower oil was spilled over a 6-9 month period (Mudge
et al., 1993, 1994, 1995; Mudge, 1995, 1997b; Salgado, 1992, 1995).
Mussels died in the intertidal shores at sites near the wreck; in other
areas where mussels survived, their lipid profiles revealed an altered
fatty acid composition reflecting the fatty acids in sunflower oil
(Mudge et al., 1995; Mudge, 1995, 1997a, 1997b; Salgado, 1992, 1995).
Mobile species that left the spill area were replaced with other
species, affecting diversity.
Sunflower oil, olive oil, rapeseed oil, and linseed oil produced
several types of adverse effects in mussels at low exposure rates in
the laboratory (Salgado, 1995; Mudge, 1995; Mudge, 1997a). These four
vegetable oils killed mussels or reduced their growth rate as much as
fivefold within 4 weeks, even at low exposure rates (1 part of oil in
1000 in a flow-through sea water system). Mussels exposed to sunflower
oil were more likely to die. Exposure to sunflower oil created
behavioral differences in the mussels, such as decreased foot extension
activity and altered gaping patterns. Interference with foot extension
activity that allows the mussels to form threads for attachment to the
substratum can dislodge mussels and endanger their survival; removal of
the oil reversed the effect (Salgado, 1995).
All four oils killed mussels in mortality studies in the
laboratory; 10% mortality was observed in mussels exposed to sunflower
oil, rapeseed oil, or olive oil for up to 4 weeks, while 70% or 80%
mortality was reported when mussels were exposed to linseed oil
(Salgado, 1995; Mudge, 1997b). No control mussels died. Mussels began
dying the second week after exposure to linseed or sunflower oil, and
later when exposed to rapeseed or olive oil. Death may have been caused
by suffocation in mussels that refused to gape in the presence of the
oil or by formation of a toxic metabolite. The death of mussels in
aerated growth tanks where anoxia (lack of oxygen) was not the cause of
death suggests that vegetable oils kill mussels through mechanisms of
toxicity.
The shells of mussels exposed to the vegetable oils in the
laboratory lacked the typical nacre lining, perhaps because of altered
behavior in the presence of oil stressors (Salgado, 1995; Mudge,
1997a). The internal shell surfaces of mussels treated with vegetable
oils were chalky in contrast to controls that exhibited an iridescent
luster. Prolonged closure of the mussels in response to oil can cause
anoxia and increase the acidity of the internal water with dissolution
of the inner shell.
Sunflower oil from the wreck of the M.V. Kimya polymerized in water
and on sediments and formed hard ``chewing gum balls'' that washed
ashore over a wide area or sank, contaminating the sediments inhabited
by benthic and intertidal communities near the spill (Mudge, 1995).
Concrete-like aggregates of sand bound together with sunflower oil
remain on the shore near the site of the M.V. Kimya spill almost six
years later (Mudge, 1995, 1997a, 1997b; Mudge et al., 1995). In
laboratory experiments with saltmarsh sediments simulating a spill over
a 35-day period, linseed oil percolated rapidly through the sediments
but sunflower oil polymerized and formed an impermeable cap, reducing
oxygen and water permeability (Mudge et al., 1995; Mudge, 1997a). In
the environment, oxygen reduction would eventually produce anoxia in
sediments with the death and removal of benthic organisms, changes in
species from a community that is aerobic to an anaerobic community, and
erosion of the saltmarsh sediments (Mudge et al., 1994, 1995).
Non-Carcinogenic Toxic Effects on Fish. Other studies have also
shown that exposure to an excess of fat or fatty acids can be
detrimental to fish, even though fish and other aquatic organisms
require certain essential fatty acids for growth and survival. Poor
growth and low feed efficiency were observed in rainbow trout fed 4% or
more of certain polyunsaturated acids (Takeuchi and Watanabe, 1979).
High levels of dietary fatty acids reduced growth in channel catfish;
while saturated, monounsaturated, or PUFA from fish oil enhanced
channel catfish growth (Stickney and Andrews, 1971, 1972). Some dietary
fatty acids inhibited the growth of common carp, but saturated and
monounsaturated acids and other classes of polyunsaturated fatty acids
from fish oil enhanced carp growth (Murray et al., 1977). More recent
papers show the relatively efficient use of high levels of dietary
lipid by warmwater and coldwater fishes, provided essential fatty acid
requirements are met (NAS/NRC, 1981a, 1983). Increased lipid intake,
however, has been associated with increased deposition of body fat.
Non-Carcinogenic Toxic Effects on Laboratory Animals. The chronic
toxic effects of petroleum oils and vegetable oils and animal fats on
laboratory animals are summarized in Appendix I, Table 2 and detailed
in the accompanying Technical Document. High levels of dietary fat have
been associated with shortened lifespan and altered reproduction in
laboratory animals (NAS/NRC, 1995). While 5% dietary fat is recommended
for most laboratory animals, growth usually increases significantly
when animals are fed higher levels of fat. Apparently, this increased
growth comes at a high cost, however, for longevity is often reduced
and reproduction may be affected adversely in animals consuming high
levels of fat.
The relationship between dietary fat intake and kidney diseases has
been demonstrated in laboratory animals (Hui, 1996a). Rats, rabbits,
and guinea pigs fed high cholesterol diets developed kidney damage.
Diets containing 2% cholesterol increased the
[[Page 54518]]
incidence or severity of coronary atherosclerosis in rats exposed
chronically to the cold (Sellers and Baker, 1960). Histological
aberrations in the small intestine and nearby lymph nodes have also
been reported in rats consuming high doses of fish oil concentrate in a
subchronic toxicology study (Rabbani et al., 1997).
Increasing the consumption of some dietary lipid components, such
as oleic acid and cholesterol, also increases the need for other fatty
acids in rats (NAS/NRC, 1995). The ratios of PUFA and polyunsaturated
to saturated fatty acids greatly influence tissue lipids and the
formation of important compounds, such as prostaglandins. The type of
fat can influence bone formation rates and fatty acid composition of
cartilage in chicks (Hui, 1996a).
Toxicity of Specific Fatty Acids and Other Constituents of
Vegetable Oils and Animal Fats. In addition to the adverse effects
produced in humans and other animals by high fat diets or by
consumption of certain classes of fats and oils, toxic effects can be
produced by constituents of some animal fats and vegetable oils,
including specific fatty acids and gossypol, and their transformation
products (Hui, 1996a; Berardi, 1980; Yannai, 1980; Mattson, 1973).
While plant breeding and processing can reduce the levels of some
constituents in the final product, the constituents are present during
the early stages of processing and storage of some vegetable oils and
may enter the environment. Although the development of varieties of
glandless, gossypol-free cottonseed and new varieties of rape seed with
little erucic acid have reduced these two constituents in some oils,
gossypol is found in crude oils and in oils derived from older
cottonseed varieties with greater resistance to disease and insects and
high amounts of erucic acid are contained in rapeseed oil used for the
manufacture of lubricants and fatty acid derivatives (Hui, 1996a,
1996b). Toxic materials can be formed during normal processing
procedures, heating, and storage or by reactions that occur when such
materials are released in the environment. Spills of crude vegetable
oils may differ greatly in their toxicity and other effects from spills
of processed vegetable oils and animal fats. Figure 1: Toxicity and
Adverse Effects of Components and Transformation Products of Vegetable
Oils and Animal Fats illustrates the variety of toxic effects that may
be caused by constituents and breakdown products of vegetable oils and
animal fats. For example, small amounts of gossypol are lethal when
they are ingested for prolonged periods despite the relatively high
LD50 values obtained in acute toxicity tests; fat
accumulated in heart muscle of weanling rats after a single day of
consuming diets containing erucic acid; and cyclopropene acids, such as
sterculic acid, are liver carcinogens in rainbow trout (Berardi, 1980;
Mattson, 1973; Hendricks et al., 1984). Phytoestrogens, which occur
naturally in some legumes and oils, including soybean, fennel, coffee,
and anise oils, exhibit estrogen-like activity in reproductive organs
of laboratory animals (Hui, 1996a; Sheehan, 1995; Levy et al., 1995).
When vegetable oils are spilled, air, moisture and heat in the
environment can cause these oils to form various harmful oxidation
products, which may be more toxic than the original product. Releases
of used oil from restaurants or releases of oil during refining may
already contain toxic oxidation products that may be further oxidized
in the environment. Cholesterol oxidation products or COPs that are
formed by autooxidation of cholesterol when it is exposed to air, heat,
photooxidation, and oxidative agents have numerous biological
activities and may play a role in the development of atherosclerosis
(Hui, 1996a). Lipid oxidation products (LOPs) that can be formed when
unsaturated fatty acids are oxidized upon exposure to oxygen, light,
and inorganic and organic catalysts have been associated with colon
cancer (Hui, 1996a; Hoffmann, 1989; Lawson, 1995).
Figure 1. Toxicity and Adverse Effects of Components and Transformation Products of Vegetable Oils and Animal
Fats
----------------------------------------------------------------------------------------------------------------
Component or transformation products Type of oil Effects
----------------------------------------------------------------------------------------------------------------
Gossypol 1,2,3 ......................... Cottonseed oil............. Cardiac irregularity in several species
of animals, death from circulatory
failure or rupture of red blood cells
and decreased oxygen-carrying capacity
in blood.
Discolors egg yolks in laying hens by
interacting with yolk iron; effect
decreased by ferrous sulfate, increased
by cyclopropene fatty acids in
cottonseed oil.
Crosslinks proteins in several species;
reduces protein quality, uncouples
respiratory-linked energy processes,
reduces activity of respiratory enzymes
and protein kinases and proteins
involved in sterol, steroid, and fatty
acid metabolism.
High LD50 in acute tests for mice and
swine, but small amounts are lethal when
ingested for prolonged period.
Death from pulmonary edema in subacute
poisoning; wasting and lack of
assimilation of food with chronic
poisoning.
Depressed appetite, loss of body weight,
diarrhea, effects on red blood cells,
heart and lung congestion, degenerative
changes in liver and spleen, various
pathological effects depending on
species.
Body weight depression, reduced sperm
production and motility in male rats;
loss of appetite, diarrhea, hair loss,
anemia, hemorrhages in stomach and
intestines, congestion in stomach,
intestines, lungs, and kidneys of rats.
Spastic paralysis of hind legs,
degeneration of sciatic nerve, rapid
pulse, cardiac effects in cats.
Posterior incoordination, stupor,
lethargy, weight loss, diarrhea,
vomiting, loss of appetite, lung and
heart congestion, hemorrhaging of liver,
fibrosis of spleen and gallbladder in
dogs.
Stupor, lethargy, loss of appetite,
spastic paralysis, decreased litter
weights, congestion of large intestine,
hemorrhaging in small intestines, lungs,
brain, and legs in rabbits.
[[Page 54519]]
Weight loss, decreased appetite, leg
weakness, reduced red blood cells,
congestion, vacuoles in liver, enlarged
gallbladder and pancreas, decreased egg
size, decreased egg hatchability,
discolored yolk in poultry.
Thumps or labored breathing, weakness,
emaciation, diarrhea, enzyme effects,
hair discoloration, dilated heart,
reduced hemoglobin, lipid in kidneys,
widespread congestion of organs in
swine.
Erratic appetite, breathing difficulties,
fatty degeneration of liver, decreased
blood clotting, and death in young
calves but no toxicity in older
ruminants.
No human toxicity in China, where
gossypol used as male contraceptive,
antifertility reversible.
Erucic Acid 2,4,5 ...................... Rapeseed oil, mustardseed Adverse effects on heart in laboratory
oil. animals; inflammation of heart in rat ,
fat deposition until fat content of
heart 3 to 4 times normal, fat droplets
visible in heart followed by mononuclear
cell infiltration and replacement of fat
and droplets with fibrous tissue in
muscle; weanling rats accumulated fat in
heart muscle after only one day; fatty
infiltration of heart absent with fully
hydrogenated rapeseed oil, indicating
effects from erucic acid; erucic acid in
heart muscle in rats exposed long-term;
changes in skeletal muscle in rats.
Lipid accumulation in hearts of rats,
hamsters, minipigs, squirrel monkeys and
ducklings; fluid accumulation around
heart and liver cirrhosis in ducklings.
Enlarged spleen, increased cell
permeability and destruction of red
blood cells in guinea pigs (erucic and
nervonic acids in rapeseed oil).
Growth suppression in rats, pigs,
chickens, turkeys, guinea pigs,
hamsters, and ducklings fed rapeseed
oil; suppressed body weight gain in rats
fed fats plus erucic acid.
Degenerative changes in liver and kidney,
fewer and smaller offspring in rats fed
high levels of rapeseed oil.
Cyclopropene Fatty Acids Cottonseed oil, kapok seed Discolors egg whites, can be removed by
2,3,4,6,7,8,9,10 . oil, cocoa butter. hydrogenation; growth suppression in
rats; reduced comb development in
roosters.
Impaired female reproduction in
laboratory animals and hens; depressed
egg production, reversible in hens;
embryomortality in hens and rats;
developmental abnormalities in rats,
increased mortality in rat pups.
Liver carcinogen in rainbow trout;
increases carcinogenic effects of other
chemicals; adverse effects on
cholesterol and fatty acid metabolism in
several species; aortic atherosclerosis
in rabbits; liver damage in rabbits and
rainbow trout.
Oxidation Products 2,4,11,12,13,14,\15\. Many vegetable oils and Cholesterol Oxidation Products (COPs):
animal fats. Numerous biological activities include
adverse effects on blood vessels,
destruction of cells, mutagenicity,
suppression of immune response,
inhibition of certain metabolic
mechanisms; may contribute to
development of atherosclerosis.
Lipid Oxidation Products (LOPs):
Associated with colon cancer; lipid
peroxides act as cancer promoters or
cocarcinogens and form crosslinks
between DNA and proteins; lipid
peroxidation correlated with severity of
atherosclerosis.
Oxidative fatty acid fraction of products
of thermal and oxidative changes from
prolonged heating of fats and oils in
laboratory studies (may not simulate
commercial heat treatment); severe heart
lesions, distended stomach, kidney
damage, hemorrhage of liver and other
tissues, reduced liver enzyme activity
in laboratory animals; reduced body
weight gain and feed consumption,
enlarged liver and kidney, damage to
thymus and sperm reservoir, diarrhea,
skin inflammation, and fur loss in
weanling rats fed heated corn and peanut
oil; reduced antioxidant tocopherol in
gastrointestinal tract of chicks fed
thermally oxidized PUFA; reports of
formation of cocarcinogens during
heating of corn oil and promotion of
chemically-induced mammary tumors.
Branched Chain Fatty Acids3,4,16........ Ruminant fats, dairy Individuals with genetic disorder
products. Refsum's syndrome: neurological
abnormalities resulting from inability
to metabolize branched chain fatty
acids.
----------------------------------------------------------------------------------------------------------------
\1\ Berardi and Goldblatt, 1980
\2\ Hui, 1996a
\3\ Hayes, 1982
\4\ Mattson, 1973
\5\ Roine et al., 1960
\6\ Phelps et al., 1965
\7\ Lee et al., 1968
\8\ Miller et al., 1969
\9\ Hendricks et al., 1980a
\10\ Hendricks et al., 1980b
\11\ Yannai, 1980
\12\ Boyd, 1973
\13\ Frankel, 1984
\14\ Artman, 1969
\15\ Andrews et al, 1960
\16\ Steinberg et al., 1971
[[Page 54520]]
6. Epidemiological Studies
Although the focus of this document is the environmental effects of
spilled vegetable oils and animal fats, a brief discussion of the
effects of these oils on human health is included for several reasons.
First, the ENVIRON report submitted by the Petitioners incorrectly
states that there are no accumulating or otherwise harmful components
in animal fats and vegetable oils that are irritating, toxic, or
carcinogenic; and that animal fats and vegetable oils are consumed
safely by wildlife and humans. The large number of human health
studies, many with a substantial population size, provide a significant
data base for examining the effects of long-term oral exposure to fats
and certain classes of fats or their components or degradation
products.
Second, humans may be exposed to spilled non-petroleum and
petroleum oils through several routes. Inhalation of harmful vapors and
dusts or mists and aerosols is often a significant route of human
exposure to spilled petroleum oils, though it is rarely an important
exposure route of less volatile vegetable oils and animal fats.
Third, humans and many animals often handle chemicals by similar
mechanisms in the body and exhibit similar toxic effects, a tenet
underlying the frequent use of animal tests in evaluations of human
health risk. For example, certain PAHs that are human carcinogens also
cause cancer in laboratory animals and in fish and other aquatic
organisms in the environment. Thus, the findings of epidemiology
studies are relevant to the evaluation of mechanisms of toxicity in
animals, particularly when the epidemiology studies are large enough to
overcome statistical limitations that are found with smaller data sets.
a. Human Health. Although fat is a major component of the human
diet, the consumption of high amounts of fat or certain types of
dietary fats and oils has been associated with several chronic diseases
(Hui, 1996a; FAO/WHO, 1994; Nelson, 1990; Katan et al., 1995). In a
number of epidemiology studies, the intake of dietary fat and some fat
types (e.g., saturated fats, unsaturated fats, polyunsaturated fatty
acids, trans-fatty acids, cholesterol) has been correlated with the
incidence of coronary artery disease. Dietary fat consumption has been
associated with the incidence of certain types of cancer, including
mammary and colon cancer, presumably because dietary fat is acting as a
cancer promoter. Dietary fat intake has also been linked to
hypertension, diabetes, and obesity (Hui, 1996a). Other studies report
that high dietary fat intake is related to altered immunity and altered
steroid excretion and may affect bone modeling and remodeling.
In many animal and human studies, dietary fat intake has been
linked to cardiovascular disease and atherosclerosis through its
effects on the levels of cholesterol and triglycerides in plasma and
the lipid composition of lipoproteins (Hui, 1996a). A 2% rise in risk
of coronary heart disease has been predicted for every 1% increase in
serum cholesterol. The American Heart Association, American Cancer
Society, and National Cancer Institute have recommended lowering fat
intake to 30% of total consumed calories in adults; the American Heart
Association also recommends limiting the intake of polyunsaturated
fatty acids to less than 10% of calories and replacing saturated acids
with monounsaturated acids (USDHHS, 1990; FAO/WHO, 1994; Hui 1996a).
b. Comparison of Effects From Oil Spills With Human Consumption of
Vegetable Oils and Animal Fats. The ENVIRON report, which was submitted
by the Petitioners, draws incorrect comparisons between the human
consumption of vegetable oils and animal fats and the environmental
effects of oil spills. The effects on humans who consume small
quantities of vegetable oils and animal fats in their foods cannot be
easily translated to environmental effects produced by oil spills.
These situations differ in many respects. A few of the differences are
highlighted below:
Differences in factors relating to the host organism:
Sensitivity; humans may not be the most sensitive species. Species
differences; while similarities in metabolism and biokinetic parameters
exist between some species, it is often unclear how effects on humans
can be translated to effects on fish. Differences in susceptibility;
there are no controls for differences in genetics, age, life-stage,
strain, gender, health, nutritional status, presence of other
chemicals, or other factors inherent to the exposed organisms.
Differences in dose-response relationships. It is unclear
how dose-response relationship can be extrapolated from humans to other
species, even if such information had been provided.
Exposure. Exposure differs in route, frequency, and
duration. Animals are exposed to large quantities of oil during an oil
spill, and the exposure may be short-term or long-term. The animals may
ingest the oil, or they may be exposed through their gills or skin.
Humans consuming foods, however, are exposed to small quantities of
oils for intermittent periods of time, and their exposure is via
ingestion only.
Differences in chemical composition. The composition of
oils used in small quantities in processed foods may differ from the
composition of the oils spilled in the environment, particularly when
the oils are acted upon by chemical and biological processes in the
environment.
Environmental factors. The effects of oil in the
environment depend on a wide variety of factors, including pH and
temperature. These factors are different from those that affect humans
consuming food oils.
Effects. Effects, such as reduced egg hatchability or
effects on molting, cannot be measured in humans.
Ecosystems. Ecosystems, food webs, and predator-prey
relationships can be affected by oil spills; these are not factors in
determining human health effects.
Statistical power of studies. Those epidemiologic studies
with large numbers of people have demonstrated possible adverse effects
from consumption of high levels of dietary fat or types of fat.
Negative studies may indicate that too few subjects were included in
the study or that confounding factors obscured the effect because of
statistical limitations of the methodology.
7. Other Adverse Effects of Oil Spills
a. Aesthetic Effects: Fouling and Rancidity. Fouling of beaches and
shoreline and rancid odors have been reported after spills of vegetable
oils and animal fats; some real-world examples are provided in section
II.D.2. Rancidity is the deterioration of fats and oils in the presence
of oxygen (oxidative rancidity) or water (hydrolytic rancidity) with
formation of off-flavors and odors (Hui, 1996b, 1996d; Kiritsakis,
1990). The hydrolysis and oxidation of spilled vegetable oils and
animal fats and decomposition of hydroperoxides leads to formation of
aldehydes, ketones, fatty acids, hydroperoxides, and other compounds
that produce off-flavors and rancid odors. Rancidity occurs especially
with oils that contain PUFA, such as linoleic acid (Hui, 1996a). Fish
oils, which contain high levels of PUFA, are especially susceptible to
oxidative rancidity and production of toxic byproducts and are often
supplemented with antioxidants to reduce their oxidation.
Unlike vegetable oils and animal fats, rancid odors have not been
reported following petroleum oil spills, although off-flavors and
tainting of fish have occurred (Crump-Wiesner, 1975;
[[Page 54521]]
Hartung, 1995). Fish collected near petroleum refineries or in
petroleum-polluted areas can be tainted (Lee, 1977), and commercial
species have been contaminated with petroleum oils (Michael, 1977).
Thousands of observations of floating tar balls and beach tar have been
tabulated over a 4-year period in a petroleum monitoring project for
marine pollution (NAS, 1985d).
b. Fire Hazards. While some petroleum oils and products present
fire and explosion hazards, most vegetable oils and animal fats do not,
unless flammable chemicals, such as hexane used during processing, are
present or temperatures are elevated. A few vegetable oils, such as
coconut oil (copra oil) are spontaneously combustible (Lewis, 1996).
Because of their low vapor pressures, some petroleum products are
highly volatile and flammable. In addition, most vegetable oils and
animal fats have a high flash point (temperature at which decomposition
products can be ignited), while the flash point for many petroleum
products is below or near room temperature.
Although most vegetable oils and animal fats do not easily catch
fire by themselves, once fires begin they are difficult to extinguish
and may cause considerable environmental damage. For example, a butter
and lard fire in Wisconsin that was apparently started by an electric
forklift resulted in the release of some 15 million pounds of melted
butter that threatened nearby aquatic resources (Wisconsin, 1991a,
1991b, 1991c; Wisconsin State Journal, 1991a, 1991b, 1991c, 1991d,
1991e).
c. Effects on Water Treatment. Oils and greases of animal and
vegetable origin and those associated with petroleum sources have long
been a concern in wastewater control (USEPA, 1979; Metcalf and Eddy,
1972). Too much oil, i.e., spills or discharges of oil and grease to a
municipal wastewater treatment system in quantities that exceed the
levels the treatment plant was designed to handle, can overwhelm the
water treatment plant that maintains sanitary conditions and removes
water pollutants that are harmful to aquatic organisms or interfere
with the recreational value of waters (Institute, 1985; Metcalf and
Eddy, 1972). Certain fatty acid products, such as quaternary amines,
may inhibit biological treatment and affect in-plant facilities and
downstream municipal sanitary sewage treatment facilities (Hui, 1996d).
Under normal operations, floating oil can be removed before
wastewater is discharged to water treatment plants, and highly variable
discharges of flow and organics can be minimized (Institute, 1985).
With large quantities of spilled oil and high organic loads, however,
these conditions may not be controlled adequately and water treatment
systems can be damaged. To prevent potential damage to water treatment
plants from oil spills, officials may halt water treatment and
interrupt water supplies, as occurred when 15 municipal drinking water
intakes were shut down following a spill of one million gallons of
diesel fuel from a collapsed storage tank at the Ashland Oil facility
in Floreffe, Pennsylvania in 1988 (USEPA, 1988).
8. FWS Comments
The FWS submitted a memorandum with the following position to the
EPA in 1994. The potential for harm from petroleum and non-petroleum
oils is equivalent; the path to injury is different. Edible non-
petroleum oils cause chronic effects with the potential of mortality.
Both petroleum and non-petroleum oil impact natural resources through
the fouling of coats and plumage of wildlife. Secondary effects from
fouling include drowning, mortality by predation, starvation, and
suffocation. The removal of edible oil is more difficult and strenuous
for wildlife due to the low viscosity of vegetable oil, which allows
deeper penetration into body plumage or fur and thorough contamination
of the wildlife.
Edible oils ingested in large quantities can cause lipid pneumonia.
Edible oil consumed by wildlife during preening or cleaning of their
coats also acts as a laxative resulting in diarrhea and dehydration.
Small amounts of edible oil on plumage can cause thermal circulation
troubles and embryo death in eggs exposed to oil through disruption of
egg/air interface (USDOI/FWS, 1994).
C. Petitioners' Claim: Animal Fats and Vegetable Oils Are Essential
Components of Human and Wildlife Diets
Petitioners claim that animal fats and vegetable oils are essential
components of human and wildlife diets.
EPA Response: While EPA agrees that some components of animal fats
and vegetable oils are essential components of human and wildlife
diets, EPA disagrees with the Petitioners that all animal fats and
vegetable oils are essential components of human and wildlife diets.
Most species require only one or two essential fatty acids. Most
animals need some level of fat to supply energy and fat-soluble
vitamins. Intake of high levels of dietary fat, some types of fat, and
essential fatty acids, however, can cause adverse effects.
While low levels of certain chemicals are essential for health,
exposure to high levels of these chemicals produces toxicity. Numerous
examples in the scientific literature demonstrate that essentiality
does not confer safety and essential elements can produce toxic
effects. Among these chemicals are vitamin A; the fatty acid a-
linolenic acid, an essential fatty acid in humans and coldwater fish;
and trace metals such as iron, manganese, selenium, and copper
(Klaassen et al., 1986; NAS, 1977a; USEPA, 1980; Rand and Petrocelli,
1985; Abernathy, 1992; Hui, 1996a; NAS/NRC 1981a).
Further, high levels of fats and oils alter the requirements for
essential fatty acids and change the balance between certain types of
lipids and fatty acids. For many species of fish and laboratory
animals, levels of essential fatty acids must be increased for the
animals to tolerate high lipid levels (NAS/NRC, 1983, 1995). High
levels of some fatty acids (n-6 PUFA, including the essential fatty
acid linoleic acid) deplete other fatty acids (n-3 PUFA, including the
essential fatty acid a-linolenic acid), thereby creating nutritional
deficiency. In addition, constituents of vegetable oils and animal fats
also affect requirements for essential fatty acids. Erucic acid, a
constituent of rapeseed oil, adversely affects reproduction in rats by
interfering with the metabolism of essential fatty acids (Roine et al.,
1960).
Animals often die from starvation after oil spills destroy their
food supply by oiling food or making it unavailable. In addition to a
reduction in food supply and a need to consume twice their normal
amount of food to maintain body temperature (Hartung, 1965; 1995),
oiled birds that are unable to float or fly cannot retrieve food from
the water that usually provides their food. Bird rescuers have
described dead birds with organs were filled with oil after eating
oiled food or consuming oil while preening their feathers to remove oil
(Croxall, 1975; Lyall, 1991; Frink and Miller, 1995). Thus, EPA finds
that Petitioners' arguments are non-persuasive and have little
relevance to the large quantities of oil released into the environment
from oil spills.
1. Nutritional Requirements for Dietary Fat
In addition to their roles in cellular structure, membrane
integrity, and microsomal enzyme function, fats play an important
nutritional role by supplying energy and essential nutrients (Rechigl,
1981; Hui, 1996b; Van Soest,
[[Page 54522]]
1982). The caloric value of fats is more than twice that of
carbohydrates or proteins (Hui, 1996a). Fats are a source of the fat-
soluble vitamins A, D, E, and K and are rich in antioxidants, including
tocopherols, such as vitamin E, and carotenes such as provitamin A.
They also facilitate the digestion and absorption of vitamins.
The nutritional requirements for dietary fat vary greatly among
species. A diet containing about 5% dietary fat is recommended for most
laboratory animals (NAS/NRC, 1995). Growth usually increases greatly in
animals fed a diet containing higher levels of fat, but lifespans are
shortened and lactation performance and reproduction adversely affected
in rats fed diets with 30% lipid (French et al., 1953). In minks, diets
with 35-40% fat have been satisfactory for meeting energy requirements,
but higher levels (44-53%) are recommended for fur development,
pregnancy and lactation (NAS/NRC, 1992.) Up to 44% fresh fat was used
in fox diets without detrimental effects (NAS/NRC, 1992). For coldwater
fish, 10% to 20% lipid is needed in diets, and higher levels of lipid
alter carcass composition by deposition of excess lipid and reduction
of the percentage of body protein (NAS/NRC, 1981a).
Nutritional requirements for fats are affected by environmental
influences and the health status of the organisms. Birds must consume
twice as much food after a spill for thermal regulation (Hartung,
1967). In laboratory animals, the requirement for certain fatty acids
(n-6 PUFA) is increased during lactation (NAS/NRC, 1995).
For many animals (cattle, goats, and sheep), vitamin and energy
requirements rather than specific dietary requirements for fat are
enumerated (NAS/NRC 1981b; NAS/NRC, 1985; NAS/NRC, 1984). Certain types
of fat are necessary for other animals. For example, sterols and
perhaps lecithin are necessary for crustaceans (NAS/NRC, 1983).
Dietary Requirements of Wild Animals. Unlike domestic animals that
are fed under regimens to maximize their productivity, wild animals and
free-ranging domestic animals may have different nutritional
requirements for their survival, growth, and reproduction (Van Soest,
1982). Diets that promote growth and obesity may also shorten life and
are undesirable for wild animals.
2. Essential Fatty Acids (EFA)
Certain unsaturated fatty acids that must be supplied in the diet
are called essential, because humans or other animals lack the enzymes
to synthesize them (Hui, 1996a; Rechigl, 1983). Two fatty acids are
considered essential in humans--linoleic acid and a-linolenic acid (Hui
1996a). These essential fatty acids are required for fetal development
and growth. Long-chain n-3 polyunsaturated fatty acids, such as a-
linolenic acid, are needed by the brain and retina; learning
disabilities and loss of visual acuity have been observed in animals
with low levels of these fatty acids. A balance of PUFA from both the
n-6 and n-3 families is needed to maintain health (Hui, 1996a).
EFA requirements differ according to species. In chickens, 1% of
the EFA linoleic acid is required; the essentiality of a-linolenic acid
has not yet been proven for poultry (NAS/NRC, 1994). Linoleic acid is
an EFA for pigs; arachidonic, which is generally added to swine diets,
can be synthesized from linoleic acid (NAS/NRC, 1988). Minks require
linoleic acid, and rabbits can develop EFA deficiency (NAS/NRC, 1992,
1977b). Silver foxes need 2 to 3 grams of EFA linoleic and linolenic
acids daily to prevent skin problems and dandruff (NAS/NRC, 1992). The
dietary EFA requirements of ruminants are about an order of magnitude
lower than those of non-ruminants (Van Soest, 1982).
Studies of fish and crustaceans demonstrate that EFA requirements
of aquatic animals vary with species and are apparently related to the
ability of the animals to convert linolenic acid (18:3w3) to highly
unsaturated fatty acids (Kanazawa et al., 1979). While some animals can
synthesize necessary fatty acids, others require them in their diets.
The n-3 fatty acids are essential for good health and growth in rainbow
trout, red sea bream, and turbot (NAS/NRC, 1981a). For chum salmon, the
requirement for linoleic and linolenic acids is 1%, or 0.5-1% for n-3
PUFA in the diet. For coho salmon, the optimal level of n-3 fatty acids
is 1-2.5%, and the optimal level of n-3 plus n-6 fatty acids appears to
be approximately 2.5%. EFA requirements can be affected by many
factors, including fat content of the diet and temperature. In fish,
EFA requirements change with temperature and culture conditions (NAS/
NRC, 1983, 1981a.)
3. Adverse Effects of High Levels of EFAs
While certain levels of fat and essential fatty acids are
necessary, higher levels can produce adverse effects. Although
requirements for linolenic acid, a n-3 polyunsaturated fatty acid, are
as high as 0.5% of total caloric intake in humans, consumption of a
diet high in the same family of fatty acids (n-3 PUFA) may cause
oxidative stress to cell membranes through lipid oxidation reactions,
thereby increasing requirements for antioxidants (Hui, 1996a).
A balance of types of lipid and various fatty acids is needed. For
example, many species of fish and laboratory animals tolerate high
levels of lipid if the essential fatty acid levels are increased. (NAS/
NRC, 1983, 1995). Similarly, a high level of other dietary components
can increase the need for certain PUFAs (n-6 PUFA) in rats, and alter
the fatty acid balance (between n-6 PUFA and n-3 PUFA) (NAS/NRC, 1995).
High levels of some fatty acids (n-6 PUFA) deplete other fatty acids
(n-3 PUFA), thereby creating adverse effects associated with
nutritional deficiency.
Compared to rodents consuming diets high in saturated fatty acids,
rodents receiving diets rich in linoleic acid--one of the two essential
fatty acids for humans--exhibited increased development of breast
tumors, including a shortened latency period for tumor appearance,
promotion of tumor growth, and increased incidence of mammary tumors
(Hui, 1996a). Once the dietary linoleic acid exceeded 4-5% of total
calories, saturated or unsaturated fats linearly increased tumor
incidence. Dietary linoleic acid enhanced the spread of mammary tumors
to lungs in rats, apparently by acting as a cancer promoter. Fish oil,
which contains n-3 PUFAs, inhibited mammary tumor development,
apparently inhibiting the effects of linoleic acid.
The importance of balance in essential fatty acids is clearly seen
in studies of coldwater fish. An optimum level of unsaturated fatty
acids is required for maximum growth of coldwater fish, and the
requirement for n-3 fatty acids may be species-specific (NAS/NRC,
1981a). EFA deficiency is characterized by poor growth as well as
numerous other symptoms, and the deficiency of most symptoms can be
reversed with certain fatty acids (n-3 PUFA); the addition of other
fatty acids (n-6 PUFA) to the diet reverses some symptoms, while others
are aggravated.
In coho salmon, extremely low and high levels of n-3 fatty acids
inhibit growth; concentrations of n-6 fatty acids above 1% also
depressed growth (NAS/NRC, 1981a). In studies of rainbow trout fed
different levels of triglycerides containing n-3 and n-6 fatty acids in
diets containing 10% lipid, growth was reduced when diets were
deficient in n-3 fatty acids, high in n-6 and low in n-3 fatty acids,
or high in both n-3 and n-6 fatty acids.
[[Page 54523]]
4. Adverse Effects of High Levels of Fats and Oils
Although fat intake is necessary to provide energy, vitamins, and
EFA, ingestion of high levels of dietary fat can cause adverse effects
in fish and aquatic species, other animals, and humans. The adverse
effects of consumption of high levels of dietary fat and certain
classes of fat by humans and animals have been discussed extensively in
section II.C.3.
5. Relevance of EFA Principles to Spills
For most animals, only one or two fatty acids are essential, and
these are not necessarily the fatty acids present in an oil spill.
Animals require only small quantities of these EFAs that are provided
in a normal diet, and these quantities must be in balance. While low
levels of one or two fatty acids are needed by some species, in several
species tested, high levels of these fatty acids produce adverse
effects by toxicity or by creating nutrient imbalances that deplete
other essential nutrients.
After a spill, high levels of animal fats and vegetable oils other
than the EFA are present in the environment. High levels of total
dietary fat, certain classes of fats, imbalances of types of fat, and
some components and breakdown products produce adverse effects in
laboratory animals and in some animals that have been examined in the
field and are associated with adverse effects in humans. Further, some
constituents of vegetable oils, such as erucic acid in cottonseed oil,
actually interfere with EFA metabolism, thereby causing adverse effects
(Roine et al., 1960).
When food is coated with oil from a spill of vegetable oils or
animal fats, animals are unable to forage or consume the food or suffer
the consequences of ingesting large quantities of oil as they consume
food. Oil-coated birds die of hypothermia or starvation when they are
unable to obtain or consume twice their normal amount of food to
provide the increased metabolic requirements needed to survive oil
spills.
Some oils, their constituents, or transformation products remain in
the environment for years. By contaminating the food source biomass,
reducing breeding animals and plants that provide future food sources,
contaminating nesting habitats, and reducing reproductive success
through contamination and reduced hatchability of eggs, oil spills can
cause long-term effects for years even if the oil remains in the
environment for relatively short periods of time.
6. FWS Comments on Essential Fatty Acids
The FWS commented that although fats and oils are used by cells of
living organisms in small amounts, too much will cause harm to
organisms through means other than toxicity. Ingestion of concentrated
vegetable oil or animal fat could cause indigestion, nausea, and
diarrhea. This could incapacitate a bird or mammal (USDOI/FWS, 1994).
D. Petitioners' Claim: Animal Fats and Vegetable Oils Are Readily
Biodegradable and Do Not Persist in the Environment
EPA disagrees with Petitioners' claim that all animal fats and
vegetable oils are readily biodegradable and notes that when
biodegradation does occur in the environment, it can lead to oxygen
depletion and death of fish and other aquatic organisms. Some products
formed by biodegradation and other transformation processes are more
toxic than the original oils and fats. While some animal fats and
vegetable oils are degraded rapidly under certain conditions, others
persist in the environment years after the oil was spilled (Mudge et
al., 1995; Mudge, 1995, 1997a, 1997b). Further, spilled animal fats and
vegetable oils can cause long-term deleterious environmental effects
even if they remain in the environment for relatively short periods of
time, because they destroy existing and future food sources, reduce
breeding animals and plants, and contaminate eggs and nesting habitats.
Every spill is different. How long the vegetable oil or animal fat
remains in the environment after it is spilled, what proportion of the
oil is degraded and at what rate, what products are formed, and where
the oil and its products are transported and distributed are determined
by the properties of the oil itself and those of the environment where
the oils is spilled. Factors such as pH (acidity), temperature, oxygen
concentration, dispersal of oil, the presence of other chemicals, soil
characteristics, nutrient quantities, and populations of various
microorganisms at the location of the spill profoundly influence the
degradation of oil.
Like petroleum oils, vegetable oils and animal fats can float on
water, settle on sediments or shorelines, and form emulsions when there
is agitation or prolonged exposure to heat or light (Crump-Wiesner and
Jennings, 1975; DOC/NOAA, 1992, 1996). Environmental processes can
alter the chemical composition and environmental behavior of the
spilled oils and influence their proximity to environmentally sensitive
areas and the environmental damage they cause.
The detrimental environmental effects of several spills of
vegetable oils and animal fats are described below and in Appendix I,
Table 4: Effects of Real-World Oil Spills. These reports provide
examples of the effects of some specific spills where death, injuries,
and damage were observed. No structured survey on the effects and
numbers of victims of spills of vegetable oils and animal fats has been
conducted (Rozemeijer et al., 1992). Because birds and other animals
show only a ``wet look'' when they are coated with vegetable oils and
animal fats, they are difficult to identify and may never be found if
they sink when they die or are consumed by predators (NAS, 1985e).
1. Chemical and Biological Processes Affecting Vegetable Oils and
Animal Fats in the Environment
Vegetable oils and animal fats that are spilled in the environment
can be transported and transformed by a wide variety of physical,
chemical, and biological processes that alter the composition of the
oil, its fate in the environment, and its toxicity. Oil that is spilled
in inland waters, such as small rivers and streams, may be especially
harmful if there are limited oxygen resources in the water body and
little dispersal of the oil (NOAA/FWS, 1996).
Whether the toxicity of these transformation products formed by
chemical and biological processes increases compared to that of the
original oil depends on the specific oil and the products that are
formed. For example, lipid oxidation products that are formed following
exposure of fats to oxygen, light, and inorganic and organic catalysts
have been associated with colon cancer; and cholesterol oxidation
products that are formed by autoxidation of cholesterol exposed to air,
heat, photooxidation, and oxidation agents have numerous biological
activities (Hui, 1996a). (See section II.B.5.d for a discussion of the
toxicity of transformation products.)
a. Chemical Processes. The fate of petroleum and non-petroleum oils
can be altered by environmental processes. Primary weathering processes
include spreading, evaporation, dissolution, dispersion,
emulsification, and sedimentation (DOC/NOAA, 1992a, 1994, 1996). The
rate and relative importance of each of these processes depends on the
specific oil that is spilled and environmental conditions that are
present and that may change over time. Wind transport, photochemical
degradation, and microbial degradation may also play
[[Page 54524]]
important roles in the transformation of petroleum oils, vegetable oils
and animal fats.
Different parts of the ecosystem are affected as the composition of
the spilled oil changes. For example, weathered petroleum oils
penetrate into marsh vegetation less than fresh oil, for weathered oil
is composed of relatively insoluble compounds and often forms mats or
tarballs (DOC/NOAA, 1994; Hartung, 1995; NAS, 1985e). Thus, weathering
decreases the potential exposure to fish through the water column while
increasing the potential exposure of species that ingest tarballs. As
the lighter fractions dissolve or evaporate, oil sinks, thereby
contaminating sediments and contributing to water column toxicity.
Spilled sunflower oil is hydrolyzed and polymerized to chewing gum
balls that can be washed ashore or can sink and cover sediments,
thereby exposing benthic and intertidal marine communities (Mudge,
1993).
Vegetable oils and animal fats can undergo several types of
chemical reactions. They can be hydrolyzed to yield free fatty acids
and diglycerides, monoglycerides, or glycerol; this hydrolysis can be
catalyzed by acids, bases, enzymes, and other substances (Hui, 1996a;
Lawson, 1995; Kiritsakis, 1990; Hoffmann, 1989). Vegetable oils and
animal fats can be oxidized to form hydroperoxides and free radicals
which perpetuate the oxidation reaction until they are destroyed by
reacting with other chemicals, such as natural or added antioxidants.
The free radicals that initiate an autoxidation reaction are formed by
decomposition of hydroperoxides, exposure to heat or light, or other
means. COPs are formed by autoxidation of cholesterol that is exposed
to air, heat, photooxidation, and oxidative agents derived from dietary
sources and metabolism (Hui, 1996a).
Several types of reactions can occur during processing, cooking, or
storage of fats and oils, including hydrogenation of unsaturated fatty
acids in oils (hardening); esterification; interesterification,
including transesterification; and halogenation (Lawson, 1995; Hui,
1996a; Hoffmann, 1989; Yannai, 1980). Thermal oxidation and
polymerization during cooking, frying, or processing operations at high
temperatures, generally between 180 deg.C to 250 deg.C, can lead to
conjugation (act of being joined) of polyunsaturated fatty acids and
cylization and the formation of volatile decomposition products.
b. Biological Processes. Petroleum oils and vegetable oils and
animal fats that are spilled in the environment can be transformed by
bacteria, yeast, fungi, and other microorganisms. Although microbial
degradation rarely occurs when there are controlled conditions during
normal storage of animal fats and vegetable oils, microorganisms can
grow on vegetable oils and animal fats and degrade them when
environmental conditions are favorable (Ratledge, 1994).
Investigations of biological approaches to remediating sites
contaminated with petroleum oils have shown that numerous environmental
factors must be carefully controlled for biodegradation to be effective
in reducing contamination from oily materials in soil (Venosa et al.,
1996; Salanitro et al., 1997). While bioremediation has been used for
soil cleanup at some petroleum-contaminated sites (e.g., in tests at
refineries, in treatment of oily sludges in oil and gas operations, and
at pipeline sites for spills of crude oil), successful cleanup requires
management of appropriate levels of applied waste to soil, aeration and
mixing, nutrient fertilizer addition according to the ratios of carbon:
nitrogen: phosphorus present, pH amendment, and moisture control to
optimize degradation by soil micoorganisms (Salanitro et al., 1997).
The extent of biodegradation apparently depends upon the type of soil
and crude oil involved.
The promise and the limitations of microbial degradation have been
highlighted in numerous studies of factors influencing the microbial
utilization of animal fats and vegetable oils (Ratledge, 1994). These
studies were conducted in experimental cultures and cannot be applied
readily to cleanups of oil spills, where control of pH, oil dispersal,
and nutrient supplementation are difficult to achieve. They are
described briefly, primarily to illustrate the complexity of
biotransformation processes, the many factors that can affect
biodegradation, and the difficulty in accurately reflecting conditions
and determining rates of biodegradation or other transformation
processes at specific spill locations. A more detailed discussion of
the microbial degradation of vegetable oils and animal fats is provided
in the accompanying Technical Document. (See Technical Document, Claims
V and VI, Biological Processes, Section A.)
Factors that affect the biodegradation of oils include pH,
dispersal of oil, dissolved oxygen, presence of nutrients in the proper
proportions, soil type, type of oil, and the concentration of
undissociated fatty acids in water. In addition to microorganisms,
other biota can also alter the chemical composition of vegetable oils
and animal fats. The reactions may depend on the species, for organisms
such as invertebrates, lack enzymes that participate in certain
metabolic pathways found in other organisms.
c. Rancidity. Biological and chemical processes can lead to the
formation of rancid products that cause off-flavors and unpleasant
odors. Rancidity results from the oxidation of unsaturated fatty acids
that are acted upon by peroxide radicals or enzymes to form a variety
of products, some of which are toxic (Hui, 1996a; Yannai, 1980).
Rancidity can also be produced by hydrolysis of triglycerides and
lipolysis by microorganisms or natural enzymes (Kiritsakis, 1990). The
hydrolysis and oxidation of spilled vegetable oils and animal fats
leads to formation of aldehydes, ketones, fatty acids, and other
compounds responsible for off-flavors and rancid odors. The rate of
rancidity increases with thermal decomposition of fats (Hui, 1996a),
although enzymatic peroxidation and oxidation of unsaturated fatty
acids by lipoxygenases can also occur in plant food stuffs even during
storage at low temperature and in the dark (Yannai, 1980).
2. Environmental Fate and Effects of Spilled Vegetable Oils and Animal
Fats: Real-World Examples
The reports in this section describe the spread of vegetable oils
and animal fats after spills into the environment and detail the
deleterious effects produced by these spills. While some aspects of
specific spills have been discussed earlier, the examples presented
below demonstrate that factors such as the nature of the oil, its
environmental fate, and proximity of the spill to environmentally
sensitive areas determine the adverse effects of spills of vegetable
oils and animal fats in the environment. Many spills are never
reported. Animals injured or killed by oils may never be found, for
they are highly vulnerable to predators or may drown and sink (USDOI,
1994; Frink, 1994; NAS, 1985e). Thus, the reports that are summarized
in Appendix I, Table 4 and below are not a comprehensive study of the
adverse environmental effects of spills of vegetable oils and animal
fats, but rather a snapshot revealing some of the deleterious effects
caused by spills of oil into the environment.
Minnesota Soybean Oil and Petroleum Oil Spills. Oil from two spills
in Minnesota killed thousands of ducks and other waterfowl and wildlife
or injured them through coating with oil. The peak of waterfowl damage
occurred
[[Page 54525]]
within two days of the breakup of ice on the Minnesota and Mississippi
rivers in the spring of 1963 (Minnesota, 1963; USDHHS, 1963). There
were two sources of oil--an estimated 1 million to 1.5 million gallons
of soybean oil that entered the Minnesota River via the Blue Earth
River when storage facilities failed at a plant in Mankato, Minnesota;
and an estimated 1 million gallons of low viscosity cutting oil that
escaped to the Minnesota River near Savage, Minnesota, from a marsh
that was flooded with oil when storage facilities failed. Oil spilled
during the winter months from mechanical failure of storage tanks or
pipelines, moved little until the breakup of ice in the spring. The
varnish-like covering of willows on the river banks showed that the
soybean oil had escaped into the river during the spring run-off.
While the petroleum oil and soybean oil slicks could not be
distinguished by field observation, laboratory analysis of samples of
oil and oil scraped from ducks revealed that soybean oil caused much of
the waterfowl loss (Minnesota, 1963). Approximately 5,300 birds were
affected or killed by oil, including 1369 live oil-soaked ducks rescued
and 1842 dead birds collected. They included lesser scaup ducks,
ringnecked ducks, coots and grebes, several other types of ducks,
gulls, and mergansers, and a cormorant. While some birds may have been
counted more than once, the numbers probably underestimate the impact
of the oil spills, because ducks covered with oil crawl into dense
cover and are hard to find.
Mammals and other dead animals were reported, including about 26
beaver, 177 muskrats, and 50 others, among them turtles, herons,
kingfisher, songbirds, other birds, skunk, squirrel, dog, and cows
(Minnesota, 1963). The death of 7,000 fish was attributed to causes
other than oil pollution, because winterkill is common in shallow
backwater areas of the river and a BOD study indicated that the sample
analyzed would not have sufficient oxygen demand to significantly
affect oxygen resources in the river. Bottom fauna used as fish food
may have been affected temporarily in localized areas.
The character of the soybean oil on and in the water changed with
time, as thick orange-colored slicks that were first observed changed
to pliable greyish and somewhat rubbery floating masses that were
stringy or somewhat rounded and were sometimes surrounded by a light
oil slick (Minnesota, 1963). Limited areas of the bottom were covered.
Oil that normally floated on the surface of the river tended to
sink to the lake bottom or settled into low areas of the river bottom
near the shoreline, apparently because of entrapment of heavy materials
in the oily mass. A sample of soybean oil collected from the bottom of
the lake contained sand, dirt, twigs, and leaves when it was analyzed
in the laboratory.
Soybean oil also mixed with sand on the beach, creating a hard
crust 3 feet above water level. White balls, apparently from soybean
oil that was once near the surface of a lake, moved toward shore and
broke up into long, white stringy material that collected on shore.
Pools of tough, milky material covered with brown scum were found in
low areas of the beach along with a hard varnish-like crust on the
beach.
Spill of Coconut Oil, Palm Oil, and Edible Materials. In 1975, a
cargo ship that was carrying primarily vegetable oils and edible raw
materials (copra or dried coconut meat, palm oil, coconut oil, and
cocoa beans) went aground on Fanning Atoll, Line Island and dumped its
cargo onto a pristine coral reef (Russell and Carlson, 1978). The
effects of the oily substances were similar to those following a
petroleum oil spill. Fish, crustaceans, and mollusks were killed.
Shifts in the algal community were observed, with excessive growth of
some types of green algae and the elimination of other algal
competitors. The effects on the algal community continued for about 11
months.
Sunflower Oil Spill in North Wales. When a cargo of unrefined
sunflower oil was spilled into the environment off the coast of
Anglesey, North Wales in January 1991, surface slicks of the oil were
formed for many miles around the ship (Mudge et al., 1993; Salgado,
1992, 1995). Some oil was hydrolyzed and polymerized to form ``chewing
gum balls'' that were washed ashore over a wide area. The denser balls
sank, allowing the sunflower oil to contact a wide range of benthic and
intertidal communities near the spill. Sunflower oil polymerized in
seawater and formed lumps that could not be degraded by bacteria.
Mussels that were near the spill died. Polymerized sunflower oil
formed a cap that reduced the permeability of sediments to water and
oxygen and killed organisms living on the sediments (Mudge et al.,
1993, 1995, Mudge, 1995). Polymerization of sunflower oil that washed
ashore produced concrete-like aggregates that still persist nearly 6
years after the spill (Mudge, 1997a, 1997b).
Rapeseed Oil Spills in Vancouver Harbor. Three small spills of
rapeseed oil caused greater losses of birds than 176 spills of
petroleum oils over a 5-year period in Vancouver harbor from 1974 to
1978 (McKelvey et al., 1980). An estimated 35 barrels of rapeseed oil
killed an estimated 500 birds, while all of the petroleum oil spills
combined oiled less than 50 birds, perhaps because the vegetable oils
lacked the strong, irritating odor of petroleum or its eye-catching
iridescence. Both petroleum and non-petroleum oils coat the feathers of
birds, destroying their waterproofing qualities and allowing water to
penetrate to the skin with loss of insulation and buoyancy, which
results in exposure, and death (Mudge, 1995; Hartung, 1967; NAS, 1985e;
Smith and Herunter, 1989; Rozemeijer, 1992).
Another spill of rapeseed oil (Canola) occurred in Vancouver Harbor
on February 26, 1989 (Smith and Herunter, 1989). During product
transfer, an estimated 400 gallons of rapeseed oil spilled into the
harbor. A thin film covered large portions of the harbor, and a patchy
slick of yellow oil from the spill site to the center of the harbor was
visible from above. It was estimated that at least 700 birds were in
the harbor at the time of the spill, including 500 diving ducks, 100
gulls, and 100 other divers.
Initially, booms were not used to contain the spill, and an attempt
to disperse the oil with multiple passes of a small tug through the
thick oil were ineffective (Smith and Herunter, 1989). EPA notes that
the trade association requested that this ineffective mechanical
dispersal be allowed as a response to spills of vegetable oil and
animal fat under the FRP rule. After several hours, booms were set up
to contain the oil and skimmer boats recovered the oil.
Cleanup was concluded 15 hours after the spill was discovered
(Smith and Herunter, 1989). Nevertheless, 88 oiled birds of 14 species
were recovered after the spill, and half of them were dead. Oiled birds
usually are not recovered for 3 days after a spill, when they become
weakened enough to be captured. Of the survivors, half died during
treatment.
The authors caution that because vegetable oils are edible, they
may not be considered as threatening to aquatic birds as petroleum
oils. However, the end result is the same. Birds die (Smith and
Herunter, 1989). The number of casualties from the rapeseed oil spills
was probably higher than the number of birds recovered, because heavily
oiled birds sink and dying or dead birds are captured quickly by
raptors and scavengers.
Smith and Herunter emphasize that containing and recovering the
spilled oil as soon as possible is critical to minimizing environmental
damage
[[Page 54526]]
(1989). Using booms, testing transfer lines, having spill detection
equipment in place, training on-site personnel, and reporting spills
immediately are essential to reducing environmental harm.
Fat and Oil Pollution in New York State Waters. Pollution of
surface waters by oils and fats from a wide variety of sources killed
waterfowl, coated boats and beaches, tainted fish, and created taste
and odor problems in water treatment plants in New York State (Crump-
Wiesner and Jennings, 1975). Sources of the fats and oils included
spills, food and soap manufacturing, refinery wastes, construction
activities, industrial waste discharges, and sanitary sewage. Grease-
like substances were seen along the shore or floating in Lake Ontario.
Grease-balls that contaminated the shoreline near Rochester and smelled
like fat or lard were analyzed and characterized as mixtures of animal
and vegetable fats with similar fatty acid contents.
Spills of Fish Oil Mixtures in South Africa. Oil that was
discharged from a fish factory effluent pipe near Bird Island, Lamberts
Bay, South Africa, the breeding ground for 5,000 pairs of Cape Gannets
and home to tens of thousands of Cape Cormorants and 500 Jackass
Penguins, killed at least 709 Cape Gannets, 5,000 Cape Cormorants, and
108 Jackass Penguins (Percy Fitzpatrick Institute, 1974). A few days
after the oiling incident, researchers found penguins covered with a
sticky, white, foul-smelling coat of oil. They were shivering on the
shore and gannet chicks, who were observed walking straight into the
oil, were dead or dying. They observed a milky white sea on one side of
the island and a frothy mixture and clots of oil thrown up on the
island. The oil smelled strongly of fish.
Damage from fish-oil pollution was detailed at two other fish
factories in South Africa (Newman and Pollock, 1973). In the rock
lobster sanctuary at St. Helena Bay, 10,000 rock lobsters and thousands
of sea urchins were killed, probably from oxygen depletion caused by
the release of organic material from the fish factory. At least 100,000
clams died near a fish factory at Saldanha Bay along with large numbers
of black mussels and prawns and some polychetes and anemones. Other
effects were also described by the authors: the sea was discolored and
smelled, water quality was poor, and the aesthetic appeal of the
beaches located near a town and popular camping site was adversely
affected.
Spill of Nonylphenol and Vegetable Oils in the Netherlands.
Thousands of seabirds, mostly Guillemots and Razorbills, washed ashore
in the Netherlands during a four-month period from December 1988 to
March 1989 (Zoun, 1991). They were covered with an oil-like substance.
Nearly all of the 1,500 sick birds that were taken to bird hospitals
died; many exhibited emaciation, aggressive behavior, bloody stools,
and leaky plumage. Autopsies and pathological examination of 30 birds
revealed hepatic degeneration and necrosis as well as aspergilliosis in
the air sacs and lungs. Chemical analysis of the feathers and organs
showed the presence of high levels of nonylphenol and vegetable oils,
such as palm oil. No source of the contaminants was established, but
they may have been discharged from a ship.
Soybean Oil Spills in Georgia From a Tanker Truck and a Vegetable
Oil Refinery. Aesthetic effects were a major concern to property owners
on an oiled cove at Lake Lanier, Georgia (Rigger, 1997). The strong,
unpleasant odor of soybean oil spilled from a tanker truck became more
rancid as the oil weathered. Rapid response action minimized the damage
and costs, although the oil adhered to boat dock floats and boats and
produced several thousand dollars in claims for cleaning boats and
docks and replacing dock floats.
In a vegetable oil refinery in Macon, Georgia, soybean oil was
released from an aboveground storage tank that was accidentally
overfilled (Rigger, 1997). Rapid response prevented significant damage
from the spilled oil, which had flowed through a storm water system and
entered a stream. Investigation of the spill incident revealed that
previous spills from the facility had entered the sanitary sewer system
and damaged the sewage treatment plant.
Wisconsin Butter Fire and Spill. In 1991, a major butter and grease
fire apparently triggered by an electric forklift destroyed two large
refrigerated warehouses at Central Storage facility in Madison,
Wisconsin and resulted in the release of large volumes of butter, lard,
cheese, meat, and other food products (Wisconsin, 1991a, 1991b, 1991c;
Wisconsin State Journal, 1991a, 1991b, 1991c, 1991d, 1991e). The
warehouses contained 15 million pounds of butter--much of it part of
the USDA surplus program. Thick, black smoke filled the air, and melted
butter and lard streamed from the burning building and threatened to
pollute a nearby creek and lake.
The quick action of firefighters, city engineers, and other
responders was credited by the company and state environmental
officials with saving a nearby creek and lake from environmental
disaster and limiting the losses and injuries from the fire (Wisconsin,
1991; Wisconsin State Journal, 1991a, 1991b, 1991c, 1991d, 1991e). If
the buttery material had flowed through storm sewers into the creek and
lake, it could have depleted the available oxygen required by walleyed
pike, bass, and other aquatic organisms living in the creek and
connecting lake and ruined a recent one million dollar cleanup effort
in the watershed.
After the cleanup was largely completed, the Wisconsin Department
of Natural Resources declared as hazardous substances the thousands of
gallons of melted butter that ran offsite and the mountain of damaged
and charred meat products spoiling in the hot sun and creating
objectionable odors. The Wisconsin DNR stated that these products posed
an imminent threat to human health and the environment.
3. FWS Comments on Degradation
Vegetable oils and animal fats may biodegrade quicker than
petroleum; however, in the short term, this advantage is neutralized by
the ability of many petroleum compounds to evaporate quickly. In
addition, the higher BOD of vegetable oils and animal fats pose an
increased risk of oxygen depletion in shallow waters and wetlands. Both
kinds of oil will degrade more slowly in low-energy waters and can
become submerged in an anoxic aquatic habitat, settle to the bottom and
into sediments, or form thick layers because the vegetable oil is no
longer being exposed to oxygenated waters or surroundings. In such
instances, the edible oil or fat will remain in the environment for a
long period of time and continue to create a risk to the natural
environment. The variability of circumstances surrounding each spill
(location, spill volume, weather, tides, water currents, effectiveness
of spill response) will have a greater influence in the short term on
environmental effects than will biodegradability. (USDOI/FWS, 1994)
E. Petitioners' Claim: Vegetable Oils and Animal Fats Have a High BOD,
Which Could Result in Oxygen Deprivation Where There Is a Large Spill
in a Confined Body of Water
Petitioners claim that vegetable oils and animal fats have a high
BOD, which could result in oxygen deprivation where there is a large
spill in a confined body of water with low flow and dilution.
EPA Response: EPA agrees with the Petitioners' claim that vegetable
oils and
[[Page 54527]]
animal fats have a high BOD, which could lead to oxygen depletion and
severe environmental consequences. (For a detailed discussion of this
topic, see section II.B.4.a.Suffocation.) EPA disagrees, however, that
oxygen depletion would occur only with large oil spills. Small spills
are sufficient to cause oxygen depletion and suffocation and death of
fish and other biota, depending on the conditions that apply at the
location of the spill. Oxygen depletion can result from reduced oxygen
exchange across the air-water surface below the spilled oil or from the
high BOD by microorganisms degrading oil (Crump-Wiesner and Jennings,
1975; Mudge, 1995). Examples of environmental damage produced by small
spills of vegetable oils and animal fats are provided above.
While a higher BOD is associated with greater biodegradability, it
also reflects the increased likelihood of oxygen depletion and
potential suffocation of aquatic organisms under certain environmental
conditions (Crump-Wiesner and Jennings, 1975). Oxygen depletion and
suffocation are produced by petroleum and vegetable oils and animal
fats. Under certain conditions, however, some vegetable oils and animal
fats present a far greater risk to aquatic organisms than other oils
spilled in the environment, as indicated by their greater BOD.
According to studies designed to measure the degradation of fats in
wastewater, some food oils exhibit nearly twice the BOD of fuel oil and
several times the BOD of other petroleum-based oils (Groenewold, 1982;
Institute, 1985; Crump-Wiesner and Jennings, 1975). While the higher
BOD of food oils is associated with greater biodegradability by
microorganisms using oxygen, it also reflects the increased likelihood
of oxygen depletion and suffocation of aquatic organisms under certain
environmental conditions (Groenewold, 1982; Institute, 1985; Crump-
Wiesner, 1975). Oil creates the greatest demand on the dissolved oxygen
concentration in smaller water bodies, depending on the extent of
mixing (Crump-Wiesner and Jennings, 1975).
FWS Comments on BOD. Decomposition of vegetable oils and animal
fats causes oxygen depletion problems for aquatic species (USDOI/FWS,
1994).
F. Petitioners' Claim: Vegetable Oils and Animal Fats Can Coat Aquatic
Biota and Foul Wildlife
EPA Response: EPA agrees with the Petitioners' claim that vegetable
oils and animal fats can coat aquatic biota and foul wildlife but
disagrees with the lack of significance accorded this potentially
devastating effect in Petitioners' ENVIRON report. Many animals and
plants die when they are coated with spilled petroleum oils or
vegetable oils and animal fats. (See section II.B.4.a. Coating with Oil
for a discussion of these effects.) Coating with oil can contaminate
existing and future food sources, destroy habitat, and damage eggs and
nesting areas, thereby inflicting environmental damage years after an
oil spill occurs (Frink and Miller, 1995).
Trustees Comments on Fouling. The biggest oversight of the ENVIRON
report, which was never subject to peer review as are journal
publications, is the insignificance given to the fouling potential of
vegetable oils and animal fats (USDOI/FWS, 1994). Wildlife
rehabilitators consider edible oils and fats to be some of the most
difficult of substances to remove from wildlife because of their low
viscosity. These less viscous oils are good wetting agents, allowing
deeper penetration into plumage or fur and creating a thoroughly
contaminated animal, as opposed to surface and intermediate
penetration. In many instances, complete removal can only be
accomplished with extremely hot water, which is detrimental because of
scalding, and excessive washing.
The FWS takes issue with statements in the ENVIRON report that
observed birds clean themselves and return to feeding areas (USDOI/FWS,
1994). Such observations are difficult to confirm without banding or
radio tagging the birds and closely observing them. It is highly
doubtful that the birds were able to clean themselves, for only
minuscule amounts of oil can be completely preened from plumage. Even
birds fouled with petroleum oils will preen and fly back to their
nests. Small amounts of oil on the birds' plumage can cause thermal
circulation trouble and smother embryos in eggs exposed to the oil.
Birds may appear to act normally, but it is not the immediate effects
of the oils but those that appear later that cause problems. Secondary
effects from fouling include drowning, mortality by predation,
starvation, and suffocation.
Both petroleum and non-petroleum oils foul the coats and plumage of
wildlife (USDOI/FWS, 1994). The risks from vegetable oils and animal
fats are magnified by their lack of repugnant smell or iridescence to
frighten wildlife away, making it more likely that wildlife will come
in contact with these oils.
III. Petitioners' Suggested Language To Amend the July 1, 1994,
Facility Response Plan Rule
This section begins with a short discussion about EPA's inland area
of jurisdiction and also provides some characterization of the amounts
of vegetable oil and animal fats produced or consumed, and reported
spills. These discussions are followed by EPA's response to the
Petitioners' specific regulatory language to amend the July 1, 1994,
facility response plan rule.
A. Background
Examples of water systems that occur in the inland area within
EPA's zone of authority are major freshwater rivers, smaller streams,
creeks, lakes and wetlands or mixed freshwater--saltwater estuary and
wetlands areas subject to tides. (See a Memorandum of Understanding
[MOU] between the Secretary of Transportation and the EPA Administrator
dated November 24, 1971 [36 FR 24080].) Many of these areas, including
wetlands and estuary areas, are often very sensitive, highly productive
areas where a large number of organisms such as shrimp, crabs, fish,
and water fowl nest, breed and feed. Lakes and larger rivers may be
used as water supplies and have drinking water and industrial intakes
that must be protected. Inland spills have a much higher potential to
contaminate both ground and surface water supplies. Some lakes,
estuaries and bays are often highly developed with industry,
recreational beaches, marinas and other highly visible areas that need
protection from oil spills.
Vegetable oil and animal fat were among the most frequently spilled
organic materials, ranking sixth and seventh respectively, and were
responsible for over 6% of all spills (384 of 6076 spills) of organic
materials reported along the coasts and major waterways in the United
States in 1973-1979 (Wolfe, 1986). Other authors estimate that at least
5% of all spill notifications are for vegetable oils and animal fats
(Crump-Wiesner, 1975). Of the 18,000 to 24,000 spills in the United
States reported annually to the National Response Center and EPA
Regions, 2-12% are from non-petroleum oils, including vegetable oils
and animal fats (USEPA/ERNS, 1995, 1996). These figures represent the
minimum number of spills; it is likely that they greatly underestimate
the actual number of spills because of significant underreporting. A
comparison was made of reports of spills in Ohio of vegetable oil and
soybean oil from January, 1984 to June, 1993 to the State
[[Page 54528]]
of Ohio Environmental Protection Agency (Ohio EPA) and to the National
Response Center (NRC). Only 7 of 27 reports (26%) to the Ohio EPA were
also reported to the NRC (USEPA, 1994a). There were a number of reports
of vegetable and soybean oil spills to the NRC that were not on the
State list (USEPA, 1994a).
B. Regulatory Language Changes Proposed by the Petitioners
Language to further clarify the definition of vegetable oil and
animal fats. EPA Response: EPA has decided not to incorporate
Petitioners' proposed definitions of ``animal fat and vegetable oils''
in the regulatory provisions of section 112.2. In issuing the final FRP
rule, EPA included a definition of ``non-petroleum oil'' in an Appendix
to the rule. (See 40 CFR part 112, Appendix E, section 1.2.3.) ``Non-
petroleum oil'' is defined to mean ``oil of any kind that is not
petroleum-based. It includes, but is not limited to, animal and
vegetable oils.'' Id.
EPA included this definition of ``non-petroleum oil'' in the rule
because the Agency established different and more flexible response
planning requirements for facilities that handle, store, or transport
non-petroleum oil, including animal fats and vegetable oils. For
example, in calculating required response resources for non-petroleum
facilities, the owner/operator of such a facility, including those
facilities which handle, store, or transport animal fats or vegetable
oils, is not required to use emulsification or evaporation factors in
Appendix E of the rule. Rather, these facilities need only: (1) Show
procedures and strategies for responding to the maximum extent
practicable to a worst case discharge; (2) show sources of equipment
and supplies necessary to locate, recover, and mitigate discharges; (3)
demonstrate that the equipment identified will work in the conditions
expected in the relevant geographic area, and respond within the
required times; and (4) ensure the availability of required resources
by contract or other approved means. 40 CFR Part 112, Appendix E,
section 7.7. Importantly, EPA does not prescribe the type or amount of
equipment that preparers of response plans for non-petroleum oil
discharges must identify. Id.
Moreover, at the time of issuing the final rule, EPA also set forth
definitions for both ``animal fat'' and ``vegetable oil'' in the
preamble to the FRP rule (59 FR 34070, 34088 (July 1, 1994)). To assist
owners and operators in distinguishing between oil types, EPA defined
``animal fat'' to mean ``a non-petroleum oil, fat, or grease derived
from animal oils not specifically identified elsewhere.'' Id. The
Agency defined ``vegetable oil'' to mean ``a non-petroleum oil or fat
derived from plant seed, nuts, kernels or fruits not specifically
identified elsewhere.'' Id. The Agency stands behind these definitions,
and because EPA is not modifying the FRP rule as requested by
Petitioners (see below), the Agency sees no need to include these
definitions in the rule provisions.
Petitioners express a concern that animal fats and vegetable oils
have been included with other types of ``non-petroleum oils,'' although
the planning requirements for owners and operators of all facilities
storing ``non-petroleum'' oils are more flexible than those
requirements for facilities storing, handling, or transporting
petroleum oil. Petitioners' main concern appears to be premised upon
the claim that vegetable oils and animal fats are ``non-toxic''
compared to other non-petroleum oils. EPA believes that Petitioners
have failed to make a demonstration that animal fats and vegetable oils
should be subject to less stringent planning requirements than other
types of non-petroleum oils. This is so for all of the reasons set
forth elsewhere in this notice.
Allow mechanical dispersal and ``no action'' options to be
considered in lieu of oil containment and recovery devices specified
for response to a worst case discharge of vegetable oil and animal
fats. EPA Response: The Agency declines this proposed language.
Although the ``no action'' and mechanical dispersal options proposed by
the Petitioners may be considered in response to an actual spill under
certain conditions, i.e., river currents too high for the effective use
of a boom, neither option would meet the intent of OPA for planning
purposes. The intent of OPA was for industry to plan for and secure the
equipment and resources needed to respond to a worst case discharge,
which may be a discharge of 1 million gallons or greater for a large
vegetable oil facility.
A ``no action'' plan would allow a large amount of oil to remain in
the environment, which would in turn cause immediate physical effects
to resources that could extend for considerable distances as the oil
spreads. This oil would have the potential to remain in the environment
for long periods of time.
One issue raised by the Petitioners is that the response to a spill
of vegetable oil or animal fat may do more harm to the environment than
a ``no action'' alternative. A consideration in the response to any
type of oil, including petroleum or vegetable oil or animal fat, is
whether the measures used in response to the spill will cause
unacceptable damage to a specific type of environment. This
determination is based on the conditions existing at the time of the
spill. Specific spill conditions will often dictate the need for
different techniques for the same water environment or shoreline
habitat. A study, which evaluated the relative impact of various
generic characteristics of response techniques in the absence of oil,
rated booming and skimming as having a ``Low'' impact in open water,
small lakes/ponds, large rivers and small rivers and streams (DOC/NOAA,
1992) and therefore, causing little environmental harm.
Mechanical dispersal of the vegetable oil or animal fat into the
water column could shut down or negatively impact drinking intakes due
to flavor changes and odors, reduce cooling efficiency in cooling
waters of power plants, contaminate food from receiving waters,
increase BOD levels, violate water quality standards, cause sludges,
and adversely impact benthic organisms and the resulting food chain in
inland areas. Oil dispersed by mechanical means may resurface and cause
further environmental damage in the same area or a different area
depending on the characteristics of the water body. (See section
II.D.2, Rapeseed Oil Spills in Vancouver Harbor on the ineffective use
of mechanical dispersal.) This Notice references studies that document
spills of vegetable oils that have remained in the water environment
for several years and that continued to kill shellfish and other
organisms.
Limit the use of containment boom to the protection of fish and
wildlife and sensitive environments: EPA's Response. Based on tests and
studies summarized in the data in this Decision Document and the
Technical Document, vegetable oils and animal fats clearly have adverse
impacts on the aquatic and terrestrial environment and its inhabitants.
EPA declines to modify the FRP rule as suggested by the Petitioners.
EPA continues to believe that an OPA required FRP must limit the
impacts of the oil through response techniques that include containment
and removal in addition to protection of priority fish and wildlife and
environmentally sensitive areas.
The Area Contingency Plan (ACP) identifies and prioritizes the fish
and wildlife and environmentally sensitive areas to be protected and
also determines the type of protection to be used when a spill occurs.
CWA section 311(j)(5)(C)(I) requires that a FRP must be consistent with
the applicable ACP, which usually requires that a
[[Page 54529]]
containment boom be positioned to protect drinking water intakes and
environmentally sensitive areas.
In addition, facility response planning must also include the use
of measures appropriate to the body of water to contain and limit and
concentrate the spread of oil for removal. The spreading rate of oil is
a function of its viscosity. Low viscosity materials spread easily over
the surface of water. At lower temperature, the oil spreads less
rapidly. Generally, vegetable oils and petroleum oils are of low
viscosity. The spread of spilled oil over a large area will hamper
recovery of the oil. The thicker the concentration of animal fat or
vegetable and petroleum oil in an area, the greater the efficiency for
oil removal. As the oil spreads over time into thinner slicks, its
removal becomes less efficient and more costly. In tidally influenced
areas, oil may move back and forth with each tide and be redeposited on
the shore line, tidal flats, and marshes and cause adverse effects.
Since vegetable oils and animal fats usually have few volatile
fractions and therefore usually do not decrease in volume through
evaporation as do many of the lighter factions of petroleum oils, most
of the quantity of vegetable oil and animal fats spilled into water
remain in the environment. When this happens, there is the potential
for adverse impacts to environmentally sensitive areas and water
intakes. Although most vegetable oils and animal fats break down more
quickly than some petroleum oils, under certain conditions and times of
the year, these oils may remain in the aquatic environment for long
periods of time, polarize and form toxic degradation products and kill
shellfish and other organisms.
If a facility storing animal fat and/or vegetable oil does not
provide for the use of containment booms in its plan to respond to a
worst case discharge, it will not have the equipment and trained
personnel available for an actual spill and many miles of shoreline and
aquatic resources over a large area of water may be impacted. Rapid and
immediate response and removal, including the use of containment booms,
offer the most effective means of minimizing the immediate and long
term effects of spills of petroleum and non-petroleum oils, including
vegetable oils and animal fats. EPA does not believe that the
Petitioners have shown why the use of containment booms should be
limited to only protecting fish and wildlife and environmental
sensitive areas. Without the use of containment booms, a worst case
discharge of vegetable oil or animal fats could cause harm not only to
fish and wildlife and environmentally sensitive areas, but also damage
the aquatic and terrestrial environment. Such a discharge could also
present risks to humans if the vegetable oil and animal fats adversely
affect drinking water intakes.
Increase the time for the arrival of on-scene response resources
for medium discharges and worst case Tier 1 response resources to 24
hours plus travel time from the currently required 12 hours including
travel arrival time: EPA's Response. A rapid response to an oil spill
is important in the recovery of as much oil product as possible. Any
oil that remains in the environment will continue to adversely impact
the aquatic and shoreline environment and cause lasting damage. (This
document contains discussions of environmental, physical and other
impacts that occur when vegetable oil and animal fats are spilled.) A
24 hour plus travel time delay in the arrival of response resources
would result in an unacceptable increase in impacts to drinking water
intakes, fish and wildlife and sensitive environments, greater response
costs, less product recovered, and increased water and other types of
pollution.
A delay in the arrival of response resources will increase the
difficulty of the removal of the spilled oil and will also result in an
increase in the cost to recover this oil. If effective containment and
cleanup procedures are initiated within an hour of a spill occurrence,
estimated removal costs are $250 per barrel (42 gallons). If two or
more hours elapse before the oil is removed, the cost can be four or
more times that amount and continue to increase with the time to
respond to the release (USEPA, 1995). The ``window of opportunity'' for
the most effective and efficient response to oil spills occurs within
the early hours after the spill.
Immediate action is required when oil spills occur on water to
prevent the oil from becoming so widely spread that containment and
cleanup become extremely expensive and a larger area of fish and
wildlife and environmentally sensitive areas are adversely affected.
There are immediate physical effects to the environment from releases
of vegetable oil and animal fat. There is the potential for additional
sensitive areas to be contaminated within the 24 hours plus travel time
proposed by the Petitioners for the arrival of response resources. This
is 12 hours plus travel time longer than the FRP requirement for
rivers, canals, inland, and near shore areas. Sensitive areas within
many additional miles would be affected with the delay in the arrival
of response resources proposed by the Petitioners since booms would not
be made available for their protection until much later. Rapid response
is imperative to limit adverse effects, protect resources, and contain
oil for removal.
Extending the time for arrival of response resources would increase
the FRP distance calculation for a facility and could result in
additional vegetable oil and animal fat facilities meeting the criteria
for substantial harm and having to prepare and submit a facility
response plan to EPA. The requirements for determination of substantial
harm in the FRP rule for facilities with 1 million gallons or above
capacity includes a calculation in Appendix C-III of 40 CFR Part 112 of
the distance an oil discharge from the facility would travel within the
time it would take for the appropriate tier of response resources to
arrive. Once the distance is calculated, the facility must determine
whether fish and wildlife and environmentally sensitive areas or
drinking water intakes are located within this distance. If so, the
facility is considered a substantial harm facility and must prepare and
submit a response plan. An additional twelve hours plus travel response
time would more than double the distance a spill could travel on water
before the arrival of response resources and therefore potentially
increase impacts to drinking water intakes and environmentally
sensitive areas and increase the number of vegetable oil and animal fat
facilities that have to prepare and submit FRPs. For the above reasons,
EPA declines to modify the FRP rule in this manner.
IV. Conclusions
The environmental effects of petroleum and non-petroleum oils,
including vegetable oils and animal fats, are similar because of
physical and chemical properties common to both. Many of the most
devastating effects of spills of petroleum oils and vegetable oils and
animal fats are physical effects, such as coating of animals,
suffocation, or starvation. Some tests measuring BOD suggest that
certain vegetable oils and animal fats may present a greater
environmental risk of suffocation to organisms than spilled petroleum
oils under certain conditions. Petroleum oils and vegetable oils and
animal fats can be transferred to the eggs of nesting birds from the
parents' feathers and smother the embryos inside. Embryos in eggs are
also killed by petroleum oils through mechanisms of toxicity; whether
non-petroleum oils also cause direct embryotoxicity has not been
evaluated in tests.
Petroleum oils and vegetable oils and animal fats, can enter all
parts of the
[[Page 54530]]
aquatic environment and adjacent shoreline. They can form a layer on
water, settle on the bottom in sediments, foul shorelines, and be
transported and distributed to other areas.
Some vegetable oils and animal fats, their components, or breakdown
products remain in the environment for years. Whether or not the oil
persists in the environment, spilled oil can have long-lasting
deleterious environmental effects. By contaminating food sources,
reducing breeding animals and plants that provide future food,
contaminating nesting habitats, and reducing reproductive success
through contamination and reduced hatchability of eggs, oil spills can
cause long-term effects years later even if the oil remains in the
environment for relatively short periods of time.
In addition to physical effects and the destruction of food and
habitat, petroleum oils and vegetable oils and animal fats, their
constituents, or degradation products can cause short-term and long-
term toxic effects in some animals. Petroleum oils contain PAHs and
benzene which are animal and human carcinogens. While vegetable oils
and animal fats contain only small quantities of PAHs, high dietary
intake of fats and certain types of fats have been associated with
increased cancer incidence in laboratory animals and humans as well as
coronary artery disease, diabetes, obesity, and altered immunity and
other effects. Lethality, impaired growth, reproductive effects, and
behavioral effects are among the subchronic and chronic toxic effects
observed in other studies of vegetable oils and animal fats.
Spills of petroleum and vegetable oils and animal fats can affect
drinking water supplies, and they have forced the closing of water
treatment systems. Rancid smells, fouling of beaches, and destruction
of recreational areas have been reported after spills of vegetable oils
and animal fats.
Small spills of petroleum and vegetable oils and animal fats can
cause significant environmental damage. Real-world examples of oil
spills demonstrate that spills of petroleum oils and vegetable oils and
animal fats do occur and produce deleterious environmental effects. In
some cases, small spills of vegetable oils can produce more
environmental harm than numerous larger spills of petroleum oils.
Because petroleum oils and vegetable oils and animal fats exhibit
similar behavior in the environment, similar methods are used to
contain them and attempt to clean them up after a spill. Because every
spill is different, decisions on what cleanup methods are most
effective and least harmful to the environment must be made case-by-
case, considering the nature of the oil, the characteristics of the
contaminated area, and the proximity of the spill to environmentally
sensitive areas.
Once oil is spilled in the environment, however, the opportunities
for reducing environmental damage and other adverse effects are
limited. Although methods for rescuing and cleaning oil-contaminated
birds, otters, and other wildlife have improved, only a small
proportion of affected animals are recovered, and even fewer of the
rescued animals survive. Further, by affecting current and future food
sources, nesting habitats, and reproduction, oil spills can damage the
environment long after the spilled oil has been removed from the
environment. Prevention measures and rapid response offer the only
effective means of minimizing the immediate, devastating effects and
long-term environmental effects of spills of petroleum and non-
petroleum oils, including vegetable oils and animal fats.
In summary, EPA finds that Petitioners' arguments about the manner
in which environmental species die or become injured following spills
of vegetable oils and animal fats, their claims about degradation of
oil in the environment, and their assertion that fats are essential to
humans and wildlife in no way obviate the need to prevent spills of
vegetable oils and animal fats that can cause lasting environmental
damage. Nor do the Petitioners' claims obviate the need to reduce
environmental damage from these spills by planning in advance for
effective response resources and actions. EPA hereby declines to modify
the July 1, 1994, Final Rule.
Dated: October 1, 1997.
Timothy Fields, Jr.,
Acting Assistant Administrator, Office of Solid Waste and Emergency
Response.
Acronym List
ACP--Area Contingency Plan
BOD--Biological Oxygen Demand
CFR--Code of Federal Regulations
COPs--Cholesterol Oxidation Products
CWA--Clean Water Act
DNA--Deoxyribonucleic Acid
DNR--Department of Natural Resources
DOT--Department of Transportation
EFA--Essential Fatty Acids
EPA--Environmental Protection Agency
ERNS--Emergency Response Notification System
FAO/WHO--Food and Agriculture Organization/World Health Organization
FR--Federal Register
FRP--Federal Response Plan
FWS--Fish and Wildlife Service
IARC--International Agency for Research on Cancer
Institute--Institute of Shortening and Edible Oils, Inc.
LC50--Lethal Concentration 50
LD50--Lethal Dose 50
LOPs--Lipid Oxidation Products
MOU--Memorandum of Understanding
NAS--National Academy of Sciences
NOAA--National Oceanic and Atmospheric Administration
NRC--Nuclear Regulatory Commission
NRC--National Response Center
OPA--Oil Pollution Act
PAHs--Polynuclear Aromatic Hydrocarbons
PCBs--Polychlorinated Biphenyls
PUFA--Polyunsaturated Fatty Acid (n-6 PUFA, including essential
fatty acid linoleic acid; n-3 PUFA, including the essential fatty
acid, a-linolenic acid)
RCRA--Resource Conservation and Recovery Act
RSPA--Research and Special Projects Administration
SPCC--Spill Prevention Countermeasure and Control
USDA--United States Department of Agriculture
USDHHS--United States Department of Health and Human Services
USDOC--United States Department of Commerce
USDOI--United States Department of Interior
USEPA--United States Environmental Protection Agency
Bibliography
Abel, P.D. (1996). Water Pollution Biology. Taylor and Francis,
London, United Kingdom, 113-163.
Abernathy, Charles O., Robert Cantilli, Julie T. Du, and Orville
A. Levander. (1992). Essentiality Versus Toxicity: Some
Considerations in the Risk Assessment of Essential Trace Elements.
In: J. Saxena, editor, Hazard Assessment of Chemicals. Hemisphere
Publishing Corp., New York, NY, Volume 8.
Albers, P.H. (1977). Effects of External Applications of Fuel
Oil on Hatchability of Mallard Eggs In: D.A. Wolfe, editor, Fate and
Effects of Petroleum Hydrocarbons in Marine Organisms and
Ecosystems. Pergamon Press, Oxford, pp. 158-163.
Albers, P.H. (1995). Oil, Biological Communities and Contingency
Planning In: L. Frink, K. Ball-Weir, and C. Smith, Editors. Wildlife
and Oil Planning. Response, Research, and Contingency Planning. Tri-
State Bird Rescue and Research, Newark, Delaware, pp. 1-9.
Alexander, Maurice M. (1983). Oil, Fish and Wildlife and
Wetlands: A Review. Northeastern Environmental Science 2 (1): 13-24.
Allen, A. and W.G. Nelson. (1983). Canola Oil As a Substitute
for Crude Oil in Cold Water Tests. Spill Technology Newsletter,
January-February, pp. 4-10.
Amdur, Mary O., John Doull and Curtis D. Klaassen. (1991).
Casarett And Doull's Toxicology. Pergamon Press, New York, NY,
Fourth Edition, pp. 12-126, 565-680.
Andrews, J.S., W.H. Griffith, J.F. Mead, and R.A. Stein. (1960).
Toxicity of Air-Oxidized Soybean Oil. J. Nutrition 70:199-210.
[[Page 54531]]
Aqua Survey, Inc. (1993). Diesel Fuel, Beef Tallow, RBD Soybean
Oil and Crude Soybean Oil: Acute Effects on the Fathead Minnow,
Pimephales Promelas. Study # 93-136, May 21, 1993.
Artman, N.R. (1969). The Chemical and Biological Properties of
Heated and Oxidized Fats. In: R. Poaletti and D. Krichevsky,
Editors, Advances in Lipid Research, pp. 245-330.
Berardi, L.C. and L.A. Goldblatt. (1980). Gossypol In: I.E.
Liener, Editor, Toxic Constituents of Plant Foodstuffs. Second
Edition, Academic Press, New York, pp. 183-237.
Boyd, E.M. (1973). Toxicity of Pure Foods. CRC Press, Cleveland,
OH, pp. 71-111.
Brekke, O.L. (1980). Edible Oil Processing--Introduction In:
American Soybean Association and American Oil Chemists' Society.
Handbook of Soy Oil Processing and Utilization. St. Louis, MO and
Champaign, IL, pp. 67-69.
Carroll, K.K. (1991) Am. J. Clin. Nutr. 53 (Suppl 4):1064S.
Cited in Hui, Y.H. (1996a). Bailey's Industrial Oil and Fat
Products, Edible Oil and Fat Products: General Application. John
Wiley & Sons, Inc., New York, NY, Volume 1, Fifth Edition, pp. 194-
196.
Chemical Hazards Response Information System (CHRIS). Department
of Transportation, U.S. Coast Guard. January, 1991.
Chemical Hazards Response Information System (CHRIS). Department
of Transportation, U.S. Coast Guard. 1995.
Clark, R.B. (1993). Marine Pollution. Clarendon Press, Oxford,
3rd Edition, Chapter 3, pp. 28-52.
Croxall, J.P. (1975). The Effect of Oil on Nature Conservation,
Especially Birds. In: Petroleum and the Continental Shelf of
Northwest Europe. v. 2: 93-101, Environmental Protection. Inst.
Petrol., London. As cited in Alexander, 1983.
Croxall, J.P. (1977). The Effects of Oil on Seabirds. Rapp. P-v.
Reun. Cons. Int. Explor. Mer 171:191-195, 1977 In: National Academy
of Sciences. Oil in the Sea. Effects, pp. 430-436.
Crump-Wiesner, Hans J. and Allen L. Jennings. Properties and
Effects of Nonpetroleum Oils. (1975). Pro. of 1975 Conference on
Prevention and Control of Pollution. American Petroleum Institute,
Washington, D.C., pp. 29-32.
Dubovkin, N.P., M.E. Tararyshkin, and L.D. Abashina. (1981).
Crude Oil and Product Research: Vapor Pressure and Critical
Parameters of Jet Fuel In: Chemistry and Technology of Fuels and
Oils. Plenum Publishing Corporation, pp. 207-210. Translated from
Russian; translated from Khimiya I Takhnologiya Topliv I Masel 17
(4):34-37, April, 1981, Consultants Bureau, New York.
Entrix, Inc. (1992). A Critical Review of Toxicity Values and an
Evaluation of the Persistence of Petroleum Products for Use in
Natural Resource Damage Assessments, Draft. Wilmington, DE. Prepared
for American Petroleum Institute. December 18, 1992, pp. 108-120.
ENVIRON Corporation. (1993). Environmental Effects of Releases
of Animal Fats and Vegetable Oils to Waterways. Arlington, VA June
3, 1993. Submitted by Petitioner.
Food and Agriculture Organization of the United Nations, World
Health Organization (FAO/WHO). (1994). Fats and Oils in Human
Nutrition. Expert Consultation, October 19-26, 1993, Rome. Published
by Food and Agriculture Organization, Rome, pp. 1-102, 113-147.
Frankel, E.N. (1984). Lipid Oxidation: Mechanisms, Products and
Biological Significance. Journal of the American Oil Chemist Society
61(12):1908-1917, December 1984.
Freedman. L.S., C. Clifford, and M. Messina. (1990). Cancer Res.
50:5710. In: Hui, Y.H. (1996a). Bailey's Industrial Oil and Fat
Products, Edible Oil and Fat Products: General Application. John
Wiley & Sons, Inc., New York, NY, Volume 1, Fifth Edition, pp. 194-
196.
French, C.E., R.H. Ingram, J.A. Uram, G.P. Barron, and R.W.
Swift. (1953). The Influence of Dietary Fat and Carbohydrate on
Growth and Longevity in rats. J. Nutr. 51:329-339. Cited in:
National Research Council, Nutrient Requirement of Laboratory
Animals., 4th Edition. National Academy Press, Washington, D.C., p.
20, 1995.
Frink, L. (1994). Statement on Regulatory Standards for the
Transportation of Edible Oil. Tri-State Bird Rescue & Research,
Inc., January 30, 1994.
Frink, L. and E.A. Miller. (1995). Principles of Oiled Bird
Rehabilitation. Wildlife and Oil Spills. Tri-State Bird Rescue &
Research, Inc., Newark, DE, pp. 61-68.
Gilman, A.G., L.S. Goodman, T.W. Rall, and F. Murad. (1985).
Goodman and Gilman's The Pharmacological Basis of Therapeutics.
Macmillan Publishing Company, Seventh Edition, pp. 1001-1003.
Goodrich, W.H. (1980). Environmental Concerns In: D.R. Erickson,
E.H. Pryde, O.L. Brekke, T.L. Mounts, and R.A. Falb, Editors,
Handbook of Soy Oil Processing and Utilization. American Soybean
Association, St. Louis, MS and American Oil Chemists' Society,
Champaign, IL, pp. 521-527.
Groenewold, J.C., R.F. Pico, K.S. Watson. (1982). Comparison of
BOD Relationships for Typical Edible and Petroleum Oils. Journal of
the Water Pollution Control Federation 54(4):398-405, April, 1982.
Hartung, R. (1965). Some Effects of Oiling on Reproduction of
Ducks. Journal of Wildlife Management 29(4):872-874.
Hartung, R. (1967). Energy Metabolism in Oil-Covered Ducks.
Journal of Wildlife Management 31:798-804.
Hartung, R. (1995). Assessment of the Potential for Long-Term
Toxicological Effects of the Exxon Valdez Oil Spill on Birds and
Mammals In: P.G. Wells, J.N. Butler, and J.S. Hughes, Editors, Exxon
Valdez Oil Spill: Fate and Effects in Alaskan Waters. American
Society for Testing and Materials, Philadelphia, PA, pp. 693-725.
Hayes, A. Wallace. (1982). Principles and Methods Of Toxicology.
Raven Press, New York, NY, pp. 1-55.
Hayes, A. Wallace. (1989). Principles and Methods of Toxicology.
Raven Press, New York, NY, Second Edition, pp. 75-76, 105-110, 169-
220.
Hazardous Substances Data Base (HSDB), National Library of
Medicine, 1997.
Hendricks, J.D., R.O. Sinnhuber, P.M. Loveland, N.E. Pawlowski,
and J.E. Nixon. (1980a). Hepatocarcinogenicity of Glandless
Cottonseeds and Refined Cottonseed Oil to Rainbow Trout (Salmo
gairdneri). Science 208:309-310.
Hendricks, J.D., R.O. Sinnhuber, J.E. Nixon, J.H. Wales, M.S.
Masri, and D.P.H. Hsieh. (1980b). Carcinogenic Response of Rainbow
Trout (Salmo gairdneri) to Aflatoxin Q1 and Synergistic
Effect of Cyclopropenoid Fatty Acids. JNCI 64:523-528.
Hendricks, J.D., T.R. Meyers, and D.W. Shelton. (1984).
Histological Progression of Hepatic Neoplasia in Rainbow Trout
(Salmo gairdneri). In: K.L. Hoover, Editor, Use of Small Fish
Species in Carcinogenicity Testing. National Cancer Institute
Monograph 65, NIH Publication Number 84-2653, National Institutes of
Health, Bethesda, Maryland, pp. 321-336, May, 1984.
Hoffmann, G. (1989). The Chemistry and Technology of Edible Oils
and Fats and their High Fat Products. Academic Press, London, pp. 1-
28, 343-363.
Hui, Y.H. (1996a). Bailey's Industrial Oil and Fat Products,
Edible Oil and Fat Products: General Application. John Wiley & Sons,
Inc., New York, NY, Volume 1, Fifth Edition, pp. 1-280, 397-439.
Hui, Y.H. (1996b). Bailey's Industrial Oil and Fat Products,
Edible Oil and Fat Products: Oils and Oilseeds. John Wiley & Sons,
Inc., New York, NY, Volume 2, Fifth Edition, pp. 1-689.
Hui, Y.H. (1996d). Bailey's Industrial Oil and Fat Products,
Edible Oil and Fat Products: Products and Application Technology.
John Wiley & Sons, Inc., New York, NY, Volume 4, Fifth Edition, pp.
1-655.
Institute of Shortening and Edible Oils, Inc. (1985). Treatment
of Wastewaters From Food Oil Processing Plants in Municipal
Facilities. October, 1985, pp. 1-18.
International Agency for Research on Cancer (IARC). (1984).
Evaluation of the Carcinogenic Risk of Chemicals to Humans:
Polynuclear Aromatic Compounds, Part 2, Carbon Blacks, Mineral Oils
and Some Nitroarenes. IARC, France, Volume 33, pp. 29-31 and 87-168.
International Agency for Research on Cancer (IARC). (1989).
Evaluation of the Carcinogenic Risk of Chemicals to Humans:
Occupational Exposures in Petroleum Refining: Crude Oil and Major
Petroleum Fuels. IARC, Lyon, France, Volume 45, pp. 13-272.
Kanazawa, A., S. Teshima, and K. Ono. (1979). Relationship
Between Essential Fatty Acid Requirements of Aquatic Animals and the
Capacity for Bioconversion of Linolenic Acid to Highly Unsaturated
Fatty Acids. Comp. Biochem. Physiol. 63B:295-298.
Katan, M. B., P. L. Zock, and R.P. Mensink. (1995). Trans Fatty
Acids and Their Effects on Lipoproteins in Humans. Annual Review of
Nutrition 15:473-493.
Kiritsakis, A.K. (1991). Olive Oil. American Oil Chemists'
Society, Champaign, Illinois, pp. 25-33, 104-127, and 157-161.
Klaassen, Curtis D., Mary O. Amdur and John Doull. (1986).
Casarett And Doull's
[[Page 54532]]
Toxicology. Macmillan Publishing Company, New York, NY, Third
Edition, pp. 11-98 and 519-635.
Kooyman, G.L., R.W. Davis, and M.A. Castellini. (1977) Thermal
Conductance of Ememrsed Prinniped and Sea Otter Pelts Before and
After Oiling with Prudhoe Bay Crude In: D.A. Wolfe, editor, Fate and
Effects of Petroleum Hydrocarbons in Marine Organisms and
Ecosystems, Pergamon Press, Oxford, pp. 143-150.
Lawson, H. (1995). Food Oils and Fats. Technology, Utilization,
and Nutrition. Chapman & Hall, New York, NY, pp. 3-27.
Lee, R.F. (1977). Accumulation and Turnover of Petroleum
Hydrocarbons in Marine Organisms In: D.A. Wolfe, Editor, Fate and
Effects of Petroleum Hydrocarbons in Marine Ecosystems and
Organisms, Pergamon Press, Oxford, pages 60-70.
Lee, D.J., J.H. Wales, J.L. Ayres, and R.O. Sinnhuber. (1968).
Synergism between Cyclopropenoid Fatty Acids and Chemical
Carcinogens in Rainbow Trout (Salmo gairdneri). Cancer Research
28:2312-2318, November, 1968.
Leighton, F.A. (1995). The Toxicity of Petroleum Oils to Birds:
An Overview. In: L. Frink, K. Ball-Weir, And C. Smith, Editors,
Wildlife and Oil Spills: Response, Research, and Contingency
Planning, Tri-State Bird Rescue & Research, Newark, Delaware, pp.
10-22.
Levy, J.R., K.A. Faber, L. Ayyash, and C.L. Hughes. (1995). The
Effect of Prenatal Exposure to the Phytoestrogen Genistein on Sexual
Differentiation in Rats. Second International Conference on
Phytoestrogens. October 17-20, 1993. Little Rock, Arkansas.
Proceedings of the Society for Experimental Biology and Medicine 208
(1):60-66, January, 1995.
Lewis, A., P. S. Daling, T. Strom-Kristiansen and P. J.
Brandvik. (1995). The Properties and Behavior of Crude Oil Spilled
at Sea. Pro. Second International Oil Spill Research and Development
Forum. International Maritime Organization, London, United Kingdom,
Volume 1, May 1995, pp. 408-420.
Lewis, R.J. (1996). Sax's Dangerous Properties of Industrial
Materials. Ninth Edition, Van Nostrand Reinhold, New York, Volume 1:
pp. xiii-xxvii, Volume 2: pp. 922, 924, 1143-1144, Volume 3: pp.
2054, 2372-2373, 2514, 2561, 2573-2574, 2894, 3340, 3367.
List, G. R. and D. R. Erickson. (1980). Storage, Stabilization
and Handling In: D.R. Erickson, E.H. Pryde, O.L. Brekke, T.L.
Mounts, and R.A. Falb, Editors, Handbook of Soy Oil Processing and
Utilization. American Soybean Association, St. Louis, MS and
American Oil Chemists' Society, Champaign, IL, pp. 272-98 and 300-
301.
Lyall, S. ``And Still the Birds Die, Out in the Poisoned Sea.''
New York Times International, April 26, 1996.
Material Safety Data Sheet (MSDS). (1997). Corn Oil. Fisher
Scientific, Fairlawn, NJ.
Mattson, F. H. (1973). Potential Toxicity of Food Lipids. In:
National Academy of Sciences, Toxicants Occurring Naturally in
Foods. National Academy of Sciences Press, Washington, D.C., pp.
189-209.
McKelvey, R.W., I. Robertson and P.E. Whitehead. (1980). Effect
of Non-Petroleum Oil Spills on Wintering Birds Near Vancouver.
Marine Pollution Bulletin 11:169-171.
Mecklenburg, T.A., S.D. Rice, and J.F. Karinen. (1977). Molting
and Survival of King Crab (Paralithodes ``Camtschatica'') and
Coonstripe Shrimp (Pandalus Hypsinothus) Larvae Exposed to Cook
Inlet Crude Oil Water-Soluble Fraction In: D.A. Wolfe, Editor, Fate
and Effects of Petroleum Hydrocarbons in Marine Organisms and
Ecosystem, Pergamon Press, Oxford, pp. 221-228.
Merck Index. (1989). 11th Edition. Merck and Co., Inc., Rahway,
NJ. Pp. 2528, 2550, 5173, 5245, 6951, 8127-8128.
Metcalf and Eddy, Inc. (1972). Wastewater Engineering:
Collection, Treatment, Disposal, Consulting Editors, V.T. Chow, R.
Eliassen, and R.K. Linsley, McGraw Hill, Inc., New York, pp. 239-
240.
Michael, A.D. (1977). The Effects of Petroleum Hydrocarbons on
Marine Populations and Communities. In: D.A. Wolfe, Editor, Fate and
Effects of Petroleum Hydrocarbons in Marine Ecosystems and
Organisms, Pergamon Press, Oxford, pages 129-137.
Miller, A.M., E.T. Sheehan, and M.G. Vavich. (1969). Prenatal
and Postnatal Mortality of Offspring of Cyclopropenoid Fatty Acid-
Fed Rats. Proc. Soc. Exp. Biol. Med. 131:61-66, 1969.
Minnesota Department of Conservation, Division of Game and Fish.
Waterfowl Mortality Caused by Oil Pollution of the Minnesota and
Mississippi Rivers in 1963. (1963). In Proceedings of the 20th
Annual Meeting of the Upper Mississippi River Conservation
Committee, pp. 149-177.
Mudge, S. M., M. A. Salgado and J. East. (1993). Preliminary
Investigations into Sunflower Oil Contamination Following the Wreck
of the M. V. Kimya. Marine Pollution Bulletin 26 (1): 40-43.
Mudge, S.M., H. Saunders and J. Latchford. (1994). Degradation
of Vegetable Oils in the Marine Environment. Countryside Commission
for Wales Report, CCW, Bangor, pp. 1-41.
Mudge, Stephen M. (1995). Deleterious Effects from Accidental
Spillages of Vegetable Oils. Spill Science and Technology Bulletin 2
(2/3): 187-191.
Mudge, Stephen M., Ian D. Goodchild and Matthew Wheeler. (1995).
Vegetable Oil Spills on Salt Marshes. Chemistry and Ecology 10: 127-
135.
Mudge, Stephen M. (1997a) Presentation, Third International
Ocean Pollution Symposium, April 6-11, 1997, Harbor Branch
Oceanographic Institution, Ft. Pierce, Florida.
Mudge, Stephen. (1997b) Can Vegetable Oils Outlast Mineral Oils
in the Marine Environment? Marine Pollution Bulletin, in press.
Murata, S., F. Tanaka, and J. Tokunaga. (1993). Measurement of
Vapor Pressure of a Series of Edible Oils. J. Fac. Agr., Kyushu
Univ. 38(1-2): 9-18.
Murray, M.W., J.W. Andrews, and H.L. DeLoach. (1977). Effects of
Dietary Lipids, Dietary Protein and Environmental Temperatures on
Growth, Feed Conversion and Body Composition of Channel Catfish. J.
Nutr. 107: 272-280. Cited in: National Research Council, Nutrient
Requirements of Warmwater Fishes and Shellfishes. National Academy
Press, pp. 9-11, 1983.
National Academy of Sciences (NAS), National Research Council
(NRC). (1977a). Drinking Water and Health. NAS, Washington, D.C.,
Volume 1, pp. 19-62, 252-253, and 265-270.
National Academy of Sciences (NAS), National Research Council
(NRC). (1977b). Nutrient Requirements of Rabbits. National Academy
Press, Washington, D.C., Second Revised Edition, pp. 2-28.
National Academy of Sciences (NAS), National Research Council
(NRC). (1981a). Nutrient Requirements of Coldwater Fishes. National
Academy Press, Washington, D.C., Number 16, pp. 6-53.
National Academy of Sciences (NAS), National Research Council
(NRC). (1981b). Nutrient Requirements of Goats: Angora, Dairy, and
Meat Goats in Temperate and Tropical Countries. National Academy
Press, Washington, D.C., Number 15, pp. 2-5 and 74-76.
National Academy of Sciences (NAS), National Research Council
(NRC). (1983). Nutrient Requirements of Warmwater Fishes and
Shellfishes. National Academy Press, Washington, D.C., Revised
Edition, pp. 2-58.
National Academy of Sciences (NAS), National Research Council
(NRC). (1984). Nutrient Requirements of Beef Cattle. National
Academy Press, Washington, D.C., 6th revised edition, pp. 2-6 and
35-36.
National Academy of Sciences (NAS). (1985c). Oil in the Sea--
Inputs, Fates and Effects. Chemical and Biological Methods. National
Academy Press, Washington D.C. pp. 89-269.
National Academy of Sciences (NAS). (1985d). Oil in the Sea--
Inputs, Fates and Effects. Fates. National Academy Press, Washington
D.C., pp. 270-368.
National Academy of Sciences (NAS). (1985e). Oil in the Sea--
Inputs, Fates and Effects. Effects. National Academy Press,
Washington, D.C., pp. 369-547.
National Academy of Sciences (NAS), National Research Council
(NRC). (1985). Nutrient Requirements of Sheep. National Academy
Press, Washington, D.C., Sixth Revised Edition, pp. 2-8 and 28.
National Academy of Sciences (NAS), National Research Council
(NRC). (1988). Nutrient Requirements of Swine. National Academy
Press, Washington, D.C., Ninth Revised Edition, pp. 2-8 and 63-66.
National Academy of Sciences (NAS), National Research Council
(NRC). (1992). Nutrient Requirements of Mink and Foxes. National
Academy Press, Washington, D.C., Number 7, Second Revised Edition,
pp. 9 and 19.
National Academy of Sciences (NAS), National Research Council
(NRC). (1994). Nutrient Requirements of Poultry. National Academy
Press, Washington, D.C., Ninth Revised Edition, pp. 11-1320-23, 27,
36-37, 40-42, 45, 69, and 75-77.
National Academy of Sciences (NAS), National Research Council
(NRC). (1995). Nutrient Requirements of Laboratory
[[Page 54533]]
Animals. National Academy Press, Washington, D.C., Fourth Revised
Edition, pp. 17-21, 60-71, 84-85, 97-100, 106-107, 126-129, and 141.
Nelson, G.J. (1990). Health Effects of Dietary Fatty Acids.
American Oil Chemists' Society, Champaign, Illinois, pp. 1-263.
Newman, G.G. and D.E. Pollock. (1973). Organic Pollution of the
Marine Environment by Pelagic Fish Factories in the Western Cape.
South African Journal of Science 69:27-29.
Oil Pollution Act (OPA) Public Law 101-380, 104 Stat. 484.
Percy FitzPatrick Institute of African Ornithology. (1974). Fish
Oil Kills Sea Birds. African Wildlife 28(4):24-25.
Phelps, R.A., F.S. Shenstone, A.R. Kemmerer, and R.J. Evans.
(1965). A Review of Cyclopropenoid Compounds: Biological Effects of
Some Derivatives. Poultry Science 44:358-394.
Rabbani, P.I., H.Z. Alam, S.J. Chirtel, R. Duvall, R.C. Jackson,
and G. Ruffin. (1997). Subchronic Toxicity of Menhaden Oil (MO) and
MaxEPA in Male and Female Rats. (Abstract). Fundamental and Applied
Toxicology, Supplement 36(1), Part 2:42-43, March, 1997. Presented
at 36th Annual Meeting of Society of Toxicology, Cincinnati, Ohio,
March 9-13, 1997.
Rand, G.M. and S.R. Petrocelli. (1985). Fundamentals of Aquatic
Toxicology: Methods and Applications. Hemisphere Publishing
Corporation, New York, NY, pp.1-109 and 124-163.
Ratledge, C. (1994). Biodegradation of Oils, Fats, and Fatty
Acids. In: C. Ratledge, Editor, Biochemistry of Microbial
Degradation. Kluwer Academic Publishers, The Netherlands, pp. 89-
141.
Rechcigl, Jr., M. (1981). CRC Handbook of Nutritional
Requirements in a Functional Context: Hematopoiesis, Metabolic
Function, and Resistance to Physical Stress. CRC Press, Inc., Boca
Raton, FL, Volume II, pp. 80-81, 148-51, 302-330, 342-43, 349, 357,
364-66, 381-82, 388, 390, 392, and 394-95.
Rechcigl, Jr., M. (1983). CRC Handbook of Naturally Occurring
Food Toxicants. CRC Press, Inc., Boca Raton, FL, pp. 15-17, 21-30,
101-104, 226.
Rescorla, A.R. and F.L. Carnahan. (1936). Ind. Eng. Chem.
28:1212-1213. In A.E. Bailey, Bailey's Industrial Oil and Fat
Products, p. 55, 1945.
Rigger, D. (1997). Edible Oils: Are They Really That Different?
Proceedings of the 1997 International Oil Spill Conference.
Sponsored by U.S. Coast Guard, U.S. Environmental Protection Agency,
American Petroleum Institute, International Petroleum Industry
Environmental Conservation Association, and International Maritime
Organization. Fort Lauderdale, Florida. April 7-10, 1997, pp. 59-61.
Roine, P., E. Uksila, H. Teir, and J. Rapola. (1960).
Histopathological Changes in Rats and Pigs Fed Rapeseed Oil.
Zeitschrift feur Erneahrungswissenschaft 1:118-124.
Rozemeijer, M.J.C., K. Booij, C. Swennen and J.P. Boon. (1992).
Harmful Effects of Floating Lipophilic Substances Discharged from
Ships on the Plumage of Birds. Netherlands Institute for Sea
Research (NIOZ), Den Burg, Netherlands, pp. 1-17, April, 1992.
Attachment to Amendments and Interpretation of the BCH Code and the
IBC Code, International Maritime Association, July 17, 1992 and
Annex 3, Draft Marine Environment Protection Committee Circular on
Harmful Effects on Birds from Contact with Animal and Fish Oils and
Fats and Vegetable Oils (Floating Lipophylic Substances).
Russell, D.J. and B.A. Carlson. (1978). Edible-Oil Pollution on
Fanning Island, Pacific Science 32(1):1-15, University Press of
Hawaii.
Salanitro, J.P., P. Dorn, M. Huesemann, K.O. Moore, I.A. Rhodes,
L.M.R. Jackson, T.E. Vipond, M.M. Western, and H.L. Wisniewski.
(1997). Crude Oil Hydrocarbon Bioremediation and Soil Ecotoxicity
Assessment. Environ. Sci. Technol. 31: 1769-1776.
Salgado, M. (1992). Contamination of the Anglesey Coastline by
Sunflower Oil from the Wreck of the M.V. Kimya. Master of Science
Thesis, School of Ocean Sciences, University College of North Wales,
Menai Bridge, United Kingdom. April, 1992, pp. 1-107.
Salgado, M. (1995). The Effects of Vegetable Oil Contamination
on Mussels. PhD Thesis, School of Ocean Sciences, University of
Wales, Menai Bridge, Gwynedd, United Kingdom. October, 1995, pp. 1-
219.
Sanders, H.L., J.F. Grassle, G.R. Hampson, L.S. Morse, S.
Garner-Price and C.C. Jones. (1980). Anatomy of an Oil Spill: Long-
term Effects from the Grounding of the Barge Florida Off West
Falmouth, Massachusetts. Journal of Marine Research 38(2): 265-380.
Sellers, E.A. and D.G. Baker. (1960). Coronary Atherosclerosis
in Rats Exposed to Cold. Can. Med. Assoc. J. 83:6-13 In: M.
Rechcigl, Editor, CRC Handbook of Nutritional Requirements in a
Functional Context, vol. II, Hematopoiesis, Metabolic Function, and
Resistance to Physical Stress, CRC Press, Inc., Boca Raton, Florida,
1981, pp. 527-528, 540.
Shaw, D.G. (1977). Hydrocarbons in the Water Column. In: D.A.
Wolfe, Editor, Fate and Effects of Petroleum Hydrocarbons in Marine
Ecosystems and Organisms, Pergamon Press, Oxford, pages 8-18.
Sheehan, D.M. (1995). Introduction: The Case for Expanded
Phytoestrogen Research. Second International Conference on
Phytoestrogens. October 17-20, 1993. Little Rock, Arkansas.
Proceedings of the Society for Experimental Biology and Medicine
208(1):3-5, January, 1994.
Smith, D.W. and S.M. Herunter. (1989). Birds Affected by a
Canola Oil Spill in Vancouver Harbour, February, 1989. Spill
Technology Newsletter, pp. 3-5 October-December 1989.
Steinberg, D. (1971). Phytanic Acid Storage Disease (Refsum's
Disease). In: J.B. Stanbury, J.B. Wyngaarden, and D.S. Fredrickson,
Editors, Metabolic Basis of Inherited Disease. 3rd Edition, McGraw-
Hill, New York. Cited in Mattson, F.H. Potential Toxicity of Food
Lipids, National Academy of Sciences, Toxicants Occurring Naturally
in Foods. National Academy of Sciences Press, Washington, D.C., pp.
189-209, 1973.
Stickney, R.R. and J.W. Andrews. (1971). Combined Effects of
Dietary Lipids and Environmental Temperature on Growth, Metabolism
and Body Composition of Channel Catfish (Ictalurus punctatus). J.
Nutr. 101:1703-1710. Cited in: National Research Council, Nutrient
Requirements of Warmwater Fishes and Shellfishes. National Academy
Press, Washington, D.C., pp. 9-11.
Stickney, R.R. and J.W. Andrews. (1972). Effects of Dietary
Lipids on Growth, Food Conversion, Lipid and Fatty Acid Composition
of Channel Catfish. J. Nutr. 102:249-258. Cited in: National
Research Council, Nutrient Requirements of Warmwater Fishes and
Shellfishes. National Academy Press, Washington, D.C., pp. 9-11.
Straughan, D. (1977). Biological Survey of Intertidal Areas in
the Straits of Magellen in January, 1975, Five Months After the
Metula Oil Spill In: D.A. Wolfe, Editor, Fate and Effects of
Petroleum Hydrocarbons in Marine Organisms and Ecosystems, Pergamon
Press, Oxford, pp. 247-260.
Szaro, R.C. and P.H. Albers. (1977). Effects of External
Applications of No. 2 Fuel Oil on Common Eider Eggs In: D.A. Wolfe,
Editor, Fate and Effects of Petroleum Hydrocarbons in Marine
Organisms and Ecosystems. Pergamon Press, Oxford, pp. 164-167, 1977.
Takeuchi, T. and T. Watanabe. (1979). Studies on Nutritive Value
of Dietary Lipids in Fish. XIX. Effect of Excessive Amounts of
Essential Fatty Acids on Growth of Rainbow Trout. Bull. Jpn. Soc.
Sci. Fish. 45:1517-1519. Cited in: National Research Council,
Nutrient Requirements of Warmwater Fishes and Shellfishes. National
Academy Press, Washington, D.C., pp. 9-11.
Tannenbaum, A. (1942). Cancer Res. 2:468. Cited in: Hui, Y.H.
(1996a). Bailey's Industrial Oil and Fat Products, Edible Oil and
Fat Products: General Application. John Wiley & Sons, Inc., New
York, NY, Volume 1, Fifth Edition, pp. 194-196.
Teal, J.M. (1977). Food Chain Transfer of Hydrocarbons, pp. 71-
77 In: Wolfe, D.A. Fate and Effects of Petroleum Hydrocarbons in
Marine Ecosystems and Organisms. Pergamon Press, New York, NY,
Chapters 8, 15, 16 and 23.
Ullrey, D.E. (1996). Personal Communication to Barbara Davis on
Nutritional Ecology of the Ruminant. June 18, 1996.
U.S. Department of Commerce (USDOC), National Oceanic and
Atmospheric Administration (NOAA). (1992a). An Introduction to Oil
Spill Physical and Chemical Processes and Information Management.
April, 1992, Chapters 2 and 3, pp. 2-1 to 2-56 and 3-1 to 3-97.
U.S. Department of Commerce (USDOC), National Oceanic and
Atmospheric Administration (NOAA). (1992b). Shoreline
Countermeasures Manual. Temperate Coastal Environments. pp. 9-23 and
37-62, December, 1992.
U.S. Department of Commerce (USDOC), National Oceanic and
Atmospheric Administration (NOAA). Memorandum of Record, June 3,
1993, from NOAA Hazardous Materials Response and Assessment
Division, June 3, 1993.
U.S. Department of Commerce (USDOC), National Oceanic and
Atmospheric Administration (NOAA). (1994). Options for Minimizing
Environmental Impacts of
[[Page 54534]]
Freshwater Spill Response. NOAA and American Petroleum Institute,
September 1994, pp. 2-11, 122-124.
U.S. Department of Commerce (USDOC), National Oceanic and
Atmospheric Administration (NOAA). (1996). Damage Assessment and
Restoration Program. Injury Assessment: Guidance Document for
Natural Resource Damage Assessment Under the Oil Pollution Act of
1990. Silver Spring, Maryland, Appendix C, Oil Behavior, Pathways,
and Exposure, pps. C-1-24 and Appendix D, Adverse Effects From Oil,
pps. D-1-69, August, 1996.
U.S. Department of Health & Human Services (USDHHS), Public
Health Service (PHS), 1963. Report on Oil Spills Affecting the
Minnesota and Mississippi Rivers, Winter of 1962-1963. Cincinnati,
Ohio, pp. 1-40.
U.S. Department of Health & Human Services (USDHHS). (1990).
Healthy People 2000. Conference Edition, pp. 119-137 and 390-436.
U.S. Department of Health & Human Services (USDHHS). Agency for
Toxic Substances and Disease Registry (ATSDR). (1995a).
Toxicological Profile for Gasoline, pp. 9-111, June, 1995.
U.S. Department of Health & Human Services (USDHHS). Agency for
Toxic Substances and Disease Registry (ATSDR). (1995b).
Toxicological Profile for Fuel Oils. pp. 9-109, June 1995.
U.S. Department of Health & Human Services (USDHHS). Agency for
Toxic Substances and Disease Registry (ATSDR). (1995c).
Toxicological Profile for Jet Fuels (JP4 and JP7). pp. 7-74, June
1995.
U.S. Department of the Interior (USDOI), Fish & Wildlife Service
(FWS). (1994). Submitted to U.S. Environmental Protection Agency,
1994. FWS Memorandum from Peter H. Albers, Leader, Contaminant
Ecology Group to Oil Spill Response Coordinator, December 29, 1993.
U.S. Department of the Interior (USDOI), Fish & Wildlife Service
(FWS). U.S. Fish and Wildlife Service Letter from Michael J. Spear,
Assistant Director, Ecological Services, to Ms. Ana Sol Gutierrez,
Research and Special Projects Administration, U.S. Department of
Transportation, April 11, 1994.
U.S. Department of Transportation (USDOT), Coast Guard (CG).
(1996). Response Plans for Marine Transportation-Related Facilities:
Final Rule. 61 FR 7890, 7907-7908, Feb. 29, 1996.
U.S. Environmental Protection Agency (USEPA), Memorandum of
Understanding between the Secretary of Transportation and the EPA
Administrator, dated November 24, 1971 (36 FR 24080).
U.S. Environmental Protection Agency (USEPA), Office of Research
and Development (ORD). (1976). Acute Toxicity of Selected Organic
Compounds to Fathead Minnows. EPA-600/3-76-097, Environmental
Research Laboratory, Office of Research and Development, U.S.
Environmental Protection Agency, Duluth, Minnesota, October, 1976,
pp 1-13.
U.S. Environmental Protection Agency (USEPA). (1978).
Identification of Conventional Pollutants. 43 FR 32857-32859, July
28, 1978.
U.S. Environmental Protection Agency (USEPA). (1979).
Identification of Conventional Pollutants, Final Rule. 44 FR 44501-
44503, July 30, 1979.
U.S. Environmental Protection Agency (USEPA). (1980). Water
Quality Criteria Documents; Availability. 45 FR 79318-79379,
November 28, 1980.
U.S. Environmental Protection Agency (USEPA), Office of Solid
Waste and Emergency Response, Office of Emergency and Remedial
Response (OSWER). (1988). The Oil Spill Prevention, Control, and
Countermeasures Program Task Force Report. May 13, 1988.
U.S. Environmental Protection Agency. (1994a). Memorandum from
Kathleen Bogan, ABB to Dana Stalcup, Oil Program Branch, USEPA, June
22, 1994.
U.S. Environmental Protection Agency (USEPA, 1994b). Oil
Pollution Prevention; Non-Transportation-Related Onshore Facilities;
Final Rule. 59 FR 34070, 3408, Appendix E, July 1, 1994.
U.S. Environmental Protection Agency (USEPA, 1994c). Request for
Data and Comment on Response Strategies for Facilities that Handle,
Store, or Transport Certain Non-Petroleum Oils. 59 FR 53742, 53743,
October 26, 1994, p. 5.
U.S. Environmental Protection Agency (USEPA), Office of Solid
Waste and Emergency Response (OSWER), Environmental Response Team.
(1995). Hazardous Material Incident Response Training Program,
Edison, NJ, 1995 Review, Section 4, pp. 1-27.
U.S. Environmental Protection Agency (USEPA), Office of Solid
Waste and Emergency Response (OSWER). Emergency Response
Notification System (ERNS) database, 1996 and ``An Overview of
ERNS,'' March, 1995.
Van Soest, P.J., Nutritional Ecology of the Ruminant. (1994).
Comstock Publishing Associates, Ithaca, pp. 1-3, 7-11, 325-336.
Venosa, A.D., M.T. Suidan, B.A. Wrenn, K.L. Strohmeier, J.R.
Haines, B.L. Eberhart, D. King, and E. Holder. (1996).
Bioremediation of an Experimental Oil Spill on the Shoreline of
Delaware Bay. Environ. Sci. Technol. 30:1764-1775.
Weiss, T.J. (1983). Food Oils and Their Use. Second Edition, Avi
Publishing Co., Inc., Westport, CT, pp. 10-13.
Whiticar, S., M. Bobra, M. Fingas, P. Jokuty, P. Liuzzo, S.
Callaghan, F. Ackerman and J. Cao. (1993). A Catalogue of Crude Oil
and Oil Product Properties. Environment Canada, Ottawa, Ontario,
1992 Edition, February 1993, pp. 111-119, 154-156, 160-165, 215-266.
Williams, T.M., J. McBain, R.K. Wilson, and R.W. Davis. (1990).
Clinical Evaluation and Cleaning of Sea Otters Affected by the T/V
Exxon Valdez Oil Spill. Sea Otter Symposium, U.S. Department of the
Interior, Biological Report 90 (12), December, 1990, Washington,
D.C., pp. 236-257.
Wisconsin, Department of Natural Resources. (1991a). Spill
Cleanup from the Central Storage and Warehouse Fire on Cottage Grove
Road in Madison. Memo of J.W. Brusca to K.R. Williams, May 14, 1991;
Central Storage Warehouse Fire/Spill Cleanup.
Wisconsin, Department of Natural Resources. (1991b). Memo from
T.J. Amman to Floyd Stutz, about May 31, 1991; Update on Clean Up
Actions following the Fire in Early May, 1991.
Wisconsin, Department of Natural Resources. (1991c). Letter from
T.J. Amman to T. Fitzgerald, Central Storage and Warehouse Co.,
Inc., August 1, 1991.
Wisconsin State Journal (1991a). Walking in Wet Concrete. May 5,
1991.
Wisconsin State Journal (1991b). Mike Flaherty. Grease Fire
Burning On. May 6, 1991.
Wisconsin State Journal (1991c). Mike Flaherty. Blaze Also Poses
Environmental Threat. May 6, 1991.
Wisconsin State Journal (1991d). Jonnel LiCari. Rain Adds to
Cleanup Woes. May 6, 1991.
Wisconsin State Journal (1991e). Mike Flaherty. Fire Assessment
Begins. May 9, 1991.
Wolfe, D.A. (1986). Source of Organic Contaminants in the Marine
Environment: Ocean Disposal and Accidental Spills In: C.S. Giam and
H.J.M. Dou, Editors, Strategies and Advanced Techniques for Marine
Pollution Studies: Mediterranean Sea. Springer-Verlag, Berlin, pp.
237-288.
Yannai, S. (1980). Toxic Factors Induced by Processing In I.E.
Liener, Editor, Toxic Constituents of Plant Foodstuffs, Academic
Press, New York, Second Edition, pp. 371-427.
Zoun, P.E.F., A.J. Baars and R.S. Boshuizen. (1991). A Case of
Seabird Mortality in the Netherlands Caused by Spillage of
Nonylphenol and Vegetable Oils, Winter 1988/1989. Sula 5 (3): 101-
103. Summary of a report, published in Dutch.
[[Page 54535]]
Appendix I--Supporting Tables
Table 1. Comparison of Physical Properties of Vegetable Oils and
Animal Fats with Petroleum Oils
Table 2. Comparison of Vegetable Oils and Animal Fats with
Petroleum Oil
Table 3. Comparison of Aqua Methods and Standard Acute Aquatic
Testing Methods
Table 4. Effects of Real-World Oil Spills
Table 1.--Comparison of Physical Properties of Vegetable Oils and Animal Fats With Petroleum Oils
----------------------------------------------------------------------------------------------------------------
Specific Gravity
Solidification at 25 deg.C unless Vapor pressure
Oil type point Solubility otherwise (mmHg)
specified
----------------------------------------------------------------------------------------------------------------
Edible Oils
----------------------------------------------------------------------------------------------------------------
Tallow.......................... 40 to 46 deg.C \1\ Insoluble in water 0.87 at 80 deg.C ..................
\1\. \3\.
Corn oil........................ 14 to 20 deg.C \4\ Insoluble in 0.916-0.921 \4\, Negligible.\6\
water; soluble in 0.91875.\5\.
acetone.1,2.
Coconut oil..................... Solid to liquid at Insoluble in 0.922 \7\......... ..................
15 deg.C, 1 water; very
atm.\7\. soluble in
ether.\1\.
Rapeseed/Canola oil............. -2 to -10 deg.C; Insoluble in 0.913-0.917 \8\... 250 deg.C,
liquid at 15 water; soluble in 0.535mmHg.\9\
deg.C.\4\. chloroform and
ether.\4\.
Fish oil........................ -2 to 4 deg.C; Insoluble in water 0.93 at 20 ..................
liquid at 15 \1\. deg.C.\7\.
deg.C.\4\.
Soybean oil..................... -10 to -16 deg.C; Insoluble in water 0.916-0.922 \4\, 250 deg.C,
liquid at 15 and acetone.\1\. 0.9175 \5\. 0.351mmHg.\9\
deg.C.\5\.
Cottonseed oil.................. 0 to -5 deg.C; Insoluble in 0.915-0.921 \4\, 250 deg.C,
liquid at 15 water; slightly 0.917 \5\. 0.317mmHg.\9\
deg.C.\4\. soluble in
alcohol.\1\.
Palm oil........................ Solid to liquid at Insoluble in 0.920-0.927 ..................
15 deg.C, 1 water.\1\. (fruit), 0.952
atm.\7\. (seed).\4\.
Lard............................ -2 to 4 deg.C \1\. Insoluble in water 0.917 \4\ <1 \1\.. ..................
or cold alcohol;
soluble in ether
and benzene.\1\.
----------------------------------------------------------------------------------------------------------------
Petroleum Oils
----------------------------------------------------------------------------------------------------------------
Diesel.......................... Liquid at 15 Insoluble in water 0.841 at 16 deg.C 38 deg.C,
deg.C, 1 atm \7\. \7\. \7\. 0.201mmHg.\9\
Fuel Oil #1 (kerosene).......... Liquid at 15 Insoluble in 0.80 \4\.......... 21 deg.C, 2.12-
deg.C, 1 atm \7\. water; miscible 26.4mmHg.\11\
with other
petroleum
solvents.\1\.
Fuel Oil 2-D.................... Liquid at 15 Insoluble in water 0.87-0.9 at 20 21 deg.C, 2.12-
deg.C, 1 atm \7\. \7\. deg.C \7\. 26.4mmHg.\11\
Crude........................... Liquid at 15 Insoluble in water 0.89 \8\.......... 37.8 deg.C,
deg.C, 1 atm \7\. \7\. 3.27mmHg.\10\
Fuel Oil #6 Residual............ Liquid at 15 Insoluble in water 0.95 approx. at 20 37.8 deg.C,
deg.C, 1 atm \7\. \7\. deg.C \7\. 0.092mmHg.\10\
Jet Fuel JP #7.................. .................. .................. .................. 260 deg.C, 2,480
mmHg.\12\
T 1............................. .................. .................. .................. 180-380 deg.C,
6,907mmHg.\13\
T 6............................. .................. .................. .................. 170-450 deg.C,
7,120mmHg.\13\
----------------------------------------------------------------------------------------------------------------
Viscosity dynamic Viscosity kinematic
Oil type (centipoises) (centistokes)
Edible Oils
------------------------------------------------------------------------
Tallow...................... 16.5 at 100 deg.C ....................
\3\
Corn oil.................... 30.8 at 40 deg.C \5\ ....................
Coconut oil................. 32.6 at 32 deg.C \7\ 29.79 at 37.8
deg.C.\14\
Rapeseed/Canola oil......... .................... 50.64 at 37.8 deg.C
\14\, 62.6 at 25
deg.C, 36.7 at 40
deg.C for RBD
Soybean Oil.\5\
Fish oil.................... .................... 32.7 at 37.8 deg.C
(cod liver 12).\14\
Soybean oil................. 28 at 40 deg.C \15\. 28.49 at 37.8 deg.C
\14\, 50.1 at 25
deg.C, 28.9 at 40
deg.C.\5\
Cottonseed oil.............. 34 at 40 deg.C \15\. 38.88 at 37.8
deg.C.\14\
Palm oil.................... ....................
Lard........................ 45 at 40 deg.C \15\. 44.41 at 37.8
deg.C.\14\
------------------------------------------------------------------------
Petroleum Oils
------------------------------------------------------------------------
Diesel...................... 11.9 at 37.8 deg.C 6.8 at 20 deg.C.\10\
\7\.
Fuel Oil #1 (kerosene)...... 1.15 at 21 deg.C \7\ 1.7 at 15 deg.C.\10\
Fuel Oil 2-D................ 1.97 at 21 deg.C \7\ 2.0 to 3.6 at 38
deg.C.\10\
Crude....................... 5.5 at 21 deg.C \7\. 5.96 at 20
deg.C.\10\
Fuel Oil 6 Residual......... 123 to 233 at 20 >130 at 40
deg.C \10\. deg.C.\10\
\1\ HSDB: Hazardous Substances Data Base. National Library of Medicine,
1997.
\2\ USDOC/NOAA, 1994.
\3\ Chemical Hazards Response Information System (CHRIS), DOT, USCG,
January, 1991.
\4\ Merck Index, 1989.
\5\ Hui, 1996a, 1996b.
\6\ Material Safety Data Sheet (MSDS), 1997, Corn Oil, Fisher
Scientific.
\7\ Chemical Hazards Response Information System (CHRIS), Department of
Transportation, U.S. Coast Guard, 1995.
[[Page 54536]]
\8\ Allen and Nelson, 1983.
\9\ Murata et al., 1993.
\10\ Whiticar et al., 1993.
\11\ U.S. Department of Health and Human Services, Agency for Toxic
Substances and Disease Registry, 1995b.
\12\ U.S. Department of Health and Human Services, Agency for Toxic
Substances and Disease Registry, 1995c.
\13\ Dubovkin et al.,1981. Translated.
\14\ Rescorla and Carnahan, 1945.
\15\ Weiss, 1983.
Table 2.--Comparison of Vegetable Oils and Animal Fats With Petroleum
Oils
------------------------------------------------------------------------
Vegetable oil/animal
fats Petroleum oils
------------------------------------------------------------------------
Chemical Properties:
Chemical Structure...... Triglycerides Alkanes,
(triacylglycerols), cycloalkanes,
cholesterol, aromatic
phospho lipids, hydrocarbons,
fatty acids, other polynuclear
components in crude aromatic
oils.1,2,3. hydrocarbons
(PAHs), other
components in crude
oils.4
Chemical Form........... Some liquids, some Some liquids, some
solids.1,5,6,7,8,9. solids.10,11,12,13
Physical Properties:
Density................. Most 0.908-0.927 at Most 0.80-0.95 at 20
20 deg. C; most deg. C; most float
float on water, on water, some
some sink.8,9,14
sink.1,5,6,7,9,14.
Solubility.............. Most insoluble in Most insoluble in
water, soluble in water, soluble in
organic organic
solvents.6,8,9. solvents.6,8, 12
Viscosity............... Wide range, depends Wide range, depends
on on temperature.8,10
temperature.1,5,7,8
,15,16.
Volatility.............. Generally small Some fractions
proportion (e.g., gasoline)
volatile, most not volatile, some not
volatile.1,5,13,17. volatile; 11-90%
volatile, depending
on type of
oil.10,11,12,18
Environmental Fate:
Environmental Oil found in water, Oil found in water,
Distribution. soil/sediment, air, soil/sediment,
biota; usually biota.4,12,24,25,26
little in ,27,28,29,30,31,32,
air.1,5,19,20,21,22 33
,23.
Persistence............. May persist in May persist in
environment for environment for
many years or many years; depends
degrade rapidly; on oil, media,
depends on oil, environmental
media, conditions where
environmental spilled.6, 30,38,39
conditions where
spilled.22,34,35,36
,37.
Chemical, Physical, and Oxidation, Oxidation,
Biological Reactions. hydrolysis, photolysis,
polymerization, weathering
photolysis, other processes; degraded
chemical reactions; by microorganisms;
degraded by petroleum
microorganisms, components taken up
metabolized by by plants and
plants and animals,
animals.1,2,3,40,41. metabolized by
macroinvertebrates
and some other
animals.4,30,33
Toxic Components, Some oils contain Many contain
Degradation Products. toxic components or benzene, PAHs, and
may be degraded to other toxic
form toxic components; may be
products.1,2,43,44, degraded to form
45. toxic
products.46,47,48
Physical Effects:
Smothering.............. Yes; suffocation Yes; suffocation
when oil blocks from oxygen
aeration at water depletion.30,47
surface or depletes
oxygen through
biodegradation.20,2
2,49,50,51,52,53.
Coating................. Yes, can cause Yes, can cause
hypothermia, hypothermia,
increased need for increased need for
food, loss of food, loss of
buoyancy, decreased buoyancy, decreased
ability to escape ability to escape
predators.22,29,36, predators.28,29,47,
37,54,55,56,57,58,5 54,55,56,57,58
9.
Egg Contamination....... Yes; can be Yes; can be
transferred from transferred from
coated parents and coated parents and
kill embryos by kill embryos by
blocking air blocking air
exchange at egg exchange at egg
surface.22,29,54,55 surface and by
,56,57,58. toxicitytion.28,29,
47,56,57,60,61,62,6
3
Food and Habitat Yes; can cause Yes, can cause
Destruction. starvation or starvation or
ingestion of oiled ingestion of oiled
food, destruction food that clogs
of future food organs, destruction
sources, of future food
destruction of sources,
habitat, community destruction of
effects.22,29,55,56 habitat, community
,57. effects.28,29,47,54
,55,56,57,58,61,64,
65
Lethality (LD50, LC50).. Results vary by Results vary by
test, organism, test, organism,
conditionsG546,47,6 conditions.46,47,66
6,67 Tests ,67,68 Tests
submitted by submitted by
Petitioners Other petitioner Other
tests: Corn oil and tests: 0.5-28 ppm
cottonseed more 96-hour LC50 static
lethal than mineral tests for some
oil in albino rats-- aromatic
55 g/kg was LD50 hydrocarbons for
for 5 days for corn selected marine
oil and for 4 days macroinvertebrates
for cottonseed oil; and fish.46,47,68
no fatalities at
130 g/kg with
mineral oil for 15
days.69 Other
tests: Several free
fatty acids
intermediate in
lethality in series
of chemicals in
fathead minnows.70
Other tests:
Mussels died after
two weeks or more
of exposure to low
levels of oils (0.3
ml/min flowrate for
oils, 300 ml/min
flowrate
seawater).19,21.
Acute Toxicity.......... Laxative, diarrhea, Laxative, decreased
lipid pneumonia, ability to escape
decreased ability predators,
to escape pneumonia; affects
predators; some lung, liver,
vegetable oils, kidney, blood,
such as safflower gastrointestinal
oil, are irritating and nervous
to human skin and systems.28,29,47,57
eyes.55,56,57,71,72.
Chronic Toxicity:
[[Page 54537]]
Cancer.................. High-fat diets and Benzene and some
diets containing PAHs are human
certain types of carcinogens;
fats increase certain crude oil
cancer incidence in fractions and
studies of petroleum products
laboratory animals sufficient evidence
and epidemiological of carcinogenicity
studies.1,73,74,75, in laboratory
76,77,78. animals and
associated with
increased cancer in
refinery
workers.47,48,79
Effects on Growth....... High levels of some Petroleum
types of fats hydrocarbons affect
increase growth and nearly all aspects
obesity but early of physiology and
death and decreased metabolism; reduced
reproductive feeding rates in
ability in several most animal species
species of animals; studied at
elevated levels of concentrations
some oils or similar to those in
components decrease spills; benthic
growth in some organisms
fish; growth especially
inhibition in sensitive; varying
mussels exposed to responses in marine
low levels of plants.28,29,38,47
sunflower
oil.1,21,35,74,78,8
0,81,82,83,84,85,86.
Reproductive and Decreased Affect broad range
Developmental Effects. reproduction or of reproductive and
growth and survival developmental
of offspring in processes;
some animals sensitivities to
ingesting high hydrocarbons vary
levels of oils; widely between
kills embryos in species and life
eggs by physical stages; significant
effects, unknown reproductive
whether toxicity impairment rarely
also seen in field
occurs.22,55,56,57, although coral,
74. mussels, fiddler
crabs,fish, birds,
crustaceans,
teleosts can be
affected, some for
years; decreased
reproductive
capacity and
malformations in
fish, birds;
reduced egg
production and
toxicity in several
bird
species.28,29,30,38
,47,59,60,61,62
Other Toxic Effects..... Effects on shells of Affect broad range
mussels exposed to of organ systems
low levels of oils, and functions;
decreased foot increased
extension activity; vulnerability to
human and some disease and
animal studies show decreased growth
correlation of high and reproductive
levels of dietary success; adverse
fats with coronary skin effects in
artery disease, workers; components
some types of affect immune and
cancer, hematopoeitic
hypertension, systems.28,29,30,38
diabetes, obesity, ,39,47,48
altered immunity,
altered steroid
excretion, effects
on bone modeling;
increased
atherosclerosis in
rats fed high
cholesterol levels;
decreased lifespan
in some animals
consuming high
levels of certain
types of oils that
increased growth
and
obesity.1,21,35,73,
74,78,86,87.
Toxicity of Components Most common chronic Single exposures to
or Degradation Products. toxic effects of benzene, a
gossypol, a component of
cottonseed oil petroleum oils, at
component, in very high
animals are cardiac concentrations
irregularity, fatal in man; can
circulatory failure cause central
or rupture of red nervous system
blood cells, and stimulation
death; erucic acid followed by
in rapeseed oil and depression and
mustardseed oil respiratory
causes cardiac failure; can
effects, fat produce nausea,
deposition in giddiness,
hearts of animals, headache,
growth suppression, unconsciousness,
anemia, and other convulsions, and
effects, affects paralysis; chronic
essential fatty exposure of humans
acids; cyclopropene to benzene can
fatty acids in produce anemia and
cottonseed and other blood effects
other oils suppress and decrease immune
growth and impair defense mechanisms;
female reproduction some PAHs,
in laboratory components of
animals, produce petroleum oils,
embryomortality in have reproductive
hens and rats, effects and cause
increase liver birth defects in
toxicity of other animals and can
chemicals, and affect skin, body
cause liver cancer fluids, and the
in rainbow trout; immune system after
oxidation products short and long-term
of animal fats and exposures in
vegetable oils-- animals, and cause
cholesterol some respiratory
oxidation products effects in workers;
can adversely some breakdown
affect the heart, products are
immune system, and mutagenic or linked
metabolism, and to
some lipid carcinogenicity.12,
oxidation products 28,29,38,47,48,66,7
may act in cancer 9,94
development and
affect
atherosclerosis.1,4
2,43,44,88,89,90,91
,92,93.
Indirect Effects............ High levels of oils Fuel oil no. 5
upset fermentation reduced herring
and digestion in population by
ruminants.\95\. decreasing amphipod
grazers that
control fungal
damage to fish
eggs.\47\
Aesthetics (Fouling, Rancid odors of Fouling of beaches
Rancidity). breakdown products; with tar balls and
fouling of beaches, weathered
polymers formed in oil.31,32,33,47
water and on
sediments and
concrete-like
aggregates of oil
and sand foul
beaches.
1,2,3,5,19,21,22,34
,35,96.
Fire/Explosion Hazard....... Usually not a Many petroleum
hazard, unless products contain
hexane or other volatile chemicals
chemicals that are flammable
present.1,2,15,17. or explosive under
certain
conditions.11,12,18
,31,39
[[Page 54538]]
Interference With Water Large amounts can Spills can interfere
Treatment. overwhelm with water
microorganisms used treatment
in water treatment processes,
plants; treatment requiring shutdown
plants must be shut of plants and
down and provision of
alternative water alternate water
supply provided to supply; can
prevent disruption contaminate
from groundwater.30,52,9
spills.96,97,98,99, 7,98,99
100.
------------------------------------------------------------------------
\1\ Hui, 1996a
\2\ Hoffmann, 1989
\3\ Lawson, 1995a
\4\ NAS, 1985a
\5\ Hui, 1996b
\6\ Hazardous Substances Data Base, National Library of Medicine, 1997
\7\ CHRIS (Chemical Hazards Response Information System), DOT, 1991
\8\ CHRIS (Chemical Hazards Response Information System), DOT, 1995
\9\ Merck Index, 1989
\10\ Whiticar et al., 1993
\11\ Dubovkin et al., 1995
\12\ USDHHS/ATSDR, 1995b
\13\ Material Safety Data Sheet on Corn Oil, 1997
\14\ Allen and Nelson, 1983
\15\ Rescorla and Carnahan, 1936
\16\ Weiss, 1983
\17\ Murata et al., 1993
\18\ USDHHS/ATSDR,1995a
\19\ Salgado, 1992
\20\ Mudge et al., 1993
\21\ Mudge, 1995
\22\ Crump-Wiesner and Jennings, 1975
\23\ Russell and Carlson, 1978
\24\ Sanders et al., 1980
\25\ Shaw, 1977
\26\ Lee, 1977
\27\ Teal, 1977
\28\ Alexander, 1983
\29\ Hartung, 1995
\30\ USDOC/NOAA, 1996
\31\ USDOC/NOAA, 1992b
\32\ Clark, 1993
\33\ NAS, 1985d
\34\ Mudge, 1997a
\35\ Mudge, 1997b
\36\ Minnesota, 1963
\37\ USDHHS, 1963
\38\ Entrix, 1992
\39\ USDOC/NOAA, 1992a
\40\ Hui, 1996d
\41\ Ratledge, 1994
\42\ Hayes, 1982
\43\ Mattson, 1973
\44\ Berardi and Goldblatt, 1980
\45\ Rechcigl, 1983
\46\ NAS, 1985c
\47\ NAS, 1985e
\48\ IARC, 1989
\49\ Mudge et al., 1995
\50\ Mudge et al., 1997b
\51\ Straughan , 1977
\52\ Groenewold et al., 1982
\53\ Institute, 1985
\54\ Michael, 1977
\55\ USDOI/FWS, 1994
\56\ Frink, 1994
\57\ Frink and Miller, 1995
\58\ Rozemeijer et al., 1992
\59\ Smith and Herunter, 1989
\60\ Albers, 1995
\61\ Leighton, 1995
\62\ Albers, 1977
\63\ Szaro and Albers, 1977
\64\ Croxall, 1975
\65\ Lyall, 1996
\66\ Klaassen et al., 1986
\67\ Rand, 1985
\68\ Mecklenburg et al., 1977
\69\ Boyd, 1973
\70\ USEPA, 1976
\71\ Gilman et al., 1985
\72\ Lewis, 1996
\73\ USDHHS, 1990
\74\ NAS/NRC, 1995
[[Page 54539]]
\75\ Tannenbaum, 1942
\76\ Carroll, 1990
\77\ Freedman, 1990
\78\ FAO/WHO, 1994
\79\ IARC, 1984
\80\ NAS/NRC, 1983
\81\ NAS/NRC, 1981a
\82\ Takeuchi and Watanabe, 1979
\83\ Stickney and Andrews, 1971
\84\ Stickney and Andrews, 1972
\85\ Murray et al., 1977
\86\ Salgado, 1995
\87\ Sellers and Baker, 1960
\88\ Frankel, 1984
\89\ Hendricks et al., 1980a
\90\ Phelps et al., 1965
\91\ Miller et al., 1969
\92\ Roine et al., 1960
\93\ Yannai, 1980
\94\ USDHHS/ATSDR, 1995d
\95\ Van Soest, 1994
\96\ Rigger, 1997
\97\ USEPA, 1978; Identification of Conventional Pollutants, 43 FR 32857-
32859, July 28, 1978
\98\ USEPA, 1979; Final Rule, Identification of Conventional Pollutants,
44 FR 44501-44503, July 30, 1979
\99\ Metcalf and Eddy, 1972
\100\ Goodrich, 1980
Table 3. Comparison of AQUA Methods and Standard Acute Aquatic Testing Methods
----------------------------------------------------------------------------------------------------------------
Method Number of species Fish size Acclimation
----------------------------------------------------------------------------------------------------------------
AQUA Report 1993.................. 1--Fathead minnow.... 0.0660.041 g, 5 days.
20.43.7 mm,
approximately 4 weeks old.
USEPA/OPP 1982 (update 1985) \1\.. 2--1 warmwater, 1 0.5-5 g, very young not (At least 2 weeks).
coldwater (2--1 used, longest no more
warmwater, 1 than twice shortest (0.5-
coldwater). 5g).
ASTM 1986......................... List of recommended 0.5-5 usually, not very 2 days or more with 100%
species. young, similar size and dilution water and
age, length of longest no maximum temperature,
more than twice shortest. change no more than 3
deg.C over 72 hours.
USEPA/OTS 1985 (update 1987)...... Fathead minnow or 21 cm Held 12 to 15 days before
other listed species. recommended length. testing; maintained in
water of quality to be
used in test at least 7
days.
USEPA/ORD 1985 (update 1991) Species depends on Age: 1-90 days {Age: 1-14 At least 24 hours in 100%
{update 1993b}\2\. regulatory days}. dilution water at
requirements. temperature range of
test.
APHA 1989......................... List; sensitive to Most sensitive life stage, Acclimate fish to lab
effluent, material, depending on test conditions at least 14
envi. conditions. purpose; longest no more days; 100% dilution
than 1.5 times length of water for at least 2
shortest. days.
OECD 1984......................... 1 or more............ Recommended total length 12 days or more; fish
for several species; exposed to water of test
21 cm for quality and temperature
fathead minnow; rationale at least 7 days.
if others.
EEC 1984.......................... 1 or more............ Recommended length 52 cm for fathead exposed to water of test
minnow. quality and temperature
at least 7 days.
----------------------------------------------------------------------------------------------------------------
Method Static test duration Aeration
AQUA Report 1993............ 48 hours............ No--Set 1.
Yes--Crude soybean
oil and diesel
fuel, set 2 aerated
for 48 hours;
others not aerated.
USEPA/OPP 1982 (update 1985) 96 hours (96 hours). (No, except aerate
reconstituted water
prior to use).
ASTM 1986................... 96 hours, except 48 May gently aerate
hours for daphnids all chambers and
and midge larvae; controls; use
record mortality at simultaneous test
24, 48, 96 hours without aeration;
for LC.50. toxicant
concentration in
aerated chamber not
more than 20% lower
than unaerated.
USEPA/OTS 1985 (update 1987) 96 hours preferred, Dilution water
mortality at 24, aerated until
48, 72, 96 hours, oxygen saturation,
LC50, 95% stored 2 days
confidence limits without further
(96 hours). aeration.
USEPA/ORD 1985 (update 1991) 24-48 hours; 96 May alter results,
{update 1993b}. hours, some states only as last
(24-96 hours, resort; none,
depends on unless dissolved
requirements). oxygen <4mg/l, at
which time gentle
single-bubble
aeration (Aeration
rate not over 100
bubbles/min in all
test solutions).
APHA 1989................... 96 hours for LC50; Avoid aerating,
24 hours, range- because aeration
finding. may alter results.
OECD 1984................... 96 hours preferred; May be used if no
mortality recorded significant loss of
at 24, 48, 72, and test substance;
96 hours and LC.50. must show test
substance
concentration at
least 80% nominal
concentration over
test period.
[[Page 54540]]
EEC 1984.................... 96 hours preferred, ....................
48 hours minimum;
morality recorded
each 24 hours and
LC.50.
------------------------------------------------------------------------
Method Test Vessels Dissolved oxygen
AQUA Report 1993............ Polyethylene buckets Protocol says not
below 4.5 mg/l (but
was below 4.5 in
100% beef tallow
and all
concentrations of
crude soybean oil,
Set 1).
USEPA/OPP 1982 (update 1985) (Glass or welded Measure
stainless steel; concentration at
polyethylene start and every 48
absorbs test hours to end; first
materials; for 48 hrs., 60-100%
other materials, saturation, then 40-
analyze toxicant 100% (Measure in
concentration). control, high,
medium, low
concentration).
ASTM 1986................... Welded stainless 60-100% saturation
steel or glass; for first 48 hours,
size and shape of 40-100% saturation
chamber may affect after 48 hours.
results if toxicant
volatilizes or
sorbs onto chamber.
USEPA/OTS 1985 (update 1987) Not contain Maintain above 4.5
substances that mg/l or at least
leached or 60% air saturation
dissolved into value.
aqueous solutions
or chemical
sorption; glass,
stainless steel,
perfluorocarbon
plastic.
USEPA/ORD 1985 (update 1991) Usually soft glass 4 mg/l minimum
{update 1993b}. {Borosilicate glass warmwater species,
or non-toxic 6 mg/l minimum
disposable plastic, coldwater species.
covered}.
APHA 1989................... No material with At or near
leachable saturation, never
substances or below 4 mg/l or 60%
adsorbs substances saturation.
from water;
stainless steel
probably best,
glass adsorbs
organics; do not
use rubber or
plastics with
fillers, additives,
stabilizers..
OECD 1984................... Chemically inert At least 60% of air
materials, suitable saturation value
capacity. throughout.
EEC 1984.................... .................... At least 60% of air
saturation value at
selected
temperature
throughout.
------------------------------------------------------------------------
Chemical Analysis of
Method Dilution Water Concentration
AQUA Report 1993............ 72 mg/l CaCO3 None reported;
(moderately hard, nominal
lab fresh water concentrations
deionized). listed in report.
USEPA/OPP 1982 (update 1985) Describe source, Describe methods,
characteristics, concentration,
pretreatment validation and
(Reconstituted blanks if done
water, soft, aged 1- (Chemical analysis
2 weeks, aerated of test solutions
before use or preferred,
natural water, especially if
hardness 40-48 mg/l aerated, material
as CaCO3; animals insoluble,
not stressed). containers not
stainless steel or
glass, or chemical
adsorbs to
container).
ASTM 1986................... Test organisms Measure
survive without concentration at
stress or grow and beginning and end
reproduce; in all chambers if
reconstituted, possible; desirable
surface, or natural to measure
water, requirements degradation
described. products and report
methods of
analysis, standard
deviation and
validation studies.
USEPA/OTS 1985 (update 1987) Drinking, natural, Measure
or reconstituted concentration in
water, 50-250 mg/l each at beginning
as CaCO3, pH6-8.5 and end; validate
preferred. analytical methods,
degradation
products not
interfere;
replicates within
20% (Concentration
in each chamber not
vary >30% from
measured at start).
USEPA/ORD 1985 (update 1991) Receiving water, Use methods in CWA
{update 1993b}. other surface Sec 304(h) for
water, ground analysis {Measure
water, soft in each test
synthetic water concentration at
{Same water, start, daily, and
culturing and end}.
dilution}.
APHA 1989................... Reconstituted or Measure
natural water; concentration in
standard water each container at
conditions for start and once
comparative during test;
toxicity, measured
sensitivity tests. concentration
within 15% of
calculated.
OECD 1984................... Drinking, natural or Must show
reconstituted concentration
water; prefer maintained and
hardness 50-250 mg measured
CaCO3 per liter, pH concentration at
6-8.5. least 80% of
nominal.
EEC 1984.................... Drinking water, Evidence from
natural water, analysis, chemical
reconstituted properties, or test
water; prefer 50- system used that
250 mg/l as CaCO3, concentration
pH 6-8.5. maintained and
within 80% of
initial
concentration.
------------------------------------------------------------------------
Method Results reported
AQUA Report 1993.................. 48-hour LC50; no confidence limits
reported, but protocol says
intervals computed.
USEPA/OPP 1982 (update 1985)...... Effect criteria, percent with
effects; 96-hour LC50, 95%
confidence limits, slope or show
LC50>100 mg/l (at least 30
organisms exposed) or >100,000
times maximum expected
environmental concentration or
estimated environmental
concentration (Methods, materials,
organisms, LC50, 95% confidence
limits, slope, calculations,
chemical analysis).
ASTM 1986......................... 24, 48, and 96-hour LC50, 95%
confidence limits, percentage died
at each concentration and controls,
calculation methods, and detailed
information on test and organisms
and findings, validation studies
for analytical methods and
accuracy.
USEPA/OTS 1985 (update 1987)...... Test procedures and conditions,
preparation of test solutions,
maximum concentration with 0%
mortality, minimum concentration
with 100% mortality, cumulative
mortality each concentration and
time, LC50 based on nominal
concentration at each time, 95%
confidence limits, concentration-
mortality curve at end, procedures
for determining LC50, mortality of
controls, test according to
guidelines.
[[Page 54541]]
USEPA/ORD 1985 (update 1991) Chemical analysis, organisms died or
{update 1993b}. effect in each chamber,
observations, LC50, 95% confidence
intervals and methods to calculate,
deviation from methods {Raw
toxicity data, relationship between
LC50 and NOAEL if NOAEL, pass/
fail}.
APHA 1989......................... LC50's for exposure times, 95%
confidence limits; mortality in
controls, describe test conditions
and methods, observations, test
material, response criteria.
OECD 1984......................... Cumulative percent mortality vs.
concentration; LC50; confidence
limits, p=0.95; where data
inadequate, geometric mean of
highest concentration with 0%
mortality and lowest concentration
with 100%.
EEC 1984.......................... Methodology, highest concentration
with 0% mortality, lowest
concentration with 100% mortality,
cumulative mortality, control,
LC50, 95% confidence limits, LC50
calculations, dose-response at end,
slope, dissolved oxygen and pH and
temperature every 24 hours.
------------------------------------------------------------------------
Method Special considerations
AQUA Report 1993.................. ....................................
USEPA/OPP 1982.................... Required to register end-use
(update 1985)..................... pesticide product introduced
directly into aquatic environment,
LC50 below or equal to maximum
expected environmental
concentration, or ingredient
enhances toxicity
(Required if insoluble; flow-through
if high BOD; 17-22 deg.C, at least
10 organisms/concentration, loading
limits; reviews statistical
analysis; invalid if aerated or not
glass or solubility problems).
ASTM 1986......................... Use flow-through if chemical has
high BOD; loading limits specified
so dissolved oxygen acceptable,
metabolic products not above
acceptable level, and no crowding;
temperature not vary > 1 deg.C; 10
organisms per concentration group.
USEPA/OTS, 1985................... Guidelines for development of test
(update, 1987).................... rules standards, test data under
Toxic Substances Control Act;
loading limits; 23 deg. 2 deg.C.
USEPA/ORD 1985.................... For National Pollutant Discharge
(update 1991)..................... Elimination System effluents;
{update 1993b}.................... definitive vs. screening tests;
loading, limits; 20 deg. C; 2
replicates, 10 organisms/
concentration.
{If pH outside 6-9, two parallel
tests, one adjusted; or static
renewal or flow-through}.
APHA 1989......................... 5 concentrations and control; 10
fish/tank, 20 fish/concentration;
species in receiving water or
similar, available for tests,
healthy in lab, important trophic
link or economic resource.
OECD 1984......................... 21-25 deg. C; carry out without pH
adjustment, adjust pH of stock
solution if necessary so
concentration not changed and no
reaction or precipitation.
EEC 1984.......................... 20-24 deg. C 1 deg.C;
carry out without pH adjustment,
adjust if necessary; interpret
results with care if stability or
homogeneity of test substance not
maintained.
------------------------------------------------------------------------
1 In some instances, other test conditions were allowed (USEPA, 1996).
Draft Amendment to Standard Evaluation Procedures, 1996 states:
Individual fish should weigh 0.1-5 g. Hardness of natural dilution water
of less than 200 mg/l as CaCO3 can be used in lieu of reconstituted
water for organic chemicals. Chemicals that are poorly soluble or with
a water solubility less than 100 ppm (<100 mg/l) should be tested up
to the maximum water solubility if certain conditions apply.
2 Final Report of Fourth Edition, August, 1993.
Table 4.--Effects of Real-World Oil Spills
----------------------------------------------------------------------------------------------------------------
Name and location of spill Oil spilled Effects
----------------------------------------------------------------------------------------------------------------
Minnesota Soybean Oil and Petroleum Oil 1 to 1.5 million gallons Killed thousands of ducks and other
Spills (1962-1963).1,2 soybean oil from storage waterfowl and wildlife or injured them
facilities, 1 million through coating; 5,300 birds injured or
gallons low viscosity died, 26 beavers, 177 muskrats.
cutting oil. Formed stringy, rubbery masses with
slicks; sank to bottom; milky material
and hard crusts of soybean oil with sand
on beaches.
Soybean oil caused much of waterfowl
loss, as shown by lab analysis of oil
scraped from ducks.
Fanning Atoll Spill (1975).\3\ Cargo ship with coconut Effects similar to petroleum oil spill.
oil, palm oil, and edible Killed fish, crustaceans, mollusks;
materials; ran aground, shifts in algal community continued for
dumped cargo onto coral 11 months.
reef.
Kimya Spill, North Wales Cargo of unrefined Killed mussels, shifts in ecological
(1991).4,5,6,7,8 sunflower oil. communities around spill.
Polymerized, covered bottom, killed
benthic organisms; formed impermeable
cap, shut out oxygen, bacteria cannot
break down; polymers remain nearly 6
years later.
Concrete-like aggregates of oil and sand
on beach.
Lab studies of mussels show small amounts
of sunflower and other vegetable oils
kill mussels after 2 weeks; affect
mussel lining.
Rapeseed Oil Spills (1974-1978).\9\ 3 small spills, total about Greater losses of birds from 3 small
35 barrels rapeseed oil. spills of rapeseed oil than 176 spills
of petroleum oils over 5 years in
Vancouver Harbor.
Killed 500 birds; petroleum spills killed
less than 50 birds.
Perhaps vegetable oils lack strong,
irritating odor of petroleum oils, so
birds do not avoid.
(1989).\10\ About 10 barrels (400 88 oiled birds of 14 species, half of
gallons) of rapeseed oil. them dead; half of rescued birds died;
casualties probably higher.
About 300 oiled Barrow's Goldeneyes
spotted 2 days after spill crowded onto
islands where they remained for 2 days--
fate unknown, but weakened birds often
die.
[[Page 54542]]
Fat and Oil Pollution in New York State Wide variety of sources.... Killed waterfowl, coated boats and
Waters (1967).\11\ beaches, tainted fish, created taste and
odor problems in water treatment plants.
Grease like substances on shore or
floating on Lake Ontario; shoreline
grease balls smelled like lard, analyzed
as mixtures of animal and vegetable
fats.
Spills of Fish Oil Mixtures near Bird Fish factory effluent pipe Killed at least 709 Cape Gannets, 5,000
Island, Lamberts Bay, South Africa near breeding ground for Cape Cormorants, and 108 Jackass
(1974).\12\ Cape Gannets. Penguins.
Penguins with sticky, white, foul-
smelling coat of oil shivering; gannet
chicks dead.
Milky white sea and clots of oil on
island smelling of fish.
Releases at two other fish factories at Two other fish factories; Two other fish factories; at one, killed
St. Helena Bay and Saldanha Bay, South storage pits and 10,000 rock lobsters and thousands of
Africa (1973).\13\ processing effluents and sea urchins probably from oxygen
off loading water from depletion; at second, killed 100,000
vessels. clams and black mussels, prawns,
polychetes, and anemones, and smelled
bad and adversely affected aesthetics of
beaches and camping site.
Soybean Oil Spills in Georgia Soybean oil from tanker Aesthetic effects at Lake Lanier; rancid
(1996).\14\ truck and soybean oil as weathered; adhered to boats and
vegetable oil refinery docks.
with overfilled At Macon, rapid response prevented
aboveground storage tank. significant damage from oil, which
flowed through storm water system and
entered stream; previous spills from
facility had entered sanitary sewer
system and damaged sewage treatment
plant.
Spill of Nonylphenol and Vegetable Oils Unknown source............. Thousands of seabirds, mostly Guillemots
in Netherlands (December,1988 to March, and Razorbills, washed ashore.
1989).\15\ 1,500 sick birds died; covered with oil,
emaciation, aggressive behavior, bloody
stools, leaky plumage; liver damage,
lung infections.
High levels of nonylphenol and vegetable
oils, such as palm oil.
Wisconsin Butter Fire and Spill Butter, lard, cheese as Released 15 million pounds of butter and
(1991).16,17,18,19,20,21,22,23 well as meat and other 125,000 pounds of cheese into the
food products. environment and damaged at least 4.5
million pounds of meat; thousands of
pounds of butter ran offsite; rapid
response prevented flow of buttery
material through storm sewers to nearby
creek and lake, where fish and other
aquatic organisms could have suffocated
from oxygen depletion.
Destroyed two large refrigerated
warehouses with $10 million to $15
million in property damage.
Cost tax payers $13 million for butter
and cheese stored under USDA surplus
program.
Damage to fire equipment from grease,
loss of business, overtime pay for 300
firefighters and responders, costs for
cleaning equipment and drains, rodent
control.
Environmental cleanup costs; thousands of
gallons of melted butter; butter and
spoiled meat declared hazardous waste.
----------------------------------------------------------------------------------------------------------------
1 Minnesota, 1963.
2 USDHHS, 1963.
3 Russell and Carlson, 1978.
4 Salgado, 1992.
5 Mudge et al., 1993.
6 Mudge et al., 1995.
7 Mudge, 1997a.
8 Mudge, 1997b.
9 McKelvey et al., 1980.
10 Smith and Herunter, 1989.
11 Crump-Wiesner and Jennings, 1975.
12 Percy-Fitzpatrick Institute, 1974.
13 Newman and Pollock, 1973.
14 Rigger, 1997.
15 Zoun et al., 1991.
16 Wisconsin, 1991a.
17 Wisconsin, 1991b.
18 Wisconsin, 1991c.
19 Wisconsin State Journal, 1991a.
20 Wisconsin State Journal, 1991b.
21 Wisconsin State Journal, 1991c.
22 Wisconsin State Journal, 1991d.
23 Wisconsin State Journal, 1991.
Appendix II--Edible Oil Regulatory Reform Act Differentiation
Edible Oil Regulatory Reform Act
Congress enacted the Edible Oil Regulatory Reform Act on November
20, 1995. The Act requires all Federal agencies (with the exception of
the Food and Drug Administration) to (1) differentiate between and
establish separate classes for animal fats and oils and greases, fish
and marine mammal oils, oils of vegetable origin, including oils from
certain seeds, nuts, and kernels, from other oils and greases,
including petroleum; and (2) apply standards to different classes of
fats and oils based on certain considerations. In
[[Page 54543]]
differentiating between the classes of fats, oils, and greases, each
Federal agency shall consider differences in the physical, chemical,
biological, and other properties, and in the environmental effects, of
the classes. These requirements apply when Federal agencies are issuing
or enforcing any regulation or establishing any interpretation or
guideline relating to the transportation, storage, discharge, release,
emission, or disposal of a fat, oil, or grease under any Federal law.
EPA's Final Rule amending the Oil Pollution Prevention regulation
(Oil Pollution Prevention; Non-Transportation-Related Onshore
Facilities; Final Rule, 59 FR 34070, July 1, 1994) was promulgated
before the Edible Oil Regulatory Reform Act was enacted; Congress did
not make the requirements of the Act retroactive. EPA is, therefore,
not obligated to evaluate the statutory criteria to determine if a
further differentiation between edible oils and other oils should be
made in its Final Rule. EPA does, however, present the following
information in support of its conclusion that spills of vegetable oils
and animal fats can indeed pose a serious risk to fish, wildlife, and
sensitive environments.
A summary of the properties and effects of vegetable oil and animal
fats are presented in Appendix I, Tables 1 and 2. Additional detailed
discussion and studies of these properties and effects are contained in
the Technical Document in support of this document.
Physical Properties. Vegetable oils and animal fats are generally
solids in water at ambient temperatures. They both have limited water
solubility but high solubility in organic solvents. They generally are
of low viscosity, have a low evaporation potential, and their specific
gravity can range from 0.87 to 0.92. Petroleum oils also have limited
water solubility and high solubility in organic solvents. They form an
emulsion in turbulent water, and they evaporate faster than edible
oils. Their specific gravity can range from 0.78 to 0.97. Data
regarding petroleum oil's solidity and viscosity vary. (See Appendix I,
Table 1. Comparison of Physical Properties of Vegetable Oils and Animal
Fats with Petroleum Oils and Table 2. Comparison of Vegetable Oils and
Animal Fats with Petroleum Oils.
Vegetable oils and animal fats and petroleum oils all have similar
physical properties. One difference is the low volatility of most
vegetable oils and animal fats, which results in less product removed
from a spill by evaporation and reduces the combustion and explosive
potential of these oils.
Chemical Properties. Animal fats and vegetable oils are water-
insoluble substances that consist predominantly of glyceryl esters of
fatty acids or triglycerides. Petroleum oils are extremely complex
mixtures of chemical compounds. Many classes of compounds are present
in petroleum, and each class is represented by many components. For
example, hydrocarbons are a major class of constituents of petroleum.
Similar behavior of fatty acids and petroleum oil in the aquatic
environment is largely a result of their predominantly hydrocarbon
character.
Biological Properties. Some vegetable oils and animal fats do
biodegrade more readily than petroleum oils; however, because their
evaporation potential is low, vegetable oils and animal fats may tend
to stay in the water in larger quantities and for longer periods of
time than petroleum oils. Under certain circumstances, vegetable oils
and animal fats can remain in the environment for periods of time
greatly exceeding their potential degradation time. Environmental
circumstances play an important part with regard to the comparative
degradation rates of petroleum and non-petroleum oils including
vegetable oil and animal fats. Both kinds of oil degrade more slowly in
low-energy and poorly oxygenated waters, and both tend to disappear
quickly in high-energy, well oxygenated, open water areas. Both
petroleum and non-petroleum oils can remain in the environment for
extended periods of time if buried under sediment or spilled in large
enough quantities to form thick layers. The high BOD of vegetable oils
and animal fats increases the rate of biodegradation but also quickly
depletes the available oxygen of the surrounding environment. This
could result in significant harm to shallow near-shore areas or
wetlands. Oxygen depletion could be as serious as toxicity with regard
to its impact on aquatic wildlife.
Environmental Effects. Certain effects of non-petroleum oils are
similar to the effects of petroleum oils because of the physical
properties common to both. Significant environmental harm from
petroleum oils, animal fats and vegetable oils, and other non-petroleum
oils can occur as a result of the following: physical effects such as
coating with oil, suffocation, contamination of eggs and destruction of
food and habitat, short and long term toxic effects, pollution and shut
down of drinking water supplies, rancid smells, fouling of beaches and
recreational areas.
Summary of Analysis after Reviewing the Act's Criteria. Based on
the significant degree of similarity between animal fats and vegetable
oils and other petroleum and non-petroleum oils, especially with
respect to negative environmental effects associated with the common
physical properties of all oils, EPA stands by its decision not to make
further changes to its July 1, 1994, Final Rule. The Final Rule already
provides a greater degree of flexibility for owners or operators of
facilities storing only non-petroleum oils, including vegetable oils
and animal fats, to devise different and more appropriate response
strategies than owners or operators of petroleum oil facilities.
[FR Doc. 97-27261 Filed 10-17-97; 8:45 am]
BILLING CODE 6560-50-P