An Analysis and Comparison of Methyl Tertiary Butyl Ether's (MTBE's) Use as a Fuel Oxygenate Against the Tenets of the Precautionary Principle

Item

Title

Eng An Analysis and Comparison of Methyl Tertiary Butyl Ether's (MTBE's) Use as a Fuel Oxygenate Against the Tenets of the Precautionary Principle

Date

2011

Creator

Eng Fowler, Diane R

Subject

Eng Environmental Studies

extracted text

AN ANALYSIS AND COMPARISON OF METHYL TERTIARY BUTYL
ETHER'S (MTBE’S) USE AS A FUEL OXYGENATE AGAINST THE TENETS
OF THE PRECAUTIONARY PRINCIPLE

by
Diane R Fowler

A Thesis: Essay of Distinction
Submitted in partial fulfillment
of the requirements for the degree
Master of Environmental Studies
The Evergreen State College
March 2011

© 2011 by Diane R Fowler. All rights reserved.

This Thesis for the Master of Environmental Studies Degree
by
Diane R Fowler
has been approved for
The Evergreen State College
by

______________________________
Maria Bastaki
Member of the Faculty

______________________________
Date

ABSTRACT
An Analysis and Comparison of Methyl Tertiary Butyl Ether's (MTBE’s) Use as a
Fuel Oxygenate Against the Tenets of the Precautionary Principle
Diane R Fowler

Fuel oxygenates, such as methyl tertiary butyl ether (MTBE), are
commonly added to gasoline to reduce air pollution by promoting more
complete burning of fossil fuels in combustion engines. However, large-scale
production and use of MTBE for this purpose has contaminated groundwater
throughout the United States, primarily as a result of spills and leaking
underground storage tanks. Shortly after MTBE's introduction as a fuel
oxygenate, anecdotal reports of acute respiratory health symptoms surfaced,
raising concerns about human health risks from exposure to inhaled MTBE
during vehicle refueling and in occupational settings. The chemical structure and
properties of MTBE suggest that its release into the environment would result in
widespread groundwater contamination and that remediation might prove
challenging. Once MTBE was discovered in groundwater, steps were taken to
replace MTBE with another fuel oxygenate, even though there was uncertainty
about MTBE’s health impacts to humans or the environment.
There are at least two schools of thought governing how or if a chemical
is introduced into the marketplace. The first, risk assessment, is the process of
quantifying the probability a chemical will cause a harmful effect to individuals
or populations. The other, the precautionary principle, states that with evidence
of threats of significant harm, even in the face of scientific uncertainty,
precautionary actions should be taken to protect public health. This thesis
examines and compares the use of MTBE as a fuel oxygenate against the tenets
of the precautionary principle. Variations in how precautionary principles are
applied are described as strong, moderate, or weak.
After reviewing the scientific literature available for MTBE, I believe its
use as a fuel oxygenate provides, at best, an example of the weak version of the
precautionary principle. Although steps were taken to discontinue its use after it
was found in groundwater, a strong version of the precautionary principle would
have required proof of “no environmental harm” prior to MTBE's introduction as
a fuel oxygenate.

TABLE OF CONTENTS
Chapter 1

Introduction and Background……………...............……………………………………..….1
Introduction…………………………....................…………………………..………….………1
Air Pollution and the Clean Air Act……....………..........…………………...……1
Extent of MTBE contamination in the United States……..........…..…8
Leaking underground storage tanks
(LUSTs)……............……….......….14

Chapter 2

Tools for Protecting Human Health: Risk Assessment and the
Precautionary Principle…………………………………….........…………………17
Introduction………………....………………………………................……….…………....17
Risk assessment…....………………………...............…………………….….…….…....17
The precautionary principle………………...………...........………….……….…...23

Chapter 3

Gasoline and Fuel Oxygenates………………...........……………………………......….29
Gasoline properties……………………....………………………..............………..……29
Gasoline additives and fuel oxygenates…………………............…....…….29
MTBE production and properties……………………….............………...…….32
Effects of fuel oxygenates on vehicle emissions……..….............……35

Chapter 4

MTBE Health Effects Studies……………………………...…….............…………...……39
Introduction………………………....................…………………………………..…....……39
Toxicology and exposure durations….…………............….……….…….……39
Human health effects and kinetics after exposure to
MTBE…………………………………………......................................…….…………….…..41
Acute…………………………………........................……………….….………..…….41
Chronic/subchronic……………………...................…..……………………….46
Possible human health benefits associated with MTBE use.......49
Evaluation of MTBE kinetics………………………………………..............………..51
Animal health effects after exposure to MTBE………….........….……..54
Acute……………………........................…………………………………………..…….54
Chronic…………………………….......................……………………………..……….57
Toxicity evaluation of MTBE metabolites………………............……...…..59
Evaluation of cancer-causing potential based on animal
studies………………….....................……………………………………….…….…..……60
Applicability of animal testing data to humans……...........……...……61
Regulatory limits……………..................……………………………….…………...…….62
Human pathways of exposure to MTBE……………………...........…..…….64
Estimates of human exposure to MTBE………………..…...........………….65
Comparison of human exposure estimates to regulatory
limits……………………………......................…………………………….……..……………67

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Chapter 5

Summary and Recommendations…………………..................…...….…………….71
Summary…………………....................………………………………..….………………….71
Recommendations………………………………..................………..……………………73

References………………………………..………….....................……………………………………….…...………………79

v

LIST OF FIGURES
Figure 1.

MTBE's chemical formula................................................................................32

Figure 2.

Formation of MTBE...........................................................................................32

vi

LIST OF MAPS
Map 1.

Areas of the United States requiring the use of reformulated
gasoline (RFG) as of May 1, 2007................................................................6

Map 2.

MTBE detections in groundwater in the United States,
1990-2009.......................................................................................................13

vii

LIST OF TABLES
Table 1 .

States participating in the Winter Oxyfuel Program as of
January, 2008....................................................................................................4

Table 2 .

Use of reformulated gasoline (RFG) in the United States
as of May 1, 2007............................................................................................7

Table 3 .

Most frequently detected volatile organic compounds (VOCs)
in U.S. aquifer samples................................................................................11

Table 4 .

Examples of the precautionary principle in environmental
laws and policy...............................................................................................24

Table 5 .

Typical properties of fuel oxygenates..........................................................30

Table 6 .

Comparison of annual U.S. production of ethanol and MTBE
as fuel oxygenates, 1990-2008.................................................................34

Table 7 .

Oxyfuel effects on twenty 1989 model year vehicles
exhaust emissions.........................................................................................36

Table 8 .

Effects of 15% MTBE fuel (2.7% wt oxygen) on older
1983-1985 and newer 1989 model year vehicles...............................37

Table 9 .

Impact of MTBE on vehicle emissions of volatile organic
compounds (VOCs) in summer and winter...........................................50

Table 10.

MTBE Minimal Risk Levels (MRLs) for humans based on animal
studies..............................................................................................................57

Table 11.

Summary of threshold doses for selected gasoline constituents........63

Table 12.

Comparison of MTBE Minimal Risk Levels (MRLs) with exposure
estimates for workers and consumers...................................................68

viii

ACKNOWLEDGEMENTS

I would like to thank my family for their love, support, and patience while
writing this thesis. It took longer than I ever could have imagined.
Specifically, I would like to thank my husband Chris for his
encouragement, and even his concern, during the course of this work. It all
helped to motivate me to finish this project. And to my two beautiful and
amazing sons, Ian and Ryan, I love you more than you could ever know.
To Harry, Dorothy, and Dave McAbee – You are always in my thoughts.
I hope you know how much you’re missed.
And to my reader and advisor Maria Bastaki, I greatly appreciate your
guidance, your willingness to share your toxicology expertise, and your
encouragement to continue my writing in spite of obstacles. You might be
almost as glad as I am to see this project completed.

ix

CHAPTER 1 – INTRODUCTION AND BACKGROUND
INTRODUCTION
Fuel oxygenates, such as methyl tertiary butyl ether (MTBE), are commonly
added to gasoline to reduce air pollution by promoting more complete burning of
fossil fuels in combustion engines. However, large-scale production and use of
MTBE for this purpose has contaminated groundwater throughout the United
States, primarily as a result of spills and leaking underground storage tanks. This
thesis examines and compares the use of MTBE as a fuel oxygenate against the
tenets of the precautionary principle.

AIR POLLUTION AND THE CLEAN AIR ACT
Gasoline-fueled engines are a major source of carbon monoxide (CO), a
colorless, odorless, and poisonous gas produced by the incomplete combustion of
carbon-containing fuels (EPA, 2011a). Elevated levels of CO have been shown to be
a human health hazard (National Science and Technology Council, 1997; EPA,
2011b). While motor vehicles built today emit fewer pollutants (60% to 80% less,
depending on the pollutant) than those built in the 1960s, cars and trucks still
account for almost half the emissions of the ozone precursors volatile organic
compounds (VOCs) and nitrogen oxides (NOx), and up to 90% of the CO emissions in
urban areas (EPA, 1970; EPA, 2011c).

1

The purpose of the Clean Air Act, originally passed by the United States
Congress in 1963, is to reduce air pollution in order to protect the environment and
human health. Under this law, the U.S. Environmental Protection Agency (EPA) set
limits on certain air pollutants and implemented a variety of programs intended to
reduce outdoor concentrations of air pollutants that cause smog, haze, acid rain,
and other problems (EPA, 2008a). The law was also intended to reduce emissions
of toxic air pollutants known to, or suspected of, causing cancer or other serious
health effects; and to phase out production and use of chemicals that destroy
stratospheric ozone (EPA, 2008a). These pollutants come from both stationary
sources, such as chemical plants, and mobile sources, such as cars and planes. This
federal legislation has undergone several amendments, most recently in 1990 (EPA,
1990). Three major threats specifically addressed in this latest amendment are acid
rain, urban air pollution and toxic air emissions (EPA, 2008b). Two of these threats,
urban air pollution and toxic air emissions, are addressed in part by the addition of
fuel oxygenates to vehicle fuel.
The 1990 Clean Air Act Amendments (1990 CAAA) created two programs,
administered by the EPA, requiring the use of fuel oxygenates (EPA, 1990). These
provisions address the continuing problem of urban air pollution, particularly with
regard to ozone (smog), carbon monoxide (CO) and particulate matter (PM-10), the
major components of urban air pollution.

2

The first program, the Winter Oxyfuel Program, began in the fall of 1992
with the objective of reducing carbon monoxide emissions in several areas of the
country where air pollutant monitoring demonstrated a persistent pattern of high
CO levels during winter months (EPA, 2008c). (Note: Denver, Colorado
implemented a winter oxyfuel program in 1988, prior to the 1990 CAAA.) During
cold weather, temperature inversions tend to trap pollutants near the ground and
inhibit dispersion. The buildup of CO is further aggravated in cold climates by
longer engine idling times from cold vehicles (National Science and Technology
Council, 1997). Under this program, the 1990 Clean Air Act Amendments required
the sale of gasoline with an oxygen content of 2.7% by weight during the cold
weather season in areas that failed to attain national ambient air quality standards
(NAAQS) for carbon monoxide. Although the 1990 CAAA does not require the use
of a specific fuel oxygenate, this level of oxygen is typically achieved by the addition
of about 15% methyl tertiary butyl ether (MTBE) or about 7.5% ethanol (by volume)
(National Science and Technology Council, 1997). Other fuel oxygenates that are
used to a lesser extent or that may potentially be used include ethyl tertiary-butyl
ether (ETBE), tertiary-amyl methyl ether (TAME), diisopropyl ether (DIPE), and
tertiary-butyl alcohol (TBA). As shown in Table 1, twenty three states were required
to implement the Winter Oxyfuel Program, but by January 2008 only six states had
continued the program (EPA, 2008d). The number of states participating in the
Winter Oxyfuel Program decreased over time as air quality improved. Once

3

wintertime air quality standards were met, the use of gasoline oxygenate was no
longer required in these areas.

Table 1. States participating in the Winter Oxyfuel Program as of
January, 2008
State

Winter Oxyfuel Program
Required, 1992

Alaska
Arizona
California
Colorado
Connecticut
District of Columbia
Maryland
Massachusetts
Minnesota
Montana
Nevada
New Jersey
New Mexico
New York
North Carolina
Ohio
Oregon
Pennsylvania
Tennessee
Texas
Utah
Virginia
Washington
Source: EPA, 2008d

Implementing Winter
Oxyfuel Program, 2008

The second program mandated by the 1990 Clean Air Act Amendments
required year-round use of reformulated gasoline (RFG) containing a minimum of
4

2.0% oxygen by weight, beginning in 1995, in selected areas having the highest
levels of tropospheric ozone. RFG is specially blended to have fewer polluting
compounds than conventional gasoline. In addition to reducing emissions of ozone
precursors, the RFG program was also intended to help reduce the emissions of
certain toxic organic air pollutants. The RFG program was initially mandated in
nine metropolitan areas with “severe” ozone problems (EPA, 2008d):
•

Los Angeles and San Diego, California;

•

Chicago, Illinois;

•

Houston, Texas;

•

Milwaukee, Ohio;

•

Baltimore, Maryland;

•

Philadelphia, Pennsylvania;

•

Hartford, Connecticut; and

•

New York City, New York.
Since then, five other areas have been classified with ‘severe' air quality

(EPA, 2008d):
•

Baton Rouge, Louisiana;

•

Atlanta, Georgia;

•

Sacramento and San Joaquin Valley, California; and

•

Washington, DC.

5

The map below (Map 1) shows the counties of nineteen states and the
District of Columbia that used RFG, either because of Clean Air Act requirements or
on a voluntary basis to achieve air quality standards. Table 2 is similar, but shows
greater detail about the voluntary or required use of RFG for each state.

Map 1. Areas of the United States requiring the use of reformulated
gasoline (RFG) as of May 1, 2007

Source: EPA, 2008d

6

Table 2. Use of reformulated gasoline (RFG) in the United States as of
May 1, 2007
State

California
Connecticut
Delaware
District of Columbia
Georgia
Illinois
Indiana
Kentucky
Louisiana
Maryland
Massachusetts
Missouri
New Hampshire
New Jersey
New York
Pennsylvania
Rhode Island
Texas
Virginia
Wisconsin
Source: EPA, 2008d

Required (at least in
certain areas) to use RFG
under 1990 Clean Air Act
Amendment

Opted to use RFG (voluntary use)
(Some states required to use RFG
in specified areas may also
voluntarily use RFG in other areas.)

In the summer of 1996, about 11 percent of the RFG sold contained ethanol
while virtually all the remainder contained MTBE (EPA, 1998a). By the late 1990s,
MTBE contamination was shown to be widespread in groundwater throughout the
United States (Squillace et al., 1999). Concerns about the unknown health risks
posed by drinking water containing MTBE prompted the Clinton administration in

7

2000 to ask the U.S. Congress to change a provision in the Clean Air Act that set the
standard for oxygen content in reformulated gasoline. The intent of this provision
was to eliminate or at least reduce the amount of MTBE in gasoline. By the summer
of 2005, the ethanol share had increased to about 53 percent, with corresponding
decreases in MTBE (EPA, 2008c).
In late 2005, the U.S. Congress passed the Energy Policy Act which amended
the 1990 Clean Air Act Amendments to remove the oxygen content requirement
and associated compliance requirements for reformulated gasoline (EPA, 2005).
Although the requirement to use fuel oxygenates has been removed, many states
continue to use oxygenates to meet air quality standards (EPA, 2008d). All states
still using fuel oxygenates now use 100% ethanol.

EXTENT OF MTBE CONTAMINATION IN THE UNITED STATES
The presence of MTBE in groundwater has been observed at least since the
mid-1980s. The 1990 Clean Air Act Amendments led to a rapid expansion in the
production and use of MTBE starting in the late 1980s (ATSDR, 1996), and it has
been used by refiners since the 1970s to increase octane when lead was banned for
this use (McCarthy & Tiemann, 2006). The first national survey on the occurrence
of volatile organic compounds (VOCs) analyzed samples of untreated ambient
groundwater collected between 1985 and 1995 (Squillace et al., 1999). It was
noted that MTBE was one of the most frequently detected VOC in both urban and
rural areas. Routine monitoring of ambient ground water between 1993 and 1998
8

noted the frequent occurrence of MTBE, typically at low levels, in shallow urban
ground water in the northeastern United States (Grady, 2001). The occurrence of
MTBE and other VOCs were also noted in surveys of community drinking water
sources in the United States between 1999-2001 (Clawges et al., 2001; Delzer &
Ivahnenko, 2003).
More recently (2006), the U.S. Geologic Survey (USGS) National Water
Quality Assessment (NAWQA) Program performed a national assessment of 55
VOCs in ground water to provide a general characterization of water-quality
conditions in the United States (Zogorski et al., 2006). The assessment of ground
water included analyses of about 3,500 water samples collected between 1985 and
2001 from various types of wells. Samples were collected at the well head, before
any treatment or blending, from 2,401 domestic wells and 1,096 public wells.
Almost 20 percent of the water samples from aquifers contained one or more of
the 55 VOCs, at a detection limit of 0.2 microgram per liter (μg/L). This detection
frequency increased to slightly more than 50 percent for the subset of samples
analyzed with a low-level analytical method and for which an order-of-magnitude
lower assessment level (0.02 μg/L) was applied. The finding that most VOC
concentrations in ground water are less than 1 μg/L is important because many
previous monitoring programs did not use low-level analytical methods and
therefore would not have detected such contamination. MTBE was the third most
frequently detected VOC (behind chloroform and perchloroethene, see Table 3 for
a complete list) and was found to have a regional or local occurrence pattern
9

(Zogorski et al., 2006). The greatest detection frequency of MTBE was in areas: (1)
with high population density; (2) where MTBE was used as an oxygenate in
reformulated gasoline, and (3) with high rates of ground-water recharge, such as in
the highly populated New England and Mid-Atlantic States. In general, MTBE did
not occur frequently with other gasoline components in ground water except when
detected at high concentrations. The detection of MTBE without other common
gasoline hydrocarbons likely is the result of MTBE’s higher solubility and greater
persistence in ground water relative to common gasoline hydrocarbons. The study
noted that the relatively frequent detections of MTBE in aquifers were not
anticipated due its relatively short and recent use (a period of approximately 10
years at the time of this study) (Zogorski et al., 2006).

10

Table 3. Most frequently detected volatile organic compounds (VOCs)
in U.S. aquifer samples
(VOCs found in about one percent or more of aquifer samples, at an assessment
level of 0.2 μg/L. Compounds are listed by decreasing detection frequency.)
Compound name

Chloroform
Perchloroethene
Methyl tert-butyl ether
Trichloroethene
Toluene
Dichlorodifluoromethane
1,1,1-Trichloroethane
Chloromethane
Bromodichloromethane
Trichlorofluoromethane
Bromoform
Dibromochloromethane
trans-1,2-Dichloroethene
Methylene chloride
1,1-Dichloroethane
Source: Zogorski et al., 2006

VOC group
trihalomethane
solvent
gasoline oxygenate
solvent
gasoline hydrocarbon
refrigerant
solvent
solvent
trihalomethane
refrigerant
trihalomethane
trihalomethane
solvent
solvent
solvent

Because of known or suspected human-health concerns, the EPA has
established Maximum Contaminant Levels (MCLs) that apply to 29 VOCs in drinking
water supplied by public water systems. In addition, some States have set MCLs for
additional VOCs and in some cases have established more stringent standards than
EPA’s values. To set an MCL for a contaminant, EPA first determines how much of
the contaminant may be present with no adverse health effects. This level is called
the Maximum Contaminant Level Goal (MCLG) and is basically a non-enforceable
public health goal. The MCL is then set as close as possible to the MCLG standards
and is the legally enforceable limit on the amount of a hazardous substance that
11

can be delivered to any user of a public water system (EPA, 2006). While the MCLG
considers only public health, the MCL considers other factors, such as the use of
best available technology, treatment techniques, and cost. The human-health
consequences of exposure to VOCs in drinking water at concentrations less than
MCLs are uncertain. Concentrations of MTBE were typically less than the lower limit
of the EPA drinking-water consumer concentration range of 20-40 parts per billion,
which is based on taste and odor thresholds. Only one drinking-water sample,
which was from a domestic well, had a concentration of MTBE equal to the lower
limit of the drinking-water consumer advisory. No Federal drinking-water standard
(MCL) currently exists for MTBE. Health-based Screening Levels (HBSLs) have been
calculated for unregulated contaminants (those with no MCLs) analyzed by the
NAWQA Program. HBSLs are estimates of benchmark concentrations of
contaminants in water that may be of potential human-health concern and are
based on health effects alone. Although HBSLs have been calculated for 15 of the
26 unregulated VOCs in this assessment, they were not calculated for the remaining
11 VOCs, which include MTBE, due to a lack of toxicity information. The NAWQA
Program also analyzed samples for three other gasoline oxygenates – tert-amyl
methyl ether (TAME), diisopropyl ether (DIPE), and ethyl tert-butyl ether (ETBE).
These VOCs were detected infrequently in samples from domestic and public wells
(Zogorski et al., 2006).
Although most detections of MTBE contamination are found in areas where
MTBE has been used as a fuel oxygenate, it is not limited to these areas. The map
12

below (Map 2), created using the NAWQA Data Warehouse Mapper, shows areas of
the United States where MTBE has been detected in groundwater samples between
1990 and 2009. Comparisons to the previous map of RFG areas illustrate MTBE
contamination is found in areas where MTBE has not been used as a fuel oxygenate.

Map 2. MTBE detections in groundwater in the United States,
1990-2009

Source: USGS, 2009
Possibilities for how this contamination spread beyond the RFG-use areas
include point sources such as leaking underground storage tanks, tank overflow
spills, leaks from transport pipelines, vehicle accidents, and improper disposal.
Potential nonpoint sources of MTBE include evaporative losses from tanks or
pipelines, incomplete combustion in automotive engines, urban storm water runoff,
exhaust from motorized watercraft, and leaks from watercraft tanks (Zogorski et al.,
13

2006). Since the contribution of leaking underground storage tanks, or LUSTs,
towards MTBE contamination is likely substantial, it is worth exploring in greater
detail.

LEAKING UNDERGROUND STORAGE TANKS
Leaking underground storage tanks (LUSTs) that contain gasoline are
believed to be the primary source of localized releases of MTBE in high
concentrations. The EPA defines an underground storage tank as “a tank (or a
combination of tanks) and connected piping having at least 10 percent of their
combined volume underground” (EPA, 2008e). Until the mid-1980s, most
underground storage tanks (USTs) were made of bare steel, which is likely to
corrode over time and allow UST contents to leak into the environment. Faulty
installation or inadequate operating and maintenance procedures also can cause
USTs to release their contents into the environment. According to the EPA, as of
March 31, 2009, there were 616,613 active underground storage tanks (at
approximately 235,000 sites) nationwide which are regulated by the UST technical
regulations (EPA, 2009a).
In order to prevent leaks from occurring, all regulated tanks and piping are
required by the EPA to have release detection (often called leak detection) so that
leaks are discovered quickly before contamination spreads from the underground
storage tank site. Leak detection methods include manual tank gauging (on tanks
2,000 gallons or less), automatic tank gauging systems, vapor monitoring, ground
14

water monitoring, and statistical inventory reconciliation (SIR). SIR uses computer
software to conduct a statistical analysis of inventory, delivery, and dispensing data
collected over a period of time to determine whether or not a tank system is
leaking. Another method is secondary containment, which involves placing a
barrier between the underground storage tank and the environment, such as a
vault, liner, or outer wall of a double-walled structure.
Despite federal and state programs to improve handling of gasoline and
other fuels in pipelines, underground and above ground storage tanks, and other
transport modes, gasoline spills and leaks still occur. Improper installation is a
significant cause of fiberglass-reinforced plastic (FRP) and steel UST failures,
particularly piping failures (EPA, 2009b). Many releases at UST sites come from
spills made during delivery and usually result from human error (EPA, 2008e).
Additionally, not all UST systems are regulated and not all components of regulated
systems are regulated (EPA, 2009c).
As of March 31, 2009, there were 482,166 confirmed releases at
underground storage tanks (EPA, 2009a). The actual number of releases is likely
much higher as not all tank leaks are reported. Although 456,677 cleanups have
been initiated and nearly 381,000 cleanups have been completed, there is a
cleanup backlog of 101,190 tanks (EPA, 2009a). Nearly all LUSTs at these sites
contain petroleum (EPA, 2008e).

15

16

CHAPTER 2 – TOOLS FOR PROTECTING HUMAN HEALTH: RISK
ASSESSMENT AND THE PRECAUTIONARY PRINCIPLE
INTRODUCTION
There are at least two schools of thought governing how or if a chemical is
introduced into the marketplace. The first, risk assessment, is the process of
quantifying the probability a chemical will cause a harmful effect to individuals or
populations. The other, the precautionary principle, states that with evidence of
threats of significant harm, even in the face of scientific uncertainty, precautionary
actions should be taken to protect public health. These two methods of protecting
human health are discussed below.

RISK ASSESSMENT
In the context of public health, risk assessment is the process of quantifying
the probability of a harmful effect to individuals or populations. A goal of risk
assessment is to estimate the extra risk caused by a toxic or carcinogenic chemical
over that which exists when exposure to the chemical does not exist (Rodricks,
2007).
For all non-carcinogenic chemicals, there is a dose threshold under which no
effects of toxicity are observed in animal studies or expected in exposed individuals.
Toxic effects are observed in a dose-dependent manner above this threshold. As
17

the dose increases above the threshold, the frequency and seriousness of those
effects also increase. This relationship is referred to as the dose-response.
According to Rodricks (2007), if for every chemical in the environment we knew the
range of ‘no-effect’ doses and the point at which toxicity begins to appear – the
point at which the threshold of toxicity is passed – we could then act to prevent
exposures from ever reaching the level at which harmful doses are created. The
problem is that data on toxicity and dose-response are only available for a small
fraction of the chemicals to which people are exposed.
Risk is the likelihood, or probability, that the toxic properties of a chemical
will be produced in populations of individuals under their actual conditions of
exposure (Rodricks, 2007). Risk assessment involves four steps: (1) hazard
identification; (2) dose response assessment; (3) exposure assessment; and (4) risk
characterization.
First, in hazard identification, all available epidemiology and experimental
toxicity data are gathered and critically evaluated in order to assess the types of
toxicity the chemical can produce. These may include acute or chronic effects,
various organs and tissues (dermal, respiratory, etc), and a variety of biological
endpoints from the most overt (death) to molecular level effects (enzyme
inhibition).
Next, a dose-response assessment quantifies the relationship between
exposure and the response observed in studies. This analysis considers the range of
18

doses where the chemical’s toxicity can be produced and the threshold of no effect.
The challenge in this step is extrapolating results from experimental animals (such
as mice or rats) to humans, and/or from higher to lower doses. There are also
differences between individuals due to genetics or other factors, which may mean
that the hazard may be higher for particular groups, often referred to as susceptible
populations. There may also be missing data. To account for uncertainties, the
lowest no-observed-effect-level (NOEL) from all available studies is assumed to be
the threshold of toxicity for the groups of subjects (human or animal) in which
toxicity data were collected. Safety factors (typically a factor of ten) are built in to
further account for uncertainties. For example, for humans, the threshold is
estimated by dividing the NOEL derived from animal studies by a factor of ten for
each reason of uncertainty, and typically is 1/100th of the animal threshold value.
Then, in exposure assessment, the condition (dose, timing and duration)
under which humans may be exposed to the chemical is evaluated. Since different
locations, lifestyles, and other factors likely influence the amount of contaminant
that is received, a range or distribution of possible values are generated. Particular
care is taken to determine the exposure of susceptible populations.
Finally, risk assessment, or risk characterization, uses the results of the
previous three steps to produce an estimate of overall risk. Because of the different
susceptibilities and exposures, this risk will vary within a population. The decisions
based on the application of risk assessment are sometimes based on a standard of

19

protecting those most at risk. If an identifiable sub-population is more susceptible
due to inherent genetic or other factors, policies are often set to protect such
groups. This is currently done under the Clean Air Act for populations such as
asthmatics.
It is important to note that the final calculated risk is still only an estimate.
Because of the approach of ten-fold safety factors, risk is more likely to be
overestimated (so the resulting estimates are more likely to be greater than the
actual risk) but some detailed analyses have shown that for specific chemicals it is
still possible that risk can be underestimated.
In summary, risk assessment is a process of estimating risk. It takes into
account all available scientific information and uses the most conservative
adjustments for uncertainties to offer as safe an estimate of risk as possible. The
information gathered in the risk assessment should identify hazards, identify the
populations potentially at risk from those hazards, and estimate the risks involved.
The products of risk assessment are typically used in efforts to reduce, limit
or eliminate the risks, also referred to as risk management. The problem with risk
management is that the techniques and approaches used are intended to minimize
the risks of the proposed activity but not to question whether the harm is
necessary, or if there might be alternatives that would avoid harm altogether.
Questioning whether the risks are necessary or if there are alternatives falls under a

20

larger decision making process that may directly or indirectly affect regulatory
change.
Risk assessment is intended to be used as a regulatory tool to show, for
example, dangerous products that should be removed from the market. At times, it
appears to have had the opposite effect. Risk assessment has been used by
industry groups to insist that harm must be proven scientifically before action is
taken to stop a process or product. There are many examples where "certainty"
about the absence of harm delayed preventative actions with potentially disastrous
results.
For example, Bovine Spongiform Encephalopathy (BSE, or more commonly,
Mad Cow Disease) was first recognized in the United Kingdom (UK) in November
1986 (DEFRA, 2008). When it was first noticed that the illness observed in cows
might be passed to humans, adequate preventative actions were not taken based
on this suspicion. Instead, it was argued that to act would cause economic hardship
among the country's producers of beef. The result was the spread of BSE and a
subsequent ban by other countries against the importation of beef from the UK.
The BSE epidemic in the United Kingdom peaked in January 1993 at almost 1,000
new cases per week (CDC, 2010). By the end of 2008, more than 184,500 cases of
BSE had been confirmed in the UK in more than 35,000 herds (CDC, 2010). BSE was
eventually brought under control by culling all suspect cattle populations.
However, human health is still impacted by the BSE outbreak. A new variant of

21

Creutzfeldt-Jakob disease (nvCJD), a form of brain damage that leads to a rapid
decrease in mental function and movement, is linked to eating BSE-contaminated
beef products (USDA Food Safety Research Info Office, 2009). nvCJD is believed to
result from a protein called a prion. Although suspect cattle have been culled, new
cases of nvCJD occur because of the long incubation time for prion diseases, which
are typically measured in years or decades.
According to Myers (2002), global warming is another example where
insistence on "scientific certainty" and focus on monetary costs has delayed
protective action. In the United States, one of the heaviest users of fossil-fuel and
where risk assessment has been widely used, little was done to move away from
fossil fuels even when there was mounting evidence that the burning of fossil fuels
was a primary cause of global warming. Priority was given to protecting national
economic interests over environmental protection as the United States signed but
did not ratify the 1997 Kyoto protocol, an international agreement that sought to
decrease human activities that contribute to ozone depletion and global warming.
Along with the United States, international trade organizations and agreements like
the World Trade Organization (WTO) and the North American Free Trade
Agreement (NAFTA) have institutionalized a non-precautionary approach to
environmental controls (Myers, 2002).
In contrast to the typical risk assessment process and perhaps as a result of
its shortcomings, an alternative approach based on precaution has been developed
22

and articulated as the precautionary principle. The goal of the precautionary
principle is to prevent harmful chemicals from ever entering the marketplace,
eliminating exposure and therefore risk.

THE PRECAUTIONARY PRINCIPLE
The precautionary principle is believed to have evolved in the early 1970s
out of the German socio-legal tradition centering on the concept of good household
management. In German, the concept is Vorsorgeprinzip, which translates into
English as precaution principle. However, it was not until the 1992 United Nations
Conference on Environment and Development that the principle received broad
international recognition. It has been evoked in a number of multilateral
agreements, international laws, and domestic laws and policies dealing with climate
change, biodiversity, endangered species, fisheries management, wildlife, trade,
food safety, pollution controls, chemicals regulation, exposure to toxics, and other
environmental and public health issues (Peterson, 2006). Table 4 highlights a few
of these agreements and policies.

23

Table 4. Examples of the precautionary principle in environmental
laws and policy
Year Name of Conference
1984 International Conferences on the
Protection of the North Sea (The North
Sea Conferences) (OSPAR Commission,
1984)
1987 Montreal Protocol on Substances that
Deplete the Ozone Layer (United Nations,
1987)
1990 Second World Climate Conference
(United Nations, 1990)
1992 Rio Declaration on Environment and
Development (The Rio Earth Summit)
(United Nations, 1992a)
1992 United Nations Framework Convention
on Climate Change (United Nations,
1992b)
1992 Maastricht Treaty (European Union,
1992)
1994 United Kingdom Biodiversity Action Plan
(Department of the Environment (UK),
1994)
1997 Kyoto Protocol (United Nations, 1997)
1998 Wingspread Statement on the
Precautionary Principle (Wingspread
Conference, 1998)
2000 Cartagena Protocol on Biosafety (United
Nations, 2000)
2000 Earth Charter (Earth Charter Commission,
2000)
2001 Stockholm Convention on Persistent
Organic Pollutants (United Nations, 2001)
2007 Registration, Evaluation, Authorisation,
and Restriction of Chemical Substances
(REACH) (European Parliament, Council,
2007)

24

Main Topic Addressed
Pollution in the North Sea

Greenhouse gases, climate
change
Climate change
Sustainable development
Greenhouse gases, climate
change
Established the European Union
(EU), named the precautionary
principle as a guide to EU
environment and health policy
Protect threatened species and
habitats by protecting and
restoring natural systems
Greenhouse gases, climate
change
How to implement the
precautionary principle in
environmental regulation
Genetically modified organisms
Environmental protection,
human rights
Certain toxic chemicals
Burden of proof placed on
industry to collect or generate
the data necessary to ensure
the safe use of chemicals (both
new and existing)

There are many definitions of the precautionary principle, but the most
widely quoted is from the 1992 Rio Declaration (United Nations, 1992a), which
states that:
"where there are threats of serious or irreversible damage, lack of full
scientific evidence shall not be used as reason for postponing cost-effective
measures to prevent environmental degradation."

While most definitions of the precautionary principle share common
features, there are some key areas of difference (Peterson, 2006). These
differences include:
•

The level of threat or harm that is sufficient to trigger application of the
principle (the threshold of harm).

•

Whether potential threats are balanced against other considerations, such
as costs or non-economic factors, in deciding what precautionary measures
to implement.

•

Whether the principle imposes an obligation to act or whether it simply
permits action.

•

Whether liability for environmental harm is assigned and, if so, who bears
the liability?
Based on these differences, different versions of the principle can be

categorized as weak, moderate or strong (Cooney & Dickson, 2005; Peterson, 2006;
Wiener & Rogers, 2002) and are outlined below (as summarized by Cameron, 2006):
25

Weak version:
The weak version is the least restrictive and allows preventative measures to
be taken in the face of uncertainty, but does not require them (e.g. 1992 Rio
Declaration; 1992 United Nations Framework Convention on Climate Change). To
satisfy the threshold of harm, there must be some evidence relating to both the
likelihood of occurrence and the severity of consequences. Some, but not all,
require consideration of the costs of precautionary measures. Weak formulations
do not preclude weighing benefits against the costs. Factors other than scientific
uncertainty, including economic considerations, may provide legitimate grounds for
postponing action. Under weak formulations, the requirement to justify the need
for action (the burden of proof) generally falls on those advocating precautionary
action. No mention is made of assignment of liability for environmental harm.
Moderate version:
In moderate versions of the principle, the presence of an uncertain threat is
a positive basis for action, once it has been established that a sufficiently serious
threat exists. For example, the United Kingdom Biodiversity Action Plan states:
"In line with the precautionary principle, where interactions are complex
and where the available evidence suggests that there is a significant chance
of damage to our biodiversity heritage occurring, conservation measures are
appropriate, even in the absence of conclusive scientific evidence that
damage will occur" (Department of the Environment (UK), 1994).

26

Usually, there is no requirement for proposed precautionary measures to be
assessed against other factors such as economic or social costs. The trigger for
action may be less rigorously defined, for example, as "potential damage", rather
than as "serious or irreversible" damage as in the weak version. Liability is not
mentioned and the burden of proof generally remains with those advocating
precautionary action.
Strong version:
Strong versions of the principle differ from the weak and moderate versions
in reversing the burden of proof. Strong versions justify or require precautionary
measures and some also establish liability for environmental harm, which is
effectively a strong form of "polluter pays". For example, the Earth Charter (2000)
states:
"When knowledge is limited apply a precautionary approach. Place the
burden of proof on those who argue that a proposed activity will not cause
significant harm, and make the responsible parties liable for environmental
harm."

Reversal of proof requires those proposing an activity to prove that the
product, process, or technology is sufficiently "safe" before approval is granted.
Requiring proof of "no environmental harm" before any action proceeds implies the
public is not prepared to accept any environmental risk, no matter what the
economic or social benefits (Peterson, 2006). At the extreme, such a requirement

27

could involve bans and prohibitions on entire classes or potentially threatening
activities or substances (Cooney, 2005).
Although different versions of the precautionary principle exist, they all
agree that when there is a reason to think – not absolute proof – that some human
activity is or might be harming the environment, precautions should be taken.
Proponents of the principle argue that its strength lies in its high degree of
generality since it may be applied to all environmental protection and health safety
issues (Ashford, 2005). Critics of the precautionary principle argue it is too general,
lacks clarity, and offers little guidance for regulatory policies (Treich, 2001). Despite
these differences, and as evidenced in Table 4 above, the precautionary principle
has become more prominent in environmental laws and regulations, and its
adoption and use is becoming more mainstream. A good example of this is the
European Union’s Registration, Evaluation, Authorisation, and Restriction of
Chemical Substances (REACH) program.

28

CHAPTER 3 – GASOLINE AND FUEL OXYGENATES
GASOLINE PROPERTIES
Gasoline is a complex manufactured mixture that does not exist naturally in
the environment. It is produced from petroleum in the refining process and
typically contains more than 150 chemicals, to include small amounts of benzene,
toluene, xylene, and sometimes lead. How the gasoline is produced determines
which chemicals are present in the gasoline mixture and how much of each is
present. The actual composition varies with the source of the crude petroleum, the
manufacturer, and the time of year. Gasoline is highly flammable, evaporates
quickly, and forms explosive mixtures with air. Most people can begin to smell
gasoline at 0.25 parts of gasoline per million parts of air (ppm). Although gasoline
does not dissolve readily in water, some of the chemicals that make up gasoline can
dissolve easily in water (ATSDR, 1995).

GASOLINE ADDITIVES AND FUEL OXYGENATES
One of the first gasoline additives was tetraethyl lead, which was phased out
when lead in automotive gasoline was banned in the United States in the early
1980s. Oxygenates are now the most common gasoline additives, used to increase
octane levels once provided by lead, and to increase oxygen levels and reduce
pollution emissions. Oxygenates are hydrocarbons that contain one or more
oxygen atoms. Oxygenates are added to motor vehicle fuels to increase the
29

combustion efficiency of gasoline, thereby reducing toxic tailpipe emissions
(particularly carbon monoxide) and allowing states to meet federal air quality
guidelines. Introducing additives that are partially oxidized promotes the complete
combustion of gasoline, so the engine emits CO 2 instead of CO. The primary
oxygenates are alcohols and ethers and include ethanol, methyl tertiary butyl ether
(MTBE), ethyl tertiary-butyl ether (ETBE), tertiary-amyl methyl ether (TAME),
diisopropyl ether (DIPE), and tertiary-butyl alcohol (TBA). Oxygenates are also used
as fuel additives to increase octane ratings. Most automobile engines require fuel
with octane ratings of 87 to 93 to avoid "knocking," a regular rapping noise within a
vehicle’s engine compartment that is usually caused by faulty fuel combustion
(Shakhashiri, 2009). Adding oxygenates to gasoline increase the octane rating of
the fuel.
As shown in Table 5, oxygenates vary in their effectiveness in reducing toxic
tailpipe emissions and several other parameters:

Table 5. Typical properties of fuel oxygenates
MTBE

CH 3 OC(CH 3 ) 3
Chemical
formula
Oxygenate
18.15
content,
percent by
weight
Octane
110
Reid vapor
8
pressure
(RVP)
Source: EIA, 2000

30

ETBE

TAME

Ethanol

CH 3 CH 2 OC(CH 3 ) 3

(CH) 3 CCH 2 OCH 3

CH 3 CH 2 OH

15.66

15.66

34.73

111
4

105
1.5

115
18

In addition to requiring that fuels burn cleaner, EPA requires areas with high
levels of smog (including but not limited to RFG areas) to reduce the vapor pressure
of gasoline in the summer months. When vapor pressure is reduced, it lessens the
volatilization of petroleum products at storage facilities and during fuel transfer.
Because MTBE-blended gasoline has a lower Reid Vapor Pressure, or RVP, than
ethanol-blended gasoline, MTBE is the preferred oxygenate in warm weather (EPA,
1998b).
The petroleum refinery industry also favors the use of MTBE over ethanol
for octane enhancement and RFG because it is less expensive and easier to use
(EPA, 1998b). MTBE is more compatible with gasoline, and can be blended at the
refinery and distributed with gasoline through pipelines. Ethanol, on the other
hand, much be shipped seperately from gasoline and added at the distribution
terminal soon before use. If ethanol-blended gasoline is exposed to water or even
water vapor (as in pipelines), ethanol will bring the water into solution and make
the gasoline unusable. Also, if ethanol-blended gasoline is stored for an extended
period, the ethanol will begin to separate from the gasoline. As a result, ethanol is
often manufactured close to the point of use or shipped by rail, increasing the cost
of its use (EPA, 1998b).

31

MTBE PRODUCTION AND PROPERTIES
Methyl tert-butyl ether (MTBE) is a colorless, flammable liquid with a boiling
point of 55°C and a density of 0.74 g/mL. MTBE’s unique Chemical Abstract Service
registry number, or CAS, is 1634-24-4 (CAS, 2009). The chemical formula for MTBE
is C 5 H 12 O and its molecular structure is shown below.

Figure 1. MTBE’s chemical formula

In MTBE one carbon atom is that of a methyl group, -CH 3 , and the other is
the central atom in a tertiary butyl group, -C(CH 3 ) 3 . MTBE is made by reacting
methanol, made from natural gas, with isobutylene (2-methyl-1-propene) in the
liquid state, using an acidic catalyst at 100°C.

Figure 2. Formation of MTBE

32

MTBE’s chemical structure determines its reactivity to other substances.
MTBE does not have hydrogen attached to oxygen or nitrogen, so it cannot form a
hydrogen bond to other molecules. It does, however, have an unbound electron
pair on its oxygen atom. This means that substances that have hydrogen bonded to
oxygen can bond to MTBE and is why MTBE, although soluble in petroleum at all
combinations, also has solubility in water, H 2 O. Therefore, any MTBE that gets to
the ground will be dissolved in rain water or other aqueous systems.
The 1990 Clean Air Act created a guaranteed market for all types of fuel
oxygenates. During the Winter Oxyfuel Program (WOP), MTBE demand increased
from 36.8 million barrels per year in 1992 to 52.4 million barrels per year by 1994
(EIA, 2009). The reformulated gasoline (RFG) program provided a further boost to
oxygenate blending and by 1997, MTBE production had increased to 71.9 million
barrels annually (EIA, 2009). For comparison, in 1970 MTBE was the 39th highest
produced organic chemical in the United States (Shakhashiri, 2009). By 1998, it had
become the fourth highest. As concerns about MTBE contamination spread,
production volumes decreased. In 2005 47.3 million barrels were produced
annually, and by 2006 this number had dropped to 30.6 million (EIA, 2009). As
shown in Table 6, as MTBE production decreased, there was a corresponding
increase in ethanol production. Ethanol production was 92.9 million barrels
annually 2005 and 116.2 million in 2006.

33

Table 6. Comparison of annual U.S. production of ethanol and MTBE
as fuel oxygenates, 1990-2008

Annual U.S. Production of Ethanol and
MTBE Fuel Oxygenates, 1990-2008

in thousand barrels

250,000
200,000
150,000
Ethanol

100,000

MTBE

50,000

1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005
2006
2007
2008

0

Source: EIA, 2009

Despite its relatively short production history, MTBE has frequently been
detected in groundwater. MTBE’s physical properties allow it to reach groundwater
and to travel faster and farther than many other common gasoline components
(Zogorski et al., 2006). Many regulators of UST programs have observed that
MTBE’s relatively high solubility allows it to dissolve into groundwater in “pulses”
that result in rapid orders of magnitude changes in groundwater concentrations
(EPA, 1998c). Pulses, which may be caused by the infiltration of rain water or rising
groundwater levels, may necessitate frequent groundwater sampling to determine
actual MTBE concentrations. In addition, the biodegradation of MTBE in
groundwater is relatively slow and MTBE can persist longer in aquifer systems
34

relative to many other gasoline compounds, such as benzene and toluene (Zogorski
et al., 2006). MTBE’s high solubility in water, low rate of adsorption to soil, and low
rate of biodegradation can make treating groundwater contaminated with MTBE
more expensive than treating groundwater that does not contain MTBE (EPA,
1998c).

EFFECTS OF FUEL OXYGENATES ON VEHICLE EMISSIONS
The use of oxygenates has been reported to have favorable impacts on air
quality (EPA, 1999). Analyses of ambient carbon monoxide measurements in some
cities with winter oxyfuel programs find a reduction in ambient CO concentrations
of about 10% (National Science and Technology Council, 1997). As illustrated in
Table 7, fuel oxygenates decrease vehicle emissions of air toxics such as benzene
and 1,3-butadiene, but increase the emissions of aldehydes (acetaldehyde from the
use of ethanol or ETBE, and formaldehyde from MTBE) and of NOx gases (National
Science and Technology Council, 1997). Acetaldehyde is a metabolite of ethanol,
and a possible carcinogen that undergoes a photochemical reaction in the
atmosphere to produce the respiratory irritant peroxylacetate nitrate (PAN)
(Ahmed, 2001).

35

Table 7. Oxyfuel effects on twenty 1989 model year vehicles exhaust
emissions
Emission

Mass
Emission b
(g/mi)
2.5
0.21
0.6
9 x 10-3
9 x 10-4
1.5 x 10-3
1.4 x 10-3

% Changes with Oxyfuel per wt % Oxygen c
3.7% Oxygen 2.7% Oxygen 2.7% Oxygen
EtOH
MTBE
ETBE

Carbon monoxide (CO)
-3.6 ± 1.3
-3.4 ± 2.4
-5.4 ± 2.7
a
Hydrocarbons (HC)
-1.3 ± 0.7
-2.4 ± 1.3
-1.9 ± 1.4
Nitrogen oxides (NOx)
+1.4 ± 1.1
+1.3 ± 2.0
+2.0 ± 2.3
Benzene
-3.1 ± 1.6
-4.1 ± 3.0
-3.5 ± 3.0
1,3-Butadiene
-1.6 ± 1.5
-0.6 ± 2.9
-1.0 ± 3.1
Formaldehyde
+5.2 ± 8.4
+5.9 ± 15.3
+6.3 ± 26.6
Acetaldehyde
+43 ± 12
-0.3 ± 13
+95 ± 25
a
= Total hydrocarbons
b
= average values for test fuels
c
= Oxyfuel effects have been normalized to 1 wt % oxygen. Uncertainties represent
95% confidence limits.
Source: National Science and Technology Council, 1997
Although NOx emissions increased for all oxygenates, the result was
statistically significant for only the ethanol fuels, the fuel set with the highest
oxygen content. Acetaldehyde emissions increased greatly for ethanol and ETBE
fuels. Except for the effects on acetaldehyde emissions, it is generally assumed the
effects of oxygenates are indistinguishable (National Science and Technology
Council, 1997). It is worth noting that acetaldehyde is not an insignigicant issue
since it also believed to be a human carcinogen.

36

Table 8. Effects of 15% MTBE fuel (2.7% wt oxygen) on older 19831985 and newer 1989 model year vehicles
Emission

CO
Current Fleet
Older Fleet
HC b
Current Fleet
Older Fleet
NOx
Current Fleet
Older Fleet

Mass Emission
(g/mi)

% Changes with Oxyfuel per wt % Oxygen

2.8
6.2

-4.1 ± 1.3
-5.2 ± 1.4

0.22
0.53

-2.2 ± 0.9
-3.4 ± 1.1

0.6
1.2

+0.5 ± 0.7
+0.5 ± 0.7

Source: National Science and Technology Council, 1997
The favorable impacts on air quality from the use of oxygenates is also
disputed. According to Interagency Assessment of Oxygenated Fuels (National
Science & Technology Council, 1997), the general decline in urban concentrations of
carbon monoxide over the past twenty years is largely attributed to stringent EPAmandated vehicle emission standards and improved vehicle emission control
technology. Newer model vehicles generally emit less pollution because of
improved emission control devices and the use of fuel injection. Emissions may also
vary from vehicle to vehicle depending upon how it is maintained and operated and
the quality of the fuel used (National Science and Technology Council, 1997). As
seen in Table 8, reductions in CO and hydrocarbon emissions from the use of fuel
oxygenate are found to be smaller in newer technology vehicles compared to older
technology and higher emitting vehicles. Older vehicles typically use carbureted
and oxidation catalyst technology, compared with the fuel injected, adapted
learning, and closed loop three-way catalyst systems commonly used in newer
37

vehicles (National Science and Technology Council, 1997). Although these older
vehicles represent a smaller fraction of the on-road fleet, there is evidence to
support they are responsible for a disproportionately large amount of urban CO
(National Science and Technology Council, 1997). Over time, as older vehicles leave
the on-road fleet, the need for fuel oxygenates will decrease.
In light of these factors, it may be hard to attribute improvement in air
quality definitively to the use of fuel oxygenates or to MTBE in particular.

38

CHAPTER 4 – MTBE HEALTH EFFECTS STUDIES
INTRODUCTION
Shortly after MTBE's introduction as a fuel oxygenate, anecdotal reports of
acute health symptoms such as eye and nose irritation, headaches, nausea, and
dizziness surfaced, leading to concerns about the human health risks from exposure
to MTBE. These health concerns were not anticipated. A review of available
literature, to include toxicological studies and epidemiological investigations, show
the body of evidence for possible health effects resulting from MTBE exposure in
both humans and animals.

TOXICOLOGY AND EXPOSURE DURATIONS
One of the basic concepts of toxicology is that all chemicals are toxic under
some conditions of exposure. The difficulty for toxicologists is to know under what
condition or level of exposure chemicals are toxic, so that measures can be taken to
limit human exposure so that toxicity can be avoided (Rodricks, 2007).
Toxicity is commonly categorized based on exposure duration – either acute,
chronic, or subchronic exposures. Acute toxicity testing involves a single high dose.
In animal testing, the acute lethal dose-50 (LD50) is the single dose of a chemical
that will, on average, kill 50% of a group of experimental animals. The LD50 has
become one standard measure of a chemical’s acute toxicity and represents the
39

dose at which animals have a 50% probability, or risk, of dying. Acute toxicity tests
in which non-lethal outcomes are sought include studies of the amounts of
chemical needed to cause skin or eye irritation or more serious damage.
Chronic exposure generally refers to dosing over a whole lifetime, or
something close to it. Subchronic exposures refer to repeated exposures for some
fraction of a lifetime. In animal toxicity studies involving rodents, chronic exposure
generally refer to daily doses over about a two-year period (rodent life-time), and
subchronic generally refers to daily doses over 90 days. The purpose of subchronic
and chronic testing is to identify the types of adverse health effects produced by a
chemical administered repeatedly, for large fractions of a lifetime, the dose at
which toxicity begins to appear, and the manner in which toxicity changes above
the minimum toxic dose (Rodricks, 2007). The maximum dose at which the
chemical produces no observable toxicity is referred to as NOEL, or “no-observed
effect level.” Risk assessors use NOEL to estimate the safe exposure level (the
reference dose, or RfD) and evaluate the likelihood of health damage in groups of
people exposed to various doses of a chemical.

40

HUMAN HEALTH EFFECTS AND KINETICS AFTER EXPOSURE TO MTBE
ACUTE
In an effort to understand the variations in reported acute health effects
from MTBE exposure, Borak et al., (1998) performed a critical literature review of
19 reports describing the results of twelve studies on the acute human health
effects of inhalation exposure to MTBE and twelve reports describing the clinical
use of parenteral MTBE (MTBE administered other than by mouth, usually injected
or implanted into the body) to dissolve cholesterol gallstones. Each study was
reviewed from three perspectives (epidemiology, industrial hygiene, and clinical
diagnostics); judged either satisfactory, limited adequacy, or unsatisfactory; and
grouped into one of three categories from most to least adequate in overall
methodology. The results of this review found those studies judged most adequate
on individual criteria and those with highest overall adequacy found no significant
association between MTBE exposure and seven "key" symptoms – headache, eye
irritation, burning of the nose and throat, cough, nausea and vomiting, dizziness,
and spaciness. As a result, it has been suggested that the major source of public
perception that MTBE poses hazards, and the principal basis for the ensuing
political debate, were the initial findings of methodologically weak studies. Borak
et al., (1998) concluded that methodologically superior studies – those designed to
rigorously test the MTBE hypothesis – found no association between exposure to
oxygenated fuels and the seven "key" symptoms.
41

Nihlen et al., (1998) attempted to assess the acute health effects of MTBE
exposure by subjecting ten healthy male volunteers to MTBE vapor for two hours at
three levels (5, 25, and 50 ppm). Each individual was exposed on three occasions
with at least two weeks between successive exposures. All subjects were first
exposed to the highest level, whereas the order of the 5- and 25-ppm exposure
levels was randomly divided. There was no control group. A symptoms
questionnaire was administered before, during, and after exposure inquiring
whether participants had discomfort in the eyes, nose, throat or airways; whether
they had difficulty breathing or experienced headache, nausea, fatigue, dizziness, or
intoxication; and whether they could smell solvent. The subjects did not indicate
any increased irritation effects or discomfort after MTBE exposure, with the
exception of solvent smell. Measurements of ocular and nasal irritation were also
performed before, during, and after exposure. No significant effects of MTBE were
seen in any measurements, to include blinking frequency, eye redness, or corneal
damage. Nasal blockage and nasal swelling are commonly reported symptoms
during exposure to airborne substances. Although a nasal swelling effect was
observed, the authors concluded there was no clear dose-effect relationship
between this symptom and MTBE exposure. The results of this study indicate no or
minimal acute effects of MTBE vapor upon short-term exposure at relatively high
levels. However, this study did discuss potential limitations, to include possible
hesitation of individuals with prior negative experiences with MTBE or of volatiles in
general to participate in chamber studies (thus excluding sensitive individuals), and
42

that short exposure durations may reduce the ability of the study to reveal any
acute effects of MTBE exposure.
The effects of MTBE on the immune system were measured by monitoring
plasma interleukin-6 levels (an indicator of immune reaction) in 22 volunteers
exposed to auto emissions derived from oxyfuels during a four-week period in late
November and early December 1992 at several locations around Fairbanks, Alaska
(Duffy et al., 1994). Blood samples were collected at the beginning of work shifts
and the end of the workday and analyzed for interleukin-6 by an immunochemical
assay. No differences in interleukin-6 levels were found between the morning and
evening blood samples.
To address some of the issues identified in the occupational and field
studies, an experimental double-blind study was conducted in 22 healthy men and
21 healthy women, who were examined for both objective and subjective effects
(Cain et al., 1994). In this study, half of the subjects were exposed sequentially to
1.7 ppm MTBE for one hour on one day, to uncontaminated air for one hour two
days later, and to 7.1 ppm of a 17-component mixture of volatile organic
compounds (VOCs) for one hour two days later. The other group of subjects was
similarly exposed in the reverse order. The subjects were able to detect the odor of
MTBE, but expressed little objection to it. Analysis of nasal lavage material and tear
fluid from the eyes revealed no statistically significant differences across the three
exposure conditions. In addition, statistical analysis of the results of questionnaires
administered every ten minutes during the various exposure conditions revealed no
43

differences for irritation of the nose or throat, dry skin or skin rash, dry or sore
throat, stuffy or runny nose, sinus congestion, cough, wheezing, chest tightness, or
shortness of breath when the subjects were exposed to MTBE or when they were
exposed to air. Neurobehavioral tests were also administered at one hour before
exposure and during the last 15 minutes of exposure. Results of statistical analysis
in these tests (analysis of variance, or ANOVA) revealed no difference across the
three conditions of exposure to MTBE, air, or VOCs. Subjects were also
administered questionnaires regarding subjective symptoms of eye irritation (dry,
itching, or irritated eyes; tired or strained eyes; burning eyes); headache; difficulty
remembering things or concentrating; feelings of depression; unusual tiredness,
fatigue or drowsiness; tension, irritability, or nervousness; dizziness or
lightheadedness; mental fatigue or “fuzziness;” pain or numbness in the hands or
wrists; and skin rash or dry skin. No differences in reporting of symptoms were
noted for exposure to MTBE versus exposure to air.
In a similar study, 19 healthy men and 18 healthy women were exposed for
one hour to clean air and 1.39 ppm MTBE in separate sessions separated by at least
one week (Prah et al., 1994). The order of exposure was randomly selected, but
because of the odor of MTBE, it is likely that the subjects were aware of the
exposure conditions. Questionnaires were administered prior to exposure,
immediately upon entering the exposure chamber, after 30 minutes of exposure,
and during the last five minutes of exposure. Responses to the questionnaires
revealed no differences between pre- and post-exposure for several conditions:
44

headache, difficulty in memory or concentration, depressed feelings, unusual
tiredness, fatigue, drowsiness, tension, irritability, nervousness, dizziness,
lightheadedness, mental fatigue, “fuzziness,” or pain, stiffness, or numbness of the
back, shoulders, neck, hands, or wrists. Tests to evaluate neurobehavioral function
were completed as baseline before entering the chamber and after 45 minutes of
exposure. No measures approached statistical significance. There were also no
differences between exposures for eye irritation, skin rash or dry skin, irritation of
the nose, cough, wheezing, chest tightness, shortness of breath, stuffy or runny
nose, or irritation of the throat. No differences were found for nasal inflammation
upon examination of nasal lavage material. Female subjects reported that the air
quality during MTBE exposure was worse than the air without MTBE. The odor
threshold was determined to be approximately 0.18 ppm. Thus, other than
detection of odor and the reported poor air quality in these experimental studies,
no reactions to exposure to MTBE were observed or reported under the conditions
of the studies. Although the exposure concentrations used in these experimental
studies were chosen on the basis of airborne concentrations of MTBE to which
commuters are exposed, the studies could not resolve whether multiple exposures,
exposure to higher concentrations, and exposure for longer durations, which are
more relevant for real-life exposure of motorists to MTBE, would have caused
cumulative effects.

45

CHRONIC/SUBCHRONIC
In a study of physician visits before, during, and after the oxygenation of
gasoline in the Philadelphia, Pennsylvania area, Joseph (2002) noted the proportion
of visits related to asthma, wheezing, and headache increased dramatically and in
association with increasing concentrations of MTBE in air during a time when
criterion pollutants were stable. This suggests that MTBE might be associated with
these symptoms, and not the air pollutants commonly measured. Joseph (2002)
reported the symptoms attributed anecdotally to MTBE use in gasoline include skin
rash, general allergy, anxiety, insomnia, cardiac symptoms, and malaise. As a
control, statistics for six diseases and symptoms thought to be unrelated to air
pollution (diabetes; essential hypertension; chronic liver disease, including alcoholic
cirrhoses and hepatitis; back pain; diverticula of the intestine; and abdominal pain)
were examined. With the exception of hypertension, none of the changes were
statistically significant. However, the increase in hypertension was very small
(4.1%), especially when compared to increases observed in symptoms attributed to
pollution. By comparison, symptoms anecdotally related to MTBE increased
between 59 and over 700 percent during the same time period. Confounding
factors and sources of bias acknowledged in this study included the possible impact
of MTBE publicity on patient and physician behavior with regard to symptom
reporting. A review of MTBE publicity revealed that coverage in Pennsylvania
tended to cover economic and regulatory aspects of gasoline, which was described

46

as reducing air pollution, so it is unlikely the increases in patient symptoms were
due to negative patient reactions to the MTBE news coverage.
To determine the extent of exposure to gasoline vapors during vehicle
refueling, Hakkola & Saarinen (2000) measured the differences in the exposure of
20 customers to gasoline and oxygenate vapors during refueling in service stations
with and without vapor recovery systems. There are two types of recovery
systems. The equipment and procedures at Stage I service stations reduce the
vapor emissions during the delivery of gasoline from road tankers into underground
storage tanks (closed conditions). Stage II vapor recovery systems reduce vapor
emission during refueling by trapping the vapor with the fuel nozzle and containing
it within the storage tank. The results of the study indicate that although the Stage
II vapor recovery system did not remove all vapors, exposure to MTBE was reduced
considerably by Stage II recovery systems (from a mean of 23.4 mg/m3 to 5.6
mg/m3 when compared to Stage I recovery systems). Although there are no
studies of long-lasting negative health effects to customers from exposure to
gasoline vapors during refueling and the time of exposure to gasoline vapors during
refueling are brief (mean refueling times were 57 seconds (range 23-207sec) at the
Stage I and 66 seconds (range 18-120) at Stage II stations), the use of fuel recovery
systems further reduce the potential for human and environmental contamination
from fuel oxygenates.
Fiedler et al., (1994) conducted a study to determine whether symptoms
associated with MTBE were reported at an increased rate among subjects known to
47

be sensitive to chemicals and in situations where exposure to MTBE was likely to be
greatest. In this study, 14 individuals with multiple chemical sensitivities, five
individuals with chronic fatigue syndrome, and six control individuals were
interviewed regarding symptoms in response to situations in which gasoline
containing MTBE was used (driving a car, gasoline stations) and not used (shopping
malls, grocery stores, office buildings, parks). The symptoms of interest included
cough, burning sensation in the nose, and gastrointestinal upset. Although multiple
chemical sensitivity subjects and chronic fatigue syndrome subjects reported more
symptoms than normal controls in some situations, no significant differences were
found among the groups for driving a car or visiting gas stations. The authors
concluded that the study did not provide clear evidence to support that an
unusually high rate of symptoms or an increase of symptoms occurred uniquely
where MTBE exposure was likely.
In a later study, Fiedler et al., (2000) again compared individuals with selfreported symptoms (SRSs) associated with MTBE (headache; nausea; and eye, nose,
and throat irritation) to a control group. In a double-blind, repeated measures,
controlled exposure, subjects were exposed for 15 min to clear air, gasoline,
gasoline with 11% MTBE, and gasoline with 15% MTBE. Relative to controls, SRSs
reported significantly more total symptoms when exposed to gasoline with 15%
MTBE than when exposed to gasoline with 11% MTBE or to clean air. However,
these differences in symptoms were not accompanied by significant differences in
neurobehavioral performance or psychophysiologic responses, nor were significant
48

differences found when subjects exposed to gasoline with 11% MTBE were
compared to clean air or to gasoline. The results of this study did not support a
dose-response relationship for MTBE exposure nor the symptoms associated with
MTBE in epidemiologic studies.

POSSIBLE HUMAN HEALTH BENEFITS ASSOCIATED WITH MTBE USE
In addition to potential risks associated with MTBE exposure, it has been
suggested that use of MTBE as a fuel oxygenate may have anticipated health
benefits. Modeled ambient air concentrations of VOCs were used to compare
baseline gasoline (pre-1990 CAAA gasoline) to three fuel mixture scenarios: summer
MTBE:RFG, winter MTBE:RFG, or MTBE oxyfuel (Spitzer, 1997). The model
predicted that the addition of MTBE to RFG or oxyfuel would decrease
acetaldehyde, benzene, 1,3-butadiene and particulate organic matter (POM), but
increase formaldehyde tailpipe emissions (Table 10.) However, the increased
formaldehyde emissions would be offset by the reduction of formaldehyde
formation in the atmosphere from other VOCs.

49

Table 9. Impact of MTBE on vehicle emissions of volatile organic
compounds (VOCs) in summer and winter
Component
Acetaldehyde
Benzene
1,3-Butadiene
Formaldehyde
POM
Total

Summer (mg/mile)
Baseline
MTBE
gasoline
RFG
8.1
7.5
108.5
71.8
13.0
12.0
15.0
16.5
5.9
5.4
150.5
112.3

Winter (mg/mile)
Baseline
MTBE
gasoline
RFG
14.4
13.4
178.4
112.3
23.0
19.6
26.6
30.8
10.5
10.0
252.9
186.1

MTBE
oxyfuel
13.4
113.2
17.9
32.6
10.1
187.2

Source: Spitzer, 1997

Based on these model emissions, and assuming total US population
exposure, the EPA predicted annual cancer risk estimates associated with tail pipe
emissions of VOCs. As reported by Spitzer (1997), an incidence of 437 annual
cancer-related deaths from use of 100% baseline gasoline year-round would decline
13% (to 379 annual cancer-related deaths) if baseline gasoline was used exclusively
in the summer and MTBE:RFG in winter. If baseline gasoline replaced MTBE in
summer and winter, the predicted cancer declined to 362 annual cancer-related
deaths (17%). The maximum decline (359 annual cancer-related deaths or 18%)
was achieved when MTBE:RFG was used exclusively in the summer and MTBE
oxyfuel in winter. Based on these predictions, use of MTBE in RFG year-round
coupled with winter use of the oxygenate in the Winter Oxyfuel Program would
result in the greatest lives saved in terms of reduced cancer-related deaths
attributable to air pollutants.

50

Similarly, Erdal et al., (1997) reported that even small MTBE-associated
reduction in peak ambient ozone levels (1-5 ppb, according to model estimates)
should yield considerable public health benefits. Ozone is a highly reactive irritant
gas that primarily affects the respiratory system. Acute responses to ozone include
respiratory symptoms, decrements in lung function, decreased athletic
performance, and biochemical and cellular changes indicating lung inflammation
(Erdal et al., 1997). MTBE use in fuel reduces ozone by reducing the emission of
other VOCs.

EVALUATION OF MTBE KINETICS
In a short-term inhalation exposure study by Lee et al., (2001) six subjects
were exposed to MTBE in gasoline in order to assess the metabolic kinetics of MTBE
and its metabolite, tertiary butyl alcohol (TBA) in the human body. Three male and
three female participants were exposed to 1.7 ppm MTBE vapor for 15 minutes in a
controlled setting. Urine void samples were collected first thing in the morning of
exposure day (pre-exposure), then periodically until the following morning,
including a sample 5-10 minutes prior to exposure. Breath and blood background
samples were collected 5-10 minutes prior to the subjects entering the test facility.
Once testing began, air and breath samples were taken concurrently during the
exposure at four minute time intervals. Post-exposure biological samples were
collected in a room with no known MTBE sources. MTBE air concentrations inside
the testing room ranged from 5510µg/m3 (1.5ppm) to 6480 µg/m3 (1.6ppm) during
51

the exposures. The elimination patterns for the six test subjects were similar.
Breath MTBE levels declined quickly following the 15-minute exposure. All postexposure breath concentrations of MTBE dropped more than 50% in ten minutes
and 69% of the absorbed doses were expired through respiration within eight hours
following exposure. Breath levels of TBA never exceeded its detection limit of 1.5
μg/m3. Blood MTBE concentrations reached its highest levels right after exposure
with a range from 4 to 10 µg/ml, then declined to background levels in most cases.
TBA reached its highest levels (5-10 µg/l) 2-4 hours after exposure and then
declined slowly. TBA did not always reach background levels within 24 hours after
exposure, the time when the last sample was collected. The half-lives of TBA in the
blood for a single female and single male subject were 10.5 and 8.0 hours,
respectively. MTBE urinary excretion rates increased immediately following
exposure and declined to background 10 to 15 hours after exposure. TBA excretion
rates reached its highest levels 6-8 hours later, returning to background levels
around 20 hours after exposure. Approximately 0.7-1.5% of the amount of MTBE
inhaled was excreted unchanged as urinary MTBE, and 1-3% was excreted as
urinary TBA within 24 hours after exposure. The ranges of MTBE half-lives is
believed to be 1-4 minutes for the lungs, 9-53 minutes for blood, 2-8 hours for
vessel rich tissue, and 14-24 hours for vessel pore or adipose (fatty) tissue. Overall,
exposure results from this study suggest MTBE and its metabolite, TBA, are
processed and removed from the human body relatively quickly (within 24 hours)
with expired air and urine comprising the main routes of excretion. Females tended
52

to process MTBE and TBA slower than males, suggesting a possible higher health
risk for females in terms of exposure.
Prah et al., (2004) measured blood, urine, and breath volumes after
fourteen male volunteers were exposed to MTBE dermally, orally, or through
inhalation. Specifically, volunteers were exposed to 51.3 µg/ml MTBE dermally in
tap water for 1 hour, drank 2.8 mg MTBE in 250 ml Gatorade, and inhaled 3.1ppm
MTBE for 1 hour. A baseline blood sample was obtained prior to exposure, and
blood and breath samples were obtained throughout the exposure and postexposure periods, to include 24-hours post-exposure samples. Participants were
exposed in random order and each of the three exposures was separated by at least
one week to minimize the physiological carryover of MTBE or TBA. Study results
indicate blood MTBE peaked between 15 and 30 minutes following oral exposure,
immediately at the end of inhalation exposure, and roughly five minutes after
dermal exposure. TBA measured in blood slowly increased and reached a plateau,
but did not return to pre-exposure baseline at the 24-hour follow-up. The dermal
and inhalation exposure experiment shows MTBE was readily absorbed and
metabolized into TBA. In contrast, the oral route of exposure demonstrated a
significant first-pass metabolism effect that resulted in proportionally more TBA and
therefore, less MTBE would be available for elimination via exhalation. This result
means risk assessment calculations should take route or exposure into
consideration. Oral exposure resulted in significantly greater MTBE metabolism
into TBA than by other routes. Uptake was slowest for the dermal exposure route.
53

In a study performed by Johanson et al., (1995), ten healthy male volunteers
were exposed to MTBE vapor at 5, 25, and 50ppm for two hours during light
physical exercise. Measurements were taken of MTBE and tertiary butyl alcohol in
inhaled and exhaled air, blood and urine. The concentration of MTBE and TBA in
blood was proportional to exposure level suggesting linear kinetics up to 50ppm.
Subjective ratings (discomfort, irritative symptoms, CNS effects); eye (redness, tear
film break-up time, conjunctival damage, blinking frequency); and nose
measurements (peak expiratory flow, acoustic rhinometry, inflammatory markers in
nasal lavage) indicated no or minimal effects of MTBE exposure.

ANIMAL HEALTH EFFECTS AFTER EXPOSURE TO MTBE
ACUTE
Acute inhalation 4-hour LC50 (lethal concentration, 50% kill) values in rats
for two grades of MTBE was determined to be 33,370 ppm (120,132 mg/m3) for
commercial MTBE (99.1% MTBE) and 39,395 ppm (141,822 mg/m3) for ARCO MTBE
(96.2% MTBE) (ARCO, 1980). An acute LC50 in mice following inhalation of MTBE for
ten minutes was determined to be 180,000 ppm (648,000 mg/m3) (Snamprogetti,
1980). The LT50 (time at which death occurs in 50% of exposed animals) in mice
following inhalation exposure to 209,300 ppm (753,480 mg/m3) MTBE was 5.6
minutes. No deaths occurred in male or female Fischer rats exposed to < 8,000 ppm
(28,800 mg/m3) for six hours (Bioresearch Labs, 1990a; Gill, 1989).

54

A 4-hour inhalation exposure of rats to high concentrations of MTBE
(>18,000 ppm, or 64,800 mg/m3) caused rapid breathing, excessive tear secretion,
nasal discharge, loss of coordination and loss of righting reflex, with respiration
gradually slowing until the rats died (ARCO, 1980). MTBE exposure at
concentrations of 8,321 ppm (29,956 mg/m3) for one hour produced labored
breathing in rats (Tepper et al., 1994) and mice (Tyl & Neeper-Bradley, 1989).
Exposure to MTBE at concentrations <3,000 ppm (10,800 mg/m3) did not produce
observable respiratory symptoms. No neurological effects were observed at 800
ppm (2,880 mg/m3) for six hours. Based on this NOAEL, an acute-duration
inhalation MRL of 2 ppm (7 mg/m3) was calculated
Some rats and mice died after being given very large amounts of MTBE by
mouth. The oral LD50 (lethal dose, 50% kill) for MTBE was found to be 3,866 mg/kg
for rats (ARCO, 1980) and 4,000 mg/kg for mice (Little et al., 1979).
No deaths occurred in rats (Bioresearch Labs, 1990b) or rabbits (ARCO,
1980) dermally exposed to MTBE.
The immediate acute effect of orally administered MTBE is on the central
nervous system. Oral ingestion of MTBE at doses > 4,080 mg/kg MTBE caused lack
of coordination, tremors, labored breathing, and loss of righting reflex in rats
(ARCO, 1980). Onset of neurological signs was rapid, but they disappeared or were
markedly reduced within 24 hours. Another study in rats reported drowsiness,
which subsided within 24 hours after a single oral dose of 400 mg/kg (Bioresearch
Labs, 1990b). A NOAEL (no observed adverse effect level) of 40 mg/kg for
55

neurological effects for acute oral exposure was identified for MTBE (Bioresearch
Labs, 1990b). Based on this NOAEL value, MTBE’s acute oral Minimal Risk Levels
(MRL) was calculated to be 0.4 mg/kg/day.
The Agency for Toxic Substances and Disease Registry (ATSDR) derives MRLs
when it determines that reliable and sufficient data exist to identify the target
organ(s) of effect or the most sensitive health effect(s) for a specific duration for a
given route of exposure to a substance (ATSDR, 2009). The MRL is an estimate of
the daily human exposure to a hazardous substance that is likely to be without
appreciable risk of adverse noncancerous health effects over a specified duration of
exposure (ATSDR, 2009). MRLs are derived for acute (1-14 days), intermediate
(>14-364 days) and chronic (365 days and longer) exposure durations, and for the
oral and inhalation routes of exposure. ATSDR has not yet identified a method
suitable for determining MRLs for dermal exposure. Although human data is
preferred, MRLs are often based on animal studies because relevant human studies
are lacking (ATSDR, 2009). To be protective of human health, the MRL may be as
much as a hundredfold below levels shown to be nontoxic in laboratory animals.
Table 11 shows MRL values for MTBE.

56

Table 10. MTBE Minimal Risk Levels (MRLs) for humans based on
animal studies
Route
Inhalation

Duration
Acute
Intermediate
Chronic
Oral
Acute
Intermediate
Source: ATSDR, 2009

MRL
2 ppm (7 mg/m3)
0.7 ppm (2.52 mg/m3)
0.7 ppm (2.52 mg/m3)
0.4 mg/kg/day
0.3 mg/kg/day

CHRONIC
The most common effect of MTBE in animals is on their nervous system.
Breathing high concentrations (> 3,000 ppm, or 10,800 mg/m3) of MTBE caused
hypoactivity, lack of coordination, lack of startle reflex, and labored breathing
(Vergnes & Morabit, 1989; Chun & Kintigh, 1993; Vergnes & Chun, 1994; Dodd &
Kintigh, 1989; Tyl & Neeper-Bradley, 1989; Chun et al., 1992; Burleigh-Flayer et al.,
1992). Inhalation of MTBE at lower concentrations (<2,000 ppm) also resulted in
hypoactivity in rats and mice. Some animals that breathed high levels (8,000 ppm,
or 28,800 mg/m3) of MTBE for several hours a day for several weeks gained less
weight than normal, probably because they ate less food while they were inactive.
A concentration of 400 ppm (1,440 mg/m3) did not produce any effects. Based on
the NOAEL of 400 ppm, an intermediate-duration inhalation MRL of 0.7 ppm (2.52
mg/m3) was calculated for MTBE.
When rats (Dodd & Kintigh, 1989), rabbits (Tyl & Neeper-Bradley, 1989), and
mice (Burleigh-Flayer et al., 1992; Chun & Kintigh, 1993) breathed high levels
57

(>3000 ppm) of MTBE intermittently for a period of time ranging from a few weeks
to 18 months, some had larger livers than normal, increased kidney and adrenal
weights, and decreased body weight gain. Some mice also developed tumors in the
liver.
Fischer 344 rats (50 of each sex/dose level) were exposed to MTBE (99%
pure) vapor in inhalation chambers at target concentrations of 0, 1440, 10880, and
28800 mg/m3 (or 0, 400, 3000, and 8000 ppm, respectively) six hours/day, five
days/week for up to two years (Chun et al., 1992; Bird et al., 1997; Mennear, 1997).
Various clinical signs of toxicity (hypoactivity, ataxia, lack of startle reflex, swollen
periocular tissue and salivation) were observed in both sexes at the two highest
dose levels. An increased incidence of renal tubular cell adenomas and carcinomas,
and of interstitial cell adenomas (Leydig cell tumors) of the testes in male rats was
noted in the mid- and high-dose groups.
Sprague-Dawley rats were given MTBE (>99% pure) in olive oil by gavage
four times per week for 104 weeks, at doses of 0, 250, or 1000 mg/kg body weight
(Belpoggi et al., 1995). There was a dose-related increase in cancers of the blood
(leukemia) and cancer (lymphoma) of some of the tissues that produce blood cells
in female rats, but not in male rats, and an increased incidence of interstitial cell
tumors of the testes in the high-dose group of males.
In a 90 day study, groups of Sprague-Dawley rats (ten males and ten females
in each test group) were gavaged 0 (corn oil), 100, 300, 900 or 1200 mg/kg of
undiluted MTBE (>99.95% pure) daily for 90 days (Robinson et al., 1990). The most
58

pronounced clinical effect was the profound anesthetic effect at the highest dose.
In female rats, elevated cholesterol levels and increased kidney weights were
observed at all levels of exposure. For male rats, kidney weights increased only at
the two highest doses (>900 mg/kg). Liver weights increased with exposures >900
mg/kg for both male and female rats.
Application of 0.5 mL or 10,000 mg/kg ARCO MTBE (96.2% MTBE) or
commercial MTBE (99.1% MTBE) to the skin of rabbits resulted in slight to severe
skin irritation (ARCO, 1980). Injection of 0.5 mL of a 1% MTBE solution
intradermally in guinea pigs also resulted in skin irritation (ARCO, 1980). Direct
application of ARCO MTBE (96.2% MTBE) or commercial MTBE (99.1% MTBE) into
the eyes of rabbits resulted in eye redness, discharge, clouding of the cornea, and
thickening of the eyelids (ARCO, 1980; Snamprogetti, 1980).

TOXICITY EVALUATION OF MTBE METABOLITES
The potential carcinogenicity of two metabolites of MTBE, formaldehyde
and tertiary-butyl alcohol (TBA) has also been examined in animals. Fischer-344
rats given 0, 1.25, 2.5, or 5 mg/mL (males) or 0, 2.5, 5, or 10 mg/mL (females) TBA in
drinking water for two years, showed increased incidence of kidney tumors in males
at the intermediate doses and increased incidence of focal renal tubule hyperplasia
in males at the high dose (Cirvello et al., 1995). In B6C3 F1 mice, 0, 5, 10, or 20
mg/mL TBA given in drinking water for two years significantly increased the
incidence of thyroid tumors in all exposed male groups and in females at the two
59

higher doses. The incidence of follicular-cell adenoma or carcinoma was slightly
higher in males at the intermediate dose and significantly higher in females at the
high dose (Cirvello et al., 1995).
Data for carcinogenic activity is ambiguous for drinking water exposure to
formaldehyde. A study by Soffritti et al., (1989) reported a dose-related increase in
the incidence of leukemia and intestinal tumors in Sprague-Dawley rats, although
the experimental data was limited. Another drinking water study on formaldehyde
by Tyl et al., (1989) using Wistar rats, found no evidence of carcinogenicity.

EVALUATION OF CANCER-CAUSING POTENTIAL BASED ON ANIMAL
STUDIES
Experimental studies provide some evidence to suggest MTBE is
carcinogenic in rats and mice at multiple organ sites after inhalation or oral-gavage
exposure (National Science and Technology Council, 1997; Belpoggi et al., 1995;
Chun et al., 1992; Bird et al., 1997; Mennear, 1997) and to regard MTBE as having
human cancer causing potential. Some studies suggested that carcinogenicity of
MTBE might be due to its two main metabolites, formaldehyde or tertiary-butyl
alcohol (TBA) (Ahmed, 2001). However, MTBE has not been classified as a
carcinogen by either the Department of Health and Human Services (DHHS), the
International Agency for Research on Cancer (IARC), or EPA.

60

APPLICABILITY OF ANIMAL TESTING DATA TO HUMANS
Animals have the same basic biological features of humans and much
empirical evidence exists to show that laboratory animals and human beings
respond similarly to chemical exposures (Rodricks, 2007). These similarities
increase the probability that results observed in a laboratory setting will predict
similar results in humans However, due to differences between species, it is not
possible to conclude that humans will absorb the same amount of MTBE as rats or
mice or that the effect will be the same. Problems of test interpretation and
extrapolation of results to human beings is an area of some controversy. However,
animals do generally serve as good models for humans and few other options for
testing chemical toxicity exist (ethics prohibit human testing). Some of the
differences can be interpreted by the identification of differences in the mechanism
of action, or metabolism among species. More often than not the mechanisms are
similar and therefore toxicity is similar.
Larger uncertainties exist in the estimates of cancer potency derived from
animal studies. The mechanisms by which MTBE causes cancer in animals are not
well understood. Animals are exposed to MTBE is much larger quantities and for
much longer periods than humans are likely to be exposed to, lessening the
likelihood that humans will have the same health outcome suggested by animal
studies. Even with this uncertainty, animal study results contribute to the overall

61

weight of evidence for MTBE carcinogenicity and suggest MTBE may pose a
potential for carcinogenicity to humans at high doses.

REGULATORY LIMITS
Based on available data, exposure limits protective of human health have
been set for MTBE. EPA has developed a Reference Concentration (RfC) of 3 mg/m3
(0.8 ppm) for inhaled MTBE (EPA 1994). The Reference Concentration (RfC) is the
threshold value for inhalation that represents the doses to which it is believed that
humans can be exposed continuously over a lifetime without experiencing adverse
effects. The Agency for Toxic Substances and Disease Registry (ATSDR) also
develops minimal risk levels (MRLs), which are defined as the “estimate of the daily
human exposure to a hazardous substances that is likely to be without appreciable
risk of adverse non-cancer health effects over a specified duration of exposure”
(ATSDR, 2000). These MRLs are similar in nature to EPA’s RfC values in that they
specify health guidance or acceptable exposure levels, but they differ in that they
are based on the most sensitive substance-induced endpoint considered to be of
relevance to humans, which may be less severe than those considered under the
EPA approach. ATSDR has established an MRL of 0.3 mg/kg/day (0.3 ppm) for
intermediate-duration oral exposures to MTBE.
A reference dose (RfD) is similar to an RfC, except instead of continuous
inhalation exposure, it refers to daily oral exposure. The EPA has not established an

62

RfD value for MTBE, but Moyer and Kostecki (2003) extrapolated an RfD value of
one based on the chronic RfC value. The table below (Table 11) compares noncancer threshold values established by EPA and ATSDR for MTBE and other selected
gasoline constituents. As indicated in this table, the threshold values for MTBE are
up to ten times greater than that for other gasoline constituents, suggesting that, in
general, MTBE has much lower non-cancer toxicity than other common gasoline
constituents.

Table 11. Summary of threshold doses for selected gasoline
constituents
Constituent

Chronic
Chronic
Acute
Intermediate
Oral RfD
Inhalation Oral MRL
Oral MRL
(mg/kgRfC
(mg/kg(mg/kg-day)
day)
(mg/m3)
day)
MTBE
1*
3
0.4
0.3
Ethylbenzene
0.1
1
NA
NA
Toluene
0.2
0.4
0.8
0.02
Xylene
2
NA
1
0.2-0.6
*Based on extrapolation from chronic RfC, NA=not available,
Source: Moyer & Kostecki, 2003

Chronic
Oral MRL
(mg/kgday)
NA
NA
NA
NA

63

HUMAN PATHWAYS OF EXPOSURE TO MTBE
MTBE or any other chemical does not pose a risk to human health unless
exposure occurs. The most likely pathway for human exposure is inhalation. For
most people, this would likely occur while pumping gasoline and breathing the
evaporative losses that occur during refueling; by breathing exhaust fumes while
driving a car; or breathing air near highways or in cities where the concentration of
MTBE in air would likely be higher. The next most likely exposure for the general
public would occur from drinking, swimming, or showering in water that has been
contaminated with MTBE. However, MTBE has a taste and smell that most people
find unpleasant so prolonged exposure through ingestion or inhalation is less likely.
On the other hand, people who consume smaller, less detectable quantities of
MTBE in drinking water over long periods of time may not be aware of their
exposure. Dermal contact may also occur through accidental spills of MTBEblended gasoline or through the use of gasoline as a solvent (Ahmed, 2001).
For manufacturing and distribution workers, service station attendants, and
auto mechanics, occupational exposure can occur at any point in the manufacture,
transportation, distribution, or use of MTBE and gasoline containing MTBE. The
duration of exposure is also likely to be higher for this group since contact with
MTBE occurs over an eight-hour workday. For the general population, MTBE
exposure would typically be brief and infrequent. For instance, refueling a vehicle

64

generally takes only a few minutes during which exposure to MTBE through
evaporative losses might occur.
Intentional exposure to MTBE can also occur during medical treatment.
MTBE can be used as an alternative to surgery to dissolve gallstones when injected
intraductally (inside the bile duct) (ATSDR, 1996).

ESTIMATES OF HUMAN EXPOSURE TO MTBE
In an occupational exposure setting, employees could be exposed to peak
levels of >50ppm during production and transportation processes, and median
levels have been measured up to 2 ppm during six hours of exposure (Nihlen et al.,
1998). Service station attendants could be exposed in the range of 0.1-1 ppm
(average 4 hours), and consumers could be exposed to 1-10 ppm (average 2
minutes) during refueling (Nihlen et al., 1998). The presence of MTBE in ambient
air, public buildings and residences can result in longer duration exposures, but at
concentrations that are quite low, in the range of 0.001 to 0.01 ppm (Balter, 1997).
In the United States, the American Conference of Governmental Industrial
Hygienists (ACGIH) recommends that the amount of workroom air be limited to a
time-weighted average of 50 ppm, but governmental agencies such as the National
Institutes for Occupational Safety and Health (NIOSH) and the Occupational Safety
and Health Administration (OSHA) have not established exposure criteria for MTBE
(NIOSH, 2008).

65

Brown (1997) compiled data on concentrations of MTBE in air for 15
difference occupational, commuting, or residential exposure categories, and
concentration in potable water were compiled from five states in MTBE-using areas
of the United States. Based on these concentrations and characteristics of the
exposed populations, average daily and lifetime average doses were estimated.
Arithmetic mean occupational doses via air were in the range of 0.1 to 1.0 mg/kgday (0.1 to 1.0 ppm), while doses from residential exposures, commuting, and
refueling were in the range of 0.0004 to 0.006 mg/kg-day (0.0004 to 0.0006 ppm).
Lifetime doses for workers were in the range 0.01 to 0.1 mg/kg-day (0.01 to 0.1
ppm). The cumulative dose distribution for the entire population of the MTBE-using
regions of the United States was estimated by combining the distributions of doses
and the numbers of people in each exposure category. In the MTBE-using areas,
arithmetic mean doses via air were estimated to be 0.0053 and 0.00185 mg/kg-day
(0.0053 and 0.00185 ppm) for the chronic and lifetime cases, respectively.
Approximately 98.5% of the population living in MTBE-using regions uses water
with concentrations affected only by atmospheric deposition, if at all, and too low
to be detected with current methods (<2 μg/liter). The remaining population uses
water with an estimated geometric mean concentration of 0.36 μg/liter, an
arithmetic mean concentration of 49 μg/l, and a 95th percentile concentration of 64
μg/liter. Doses via ingestion, inhalation, and dermal absorption were included. The
estimated arithmetic mean dose for the population exposed via water was 1.4 ×
10−3mg/kg-day.
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COMPARISON OF HUMAN EXPOSURE ESTIMATES TO REGULATORY
LIMITS
There are few regulatory limits for MTBE. However, there are protective standards
in place to limit human exposure to MTBE. Table 12 compares Minimal Risk Levels,
or MRLs, developed for MTBE with exposure values available in published literature
showing the amounts of MTBE people are likely to encounter in occupational or
ambient settings.

67

Table 12. Comparison of MTBE Minimal Risk Levels (MRLs) with
exposure estimates for workers and consumers
Exposure
Route

Exposure
Duration

MRL
(ATSDR, 2009)

Exposure
Estimate

Exposed Group

Inhalation

Acute

2 ppm =
2 mg/kg

0.1 – 1.0
mg/kg/day
(Brown, 1997)
>50 ppm
(Nihlen et al.,
1998)

Occupational

2 ppm
(Nihlen et al.,
1998)
0.1-1 ppm
(Nihlen et al.,
1998)
1-10 ppm
(Nihlen et al.,
1998)
0.001-0.01
ppm (Balter,
1997)

Intermediate
Chronic

0.7 ppm =
7 mg/kg
0.7 ppm =
0.7 mg/kg

0.0004 – 0.006
mg/kg/day
(Brown, 1997)
NA

Occupational –
peak levels during
production &
transportation
Occupational –
median during 6
hours of exposure
Occupational –
service station
attendants
average 4 hours
Consumers during
refueling average
2 minutes
Residential –
ambient air,
public buildings, &
residences
Residential

Exposure
Estimate
> MRL?
NO
YES

EQUAL
NO

MAYBE
NO

NO

NA

0.01 – 0.1
Occupational
NO
mg/kg/day
lifetime
(Brown, 1997)
.0053
Residential
NO
mg/kg/day
(Brown, 1997)
0.00185
Residential
NO
mg/kg-day
lifetime
(Brown, 1997)
Oral
Acute
0.4 mg/kg/day 1.4 x 10-3
Residential
NO
mg/kg/day
(Brown, 1997)
Intermediate 0.3 mg/kg/day NA
NA
For Duration, Acute = 1 to 14 days, Intermediate = 15 to 364 days, and Chronic = >1 year.

68

Based on these exposure scenarios and available data, the MRL for MTBE
would be exceeded in certain occupational settings. According to published
exposure estimates, the vast majority of the population is unlikely to encounter
MTBE at levels considered harmful to human health. Exposure thresholds for
consumers were only exceeded during vehicle refueling, and these exposures are
typically very brief (average 2 minutes).

69

70

CHAPTER 5 SUMMARY AND RECOMMENDATIONS
SUMMARY
The Clean Air Act Amendments of 1990 mandated the use of fuel
oxygenates in two programs. The Winter Oxyfuel Program began in the fall of 1992
and required the use of oxygenated fuel in cold winter months, and year-round use
of reformulated gasoline was required beginning in 1995. MTBE production
increased substantially after these programs were implemented, from 36.8 million
barrels per year in 1992 to 71.9 million barrels annually by 1997 (EIA, 2009).
The presence of MTBE in groundwater has been observed at least since the
mid-1980s. The first national survey on the occurrence of volatile organic
compounds (VOCs) in untreated ambient groundwater analyzed samples collected
between 1985 and 1995 (Squillace et al., 1999). MTBE was one of the most
frequently detected VOC in both urban and rural areas. Routine monitoring of
ambient ground water between 1993 and 1998 noted the frequent occurrence of
MTBE, typically at low levels, in shallow urban ground water in the northeastern
United States (Grady, 2001). The occurrence of MTBE and other VOCs were also
noted in surveys of community drinking water sources in the United States between
1999-2001 (Clawges et al., 2001; Delzer & Ivahnenko, 2003).
Shortly after MTBE's introduction as a fuel oxygenate, anecdotal reports of
acute health symptoms such as eye and nose irritation, headaches, nausea, and
dizziness surfaced, leading to concerns about the human health risks from

71

exposure to MTBE. A review of available literature, to include toxicological studies
and epidemiological investigations, show the body of evidence for possible health
effects resulting from MTBE exposure in both humans and animals. The most likely
pathway for human exposure to MTBE is through inhalation.
A review of nearly a dozen human health effects studies evaluating the
association between MTBE exposure and symptoms found that although the
reporting of symptoms anecdotally related to MTBE exposure did increase after the
MTBE reformulated fuel (RFG) program began (Joseph, 2002), no clear evidence or
significant association was found between exposure and adverse health effects
(Borak et al., 1998; Moolenaar et al., 1996; Brown, 1997; Fiedler et al., 1994; Cain et
al., 1994, Prah et al., 1994; Duffy et al., 1994; Nihlen et al., 1998). The MTBE
metabolite tertiary-butyl alcohol (TBA) is processed and removed from the human
body within 24 hours (Lee et al., 2001) and there was no suggestion of adverse
health impacts from this mechanism.
There was some evidence to suggest MTBE is carcinogenic in rats and mice
at multiple organ sites after inhalation or oral-gavage exposure (National Science
and Technology Council, 1997; Belpoggi et al., 1995; Chun et al., 1992; Bird et al.,
1997; Mennear, 1997). For MTBE metabolites, there was a slight increase in
leukemia and intestinal tumors in Sprague-Dawley rats (Soffritti et al., 1989), but
not in Wistar rats (Tyl et al., (1989). Animal testing has suggested that MTBE may
have the potential to cause cancer in humans at high doses, but MTBE has not been
classified as a carcinogen by either the Department of Health and Human Services,
72

the International Agency for Research on Cancer, or EPA. Instead, it has been
suggested that the use of MTBE as a fuel oxygenate may have anticipated health
benefits by reducing the number of cancer-deaths attributable to air pollutants
(Erdal et al., 1997; Spitzer, 1997).

RECOMMENDATIONS
The precautionary principle states that with evidence of threats of
significant harm, even in the face of scientific uncertainty, precautionary actions
should be taken to protect public health and the environment. After reviewing the
scientific literature available for MTBE, there is not compelling evidence to suggest
that exposure to MTBE causes adverse health effects, especially under the
conditions most people would likely be exposed (inhalation in small doses for brief
periods of time). Since the threats of harm are relatively small, the use of MTBE as
a fuel oxygenate provides, at best, an example of the weak version of the
precautionary principle.
In the weak version of the precautionary principle, preventative measures
can be taken in the face of uncertainty, but they are not required. With regard to
harm, there must be some evidence that the threat is likely to occur and have some
degree of severity in consequences. This version also includes consideration of the
costs of the precautionary measure. And finally, the requirement to justify the
need for action (the burden of proof) generally falls on those advocating
73

precautionary action. The case of MTBE fits all of these criteria. Actions to
discontinue use of MTBE as a fuel oxygenate were taken after it was found in
groundwater, even though there was uncertainty about MTBE’s health impact to
humans or the environment. MTBE’s chemical structure and properties suggested
that its release into the environment would result in widespread contamination in
groundwater and that remediation might prove challenging. MTBE was chosen as
the primary fuel additive largely based on cost and availability. And finally, once
MTBE was brought into widespread use and complaints surfaced about potential
health effects from exposure to MTBE, it was the public who signed petitions and
lobbied for its removal as a fuel oxygenate (Erdal & Goldstein, 2000).
According to Cameron (2006), strong versions of the precautionary principle
justify or require precautionary measures be taken, and when knowledge is limited,
those who argue a proposed activity are responsible for demonstrating that the
proposed activity is sufficiently “safe” before approval is granted. A stronger case
could have been made for MTBE adhering to the precautionary principle had the
following actions been taken. First of all, studies about the potential health impacts
from exposure to MTBE should have been conducted and assessed fully prior to its
use. As mentioned, the presence of MTBE in groundwater has been observed at
least since the mid-1980s. However, its use as a fuel oxygenate came much later
(1992) and the majority of health studies I located that addressed potential human
health impacts from exposure to MTBE started after reports of health complaints
emerged in Alaska and elsewhere in late 1992. If this had been done, the decision
74

to use MTBE would have been made with the full spectrum of information available
and not driven primarily by economic factors. Analysis of MTBE health effects data
showed little evidence of harm. Armed with this information, the introduction of
MTBE as a fuel oxygenate could have been better supported and therefore would
have garnered greater public awareness and support. Appropriate precautions
could then be taken to mitigate some of these health risks. For example, exposure
to MTBE-containing fuels is reduced through the use of vapor recovery systems at
gas refueling stations.
The issue of leaking underground storage tanks needs to be addressed.
Leaking tanks that continue to add MTBE-containing gasoline into groundwater
should be removed or cleaned up so that their contents are no longer threats to the
environment or human health. There are other components of gasoline (like
benzene) that have known health risks that far exceed those of MTBE. The public
debate about MTBE-contamination in groundwater has brought to light (or at least
refocused attention) on a much larger issue about how these tanks are being
managed. Great strides in environmental protection could be made if this issue
alone was addressed.
Precautionary action also includes the consideration of alternatives. For
example, emission control devices such as filters and catalytic converters capture
and prevent carbon monoxide emissions without the use of fuel oxygenates.
Changes to the way gasoline is formulated may have reduced the harmful
properties of fuel emissions without the need for fuel oxygenates. Policy changes
75

to encourage drivers to decrease the number of vehicle miles driven may have also
helped to decrease emissions, regardless of the gasoline formula or whether an
oxygenate was added. And if a fuel oxygenate were used, it would at least have
been evaluated against all available fuel oxygenates and selected based on its
usefulness to lower harmful fuel emissions without associated health risks.
When concerns about MTBE surfaced, the reaction was to switch
oxygenates, presumably to one with less risk. However, concerns with ethanol have
surfaced. MTBE-contaminated groundwater is widespread and will presumably be
compounded with the spread of contamination from ethanol-containing fuel
because the problem of leaking underground storage tanks remains. Only when the
validity of solving emissions problems through the use of fuel oxygenates is
questioned will the underlying problem become clear. The problem is fuel driven.
Despite improved technologies, emissions are still problematic due to increases in
the number of cars and vehicle miles driven. The use of fuel oxygenates may have
kept harmful emissions from worsening, but it is not a solution. A better method
for reducing emissions would be to reduce fossil fuel use.
The possibility exists that in the end, MTBE may have achieved greater air
quality benefits with fewer human health impacts than ethanol. If underground
storage tanks had not spread MTBE contamination to the extent that it did and the
public had not reacted so strongly, I believe MTBE would still be in use but still not
quantified in terms of health risk.

76

At the time of this writing, chemical policy in the United States is changing
and moving towards a more precautionary approach. With the European Union’s
adoption of the precautionary principle in its Registration, Evaluation, Authorisation
and Restriction of Chemical substances (REACH) program, the world has had an
opportunity to see the precautionary approach work in a large public forum. This
program attempts to improve the knowledge gap that exists for the majority of
chemicals in commerce and calls for toxicity testing of new chemicals prior to their
introduction in the market. It also requires testing of existing chemicals starting
with those of high production volume. Within the United States, there is already
evidence that precautionary principles will be brought to the forefront of
environmental planning and management. The work of several western states to
create climate change policies more stringent and protective than those put forth
by the federal government has drawn the attention of the new administration. In
our own State of Washington, direct mention of the precautionary principle is now
found on the websites of several state agencies: Department of Ecology,
Department of Fish and Wildlife, Department of Health, Department of Natural
Resources, Puget Sound Partnership, and Washington State Board of Health (State
of Washington, 2009).
Evaluating MTBE’s use as a fuel oxygenate against precautionary principles
provides a lesson that can help guide future policy decisions, as it encourages
actions that are more protective of human and environmental health.

77

78

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