[Senate Hearing 106-546]
[From the U.S. Government Publishing Office]
S. Hrg. 106-546
BLUE RIBBON PANEL FINDINGS ON MTBE
=======================================================================
HEARING
BEFORE THE
SUBCOMMITTEE ON CLEAN AIR, WETLANDS,
PRIVATE PROPERTY, AND NUCLEAR SAFETY
COMMITTEE ON
ENVIRONMENT AND PUBLIC WORKS
UNITED STATES SENATE
ONE HUNDRED SIXTH CONGRESS
FIRST SESSION
__________
OCTOBER 5, 1999
__________
Printed for the use of the Committee on Environment and Public Works
U.S. GOVERNMENT PRINTING OFFICE
63-233 CC WASHINGTON : 2000
_______________________________________________________________________
For sale by the U.S. Government Printing Office
Superintendent of Documents, Congressional Sales Office, Washington, DC
20402
COMMITTEE ON ENVIRONMENT AND PUBLIC WORKS
ONE HUNDRED SIXTH CONGRESS
JOHN H. CHAFEE, Rhode Island, Chairman
JOHN W. WARNER, Virginia MAX BAUCUS, Montana
ROBERT SMITH, New Hampshire DANIEL PATRICK MOYNIHAN, New York
JAMES M. INHOFE, Oklahoma FRANK R. LAUTENBERG, New Jersey
CRAIG THOMAS, Wyoming HARRY REID, Nevada
CHRISTOPHER S. BOND, Missouri BOB GRAHAM, Florida
GEORGE V. VOINOVICH, Ohio JOSEPH I. LIEBERMAN, Connecticut
MICHAEL D. CRAPO, Idaho BARBARA BOXER, California
ROBERT F. BENNETT, Utah RON WYDEN, Oregon
KAY BAILEY HUTCHISON, Texas
Jimmie Powell, Staff Director
J. Thomas Sliter, Minority Staff Director
------
Subcommittee on Clean Air, Wetlands, Private Property, and Nuclear
Safety
JAMES M. INHOFE, Oklahoma, Chairman
GEORGE V. VOINOVICH, Ohio BOB GRAHAM, Florida
ROBERT F. BENNETT, Utah JOSEPH I. LIEBERMAN, Connecticut
KAY BAILEY HUTCHISON, Texas BARBARA BOXER, California
(ii)
C O N T E N T S
----------
Page
OCTOBER 5, 1999
OPENING STATEMENTS
Bennett, Hon. Robert F., U.S. Senator from the State of Utah..... 10
Boxer, Hon. Barbara, U.S. Senator from the State of California... 3
Chafee, Hon. John H., U.S. Senator from the State of Rhode Island 2
Inhofe, Hon. James M., U.S. Senator from the State of Oklahoma... 1
Lieberman, Hon. Joseph I., U.S. Senator from the State of
Connecticut.................................................... 39
Voinovich, Hon. George V., U.S. Senator from the State of Ohio... 20
WITNESSES
Campbell, Robert H., chairman and chief executive officer,
Sunoco, Inc.................................................... 28
Letter, to Senators Inhofe and Graham........................ 55
Prepared statement........................................... 53
Responses to additional questions from Senator Inhofe........ 56
Summary, Blue Ribbon Panel Recommendations on MTBE........... 41-47
Garn, Hon. Jake, vice chairman, Huntsman Corporation, Salt Lake
City, UT....................................................... 25
Prepared statement........................................... 71
Greenbaum, Daniel S., president, Health Effects Institute,
Cambridge, MA, and former chair, Blue Ribbon Panel on the Use
of Oxygenates in Gasoline...................................... 11
Prepared statement........................................... 40-48
Responses to additional questions from:
Senator Boxer............................................ 50
Senator Inhofe........................................... 48
Senator Lieberman........................................ 52
Kenny, Michael P., executive officer, California Air Resources
Board, Sacramento, CA.......................................... 26
Letters:
To EPA Assistant Administrator, Robert Perciasepe........ 63
To EPA Director of Mobile Sources, Margo Oge............. 70
Prepared statement........................................... 57
Responses to additional questions from Senator Inhofe........ 59
ADDITIONAL MATERIAL
Articles:
MTBE Groundwater Impacts in South Lake Tahoe, CA............. 87
Former Senator Garn Tells Senate Panel to Save Fuel Additive
MTBE....................................................... 85
Comments, National Research Council Report....................... 77-81
Letters:
To Margo T. Oge, Director, Office of Mobile Sources, from
Michael P. Kenny........................................... 70
To Senators James M. Inhofe and Bob Graham, from Robert H.
Campbell................................................... 55
To EPA Assistant Administrator Robert Perciasepe from Michael
P. Kenny................................................... 63-69
To Senator Bob Graham from Robert Baer....................... 87
Report, Public Health Goal for Methyl Tertiary Butyl Ether (MTBE)
in Drinking Water..............................................88-177
Statements:
Association of Metropolitan Water Agencies and American Water
Works Association.......................................... 81
Bergson, Ivo, South Tahoe Public Utility District............ 87
Hall, Steve, executive director of the Association of
California Water Agencies.................................. 82
Lyondell Chemical Company--Summary of Dissenting Report...... 48
Santa Clara Valley Water District............................ 85
Summary, The Blue Ribbon Panel on Oxygenates in Gasoline--
Executive Summary and Recommendations.......................... 41-47
BLUE RIBBON PANEL FINDINGS ON MTBE
----------
TUESDAY, OCTOBER 5, 1999
U.S. Senate,
Committee on Environment and Public Works,
Subcommittee on Clean Air, Wetlands, Private Property, and
Nuclear Safety,
Washington, DC.
The subcommittee met, pursuant to notice, at 9:30 a.m., in
room 406, Senate Dirksen Building, Hon. James N. Inhofe
(chairman of the subcommittee) presiding.
Present: Senators Inhofe, Bennett, Voinovich, Boxer, and
Chafee [ex officio].
OPENING STATEMENT OF HON. JAMES M. INHOFE,
U.S. SENATOR FROM THE STATE OF OKLAHOMA
Senator Inhofe. The subcommittee will come to order.
At today's hearing we are going to examine the
recommendations of the Environmental Protection Agency's Blue
Ribbon Panel Advisory Committee on the use of Oxygenates in
Gasoline on MTBE.
MTBE is a fuel additive used to add oxygen to gasoline. The
Clean Air Act requires reformulated gasoline, RFG, to contain 2
percent oxygen by weight. MTBE is used in over 85 percent of
the RFG, and ethanol is the second largest at 8 percent. The
requirement for RFG began in 1995, as mandated by the 1990
Clean Air amendments.
In the last few years, MTBE has been found in drinking
water sources, and it is my understanding that the great
majority of the levels found are well below the public health
concerns, although they create a problem with odor and taste.
Because of these water-related concerns, the use of MTBE has
been questioned. In March 1999, Governor Gray Davis issued an
executive order that will eliminate MTBE from California's
gasoline by the end of 2002.
There are various legislative options in Congress for
dealing with MTBE. These range from an outright ban, to phase-
out, to making oxygenates optional.
Over the last 2 years the full committee has held two
hearings addressing the concerns in California; today is the
first time for our subcommittee to consider the MTBE program
nationwide. We will be hearing from members of the Blue Ribbon
Panel and other representatives.
The EPA's Blue Ribbon Panel issued their report on July 29,
1999. The findings of the report have, in my opinion, been
mischaracterized by both the press and the Senate. It is my
understanding that the panel's recommendation for an orderly
phase-down in the use of MTBE was dependent upon the repeal of
the Federal oxygenate mandate. It is my hope that the ultimate
goal of today's hearing is for the members of the committee to
understand fully what the report says and does not say
regarding MTBE.
Recently the Department of Energy identified several areas
of concern for the U.S. refining industry, including the
uncertainty of the role of oxygenates, particularly MTBE in
gasoline. I think it is important that we do not jump to any
rash conclusions out of unfounded fear or unjustified claims of
fuel alternatives. We should not act in haste on the MTBE issue
because the potential impacts to the consumer are significant.
The safeguarding of the nationwide supply and distribution of
gasoline must be a key consideration in any action that is
taken to address MTBE.
I believe that one of the most important lessons to be
learned from the current situation is that prescriptive
mandates reduce flexibility and may lead to unintended
consequences.
There are a number of issues and questions that I would
like addressed, both today and in the coming weeks and months.
First, what are the health concerns of MTBE--not the talk,
but the real health concerns?
Are there benefits to the air from MTBE or other
oxygenates, and are they necessary?
Are there specific negative environmental effects from
MTBE?
What is the impact of MTBE and other oxygenates on the fuel
supply and delivery system?
Since MTBE was required under the Clean Air Act, if we ban
or phase out, should we compensate for stranded cost of
investment of the MTBE producers?
And last, what impact will States' efforts to address MTBE
have on the gasoline and distribution system?
Senator Inhofe. We have an excellent slate of witnesses
today, including the chairman of the Blue Ribbon Panel and
former Senator Jake Garn. This is probably not the last time we
will address the MTBE or oxygenates issue. We will probably be
having a hearing on the environmental effects of ethanol.
Senator Chafee, do you have an opening statement you would
like to make?
OPENING STATEMENT OF HON. JOHN H. CHAFEE,
U.S. SENATOR FROM THE STATE OF RHODE ISLAND
Senator Chafee. I do.
I am delighted that you are having this hearing, Mr.
Chairman.
I want to welcome our witnesses, especially our former
colleague from Utah, Senator Jake Garn. It's so nice to see you
here once again.
The full committee held a hearing on MTBE last year. Since
then, as you mentioned, much has happened. In March, Governor
Davis in California ordered the State to phase out MTBE use by
the end of 2002.
In July, the Blue Ribbon Panel issued its report on the use
of oxygenates in gasoline. Those findings have served to guide
the debate about the future of MTBE, the 2 percent mandate, and
the problems with leaking underground storage tanks.
In August, the future of MTBE was even debated on the
Senate Floor. In that debate I urged the Senate to move forward
cautiously, guided by the recommendations of the Blue Ribbon
Panel. It is important that we not rush to judgment, as you
indicated, Mr. Chairman, or make hasty decisions, but I believe
we have to address this problem. The future of the program, the
progress we've made on air quality and public confidence in our
water supply, all depend upon resolving this question about the
use of oxygenates in gasoline.
I want to stress that this is not a ``California only''
problem. MTBE has been found in water supplies in 26 States,
including my State of Rhode Island. Much of it comes from
leaking underground storage tanks, which were required by law
to be upgraded or closed by December 22, 1998. MTBE
contamination of water is most acute in the 17 States that use
reformulated gasoline.
Air quality benefits of reformulated gasoline have been
substantial. Toxics and ozone-forming compounds have been
reduced dramatically.
Last year, in a full committee hearing, I called for the 2
percent mandate to be lifted. I am glad to see that the Blue
Ribbon Panel agreed with me in that recent report. We look
forward to hearing what they have to say.
I want to thank you again, Mr. Chairman, and I would submit
this entire statement for the record.
Senator Inhofe. Thank you, Chairman Chafee.
Senator Boxer.
OPENING STATEMENT OF HON. BARBARA BOXER,
U.S. SENATOR FROM THE STATE OF CALIFORNIA
Senator Boxer. Thank you so much to both my chairmen, my
subcommittee chair and the full committee chair. I am really
glad to have the opportunity to make some remarks.
It is a very serious issue. I think I have a slightly
different view than my friends, and I want to lay it out, if I
might.
After I asked Administrator Browner to phase out MTBE, she
appointed the Blue Ribbon Panel, and I am very pleased that my
reading of the panel's report suggests my view, that we would
be better off without MTBE. Specifically, on the question of
whether MTBE use should continue, the panel report states:
The panel agreed broadly that in order to minimize current
and future threats to drinking water, the use of MTBE should be
reduced substantially. Several members believe that the use of
MTBE should be phased out completely.
I first formed a view that we should phase out MTBE in
1997, after the city of Santa Monica lost 71 percent of its
drinking water supply due to MTBE contamination. And I want to
say to both my Chairmen, I can assure you that if one of the
cities in your State was faced with that situation, of losing
71 percent of their water supply, I think perhaps you would be
closer to my view.
Now, on August 4, 1999, the majority of the U.S. Senate
joined with me in expressing the view that we should phase out
MTBE. We adopted my Sense of the Senate; it provided that ``The
United States should phase out MTBE in order to address the
threats that MTBE poses to public health and the environment.''
And I would like to place the text of this Sense of the Senate
into the hearing record, Mr. Chairman, if I might.
Senator Inhofe. Without objection.
Senator Boxer. Thank you.
Senator Boxer. The Sense of the Senate counted Senator
Crapo, Chairman of the Environment and Public Works Drinking
Water Subcommittee, among its cosponsors, and for good reason.
This issue is, first and foremost, a drinking water issue,
because MTBE is contaminating drinking water.
I would like to place into the hearing record the testimony
of the Association of California Water Agencies, the Santa
Clara Valley Water District, and the South Tahoe Public Water
Utility District.
Senator Inhofe. Without objection.
Senator Boxer. Thank you so much, Mr. Chairman.
Senator Boxer. These agencies wanted to testify today, but
there wasn't time to have a panel on water quality, so I am
putting their statements in the record.
Why does MTBE pose a threat to drinking water and public
health? First, in 1997, MTBE was the second-most produced
chemical in the United States, so it's out there, in the
environment, in huge quantities.
Second, MTBE is classified by the EPA as a possible human
carcinogen. The University of California has also concluded
that MTBE is an animal carcinogen and has the potential to
cause cancer in humans.
I would like to place a peer-reviewed MTBE report, prepared
by the California Office of Environmental Health Hazard
Assessment, in today's hearing record. I would like to place,
Mr. Chairman, a peer-reviewed MTBE report prepared by the
California Office of Environmental Health Hazard Assessment in
today's hearing record.
Senator Inhofe. Without objection, so ordered.
Senator Boxer. Thank you.
This report details and summarizes the health studies
underlying the agency's recommendation, that California adopt
an MTBE public health drinking water standard of 13 parts per
billion. This standard is more protective than EPA's current
non-binding standard of up to 40 parts per billion. So
California is way ahead, in my view, in terms of protecting the
public health, way ahead of where we are at the EPA, and I am
very disappointed about that.
To summarize what I've said so far, MTBE is dangerous and
it is widely used. Another reason is that it is also very hard
to control. When MTBE leaks from an underground storage tank,
from a motorboat, or from a gas tank after a car accident, into
the groundwater, it moves through that water very fast and very
far. It extends well beyond the area of a typical gasoline
groundwater plume.
Also, unlike the other constituents of gasoline, it resists
degrading once it is in the water. Moreover, it only takes a
very small amount of this widely-used chemical to contaminate a
drinking water source. For example, in Maine--I'm not talking
about California, in Maine--about 7 to 12 gallons of gas
containing MTBE spilled during a car accident and contaminated
24 nearby private drinking water wells. Twelve of those wells
showed contamination above Maine's MTBE drinking water
standard. And it takes even less MTBE to render water
undrinkable.
MTBE causes water to take on the taste and smell of
turpentine at very low levels. Consumers can taste MTBE in
their water at as low as 5 parts per billion. That is
equivalent to less than a tablespoon of MTBE in an Olympic-size
pool.
I have an example of this from Santa Monica. This is what
their water smells like. I thought it would be interesting to
smell it.
[Laughter.]
Senator Boxer. If you could pass it on to Senator Bennett.
I think it's important, because--here's the point I'm
trying to make--even at 5 parts per billion, this stuff ruins
the water in terms of your perception of it. People will not
drink it if it smells that way. It smells like turpentine.
What is the extent of MTBE contamination in the Nation?
And, Mr. Chairman, I am winding down, you will be happy to
know. Since the Santa Monica catastrophe, South Lake Tahoe, CA
has lost 13 of its 34 drinking water wells to MTBE
contamination. Santa Clara County in the Silicon Valley has
detected MTBE at over 400 groundwater sites, many of which are
near public water supply wells. In 1998, a study conducted by
Lawrence Livermore determined that MTBE is leaking at 10,000
sites in California.
But MTBE contamination is not just a California problem, as
I have said before. Maine has determined that between 1,000 and
4,300 private wells may contain MTBE. In New Hampshire, MTBE
has been detected in more than 100 public wells and water
supplies. Suffolk County Water Utility in New York, which
serves 1.2 million customers entirely with groundwater, tells
me that 80 percent of its wells show detectable levels of MTBE.
Overall, the panel report states that the USGS estimates
that between 5 and 10 percent of drinking water supplies now
show MTBE contamination. I believe that is a low-end estimate,
and I can get into why I believe that, but I won't go into it
in the statement.
So again, to summarize, the chemical is out there; it's out
there in large quantities; it has the potential to cause cancer
in humans; it can render drinking water undrinkable, as I think
you would agree, at very low levels. And one more point. We
know that the potential cleanup costs are already astronomical.
A University of California study in 1998 estimated cleanup
costs could run as high as $1.5 billion just in California. Mr.
Chairman, we all care about balancing the budget. Why would we
want to put more of this stuff out there when we already know
the cleanup costs are $1.5 billion?
Now, I had further discussions. The authors of the studies
believe they have underestimated the cleanup costs. They
believe they could be 20 to 30 percent higher than that
estimate.
Some argue that replacing gasoline storage tanks is the
answer, but even new tanks have problems. A July 22, 1999 study
by Santa Clara Valley Water District, in fact, found that many
of its new tanks are leaking. The study reviewed a total of 28
sites with fully upgraded storage tank systems, to observe
whether MTBE had leaked. MTBE was detected in groundwater at 13
of these sites at concentrations ranging from 1 part per
billion to 200,000 parts per billion. I would like to place
that study into the record.
Senator Inhofe. Without objection.
Senator Boxer. So upgrading the tanks isn't the full
answer, and neither will legislation which would amend the
Clean Air Act to eliminate the oxygen requirement, but not ban
MTBE--that's not the answer.
The argument behind such legislation is that if we give oil
companies the flexibility to make reformulated gas without an
oxygenate, they will voluntarily stop using MTBE. A story from
the San Francisco Bay area, however, shows we can't rely upon
the oil companies to voluntarily stop using it.
Even though oxygenated gas is not required to be used in
the San Francisco Bay area, in May of this year it was
disclosed that Chevron and Tosco were adding large quantities
of MTBE to their gasoline in order to stretch gasoline
supplies. So they didn't have to do it; they know the
controversy--Governor Davis had already acted to say he was
going to phase it out, and they used it anyway.
And I would like to place an L.A. Times story detailing
this incident into the record at this time.
Senator Inhofe. Without objection.
Senator Boxer. As a result of the action of Chevron and
Tosco, an area of California we could have hoped would be
spared MTBE contamination may now also face significant threat.
In conclusion, I believe there are two ways to end MTBE
use.
First, Congress should pass a phase-out schedule; or
second, Administrator Browner could use her emergency authority
to phase it out, and I'm very sorry that she hasn't done so.
I have introduced legislation which would phase out MTBE in
stages beginning January 1, 2000, and adopting equal interim
reductions each year until the phase-out deadline is completed
on January 1, 2003. The DOE predicts it would take
approximately 4 years to allow refiners to re-tool their
facilities and increase ethanol production in the United States
in order to implement such a phase-out, so my bill is in the
ball park in terms of its timeframe.
MTBE is destroying water supplies throughout the Nation.
MTBE cleanup costs are astronomical. MTBE is harming our lakes.
MTBE is dangerous to your health. MTBE should be phased out.
Clean air is crucial to the health of our citizens; so is a
safe drinking water supply. We need to do both--not one, but
both.
Thank you, Mr. Chairman.
[The prepared statement and article submitted by Senator
Boxer follow:]
Statement of Hon. Barbara Boxer, U.S. Senator from the
State of California
Good morning, Mr. Chairman. Thank you for holding this hearing
today.
After I asked Administrator Browner to phase out MTBE, she
appointed the Blue Ribbon Panel. I am pleased that panel report
supports my view that we would be better off without MTBE.
Specifically, on the question of whether MTBE use should continue,
the panel report states that:
[t]he Panel agreed broadly that, in order to minimize current
and future threats to drinking water, the use of MTBE should be
reduced substantially. Several members believed that the use of
MTBE should be phased out completely.
I first formed the view that we should phase out MTBE in 1997 after
the City of Santa Monica lost 71 percent of its drinking water supply
due to MTBE contamination.
On August 4, 1999, the majority of the Senate joined with me in
expressing that view by adopting my Sense of the Senate on this issue.
That Sense of the Senate provided that the United States should ``phase
out MTBE in order to address the threats MTBE poses to public health
and the environment.''
I would like to place the text of this Sense of the Senate into the
hearing record.
The Sense of the Senate counted Senator Crapo, chairman of the
Environment and Public Works' drinking water subcommittee, among its
cosponsors.
And for good reason.
This issue is, first and foremost, a drinking water issue.
I would like to place into the hearing record the testimony of the
Association of California Water Agencies, the Santa Clara Valley Water
District and the South Tahoe Public Water Utility District.
These agencies requested to testify here today. They support
phasing out MTBE completely.
Why does MTBE pose a threat to drinking water and public health?
First, in 1997, MTBE was the second most-produced chemical in the
United States. It's out there in our environment in huge quantities.
Second, MTBE is classified by the EPA as a possible human
carcinogen. The University of California has also concluded that MTBE
is an animal carcinogen, and has the potential to cause cancers in
humans.
I would like to place a peer reviewed MTBE report prepared by the
California Office of Environmental Health Hazard Assessment in today's
hearing record.
This report details and summaries the health studies underlying the
agency's recommendation that California adopt a MTBE public health
drinking water standard of 13 parts per billion.
That standard is more protective than EPA's current nonbinding
standard of up to 40 parts per billion.
So MTBE is dangerous and widely used.
It is also very hard to control.
When MTBE leaks from an underground storage tank, from a motor boat
or from a gas tank after a car accident into groundwater, it moves
through that water very fast and very far.
It extends well beyond the area of a typical gasoline groundwater
plume.
Also, unlike the other constituents of gasoline, it resists
degrading once in water.
Moreover, it only takes a very small amount of this widely used
chemical to contaminate a drinking water source.
For example, in Maine about 7 to 12 gallons of gasoline containing
MTBE spilled during a car accident and contaminated 24 nearby private
drinking water wells. Twelve of those wells showed contamination above
Maine's MTBE drinking water standard.
And, it takes even less MTBE to render water undrinkable.
MTBE causes water to take on the taste and smell of turpentine at
very low levels. Consumers can taste MTBE in their water at as low as
five parts per billion.
That is equivalent to less than a tablespoon of MTBE in an Olympic
size pool.
What is the extent of MTBE contamination in the nation?
Since the Santa Monica catastrophe, South Lake Tahoe, California
has lost 13 of its 34 drinking water wells to MTBE contamination. Santa
Clara County, in the Silicon Valley, has detected MTBE at over 400
groundwater sites, many of which are near public water supply wells.
A 1998 study conducted by Lawrence Livermore determined that MTBE
is leaking at approximately 10,000 sites in California.
But MTBE contamination is not just a California problem.
Maine has determined that between 1,000 and 4,300 private wells may
contain MTBE. In New Hampshire, MTBE has been detected in more than 100
public wells and water supplies. Suffolk County Public Water Utility in
New York, which serves 1.2 million customers entirely with groundwater,
tells me that 80 percent of its wells show detectible levels of MTBE.
Overall, the panel report states that the United States Geological
Survey estimates that between 5 and 10 percent of drinking water
supplies now show MTBE contamination. And, I believe that this is a
low-end estimate.
So again, to summarize so far, the chemical is out there, it is out
there in large quantities, it has the potential to cause cancer in
humans, and it can render drinking water undrinkable at very low
levels.
We also know that the potential cleanup costs are already
astronomical.
In 1998, a University of California study estimated that cleanup
costs could run as high as 1.5 billion in California alone.
Based upon further discussions, the authors of the study now
believe that the cleanup costs are about 20 to 30 percent higher than
that estimate.
Some argue that replacing gasoline storage tanks is the answer.
But even the new tanks have problems, a fact acknowledged by the
panel.
A July 22, 1999 study by the Santa Clara Valley Water District, in
fact, found that many of its new tanks are leaking. The study reviewed
a total of 28 sites with fully upgraded storage tank systems to observe
whether MTBE had leaked from those tanks.
MTBE was detected in groundwater at 13 of these sites at
concentrations ranging from 1 part per billion to 200,000 part per
billion.
I would like to place that study into the hearing record.
Upgrading the tanks won't solve the problem.
And neither will legislation which would amend the Clean Air Act
(CAA) to eliminate the oxygen requirement, but not ban MTBE.
The argument behind such legislation is that if we give oil
companies the flexibility to make reformulated gasoline without an
oxygenate, they will voluntarily stop using MTBE.
A story from the San Francisco Bay area, however, shows why we
can't rely upon the oil companies to voluntarily stop using MTBE.
Even though oxygenated gasoline is not required to be used in the
Bay Area, in May of this year it was disclosed that Chevron and Tosco
were adding large quantities of MTBE to their gasoline in order to
stretch gasoline supplies.
I would like to place a Los Angeles Times story detailing this
incident into the record.
As a result of Chevron and Tosco's action, an area of California we
could have hoped would be spared MTBE contamination may also now face
significant threat.
I believe that there are two ways to end MTBE use.
First, Congress should pass a phase out schedule. Second,
Administrator Browner should use emergency authorities to phase it out.
I have introduced legislation which would phase out MTBE in stages
beginning on January 1, 2000, and adopting equal interim reductions
each year until the complete phase-out deadline of January 1, 2003.
The Department of Energy predicts that it would take approximately
4 years to allow refiners to retool their facilities and increase
ethanol production in the United States in order to implement such a
phase out--so my bill is in the ballpark.
MTBE is destroying water supplies throughout the nation. MTBE
cleanup costs are astronomical. MTBE is harming our lakes. MTBE is
dangerous to health. MTBE should be phased out.
Clean air is crucial to our health. So is a safe drinking water
supply. We need both--not one, but both.
Thank you.
______
[From the Los Angeles Times, May 7, 1999]
MTBE Put In Gas
(By Jennifer Warren)
Sacmamento--Just as Gov. Gray Davis Was declaring MTBE an
environmental hazard and ordering it phased out of gasoline, two oil
companies were increasing amounts of the controversial ad?ditive in gas
sold in Northern California.
Officials at Chevron Corp. and Tosco Corp. confirmed the boost in
MTBE, saying it was necessary to stretch their gasoline supply after
refinery fires and marketplace factors reduced production.
The move enabled the companies to keep a high volume of their
gasoline flowing to market in March and April, when pump prices spiked
to more than $2 a gallon in some parts of California.
Chevron and Tosco officials defended the move as a temporary
measure to help them serve customers during a short-term emergency. And
while MTBE--a possible carcinogen--is scheduled to be banned in
California, adding more of it to gasoline now is not illegal.
Critics, including a state senator, condemned the tactic, accusing
the companies of putting profits ahead of public fears of a chemical
that has contaminated drinking water wells throughout the state.
They also call the move hypocritical because both oil companies
have been leaders in making MTBE-free gasoline. Last month, Tosco held
a press conference to publicize its delivery of MTBE-free gasoline to
Union 76 stations in the Lake Tahoe area. It also sells MTBE-free gas
in three Bay Area counties.
Chevron, meanwhile, had been supplying MTBE-free gasoline to much
of Northern California. About half of the gasoline produced at its
Richmond refinery is typically made without MTBE.
``These are companies that have been making MTBE-free gas for quite
awhile, so why are they doing this?'' said state Sen. Don Perata (D-
Alameda). ``It's pure economics. The price is high and they're
stretching their supply by adding more MTBE. . . . It's hard not to be
cynical about it.''
Assembly Speaker Antonio Villaraigosa (D-Los Angeles) expressed
similar concerns: ``They seem to be sending mixed signals here. There's
no formal MTBE ban yet, but this is obviously taking us in the wrong
direction.''
MTBE is a key component of ``cleaner-burning gasoline,'' which has
laden used in most of California's 24 million vehicles since 1996,.
While credited with reducing auto emissions, MTBE has leaked from
underground storage tanks to contaminate drinking water from Santa
Monica to Lake Tahoe. It also taints lakes by entering the water from
two-stroke engines such as those that power water scooters.
Although other components of gasoline also seep from subterranean
tanks, MTBE is a particular peril because it travels into ground water
so quickly. Its health effects on humans are poorly understood, but it
has been shown to cause cancer in mice and rats.
Responding to a rising clamor, the Governor declared in late March
that MTBE poses a ``significant risk'' to the environment and ordered
it phased out in California by the end of 2002.
Davis was traveling Thursday and had no immediate comment on the
new developments. A spokeswoman noted that Davis has publicly urged
companies to voluntarily remove MTBE from gasoline before the deadline.
The boost in MTBE usage by Chevron and Tosco came to light after
Perata--acting on a tip--asked an East Bay water district to take
samples of gasoline at three service stations in early April. The
samples showed that various grades of gas at the stations--in San
Francisco and Oakland--contained levels of MTBE as high as 15 percent,
the legal limit.
Company officials did not dispute the findings, and acknowledge
that they represent an increase. MTBE typically makes up about 10 to 11
percent of Tosco's gasoline, while much of Chevron's Northern
California gas had previously contained no MTBE, officials said. The
exception to that is in Sacramento, where clean air rules mandate an 11
percent concentration of the smog-fighting additive.
Mixing in more MTBE was one of many steps the companies took in
response to a gas supply shortage that hit in March, officials said.
The shortage was caused in part by a Feb. 23 explosion that closed
Tosco's Martinez refinery and a fire at Chevron's Richmond refinery on
March 25.
Al Jessel, a Chevron fuels specialist, said the fire cut the
refinery's capacity by 10 percent to to 15 percent, forcing officials
to hunt for ways to stretch supply. In addition to blending in more
MTBE, Chevron ``bought every gallon of gasoline we could find from
anyone anywhere in the world.''
If the company had not added more MTBE, the result would have been
an even tighter supply and even higher prices, Jessel said.
``We had to make a balance in our minds between having, MTBE-free
gas and running out of gas and being unable to supply our customers,''
said Jessel, adding that Chevron has since found new sources of
gasoline and is no longer mixing in more MTBE.
At Tosco, spokesman Duane Bordvick said his company went to similar
lengths to cope with the supply crunch. He took issue with critics who
suggest that adding more MTBE was an environmental sin.
``Tosco is doing an awful lot to get MTBE out of gasoline. We've
been a leader in the industry,'' Bordvick said. ``But I don't think
increasing it up to the legal limit over a period of days has any
impact.''
At Communities for a Better Environment, staff scientist Azibuike
Akaba disagreed and called the companies' action ``extremely
irresponsible.''
``We've already got a terrible contamination problem with MTBE,''
said Akaba, whose San Francisco-based nonprofit group has been a critic
of MTBE since 1991. ``The more they put in, the worse it gets.''
Senator Inhofe. Thank you, Senator Boxer.
Senator Bennett.
OPENING STATEMENT OF HON. ROBERT F. BENNETT,
U.S. SENATOR FROM THE STATE OF UTAH
Senator Bennett. Thank you, Mr. Chairman. I am going to
look forward to the testimony of the witnesses.
I hope when we finally come down to a decision here, it is
based on sound science, based on a full understanding of all of
the aspects of the issue. I cannot help but reflect on an
experience that occurred before I came to the Congress but that
nonetheless, I think, had lasting impact. This was the concern
about Alar on apples, and the Congress received a great deal of
testimony, some of it from Academy Award-winning actresses,
about the terrible effects on human health from Alar being
sprayed on apples. Congress reacted to that testimony, and Alar
was banned. The apple crop for that particular season was
ruined.
I talked with the individual in Utah who handles food for
the homeless, and he said, ``That was a great boon for us,
because we received all the apples that could not be sold in
the supermarkets that were perfectly wonderful food, that had
no contamination to them at all, and had been taken off the
market as a result of panic. And that was fine, in that we had
food to distribute to the homeless, but once the science caught
up with the rhetoric, we found out we had made a serious
mistake.''
I get very nervous anytime we get into any of these kinds
of hearings, to make sure that the science catches up with the
rhetoric. And if we come out with a sound scientific answer
this morning as a result of the balanced witnesses we're going
to hear, I will be very grateful and I will be happy to support
an appropriately scientific answer to what is a very troubling
and difficult kind of question.
Thank you, Mr. Chairman.
Senator Boxer. Would the Senator yield for one point?
I would not send this to a homeless shelter. I mean, you're
talking about a different situation. You're talking about a
city that has 71 percent of its water supply finished, closed
off, shut down. You're not talking about theory here.
Also, I hope my friend would read the scientific reports
that we have placed in the record.
Senator Bennett. I will read those.
Senator Boxer. I think it's part of the balance that he's
looking for.
Senator Bennett. I will read the scientific report.
I have relatives who live in Santa Monica. They continue to
drink the water, but I'll look forward to hearing from them,
I'm sure, as this thing goes on.
Senator Boxer. Well, we do deliver clean water to those
people. Those wells are closed, but the rest of it is fine.
Senator Inhofe. Our first witness was the chairman of the
Blue Ribbon Panel. Mr. Greenbaum, we appreciate very much your
being here today. As you can see, there are some clarifications
that we are looking to you to take care of for us.
We're going to have four witnesses today. What we're going
to do is ask the witnesses to try to confine their opening
statements to 5 minutes, and we will use the lighting system
here. However, your entire statement will be entered in as a
part of the record.
We will also have 5-minute rounds, and we will try to hold
ourselves to that same timeframe.
Mr. Greenbaum.
STATEMENT OF DANIEL S. GREENBAUM, PRESIDENT, HEALTH EFFECTS
INSTITUTE, CAMBRIDGE, MA, AND FORMER CHAIR, BLUE RIBBON PANEL
ON THE USE OF OXYGENATES IN GASOLINE
Mr. Greenbaum. Mr. Chairman, thank you very much. To you,
Mr. Chairman, and Chairman Chafee and other members of the
committee, I am pleased to have the opportunity to be here. I
have to say, sitting here and listening to your opening
statements, I felt for a moment that I was back at the first
meeting of the Blue Ribbon Panel because some of the same
issues and questions were placed on the table, as you might
guess. We made an effort to try to bring a group of people
together to try to look at this issue, look at the facts of
this issue, and hopefully I can share with you some of that in
my testimony and then answer questions as we go through the
session this morning.
In the wake of the detection of MTBE in drinking water
supplies, as Senator Boxer said, in both Maine and California
and elsewhere, Administrator Browner convened the Blue Ribbon
Panel to investigate the facts of the situation and to
recommend actions to achieve both clean air and clean water.
The Panel consisted of experts on air, water, and public
health, as well as representatives of the oil, ethanol, and
MTBE industries, and the environmental community. We began our
work in January of this year and we conducted an in-depth
investigation of the air quality, water quality, fuel supply,
and price issues surrounding the use of oxygenates in gasoline.
We held six meetings in 6 months, including field meetings in
New England and California. We heard from experts, we reviewed
dozens of both existing and new studies of oxygenates in
gasoline.
Based on that review the Panel found, first, that RFG has
provided substantial reductions in the emissions of a number of
air pollutants from motor vehicles, in most cases resulting in
emission reductions that exceed those required by law.
Second, we found that there have been growing detections of
MTBE in drinking water across the country, with between 5
percent and 10 percent of drinking water supplies in RFG areas
showing detectable amounts of MTBE. There have not, at the same
time, been increases in detections of the other portions of
gasoline which behave fundamentally differently than MTBE in
groundwater.
The great majority of the MTBE detections have been below
levels of public health concern, as you yourself said in your
opening comments, Mr. Chairman. With approximately 1 percent
rising to levels above 20 parts per billion, and some
instances, such as Santa Monica--although rare--of levels of
100 parts per billion and higher.
Detections at these lower levels, however, have raised
consumer taste and odor concerns, and they have caused water
suppliers to stop using some water supplies and to incur the
costs of treatment and remediation.
The third thing we found is that the major source of this
contamination appears to be releases from underground gasoline
storage systems. These systems have been upgraded in the past
decade, and that has likely resulted in reduced risk of leaks.
However, approximately 20 percent of the storage tanks have not
yet been upgraded. As well, there continue to be reports of
releases from some upgraded systems due to inadequate design,
installation, maintenance, and operation.
In addition, under the law under which USEPA regulates
these tanks, they do not currently have the authority to
regulate many fuel storage systems beyond those we see in
gasoline stations.
Based on these facts, the Panel evaluated a range of
alternatives for addressing the problems, and we recommended
that EPA work with you in Congress and the States to implement
a four-part integrated--and that's an important term here--
integrated package of reforms to ensure that water supplies are
better protected, while the substantial reductions in air
pollution that have resulted from RFG are maintained.
Specifically, the Panel recommended, No. 1, a comprehensive
set of improvements to the Nation's water protection programs,
including over 20 specific actions to enhance underground
storage tanks, safe drinking water, and private well protection
programs. The Panel considered these necessary to prevent
future water contamination, but not sufficient in and of
themselves to ensure that the problem will be solved.
We recommended further that we agreed broadly that the use
of MTBE should be reduced substantially, with some members
supporting its complete phase-out, and that Congress should act
to provide clear Federal and State authority to regulate and/or
eliminate the use of MTBE and other gasoline additives that
might threaten drinking water supplies.
Third, recognizing that MTBE was a very important part of
the Nation's fuel supply, we recommended that Congress act to
remove the current Clean Air Act requirement that 2 percent of
RFG by weight consist of oxygen, to ensure that adequate fuel
supplies can be blended in a cost-effective and timely manner,
while reducing the use of MTBE.
And fourth, we recommended that EPA seek mechanisms to
ensure that there is no loss of the current air quality
benefits as the use of MTBE declines.
Now, although the Panel agreed broadly in its
recommendations, two members--while agreeing with most
recommendations--did have concerns over specific provisions,
and I feel it my duty as Chairman to share those with you here.
The MTBE industry representative on the Panel felt that the
water protection reforms that we proposed were sufficient to
protect water supplies, and was concerned that the Panel had
not adequately considered the air quality benefits of
oxygenates.
The ethanol industry representative was concerned that the
Panel's recommendation to lift the oxygen requirement did not
adequately reflect the benefits of using oxygenates.
Copies of their statements are attached to the executive
summary and in the final report.
In sum, the Panel found that we have a successful, cleaner-
burning gasoline program in place, but we need to take action
to ensure that the detections of MTBE in drinking water that we
have seen, and which fortunately in the great majority of cases
have not yet been a public health concern, do not continue to
grow.
We have provided to the committee the executive summary, as
well as the full report of the Panel, as now available on the
World Wide Web, and I thank you for this opportunity to
testify. I would be glad to answer any questions.
Senator Inhofe. Thank you, Mr. Greenbaum. We will have
rounds of questions.
You know, all of this started, I guess, when Senators Dole
and Daschle, in the 1990 amendments to the Clean Air Act, put
the requirement in for oxygenates. I think that's getting down
to the core of the problem. That's Dole and Daschle from the
beautiful corn States of Kansas and South Dakota.
What did the Panel find in relation to the air benefits
from MTBE? I think this is getting down to the crux of the
problem, because it's my understanding that your Panel called
for the repeal of the Federal oxygen content mandate. When you
talk about the phase-down in the use of MTBE, it was dependent
upon the repeal of the Federal mandate, is that correct? Could
you elaborate on that?
Mr. Greenbaum. Yes, I will.
First of all, we on the Panel understood that the RFG
program as enacted into law, including the oxygen mandate, has
been a tremendous air quality success. And as a result, it has
been one that has greatly aided a number of people in their air
pollution exposure across the country.
The benefits of the oxygenates themselves, both MTBE and
ethanol, in that have been substantial in getting that program
up and running. I think it is fair to say that at the time,
there were no other proposals on the table that would provide
fuels as clean that could provide similar air quality benefits.
What has occurred, and what the Panel saw, was that today
the refining industry has emerged with fuel formulations that
would contain no oxygenate at all, and that would meet or
exceed the current performance of RFG. I don't think that was
in place, necessarily, in 1990; I think that that's something
that we've seen emerge, and I think in the end it was a
challenge for the Panel. We didn't totally agree on the air
quality benefits of MTBE specifically, in part because although
they have played a role, it seems clear that there are other
formulations of fuel that are available that could provide the
same benefits as the ones with MTBE.
We did feel, particularly in the area of air toxics
reductions, that MTBE and the oxygenate presence--both MTBE and
ethanol--had contributed in some way to that, but the Panel
recommended that if you remove the oxygen mandate and reduce
the amount of MTBE, and at the same time made sure that the air
quality requirements stayed strong, that you could see the fuel
supply provide fuel that was cost-effective and provide the
same air quality benefits, but without the problems with high
levels of MTBE.
That was a long answer, Senator, I'm sorry.
Senator Inhofe. No, it's a good answer. I just want to be
sure that we're all clear, that if the MTBE is phased out, did
the Panel have any recommendation to replace that? Or was it
for a replacement of the 2 percent oxygenate mandate? In other
words, did they have the idea of phasing this out and then
replacing it with something else, or phasing it out and also
phasing out the 2 percent mandate?
Mr. Greenbaum. First of all, to clarify, the Panel as a
whole called for phasing down the use of MTBE, not phasing it
out, although there were members who thought we should phase it
out, but that was not the majority opinion of the Panel. In
other words, reduce its use substantially; that's what we
called for.
We did not pick one alternative that was ``the best''
alternative. We felt that that would depend on a complex
mixture of decisions, including decisions at each refinery,
decisions about the availability of fuel blending stocks, and
decisions about what else within the gasoline already that
neither the Panel, we thought, or the Federal Government should
necessarily dictate. We thought that one of the alternatives
that would come in to meet this would be increased use of
ethanol. We thought another one would be increased use of
components of existing gasoline, particularly alkylates, which
are in gasoline currently and would have to be increased in
production. And the Panel did not rule out the possibility of
continued lower-level use of MTBE, in part because we saw in
areas of the country where it had been used at lower levels, we
did not see the same level of contamination.
In order to provide the flexibility necessary for that
range of alternatives to be chosen in a cost-effective fashion
by the refining industry to meet the air quality needs, we felt
it was essential that the 2 percent mandate be lifted that in
some parts of the country it might still be 2 percent or even
more, where ethanol was available, and could even grow in its
use; in other parts of the country, other parts of crude oil
would be used. In some components of it, smaller levels of MTBE
might continue to be used.
Senator Inhofe. Did your Panel look into the idea that if
you are replacing MTBE, you could be replacing it with
something that is as toxic or more toxic than MTBE is--benzene?
Mr. Greenbaum. Well, we were concerned with that, and
called for immediate review of the health effects of all of the
alternatives that might mean an increase in supply, including
ethanol, including alkylates, and including aromatics like
benzene, which might increase in supply.
First of all, we felt that benzene is already capped in its
use in reformulated gasoline; and that second, if at the same
time you were tightening the air quality requirements to ensure
that we kept the same level of good performance that we've had
from existing RFG, that that would in itself keep the lid on
some of the levels of more toxic components of gasoline that
might increase, like benzene.
Senator Inhofe. Yes.
Senator Chafee.
Senator Chafee. Thank you, Mr. Chairman.
Let's see if I understand what you're recommending. As I
understand it, you are recommending that we give up the 2
percent oxygen by weight, is that correct?
Mr. Greenbaum. That's right.
Senator Chafee. And leave it up to each State as to how
they want to handle this situation, whether they want to have
some kind of an oxygen requirement, is that correct?
Mr. Greenbaum. Well, we actually called for each State's
and EPA's authority to be clarified as to how they could
regulate additives to gasoline that might cause a threat to
groundwater. And in essence that might mean that a State could
continue to require oxygen, per se, but more importantly the
question was, did they want to regulate the use of additives
that might affect groundwater, which was really the crux of our
concern.
Senator Chafee. Now, it seems to me that an important part
of all this is that we ought to get on with this upgrading of
the tanks, the underground storage tanks, and the surface
tanks, too. But then you mentioned somewhere in your testimony
that older outboards on recreational boats are contributing to
this, likewise.
Mr. Greenbaum. Yes. I actually have that in my formal
testimony; to keep within the 5 minutes, I didn't comment on
that.
There's no question that the tank systems--we have to
complete the upgrade that we already started back in 1988, but
really have to go much further than that with the tank system
than we have. First of all, to complete it, but second, for the
tanks, the standards for those tanks were put in place in 1988,
prior to any knowledge that there would be high levels of use
of MTBE in the fuel. The oxygen requirement didn't pass until
1990.
MTBE, as we have heard and as our Panel heard in detail
from hydrogeologists, behaves substantially differently in
groundwater than the other components of gasoline. Therefore,
the consequences of a leak from an underground tank are
greater, and the standards almost certainly would have been
looked at more tightly in 1988 if we knew MTBE was in place,
and probably need to be revisited.
So even within the tank program, there are things that need
to be done to really tighten those standards, which cannot be
done overnight. They need to be done.
Second, there are tanks that have been upgraded that are
leaking. That's not because they weren't properly designed,
necessarily, although in some cases they weren't well designed;
they may have been misinstalled, they may have been improperly
used. But we have had evidence of cases of that in Maine,
Delaware, and California already. Not every tank, but some of
the tanks will continue to leak.
Third, and I think this gets more focused to the point of
your question, Senator Chafee, once you put this material in
gasoline, there are a number of ways it can get into the
groundwater and into the surface water. It can happen if leaks
occur, if a tanker truck turns over, which does happen on
highways; I saw that when I was Commissioner in Massachusetts.
If a car accident occurs or a truck accident occurs, it can
happen in a number of situations. It also comes out of
motorboats, and we saw evidence in a number of surface waters
of seasonal peaks in MTBE levels in waters because of older
boat engines.
So it gets into the water in a number of ways. The single
largest source of that has been underground tanks, but we
shouldn't neglect the fact that there are other possible ways.
Senator Chafee. What is your answer to this statement? I
have a memo here, and it says as follows: ``The oxygen
requirement is a redundant mandate that costs consumers over $1
billion a year.''
Mr. Greenbaum. Well, I'm not sure of the source of that. I
can't go back to a specific economic analysis that would tell
me that.
I think, as I said earlier, it is not clear to me, looking
backwards with 20-20 hindsight, that in 1990 there was another
way to get to the kind of clean fuel we have, other than by the
way that law was put in place. I think where we are today,
technology has changed and the options have changed, and there
are more options available to us for producing very clean
gasoline than were available then. Whether there is an extra
cost that consumers have incurred over time or not, I can't
guarantee. I do know that most of the estimates of the
increased cost of RFG, which were not just because of the
oxygenates, ended up being in the $0.01 to $0.02 per gallon
range, once that was actually implemented.
So I don't think we were talking about large increases in
cost.
Senator Chafee. Thank you, Mr. Chairman.
Senator Inhofe. Let me ask about the leakage in these
newly-installed underground tanks, like what percentage of them
do have leaks, and what could be done to stop these leaks. Was
it from installation? Was any kind of a study done? Because if
it gets down to a point where we're going to have to be looking
at regulation for the installation of these tanks, it will be
important to know that.
Mr. Greenbaum. There were only the beginnings of such
studies, since many of the tanks didn't get upgraded until the
latter part of the last decade, with a deadline of 1998. We did
have one review done by the California Water Resources Board of
a series of tanks in trying to identify what percentage were
leaking and what the nature of the problems was, and they had
the same interest, to try to understand whether they could
tighten the rules, whether they could make it better. And we
can certainly refer you to that.
There was also this survey by the Santa Clara Water
District that Senator boxer mentioned. Because we've only had 3
to 5 years, really, of experience with most of these tanks
being upgraded, we probably don't have the full range of
experience necessary. One of the things the Panel called for
was an immediate look to try to build that data base.
Senator Inhofe. Would you submit that for the record, the
reports of the analysis in California?
Mr. Greenbaum. We certainly will do that.
Senator Inhofe. Senator Boxer.
Senator Boxer. Thank you, Mr. Chairman. Thank you for
pressing the issue of the tanks, because it is really stunning
to realize that in Santa Clara they put in all these new tanks,
and they still have the leakage. It's very troubling.
I want to thank you very much for all the work you did and
the committee did, the Blue Ribbon Panel. I think the fact that
you had a member from the MTBE industry on there and a member
from the ethanol industry on there says that there was quite a
tug of war going on, and I know that makes it very, very
difficult to come to some firm conclusion.
Again, I want to read the conclusion that you came to,
because I think it is very clear:
The Panel agreed broadly that in order to minimize current
and future threats to drinking water, the use of MTBE should be
reduced substantially. Several members believed that the use of
MTBE should be phased out completely.
That's pretty clear guidance for this committee, I hope.
I wanted to probe a little bit about this recommendation.
Without identifying who, because that's not important,
approximately how many felt it ought to be phased out? And I'm
not counting the two--I don't think it's fair to count the two
who had a special economic interest, because obviously the
ethanol person would say, ``phase it out,'' and the MTBE person
would say, ``don't.''
So without that, how many of that 11 left would you say
said, ``phase it out''?
Mr. Greenbaum. Well, first of all, I think it's fine not to
count those two. Actually, as I said in my comments, the
representative of the MTBE industry did not think that we
needed to go to the next stage of reductions, that the
upgrading of the tanks and the other recommendations were
sufficient.
To my recollection, there were four or five members, all
from California--no, not all from California, four or five
members of the Panel who felt they were most comfortable with a
phase-out. The remainder of the Panel felt that a substantial
reduction was adequate.
Senator Boxer. OK.
Mr. Greenbaum. But the whole panel could not agree on--
Senator Boxer. I understand.
But I think that's important, Mr. Chairman, to recognize
that, if you take away the ethanol and the MTBE people, because
frankly, I think they have a particular view on the point. I
think that's pretty interesting, because that is a large number
who would say, ``phase it out.''
Now, out of those who said there ought to be a substantial
reduction, what is a ``substantial'' reduction? What does that
mean? Does that mean reduce the amount by 25 percent, 50
percent, 60 percent, 70 percent? What does that mean? It's kind
of a fuzzy word.
Mr. Greenbaum. Well, we actually did--in our
recommendations we did not set a specific number because we
felt, I think, more broadly that the setting of specific
numbers in this process has been part of the problem rather
than part of the solution. But we did give an example of such a
substantial reduction, which would be moving back to the
historical levels in which MTBE was used as a lead and other
additive replacement prior to the introduction of RFG. It was
used in those situations, on average across the whole fuel
supply, at about 2 percent of the fuel supply, although in some
cases it was higher and in some cases it wasn't used at all.
But on average--
Senator Boxer. So the average was about 2 percent. And what
is it now?
Mr. Greenbaum. Well, in the RFG areas it is required to be
11 percent--I'm speaking, by the way, by volume here, 2 percent
by volume versus 11 percent by volume.
Senator Boxer. OK. Well, that's very important guidance,
Mr. Chairman. That is a substantial reduction.
Mr. Greenbaum. That would be a substantial reduction. We
were not prepared, because of the nature of the issue in
different parts of the country, to say that that's what should
be happening in every single location, but it was one example
that we could give.
Senator Boxer. OK.
Now, here's a point I want to get at. If you eliminate the
2 percent requirement for oxygenates, but you don't ban MTBE,
what assurance is there that MTBE won't be used? Because I gave
you the example of San Francisco, which was completely shocking
to people, where we did not need, because we were meeting the
clean air requirement, to have MTBE. The oil companies, after
learning that Gray Davis wanted to phase this out and the
legislature wanted to phase it out and all the rest, decided it
was the cheapest way to expand their gasoline supplies. It was
stunning to people that they did that.
So my question is, if you don't ban MTBE but you list the
oxygenate requirement, there's no guarantee that this
substantial reduction is going to take place, wouldn't you
agree, given the facts of what happened in San Francisco?
Mr. Greenbaum. Well, I don't want to suggest that I know
all the details of the situation in San Francisco, although I
will say that the Panel happened to be having its meeting in
California on the day that two things occurred simultaneously,
No. 1, that Governor Davis made his announcement, and No. 2,
that there was a major fire, the second in a short period of
time, in one of the refineries in California.
While I would agree that it was unusual that the use of
MTBE went up within 2 months of Governor Davis calling for its
reduction, I would also suggest, based on what we as the Panel
understood, that the situation in California was unique in the
sense that the supply of gasoline from crude oil was
substantially reduced because of the incidents in these two
refineries.
Having said that, I think the general evidence that the
Panel saw and the analyses that the Department of Energy has
done, which are in the record and are summarized in our final
report and can be provided, suggested that if you solely
removed the mandate, that economic forces probably would reduce
the amount of MTBE but continue to use it at fairly high
levels, because it is a relatively cost-effective blending
component for gasoline, very high octane and very clean.
The factor that the Panel knew would be a factor in
industry decisionmaking, but which we couldn't quantify, is the
growing concerns that a variety of people in industry have
raised about the future liability for cleanup costs for
industry of using MTBE, and that in and of itself is often a
driver to get industry to reduce its use. And I think some
companies are already trying to figure out, without the 2
percent mandate, how to reduce the use.
Having said that, the Panel did not feel that just lifting
the mandate was sufficient, and that's why we called for
Congress to clarify both Federal and State authority to
regulate and/or eliminate the use of MTBE and similar
additives. In other words, we were not calling for a ban, but
we were calling for clarity on what the authority would be to
ensure that you could get a reduction over time if the market
didn't provide that.
Senator Boxer. I appreciate that.
Two more quick questions----
Senator Inhofe. I'm really sorry, I'm going to have to cut
you off because you've gone over----
Senator Boxer. Other people went over. You went over it,
and so did Senator Chafee.
Senator Inhofe. No, I'm really trying to be fair with
everyone.
Senator Boxer. Well, then, can I ask this when you finish
everybody else? I have two more questions.
Senator Inhofe. How about 1 more minute, all right?
Senator Boxer. Fair enough.
Here's the point. You're right about litigation. In Santa
Monica--and this goes to the point raised by my good friend and
colleague, Senator Bennett--in Santa Monica, they shut down 71
percent of the water supply. Do you know where they're getting
the water from to serve your family or friends? From the
Colorado River.
Now, we are already over our allocation. This is a real
serious problem for us. That is not a solution. And by the way,
they are in litigation, trying to get the oil companies to pay
for this importation of water.
We all love local government here. I served in local
government. This is putting the burden on them for some mistake
we made here.
So the bottom line is, the cost of this cleanup is enormous
and it leads to litigation, and therefore we should ban MTBE.
And the last question I have deals with the fact that
this--I think it's good to focus on the leaking tanks; the
chairman is right on that point. However, that's not the only
way this stuff gets in the water. We already talked about the
use of MTBE and the boats and it goes in the lakes. When we
transfer the fuel at transfer stations, it leaks. There was a
car accident in Maine that contaminated 24 wells.
So it isn't just a matter of the underground tanks. We have
other ways for MTBE to get in, is that correct, into the water
supply?
Mr. Greenbaum. I think I said that in response to Senator
Chafee's question. There clearly are other ways. Our best
estimate was that the great majority of the problems have been
tanks, but that there are a number of other ways in which it
can get in, the major ones being spills, accidents, and boats.
Senator Boxer. All right.
Thank you very much, Mr. Chairman.
Senator Inhofe. Thank you.
Before going to Senator Bennett, did you have an opening
statement to make, Senator Voinovich?
OPENING STATEMENT OF HON. GEORGE V. VOINOVICH,
U.S. SENATOR FROM THE STATE OF OHIO
Senator Voinovich. I will just submit it for the record.
Senator Inhofe. All right.
[The prepared statement of Senator Voinovich follows:]
Statement of Hon. George V. Voinovich, U.S. Senator from the State of
Ohio
Mr. Chairman, I am pleased you are conducting this hearing on the
EPA's Blue Ribbon Panel findings on the use of oxygenates in gasoline.
Throughout my 33 years of public service, I have been committed to
preserving our environment and the health and well-being of our
citizens. While in the Ohio House of Representatives, I was responsible
for creating the Environment and Natural Resources Committee and was
honored to serve as vice chair of that committee.
I am proud that the State of Ohio realized significant improvements
in air quality in recent years. When I first entered office as Governor
in 1991, most of Ohio's urban areas were not attaining the 1-hour ozone
standard. By the time I left office in 1998, all cities had attained
the standards, except one. However, earlier this year EPA proposed a
rule to revoke the 1-hour standard for the last nonattainment area.
Overall, the ozone level in Ohio has gone down by 25 percent. In
many urban areas, it has gone down by more than 50 percent in the past
20 years. My point is that Ohio is doing its part to provide cleaner
air and a healthier environment for its citizens. For instance, Ohio's
public utilities spent $3.7 billion on air pollution controls through
1995, more than the combined expenditures of all the Northeast states.
As I said, all of our urban areas but one have met the one-hour
ozone standard. And one of the things we did in Ohio to achieve this
was to implement an emission testing program. This was not an easy task
and I took a lot of heat for it. As a matter of fact, I had to veto a
bill passed by the state legislature which would have removed the E-
Check program because it was so unpopular and the legislature did not
want to take the heat for it. But my Administration thought this
program would best help us attain the National Ambient Air Quality
Standards.
Ohio could have chosen to opt into the reformulated gasoline
program as one option to reach the NAAQS standards, but we were not
mandated to use it. However, other areas of the country are required to
participate in the reformulated gasoline program to help them comply
with air standards.
I think most state and local governments are willing to take the
necessary steps to make the air we breathe cleaner. However, we need to
make sure that the right hand knows what the left hand is doing. We
want to make sure that as we are trying to reduce pollution in one
source, such as air, we aren't affecting other sources, such as
drinking or ground water. We need to make sure there is proper analysis
and sound science behind the decisions we make whether they are
regulatory standards or legislative requirements.
Quite frankly, I am concerned we are here today. I am concerned
that in 1990 Congress acted to put the 2 percent mandate in the
reformulated gasoline program without showing the necessary scientific
reason for doing so. I am concerned that there was no analysis of the
costs, benefits or risks behind this provision before it was enacted
into law.
However, I am not convinced that EPA's Blue Ribbon Panel provides
us with the adequate cost, benefit or risk analysis behind their
recommendations either. We need to know more information before we
start off on a new course of action. And we need to know whether the
same money should be spent in this area or on other priority
environmental problems.
I'm not here to say whether these recommendations are wrong or
right, but that we need more information to determine whether this is
the right path to follow.
I think that something should be done. However, I propose that
states should have the flexibility to determine how to handle this
problem in their own states.
Today we have an example of where a mandate was made without
adequately studying the potential risks that it could impose or the
science behind it. However, before we jump forward with extensive
suggestions on how to fix the problem, there needs to be careful
analysis of the costs, benefits and risks that would be incurred by
these proposals.
Thank you, Mr. Chairman. I look forward to today's testimony.
Senator Inhofe. Senator Bennett.
Senator Bennett. Thank you, Mr. Chairman.
Mr. Greenbaum, I come to your final statement. You say,
``In sum, the Panel found that we have a successful, cleaner-
burning gasoline program in place, but need to take action to
ensure that the detections of MTBE in drinking water that we
have seen, and which fortunately in the great majority of cases
have not been a public health concern, do not continue to
grow.''
Let's parse that statement. Let's go through that sentence
very carefully, because that is your summary of everything else
you say.
We must ``take action'' that ``the detections of MTBE in
drinking water that we have seen . . . do not continue to
grow.'' I assume from that you're saying that MTBE, however
noxious it may be, is not toxic? Is that a correct statement?
If not, correct me. But that's what I read into what you're
saying: this is unpleasant; it can cause people to not want to
drink the water; it can cause great difficulty, but it's not
killing anybody--at least, not yet.
Mr. Greenbaum. The ``not yet'' is important, I think.
Senator Bennett. OK.
Mr. Greenbaum. I think that at the levels at which it has
been seen in most water supplies, everyone would agree that it
is not toxic. My institution, the Health Effects Institute,
actually conducted a comprehensive review of the science of
MTBE, asked for by the White House and Centers for Disease
Control in 1996, and I think it is fair to say that while there
are questions about the toxicity of MTBE, it does not rise to
the same level of toxicity as things like benzene, which are
already in gasoline.
Having said that, there are levels at which everybody would
agree it would not be safe. The levels that were reached in
Santa Monica were 600 parts per billion. The levels at one set
of private wells in Delaware were several hundred parts per
million. So we have seen only the tip of the iceberg in terms
of health or toxicity effect concerns. That's fortunate, and
that's good. I think the Panel felt that we could not be
assured that we wouldn't see continuing problems with that, and
growth of that number of wells, and that's why we felt that we
needed to take action now.
Senator Bennett. You do not call for a ban. You call for a
reduction, which would further support the notion that only in
high concentrations is it toxic, and that a certain level is
tolerable. Am I correctly summarizing your science here?
Mr. Greenbaum. I think that's correct. The health basis for
banning a chemical normally requires considerably more clear-
cut evidence of the health concerns relating to that chemical
than we have for MTBE. And that was a conscious discussion of
the Panel.
Just to give you one example of that, benzene, which is in
gasoline, is identified by both national and international
cancer agencies as a known human carcinogen. MTBE is neither a
known human carcinogen, or even a probable human carcinogen. At
this stage it is in the ``possible'' category. In other words,
there are some animal tests that show that it causes cancer,
but there are questions about those tests.
Senator Bennett. OK. So I am interested that you did not
call for a total ban on these reasons.
Now, let's go to the other side of your examination. You
found that we do have cleaner air because of MTBE, and I would
ask, if MTBE were banned, what alternatives would you recommend
in order to achieve the level of clean air? Are we talking
about more ethanol, so that the corn farmers can rejoice? Or do
we have something else that we can turn to?
Mr. Greenbaum. Well, we actually found that clearly, RFG as
a whole has had substantial air quality benefits. MTBE has been
one of the components of that, but on the Panel we could not
ascribe with agreement any particular amount of benefit to MTBE
providing that benefit versus ethanol providing that benefit,
and that's based on the availability of data. The data is not
clear enough and clean enough to be able to do that.
But there's no question that the fuel that has been out
there with the oxygen has provided substantial air quality
benefits. The challenge for the Panel was to try to answer your
question: so if we take this stuff out, what's going to happen?
We felt there were several scenarios that could occur. One of
them would be increased use of ethanol. One of them would be
increased use of the alkylate component refined from crude oil,
which has very high octane and is generally clean. One of the
scenarios could be increased use of aromatics, like benzene,
which are things that we have been trying to reduce the use of
in gasoline.
The Panel did not feel that it could choose the best of
those alternatives, because each has strengths and weaknesses,
but rather felt that what we needed to do was make sure that
the requirements for RFG are stringent enough that we are
assured that as the fuel goes forward, no matter what a refiner
decides to do--whether they decide to use ethanol, whether they
decide to use alkylates, or whether they decide to continue to
use lower amounts of MTBE plus some of these other things--that
you continue to have the air quality benefits. And the Panel
felt that that was possible, given what we had seen in evidence
before us.
Senator Bennett. Thank you, Mr. Chairman.
Senator Inhofe. Thank you, Senator Bennett.
Senator Voinovich.
Senator Voinovich. Following up on Senator Bennett's line
of questioning, if you eliminated the 2 percent requirement and
banned MTBE, and you have reformulated gasoline, is there any
guarantee that in order to achieve the same benefits to the
air, that you wouldn't substitute something else that would be
just as harmful?
Mr. Greenbaum. Well, I think that's a very key question,
Senator, and I think--because one of the possibilities would be
that you would see some degree of increase from refiners in
some of the refineries of the use of aromatics in the fuel,
particularly things like benzene, which is very high octane.
That's the kind of thing we've been trying to reduce; in fact,
the refiners have reduced benzene below those required by the
Clean Air Act and by EPA regulations.
And I think that goes to the fourth key recommendation
which the Panel made, which was that you could only do these
things if you, at the same time, ensured that the air quality
requirements that were originally put out in the act were
tightened sufficiently to require continued benefits equal to
those we've actually had in the fuel, and that's what our
fourth recommendation was. If you don't do that, then the
concern that you raised is very real. I think there is a chance
that you wouldn't see a return to pre-RFG days because there is
a limit on how much benzene can be in the fuel, but you would
see an increase in some of the components that contribute to
air toxics and other emissions.
Senator Voinovich. So the fact is, to maintain the same
improvement in the air quality that you're getting from MTBE,
you are really not sure if you eliminated it what else you
would have to do, and you're not sure whether that might have
more harmful impact on the water than MTBE?
Mr. Greenbaum. Well, the issue of water--actually, we did
look at the alternatives and we looked at the question of what
those alternatives might have, not only for air quality
impacts, but also water impacts. It would have been crazy for
us not to look at it, given the experience we have had with
MTBE.
I think there are two things there. First, most of the
other components of gasoline, including the aromatics and the
alkylates, actually, when they get into groundwater, they are
not as soluble in groundwater as either MTBE or ethanol, and
biodegrade more readily than MTBE. So our impression was that
you would not be worsening the situation if you used more of
crude oil components for the gasoline as a replacement for
MTBE. The water situation would not be any worse than it has
been historically, with leaks of gasoline.
With ethanol, ethanol is highly soluble in water, more so
than any of the other compounds we considered, but it is also
highly biodegradable, meaning that the bacteria in soil prefer
to drink ethanol than drink benzene; I guess that's probably
one way of putting it.
[Laughter.]
Mr. Greenbaum. There are laboratory studies that confirm
that. There are no field studies that say, ``Well, what does
that mean when you get out in the field?'' We saw estimates,
projections that were made, that suggested that what would
happen with large volumes of ethanol in the fuel, is that you
would see very rapid biodegradation of the ethanol. The ethanol
would never move very far away from wherever the spill or the
leak was. But you might see other components of the gasoline,
like benzene, move further than they would otherwise move,
because they wouldn't be biodegraded right away, and they might
go as far as 30 percent further, but that is not tested in the
field at this stage. That was something that we put in our
report, and we called for an immediate look at that question
before you went to a very broad use of ethanol.
Now, to be clear, ethanol can grow in its use, but it would
also need infrastructure investment. The ethanol industry
appeared before us and it was clear that they were prepared to
make that, but overnight you would not see more ethanol--you
know, dramatic increases in ethanol. You would see some
increases.
Senator Voinovich. OK.
The last question I have is this. I read your summary, and
it looks like you are making all kinds of recommendations to
the Federal level or the State level. It sounds to me like
there was no mention in it about the cost to do everything that
was recommended. The dissenting opinion at the end said that if
this happened and they eliminated it, that it would increase
the cost of gasoline by $1 billion to $3 billion. The money
side of this wasn't involved.
Wouldn't the best solution be to give EPA the flexibility
to work with State people where they did have a problem to try
to come up with something that would best respond to the needs
of the particular community, rather than having some new
Federal administration getting into all of this, and so on? In
other words, in your report you also say that if we did a
better job, for example, dealing with storage tanks, that the
primary source of this is leaking storage tanks. Now, in my
State we have a very aggressive program that we started to get
these out of the ground and replace them with things that are
getting the job done.
The point is that this problem is localized, isn't it, in
certain places in the country? And rather than come up with
some gigantic new program, why don't we give the EPA
flexibility to deal with the problem in the areas that have
problems, and let them look at the alternatives, let the States
come back with recommendations, and let them approve it or
disapprove it, having to weigh the issue of clean air versus
the issue of water? And leave it at that.
Mr. Greenbaum. Well, there are a number of ways that one
can address the sets of issues that we recommended. I think
that embodied at the core of our recommendations was the
recommendation that Congress act to clarify the authority of
both EPA and the States to deal with these problems, because we
do think there are going to be needs for some State flexibility
and some ability to address this on a localized basis, in some
cases going further than in others. And if anything, the Panel
was suggesting moving away from a broad-based Federal
requirement, the 2 percent requirement, because it--in and of
itself--is an imposition in some ways on the entire system.
But having said that, I think the biggest concern counter
to that that requires some careful interaction and thinking
between the Federal Government and the States is the issue of
not fractionating our fuel supply in so many different pieces
that we end up with what some have called ``boutique fuels'' in
different States and in different situations, where you would
have--as you would know, Senator, if your constituents in Ohio
have to pay one thing for fuel because you have one type of
fuel, and they went across the border into another State and
got much cheaper fuel, it would get very complicated very fast.
And one of our strengths is having a national fuel supply.
So when we go to dealing with this, we have to be thinking
about how we maintain that consistency while still giving
States the authority and the flexibility to deal with their
localized problems, and also while ensuring that the States
have taken the actions to clean up their tanks as they should.
Senator Inhofe. Thank you, Mr. Greenbaum. We appreciate
your being here and what you have contributed.
Senator Inhofe. We will now ask panel No. 2 to come
forward. It will be the Honorable Jake Garn, our former
colleague, who is vice chairman of Huntsman Corporation; Mr.
Michael Kenny, executive officer, California Air Resources
Board; and Mr. Bob Campbell, CEO of Sunoco, Inc.
Again, we will ask you to try to confine your opening
remarks to 5 minutes, and then we will try to exercise the same
discipline from this end of the table.
Senator Garn.
STATEMENT OF HON. JAKE GARN, VICE CHAIRMAN, HUNTSMAN
CORPORATION, SALT LAKE CITY, UT
Mr. Garn. Thank you, Mr. Chairman. I am pleased that you
have called these hearings and are willing to expand from the
BRP and take additional testimony.
I am vice chairman of the Huntsman Corporation, which is
the largest privately-owned chemical company in the United
States, and we are a major producer of MTBE and a member of the
Oxygenated Fuels Association. Huntsman's decision to get into
the MTBE business was on the basis of clean air.
Huntsman is a unique company. One of the reasons we can do
the things we do is because we are privately-held. John
Huntsman has given $150 million in cash to the University of
Utah to create the Huntsman Cancer Institute. He is committed
to solving the problem of cancer, and knowing John, I have no
doubts he will probably over a number of years be able to
accomplish that.
I bring that out because in all of our plants in the United
States and around the world, I don't think you would find a
company that is more socially responsible, has put their money
where their mouth is in health and safety of their employees,
the surrounding communities, and so on, and it really is a
remarkable record. So I wanted you to understand the context in
which I am speaking today.
We agree with much of what the Panel has found. For
example, we agree that more research and monitoring is
necessary concerning the health effects of not only MTBE, but
also other constituents of gasoline. We agree that timely
actions need to be taken to significantly enhance Federal and
State gasoline storage programs. We also support the BRP
finding that Congress must act to expand resources available to
ensure safe drinking water supplies.
However, we have strong concerns about several of the BRP's
conclusions. Most importantly, we disagree strongly that there
is sufficient justification to recommend a substantial
reduction in the use of MTBE. As described in greater detail in
our written submission, we believe the BRP left many important
questions unanswered. Unfortunately, the BRP is gone, and the
responsibility to answer these questions falls to Congress, and
to this subcommittee in particular. Until those questions are
answered, we believe it is inappropriate to move forward with
any effort to amend the Clean Air Act to reconfigure the
reformulated gasoline program.
We appreciate this opportunity to contribute our thoughts
on how Congress should endeavor to answer these remaining
important questions.
Today I want to focus on a few of the many issues raised by
the BRP in some greater detail.
We believe that the BRP's conclusion to phase down the use
of MTBE is not supported by their own deliberative process. For
example, the BRP made no finding with respect to the health
effects due to MTBE exposure, and this result is not
surprising, given that extensive research conducted over a
number of years has indicated that MTBE exposure levels
necessary to cause injury in animals are thousands and
thousands of times greater than those humans could conceivably
be exposed to. Therefore, an array of organizations has
concluded that MTBE is not a human carcinogen. These include
the Department of Health and Human Services, the World Health
Organization's International Agency for Research on Cancer, the
National Academy of Sciences, and California's Office of
Environmental Health Hazard Assessment.
Consistent with our own beliefs about cancer research,
Huntsman supports the notion that much more research should be
done, just as BRP recommended. However, with a clear consensus
to date regarding the lack of adverse health consequences of
MTBE exposure, and with substantial health benefits relating to
clean air hanging in the balance, we cannot support BRP's
conclusion regarding phase-down of the additive.
While we are on the subject of health benefits, Huntsman
also believes that the BRP underestimated the air quality
improvements attributable to the use of oxygenates like MTBE.
EPA has written that oxygenates substantially reduce toxics and
dilute or displace other fuel components, like sulfur, which in
turn reduce emissions of the smog precursors. EPA has found
that oxygenates like MTBE improve the performance of on-board
automobile air pollution control devices. In short, the real
world benefits of MTBE usage have exceeded even the most
optimistic predicted results. By failing to give credit where
credit is due for real world performance, BRP underestimated
the environmental benefits of MTBE.
We also believe that BRP may have underestimated the
effectiveness of enhanced underground storage protection as an
appropriate response. Even Senator Feinstein observed during
Floor consideration of an appropriations matter some 2 weeks
ago, ``The major way MTBE gets into groundwater is from
defective underground tanks storing petroleum products.'' She
has offered fixes to the UST program as a way to stop the
contamination of drinking water by the gasoline additive MTBE.
Lastly, we are concerned that BRP simply paid too little
attention to the potential consequences of shifting to
alternative fuel additives to MTBE. As we all know, the primary
alternative to MTBE is ethanol. We have several concerns about
the viability of ethanol production constraints, and trouble
with pipeline deliveries make ethanol a logical and logistical
nightmare to use as a basis for the fuel supply of the United
States.
Mr. Chairman, I notice the red light has come on, and I
would simply refer to my detailed statement which you have
already offered to put in the record. When I was chairman of
the Senate Banking Committee I was very strict about time, and
so I will be happy to respond to questions after the other
witnesses, but when that red light comes on, I stop.
Senator Inhofe. Good for you, Senator.
[Laughter.]
Senator Inhofe. Thank you.
Mr. Kenny.
STATEMENT OF MICHAEL KENNY, EXECUTIVE OFFICER, CALIFORNIA AIR
RESOURCES BOARD, SACRAMENTO, CA
Mr. Kenny. Thank you, Chairman Inhofe and members of the
subcommittee. I am happy to be here today to present the
California perspective on behalf of Governor Gray Davis, the
California Environmental Protection Agency, and the California
Air Resources Board.
As the Blue Ribbon Panel report noted, California has its
own reformulated gasoline program, which was established to
deal with California's unique air quality problems.
California's RFG program differs from the Federal program in a
number of ways, and I think it's important to look at those.
The California program limits the sulfur and aromatic
content of gasoline, while the Federal program does not.
California's program also utilizes a predictive model that
enables refiners to market innovative fuel formulations that
vary from California's gasoline specifications, as long as
refiners can demonstrate through the model that the
formulations provide the required air quality benefits.
So far, the California RFG program has been immensely
successful. Peak ozone levels in the State of California have
been reduced by about 10 percent, and airborne benzene, a
highly potent toxic, has been reduced by about 50 percent.
Unfortunately, the continuing controversy over MTBE has
overshadowed the success of this program. Two California
cities, Santa Monica and South Lake Tahoe, have seen their
domestic water supplies decimated by MTBE contamination, and
MTBE has been found in groundwater at several thousand leaking
underground tank sites in California.
The Blue Ribbon Panel report documents that MTBE
contamination is truly a national problem.
California took its own proactive steps last March.
Governor Gray Davis declared that MTBE is an environmental
risk, and he ordered it to be eliminated from California
gasoline by the end of 2002. Perhaps the single most crucial
factor affecting California's ability to eliminate MTBE use is
the Federal 2 percent oxygenate requirement. The Blue Ribbon
Panel recommendation on this was to eliminate that requirement.
It is absolutely critical for California that that 2 percent
requirement be eliminated.
California does not believe there is a technical or
scientific basis for requiring the addition of oxygen to
gasoline. It is possible to make California RFG without oxygen,
and it is much more cost-
effective to let each refiner decide for itself whether to use
those oxygenates.
About 70 percent of the California gasoline market is
subject to the Federal 2 percent oxygen rule, and in the other
30 percent of the market, three refiners have produced and sold
non-oxygenated gasolines that provide all of the air quality
benefits required by California reformulated gasoline.
California has shown that it can deliver the full benefits
of its world-leading RFG program without an oxygen requirement.
Once MTBE is eliminated in California, the only feasible
oxygenate will be ethanol. If the 2 percent oxygen rule remains
in effect, ethanol will be effectively mandated for 70 percent
of California gasoline. California, in just 3 years, would need
about half the amount of ethanol that is currently produced in
the midwestern States.
The Blue Ribbon Panel report acknowledges the large
investment in infrastructure that would be needed to meet this
large demand. The California Energy Commission estimated that
the elimination of MTBE could add as much as $0.06 to $0.07 per
gallon to gasoline costs if the oxygen requirement remains in
effect. This would cost California motorists about $840 million
a year, without producing any additional air quality benefit.
In contrast, elimination of the 2 percent requirement would
allow gasoline costs to remain stable, and possibly decline.
Some have portrayed this as opposition to the use of
ethanol. It's not. Even if the Federal oxygenate requirement is
eliminated, we know that ethanol usage in California will
increase exponentially; however, California should not trade
its dependence on MTBE for a similar dependence on ethanol.
Instead, we should strive for a diverse and stable RFG
marketplace featuring a range of ethanol-based and
nonoxygenated formulations. Such fuels will continue to achieve
all the air quality benefits, but at less cost to the consumer.
I urge the committee to support the Blue Ribbon Panel's
recommendation to eliminate the 2 percent requirement, and I
especially urge you to support legislation by Senator Feinstein
and by Representative Bilbray that would provide California
with an early exemption from the requirement.
Action this year is crucial. Refiners need about 3 years to
plan and complete the plant modifications that are needed to
make non-MTBE gasoline by the end of 2002. To meet this
challenging timeline, refiners need to know now whether they
will have to continue to use 2 percent oxygen or have the
flexibility to produce non-oxygenated formulations.
In closing, I would like to emphasize that California, as
an arid State, is more dependent that most other States on our
groundwater resources. Consequently, we crucially need the
flexibility to produce RFG without oxygenates. Equally
important, California RFG can be produced that maintains, and
even improves upon, current air quality benefits, and we can do
so at less cost if oxygenates are not required.
Thank you for agreeing to hear my testimony, and I would be
happy to answer any questions.
Senator Inhofe. Thank you, Mr. Kenny.
Mr. Campbell.
STATEMENT OF ROBERT H. CAMPBELL, CHAIRMAN AND CHIEF EXECUTIVE
OFFICER, SUNOCO, INC.
Mr. Campbell. Good morning, Mr. Chairman and members of the
committee. My name is Bob Campbell, and I am chairman and CEO
of Sunoco, Inc. My company is one of the largest refiners and
marketers of gasoline on the east coast of the United States.
In this region we produce and distribute more of the clean-
burning RFG required by the Clean Air Act than by any other
company, so consequently we have learned firsthand about the
benefits and the burdens of the existing program.
We are also a manufacturer and consumer of MTBE, and we
have been using it since 1980 for its high-octane qualities.
After the Clean Air Act Amendments of 1990 were passed we
constructed a world-class MTBE plant in Texas; consequently, we
know about all there is to know about the use of that additive
in gasoline.
In addition, we are also a major supplier of conventional
gasoline in mid-America, and here we don't use MTBE, but we are
a major buyer and blender of ethanol in gasoline. So we have
extensive firsthand knowledge of both the benefits and
limitations of ethanol in motor fuel.
Dr. Greenbaum has given an excellent summary of the
deliberations and recommendations of the Panel, and those
recommendations I wholeheartedly endorse. As you know, of
course, we are now planning on implementation of those
recommendations. Some of them require legislative action.
Public concern is, of course, about the taste and smell of
drinking water containing small amounts of MTBE.
Putting aside the complex question of MTBE as a health
hazard, it should clearly not be getting into drinking water.
But regardless of how much money is spent on tank replacement
and inventory control, gasoline handled by 190 million drivers
will inevitably be spilled, and we now know how persistent a
contaminant MTBE can be in water.
California, as it so often has done, has led the way in
defining a process for eliminating the problem. Critical to
that, of course, is relief from the existing 2 percent oxygen
mandate.
But one needs to remember that MTBE is principally used on
both coasts, both the east and west coast of the United States.
In fact, more MTBE is used in the 11 east coast States
comprising the ozone transport region than in California--
130,000 barrels a day versus 100,000 barrels. And I can assure
you that people in Boston and Philadelphia are just as adamant
about the quality of their drinking water as the people are in
Sacramento and Santa Monica.
Consequently, my plea to you today is to help us solve the
equally serious problem of MTBE in the Northeast, and I believe
that to accomplish that we need a regional solution. If the
proposed legislation deals only with California, I can assure
you that several of the Northeastern States are poised to enact
their own local solutions. The result will be a patchwork quilt
of local initiatives and regulations, and that will be a
nightmare for companies attempting to reliably supply low-cost,
high-quality gasoline to consumers in the 11-State region.
The bottom line is that we can solve the problem in the
Northeast in a manner similar to California only if we are also
given relief from the 2 percent oxygen mandate. If you will do
that, then we will be able to continue to supply RFG to those
areas requiring it in an economic manner, in reliable
quantities, with the same air quality benefits; and that
reformulated gasoline will have substantially less amounts of
MTBE.
I will tell you quite honestly that even with all our
company's experience in blending ethanol in gasoline in mid-
America, I don't know how to accomplish, in a real world
practical manner, the same result in a northeast RFG system.
Ethanol in RFG is successfully blended in the Chicago area
because it's a relatively small proportion of the supply from
the manufacturers in that region. In my opinion, if the 2
percent mandate remains and we are forced to directly
substitute ethanol for MTBE in the large RFG volume areas in
the northeast, we're going to have a disastrous scenario for
both the supplier and the consumer. Obviously, there are two
very practical problems with ethanol as a blending component on
the east and west coast. No. 1, of course, is the need for a
reliable, adequate supply and the transportation issues between
where it is currently manufactured today, and where it would be
primarily used. Obviously, it has an affinity for water, and it
can't be transported in common carriers, so you would have to
put it in rail cars and trucks for both coasts.
Let me tell you exactly what I told the Blue Ribbon Panel
this spring. Given enough time and money, an enterprising
ethanol industry can expand production and create new logistics
systems to address the problem. But the added cost will be
immense and unnecessary.
Solving the logistics problem, however, will still not
address ethanol's second and most critical defect, its high
vapor pressure when blended into gasoline. The one thing we
have learned in the past 10 years is that the most crucial
characteristic of a successful RFG program is vapor pressure,
or volatile organic compound--VOC--control. Higher vapor
pressure means higher increased VOC emissions, which leads to
more ozone pollution. It's as simple as that.
The next generation of RFG in January 2000 has even more
stringent restrictions on vapor pressure than current.
Consequently, blending ethanol into future RFG would severely
compound both the environmental and the supply problems. It is
my view that ethanol cannot be practically used on the east or
west coast in the summertime period because of its low vapor
pressure requirement and the high percentage of RFG that must
be produced in those regions.
The solution? Legislation is needed to solve the oxygenate
problem where it exists, in California and the ozone transport
region of the east coast, because 75 percent of the RFG is
there and 90 percent of the MTBE consumed is there. And we just
ask you to give these regions three things: the authority to
regulate the use of oxygenates when water quality impacts are
substantiated; a waiver of the 2 percent oxygen mandate for
RFG; and the requirement that no current clean air benefits be
compromised as a result of these changes to the Federal fuel
program.
I very much appreciate the opportunity to share these
thoughts with you and look forward to any questions you ladies
and gentlemen may have.
Senator Inhofe. Thank you, Mr. Campbell.
In deference to a scheduling problem that Senator Boxer
has, I will go ahead and allow her to go first in her
questioning, if she will agree to stay within 5 minutes.
[Laughter.]
Senator Boxer. Mr. Chairman, you have that promise.
I just have some statements to make, and I thank you so
much for accommodating me. I know it's a ``good news-bad news''
thing for the chairman; he has to hear me first, but then I
leave.
[Laughter.]
Senator Boxer. So it's a much happier situation to have
four, versus no one on this side.
Senator Inhofe. Of course, we don't have any responsibility
for the lack of interest on that side.
[Laughter.]
Senator Boxer. No, they have given me their mandate, so I
speak with that.
Let me simply say a few things. Senator Voinovich made a
very good point. He said, ``You know, the problem is localized,
isn't it true?'' ``Yes. It's where MTBE is used.'' So what I'm
trying to do is do you a favor, tell you to avoid the heartache
of what is happening to us.
And I want to thank Mr. Campbell for pointing out that the
use of MTBE is really exploding in the Northeast. I want to
spare them the problem. For me, you lift the oxygenate--Mr.
Kenny, thank you for your clear explanation.
We are in good shape in California because our Governor has
banned MTBE. We're OK, so I can relax on that point. But I do
feel I want to spare the rest of the country the problem of
shutting down water supplies. It's just dreadful, and then
facing lawsuits and all the rest--it's very important.
Let me say to Senator Garn, thank you for your clear
testimony. I know that you feel strongly about your product. I
would say to you that your company giving money to cure cancer
is laudable. I think that he ought to take a look, however, at
this study that seems to be dismissed here, and I want to spend
a minute just telling you about it, because when Senator
Bennett says, ``Isn't it true the Panel found that MTBE is not
killing anybody,'' and to quote him, ``at least not yet,''
that's far from a ringing endorsement, frankly. If somebody
says, ``It's not killing you, not yet,'' I'd say that's not an
answer.
I would suggest----
Mr. Garn. Senator Boxer----
Senator Boxer. I have very little time and you will be able
to respond. I won't even be here, so you can say anything you
want and I won't be here.
Mr. Garn. No, I wanted you to hear what I have to say.
Senator Boxer. We'll meet in my office after. You just call
and we'll talk.
But here's the situation. There was an Italian study that
was made that shows that MTBE causes cancer in animals. It was
very controversial, so it was peer-reviewed, and it was peer-
reviewed by a very good group of people that was put together
by the California Office of Health Hazard Assessment. And the
people on there were very, very prominent people. They came
from universities, the EPA, San Diego State, CALEPA, etc., the
Air Board. And they essentially peer-reviewed that study and
said it was right, and came to the conclusion that MTBE has the
potential to cause cancer in humans. Now, look, you drink it
now, and we're not sure, but it has the potential.
So I would say that if we can meet the Clean Air Act
requirement without it, my goodness, let's do it. And as I
said, I like the way this thing is moving. We've got the Blue
Ribbon Panel here calling for a phase-out--excuse me, I would
say a substantial reduction, with four or five of them calling
for a phase-out. So I like what I'm hearing in terms of the
direction that we're going. I appreciate what Governor Davis
has done. We are on the cutting edge in terms of reformulated
gasoline; we're proving that a lot can be done without MTBE.
I just think that to me, as my kids would say, it's a ``no-
brainer.'' You have a very controversial chemical; it's showing
up in the water supply; the new tanks are continuing to leak,
so that's not the answer, and I would show you the study in
Santa Clara.
So bottom line is, I think the road is clear. If we want to
lift the oxygenate requirement, fine. I would add to that,
banning MTBE, because I worry that if we don't clearly ban it,
that it still will show up. I want to spare the rest of the
country the agony we've gone through.
Again I want to say to Senator Garn, we will talk, we'll
spend a half hour together going over whatever the issues are
that you feel I am misinformed on. But I do feel comfortable
with my position, and I do thank you for your graciousness, Mr.
Chairman.
Senator Inhofe. Thank you, Senator Boxer.
Senator Garn, on my time if you would like to respond?
Mr. Garn. Well, the thing that I wanted to say, Senator
Boxer, is that my political career started as the Water
Commissioner of Salt Lake City. For 4 years I had the
responsibility of delivering clean water to 375,000 people, so
I know a great deal about water and water supplies, leaking
tanks, and all of those problems. And I am not here just to
defend MTBE. My position is simply that if I thought banning
any one chemical would solve the problem, I would be for that--
--
Senator Boxer. Even though you work for a company that
makes the chemical?
Mr. Garn. That's correct.
Senator Boxer. Well, that's very, very good.
Mr. Garn. But on the basis of adequate science, not
opinions----
Senator Boxer. Of course.
Mr. Garn [continuing]. Because with gasoline you have
benzene, you have toluene, you have alkylates, there are all
sorts of things.
Senator Boxer. Of course.
Mr. Garn. It would not make me feel more comfortable to
take MTBE out, and then have others of these chemicals leaking
into the groundwater.
Senator Boxer. I understand.
Mr. Garn. We had multiple problems in our canyons and
watersheds, of groundwater leakage and other difficulties.
That's the only thing I wanted you to understand, where I am
coming from personally. I voted against the 1990 Clean Air Act
Amendments, for whatever that is worth. I wasn't sure we should
be creating problems all over the country with uniform
solutions. But until there is adequate science, we should not
act. I'll give you an example. In Park City, UT, when I was
still in the Senate, the EPA closed down a subdivision--no FHA
loans, no new building construction, talking about moving
people out of it--and I said, ``Do you have the science to
prove that lead is actually getting into these homes, and
children are at risk?'' So having been chairman of their
appropriations subcommittee, I was in a position to say,
``Stop. We will have scientific studies.'' We even blood-tested
all of the children that lived in that entire subdivision.
There was no lead contamination; EPA's case was absolutely
wrong. We solved the problem by putting 6 inches of topsoil in
everybody's yard, instead of closing down the subdivision and
causing great economic harm, the reduction in half of their
housing prices, and so on and so forth.
That is essentially what I was trying to say in my
statement. Let's not rush to judgment. Too many times in the 18
years I spent in this body we did. Let's get the science. You
eliminate MTBE; you've still got a problem in California with
leaking tanks.
So first of all I think we ought to make sure that we
eliminate the source, to begin with, and have adequate science.
I don't want to drink ethanol. I don't want to drink benzene. I
don't want to drink MTBE.
Senator Boxer. I'm not suggesting you do.
Senator Inhofe. Reclaiming my time, Senator Boxer.
Mr. Kenny, I understand that the California Air Resources
Board has raised air quality concerns about replacements for
MTBE. I would like to ask you what your concerns are in terms
of air quality changes that would take place if you did away
with, or dramatically reduced, the MTBE and did not repeal the
requirement for oxygenates.
Mr. Kenny. Thank you, Senator. The concern we have is that
if you have a requirement to use oxygenates, and MTBE is not
available, then what would happen more than likely is that the
only alternative oxygenate that would be available would be
ethanol. And our concern with regard to ethanol is that high
uses of ethanol in the summertime would result in greater
volatility of the gasoline, and the concern that we then see is
potentially degraded air quality as a result of the evaporative
emissions that would come from that gasoline. So we are very
concerned about that.
There are ways to address that. The way it is commonly
addressed is that you lower the vapor pressure of the base fuel
that the ethanol is mixed into. When that occurs, then you can
basically adjust and keep your RVPs down to a lower level. The
difficulty with that, however, is that it is extremely
expensive to lower that vapor pressure.
Senator Inhofe. Now, when you say ``extremely expensive,''
I would like to get something in the record here as to what
we're talking about, what type of framework in which we could
characterize the expense.
Mr. Kenny. It's going to be in excess of $0.06 per gallon
of gasoline sold, at a minimum.
Senator Inhofe. Thank you.
Senator Chafee.
Senator Chafee. I'm all set, thank you.
Senator Inhofe. All right.
Senator Bennett.
Senator Bennett. Thank you, Mr. Chairman.
I am interested in this discussion about removing the 2
percent requirement. Going back to my business career, I am
always in favor of what I call ``performance codes'' as opposed
to ``specification codes.'' If I can describe it in an analogy,
the old building codes required copper pipe, and they were
written before anybody had invented PVC. You came along and
said, ``Well, we can now give you a tubing or piping into your
house that is cheaper, lighter, better in terms of its ability
to withstand pressure per square foot, but the building code
says you can't use it, because in the name of `safety' we have
to have copper pipe.''
So if you go to a performance code that just says ``you
have to have this outcome,'' and let the market respond to the
performance requirement instead of the specific requirement in
a specification code, you get the best of all possible worlds.
And I think had I been in the Senate, I probably would have
voted against the specification code and would have said, ``No,
we just want clean air within these parameters,'' and allow Mr.
Campbell and whoever else to come up with the ability to do
that.
Now, I think that's what I'm hearing you say, Mr. Kenny, is
that we want a performance code, not a specification code.
Mr. Kenny. That's correct, Senator Bennett. In fact, in
California with our gasoline specifications, we do provide for
a performance method as opposed to simply specifications.
Senator Bennett. Yet at the same time, if a refiner like
Mr. Campbell comes forward and says, ``We can meet that
performance code with the use of MTBE,'' you have just added a
specification code component to your performance code, and you
do sell on the basis that ``MTBE is contaminating our
groundwater.'' Is that correct?
Mr. Kenny. That is correct.
Senator Bennett. OK.
We come back to the question of the Blue Ribbon Panel, my
question to Mr. Greenbaum, and the clear statement in their
summary position, which agrees with Senator Garn. He says we
should ``take action to ensure that the detections of MTBE in
drinking water that we have seen do not continue to grow.'' And
implicit in that and in his answer to me, he confirmed the same
thing, the point Senator Garn has made, which is that there is
no science to indicate that this--however unpleasant and
noisesome it may be--is toxic, and he agreed with that; at
least I heard him agree with that in his comment here.
Now, I know Governor Davis has taken the position that he's
taken, and you are here as his agent, and I wouldn't expect you
to do anything but support that posture. But from the
standpoint of the Congress, if we adopt a performance code and
couple that with a performance code with respect to underground
tanks, we may be achieving the requirement of the Blue Ribbon
Panel.
Mr. Kenny, I know you don't think we are. I can tell that
from your body language. But do any of the other witnesses have
a comment?
Mr. Garn.
Mr. Garn. Senator Bennett, if I could just make a comment.
When this issue first started to arise in California a couple
of years ago, I had several conversations with Governor Wilson
about the issue, and his position was quite different from
Governor Davis in the fact that he--as I have tried to present
today--wanted to ``wait for the science,'' and that was his
position. He said, ``Jake, I don't know what action I will
take; there is not sufficient evidence yet, and I am
particularly waiting for the California Office of Environmental
Health Hazard Assessment report before I make any decision,''
even though he was being pushed very hard in the summer of 1998
to do something.
Well, that office came up and voted in December 1998 that
MTBE should not be considered a carcinogenic or developmental
or reproductive toxicant. That happened in December, and that's
the report he was waiting for. Of course, he was not in office.
But again, I just have to keep making the point over and over
again, I don't think you are in a position yet--meaning you,
the Congress--to make a decision until there is a great deal
more evidence, not only on MTBE, but the same scrutiny applied
to all the other ingredients of gasoline that could be a
problem. I just can't come to the conclusion that even if we
banned MTBE, that we have solved the problem that we all agree
is a problem.
Mr. Kenny. Mr. Chairman, if I could clarify one point.
Senator Inhofe. Surely.
Mr. Kenny. With regard to the Office of Environmental
Health Hazard Assessment, there have been references to the
fact that they voted that MTBE is not a human health
carcinogen. I don't think that's quite accurate. I think it's
probably more accurate to say that they took the matter up, and
they voted 3 to 3, so they were unable to reach a decision.
Senator Bennett. Thank you for that clarification.
Mr. Campbell.
Mr. Campbell. Senator, a couple comments.
First of all, about tanks. There has been a leaking
underground storage tank program in effect for 10 years; I
think virtually every major oil company has replaced them. The
liability of delivering to a tank which has not been replaced
would be horrendous.
Part of today's problem is the fact that there have been
over 20 percent of those tanks that are covered by the program
that have not been replaced. They continue to ask for
exemptions; that needs to be stopped.
Second thing, we've been told by EPA that there are more
tanks that are exempted from the program than are currently in
it--municipal, State, Federal, farms, small business. So
completing that program is not going to be the answer. There is
a tremendous number of exemptions out there.
Secondly, to those of us who have spent hundreds of
millions of dollars replacing tanks, it's not a perfect system.
Invariably there are some leaks. I hate to say this, but we are
probably going to have continuing leaks of some amount. The
Senator points out that the real answer would be to solve the
leakage problem entirely. What I'm saying is that from
practical reality, in all probability that's not possible.
So we have to deal with--if in fact there is a leak, what
is done to remediate that? And we find that the remediation of
gasoline based on crude oil occurs much more readily than when
you put in some chemicals.
And I would like to mention one more thing about the health
issue. The chemical companies, including my own, manufacture
MTBE. The refiners use it because we're required to. The
consumer gets upset because their drinking water smells or
tastes funny. And trying to tell them that it's not a health
effects issue is an impossible task. If it smells funny and
tastes funny, as far as they are concerned, your health effects
study is incorrect. And continuing to supply that kind of
product to the consumers is a liability that few companies are
going to want to shoulder.
Senator Bennett. I don't in any way to support water that
smells and tastes funny, and I know the former Water
Commissioner doesn't, either.
Thank you, Mr. Chairman.
Senator Voinovich. Just for the record, in response to
Senator Boxer's statement that MTBE has not been listed as a
carcinogen by either the National Institute of Environmental
Health Sciences or the International Agency for Research on
Cancer--and I understand, Mr. Kenny, that California has not
listed it as a carcinogen under Proposition 65--I think we need
to make that clear, because so often around here somebody gets
a report, and before you know it, it's cancerous, and off we
go, getting back to Senator Garn's good science.
If we eliminated the 2 percent and did not ban MTBE, and
basically said, ``You figure it out in California, and you
figure it out on the east coast,'' if we came up with that
result, would that cause chaos in the gasoline industry across
this country?
Mr. Kenny. I don't think it would, Senator. I think the
optimal situation here is one in which the 2 percent
requirement is no longer in effect, and in California, MTBE is
banned. So what would occur is that in California the
performance standards would be in place.
I think with regard to the rest of the country, the issue
would be how to maintain the air quality benefits that are
currently being achieved from reformulated gasoline. In
California we can maintain those air quality benefits because
we have actually had fairly substantial investment by the
refiners in upgrading the refineries, so that the cleaner
gasoline can be produced.
I don't know if that could be said in exactly the same
degree for the rest of the country.
Mr. Campbell. Senator, in general the United States, with
our 50 States, we have relatively few regions--we call
``pads''--we have West Coast, Gulf Coast, mid-America, and
eastern regions, so consequently that's why we talked about the
need for a regional approach. Because refiners and marketers
and distributors who supply regions would have tremendous
difficulty if you had a patchwork quilt within a region--this
State wanted that, this other State wanted something entirely
different. That's why we are saying, in the Northeast--please
remember, MTBE is predominantly a West Coast/East Coast issue.
The West Coast is being addressed with California. In the case
of the East Coast, what we have done is turn to the
environmental directors in the States and some of the
organizations, like NESCOM and MIRANA, and said, ``Help us from
the standpoint of establishing the standard so that we can have
a regional fuel'' so that companies like my own and other
companies will be able to distribute it reliably and with
relatively low cost. That's the intent.
Senator Voinovich. OK. If we didn't ban MTBE--if we
eliminate the 2 percent and just say, ``You work it out on a
regional basis,'' or any way you could--do you think that's a
practical approach?
Mr. Campbell. Well, I don't, because I think there is so
much focus on MTBE now in the individual States, the fact that
it does cause odor and taste in water, that some of the States
are almost ready to ban it themselves, much in the same manner
as California.
Before the EPA Blue Ribbon Panel report came out, a number
of States were ready to take action banning it themselves----
Senator Voinovich. The question is this. Do you think the
Federal Government should ban MTBE?
Mr. Campbell. No. I voted with the Panel to say that what
we ought to do, first of all, is to have a substantial
reduction--it was expected to be in the neighborhood of 75
percent less. The reason I say that was because for more than a
decade, that was the level that was used generally throughout
the industry as an octane-enhancer, and there were literally no
complaints that anybody heard of. Only when we received the 2
percent oxygen mandate and the gasoline went from roughly 2
percent to 11 or 12 percent, or even higher, it seems to many
of us that that's when the complaints began to surface.
So what we said was--and Dan Greenbaum has pointed out to
us how difficult it is to totally ban a chemical--that what we
ought to do is go from 11 to 15 percent down to 2 percent,
which is where we were for many years----
Senator Voinovich. But if you eliminated the 2 percent, you
could do that?
Mr. Campbell. I'm talking 2 volume percent of MTBE, not 2
oxygen percent.
Senator Voinovich. OK. If you eliminated the 2 percent, you
could still----
Mr. Campbell. You would have to deal with the issue,
though, Senator, of the States saying, ``I don't care if you
have a 2 percent mandate or not, I don't want MTBE in my
State,'' and I think that's what we see occurring in kind of a
patchwork quilt fashion on the east coast of the United States.
So what we are trying to do is get them to put it together in a
regional effect, and I think that you're going to have to deal
with the issue of substantial reduction of MTBE. That's one
person's opinion, in order to have the States satisfied.
Senator Voinovich. Well, if you eliminate the oxygenate
requirement, then you can do what you want with it, can't you?
Mr. Campbell. What I'm saying is--and I apologize if I'm
not saying it clearly--if you eliminate the oxygenate
requirement, and you still permit the use of MTBE, and you give
no guidance as to the upper limit, my concern is that some of
the States might end up saying that they want either zero, or
begin to set their own limit on this.
Senator Voinovich. Well, so your answer to the question is
that you think that you ought to eliminate it, period?
Mr. Campbell. Eliminate MTBE?
Senator Voinovich. Yes.
Mr. Campbell. No--where I'm coming from is to say that what
we ought to do is go back to where we were. I think we will be
able to----
Senator Voinovich. Where we were before the 2 percent
requirement for oxygen?
Mr. Campbell. Before the 2 percent oxygen, yes, sir.
Senator Voinovich. OK. Fine. And then you would decide
regionally how you would handle it?
Mr. Campbell. That's right.
Senator Voinovich. And would you need the Federal
Government to sit down and negotiate that in a region for you?
Mr. Campbell. No, but we would need the Federal Government
to deal with the 2 percent mandate. But I don't think you need
the Federal Government to handle the gasoline formula
regionally. I think you can look to the environmental
organizations within those sections of the country to come up
with what they desire for that region.
Senator Voinovich. OK.
Another question, just to finish up. We have this great
issue of ethanol, because there are lots of States that are
involved in it, my State and lots of others. If you eliminated
the 2 percent oxygenate requirement, would gasoline still
contain ethanol? Or would that disappear?
Mr. Campbell. I believe that gasoline would still contain
ethanol. In fact, I believe that ethanol will increase in
gasoline in the future. The reason I say that--assuming some
MTBE comes out of the system, and you get down to a lower
level--we're also going to be reducing sulfur from gasoline, in
all probability. You do that, and you're going to lower the
octane pool in this country. The way the refiners will turn in
order to correct that, more and more will be turning to
ethanol.
So my expectation is, if you eliminate the 2 percent
mandate, oxygenate mandate, ethanol consumption in fuel in the
United States will go up.
Senator Voinovich. Probably immediately, because a lot of
people wouldn't use the MTBE? Some would substitute it?
Mr. Campbell. Some would substitute ethanol where you don't
have the RFG program.
Senator Voinovich. Thank you.
Senator Inhofe. Our time has expired. I thought I had it
pretty well sorted out in my mind until Senator Voinovich
started asking these questions, so let me ask this just for my
own clarification.
If we went back to the pre-1990 amendments, where they did
not have the oxygenate requirement, we still had the additive
in there at that time, but it was used as an octane enhancer,
and there wasn't a problem with the ``patchwork,'' as you have
explained it.
Why would there be that problem now if there wasn't before,
if they were to repeal what they did in 1990?
Mr. Campbell. There would not. You are right, there would
not. I misunderstood the Senator's question. What you're saying
is that if you repeal the 2 percent mandate and you go back to
where we were, back prior to the 1990 amendments, and you
essentially permitted the companies to blend whatever they
needed to blend to meet some requirement from the standpoint of
performance, to go back to Senator Bennett, the chances are
that you would be back at the 2 volume percent MTBE in
gasoline, and back at----
Senator Inhofe. As opposed to 11?
Mr. Campbell. As opposed to 11.
I think the concern is that, certainly in California and
increasingly on the east coast, there is a call for the banning
of MTBE. If you talk to the water people, the thought of
saying, ``Let's go from 11 percent to 2 percent, and the
problem is solved,'' they will say to you that that just means
it's going to take five times longer to get to the same problem
level; you didn't solve it back in those earlier days.
I think you will end up having a cry for some maximum
ceiling of MTBE in gasoline. But by eliminating the oxygenate
mandate, trying to go back to the 1980 or 1990 period of time,
I think you would solve much of the problem.
Senator Inhofe. All right.
Well, I thank you very much. I appreciate all of you coming
and being present and testifying. You will be receiving
questions in writing, which we will ask you to submit for the
record.
Senator Inhofe. We are in recess.
[Whereupon, at 11:23 a.m., the subcommittee was adjourned,
to reconvene at the call of the chair.]
[Additional statements submitted for the record follow:]
Statement of Hon. Joseph I. Lieberman, U.S. Senator from the State of
Connecticut
Thank you, Mr. Chairman, for holding today's hearing on the results
of the EPA's Blue Ribbon Panel on Oxygenates in Gasoline. I look
forward to hearing from today's witnesses on this very important issue.
The 2 percent oxygenate requirement was included as part of the
reformulated gasoline program (RFG), an effort to address smog
pollution from mobile sources. Nine areas with the worst smog
problems--including parts of Connecticut--were required to use cleaner
burning gasoline. Other areas opted in voluntarily. Overall, RFG has
produced significant benefits--reducing volatile organic compounds,
carbon monoxide, and mobile air toxics--in many cases exceeding the
standards required by law.
Unfortunately, the oxygenate requirement has had some unforseen
consequences as well. MTBE, the most widely used oxygenate, has been
found in the water supply in more than 20 states and in several states
occurs in concentrations high enough to cause the shutdown of wells. In
my home State, Connecticut, at least 200 wells have been identified as
contaminated by MTBE, raising serious health concerns.
However, even as we contemplate federal action to address the
serious issue of MTBE contamination of water quality, we must not
sacrifice the clean air benefits gained through the use of oxygenates.
Thus, the challenge that faces us today is one of preserving the
advances we have made in air quality while acting to increase
protection of our nation's water supplies.
Foremost among our responsibilities at the federal level should be
allowing states to address concerns about MTBE within the confines of
the RFG program. I therefore support a national approach to this issue,
giving states flexibility in dealing with MTBE and other oxygenates in
gasoline by removing the federal oxygenate requirement. However,
because the Blue Ribbon Panel, NESCAUM, and others have confirmed that
oxygenates sometimes help gasoline exceed current standards, I also
feel strongly that any legislation we consider must maintain existing
air quality benefits. This could be included in revised performance
criteria for gasoline. Perhaps some of the witnesses will have
suggestions as to how to accomplish this most effectively.
I would also like to point out that Connecticut has taken
significant steps to address another source of MTBE pollution, leaking
underground storage tanks. As of February 1999, 15,450 leaking tanks
had been closed in Connecticut and 1,818 cleanups were initiated. In
addition, the Connecticut Department of Environmental Protection just
announced a state program to assist homeowners in identifying and
remediating leaky tanks.
I look forward to hearing from the witnesses about how we can best
use the Panel's findings to solve the problem of MTBE contamination of
drinking water.
______
Statement of Daniel S. Greenbaum, Chair, Blue Ribbon Panel on
Oxygenates in Gasoline and President, Health Effects Institute
Mr. Chairman, and members of the Committee, thank you for the
opportunity to appear before you today to provide you with the results
of the work of the Blue Ribbon Panel on Oxygenates in Gasoline. I have
attached a copy of the Executive Summary and Recommendations of the
Panel, which were issued on July 27, 1999.
In the wake of the detection of the additive MTBE (Methyl Tertiary
Butyl Ether) in drinking water supplies in Maine, California, and
elsewhere, the Blue Ribbon Panel was convened by U.S. EPA Administrator
Browner to investigate the facts of the situation and recommend actions
to achieve both clean air and clean water. The Panel consisted of
experts on air and water quality, as well as representatives of the
oil, ethanol, and MTBE industry and the environmental community (see
attached list).
The Panel, began its work in January of this year, and conducted an
in-depth investigation of the air quality, water quality, fuel supply,
and price issues surrounding the use of oxygenates in gasoline, holding
six meetings in 6 months (including field meetings in both New England
and California), hearing from experts, and reviewing dozens of existing
and new studies of oxygenates in gasoline.
Based on that review the Panel found:
1. RFG has provided substantial reductions in the emissions of a
number of air pollutants from motor vehicles, most notably volatile
organic compounds (precursors of ozone), carbon monoxide, and mobile-
source air toxics (benzene, 1,3-butadiene, and others), in most cases
resulting in emissions reductions that exceed those required by law.
2. There have been growing detections of MTBE in drinking water,
with between 5 percent and 10 percent of drinking water supplies in RFG
areas showing detectable amounts of MTBE. The great majority of these
detections to date have been below levels of public health concern,
with approximately one percent rising to levels above 20 ppb and some
instances, although rare, of levels above 100ppb. Detections at lower
levels have raised consumer taste and odor concerns that have caused
water suppliers to stop using some water supplies and to incur costs of
treatment and remediation. The contaminated wells include private wells
that are less well protected than public drinking water supplies and
not monitored for chemical contamination. There is also evidence of
contamination of surface waters, particularly during summer boating
seasons.
3. The major source of groundwater contamination appears to be
releases from underground gasoline storage systems (UST). These systems
have been upgraded over the last decade, likely resulting in reduced
risk of leaks. However, approximately 20 percent of the storage systems
have not yet been upgraded. There continue, as well, to be reports of
releases from some upgraded systems, due to inadequate design,
installation, maintenance, and/or operation. In addition, U.S. EPA does
not currently have the authority to regulate many fuel storage systems
(e.g. farms, small above-ground tanks).
Beyond groundwater contamination from UST sources, the other major
sources of water contamination appear to be small and large gasoline
spills to ground and surface waters, and recreational water craft--
particularly those with older motors--releasing unburned fuel to
surface waters.
Following its investigation, the Panel evaluated a range of
alternatives for addressing these problems, and recommended that U.S.
EPA work with Congress and the states to implement a 4-part integrated
package of reforms to ensure that water supplies are better protected
while the substantial reductions in air pollution that have resulted
from RFG are maintained. Specifically, the Panel:
Recommended a comprehensive set of improvements to the
nation's water protection programs, including over 20 specific actions
to enhance Underground Storage Tank, Safe Drinking Water, and private
well protection programs. The panel considered these necessary, but not
sufficient in and of themselves, to prevent future water contamination.
Agreed broadly that use of MTBE should be reduced
substantially (with some members supporting its complete phase out),
and that Congress should act to provide clear federal and state
authority to regulate and/or eliminate the use of MTBE and other
gasoline additives that threaten drinking water supplies;
Recommended that Congress act to remove the current Clean
Air Act requirement--that 2 percent of RFG, by weight, consist of
oxygen--to ensure that adequate fuel supplies can be blended in a cost-
effective manner while reducing usage of MTBE; and
Recommended that EPA seek mechanisms to ensure that there
is no loss of current air quality benefits as the use of MTBE declines.
The Panel also called for accelerated research into the air, water
and health characteristics of all compounds whose use would likely
increase as replacements for MTBE, including aromatics, alkylates, and
ethanol.
Although the Panel agreed broadly on its recommendations, two
members, while agreeing with most recommendations, had concerns with
specific provisions: the MTBE industry representative felt that the
water protection reforms proposed by the Panel were sufficient to
protect water supplies and was concerned that the Panel had not
adequately considered the air quality benefits of oxygenates, and the
ethanol industry representative was concerned that the Panel's
recommendation to lift the oxygen requirement did not adequately
reflect the benefits of using oxygenates. (Their statements are
attached to the Executive Summary and Recommendations).
In sum, the Panel found that we have a successful cleaner-burning
gasoline program in place but need to take action to ensure that the
detections of MTBE in drinking water that we have seen--and which
fortunately in the great majority of cases have not been of public
health concern--do not continue to grow.
The Panel's full report, including background issues summaries on
all of the data the Panel reviewed, is now available on the World Wide
Web at the Panel's home page: http://www.epa.gov/oms/consumer/fuels/
oxypanel/blueribb.htm.
Thank you again for this opportunity to testify. I would be pleased
to answer any of the Committee's questions.
______
The Blue Ribbon Panel on Oxygenates in Gasoline--Executive Summary
and Recommendations
introduction
The Federal Reformulated Gasoline Program (RFG) established in the
Clean Air Act Amendments of 1990, and implemented in 1995, has provided
substantial reductions in the emissions of a number of air pollutants
from motor vehicles, most notably volatile organic compounds
(precursors of ozone), carbon monoxide, and mobile-source air toxics
(benzene, 1,3-butadiene, and others), in most cases resulting in
emissions reductions that exceed those required by law. To address its
unique air pollution challenges, California has adopted similar but
more stringent requirements for California RFG.
The Clean Air Act requires that RIO contain 2 percent oxygen, by
weight. Over 85 percent of RFG contains the oxygenate methyl tertiary
butyl ether (MTBE) and approximately 8 percent contains ethanol--a
domestic fuel-blending stock made from grain and potentially from
recycled biomass waste. There is disagreement about the precise role of
oxygenates in attaining the RFG air quality benefits although there is
evidence from the existing program that increased use of oxygenates
results in reduced carbon monoxide emissions, and it appears that
additives contribute to reductions in aromatics in fuels and related
air benefits. it is possible to formulate gasoline without oxygenates
that can attain similar air toxics reductions, but less certain that,
given current federal RFG requirements, all fuel blends created without
oxygenates could maintain the benefits provided today by oxygenated
RFG.
At the same time, the use of MTBE in the program has resulted in
growing detections of MTBE in drinking water, with between 5 percent
and 10 percent of drinking water supplies in high oxygenate use areas
\1\ showing at least detectable amounts of MTBE. The great majority of
these detections to date have been well below levels of public health
concern, with approximately one percent rising to levels above 20 ppb.
Detections at lower levels have, however, raised consumer taste and
odor concerns that have caused water suppliers to stop using some water
supplies and to incur costs of treatment and remediation. The
contaminated wells include private wells that are less well protected
than public drinking water supplies and not monitored for chemical
contamination. There is also evidence of contamination of surface
waters, particularly during summer boating seasons.
---------------------------------------------------------------------------
\1\ Areas using RFG (2 percent by weight oxygen) and/or Oxyfuel
(2.7 percent by weight Oxygen)
---------------------------------------------------------------------------
The major source of groundwater contamination appears to be
releases from underground gasoline storage systems (UST). These systems
have been upgraded over the last decade, likely resulting in reduced
risk of leaks. However, approximately 20 percent of the storage systems
have not yet been upgraded, and there continue to be reports of
releases from some upgraded systems, due to inadequate design,
installation, maintenance, and/or operation. In addition, many fuel
storage systems (e.g., farms, small above-ground tanks) are not
currently regulated by U.S. EPA. Beyond groundwater contamination from
UST sources, the other major sources of water contamination appear to
be small and large gasoline spills to ground and surface waters, and
recreational water craft--particularly those with older motors--
releasing unburned fuel to surface waters.
the blue ribbon panel
In November, 1998, U.S. EPA Administrator Carol M. Browner
appointed a Blue Ribbon Panel to investigate the air quality benefits
and water quality concerns associated with oxygenates in gasoline, and
to provide independent advice and recommendations on ways to maintain
air quality while protecting water quality. The Panel, which met six
times from January-June 1999, heard presentations in Washington, the
Northeast, and California about the benefits and concerns related to
RFG and the oxygenates; gathered the best available information on the
program and its effects; identified key data gaps; and evaluated a
series of alternative recommendations based on their effects on:
air quality
water quality
stability of fuel supply and cost
the findings and recommendations of the blue ribbon panel
Findings Based on its review of the issues, the Panel made the
following overall findings:
The distribution, use, and combustion of gasoline poses
risks to our environment and public health.
RFG provides considerable air quality improvements and
benefits for millions of U.S. citizens.
The use of MTBE has raised the issue of the effects of
both MTBE alone and MTBE in gasoline. This panel was not constituted to
perform an independent comprehensive health assessment and has chosen
to rely on recent reports by a number of state, national. and
international health agencies. What seems clear, however, is that MTBE,
due to its persistence and mobility in water, is more likely to
contaminate ground and surface water than the other components of
gasoline.
MTBE has been found in a number of water supplies
nationwide, primarily causing consumer odor and taste concerns that
have led water suppliers to reduce use of those supplies. Incidents of
MTBE in drinking water supplies at levels well above EPA and state
guidelines and standards have occurred, but are rare. The Panel
believes that the occurrence of MTBE in drinking water supplies can and
should be substantially reduced.
MTBE is currently an integral component of the U.S.
gasoline supply both in terms of volume and octane. As such, changes in
its use, with the attendant capital construction and infrastructure
modifications, must be implemented with sufficient time, certainty, and
flexibility to maintain the stability of both the complex U.S. fuel
supply system and gasoline prices.
The following recommendations are intended to be implemented as a
single package of actions designed to simultaneously maintain air
quality benefits while enhancing water quality protection and assuring
a stable fuel supply at reasonable cost. The majority of these
recommendations could be implemented by-federal and state environmental
agencies without further legislative action, and we would urge their
rapid implementation. We would, as well, urge all parties to work with
Congress to implement those of our recommendations that require
legislative action.
Recommendations to Enhance Water Protection
Based on its review of the existing federal, state and local
programs to protect, treat, and remediate water supplies, the Blue
Ribbon Panel makes the following recommendations to enhance,
accelerate, and expand existing programs to improve protection of
drinking water supplies from contamination.
Prevention
1. EPA, working with the states, should take the following actions
to enhance significantly the Federal and State Underground Storage Tank
programs:
a. Accelerate enforcement of the replacement of existing tank
systems to conform with the federally-required December 22, 1998
deadline for upgrade, including, at a minimum, moving to have all
states prohibit fuel deliveries to non-upgraded tanks, and adding
enforcement and compliance resources to ensure prompt enforcement
action, especially in areas using RIG and Wintertime Oxyfuel.
b. Evaluate the field performance of current system design
requirements and technology and, based on that evaluation, improve
system requirements to minimize leaks/releases, particularly in
vulnerable areas (see recommendations on Wellhead Protection Program in
2. below)
c. Strengthen release detection requirements to enhance early
detection, particularly in vulnerable areas, and to ensure rapid repair
and remediation
d. Require monitoring and reporting of MTBE and other ethers in
groundwater at all UST release sites
e. Encourage states to require that the proximity to drinking
water supplies, and the potential to impact those supplies, be
considered in land-use planning and permitting decisions for siting of
new UST facilities and petroleum pipelines.
f. Implement and/or expand programs to train and license UST
system installers and maintenance personnel.
g. Work with Congress to examine and, if needed, expand the
universe of regulated tanks to include underground and above ground
fuel storage systems that are not currently regulated yet pose
substantial risk to drinking water supplies.
2. EPA should work with its state and local water supply partners
to enhance implementation of the Federal and State Safe Drinking Water
Act programs to:
a. Accelerate, particularly in those areas where RFG or Oxygenated
Fuel is used, the assessments of drinking water source protection areas
required in Section 1453 of the 1996 Safe Drinking Water Act
Amendments.
b. Coordinate the Source Water Assessment program in each state
with federal and state Underground Storage Tank Programs using
geographic information and other advanced data systems to determine the
location of drinking water sources and to identify UST sites within
source protection zones.
c. Accelerate currently-planned implementation of testing for and
reporting of MTBE in public drinking water supplies to occur before
2001.
d. Increase ongoing federal, state, and local efforts in Wellhead
Protection Areas including:
enhanced permitting, design, and system installation
requirements for USTs and pipelines in these areas;
strengthened efforts to ensure that non-operating USTs are
properly closed;
enhanced UST release prevention and detection
improved inventory management of fuels.
3. EPA should work with states and localities to enhance their
efforts to protect lakes and reservoirs that serve as drinking water
supplies by restricting use of recreational water craft, particularly
those with older motors.
4. EPA should work with other federal agencies, the states, and
private sector partners to implement expanded programs to protect
private well users, including, but not limited to:
a. A nationwide assessment of the incidence of contamination of
private wells by components of gasoline as well as by other common
contaminants in shallow groundwater,
b. Broad-based outreach and public education programs for owners
and users of private wells on preventing, detecting, and treating
contamination;
c. Programs to encourage and facilitate regular water quality
testing of private wells.
5. Implement, through public-private partnerships, expanded Public
Education programs at the federal, state, and local levels on the
proper handling and disposal of gasoline.
6. Develop and implement an integrated field research program into
the groundwater behavior of gasoline and oxygenates, including:
a. Identifying and initiating research at a population of UST
release sites and nearby drinking water supplies including sites with
MTBE, sites with ethanol, and sites using no oxygenate;
b. Conducting broader, comparative studies of levels of MTBE,
ethanol, benzene, and other gasoline compounds in drinking water
supplies in areas using primarily MTBE, areas using primarily ethanol,
and areas using no or lower levels of oxygenate.
Treatment and Remediation
7. EPA should work with Congress to expand resources available for
the up-front funding of the treatment of drinking water supplies
contaminated with MTBE and other gasoline components to ensure that
affected supplies can be rapidly treated and returned to service, or
that an alternative water supply can be provided. This could take a
number of forms, including but not limited to:
a. Enhancing the existing Federal Leaking Underground Storage Tank
Trust Fund by fully appropriating the annual available amount in the
Fund, ensuring that treatment of contaminated drinking water supplies
can be funded, and streamlining the procedures for obtaining funding.
b. Establishing another form of funding mechanism which ties the
funding more directly to the source of contamination.
c. Encouraging states to consider targeting State Revolving Funds
(SRF) to help accelerate treatment and remediation in high priority
areas.
8. Given the different behavior of MTBE in groundwater when
compared to other components of gasoline, states in RFG and Oxyfuel
areas should reexamine and enhance state and federal ``triage''
procedures for prioritizing remediation efforts at UST sites based on
their proximity to drinking water supplies.
9. Accelerate laboratory and field research, and pilot projects,
for the development and implementation of cost-effective water supply
treatment and remediation technology, and harmonize these efforts with
other public/private efforts underway.
Recommendations for Blending Fuel for Clean Air and Water
Based on its review of the current water protection programs, and
the likely progress that can be made in tightening and strengthening
those programs by implementing Recommendations 1-9 above, the Panel
agreed broadly, although not unanimously, that even enhanced protection
programs will not give adequate assurance that water supplies will be
protected, and that changes need to be made to the RFG program to
reduce the amount of MTBE being used, while ensuring that the air
quality benefits of RFG, and fuel supply and price stability, are
maintained.
Given the complexity of the national fuel system, the advantages
and disadvantages of each of the fuel blending options the Panel
considered (see Appendix A), and the need to maintain the air quality
benefits of the current program, the Panel recommends an integrated
package of actions by both Congress and EPA that should be implemented
as quickly as possible. The key elements of that package, described in
more detail below, are:
Action agreed to broadly by the Panel to reduce the use of
MTBE substantially (with some members supporting its complete phase
out), and action by Congress to clarify federal and state authority to
regulate and/or eliminate the use of gasoline additives that threaten
drinking water supplies;
Action by Congress to remove the current 2 percent oxygen
requirement to ensure that adequate fuel supplies can be blended in a
cost-effective manner while quickly reducing usage of MTBE; and
Action by EPA to ensure that there is no loss of current
air quality benefits.
The Oxygen Requirement
10. The current Clean Air Act requirement to require 2 percent
oxygen, by weight, in RFG must be removed in order to provide
flexibility to blend adequate fuel supplies in a cost-effective manner
while quickly reducing usage of MTBE and maintaining air quality
benefits.
The panel recognizes that Congress, when adopting the oxygen
requirement, sought to advance several national policy goals (energy
security and diversity, agricultural policy, etc.) that are beyond the
scope of our expertise and deliberations.
The panel further recognizes that if Congress acts on the
recommendation to remove the requirement, Congress will likely seek
other legislative mechanisms to fulfill these other national policy
interests.
Maintaining Air Benefits
11. Present toxic emission performance of RFG can be attributed, to
some degree, to a combination of three primary factors: (1) mass
emission performance requirements, (2) the use of oxygenates, and (3) a
necessary compliance margin with a per gallon standard. In Cal RFG,
caps on specific components of fuel is an additional factor to which
toxics emission reductions can be attributed.
Outside of California, lifting the oxygen requirement as
recommended above may lead to fuel reformulations that achieve the
minimum performance standards required under the 1990 Act, rather than
the larger air quality benefits currently observed. In addition,
changes in the RFG program could have adverse consequences for
conventional gasoline as well.
Within California, lifting the oxygen requirement will result in
greater flexibility to maintain and enhance emission reductions,
particularly as California pursues new formulation requirements for
gasoline.
In order to ensure that there is no loss of current air quality
benefits, EPA should seek appropriate mechanisms for both the RFG Phase
II and Conventional Gasoline programs to define and maintain in RFG II
the real world performance observed in RFG Phase I while preventing
deterioration of the current air quality performance of conventional
gasoline.\2\
---------------------------------------------------------------------------
\2\ The Panel is aware of the current proposal for further changes
to the sulfur levels of gasoline and recognizes that implementation of
any change resulting from the Panel's recommendations will, of
necessity, need to be coordinated with implementation of these other
changes. However, a majority of the panel considered the maintenance of
current RFG air quality benefits as separate from any additional
benefits that might accrue from the sulfur changes currently under
consideration.
---------------------------------------------------------------------------
There are several possible mechanisms to accomplish this. One
obvious way is to enhance the mass-based performance requirements
currently used in the program. At the same time, the panel recognizes
that the different exhaust components pose differential risks to public
health due in large degree to their variable potency. The panel urges
EPA to explore and implement mechanisms to achieve equivalent or
improved public health results that focus on reducing those compounds
that pose the greatest risk.
Reducing the Use of MTBE
12. The Panel agreed broadly that, in order to minimize current and
future threats to drinking water, the use of MTBE should be reduced
substantially. Several members believed that the use of MTBE should be
phased out completely. The Panel recommends that Congress act quickly
to clarify federal and state authority to regulate and/or eliminate the
Use of gasoline additives that pose a threat to drinking water
supplies.\3\
---------------------------------------------------------------------------
\3\ Under Sec. 211 of the 1990 Clean Air Act, Congress provided EPA
with authority to regulate fuel formulation to improve air quality. In
addition to EPA's national authority, in Sec. 211(c)(4) Congress sought
to balance the desire for maximum uniformity in our nation's fuel
supply with the obligation to empower states to adopt measures
necessary to meet national air quality standards. Under Sec. 211(c)(4),
states may adopt regulations on the components of fuel, but must
demonstrate that (1) their proposed regulations are needed to address a
violation of the NAAQS and (2) it is not possible to achieve the
desired outcome without such changes.
The panel recommends that Federal law be amended to clarify EPA and
state authority to regulate and/or eliminate gasoline additives that
threaten water supplies. It is expected that this would be done
initially on a national level to maintain uniformity in the fuel
supply. For funkier action by the states, the granting of such
authority should be based upon a similar two-part test:
(1) states must demonstrate that their water resources are at risk
from MTBE use, above and beyond the risk posed by other gasoline
components at levels of MTBE use present at the time of the request.
(2) states have taken necessary measures to restrict/eliminate the
presence of gasoline in the water resource. To maximize the uniformity
with which any changes are implemented and minimize impacts on cost and
fuel supply, the panel recommends that EPA establish criteria for state
waiver requests including but not limited to:
a. Water quality metrics necessary to demonstrate the risk to
water resources and air quality metrics to ensure no loss of benefits
from the federal RFG program.
b. Compliance with federal requirements to prevent leaking and
spilling of gasoline.
c. Programs for remediation and response.
d. A consistent schedule for state demonstrations, EPA review, and
any resulting regulation of the volume of gasoline components in order
to minimize disruption to the fuel supply system.
---------------------------------------------------------------------------
Initial efforts to reduce should begin immediately, with
substantial reductions to begin as Soon as Recommendation 10 above--the
removal of the 2 percent oxygen requirement--is implemented.\4\
Accomplishing any such major change in the gasoline supply without
disruptions to fuel supply and price will require adequate lead time--
Up to 4 years if the use of MTBE is eliminated, sooner in the case of a
substantial reduction (e.g. returning to historical levels of MTBE
use).
---------------------------------------------------------------------------
\4\ Although a rapid, substantial reduction will require removal of
the oxygen requirement, EPA should, in order to enable initial
reductions to occur as soon as possible, review administrative
flexibility under existing law to allow refiners who desire to make
reductions to begin doing so.
---------------------------------------------------------------------------
The Panel recommends, as well, that any reduction should be
designed so as to not result in an increase in MTBE use in Conventional
Gasoline areas.
13. The other ethers (e.g. ETBE, TAME, and DIPE) have been less
widely used and less widely studied than MTBE. To the extent that they
have been studied, they appear to have similar, but not identical,
chemical and hydrogeologic characteristics. The Panel recommends
accelerated study of the health effects and groundwater characteristics
of these compounds before they are allowed to be placed in widespread
use.
In addition, EPA and others should accelerate ongoing research
efforts into the inhalation and ingestion health effects, air emission
transformation byproducts, and environmental behavior of all oxygenates
and other components likely to increase in the absence of MTBE. This
should include research on ethanol, alkylates, and aromatics, as well
as of gasoline compositions containing those components.
14. To ensure that any reduction is adequate to protect water
supplies, the Panel recommends that EPA, in conjunction with USGS, the
Departments of Agriculture and Energy, industry, and water suppliers,
should move quickly to:
a. Conduct short-term modeling analyses and other research based
on existing data to estimate current and likely future threats of
contamination;
b. Establish routine systems to collect and publish, at least
annually, all available monitoring data on:
use of MTBE, other ethers, and Ethanol,
Llevels of MTBE, Ethanol, and petroleum hydrocarbons
found in ground, surface and drinking water,
Ltrends in detections and levels of MTBE, Ethanol,
and petroleum hydrocarbons in ground and drinking water;
c. Identify and begin to collect additional data necessary to
adequately assist the current and potential future state of
contamination.
The Wintertime Oxyfuel Program
The Wintertime Oxyfuel Program continues to provide a means for
some areas of the country to come into, or maintain, compliance with
the Carbon Monoxide standard. Only a few metropolitan areas continue to
use MTBE in this program. In most areas today, ethanol can and is
meeting these wintertime needs for oxygen without raising volatility
concerns given the season.
15. The Panel recommends that the Wintertime Oxyfuel program be
continued (a) for as long as it provides a useful compliance and/or
maintenance tool for the affected states and metropolitan areas, and
(b) assuming that the clarification of state and federal authority
described above is enacted to enable states, where necessary, to
regulate and/or eliminate the use of gasoline additives that threaten
drinking water supplies.
Recommendations for Evaluating and Learning From Experience
The introduction of reformulated gasoline has had substantial air
quality benefits, but has at the same time raised significant issues
about the questions that should be asked before widespread introduction
of a new, broadly-used product. The unanticipated effects of RFG on
groundwater highlight the importance of exploring the potential for
adverse effects in all media (air, soil, and water), and on human and
ecosystem health, before widespread introduction of any new, broadly-
used, product.
16. In order to prevent future such incidents, and to evaluate of
the effectiveness and the impacts of the RFG program, EPA should:
d. Conduct a full, multi-media assessment (of effects on air,
soil, and water) of any major new additive to gasoline prior to its
introduction.
e. Establish routine and statistically valid methods for assessing
the actual composition of RFG and its air quality benefits, including
the development, to the maximum extent possible, of field monitoring
and emissions characterization techniques to assess ``real world''
effects of different blends on emissions
f. Establish a routine process; perhaps as a part of the Annual
Air Quality trends reporting process, for reporting on the air quality
results from the RFG program.
g. Build on existing public health surveillance systems to measure
the broader impact (both beneficial and adverse) of changes in gasoline
formulations on public health and the environment.
Appendix A
In reviewing the RFG program, the panel identified three main
options (MTBE and other ethers, ethanol, and a combination of alkylates
and aromatics) for blending to meet air quality requirements. They
identified strength and weaknesses of each option:
MTBE/other ethers: A cost-effective fuel blending component that
provides high octane, carbon monoxide and exhaust VOCs emissions
benefits, and appears to contribute to reduction of the use of
aromatics with related toxics and other air quality benefits; has high
solubility and low biodegradability in groundwater, leading to
increased detections in drinking water, particularly in high MTBE use
areas. Other ethers, such as ETBE, appear to have similar, but not
identical, behavior in water, suggesting that more needs to be learned
before widespread use
Ethanol: An effective fuel-blending component, made from domestic
grain and potentially from recycled biomass, that provides high octane,
carbon monoxide emission benefits, and appears to contribute to
reduction of the use of aromatics with related toxics and other air
quality benefits; can be blended to maintain low fuel volatility; could
raise responsibility of increased ozone precursor emissions as a result
of commingling in gas tanks if ethanol is not present in a majority of
fuels; is produced currently primarily in Midwest, requiring
enhancement of infrastructure to meet broader demand; because of high
biodegradability, may retard biodegradation and increase movement of
benzene and other hydrocarbons around leaking tanks.
Blends of Alkylates and Aromatics: Effective fuel blending
components made from crude oil; alkylates provide lower octane than
oxygenates; increased use of aromatics will likely result in higher air
toxics emissions than current RFG; would require enhancement of
infrastructure to meet increased demand; have groundwater
characteristics similar, but not identical, to other components of
gasoline (i.e. low solubility and intermediate biodegradability)
Appendix B
Members of the Blue Ribbon Panel
Dan Greenbaum, Health Effects Institute, Chair
Mark Buehler, Metropolitan Water District, So. California
Robert Campbell, Chairman and CEO, Sunoco Inc.
Patricia Ellis, Hydrogeologist, Delaware Department of Natural
Resources and
Environmental Conservation
Linda Greer, Natural Resources Defense Council
Jason Grumet, NESCAUM
Anne Happel, Lawrence Livermore Nat. Lab
Carol Henry, American Petroleum Institute
Michael Kenny, California Air Resources Board
Robert Sawyer, University of California, Berkeley
Todd Sneller, Nebraska Ethanol Board
Debbie Starnes, Lyondell Chemical
Ron White, American Lung Assoc.
Federal representatives (Non-Voting)
Robert Perciasepe, Air and Radiation, US EPA
Roger Conway, US Dept. of Agriculture
Cynthia Dougherty, Drinking Water, U.S. EPA
William Farland, Risk Assessment, US EPA
Barry McNutt, US DOE
Margo Oge, Mobile Sources, US EPA
Samuel Ng, Underground Tanks, US EPA
Mary White, ATSDR
John Zogorski, USGS
______
Todd C. Sneller, Member, EPA Blue Ribbon Panel--Summary of
Dissenting Opinion
In its report regarding the use of oxygenates in gasoline, a
majority of the Blue Ribbon Panel on Oxygenates in Gasoline recommends
that action be taken to eliminate the current oxygen standard for
reformulated gasoline. Based on legislative history, public policy
objectives, and information presented to the Panel, I do not concur
with this specific recommendation. The basis for my position follows:
1. The Panel's report concludes that aromatics can be used as a
safe and effective replacement for oxygenates without resulting in
deterioration in VOC and toxic emissions. In fact, a review of the
legislative history behind the passage of the Clean Air Act Amendments
of 1990 clearly shows that Congress found the increased use of
aromatics to be harmful to human health and intended that their use in
gasoline be reduced as much as technically feasible.
2. The Panel's report concludes that oxygenates fail to provide
overwhelming air quality benefits associated with their required use in
gasoline. The Panel recommendations, in my opinion, do no accurately
reflect the benefits provided by the use of oxygenates in reformulated
gasoline. Congress correctly saw a minimum oxygenate requirement as a
cost effective means to both reduce levels of harmful aromatics and
help rid the air we breathe of harmful pollutants.
3. The Panel's recommendation to urge removal of the oxygen
standard does not fully take into account other public policy
objectives specifically identified during Congressional debate on the
1990 Clean Air Act Amendments. While projected benefits related to
public health were a focal point during the debate in 1990, energy
security, national security, the environment and economic impact of the
Amendments were clearly part of the rationale for adopting such
amendments. It is my belief that the rationale behind adoption of the
Amendments in 1990 is equally valid, if not more so, today.
Congress thoughtfully considered and debated the benefits of
reducing aromatics and requiring the use of oxygenates in reformulated
gasoline before adopting the oxygenate provisions in 1990. Based on the
weight of evidence presented to the Panel, I remain convinced that
maintenance of the oxygenate standard is necessary to ensure cleaner
air and a healthier environment. I am also convinced that water quality
must be better protected through significant improvements to gasoline
storage tanks and containment facilities. Therefore, because it is
directly counter to the weight of the vast majority of scientific and
technical evidence and the clear intent of Congress, I respectfully
disagree with the Panel recommendation that the oxygenate provisions of
the federal reformulated gasoline program be removed from current law.
______
Lyondell Chemical Company--Summary of Dissenting Report
While the Panel is to be commended on a number of good
recommendations to improve the current underground storage tank
regulations and reduce the improper use of gasoline the Panel's
recommendations to limit the use of MTBE are not justified.
Firstly, the Panel was charged to review public health effects
posed by the use of oxygenates, particularly with respect to water
contamination. The Panel did not identify any increased public health
risk associated with MTBE use in gasoline.
Secondly no quantifiable evidence was provided to show the
environmental risk to drinking water from leaking underground storage
tanks (LUST) will not be reduced to manageable levels once the 1998
LUST regulations are fully implemented and enforced. The water
contamination data relied upon by the panel is largely misleading
because it predates the implementation of the LUST regulations.
Thirdly, the recommendations fall short in preserving the air
quality benefits achieved with oxygenate use in the existing RFG
program. The air quality benefits achieved by the RFG program will be
degraded because they fall outside the control of EPA's Complex Model
used for RFG regulations and because the alternatives do not match all
of MTBE's emission and gasoline quality improvements.
Lastly, the recommendations will impose an unnecessary additional
cost of I to 3 billion dollars per year (3-7 c/gal. RFG) on consumers
and society without quantifiable offsetting social benefits or avoided
costs with respect to water quality in the future.
Unfortunately, there appears to be an emotional rush to judgment to
limit the use of MTBE. For the forgoing reasons, Lyondell dissents from
the Panel report regarding the following recommendations:
The recommendation to reduce the use of MTBE substantially
is unwarranted given that no increased public health risk associated
with its use has been identified by the Panel.
The recommendation to maintain air quality benefits of RFG
is narrowly limited to the use of EPA's RFG Complex Model which does
not reflect many of the vehicle emission benefits realized with
oxygenates as identified in the supporting panel issue papers.
Therefore, degradation of air quality will occur and the ability to
meet the Nation's Clean Air Goals will suffer under these
recommendations.
______
Responses by Daniel Greenbaum to Additional Questions from
Senator Inhofe
Question 1. How many members of the Blue Ribbon Panel individually
endorsed removing the oxygenate mandate?
Response. Of the 13 members of the Blue Ribbon Panel, 11 explicitly
endorsed the removal of the oxygen mandate.
Question 2. On August 12, Carol Browner held a public briefing on
the Executive Order No. 13101 to promote the use of agricultural crops
and forestry products in developing fuels, electricity, and industrial
products. As part of this briefing, Administrator Browner said that the
Administration would not support any reopening of the Clean Air Act
that did not ``preserve all of the opportunities that exist for
ethanol.'' Is this also the position of the Blue Ribbon Panel? Is this
EPA position consistent with the Panel's recommendations?
Response. The Panel did not have the expertise nor the charge to
fully review all of the existing incentive programs for the use of
ethanol and thus did not explicitly endorse any particular approach. We
did, in recommending the lifting of the oxygen mandate (recommendation
10) state:
The panel recognizes that Congress, when adopting the oxygen
requirement, sought to advance several national policy goals
(energy security and diversity, agricultural policy, etc) that
are beyond the scope of our expertise and deliberations.
The panel further recognizes that if Congress acts on the
recommendation to remove the requirement, Congress will likely
seek other legislative mechanisms to fulfill these other
national policy interests.
Question 3. The ethanol industry has stated that it could bring
substantial new production capacity online in a short time frame. They
estimate that new capacity could be built in 3 years to meet MTBE
demand--nearly double current ethanol production. Did the Blue Ribbon
Panel reach a consensus or evaluate the ability of the ethanol industry
to replace MTBE demand within this ambitious 3 year window?
Response. The Panel did review the ability of the Ethanol industry
to increase its capacity, and concurred that there could be a rapid
increase in capacity (perhaps 20 percent) quite quickly because of
existing permitted but unused capacity. The Panel could not agree on
the timing for the industry to substantially increase its capacity
(i.e. doubling) because of questions about the ability of existing and
likely future rail and shipping infrastructure to transport the
increased volumes in a timely and cost-effective manner to the East and
West coasts.
Question 4. The report seems to imply that 20 parts per billion of
MTBE in drinking water would be cause for ``public health concern.''
What scientific evidence did the Blue Ribbon Panel examine which
indicated that 20 parts per billion of MTBE in drinking water, even if
exposed for a lifetime, causes human beings to become sick?
Response. Actually the Panel did not make a determination that
levels above 20 ppm would be a cause for public health concern. Rather,
we used that level to indicate the lower level of the advisory issued
by EPA (and also incorporated in the majority of standards in those
states that have set standards). This range--20-40 ppm--was selected by
U.S. EPA and the states based primarily on knowledge that at these
levels taste and odor concerns would arise among users, and that based
on existing evidence, adverse health effects are not likely to occur at
or below these levels.
Question 5. The Blue Ribbon Panel Report indicates that several
states have set guidelines for MTBE in drinking water under 100 parts
per billion on the basis of health concern. To your knowledge, did any
of the administrators in these states have better or more complete
scientific information regarding MTBE health effects than does the
federal EPA?
Response. The only health data which has been used by states that
was not incorporated in the EPA advisory was that used by California to
set its Water Quality Goal at 13 ppm. This was based on the study of
Belpoggi, et al cited in the Panel's report which found an increase in
leukemia/lymphoma in laboratory rats that ingested relatively high
levels of MTBE for a lifetime. Because of questions about the
interpretation of this study, neither the International Agency for
Research on Cancer, nor the National Institute of Environmental Health
Sciences (in preparing its Biannual Report to Congress on carcinogens)
felt that this study was adequate to be used for human risk assessment
purposes.
Question 6. How much of the MTBE problem in California is caused by
the recreational use of the water reservoirs?
Response. Although the Panel did not have a precise quantitative
estimate of this, by far the vast majority of the contamination in
California involved leaking underground fuel storage systems, with
perhaps a rough estimate of 10 percent of the problems involving water
craft.
Question 7. On July 27, 1999, the Blue Ribbon Panel issued its
recommendations on the use of MTBE. In the Executive Summary, the Panel
made several recommendations to enhance, accelerate, and expand
existing programs to improve the protection of drinking water supplies.
Recommendation No. 6 proposes the development of an integrated field
research program to study the groundwater behavior of gasoline and
oxygenates, including ethanol. Is it somewhat premature to promote
substitutes for MIBE until this research on oxygenates is completed?
Response. It would definitely be premature to move to other
oxygenates that are ethers (e.g. ETBE, TAME) and the Panel recommended
explicitly in Recommendation 13 that these not be placed in wider use
until fully tested. The Panel did have some water behavior information
on other alternatives to MTBE--ethanol and other components refined
from crude oil (e.g. alkylates). The other components from crude oil
clearly have characteristics that would make them less likely to
contaminate groundwater than even the existing components of gasoline.
The Panel also saw some evidence that the high biodegradability of
ethanol might cause somewhat longer plumes of benzene and other
components of gasoline--thus the recommendation for field studies--but
did not identify likely problems comparable to those experienced with
MTBE.
______
Responses by Daniel Greenbaum to Additional Questions from
Senator Boxer
Question 1. The Panel report concluded that MTBE presents a risk to
drinking water and that its use should therefore be substantially
reduced, with some members supporting a complete phase out. As a means
of dealing with this drinking water threat, the Panel prescribes this
solution:
The Panel recommends that Federal law be amended to clarify
EPA and state authority to regulate and/or eliminate gasoline
additives that threaten water supplies. It is expected that
this would he done initially on a national level to maintain
uniformity in the fuel supply. For further action by the
states, the granting of such authority should be based upon a
similar two part test: (1) states must demonstrate that their
water resources are at risk from MTBE use, above and beyond the
risk posed by other gasoline components at levels of MTBE use
present at the time of the request. (2) states have taken
necessary measures to restrict/eliminate the presence of
gasoline in the water resource.
Isn't it true that merely providing EPA and/or the states with the
authority to regulate MTBE use may lead to no change in the prevalence
of MTBE in our fuel supply?
Doesn't the requirement that states prove that MTBE is causing a
problem stand in the way of states stepping forward to take
preventative measures to deal with what the Panel has acknowledged is a
known threat?
If, as the Panel acknowledges in its report, MTBE poses a threat to
drinking water requiring that its use be substantially curtailed or
terminated, why didn't the Panel recommend that Congress take direct
action to restrict MTBE use? Isn't this the only way to ensure that
MTBE use is ``substantially reduced?''
Response. There are several factors that will likely lead to a
reduction in the use of MTBE: (1) the lifting of the oxygen mandate
(thus allowing refiners to use readily available non-oxygenated, or
less-oxygenated blends); (2) the increasing liability of refiners for
the contamination caused by MTBE (and a desire to prevent the growth of
these liabilities) and (3) active regulatory efforts by state and
federal regulators to require reduced use of MTBE. Since a number of
state have or are poised to take regulatory action, the Panel saw it as
critical that they have the clear authority to regulate constituents of
gasoline, and fully expect that with the authority they will move to
take action.
As to the need for states to show that they have taken appropriate
water protection actions before restricting use, it seemed to the Panel
that states that have already taken appropriate action to prevent leaks
should have no problem meeting these tests, while those that have not
cleaned up their underground tanks should be expected to do that before
being authorized to reduce or ban any particular part of fuel.
As to Congress taking direct action to reduce the use of MTBE, this
is of course at the discretion of Congress to enact. The Panel felt
that the details of any such reduction, because of the complex
interactions among air quality, water protection, fuel supply and cost,
and the fundamentally different groundwater situations in different
states, would not best be mandated in a ``one-size-fits-all'' manner.
Question 2. You note in your testimony that you believe the San
Francisco incident (where Tosco and Chevron were found to be adding
large amounts of MTBE to their gasoline) was ``unique.'' Do we know how
much MTBE is used in attainment areas? It was my understanding that the
only reason we discovered what was going on in San Francisco was
because private parties tested the gasoline for MTBE. In other words,
do we have a basis upon which to say whether the San Francisco incident
was truly unique?
Response. The Panel did review existing data collected for the
petroleum industry on levels of MTBE used in both RFG and non-RFG
areas, and found that in general the use of MTBE in attainment areas is
quite low, with some refiners using none, some refiners using as much
as 5-8 percent in their premium blends, and overall perhaps 1 percent
of the fuel by volume containing MTBE. The uniqueness of the San
Francisco situation comes from the fact that the California fuel
market, because of the tighter CalRFG fuel requirements, is served by
only a limited number of refineries making only California-acceptable
fuel. Because of its relative isolation, this market was particularly
vulnerable to the two refinery incidents earlier this year, resulting
in lower available fuel, and higher demand for MTBE to make up for lost
octane content.
Question 3. You note in your testimony that ``I think the general
evidence that the Panel saw and the analyses that the Department of
Energy has done . . . suggested that if you solely removed the mandate,
that economic forces probably would reduce the levels of MTBE but
continue to use it at fairly high levels, because it is a relatively
cost-effective blending component for gasoline, very high octane and
very clean.'' (Transcript at 17) By this do you mean that substantial
MTBE use may continue even if the oxygenate requirement were lifted?
Response. Yes, the analyses we saw would suggest that MTBE use
would continue at relatively high levels if left only to direct market
forces, although the DOE analysis did not factor in the growing
liability concerns of refiners mentioned in 1. above, which would
likely also drive down usage once the mandate is lifted. This is why
the Panel also called for clarification of federal and state authority
to regulate and/or eliminate MTBE use.
Question 4. You note in response to Senator Bennett's question
about the health risks associated with MTBE that ``MTBE is neither a
known human carcinogen, or even a probable human carcinogen. At this
stage it is in the `possible' category. In other words, there are some
animal tests that show that it causes cancer, but there are questions
about those tests.''
Your answer seems to imply that MTBE has been disproven to be a
known human carcinogen. Isn't it accurate to say that MTBE has not been
so designated because the scientific studies required to make that
determination simply have not been performed?
You raise questions concerning the health tests that were performed
which have found MTBE to be an animal carcinogen. Are you referring to
the Belpoggi oral exposure study?
Are you aware that the California Office of Environmental Health
Hazard Assessment reviewed that study in the context of establishing a
drinking water public health standard for MTB and determined that the
``study is valid, not critically flawed, and is consistent with
reported results'' and that the quality of the study was ``as good or
better than those typically available for chemical risk assessment.''
See Public Health Goal for Methyl Tertiary Butyl Ether (MTBE) in
Drinking Water, Office of Environmental Health Hazard Assessment,
California Environmental Protection Agency, March 1999, pp. 89-90.
Response. I was careful in my testimony to not say that MTBE has
been disproven to be a carcinogen but rather to indicate that it is
possible it is a carcinogen, but that the studies done to date have not
been deemed adequate by state, national or international bodies to
raise it into the probable or known human carcinogen category.
I was referring to two sets of questions about the animal tests of
carcinogenicity: first, that the kidney tumors seen in some of the rat
experiments may be unique to rats (and thus do not suggest human
carcinogenicity), and second, that the combining of the leukemia and
lymphoma cases in the Belpoggi study to arrive at a statistically
significant increase in cancers may not have been appropriate. I am
aware of the review of the Belpoggi study conducted by the California
OEHHA, but also of the reviews of MTBE carcinogenicity conducted by
both the International Agency for Research on Cancer (IARC), and the
National Institute of Environmental health Sciences (in preparing their
Biannual Report to Congress on Carcinogens), which concluded that the
current evidence, including the Belpoggi study, was not adequate to go
beyond the ``possible'' carcinogen category.
Question 5. I am interested to hear about why some members of the
Panel recommended ``substantial reductions'' in MTBE use, while other
members recommended a complete elimination of use.
How many members of the panel recommended a complete MTBE phase
out? What were the reasons they gave for that view?
Response. The majority of the Panel supported a substantial
reduction in MTBE use and the granting of authority to EPA and the
states to go beyond that if water protection justified the need. While
I have not polled every member for their specific reasons, most cited a
desire to reduce the risk, but continuing uncertainty as well from the
groundwater data we had seen about whether MTBE at lower, historical
levels, posed the same groundwater risks. Five of the Panel members
indicated support for phasing out MTBE altogether, largely due to a
concern that the data did not allow us to identify a safe level.
Question 6. You note in your testimony that one possible strategy
for curing the MTBE problem would be to restrict MTBE use to pre-RFG
levels (2 percent of volume). This recommendation, as I understand it,
is based in past upon the theory that we only came to see MTBE
contamination in the years following the implementation of the RFG
program.
Isn't it possible, however, that we came to see MTBE contamination
at this later time not because MTBE use had increased dramatically
after the imposition of RFG program, but because we began to replace
underground storage tanks during roughly the same time that MTBE use
was increasing? It is my understanding that we often don't discover
MTBE contamination until the tanks are removed.
Response. You are right that the interaction between the
replacement of tanks and the increased use of MTBE makes it difficult
to precisely identify what contamination was or still is occurring. My
testimony, however, was based on the USGS data presented to the Panel
and summarized in our report that showed that for the over 2,000 wells
they monitor in non-RFG areas (where MTBE has been present but at lower
levels) the rate of MTBE contamination has been identical to that of
other components of gasoline (about 2 percent).
Question 7. In any event, if we know that a relatively small amount
of MTBE can contaminate a drinking water source, how can we justify
continuing to allow any of it to be used?
Response. We know for a fact that when MTBE use is high that there
is a high probability of its contaminating water supplies. At the same
time there are a number of substances, including benzene,
trichloroethylene, and others, which are in everyday use in this
country, and which contaminate a smaller number of water supplies, yet
we have not banned their use. Rather, we have sought, when the risk is
smaller, to prevent the contamination by tighter controls on placement
and construction of underground storage systems, and by seeking, over
the long term, substitutes that can reduce their use.
Question 8. How long and how extensive is the testing for MTBE
contamination throughout the country?
Response. Contamination testing for MTBE in water supplies is about
to be extended dramatically under rules recently promulgated by EPA
under the Safe Drinking Water Act. I do not believe there is any time
limit on these testing rules, although that should be confirmed by EPA.
Question 9. Can we solve the MTBE problem by simply upgrading all
of our underground storage tanks?
Response. All but one member of the Panel felt that while it was
important to continue to upgrade underground fuel storage systems,
upgrading alone was not sufficient to protect water supplies, and thus
the Panel called for the substantial reduction of the use of MTBE, the
removal of the oxygen mandate, and the tightening of the air quality
standards to ensure continuation of the current RFG benefits.
______
Responses by Daniel Greenbaum to Additional Questions from
Senator Lieberman
Question 1. If Congress were to lift the requirement on oxygenate
content, what options does the Panel propose for retaining current air
quality performance of current reformulated gasoline blends?
Specifically, if the oxygenate requirement were lifted, how can we best
preserve the current performance level of air quality improvements as
states move to adopt the haze 2 requirements for reformulated gasoline
in the year 2000?
Response. While the Panel did not recommend any specific mechanism
for retaining current air quality performance, it did note several
approaches that could be used. Recommendation 11 notes:
There are several possible mechanisms to accomplish this. One
obvious way is to enhance the mass-based performance
requirements currently used in the program. At the same time,
the panel recognizes that the different exhaust components pose
differential risks to public health due in large degree to
their variable potency. The panel urges EPA to explore and
implement mechanisms to achieve equivalent or improved public
health results that focus on reducing those compounds that pose
the greatest risk.
Question 2. One dissenting opinion on the Blue Ribbon Panel Report
raised concerns that lifting the oxygenate requirement could lead to
increased use of aromatics. Because aromatics and alkylates can
increase volatile organic compounds (VOC) and air toxic emissions, the
dissenter suggested that the oxygenate standard is needed. What
protections could be put in place to ensure that current RFG
performance with regard to air toxic emissions levels is retained if
the oxygenate requirement is lifted?
Response. Either of the mechanisms mentioned above could be used to
ensure that the use of aromatics does not rise to a level that could
reduce air quality benefits. That could take the form, as it does in
CalRFG, of a cap on aromatics content, or of specific risk-based caps
on specific aromatics (e.g. reducing the current 1 percent cap on
benzene even further).
Question 3. Could you qualify the relative risk of MTBE compared to
the many other hazardous constituents in gasoline?
Response. In general, the cancer potency of MTBE, if it is
ultimately classified as a carcinogen, has been estimated to be lower
than that of several substances in gasoline or in automotive emissions.
Overall, the Northeast States for Coordinated Air Use Management (in a
report cited in the Blue Ribbon panel's report), estimated that
gasoline with MTBE would pose an approximately 12 percent lower cancer
risk than gasoline without MTBE.
______
Statement of Robert H. Campbell, Chairman and CEO of Sunoco, Inc.
Good Morning Mr. Chairman and members of the committee. My name is
Bob Campbell, and I am Chairman and CEO of Sunoco, Inc.--a company that
is one of the largest refiners and marketers of gasoline on the East
Coast of the U.S.
In this region, we produce and distribute more of the clean-burning
reformulated gasoline required by the Clean Air Act than any other
company. Consequently, we've learned firsthand about the benefits and
burdens of the existing RFG Program.
My company is both a manufacturer and consumer of MTBE. We have
used the chemical since the early 1980s for its high-octane properties
in our gasoline. After the 1990 Clean Air Act Amendments were enacted,
we, in partnership with others, invested nearly a quarter of a billion
dollars to build a second plant--a world scale MTBE plant to supply our
newly created additional needs for the oxygenate. Consequently, we know
about all there is to know about the use of this additive in gasoline.
We are also a major supplier of conventional gasoline in the mid-
America Region of the U.S.-Gasoline supplied from our Toledo, Ohio
refinery system. Here we do not use MTBE, but rather we are a major
buyer and blender of ethanol in gasoline. Therefore, we have extensive
firsthand knowledge of both the benefits and limitations of ethanol in
motor fuels.
Finally, through my membership on the EPA's Blue Ribbon Panel on
oxygenates, I have been totally immersed over the past several months
in the debate over the future of MTBE and ethanol in the RFG Program.
I offer this introduction so you will understand why I am very
pleased to be given the opportunity to share my experiences and
opinions with this committee.
Dr. Greenbaum has given an excellent summary of the deliberations
and the recommendations of the Blue Ribbon Panel, and I'd like to
salute Dan for his extraordinary accomplishment in moving a very
diverse, fourteen member committee through a thicket of prickly issues
to a remarkable consensus. Dan helped us develop an excellent database
and a set of recommendations that I wholeheartedly endorse.
As you know, we are now embarking on the implementation of those
recommendations--some of which require legislative action. Public
concern about MTBE in drinking water is clearly the triggering event
for the call for action. Putting aside the complex question of MTBE as
a hazard to human health, it clearly should not be getting into
drinking water. But regardless of how much money is spent on tank
replacement and inventory control, gasoline handled by 190 million
drivers will inevitably be spilled, and we now know how persistent a
contaminant in water MTBE can be.
California--as it so often does--has led the way in defining the
process for the elimination of this environmental problem. As you know,
last March Governor Davis announced a 4-year program designed to
eliminate MTBE from gasoline and yet preserve the air quality goals of
the State. Critical to the achievement of that program is relief from
the existing 2 percent oxygen mandate. I support Governor Davis'
initiative for dealing quickly with a complex and often emotional
problem.
But one needs to remember that MTBE is principally used on both the
West and East Coasts of the United States. In fact more MTBE is used in
the 11 East Coast states comprising the Ozone Transport Region than in
California (130,000 vs 100,000 barrels per day). I can assure you that
the citizens of Boston and Philadelphia are just as adamant about
protecting their drinking water as the folks in Sacramento and Santa
Monica. Consequently, my plea to you today is to help us solve the
equally serious problem of MTBE in the Northeast--and to do that we
need a regional solution.
I know and understand that California's efforts are better
coordinated than the group of East Coast States on this subject. But,
if the current proposed legislation deals only with California, I can
assure you that several of the northeastern States are poised to enact
their own local solutions. The result will be a patchwork quilt of
local initiatives or regulations. This will be a nightmare for
companies attempting to reliably supply low cost, high quality gasoline
to consumers in the 11-State region.
Before the EPA Panel published its findings and recommendations,
several northeast States initiated their own legislative solution. We
asked them to wait, and give us a chance to solve the problem
collectively rather than individually. That is why I'm here today. I
have no interest in doing anything that would delay or disrupt the
Bilbray proposal. But we on the East Coast need to use that same
legislative momentum to deal with the equally thorny problem in our
region.
The bottom line is we can solve the problem in the Northeast in a
manner similar to California only if we are also given relief from the
2 percent oxygenate mandate. If you will do that, we will be able to
continue to supply RFG to those areas requiring it, in an economic
manner, in reliable quantities, with the same air quality benefits.
That reformulated gasoline will contain substantially reduced volumes
of MTBE (the Panel called for ``substantial reduction'' not the
elimination of MTBE).
I will tell you quite honestly, that even with all our experience
in blending ethanol in gasoline in mid-America, I don't know how to
accomplish in a real world, practical manner the same result in the
northeast RFG system. Ethanol in RFG is successfully blended in the
Chicago area, because it is a relatively small proportion of the supply
from the manufacturers in that region. In my opinion, if the 2 percent
mandate remains, and we are forced to directly substitute ethanol for
MTBE in the large RFG volume area of the Northeast, we will have a
disaster scenario for both the supplier and the consumer.
My reasoning for saying that is as follows: there are two very
practical problems associated with ethanol as a blending component in
East and West Coast reformulated gasolines. The first problem is the
difficulty of adequate supply and economic transportation of ethanol
from its point of manufacture (primarily the Midwest) to where it would
be needed for blending (the East and West coasts). Because of its
affinity for water, ethanol cannot be transported in common carrier
pipelines and would have to be transported by rail or truck to both
coasts. Let me repeat here exactly what I told the Blue Ribbon Panel
this spring: Given enough time and money, an enterprising ethanol
industry can expand production and create new logistics systems to
address the problem. But the added cost will be immense and
unnecessary.
Solving the logistics problem will still not address ethanol's
second, and most critical, defect--it's high vapor pressure when
blended into gasoline. The one thing we have learned in the past 10
years is that the most crucial characteristic of a successful RFG
Program is vapor pressure or ``Volatile Organic Compound (VOC)''
control. Higher vapor pressure means increased VOC emissions which
leads to more ozone pollution. The next generation of RFG--Beginning
January 1, 2000--has even more stringent restrictions on vapor pressure
than current RFG. Consequently, blending ethanol into future RFG would
severely compound the environmental and supply problems. It is my view
that ethanol cannot be practically used on the East or West Coast in
the summertime period because of the low vapor pressure requirement and
the high percentage of RFG that must be produced in those regions.
The solution--Legislation is needed to solve the oxygenate problem
where it exists--in California, and in the ozone transport region of
the East Coast. That is where 75 percent of all the RFG in the country
is used, and where almost 90 percent of the MTBE is present in
gasoline. That is also where water quality complaints from consumers
have been most vocal. We need your help to fix what's broken. I ask you
to give these two regions three things:
The authority to regulate the use of oxygenates when water
quality impacts are substantiated.
A waiver of the 2 percent oxygenate mandate for RFG.
The requirement that no current clean air benefits be
compromised as a result of these changes to the Federal fuel program.
Congressman Jim Greenwood of Pennsylvania is attempting to advance
this precise solution in the House Commerce Committee. Prompt, parallel
action in your committee can help avoid the transportation fuel crisis
that I see on the horizon, and I urge you to move quickly.
I appreciate the opportunity to share these thoughts with you, and
I look forward to any questions you may have.
______
Sunoco, Inc.,
Philadelphia PA, November 5, 1999.
Hon. James M. Inhofe,
Hon. Bob Graham,
U.S. Senate,
Washington, DC.
Dear Senators: I appreciate the opportunity you provided me to
appear before your Subcommittee regarding the EPA's Blue Ribbon Panel
on oxygenates.
As I testified, I support the recommendation of the Panel and
consider the report to be the definitive study of the problems
associated with the oxygenated fuel program. I also agree that
congressional action is required for many of the corrections which are
needed. This is a complex issue with many implications for energy and
environmental policy, and it is certainly timely for your committee to
begin to address it. Action is needed now.
I have offered answers to the questions you sent me on the attached
sheet and I will be pleased to amplify these or address other concerns
as you see fit.
I would also like to respond to a question that was posed to me at
the hearing which I believe can be more clearly answered in a written
response. Senator Voinovich asked whether simply granting states the
authority to regulate oxygenates would solve the MTBE problem. If my
answer seemed somewhat equivocal, it is only because our discussions on
this topic during the Panel's deliberations left me believing that the
states would like some policy guidance on how to proceed. No one--state
regulators, refiners or consumers--want to create boutique, individual
state fuel formulas. Consequently, the Panel actually recommended that
what was needed was ``. . . action by Congress to clarify federal and
state authority . . .'' in this area.
I believe that a legitimate Congressional function would be to
codify the principle findings of the Panel as policy guidelines for
state actions. Congressman Jim Greenwood has begun work on an amendment
which captures this concept and clearly establishes the future roles
for EPA and the states in regulating fuel oxygenates without risking a
multiplicity of state fuel formulations. A copy of a recent draft of
this amendment is attached for your review.
Thank you again for the opportunity to testify. Please feel free to
contact me if further information is needed.
Sincerely,
Robert H. Campbell.
______
Sec. 2. State Waiver of Oxygen Requirements
Section 211 of the Clean Air Act (42 U.S.C. 7545) is amended by
adding the following new subsection at the end thereof:
``(p) Waiver of Oxygen Requirements.--
``(1) In General.--Upon the petition of any State referred to in
section 184(a), the Administrator shall waive or reduce (in accordance
with the State petition) any oxygen content requirement in effect under
subsection (k) for that State.
``(2) Action by Environmental Protection Agency.--Not later than
180 days after the date of receipt of a petition submitted under
paragraph (1), the Administrator shall grant the petition. If, by the
date that is 180 days after the date of receipt of a petition submitted
under paragraph (1), the Administrator has not granted the petition,
the petition shall be deemed to be granted.
``(3) Federal Control of Fuel Oxygenates.--The regulations under
this section shall be revised by January 1, 2001, to provide a schedule
for the reduction of the use of methyl tertiary butyl ether (MTBE) in
reformulated gasoline (as defined in subsection (k)), introduced into
commerce in any state for which a waiver or reduction is in effect and
referred to in section 184(a). By January 1, 2005 the maximum content
of MTBE by volume for all gasoline, shall be no more than 5 percent.
Reductions below this amount, or on a schedule different than that set
out by regulation, may only be authorized upon petition to the
Administrator by a state for which a waiver or reduction is in effect
under this subsection, and only upon a finding that further reduction
of MTBE use is necessary to protect human health or the environment.
``(4) Air Toxic Emission Control Enhancement Requirement.--No
manufacturer or processor of any fuel or fuel additive may sell, or
offer for sale, or introduce into commerce any reformulated gasoline
(as defined in subsection (k)) for resale in any State for which a
waiver or reduction is in effect under this subsection unless the
aggregate emissions of toxic air pollutants from baseline vehicles when
using baseline gasoline shall be reduced by an annual average of at
least 27 percent.
``(5) Assurance of Adequate Fuel Supply.--Any regulation for
modification of fuel properties in this subsection shall be consistent
with reasonable schedules for necessary refinery investment projects
and appropriate fuel distribution system modifications to assure
adequate supply for the states defined in section 184(a).
______
Responses by Robert H. Campbell to Additional Questions From
Senator Inhofe
Question 1. Are both the elimination of the 2 percent by weight
oxygen mandate and a goal of no backsliding on current air quality
levels achievable goals for the refining industry? How could this be
accomplished?
Response. Refiners can adjust to the elimination of the 2 percent
oxygenate mandate while maintaining current air quality benefits. The
experience of the industry in California is instructive. CARB
regulations for fuel composition have for years focused on emission
standards, not on government-specified formulas for various fuel
components. Given federal emission targets, refiners will individually
adjust fuel components and plant processes to produce gasoline which
can meet these requirements.
Regarding the concern about ``backsliding'' from current levels of
air toxics improvements, we would prefer that the Congress set any new
minimum standards rather than allow state-by-state results predicated
on unaudited baseline data.
Question 2. The refining industry will be facing a number of fuel
initiatives over the next few years including reducing the sulfur
content of gasoline and diesel fuel. Congressional action to remove the
2 percent oxygen mandate for RFG would provide more flexibility for the
industry to meet these challenges. In contrast, renewable fuels
mandates would place further constraints on the industry. Should
Congress and EPA provide more, not less flexibility to the refining
industry?
Response. Without question, it is preferable to have more
operational flexibility to achieve regulatory environmental goals. The
domestic refining industry is presently challenged by two serious
constraints: (1) limited capital for non-productive investment
requirements; and (2) current refinery operations at nearly 100 percent
of operating capacity. When you overlay the multiple impacts of
mandated MTBE reduction on top of the imposition of severe sulfur
reduction in gasoline, the stage is set for a ``train wreck'' in the
domestic fuel supply system absent some Congressionally--required
coordination of these schedules. The introduction of yet another,
simultaneous fuel composition change--a mandated ethanol content--will
severely exacerbate this problem.
Question 3. The Northeast States for Coordinated Air Use Management
(NESCAUM) recently released a strategy to reduce MTBE use in the
Northeast. NESCAUM recommends that EPA propose regulations to cap the
MTBE content in gasoline over a three-year period to minimize adverse
impacts. NESCAUM is very concerned that changes to gasoline formulation
be implemented with adequate lead-time to avoid supply instability and
unacceptable increases in gasoline prices. What do you think of the
proposal's three-year lead-time?
Response. We support NESCAUM's overall approach to addressing the
MTBE issue and believe that crafting a regional solution for the Ozone
Transport Region is a reasonable and achievable Congressional goal.
When coupled with a mechanism to deal with the California MTBE problem,
this two-region approach would address the geographic areas where 90
percent of all MTBE is used.
Congressman Greenwood's proposed MTBE amendment has been prepared
with ongoing input from NESCAUM. This proposal would allow for a four-
year transition period to achieve a new maximum use cap on MTBE. We
believe that 4 years may be a more realistic time frame and this view
is shared by most of the refining industry. Again, with the
simultaneous imposition of new sulfur reduction rules, more time to
comply with both of these mandates is essential.
Question 4. I understand that there are vapor pressure issues and
increased vehicle emissions associated with replacing MTBE volumes with
ethanol. What adjustments and investments would be necessary at a
refinery in order to produce gasoline for blending with ethanol?
Response. The most serious limitation with ethanol is its high
vapor pressure when mixed with gasoline. Consequently, the vehicle
emissions of smog precursors increase if MTBE is replaced by ethanol
without making any refinery changes. In order to blend ethanol into
gasoline and meet the vapor pressure specification, a refiner must
first reduce the vapor pressure of the base gasoline by distilling out
the pentane fraction. This approach can allow the final ethanol blended
gasoline to meet the vapor pressure specification, but according to
testimony at the BRP, it also reduces the amount of gasoline by about 5
volume percent. This represents not only a major reduction in the U.S.
gasoline pool, but it also eliminates the most environmentally
beneficial fraction of the refining process.
While the cost for distillation columns within a refinery is quite
significant, it only represents a portion of the total investment that
is needed in order to replace MTBE with ethanol. Significant investment
is needed at each terminal and some expenditure will be needed at each
retail site because of the necessity of splash blending ethanol near
ultimate distribution points.
By comparison however, the worst case scenario for refiners and for
consumers would be to limit or ban MTBE usage while maintaining the 2
percent oxygenate mandate. Every regulatory body which has considered
this option--EPA, CARB and NESCAUM--uniformly rejects this approach
because of unavoidable impacts on the price and supply of gasoline.
______
Statement of Michael P. Kenny, Executive Officer, California Air
Resources Board
Thank you, Chairman Inhofe and members of the subcommittee for
holding today's hearing on The Report of U.S. EPA's Blue Ribbon Panel
on Oxygenates in Gasoline. As the California state representative on
the panel, I am pleased to be here on behalf of Governor Gray Davis,
the California Environmental Protection Agency and the California Air
Resources Board to discuss our state's perspective on the report and
its findings.
As the report noted, California has its own reformulated gasoline
program, which was established by the Air Resources Board to deal with
California's unique air-quality problems. California's RFG program
differs from the federal program in a number of ways.
Most notably, the California program contains limits on the sulfur
and aromatic content of gasoline, while the federal program does not.
California's program also utilizes a predictive model that enables
refiners to market innovative fuel formulations that vary from
California's gasoline specifications, as long as refiners can
demonstrate using the model that the formulations provide the required
air-quality benefits.
The California RFG program has been an unqualified success.
Analyses of weather data and air pollution levels indicate that,
following its introduction in 1996, California RFG reduced peak ozone
levels in Los Angeles by about 10 percent. Airborne benzene levels
throughout California decreased by 50 percent.
California RFG reduces smog-forming emissions from motor vehicles
by 15 percent, and it reduces cancer risk from exposure to motor
vehicle toxics by about 40 percent. These are about twice the air-
quality benefits produced by Phase 1 Federal RFG, and they still exceed
somewhat the benefits of Phase 2 Federal RFG, which will be introduced
in much of the country in January 2000.
Unfortunately, the continuing controversy over MTBE has
overshadowed the success of California RFG. Two California cities,
Santa Monica and South Lake Tahoe, have seen their domestic water
supplies decimated by MTBE contamination, and MTBE has been found in
groundwater at several thousand leaking underground tank sites in
California. But, as the Blue Ribbon Panel report emphasized, MTBE
contamination is truly a national problem. The USGS/EPA Northeastern
study found that MTBE is detected 10 times more often in community
drinking-water systems in areas using oxygenated fuels than in areas
using non-oxygenated fuels.
California took its own proactive steps to remedy its MTBE problem
this past March, when Governor Davis declared MTBE to be an
environmental risk and ordered its elimination from California gasoline
by the end of 2002. Governor Davis followed the recommendation of a
comprehensive assessment of MTBE by the University of California.
We are extremely pleased with the Blue Ribbon Panel's
recommendations for a substantial reduction of MTBE use, and for a
clarification of both federal and state authority to eliminate the use
of additives that threaten drinking water supplies. Both
recommendations back up Governor Davis' order. However, perhaps the
single most crucial factor affecting California's ability to eliminate
MTBE use is the federal 2 percent oxygen requirement. The Blue Ribbon
Panel's recommendation for the elimination of that requirement is
absolutely critical for both the environmental and economic well-being
of California. I would like to discuss this recommendation in more
detail.
California does not believe that there is a technical or scientific
basis for requiring the addition of oxygen to gasoline. Oxygenates are
an important tool for making reformulated gasoline, and in general,
oxygenates should remain an option that is available to refiners. But
there is absolutely no reason to mandate them. It is possible to make
both California and federal reformulated gasoline without oxygen, and
it is much more cost-effective to let each refiner decide for itself
whether to use oxygenates.
About 70 percent of the California gasoline market is subject to
the federal 2 percent oxygen rule. In the other 30 percent of the
market, at least three refiners have produced and sold non-oxygenated
gasoline that provides all the air-quality benefits required of
California RFG. In 1998, a substantial amount of the remaining gasoline
in that market contained less than 2 percent oxygen. The Blue Ribbon
Panel report pointed out that California's predictive model, along with
its sulfur and aromatics requirements, ensure that non-oxygenated
formulations developed by refiners provide the same air-quality
benefits as standard California RFG formulations.
The same cannot be said of Phase 1 Federal RFG--the Blue Ribbon
Panel report notes the concern that the elimination of oxygenates could
cause a backsliding of benefits due to the higher use of aromatics.
There is a need for U.S. EPA and the Congress to address this issue,
but please understand: It does not apply to California. California has
shown that it can deliver the full benefits of its world-leading RFG
program without an oxygen requirement of any kind.
The federal oxygen rule has awkwardly bifurcated California into
two states.
In San Francisco, which is not subject to the requirement, it is
possible to buy non-oxygenated gasoline. This non-oxygenated gasoline
is California RFG; it meets all our requirements. However, if an oil
company were to try to sell that gasoline two hours up the highway in
Sacramento or six hours away in Los Angeles, it would be in violation
of federal law even though the non-oxygenated gasoline provides the
same air-quality benefits as the oxygenated gasoline mandated in
Sacramento and Los Angeles.
Once MTBE is eliminated in California, the only feasible oxygenate
will be ethanol. If the 2 percent oxygen rule remains in effect,
ethanol will be effectively mandated in 70 percent of California
gasoline. California welcomes the prospect of increased ethanol use
that will almost certainly occur even without a federal mandate. The
continuance of an oxygen requirement in California, however, raises
serious economic questions.
In just 3 years, California would need about half of the amount of
ethanol as the amount currently produced in the midwestern states. The
Blue Ribbon Panel report acknowledges the large investment in
infrastructure that would be needed over the next 3 years to meet this
large demand. There is a cost to this:
The California Energy Commission estimates that the elimination of
MTBE would add 6 to 7 cents a gallon to gasoline costs if the oxygen
requirement remains in effect. This would amount to an average cost of
$40 per year per California motorist, or $840 million per year to
California motorists as a whole. Elimination of the requirement would
allow gasoline costs to remain stable and possibly decrease by one cent
a gallon. It is patently unfair--and makes no economic sense--to saddle
California motorists with this extra $840 million cost, particularly
because it would not even buy a single pound of additional air-quality
benefits.
Let me be absolutely clear: This is not an ethanol issue. It is
about the free marketplace. We expect ethanol to gain a new importance
in California. But the market--not federal rules--should determine how
much ethanol is used in California. In addition to the economics, it
also is a matter of common sense. We have seen what happened when
California and the nation in general became too dependent on a single
additive, MTBE. Why should California simply trade its dependence on
MTBE for an identical dependence on ethanol, when we can have a diverse
and stable RFG marketplace featuring a range of ethanol-based and non-
oxygenated formulations?
This past spring, California asked U.S. EPA for a waiver from the 2
percent oxygen requirement. We have exchanged technical correspondence
with U.S. EPA on this issue and we are still awaiting their decision.
At the same time, California continues to support legislation by
Senator Feinstein and Representative Brian Bilbray (S. 266/H.R. 11)
that, at the very least, would exempt California and possibly other
states from the requirement.
I urge the committee to support the Blue Ribbon Panel's
recommendation to eliminate the 2 percent requirement, and I especially
urge you to support legislation that would provide California with an
early exemption from that requirement. Refiners need to make decisions
regarding plant modifications needed to produce non-MTBE gasoline by
the end of 2002. Bear in mind that refinery modifications can take 2\1/
2\ to 3 years or longer to complete--environmental reviews and
permitting typically take 12 to 18 months, engineering work takes 6 to
12 months, and construction can take 12 to 24 months. In order to
complete these plant modifications within 3 years, refiners need to
know now whether they will have to continue to use 2 percent oxygen or
have the flexibility to produce non-oxygenated formulations.
In closing, I would like to emphasize that California has the need
and the capability to produce RFG without an oxygen requirement.
As an arid state, we are more dependent than most other states on
our groundwater resources, and we have an RFG program in place that can
ensure the use of non-oxygenated fuel without sacrificing air-quality
benefits.
Thank you once again for providing me with the opportunity to
testify here today.
______
Responses of Michael Kenny to Additional Questions from Senator Inhofe
Question 1. I understand this past July the California Energy
Commission recommended Governor Davis not to advance the removal of
MTBE from California's gasoline any earlier than December 31, 2002.
They also asked that this date not apply to downstream locations such
as pipelines, terminals and service stations. These downstream
locations should have a later MTBE-free compliance date. CEC listed
several reasons, including time for refinery modifications and terminal
modifications to add ethanol-blending facilities. What is your reaction
to this schedule? Is it appropriate, unnecessarily long, and too short?
Response. We agree with the CEC report, which recommended the
staged approach that was used for the implementation of California
Phase 2 Reformulated Gasoline (CaRFG2) in 1996. That approach allowed
an additional 90 days from the compliance date at the refinery to the
compliance date at the service station. This is precisely what we are
proposing in the California Phase 3 RFG (CaRFG3) regulations which will
be considered for adoption by the ARB on December 9, 1999. (The staff
report has been publicly available since October 22, 1999.)
Question 2. I understand that CARB has raised air quality concerns
about replacements for MTBE. What are your concerns?
Response. The air quality concerns raised by the ARB staff were
presented in a letter dated July 9, 1999 to Mr. Robert Perciasepe,
Assistant Administrator for Air and Radiation, U.S. EPA. These concerns
were further explained in a letter dated September 20, 1999 to Ms.
Margo Oge, Director, Office of Mobile Sources, U.S. EPA. Both letters
are attached. Basically, as explained in the letters, more air quality
benefits can be attained after the elimination of the use of MTBE, if
the two weight percent oxygen requirement for federal reformulated
gasoline is removed.
Specifically, for the use of ethanol as a replacement for MTBE, the
use of ethanol in RFG results in an increase in volatility that must be
offset to avoid the loss of emission benefits. This would mean that all
pentanes would have to be removed at a significant cost. In my
testimony I had indicated that the cost would be about 6 cents per
gallon. Upon further evaluation, we now estimate the cost to be no more
than 3 cents per gallon.
Question 3. If EPA granted California's request for a waiver of the
2 percent by weight oxygen content requirement for federal RFG, would
the state's concerns with MTBE be eliminated? What is the status of the
waiver request at the Agency? Why is it taking so long?
Response. The concerns with MTBE do not change with a waiver from
the federal RFG oxygen requirement. A waiver from the oxygen mandate in
federal RFG sold in California would provide the most expeditious and
least-costly phase-out of MTBE in California.
The regulatory mandate imposed by the U.S. EPA pursuant to the
federal Clean Air Act requires that federal RFG contain at least 2.0
percent by weight oxygen year-round. About 70 percent of all gasoline
sold in California is subject to the federal reformulated gasoline
requirements.
The CaRFG2 requirements result in greater emission benefits than
federal RFG, but do not require a minimum concentration of oxygen in
all gasoline. Application of the current minimum oxygen content
requirement serves no essential purpose in meeting California's air
quality goals to reduce ozone and particulate matter precursors, and
toxic pollutant emissions, from vehicles. The results of the University
of California study, a National Research Council study, and a U.S. EPA
Blue Ribbon Panel report all support the position that oxygen is not
necessary for reformulated gasoline to provide the same or better ozone
benefits as gasoline containing oxygen.
The request for a waiver is currently being evaluated by the U.S.
EPA. Although it is crucial to hear as soon as possible, we have no
information on when a decision will be made.
Question 4. Related to this issue, I understand that last Thursday
an amendment was added to H.R. 11, a reformulated gasoline bill that is
specific to California, in the House Health and Environment
Subcommittee. This amendment purported to maintain the air quality
benefits of reformulated gasoline if the oxygen content mandate is
lifted. Does CARB believe that such an amendment was needed? Do you
believe that this amendment improved CARB's ability to develop new
gasoline formulations to improve air quality, or tied its hands by not
only telling you what the goal would be for the gasoline formulation,
but also prescriptive requirements on how to do it?
Response. The amendment would have little impact in California
because Senate Bill 989 (Sher), signed by Governor Davis on October 10,
1999, already requires the ARB to ensure that the CaRFG3 regulations
maintain or improve upon emissions and air quality benefits achieved by
CaRFG2 as of January 1, 1999--both for ozone precursors identified in
California's ozone SIP, and for air toxic compounds. These are the same
emissions targeted by the federal RFG program.
Question 5. In your testimony, you mention that it is possible to
make California reformulated gasoline without oxygen. Is it feasible to
increase the production of such non-oxygenated RFG without providing
refiners more regulatory flexibility?
Response. Currently, some gasoline is sold in California without
oxygen in areas of the state not subject to the federal RFG
requirements. In the short term, it is not feasible to substantially
increase production of non-oxygenated gasoline if the federal oxygen
mandate requires oxygen to be used in 70 percent of the state's
gasoline. We expect that the production of non-oxygenated gasoline
would increase substantially in the near term with a waiver from the
federal RFG oxygen requirement. The proposed CaRFG3 regulations would
also improve compliance flexibility and would significantly reduce the
loss in production associated with the loss of MTBE as a blending
component.
Question 6. Is it true that refiners have said that it is not cost-
effective to expand production of non-oxygenated RFG without adding
greater flexibility to the fuel regulations? Have you assessed the air
quality impacts of affording refiners this greater flexibility?
Response. Eliminating MTBE from California gasoline will result in
a loss in gasoline production, and additional flexibility would
mitigate the loss in volume, therefore lowering the overall cost of
compliance.
In developing its CaRFG3 proposal, the staff was sensitive to the
loss in production volume, and some of the proposed changes to the
CaRFG3 specifications were made to help refiners recover volume.
Specifically, the proposed increase to the T90 and T50 specifications
were made to provide refiners with flexibility to increase gasoline
production. The staff was able to provide this flexibility while
preserving the emission benefits of the current program because of the
proposed tightening of the specifications for sulfur and benzene.
The emission benefits of the proposed CaRFG3 regulations are
described in the responses to questions 7 and 9.
Question 7. More specifically, the ARB draft specifications propose
relaxing five of eight categories of regulated fuel parameters. Does
your analysis of non-oxygenated RFG, which concludes that such fuel can
provide the same air quality benefits as oxygenated fuels include a
consideration of the environmental impacts of relaxing these
parameters?
Response. Our analysis fully considers the impacts of the proposed
CaRFG changes. The following table provides a summary of the current
CaRFG2 and proposed CaRFG3 standards.
Table 1.--Current and Proposed CaRFG Property Limits
----------------------------------------------------------------------------------------------------------------
Flat Limits Averaging Limits Cap Limits
Property -----------------------------------------------------------------------------
CaRFG 2 CaRFG 3 CaRFG 2 CaRFG 3 CaRFG 2 CaRFG 3
----------------------------------------------------------------------------------------------------------------
RVP, psi, max..................... 7.0 7.0(1) none none 7.0 6.4-7.2
Benzene, vol. %, max.............. 1.00 0.80 0.80 0.70 1.20 1.10
Sulfur, ppmw, max................. 40 20 30 15 80 60/30(2)
Aromatic HC, vol. %, max.......... 25 25 22 22 30 35
Olefins, vol. %, max.............. 6.0 6.0 4.0 4.0 10 10
Oxygen, wt. %..................... 1.8 to 2.2 1.8 to 2.2 none none 0-3.5 0-3.5(3)
T50 F, max........................ 210 211 200 201 220 225
T90 F, max........................ 300 305 290 295 330 335
Driveability Index................ none 1225 none none none none
----------------------------------------------------------------------------------------------------------------
\1\ Equal to 6.9 psi if using the evaporative element of the Predictive Model.
\2\ 60 ppmw will apply 12/31/2002; 30 ppmw will apply 12/31/2004.
\3\ 3.7 wt% if gasoline contains no more than 10 vol % ethanol.
For each batch of gasoline being shipped from a refinery, a refiner
can choose to meet the flat or averaging limits for each property shown
in the table. But most refiners comply by using the California
Predictive Model, which was developed from thousands of emissions data
points generated in tests evaluating the emissions impacts of gasoline
properties. A refiner using the Predictive Model selects a set of
alternative specifications for the regulated properties, never
exceeding a cap limit and indicating whether each alternative limit is
a flat or averaging limit. The Predictive Model compares the emissions
performance from these alternative limits with the emissions
performance from the corresponding limits in the table above. The set
of alternative specifications is only allowed if the Predictive Model
shows there will be no increase in emissions of HC, of NOX,
and of potency-weighted toxics compared to emissions from the limits
specified in the regulations. For instance, a refiner might identify a
less stringent aromatics limit in conjunction with a more stringent
sulfur limit, so that the HC reductions associated with the sulfur
limit offset the HC increase from the change in aromatics. Under the
Predictive Model, gasoline formulations meeting the HC, NOX
and toxics emissions criteria are allowed whether the oxygen is zero or
3.5 wt.%--except when oxygenates are mandated in greater Los Angeles in
the winter.
As can be seen from the table, the CaRFG3 proposal would lower the
flat, averaging and cap limits for two properties (sulfur and benzene)
and raise the flat, averaging and cap limits for two other properties
(T50 and T90). The aromatics cap would go up, but there would be no
change in the aromatics flat and averaging limits. There would be no
change for olefins, essentially no change for oxygen, refiners could
vary RVP using the Predictive Model for the first time, and a new
Driveability Index flat limit would be added.
The increases in stringency for sulfur and benzene in CaRFG3 would
offset the relaxations for T50 and T90. The CaRFG3 Predictive Model can
be used to directly compare the emissions impact of the CaRFG2 flat
limits with the CaFRG3 flat limits. This comparison shows the CaRFG3
specifications reduce NOX by 3.3 percent, exhaust
hydrocarbons by 0.9 percent, and potency-weighted toxics by 1.1
percent. This translates to additional reductions of 4 tons per day of
hydrocarbon and 27 tons per day of NOX, compared to the
CaRFG2 requirements. Furthermore, our analysis of effects on other
media in our staff report concludes that there are no substantial
adverse effects associated with the compounds expected to be used to
replace MTBE.
Question 8. You stated in your testimony that the concerns about
backsliding and aromatics do not apply to California. Does that mean
that non-oxygenated RFG in California will not contain higher aromatic
levels in comparison to oxygenated RFG? Could you explain in detail how
the effects of non-oxygenated RFG are different for California?
Response. Unlike other states, California imposes a specific limit
on aromatics content as part of the CaRFG standards. Following
elimination of the federal RFG oxygen mandate, the CaRFG aromatics
limits would continue to apply in California. As indicated in the
response to the previous question, the proposed CaRFG3 flat and
averaging limits for aromatics are the same as the current CaRFG2
limits. The ARB is proposing a limited relaxation of the cap limit for
aromatics, and this means refiners using the Predictive Model could
identify a higher alternative aromatics limit under CaRFG3 than they
can now under CaRFG2. However, refiners can only identify the higher
aromatics level if they simultaneously make sufficient reductions in
the alternative limits for other properties for the Predictive Model to
show there will not be an overall increase in HC, NOX, and
potency-weighted toxics emissions. The question of potential
backsliding for the gasoline actually sold in the state is addressed in
the response to the next question.
Question 9. Are there backsliding issues for non-oxygenated RFG
related to fuel parameters other than aromatics? For instance, what are
the emissions impacts of the increased levels of toxics in non-
oxygenated RFG? What are the emissions impacts of higher olefin levels
in such fuel? What are the overall air quality impacts of increased CO
emissions from non-oxygenated RFG? Are these issues included in your
analysis?
Response. As discussed above, refiners using the California
Predictive Model can only apply alternative specifications that the
Model shows will achieve reductions in emissions of HC, NOX
and toxics that are essentially equivalent to the emissions reductions
from the flat and averaging limits in the regulation. Any specification
changes that increase potency-weighted toxics will have to be offset by
other changes that achieve an equivalent reduction. Additionally, the
proposed CaRFG3 Predictive Model will account for the contribution of
CO emissions make towards ozone formation.
In making sure that the CaRFG3 proposal is consistent with the
anti-backsliding requirements of Senator Sher's SB 959, we compared
emissions from 1998 average California gasoline to emissions from
gasoline formulations we expect to be produced under the CaRFG3
proposal. These projected CaRFG3 formulations included gasoline with
oxygen at different levels and with no oxygen, and reflected the same
compliance margins as were seen in 1998 gasoline. Table 2 shows the
results of the staff 's analysis. Note that as oxygen is increased,
NOX benefits decrease. The zero oxygen fuel provides almost
5 percent greater emissions reductions (about 38 additional tons per
day) over a fuel with 3.5 percent oxygen.
For hydrocarbons, the difference between the fuels is similar when
accounting for the CO reduction from the oxygenated fuel as equivalent
evaporative hydrocarbon emissions. The data further demonstrate that
the federal RFG minimum oxygen mandate precludes the use of fuels that
do not contain oxygen and achieve greater emission benefits,
principally in terms of NOX reductions.
Table 2.--Expected Change in Emissions (2005) 1998 Average In-Use Fuel Versus Three Fuels Based on Alternative
Specifications Using the Proposed CaRFG3 Predictive Model
----------------------------------------------------------------------------------------------------------------
2.7 Percent 3.5 Percent
1998 In-Use Zero Oxygen Oxygen [In Oxygen [In
Fuel [In percent] percent] percent]
----------------------------------------------------------------------------------------------------------------
NOX............................................. 0.3% -5.4% -1.7% -0.7%
Hydrocarbons:
Exhaust....................................... -3.6 -1 .7 -6.0 -6.0
Evaporative................................... -6.6 -12.6 0 0
Carbon Monoxide................................. 0 0 -4.2 -8.9
Toxic \1\....................................... -7.9 -14.7 -15.6 -15.7
----------------------------------------------------------------------------------------------------------------
\1\ Potency weighted.
The reduction in NOX benefits as oxygen is increased
stems from the fact that a refiner using the Predicitve Model must
simultaneously achieve the necessary emissions performance for HC,
NOX and potency-weighted toxics. When oxygenates are not
used, the greatest challenge presented by the CaRFG3 standards will
typically be the need to achieve equivalent HC emissions reductions.
The formulations that are most cost-effective in meeting HC equivalency
will achieve somewhat greater reductions in NOX and toxics
than are required under the Predictive Model. This is not the case when
oxygenates are used, because of the NOX increases associated
with oxygen.
Table 2 also shows that the oxygenated fuels have lower CO
emissions than the non-oxygenated fuel. However, CO attainment is a
problem in the winter only and the Clean Air Act addresses CO
attainment in the wintertime oxygenate requirements of Section 211 (m)
rather than in the Section 211 (k) federal RFG program. Both the CaRFG2
and the CaRFG3 regulations mandate oxygen in the wintertime in the
southern California CO nonattainment areas, and these requirements
cannot be eliminated without U.S. EPA approval of a SIP revision.
Question 10. ARB's analysis of the CEC study maintains that there
is a considerable cost to consumers attributable to fuels oxygenated
with ethanol (6-7 cents). Is that a short- or long-term price impact?
How do the long-term scenarios compare for ethanol and non-oxygenated
RFG?
Response. The CEC estimate of six to seven cents per gallon is
based on an intermediate-term analysis (approximately 3 years). The CEC
has also defined a long-term period to be six years. More importantly,
this long-term period allows for the same supply and demand balances to
be achieved as in the intermediate-term, but allows refiners to make
major process unit modifications such as equipment replacement or
capacity expansions. The CEC estimates that the costs associated with
the replacement of MTBE with ethanol during this period range from 2 to
3 cents per gallon. For the non-oxygenated gasoline case, the range is
0.9 to 3.7 cents per gallon. The long-term analysis is the most
pertinent because this is what is happening with the elimination of
MTBE in California under the proposed CaRFG3 program.
Question 11. The CEC report also says that ``[i]f the scope of
replacing MTBE were to be broadened to include the elimination of all
oxygenates from gasoline, the cost impact for consumers would be the
greatest, regardless of the length of time allowed for the
transition.'' How does this affect the ARB analysis for non-oxygenated
RFG and pump prices? How can we be assured that refiners will use just
enough ethanol and just enough non-oxygenated RFG to keep prices from
spiking, particularly considering that it might not be in the refiners
best interest to find that balance?
Response. The CEC report states that the cost would be greatest if
all oxygenate were eliminated from gasoline, but following that
statement, the report states that the long-term cost would be at the
high end of the range (up to 3.7 cents per gallon). This is one cent
higher than the high estimate for using ethanol to replace MTBE. The
low end of the range is also one cent lower than the ethanol case.
There is a big difference between eliminating the oxygen mandate
and imposition of a ban on all oxygenates. It is important for refiners
to have the flexibility to use an oxygenate (expected to be ethanol)
where it makes economic sense to do so. Providing flexibility will not
guarantee that prices will not spike during times when supply shortages
occur. Flexibility should lower the average cost of producing fuel, and
enable supply shortages to be remedied more quickly.
If there were no oxygen requirement, our discussions with refiners
have led to the conclusion that some gasoline would be made with
ethanol and some would not. This would reduce California's dependence
on ethanol and would improve refiners' ability to use other gasoline
blendstocks.
In the event of a supply disruption of ethanol or other gasoline
blendstocks, refiners would have more options to produce gasoline. With
more options available, the likelihood of a price spike and the
severity of the spike would be reduced.
Question 12. Could you address ARB's recent Urban Airshed Modeling
which demonstrates that non-oxygenated fuels result in higher ozone and
CO emissions than oxygenated fuels, and will result in backsliding?
Response. There was an error in the draft analysis. The error was
in the assumptions made for the compositions of the non-oxygenated fuel
and the 5.7 percent ethanol fuel that affected the prediction of ozone,
but did not substantially affect the performance relative to toxic
compounds of interest.
The errors in the fuel composition have since been corrected and
the results now show that there are no significant differences in ozone
forming potential between oxygenated and non-oxygenated gasoline. The
analysis was based on CaRFG2 fuels and not CaRFG3 fuels. These results
are consistent with the findings of the U.S. EPA Blue Ribbon panel and
the NRC that there are no statistically significant differences in
ozone forming potential when comparing different reformulated
gasolines.
It also shows, as we expect, that CO emissions are lower with an
oxygenated fuel. As discussed earlier, the wintertime oxygen
requirement would still apply in the South Coast as long as it remains
in non-attainment of the ambient air quality standards for CO.
______
Air Resources Board,
Sacramento, CA, July 9, 1999.
Mr. Robert Perciasepe,
Assistant Administrator for Air and Radiation,
U.S. Environmental Protection Agency,
Washington, DC.
re: support materials for california's request for a waiver from the
requirement that federal rfg contain at least 2 percent oxygen year-
round
Dear Mr. Perciasepe: I am attaching a set of supplemental materials
in support of California's request for a waiver under Clean Air Act
section 211 (k)(2)(B) from the requirement that federal reformulated
gasoline contain at least 2.0 volume percent oxygen year-round. This
waiver request was made in Governor Davis's April 12, 1999 to
Administrator Carol Browner. The materials I am now transmitting are
identical to the materials I gave you on June 21, 1999, except that
Attachment 1 has been updated to reflect the emissions comparison based
on the federal complex model.
I believe that our analysis presents a substantial and compelling
justification for the requested waiver. Please call me at (916) 445-
4383 if you have any questions. Your staff can address any questions to
Dean Simeroth at (916) 322-6020 on technical issues, and to Tom
Jennings at (916) 323-9608 on legal issues.
Sincerely,
Michael P. Kenny.
______
Basis for a Waiver From the Federal RFG 2.0 Percent Oxygen Requirement
For California As Authorized in CAA Sec. 211(k)(2)(B)
California believes that U.S. EPA can and should waive the year-
round 2.0 percent by weight (wt.%) oxygen requirement for federal
reformulated gasoline (RFG) in each of California's three federal RFG
areas. This waiver is justified by the technical analysis of the
California Air Resources Board (ARB) that maintaining the federal 2.0
wt. percent oxygen requirement after MTBE has been phased out of
California gasoline will diminish the extent to which the California
RFG regulations can achieve emission reductions over and above the
reductions achieved by the federal program. This loss of additional
benefits from the California program will interfere with attainment of
the national ambient air quality standards for ozone, PM10
and PM2.5 in California's federal RFG areas.
Because California faces the most intractable air pollution
problems in the nation, the ARB has designed the California RFG (CaRFG)
program to achieve significantly greater overall emission reductions
than those resulting from the federal RFG program. ARB is now
developing its Phase 3 CaRFG rules. This is being done to eliminate the
State's reliance on MTBE--which has been found to present an
unacceptable threat to water supplies--and to enhance the emission
reductions that the CaRFG program contributes to the State
Implementation Plan (SIP). ARB's assessment shows that revised
California rules accommodating a federal RFG requirement for 2.0 wt.
percent oxygen in the fuel year-round will necessarily be less
effective in reducing vehicular emissions than would be the case if the
rules could be based on oxygen-content flexibility. This loss of
additional potential emission reductions from CaRFG would delay
attainment of the ozone standards in all three of California's federal
RFG areas, and threaten eventual attainment of the ozone and
PM2.5 standard in the Los Angeles region.
The CAA Sec. 211(k)(2)(B) waiver provision.--CAA Sec. 211(k)(2)(B)
expressly authorizes U.S. EPA to waive the federal RFG year-round 2.0
wt. percent minimum oxygen requirement, in whole or in part,
. . . upon a determination by the Administrator that
compliance with such requirement would prevent or interfere
with the attainment by the area of a national ambient air
quality standard.
California's need for additional emission reductions in its three
federal RFG areas. The emission reductions from the CaRFG program are
critical to attainment of the national ozone standards, and are
essential to compliance with the PM10 and PM2.5
standards. California needs to add measures to its ozone SIP to assure
attainment, and any loss of reductions of NOX or ozone-
forming hydrocarbons will interfere with the timely attainment of both
the ozone standards.
Additional emission reductions achieved by the CaRTG rules.--The
current CaRFG rules, which have been applicable since 1996, require
reductions in emissions of NOX and toxics that are
substantially greater than the emissions reductions that will be
required by the federal RFG Phase II rules that apply starting January
2000. Attachment 1 provides a comparison of the emission benefits of
the two sets of rules, based on application of U.S. EPA's Complex
Model. The NOX emissions reductions from the California
program are more than twice the reductions required by federal RIG
Phase II--the CaRFG rules achieve an additional overall NOX
reduction of 8 percent. The toxics emissions reductions from the
California program, on a potency-weighted basis, are about 20 percent
greater than the corresponding emissions reductions from federal RFG
Phase II. The VOC emission reductions required by the two programs arc
roughly equal.
alternative scenarios for phase 3 carfg
On March 26, 1999, Governor Davis issued Executive Order D-5-99,
which outlines California's action plan for removing MTBE from all
California gasoline by December 31, 2002 at the latest. California is
phasing out MTBE because of the threat it presents to the State's
groundwater, surface water, and drinking water systems. ARB has
initiated in Phase 3 CaRFG rulemaking with two fundamental objectives
in mind--to make the total removal of MTBE from the State's gasoline
feasible and practical, and to preserve or enhance the emission
reductions achieved by the existing program after the phaseout of MTBE.
The Phase 3 CaRFG regulations will ultimately be implemented in one
of two
distinctly different regulatory environments. In one, the year-round
2.0 wt. percent oxygen requirement would continue to be mandated by the
federal RFG regulations, applicable to about 70 percent of all of
California's gasoline. In the other regulatory environment, affirmative
action on California's waiver request by U.S. EPA--and/or action by
Congress--would allow for oxygen flexibility. ARB technical staff have
analyzed likely scenarios for a Phase 3 CaRFG program under the two
environments and the results of this analysis are contained in
Attachment 2.
If the federal RFG 2.0 wt. percent oxygen mandate is maintained
after the phase-out of MTBE, it is clear that ethanol would be the only
practical oxygenate. Three scenarios have been identified: (1) No use
of MTBE and federal oxygen flexibility;
(2) No use of MTBE and a federal RFG 2.0 wt. percent oxygen mandate met
by 5.7 vol. percent ethanol; and (3) No use of MTBE and a federal RFG
2.0 wt. percent oxygen mandate met by 10 vol. percent ethanol. For each
scenario, staff started with a hypothetical gasoline meeting all of the
``flat'' limits in the current CaRFG regulations. The staff next
identified the changes in gasoline properties that refiners would
necessarily have to make under the scenario, and identified the
emissions impact of these changes. The staff then identified potential
changes to the CaRFG standards that could be made to preserve the
emissions benefits of the current program and to enhance those benefits
to the extent feasible. Staff evaluated the feasibility of these
changes to the CaRFG standards and their overall emissions impact. The
underlying details supporting the analyses are attached.\1\
---------------------------------------------------------------------------
\1\ The California Predictive Model was used for projecting exhaust
emissions impacts and the Complex Model was used for evaporative
emissions. The Predictive Model is the tool in the CaRFG regulations
for allowing alternative CaRFG formulations that achieve equivalent
exhaust emissions reductions. It is more useful than the federal
Complex Model in determining the future emissions impacts of California
gasoline for purposes of CAA Sec. 211(k)(2)(B) waiver analysis, because
the underlying fleet more closely represents the future California
fleet. As required under CAA Sec. 211(k)(10)(A), the Complex Model is
based on representative 1990 vehicle technology. This limitation is not
present in the oxygen waiver provision. The Predctive Model does not
have an evaporative emissions element because the CaRFG limit for RVP--
the parameter affecting evaporative emissions--is not allowed to vary.
---------------------------------------------------------------------------
The analyses of the scenarios demonstrate that California's ability
to have oxygen flexibility should result in technologically feasible
increased reductions of NOX of 1.5 percent and toxics of 2.5
percent for CaRFG after the phase-out of MTBE. The scenarios for using
ethanol to meet a federal RFG 2.0 wt. percent year-round oxygen mandate
show that essentially all pentanes would have to be removed from
gasoline just to preserve the existing hydrocarbon benefits. Also,
taking sulfur down to zero--compared to 10 ppm for the oxygen
flexibility scenario--still does not achieve the same NOX or
toxics reductions. Additional changes to other CaRFG specifications
would have to be made to provide these benefits. For 10 percent
ethanol, it simply may not be possible at any cost to achieve the same
benefits as the oxygen flexibility scenario. Finally, the zero sulfur
requirement in both of the ethanol scenarios will make imports
difficult if not possible.
The loss of NOX benefits that would result from
maintenance of the federal RFG 2.0 wt. percent oxygen mandate would
prevent or interfere with attainment of the federal ozone,
PM10 and PM2.5 ambient standards in California's
federal RFG areas. There is accordingly a sound technical and legal
basis for U.S. EPA to waive the federal RFG year-round 2.0 wt. percent
oxygen requirement for California's federal RFG areas. However, because
the use of oxygen during the winter months does not threaten ozone
attainment, it may be possible to retain a lesser oxygen averaging
requirement. A waiver that retains an oxygen requirement of 2 wt.
percent for the four winter months which is approximately 0.6 wt.
percent, averaged over a year, and which allows any given fuel to
contain zero and 3.5 wt. percent oxygen, would therefore be
appropriate.
______
Attachment 1
Model Predictions are Computed for the Following Fuel Property Values
----------------------------------------------------------------------------------------------------------------
CA Mean Actual
CCA CA Phase Predictive 1996 CA EPA Phase CA Phase
Property Baseline 2 Avg. Model Mean Fuel II RFG I Limits
Limits Limits Properties
----------------------------------------------------------------------------------------------------------------
RVP......................................... 8.7 7.0 7.0 6.8 6.7 7.8
E200/T50.................................... 41/218 50/200 49/01 51/197 49/202 44/212
E300/T90.................................... 83/329 92/20 88/307 89/302 87/311 83/330
Aromatics................................... 32 22 24 23 25 34
Olefins..................................... 9.2 4 5.8 3.9 11 11
Oxygen...................................... 0 2 1.9 2.07 2.1 0
Sulfur...................................... 339 30 28 20 150 151
Benzene..................................... 1.53 0.8 0.7 0.55 0.95 2.0
----------------------------------------------------------------------------------------------------------------
Model Predictions (Percent Change Relative to Clean Air Act Baseline Fuel)
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
EPA COMPLEX MODEL PREDICTIONS ARB PREDICTIVE MODEL PREDICTION
-----------------------------------------------------------------------------------------------------------------------------------------------------------------
CA Phase 2 Avg.
Pollutant CA Phase 2 Avg. CA Mean Actual 1996 CA CA Phase 2 Avg. CA Mean Actual 1996 CA Limits Relative
Limits Predictive Model Mean Fuel EPA Phase II RFG Limits Predictive Model Mean Fuel EPA Phase II RFG to CA Phase 1
Limits Properties Limits Properties Limits
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Exhaust VOC................... -18.3........... -18.0........... -19.1........... -18.1........... -30.0........... -29.2........... -30.6........... -22.5........... -17.4
Evap VOC...................... -44.4........... -44.4........... -47.4........... -48.8........... -45.3........... -45.3........... -50.7........... -53.3........... -28.1
-----------------------------------------------------------------------------------------------------------------------------------------------------------------
Total VOC................. -28.2........... -28.1........... -29.9........... -29.8........... -35.4........... -34.9........... -37.7........... -33.5........... -21.2
NOX........................... -14.6........... -13.9........... -14.6........... - 6.8........... -11.6........... -11.0........... -12.1........... - 5.0........... - 7.0
Exhaust Benzene............... -42.3........... -42.7........... -46.1........... -35.9........... -51.7........... -50.7........... -54.6........... -38.8........... -50.8
Evap. Benzene................. -68.2........... -72.0........... -79.0........... -64.3........... -47.7........... -54.2........... -64.0........... -37.9........... -60.0
Acetaldehyde.................. -21.0........... -17.8........... -19.3........... -15.6........... 4.5.......... 6.5.......... 5.1.......... 6.8.......... 8.2
Formaldehyde.................. 18.1.......... 16.7.......... 21.5.......... 7.8.......... 43.1.......... 46.0.......... 46.6.......... 34.0.......... 29.7
1,3-Butadiene................. -33.3........... -18.0........... -32.2........... - 8.8........... -34.1........... -26.2........... -36.3........... - 9.9........... -31.3
POM........................... -18.3........... -18.0........... -19.1........... -18.1........... Not Estimated... Not Estimated... Not Estimated... Not Estimated... Not Estimated
-----------------------------------------------------------------------------------------------------------------------------------------------------------------
Total Toxics.............. -34.5........... -34.1........... -37.0........... -28.4........... Not Calculated.. Not Calculated.. Not Calculated.. Not Calculated.. Not Calculated
PWT....................... Not Calculated.. Not Calculated.. Not Calculated.. Not Calculated.. -43.2........... -39.6........... -44.1........... -26.6........... -41.8
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
______
Attachment 2
scenario 1: no use of mtbe and no federal year-round 2.0 wt.%
oxygen mandate
Step 1. Initial impact
(a) Variations from current flat specifications: Reduce oxygen
content from 2.0 to 0.0 (due to removal of MTBE)
(b) Initial impact, emissions and other:
NOX: -0.5%
THC: +3%
CO: +10%
Toxics: -0.5%
Loss of 11% volume.
Step 2. Changes to CaRFG standards
Reduce RVP standard by 0.2 psi, from 7.0 to 6.8 psi.
Reduce sulfur standard by 30 ppm, from 40 ppm to 10 ppm.
Step 3. Feasibility
Requires some capital investment and an increase in operating costs
to reduce RVP by 0.2 psi and reduce sulfur to 10 ppm, but both are
feasible.
The 11 percent lost volume will have to be made up by importing or
increasing production of alkylates (blendstocks), or importing fully
complying gasoline.
Step 4. Cumulative emissions impact
NOX: -1.5%
THC: -0.3% (includes loss of reduction in ozone-forming
potential from loss of CO emission reductions from 2.0 wt
percent oxygen)
CO: +10 percent (doesn't apply when in CO winter
nonattainment area)
Toxics: -2.5 percent
Winter oxygenates where required, using ethanol at 2.0 wt. percent
oxygen:
CO: -0 percent
RVP: Summertime limits nor applicable
scenario 2: no use of mtbe but federal year-round 2.0 wt. percent
oxygen mandate met with 5.7 vol percent ethanol
Step 1. Initial impact
(a) Variations from current flat specifications:
RVP increases 1 psi from 7.0 to 8.0 psi (due to ethanol
effect)
(b) Initial impact, emissions and other:
NOX: neutral
THC: +13 percent (from 1.0 psi increase in RVP)
CO: neutral
Toxics: +5.7 percent
Loss of 6 percent volume
Step 2.A. Changes to CaRFG standards equivalent to changes for no
oxygen mandate (Scenario 1)
Reduce RVP standard by 0.2 psi, from 8.0 to 7.8 psi.
Reduce sulfur standard by 30 ppm, from 40 ppm to 10 ppm.
Step 2.B. Changes to CaRFG standards to achieve the same benefits as
the no oxygen mandate (Scenario 1)
Further reduce RVP by 0.8 psi, from 7.8 to 7.0 psi.
Further reduce sulfur by 10 ppm, from 10 ppm to zero.
Step 3. Feasibility
A. Feasibility of Step 2.A. changes is same as in Scenario 1
B. Reduction of RVP would necessitate removal of all pentanes. This
is more expensive than in Scenario 1 and results in a loss of volume of
about 4 percent. Reducing sulfur to zero is technically very difficult
and would effectively preclude gasoline imports, as little or none
available with zero sulfur. The overall 10 percent lost volume will
have to be made up by importing or increasing production of alkylates
(blendstocks), or importing fully complying gasoline.
Step 4. Cumulative emissions impact
Step 2.A
NOX: -1 percent
THC: +8.8 percent
CO: neutral
Toxics: +3.3
Step 2.B
NOX: -1.3 percent
THC: -1 percent
CO: neutral
Toxics: -1 percent
Winter oxygenates where required, using ethanol:
CO: -0 percent
RVP: Summertime limits not applicable
scenario 3: no use of mtbe but federal year-round 2.0 wt. percent
oxygen mandate met with 10 vol percent ethanol
Step 1. Initial impact
(a) Variations from current flat specifications
RVP increases I psi from 7.0 to 8.0 psi (due to ethanol
effect)
(b) Initial impact, emissions and other
NOX: +2.6 percent
THC: +12 percent (from 1.0 psi increase in RVP)
CO: -5 percent
Toxics: +6.7 percent
Loss of 1 percent volume
Step 2.A. Changes to CaRFG standards equivalent to changes for no
oxygen mandate (Scenario 1)
Reduce RVP standard by 0.1 psi, from 7.9 to 7.8 psi (after
allowing a 0.1 psi credit for impact of CO reduction on ozone)
Reduce sulfur standard by 30 ppm, from 40 ppm to 10 ppm.
Step 2.B. Changes to CaRFG standards to achieve same benefits as the no
oxygen mandate (Scenario 1)
Further reduce RVP by 0.6 psi, from 7.8 to 7.2 psi
Further reduce sulfur by 10 ppm, from 10 ppm to zero
Step 3. Feasibility
A. Feasibility of Step 2.A. changes is same as in Scenario I
B. Reduction of RVP by 0.7 psi would necessitate removal of all
pentanes. This is more expensive than in Scenario 1 and results in a
loss of volume of about 5 percent. Reducing sulfur to zero is
technically difficult and would effectively preclude all gasoline
imports, as little or none available with zero sugar.
Step 4. Cumulative emissions impact
Step 2.A
NOX: +1.6 percent
THC: +7.2 percent
CO: -5 percent
Toxics: +4.4 percent
Step 2.B
NOX: +1.3 percent
THC: neutral
CO: -5 percent
Toxics: +1.2 percent
Air Resources Board,
Sacramento, CA, July 9, 1999.
Ms. Margo T. Oge,
Director, Office of Mobile Sources,
U.S. Environmental Protection Agency,
Washington, DC.
Dear Ms. Margo: This is in response to your August 6, 1999, letter
posing several follow-up questions to my July 9, 1999, submission of
supplemental data regarding our request for a waiver from the oxygen
requirement of the federal RFG program.
The response provided below fully addresses each of your questions.
We are hopeful that this supplemental information will allow you to
expeditiously provide California the waiver it needs to remove methyl
tertiary butyl ether (MTBE) from gasoline without impeding our ability
to expeditiously attain federal national ambient air quality standards.
For ease of reference, I am providing your original questions followed
by our response.
Question 1. Based on our review we understand that the federal
requirement of 2.0-wt percent oxygen can be met with 5.7-vol percent
ethanol (your Scenario 2). For Scenario 2 you state that the reductions
in NOX for this level of ethanol fall short of your
NOX reduction goal of 1.5 percent by 0.2 percent even with
reduction of sulfur to 0 ppm. Have you considered the potential impacts
of other fuel parameters, such as aromatics and olefins?
Response. Our analysis demonstrated that maintaining the oxygen
mandate reduced potential additional NOX emissions
reductions that might otherwise be achieved in a cost-effective manner
that preserved essential flexibility in meeting California reformulated
gasoline regulations. We recognized that compliance with the
specifications could be met by changing other properties. The
demonstration was to show that the oxygen mandate restricts our ability
to achieve the greatest possible NOX emissions reductions.
Our analysis stressed the effects of RVP and sulfur for setting new
baseline fuel specifications because emissions are most sensitive to
these parameters and when either is reduced, emissions of regulated
pollutants tend to go down. If the other properties were changed,
emissions of one or more pollutants would decrease (usually to a much
smaller degree) but emissions of at least one other pollutant would
increase. Therefore, these other parameters are much less useful in
making complying fuels with the needed NOX reductions.
Question 2. For Scenario 2 the staff analysis states that all
pentanes would need to be removed to reduce RVP from 7.8 to 7.0 psi to
preserve existing hydrocarbon benefits. Yet the staff analysis
indicates a reduction in hydrocarbons of 1.0 percent which is beyond
the 0.3 percent reduction projected for your Scenario 1 in which there
is 0.0 wt percent oxygen in the fuel. Are we correct in assuming that
Scenario 2 would exceed hydrocarbon reduction goals? If so, could RVP
be reduced by less than 0.8 psi for the 5.7-vol percent ethanol case?
Response. Yes, the hydrocarbon estimate in Scenario 2 is lower then
the 0.3 percent reduction shown in Scenario 1. However, hydrocarbon
emissions are very sensitive to changes in RVP. If RVP was increased by
just 0.1 psi, then the current evaporative emissions model predicts
there would be a 3.5 percent increase in the hydrocarbon evaporative
emissions. Even such a small change in RVP would lead to an increase in
hydrocarbon emissions and would not be practical because it would not
preserve the emission benefits.
Question 3. Your letter states that ARB would consider appropriate
a waiver of the 2.0 wt percent oxygen requirement based on averaging.
That is, a minimum of 2.0-wt percent oxygen would be required for the
four winter months, and for the remaining months any given fuel could
contain from 0 to 3.5-wt percent oxygen. If the minimum oxygen
requirement of 1.5 wt percent were eliminated, would that change the
results and/or conclusions of your analysis?
Response. No, solely removing the 1.5 wt percent minimum oxygen
requirement and keeping the 2.0 wt percent oxygen average would not
change the conclusions of our analysis.
If the 2.0-wt percent average were required, with no minimum, a
significant percentage of the summer gasoline would still require
oxygen. If the oxygen level for the four winter months were at the 3.5
percent level, then to average 2.0 percent, the oxygen content in RFG
for the remaining months would still have to average about 1.25 percent
oxygen. In reality, given the California gasoline distribution system,
such an approach would provide very little flexibility to produce non-
oxygenated RFG. Thus, it would still be very difficult to achieve
additional cost/effective NOX reductions during the summer.
Question 4. Your July 9 letter frequently cites concerns that the
2.0 wt percent oxygen mandate will create barriers to implementation of
``Phase 3 CaRFG regulations''. Please clarify, in light of the fact the
ARB has not yet finalized the Phase 3 regulations, what assumptions
were made about the Phase 3 fuel in the analysis.
Response. There was no need to assume anything for Phase 3 CaRFG
other than there still exists a need for further reductions in
emissions. The only assumptions in the analysis were that reductions of
sulfur and RVP could provide additional emissions benefits in complying
with our current or future regulations. No matter which scenario you
consider or which properties you vary, the ability to reduce
NOX and evaporative hydrocarbon emissions or maintain the
existing emissions benefits is greater without oxygen.
Question 5. Please provide information of how CO and THC changes
were calculated.
Response. The changes were calculated using the existing Predictive
Model for exhaust, and the proposed evaporative model which is being
developed as part of a revised Predictive Model. Both the current
Predictive Model and the initial draft model for public comment are
available on the ARB Cleaner Burning Gasoline web page. The evaporative
hydrocarbon results from the evaporative portion of the initial draft
model and the exhaust hydrocarbon results from the current Predictive
Model were combined by using the ARB EMFAC7G inventory weightings of
exhaust and evaporative emissions. Weights were calculated for the
inventory years; 1996, 2000, and 2005. The weights were averaged to
provide a composite weight. The NOX portion of the analysis
was generated using the current Predictive Model.
For CO, we used the relationship that increasing fuel oxygen by 2
percent in results approximately a 10 percent reduction in exhaust CO.
This is consistent with the estimates from the Auto/Oil research
program. This is also consistent with estimates of the effectiveness in
reducing ambient concentrations of CO for the wintertime oxygen
program. The analyses of the ambient data for sites-primarily impacted
by motor vehicles emissions estimated the reductions in CO to be
between 7 percent and 12 percent.
Question 6. Has ARB considered the effect on ozone associated with
reduction in CO emissions associated wig oxygen levels above 2.0 wt
percent? If so, please provide information on how such reductions were
accounted for.
Response. We accounted for reductions in CO by converting tons of
CO into tons of equivalent evaporative hydrocarbons emissions. We used
the Maximum Incremental Reactivity (MIR) factors to adjust the ozone
reactivity differences for CO and evaporative emissions to be on the
same basis. The MIR factor for CO was 0.07 and the average MIR for
evaporative emissions was about 2.2. This yields a conversion factor of
approximately 31.4 to 1. Or, it takes about a reduction of 31.4 tons of
CO to offset an increase of 1 ton of evaporative emissions. We used a
revision of the Predictive Model, discussed in the response to Comment
5, that includes an evaporative emissions component to estimate the
fuel property effects on THC. We then compared the reactivity weighted
CO and THC to adjust the THC emissions accordingly.
Sincerely,
Michael P. Kenny.
______
Statement of Hon. Jake Garn, Vice-Chairman, Board of Directors,
Huntsman Corporation
i. introduction and summary
Good morning, Mr. Chairman, Senator Chafee, and other distinguished
Members of the Committee. I am pleased to have this opportunity to
appear before the Subcommittee this morning.
My name is Jake Garn. I am appearing on behalf of the Huntsman
Corporation, headquartered in Salt Lake City, Utah. I am vice-chairman
of the Board of Directors of Huntsman. Huntsman is the largest
privately-owned chemical company in the United States. Huntsman is the
one of the largest domestic manufacturer of MTBE for the merchant
market and is a member of the Oxygenated Fuels Association which
represents manufacturers of oxygenates used in fuels. Huntsman's
decision to make additives that clean our air is consistent with this
Corporation's longstanding commitment to socially responsible actions
designed to improve the lives of all Americans. The Huntsman family has
contributed over $150 million to state-of-the-art cancer research
facilities, home to over 300 of the world's top researchers. Our belief
in protection of human health and the environment is no mere slogan; it
is a promise we have made to our community.
On behalf of the Huntsman Corporation, I want to commend the
Chairman Inhofe and Chairman Chafee for convening the Subcommittee to
examine the findings and recommendations of the Blue Ribbon Panel. As
the manufacturer of a significant amount of MTBE, we have an obvious
interest in the BRP's findings and recommendations and, perhaps more
importantly, in the actions Congress may take based on those
recommendations.
We agree with much of what the Blue Ribbon Panel concluded. For
example, we agree that more research and monitoring is necessary
concerning the health effects of not only MTBE, but also other
constituents of gasoline. However, we have strong concerns with several
of the BRP's conclusions. Most importantly, we disagree strongly that
there is sufficient justification to recommend a substantial reduction
in the use of MTBE. As described in greater detail below, we believe
that the BRP left many important questions unanswered. Unfortunately,
the BRP is gone and the responsibility to answer these questions falls
to the Congress, and to this Subcommittee in particular. Until those
questions are answered, we believe it is inappropriate to move forward
with any effort to amend the Clean Air Act to modify the reformulated
gasoline program. We appreciate this opportunity to contribute our
thoughts on how Congress should endeavor to answer these remaining
important questions.
ii. huntsman and mtbe
Huntsman Corporation is one of the largest producers of MTBE in the
United States. It has been producing MTBE since early 1998 when it
acquired Texaco's MTBE-producing facility in Beaumont, Texas. The
company sells its MTBE product to refiners who, in turn, use it to meet
the requirements of the Clean Air Act.
iii. the blue ribbon panel recommendations
As you know, in 1998 EPA Administrator Browner appointed a Blue
Ribbon Panel (BRP) to investigate the air quality benefits and water
quality concerns associated with oxygenates in gasoline, and to provide
independent advice and recommendations on ways to maintain air quality
while protecting water quality. The BRP met on several occasions and
issued its final report in July 1999. Mr. Greenbaum, the chairman of
the BRP, is better qualified to describe the work of the Panel and to
summarize its findings and recommendations. I would like to take this
opportunity to explain why Huntsman agrees with some--but not all--of
those findings and recommendations.
A. Points of Agreement
The BRP made a number of findings and recommendations with which
Huntsman Corporation agrees. They are, in significant part, the
following:
that MTBE has been detected in a number of water supplies
nationwide, primarily causing consumer odor and taste concerns that
have led water suppliers to reduce use of those supplies. The Panel
further found that incidents of MTBE in drinking water supplies at
levels well above EPA and State guidelines have occurred, but are rare;
that MTBE is currently an integral component of the U.S.
gasoline supply both in terms of volume and octane, and as such,
changes in its use, with the attendant capital construction and
infrastructure modifications, must be implemented with sufficient time,
certainty, and flexibility to maintain the stability of both the
complex U.S. fuel supply system and gasoline prices;
that the BRP's recommendations were intended to
``simultaneously'' maintain air quality benefits while enhancing water
quality protection and assuring a stable supply at reasonable cost;
that EPA should take actions to enhance significantly the
Federal and State Underground Storage Tank programs;
that EPA should work with its State and local water supply
partners to enhance implementation of the Federal and State Safe
Drinking Water Act programs;
that EPA should work with States and localities to enhance
their efforts to promote lakes and reservoirs that serve as drinking
water supplies by restricting use of recreational water craft,
particularly those with older motors;
that EPA should work with other Federal agencies, the
States, and private sector partners to implement expanded programs to
protect private well users;
that we should expand public education programs at the
Federal, State, and local levels on the proper handling and disposal of
gasoline;
that we should develop and implement an integral field
research program into the groundwater behavior of gasoline and
oxygenates;
that EPA should work with Congress to expand resources
available for the up-front funding of the treatment of drinking water
supplies contaminated with MTBE and other gasoline components to ensure
that affected supplies can be rapidly treated and returned to service,
or that an alternative water supply can be provided;
that States should reexamine and enhance State and Federal
``triage'' procedures for prioritizing remediation efforts at UST sites
based on their proximity to drinking water supplies;
that we should accelerate laboratory and field research,
and pilot projects, for the development and implementation of cost-
effective water supply treatment and remediation technology, and
harmonize these efforts with other public/private efforts underway; and
that we should identify and begin to collect additional
data necessary to adequately assess the current and potential future
State of contamination.
B. Points of Disagreement
However, there is one important recommendation of the BRP with
which we emphatically do not agree. The BRP recommended that ``in order
to minimize current and future threats to drinking water, the use of
MTBE should be reduced substantially.'' The BRP also recommended that
the current Clean Air Act mandate requiring 2 percent oxygen, by
weight, in RFG must be removed in order to provide flexibility to blend
adequate fuel supplies in a cost-effective manner while quickly
reducing usage of MTBE and maintaining air quality benefits. As a
member of the Oxygenated Fuels Association, Huntsman Corporation has
supported refiner flexibility through removal of the oxygen standard as
long as adequate assurances of no air quality backsliding are provided.
Concurrently, we have encouraged EPA to review its authority under
existing law to provide such flexibility. However, we must object
strongly to the suggestion that there is a sufficient basis of
knowledge upon which to base a recommendation to limit the amount of
use of MTBE, an effective tool to reduce air pollution.
C. Comments on the BRP's Recommendation to Reduce Substantially the Use
of MTBE
We believe several comments are in order concerning the BRP's
recommendation to reduce substantially the use of MTBE. I hope what is
evident from the following discussion is that Huntsman Corporation does
not challenge the mandate of the BRP or the great majority of its
findings and recommendations. Instead, Huntsman believes that for a
variety of reasons, the BRP was unable to finish the job, and it now
falls to Congress to answer the remaining questions, including both
questions of fact and questions of policy.
1. The BRP Made No Finding Concerning Health Effects of
Exposure to MTBE
It is important to note that the BRP did not make any finding
concerning the health effects of exposure to MTBE. The Panel
acknowledged that was not constituted to perform an independent
comprehensive health assessment. Of course, it could not perform such
an assessment and report to EPA in the limited time available to it.
Instead, the Panel chose to rely on ``recent reports by a number of
state, national, and international health agencies.''
We now understand that there is negligible risk associated with
exposure to levels of MTBE being reported in drinking water supplies.
It is instructive to review the status of reports by state, national
and international health agencies.
There is currently no regulated standard for MTBE in drinking water
under the Federal Safe Drinking Water Act. EPA has published an
Advisory document on MTBE which recommends that keeping levels of
contamination in the range 20 to 40 micrograms per liter or below ``to
protect consumer acceptance of the water resource would also provide a
large margin of exposure (safety) from toxic effects.''\1\ By its
authority under the Federal Safe Drinking Water Act, EPA recently
issued a regulation requiring most public water systems to monitor
levels of a number of unregulated contaminants, including MTBE.\2\ EPA
will use this information, together with the results of research on the
human health effects of MTBE, to determine whether it should regulate
the amount of MTBE permissible in drinking water.
---------------------------------------------------------------------------
\1\ Drinking Water Advisory: Consumer Acceptability Advice and
Health Effects Analysis on Methyl Tertiary-ButylEther (MTBE), U.S.
Environmental Protection Agency (December 1997) at 2.
\2\ 64 Fed. Reg. 50556 (September 17, 1999)(to be codified at 40
C.F.R. Sec. Sec. 9.1, 141.35, 141.40, 142.16 and 142.15).
---------------------------------------------------------------------------
For over a decade, scientists have studied MTBE to identify its
toxic properties and to determine whether they might be manifest in
people exposed to small concentrations in air and water. MTBE, like all
other chemicals, has the ability to cause some injury at sufficiently
high dosages. Extensive research has indicated that the MTBE doses
required to produce illness in laboratory animals are thousands of
times greater than those humans could conceivably be exposed to.
Furthermore, MTBE has been shown to be incapable of impairing
fertility, or of damaging the developing fetus. Also, based on numerous
tests, MTBE is incapable of damaging the genetic structure of cells,
greatly reducing the chance that it might affect numerous bodily
processes controlled by a person's DNA.
As explained earlier in this testimony, Huntsman agrees that there
should be more research on the health effects of exposure to all the
constituents of gasoline, including MTBE. Indeed, wherever MTBE is
detected, there are likely to be other, potentially more harmful
constituents of gasoline present. However, there is not yet sufficient
evidence of harmful health effects from MTBE. The BRP accurately
reflects this absence of such evidence. Without such evidence, and in
light of the overwhelming evidence of benefits from the use of MTBE in
gasoline, it is not appropriate to recommend that the use of MTBE be
reduced substantially.
The latest scientific evidence concerning the health effects of
MTBE must be considered together with the most recent information
concerning the scope of MTBE contamination in drinking water. There is
evidence to indicate that MTBE contamination of drinking water sources
is limited to geographic pockets within the United States, and that the
number of gasoline effected wells that exceed national guidelines and
State primary and secondary drinking water standards is small. The
Water Contamination Issue Summary shows primary and secondary drinking
water standards and action levels for States that have them. The
average secondary standard (aesthetically based) is over 20 ppb and the
average primary standard (health based) is over 50 ppb. Yet, Table 1 of
the same report shows that only 1 percent-2 percent of all wells tested
so far exceed 5 ppb of MTBE. Therefore, the number of wells that exceed
State standards is small enough to be manageable.
2. The BRP Underestimated the Air Quality Benefits of
Oxygenates
Huntsman Corporation is also concerned that the BRP underestimated
the air quality benefits of oxygenates. The BRP recommendations are
predicated on the regulatory requirements established in EPA's existing
RFG rules. They fail to recognize that the RFG program (with MTBE as
the oxygenate of choice in 80 percent of the market) has exceeded by
nearly double the requirements of EPA's regulations. By underestimating
such benefits, it is easier for the BRP to assume that other fuel
formulations can achieve the same, or better, air quality benefits.
According to EPA's May 24, 1999 RFG Fact Sheet, oxygenates such as
MTBE substantially reduce toxics such as benzene and other aromatics.
Oxygenates also dilute or displace other fuel components like sulfur,
which in turn reduce emissions of the smog precursors VOC and
NOx. They also provide additional reductions in the
distillation temperatures of gasoline. These improvements are important
in reducing vehicle exhaust emission, particularly during the first few
minutes of cold engine operation when the catalytic converter is not
fully operational.
Unfortunately, the BRP underestimated the real-world air quality
benefits of MTBE (and oxygenates, in general) in its narrow application
of emission prediction models. Air quality predictions using these
models ignore many of the remaining benefits that were identified
during the Panel's meetings and presented in the Air Quality Issue
Summary.
Throughout the recent debate, it has been convenient to ignore a
large portion of oxygenate air quality benefits, to ascribe them to
other fuel parameters, or to discount them altogether in favor of
automotive technology advances. Real world impacts, such as the
contribution of oxygenates to improved combustion before a vehicle's
catalytic converter achieves normal operating efficiency, have been
largely ignored. Similarly, the ``leaning-out'' benefits of off-road
gasoline engines without catalytic converters have remained unaccounted
for even though their percent share of the total emissions picture
continues to rise. The benefits of lower combustion deposit formation
and associated decrease in particulate emissions are also not
quantified. Indirect oxygenate dilution benefits of undesirables such
as olefins, sulfur and aromatics are typically discounted by the
suggestion that refiners will find some other way to achieve them. The
same is true for positive drivability impacts associated with improved
oxygenated fuel midrange volatility. In their eagerness to obtain
oxygenate flexibility, refiners have clearly misrepresented the degree
of difficulty involved in replacing MTBE.
The risk of backsliding on the air quality gains of the last decade
looms large in the horizon. This fact is demonstrated by recent claims
by California refiners that they face great difficulty in achieving the
actual air quality benefits of that state's clean burning gasoline
(CBG) without MTBE, according to an August 20, 1999 ``Inside CalEPA''
article. Regulators are not clear on how to preserve the air quality
benefits of CBG without MTBE.
Several years ago, EPA asked the National Research Council (NRC) to
(1) assess whether the existing scientific information allows a
comparison of the ozone forming potential of automotive emissions
obtained with different reformulated gasolines, and (2) evaluate the
impact of applying the ``ozone forming potential'' approach to air
quality on the overall assessment of oxygenate benefits within the RFG
program.
The NRC's recent report on Ozone-Forming Potential of Reformulated
Gasoline raises serious questions regarding the contribution of cleaner
burning facts to the nation's air quality program in general, and the
specific contribution of oxygenates in cleaner burning gasoline
formulation. The NRC report correctly captures the impact of the
substantial advances in automotive emissions controls over the past
decades. However, it diminishes the value of fuel controls by ignoring
real-world impacts and focusing exclusively on direct oxygenate impacts
on ozone. A more detailed discussion of the NRC report was prepared by
the Oxygenated Fuels Association, of which Huntsman is a member, and is
attached as Appendix A.
3. The BRP Did Not Have the Most Up-to-date Information on
the Underground Storage Tank Program
The BRP presented detailed recommendations aimed at making the
Underground Storage Tank (UST) program more effective. Huntsman
Corporation agrees with those recommendations. Unfortunately, when the
BRP made its recommendations, it did not have the most up-to-date
information on the effectiveness of the UST program. Had the BRP had
this information, its recommendation would still have been appropriate,
but it would have had even less basis upon which to recommend a
substantial reduction in the use of MTBE.
Most MTBE detections in groundwater were found prior to the UST
regulation implementation deadline (December 1998). The MTBE
contamination data presented by the USGS and reviewed by the BRP was
collected between 1988 and 1998 when underground storage tanks were
only 25 percent to 50 percent in compliance with EPA's regulations.
Data presented by the Association of State and Territorial Solid Waste
Management Officials (ASTSWMO) show that less than 50 percent of all
USTs were in compliance prior to 1998 and that as recently as 1996 only
30 percent were in compliance.\4\
---------------------------------------------------------------------------
\4\ Sausville, Paul, Dale Marx and Steve Crimaudo: A Preliminary
State Survey with Estimates Based on a Survey of 17 State Databases of
Early 1999, ASTSWMO UST Task Force, 11th Annual EPA UST/LUST National
Conference, March 15-17, 1999, Daytona Beach, Florida.
---------------------------------------------------------------------------
There is also evidence that the risk of drinking water
contamination by MTBE and other gasoline constituents has been greatly
reduced with the onset of UST regulation compliance. The University of
California at Davis study\5\, part of which was presented to the BRP
March 25 & 26, 1999, showed that tank failure rates decrease by over 95
percent (from 2.6 percent failures per year for non-upgraded tanks to
0.07 percent per year for upgraded tanks) once tanks were upgraded to
the current UST regulations. Also, with the required installation of
early leak detection monitors, the time between when a leak occurs and
when it is detected should be significantly reduced. As a result, the
amount of gasoline released from a site before it has been remediated
is minimized. Both of these effects combined should lead to substantial
reductions in the amount of MTBE and other gasoline components that
escape undetected.
---------------------------------------------------------------------------
\5\ Keller, Arruro, et. al Health and Environmental Assessment of
MTBE, Report to the Governor and Legislature of the State of California
as Sponsored by SB 521, November 1998.
---------------------------------------------------------------------------
4. The BRP Failed to Adequately Assess Alternatives to MTBE
One of the most disturbing shortcomings of the BRP's report is its
failure to provide an analysis of the alternatives to MTBE. The BRP's
recommendation to reduce the use of MTBE is of little use to
policymakers if there is no credible alternative. It is our view that
potential alternatives should be evaluated according to the same
criteria by which MTBE is judged, to wit:
whether the alternative yields the same real air quality
benefits as MTBE;
whether the alternative presents no significant risk to
human health and the environment; and
whether the alternative is preferable from the standpoint
of cost and availability.
Huntsman Corporation agrees with the BRP recommendation to more
fully investigate any major new additives to gasoline prior to their
introduction. We would expect that this process should apply to the
alternatives already identified by the panel, namely ethanol,
alkylates, and aromatics. We should be hesitant to accept expanded use
of these alternatives without more rigorous analyses of their
respective impacts on human health, air and water quality, as well as
gasoline supply and price.
It is especially disturbing that the most often suggested
alternative to MTBE--ethanol--has not been subjected to a more rigorous
analysis under the criteria set out above. For example, there are
serious questions as to whether ethanol yields the same real/air
quality benefits as reformulated gasoline using MTBE. Ethanol has a
higher volatility; it evaporates more readily, creating more air
pollution. EPA has acknowledged that the increased use of ethanol will
result in increased emissions of nitrous oxides (NOx). And
in addition to contributing to ozone exceedences, emissions of
NOx contribute to elevated ambient levels of nitrogen
dioxide and fine particulate matter, both of which are criteria
pollutants for which EPA has established national ambient air quality
standards.
Even assuming that there are some air quality benefits from the use
of ethanol, those benefits as likely to be outweighed by the
environmental costs of growing more corn and other ethanol feedstocks.
The production of corn in the United States involves substantial
applications of fertilizers, herbicides and pesticides. It would be
interesting to compare the current incidence of MTBE contamination in
drinking water supplies with the incidence of drinking water supplies
contaminated with atrazine and other farm chemicals if corn production
were to expand to the level necessary to produce enough ethanol to
replace MTBE as an oxygenate in reformulated gasoline.
The BRP also failed to consider important issues related to the
cost and availability of alternatives to MTBE, especially ethanol.
First, ethanol production results in a net negative energy yield; it
has been proven that it takes more energy to make a gallon of ethanol
than you get from that gallon of ethanol. According to the Department
of Agriculture, it takes 75,000 to 95,000 Btu's for a gallon of
ethanol, and yet the gallon of ethanol yields only 76,000 Btu's.
Second, each gallon of ethanol receives a tax subsidy of 54 cents.
In a March 1997 letter report, the U.S. General Accounting Office
estimated that the subsidy for alcohol fuels reduced motor fuels excise
tax revenues by about $7.1 billion from fiscal years 1979 to 1995.
Congressman Bill Archer, Chairman of the House Ways and Means
Committee, has estimated that the ethanol tax credit will cost American
taxpayers approximately $2.4 billion between 1997 and 2000.
In addition, expanded ethanol production will increase the cost of
gasoline at the pump, and will add to consumers' grocery bills. The
cost of gasoline at the pump will increase because there will be less
competition among fuel additives. The cost of food products will
increase because as the demand for corn increases, the cost of corn
used as animal feed will increase. Thus, the price of pork, beef and
chicken in the supermarket will increase.
Finally, there is no guarantee that ethanol can replace MTBE as the
oxygenate of choice without creating serious supply disruptions and, as
a result, price increases. Because of its physical characteristics,
ethanol cannot be blended with gasoline at the refinery and shipped by
pipeline or barge to the marketplace. It must be transported separately
and blended with gasoline near the location where it is to be sold to
consumers. This limitation on the ability to transport gasoline with
ethanol presents additional risks of supply disruptions and price
dislocations. Right now, ethanol is being supplied to metropolitan
areas in the vicinity of the ethanol producing facility with reasonable
reliability. It remains to be seen whether ethanol could be transported
nationally in a reliable and cost-effective fashion.
Ultimately, the net impact of whatever decision is taken will be
reflected in the economics of the marketplace. There can be no doubt
that the mandated use of oxygenates, primarily achieved by MTBE use,
extends the nation's fuel supply. This helps keeps prices in check and
helps overcome localized spot shortages when they do occur. The recent
California experience of increased MTBE use during gasoline shortages
brought about by refinery hardware problems serves as a clear reminder
of that fact. California Energy Commission studies showed a cost of 3-7
cents per gallon to remove MTBE from California's gasoline, assuming
essentially unlimited and reasonably priced supplies of clean burning
replacement blendstocks of ethanol and alkylate.
The true economic impact of a national phase down (or phase-out) of
MTBE is likely to be dramatically higher, depending on the specifics of
the action taken. MTBE makes up 10 to 15 percent of gasoline volume in
RFG markets. With refinery capacity utilization currently running at 98
to 99 percent in the U.S., it is not difficult to see that drastic
action could have catastrophic consequences. Members of Congress should
insist on fully defining this price and supply risk to the American
motoring public before it considers modification of the Clean Air Act.
iv. conclusion
Again, on behalf of the Huntsman Corporation, I would like to thank
the Subcommittee for this opportunity to present our views on this
important issue. We respect the work that the Blue Ribbon Panel has
conducted and agree with many of its recommendations. At the same time,
we feel strongly that the Blue Ribbon Panel's report is only the
first--albeit important--step toward addressing the problem of
contamination of drinking water supplies. We hope we have identified
some of the important questions that the BRP has highlighted and which
remain to be fully answered. Until those questions are answered, we
believe there is no sound basis upon which to limit the use of a
chemical--MTBE--which has helped to achieve important air quality
goals.
______
APPENDIX A.--COMMENTS ON: NATIONAL RESEARCH COUNCIL REPORT
An Analysis of the National Research Council's Report on Ozone-Forming
Potential of Reformulated Gasoline
summary
The recently issued report by the NRC's Committee on Ozone-Forming
Potential of Reformulated Gasoline, raises serious questions regarding
the contribution of cleaner burning fuels to the nation's air quality
improvement programs. The study questions the effectiveness of the
reformulated gasoline program in general, and the specific contribution
of oxygenates (such as MTBE and ethanol) in cleaner burning gasoline
formulations. Several of the study's conclusions appear to contradict
real-world air quality monitoring results and are inconsistent with
previously held beliefs that the use of RFG significantly improves air
quality.
The NRC Committee searches for certainty in the complex field of
fuel contributions to atmospheric impacts, where few simple, direct
cause-and-effect answers exist. The NRC report correctly captures the
impact of the substantial advances in automotive emissions controls
over the past decades. However, it improperly diminishes the value of
fuel controls by ignoring real-world impacts and focusing exclusively
on direct oxygenate impacts on ozone. More specifically, the report
suffers from several fundamental drawbacks:
It ignores real world air quality shifts associated with
cleaner burning oxygenated fuels. EPA data based on actual RFG air
quality surveys clearly indicate that, since 1995, the reformulated
gasoline program has delivered emissions benefits substantially
exceeding the minimum anticipated requirements. While vehicle
technology advances have contributed the lion's share of the ambient
air quality gains recorded since the 1960's, it is difficult to see how
vehicle controls have changed substantially since the introduction of
RFG. Furthermore, although the NRC report briefly alludes to real-world
conditions when the vehicle emissions controls may not be active (i.e.,
cold start) or are not operational (high emitters), it largely bases
its conclusions on laboratory controlled engine testing on low emitters
(newer, well-maintained vehicles) under equilibrium conditions, where
fuel contributions are appreciably diminished.
It attempts to identify an exclusive, direct oxygen
contribution to ozone abatement, similar to the one seen for carbon
monoxide. Such an impact can not be supported on newer vehicles
featuring advanced emission controls. However, understanding the
indirect pathways by which oxygenates impact ozone, is essential to the
overall assessment of oxygenate benefits. The report does not credit
oxygenates for indirect impacts on other key fuel parameters that do,
in turn, impact VOC and NOx emissions. By diluting gasoline
sulfur, olefins, aromatics and benzene, and lowering gasoline mid-range
volatility, oxygenates substantially (albeit indirectly) impact ozone
precursor formation. Furthermore, oxygenates allow refiners octane
flexibility to implement operating changes that reduce gasoline benzene
and aromatics content. When these indirect VOC and NOx ozone
precursor reductions are considered along with Carbon Monoxide
reductions, NRC's focus solely on direct ozone impacts appears
oversimplified and misleading.
The Committee clearly exceeded its primary task (i.e.,
assess RFG ozone impacts) to evaluate impacts on other pollutants such
as carbon monoxide, air toxics, etc. A comprehensive review of RFG and
oxygenate benefits is ordinarily welcomed; however, the NRC report is
largely superficial in presenting oxygenate impacts on these other key
pollutants. The report does grant that ``the most significant advantage
of oxygenates in RFG appears to be a displacement of some toxics (e.g.,
benzene) from the RFG blend, which results in a decrease in toxic
emissions.'' This substantially understates the facts: according to
EPA, oxygenates are responsible for approximately two thirds of the
large overcompliance reported in air toxics since the introduction of
the RFG program. Similarly, oxygenates are directly responsible for a
10-15 percent reduction in CO. As a result of focusing only on direct
ozone impacts and the inadequate treatment of non-ozone pollutants, the
NRC report leads to the improper conclusion that oxygenates have no air
quality benefits.
Lastly, the report leads to the erroneous conclusion that
fuel controls may not play a key role in future air quality strategies.
A key premise of the current RFG program is that reformulated fuel and
vehicle controls contribute to emissions reductions in a mutually
complementary way, i.e., they have been designed to function as a
closely interactive system. In very simple terms, poorly performing
vehicles are likely to pollute more and the fuel's role in optimizing
vehicle performance is critical. The need for lower sulfur, improved
distillation index controls and reduced combustion chamber deposits
(CCD) are all testaments of the close coupling between fuel controls
and vehicle technologies. Furthermore, in dismissing fuel contributions
as potentially ``small,'' the report ignores the regulatory dilemma of
identifying additional and/or alternative air quality controls in the
face of ever increasing vehicle miles traveled and continued pressure
to improve ambient air quality. Ozone control strategies often depend
on small incremental reductions in VOC or NOx emissions,
which should be evaluated in terms of their magnitude and cost
effectiveness versus remaining candidate controls, and not already
implemented strategies.
background
At the request of Congress, the U.S. Environmental Protection
Agency (EPA) asked the National Research Council (NRC) to:
Assess whether the existing scientific information allows
a comparison of the ozone forming potential of automotive emissions
obtained with different reformulated gasolines,
Evaluate the impact of applying the ``ozone forming
potential'' approach to air quality on the overall assessment of
oxygenate (i.e., methyl tertiary-butyl ether and ethanol) benefits
within the RFG program.
The NRC report's conclusions were unexpected. While the study
concedes that ground level ozone has declined by more than 10 percent
since 1995, it claims that it is not possible to attribute a
significant portion of these benefits to the introduction of
reformulated gasoline during this period. Instead, the NRC study
concludes that overall emissions of ozone precursors have substantially
decreased in recent decades, largely as a result of better emissions
control systems on vehicles. Furthermore, given the declining
contribution of fuel formulations to air quality, the study concludes
that, the direct contribution of oxygenates to ozone reduction is very
small. Last, the NRC finds that evaluating fuel formulations based on
their ozone reactivity potential (rather than strictly comparing mass
emissions) does not alter the study's conclusions, even though it
acknowledges that the ozone forming potential of carbon monoxide in
exhaust emissions is large and has not been comprehended in existing
fuel evaluation tools.
discussion
Real World Emissions Performance
The NRC study acknowledged that ambient monitoring data demonstrate
that RFG successfully helps reduce ozone levels, and lowers overall
ambient air toxics levels. According to EPA data, Phase I RFG areas
have performed better than planned:
VOC reductions average 36 percent in the south and 17
percent in the north (goal is 15 percent);
Air toxics reductions average 22 percent (goal is 16.5
percent when averaging)
NOx reductions average 3 percent (goal is 1.5
percent when averaging);
Ambient benzene levels have decreased by 43 percent.
EPA's RFG Survey Group has estimated the average vehicle emission
reductions by using fuel surveys for each of the cities in the Federal
RFG Phase I program:
Reductions in toxics from vehicles for all RFG cities far
exceed the Performance Standard and that the average reduction is about
double the requirement. More specifically, reductions in cities with
RFG/MTBE blends exceed 35 percent in most cases while the average
reduction for the four cities using RFG/ethanol blends is only about 27
percent. It would appear that the 2 percent oxygen standard and the
benzene standard in RFG combine to provide a reduction in toxic
emissions that is much greater than the Phase 1 Performance Standard as
well as the Phase 2 Performance Standard for the year 2000 (22 percent
minimum average reduction). Without the oxygen requirement, the toxic
reductions with RFG would be expected to decrease to near the
performance standard.
NOx reductions with RFG are more than double
(in many cases more than triple) the Performance Standard required by
CAA regulations (1.5 percent reduction). In most cases, the
NOx reductions with the MTBE/RFG blends are a few percentage
points greater than that observed with the cities using ethanol blends.
Low RVP fuels actually increase NOx emissions and are, thus,
ineffective program for reducing peak ozone.
VOC reductions for RFG cities generally exceed the
corresponding performance standard by 1.5 to 8 percent. The performance
standard for VOC reduction is more severe for southern cities as
compared to northern cities. The cities using RFG with ethanol are all
located in the north while low RVP cities (Atlanta, St. Louis, Phoenix,
etc.) are mostly located in the south. There is little difference
between RFG made with ethanol and MTBE in reducing VOC emissions.
However, low RVP gasoline only provides about two-thirds of the VOC
reduction as that observed for southern RFG cities.
Based on ambient monitoring data, RFG areas have performed better
than conventional gasoline areas (including lower vapor pressure areas)
in lowering the frequency of ozone exceedances as shown in Figure 1. By
focusing on percent change, the effects of fleet turnover, weather,
economic activity and related factors cancel out in the comparison. The
control data set used was conventional gasoline areas because fuel
standards did not change in those areas.
Figure 2 shows that MTBE is less likely to form ozone than most
gasoline components. Only benzene, which is reduced in RFG, has a lower
potential. Limited Auto/Oil results comparing ``matched'' oxygenated
and a non-oxygenated reformulated gasoline blends showed that the
oxygenated fuel had a 5-7 percent lower ozone forming tendency. It is
noted that the results of that study likely underpredict the ozone
reactivity impact, since despite efforts to control the experimental
design, the oxygenated fuel had an octane value of 2.4 numbers above
that of the non-oxygenated fuel. If the fuels had been octane balanced,
the differences in emissions would have been even greater in favor of
the cleaner burning oxygenated gasoline.
Indirect Performance Benefits of Oxygenates
The NRC study examined the direct impacts of oxygen on VOC and
NOx. The Committee did not attempt to identify the
significant indirect benefits of oxygenate blending to RFG. The Table
below provides a simplified roadmap to understanding the relative
direct and indirect contributions of oxygenate blending to reduced
gasoline emissions.
The NRC's main focus was on the direct impact of oxygenates on VOC
and NOx. As shown on the table above, this is correctly
judged to be a rather insignificant impact. The primary fuel impacts on
VOC are vapor pressure (RVP), midrange distillation (T50) and sulfur
content. For NOx, the primary impact variables are olefin
content and sulfur. The assumed oxygen level in this Table is 2 weight
percent; at this level the NOx impact is negligible.
However, as the NRC report points out, at 3.5 weight percent oxygen
(i.e., maximum ethanol) can lead to increased NOx emissions.
The problem with the NRC analysis is that it fails to recognize the
large indirect impacts that oxygenate addition would have on a typical
conventional fuel:
10-15 percent dilution impact in sulfur, olefins,
aromatics and benzene
15-20 degree Fahrenheit depression in T50
4-7 degree Fahrenheit reduction in T90
6-8 volume percent reduction in aromatics content
0.2-0.3 volume percent reduction in benzene
Oxygenates do not contain sulfur, olefins aromatics or benzene;
they dilute their presence in the RFG blend. Dilution is very important
to allow refiners to achieve the RFG air standards while maintaining
fuel quality. High oxygenate octane values contributes to aromatics
reduction by permitting lower severity in the key catalytic reforming
step. Without oxygenate blending, most refiners would find it extremely
difficult to produce satisfactory RFG in the premium grade, and
probably in the mid-range grade. Such blending advantages for MTBE were
unaccounted for in the NRC study.
It should be noted that of the four pollutants listed above, only
CO is directly impacted in a very large way by oxygenates. However,
this diminish our view of the value of oxygenates in generating overall
pollution reduction benefits:
While there is no direct impact on VOC, the indirect effects of
lowering midrange distillation, diluting and replacing aromatics, and
reducing sulfur combine to yield a sizable VOC reduction benefit,
estimated at approximately 10-15 percent of the total RFG VOC
reduction.
Similarly, the combined impact of indirect aromatics and benzene
reductions resulting from dilution and refinery operating adjustments
is equally large at approximately 20 percent of the overall RFG air
toxics benefit.
The large direct contribution of oxygenates to CO reduction is
amplified by indirect benefits accruing as a result of the reduction in
sulfur and T50. As a result, the portion of RFG's CO reduction benefits
attributable to oxygenate use exceeds 30 percent.
Of the four pollutants listed, only oxygenate contributions to
NOx could be described as ``small.'' This is because the
oxygenate benefits are primarily accruing as a result of the 10-15
dilution expected in sulfur and olefins content via dilution.
The discussion above is not aimed at fully comprehending all the
indirect benefits of oxygenates. For example, reduction in fuel
aromatics content should result in lower fuel combustion chamber
deposit forming tendency, which will, in turn, result in additional air
quality benefits. Furthermore, while the NRC acknowledges that ``as VOC
emissions from mobile sources continue to decrease in the future, CO
will become proportionately an even greater contributor to ozone
formation,'' it fails to credit the large direct contribution of
oxygenates in this area.
In conclusion, it would appear that the assessment of oxygenates in
cleaner burning gasolines is largely dependent on the reviewer's
definition of the action pathways or mechanisms included in the
accounting of air quality impacts. While there can be little doubt that
oxygenates have a substantial favorable impact on the remaining fuel
properties, the NRC study (like the University of California study
before it) does not credit oxygenates with any of the emissions shifts
associated with these secondary fuel impacts. While it can be argued
that such oxygenate benefits can be replaced and thus should not be
credited entirely to oxygenate use, there exists no basis to completely
discount indirect oxygenate impacts. Moreover, by failing to focus on
real world performance results, reviewers such as the NRC have tended
to underestimate the fuel's contribution to the air quality gains of
the recent past. This, in turn, risks projecting the erroneous view
that there is limited value in the fuel component of what has
heretofore been a very successful partnership between reformulated
gasoline and vehicle emissions controls.
______
Statement of Association of Metropolitan Water Agencies and American
Water Works Association
The Association of Metropolitan Water Agencies (AMWA) and the
American Water Works Association (AWWA), on behalf of the nation's
drinking water suppliers and their consumers, offer this statement
regarding methyl tertiary butyl ether (MTBE).
AMWA is a nonprofit organization comprised of the nation's largest
publicly-owned drinking water suppliers, represented by their city
water commissioners and chief executive officers. Together, AMWA
members serve clean, safe drinking water to over 120 million people.
AWWA is the world's largest and oldest scientific and educational
association representing drinking venter supply professionals. The
association's 56,000 members are comprised of administrators, utility
operators, professional engineers, contractors, manufacturers,
scientists, professors and health professionals. The association's
membership includes over 4,200 utilities that provide over 80 percent
of the nation's drinking. Since our founding in 1881, AWWA and its
members have been dedicated to providing safe drinking water.
AMWA and AWWA subscribe to the recommendations set forth by the
Blue Ribbon Panel on Oxygenates in Gasoline in their July 1997 report,
with one very significant exception: the associations feel strongly
that MTBE should be completely phased out.
MTBE is a known animal carcinogen and potential human carcinogen.
Little else is known about its health effects. What we do know is that
it has been found in 5 to 10 percent of drinking water supplies in high
oxygenate use areas. MTBE has been found in city water supplies in
California, New York, New Jersey, Massachusetts, Maine, and other
states.
MTBE occurs mostly at low levels, and even at extremely low levels
MTBE produces taste and odor concerns among consumers. Most consumers
perceive drinking water with an unpleasant taste or odor as being
unhealthy, and in some cases the water may very well be unsafe to
drink. The bottom line is that consumers will not tolerate MTBE in
their water.
The effect of these perceptions, accurate or not, is that consumers
purchase bottled water costing 500 to 1,000 times more than tap water.
And cities like Santa Monica and South Tahoe have abandoned otherwise
usable ground water and surface supplies and turned to other sources
usually at enormous expense. An alternative is to treat MTBE-
contaminated water, but this comes with extraordinary cost. What's
more, MTBE contaminates private wells, which are less well-protected by
Federal or State regulations, if at all.
In addition to the complete phase out of MTBE use, AMWA ant AWWA
support the recommendations of the Blue Ribbon Panel, particularly:
Enhancing Federal and State underground storage tank
programs, including:
Lhaving all states prohibit fuel deliveries to non-
upgraded tanks,
adding enforcement and compliance resources to ensure
prompt action,
strengthening early detection and remediation
mechanisms,
Lrequiring monitoring and reporting of MTBE at all
storage tank release sites, and
Lencouraging states to require that land-use planning
consider the impact of underground storage tanks on water supplies;
Enhancing the focus on MTBE in the Safe Drinking Water
Act's source water assessment program, contaminant monitoring
initiatives, and wellhead protection program?
Encouraging State and local governments to restrict the
use of gasoline-powered water craft in lakes and reservoirs that serve
as drinking water supplies;
Expanding programs to protect private well users;
Expanding public education programs on the proper handling
and disposal of gasoline,
Developing and implementing a research program into the
groundwater behavior of gasoline and oxygenates;
Expanding Federal resources for the treatment of drinking
water supplies contaminated with MTBE and other gasoline and for
securing an alternative source of water, if necessary;
Researching or increasing research on other ethers and
oxygenates to determine their health effects and environmental
behaviors; and
Estimating the current and likely future threats of MTBE
contamination and establishing a system of collecting data on MTBE,
other ethers, Ethanol, and petroleum hydrocarbons.
The nation's drinking water suppliers are deeply concerned about
MTBE contamination. The additive poses a very significant threat to
health, the environment, and the continued provision of affordable,
safe drinking water.
______
Statement of Steve Hall, Executive Director of the Association of
California Water Agencies
Mr. Chairman, members of the subcommittee, my name is Steve Hall
and I am the Executive Director of the Association of California Water
Agencies (ACWA). I am pleased to submit this statement to share the
California Water community's concerns with the continued mandated use
of MTBE in reformulated gasoline in California. ACWA represents over
440 urban and agricultural water utilities throughout the State of
California, which deliver more than 90 percent of the water distributed
in California.
MTBE is a known animal carcinogen and potential human carcinogen.
Existing health studies are inadequate to determine the risk posed by
MTBE in drinking water. Yet, it has become the third most common
chemical manufactured in the United States. It constitutes about 11
percent of the gasoline in areas such as Los Angeles, San Diego, and
Sacramento. The University of California estimated that as many as
10,000 wells may be contaminated with MTBE in California. This could
have a huge impact on the State's water resources and on the cost to
consumers of providing alternate drinking water supplies.
Our consumers can taste MTBE in their water at extremely low
concentrations, in the range of 5 parts per billion (this is equivalent
to less than a tablespoon of MTBE in an Olympic-sized pool). If our
consumers taste a chemical that is a known animal carcinogen and
potential human carcinogen, they very often choose to buy bottled water
at a cost of 500 to 1,000 times more than the cost of tapwater. Also,
MTBE is a man-made chemical. There is no good reason why it should be
present in our drinking water.
MTBE is a unique contaminant in water. It spreads into our drinking
water aquifers faster than nearly all other constituents in water. It
moves faster than regulatory agencies can track it and faster than
water utilities can drill new wells to replace the contaminated
supplies. Unlike most organic chemicals, MTBE does not biodegrade
rapidly in water. Once it has leaked into our groundwater or spilled
into our drinking water reservoirs, it persists.
A recent study conducted by the University of California has
recommended that use of MTBE be eliminated in California. The Governor
of California acting on this recommendation issued Executive Order D-5-
99 to phase out the gasoline additive by December 31, 2002. However,
this executive order cannot be properly implemented under existing
Federal requirements for mandatory use of oxygenates within the Clean
Air Act. Changes to Federal law are needed to implement Governor Davis'
executive order to phase out MTBE.
Water suppliers in California have already been severely impacted
by MTBE. The city of Santa Monica lost 50 percent of its well
production capacity and has had to switch to more expensive imported
water from Northern California. South Tahoe Public Utilities District
has lost one third of its well capacity. Unfortunately, South Tahoe has
no imported water to replace its lost supplies and is at risk of water
shortages. Many other utilities throughout the State have shut down
wells or bypassed water supply reservoirs rather than risk having the
fast-moving, persistent MTBE making its way into consumers' taps.
MTBE has also impacted individuals with private wells. Residents of
the city of Glenville were drinking water with MTBE levels as high as
20,000 parts per billion, which is 1,000 times greater than the
California Public Health Goal of 13 parts per billion. These documented
contamination incidents are likely to be a preview of future cases.
The primary source of groundwater contamination by MTBE is leaking
underground storage tanks. While ACWA supports increased upgrading,
monitoring and enforcement of underground fuel tanks, these actions
alone will not solve the MTBE problem. A recent study conducted by the
Santa Clara Valley Water District examined 28 underground storage tanks
with no reported leak history and all of which met 1998 upgrade
standards. The District found that 13 of the 28 tanks had leaked MTBE
into the soil or underlying groundwater. This study shows that
upgrading underground storage tanks will not stop MTBE from entering
the environment and contaminating drinking water sources.
The cost of removing MTBE through treatment is very high. The
University of California has estimated these treatment costs to range
from $3450 million to $1.5 billion in California alone. Other existing
treatment processes would be even more expensive (see Figure 1).
To develop new, less expensive treatment technology, an MTBE
Research Partnership was created by the Association of California Water
Agencies, the Western States Petroleum Association, and the Oxygenated
Fuels Association. The Partnership focuses on developing new, cost-
effective treatment technology to handle existing contaminated drinking
water supplies and developing source protection technology to protect
uncontaminated sources. This is a cooperative step in the right
direction.
ACWA has also supported all major State legislation on MTBE,
including bills by Kuehl/Hayden, Sher, Mountjoy, and Cunneen. However,
California MTBE legislation cannot override the Federal mandate for the
use of an oxygenate like MTBE.
The oxygenate requirement in Federal law is not necessary to meet
clean air standards. California has demonstrated that it can meet all
of the health and air requirements of the Clean Air Act without the use
of MTBE. With the elimination of MTBE, it will be possible to have both
clean air and clean water.
About 50 years ago, the pesticide DDT came into widespread use
throughout the world to control mosquitoes. It saved millions of lives
by preventing Malaria. Then we found that DDT had unintended
consequences on the environment and it had to be phased out. MTBE is
similar. It has clearly helped clean up the air; however, there have
been unintended consequences to the drinking water. It is time to
phaseout MTBE.
[From Oxygenated Fuels Association, Inc., October 5, 1999]
Former Senator Garn Tells Senate Panel to Save Fuel Additive MTBE--
Cleaner Fuel, Cleaner Air, Lower Costs Cited as Reasons to Stop Effort
to Ban
Arlington, Va.--Former Senator Jake Garn (R-UT) today told the
Clean Air, Wetlands, Private Property, and Nuclear Safety Subcommittee
of the Senate Environment and Public Works Committee that the push to
ban or phase-down MTBE will undermine our nation's clean air progress
and do nothing to improve clean water standards.
``MTBE has an unparalleled record of cleaning up the air that we
all breathe. Banning MTBE will reverse its successful record of
cleaning our air--a success which has been accelerating since passage
of the 1990 Amendments to the Clean Air Act,'' Garn testified. He also
noted, ``Banning MTBE is certainly no substitute for proper enforcement
of State and Federal rules which ensure the integrity of underground
gasoline storage tanks.''
MTBE has been the fuel oxygenate of choice for most refiners
because it effectively reduces air pollutants like toxic lead and
cancer causing benzene from car emissions. In addition, MTBE has helped
keep the cost of cleaner burning gasoline down. Various studies have
concluded that banning or restricting MTBE will lead to higher pump
prices and gasoline shortages.
The focus of much of today's hearing was leaking underground
storage tanks. Trace amounts of MTBE in some sources of drinking water
have caused calls for the banning of MTBE in fuel. Mr. Garn testified
today that it's the tanks and not MTBE that needs to be the focus of
attention in this debate.
In his testimony today, Senator Garn was representing Huntsman
Corporation, where he serves as Vice Chairman of the Board of
Directors. Huntsman is the largest, privately-owned chemical company in
the U.S. and a major supplier of MTBE for America's clean fuels
program. Huntsman Corporation is a member of the Oxygenated Fuels
Association (OFA).
Speaking on behalf of OFA, Executive Director Terry Wigglesworth
said she was confident that the Clean Air, Wetlands, Private Property,
and Nuclear Safety Subcommittee of the Senate Environment and Public
Works ``will consider all of the evidence provided today, and will come
to an appropriate conclusion based on science and fact.
______
Statement of Santa Clara Valley Water District
The Santa Clara Valley Water District is the water resource
management agency serving the wholesale water supply and flood
protection needs of the 1.6 million residents in Santa Clara County,
California, with its thriving Silicon Valley economy. In fulfilling its
water supply mission, SCVWD owns and operates ten reservoirs (total
capacity of approximately 163,000 acre feet), three water treatment
plants (total capacity 220 million gallons per day), and 393 acres of
groundwater recharge ponds. SCVWD is also responsible for protecting
water quality of its local groundwater basin that provides
approximately 50 percent of the County's water supply needs.
The Santa Clara Valley Water District is implementing a
comprehensive program to address Methyl Tertiary Butyl Ether (MTBE)
contamination in its water supplies and has been recognized as a leader
in the water community on this issue. We have reviewed the findings and
recommendations from The Blue Ribbon Panel on Oxygenates in Gasoline
and generally agree with the recommendations addressing water
contamination. In fact, SCVWD is implementing where it can many of the
Blue Ribbon Panel's recommendations at the local level, and supporting
their implementation at the State level. Because of its chemical
properties and widespread use in California, SCVWD has taken the
position that MTBE should be completely removed from gasoline.
SCVWD has been monitoring its water sources for MTBE over the past
several years and continues to find it. Monitoring of our imported
supplies from the Sacramento-San Francisco Bay-Delta periodically shows
concentrations of 1-2 parts per billion (ppb). Monitoring has also
shown concentrations up to 24 ppb at three of our local surface water
reservoirs where we allow motor-powered watercraft recreation.
Our greatest concern, however, continues to be contamination of
local groundwater basins from leaking underground storage tanks. The
SCVWD operates a Leaking Underground Storage Tank Oversight Program
(LUSTOP) to assist State regulators in this area. Most of the
underground storage tank sites that are listed as cases in our LUSTOP
program have monitored for MTBE and a total of 425 sites have detected
MTBE, many at very high levels as shown on the accompanying graph.
Almost 60 percent of the sites with detections show MTBE greater than
100 ppb. This phenomenal rate of MTBE contamination is in the shallow
groundwater aquifers. Our concern is that this contamination will
eventually impact water supply wells deeper in the aquifer. So far,
only one water supply well in the County has been impacted; however,
the source investigation of this impacted well depicts another problem
with MTBE. Because of its high mobility, MTBE plumes are very
challenging to define and clean up since they can be long and narrow. A
very detailed investigation of the local geology is required to
properly assess the impact. The evidence developed to date indicates
that a nearby gasoline station with a state of the art, upgraded
underground storage tank system, is the source of contamination for
this well. Because of MTBE's mobility, we do not believe the current
data set fully represents the severity of MTBE contamination from
leaking tanks since this data was gathered from current fixed
monitoring wells at each site and most sites are not fully
investigated.
The SCVWD also initiated a pilot study, which we have included with
this testimony, to better determine the ability of upgraded tank
systems to adequately contain MTBE. A total of 28 sites with fully
upgraded underground storage tank systems were investigated to
determine MTBE occurrence originating from these sites. None of these
sites have previously shown signs of leakage. Groundwater was
encountered at 27 sites and MTBE was detected in groundwater in 13 of
these 27 sites at concentrations ranging from 1 ppb to 200,000 ppb.
Concentrations over 1,000 ppb were detected at 5 sites. These data
indicate that MTBE may be present in groundwater at approximately 50
percent of the underground storage tank facilities that meet 1998
upgrade requirements. This information is consistent with the
conclusions of an advisory panel to the Governor of California that
concluded there is evidence of MTBE occurrence from new and upgraded
underground storage tank systems. The SCVWD study is the first to
gather hard data on this issue.
Given the widespread contamination of the shallow groundwater
basins from leaking underground storage tanks, the mobility and
persistence of MTBE, and stringent California drinking water quality
standards for MTBE, we have serious concerns that large portions, or
perhaps all of our groundwater basins could become unusable as a water
supply source due to MTBE contamination if its use continues
indefinitely. Therefore, we feel that MTBE, and other ether oxygenates
with similar chemical properties, should be removed from gasoline, and
we support the findings and conclusions of The Blue Ribbon Panel on
Oxygenates in Gasoline.
______
South Tahoe Public Utility District,
South Lake Tahoe, CA, October 4, 1999.
Hon. Bob Graham,
Subcommittee on Clean Air, Wetlands, Private Property and Nuclear
Safety,
Committee on Environment and Public Works,
U.S. Senate,
Washington, DC.
Dear Senator Graham: On behalf of the South Tahoe Public Utility
District, I write to request that the enclosed statement be included in
the formal record of the proceedings related to the Subcommittee's
October 5, 1999 hearing into Federal requirements associated with
oxygenates and the Clean Air Act.
Over the past several years, the District has worked diligently,
and at great taxpayer expense, to respond to the serious health threats
created from the use of the oxygenate MTBE. We believe our experiences
with both the tank technology and the chemical and physical attributes
of MTBE are especially relevant to the Subcommittee's review of the
status of this Federal mandate.
In advance, thank you for including our comments in the record. If
you or your staff have any questions, please let me know or contact
Eric Sapirstein at (202) 466-3755.
Sincerely yours,
Robert Baer,
General Manager.
______
MTBE Groundwater Impacts in South Lake Tahoe, CA, Ivo Bergsohn, C.HG.,
Hydrogeologist, South Tahoe Public Utility District
Methyl Tertiary-Butyl Ether (MTBE) plumes associated with gasoline
releases from Service Station operations, in conjunction with water
well construction practices and hydro-geologic conditions prevalent in
the south shore area of the Tahoe Basin has resulted in the shut-down
of 12 (12) of the thirty-four (34) municipal water supply wells owned
and operated by the South Tahoe Public Utility District (District).
Because of the known environmental behavior and low taste and odor
thresholds for MTBE, District wells were put off-line to prevent the
migration of MTBE plumes toward District wells and the drawdown of
contaminants into deeper portions of the alluvial aquifer. A case
example from the South Y Area is presented to show the potential extent
of an MTBE plume in a dynamic groundwater environment and its impact on
nearby water supply wells.
Groundwater production in the South Y Area is predominantly from a
water table aquifer system formed in glacial outwash deposits
consisting of fine to medium sands interbedded with silt and clay. A
thick section of bedded clay, interpreted as representing Older Lake
Bed Deposits, forms a regional aquitard beneath the water table aquifer
at depths of approximately 90 to 135 feet across the area. Interbeds of
low permeability silt within the outwash deposits form local semi-
confined aquifer and perched water table conditions. The water table is
relatively shallow and typically occurs at depths less than 30 feet.
During seasonal high water table conditions, perched portions of the
water table aquifer may rise to within 10 feet of land surface. Because
of the historically excellent chemical quality of the water in the
shallow system, the majority of the water supply wells completed in the
area either wholly or, in part, pump groundwater from the water table
system.
Results of contaminant assessment investigations performed in the
South Y Area have identified a diving MTBE plume in the water table
aquifer system. The delineated plume extends approximately 1,500 feet
along its long axis and approximately 650 feet across its short axis.
Along its extent, the plume is believed to vary from approximately 25
to 40 feet in thickness. Within the plume and away from the source
area, the area of highest MTBE concentration progressively moves
downward through the aquifer. Immediately beneath the source area,
highest MTBE concentrations are found within the upper 30 feet of the
aquifer system. Approximately 600 feet away from the source area, high
MTBE concentrations are found in well samples collected from
intermediate portions (30-60') of the aquifer system. At distances of
approximately 1,000 feet away from the source area, high MTBE
concentrations are found in well samples collected from deep portions (
>60') of the aquifer system and at depths as great as 85 to 90 feet.
Comparison of water level measurements from monitoring well clusters
across the area show a strong downward vertical gradient. The observed
vertical gradients are believed to be due to a combination of
hydrogeologic effects, including seasonal recharge events and the
presence of higher conductivity materials at depth, and pumping effects
from nearby District water wells.
The delineated MTBE plume has had a significant impact on District
wells in the South Y Area. MTBE has been detected in the Tata No. 4
Well since this well was first sampled for MTBE in June 1996.
Operational demands required the continued pumping of this well. In
July 1998, MTBE concentrations increased to above the current
California Department of Health Service (DHS) action level of 35 ppb
and the well was immediately shut-down.
Following this well shut-down, very low levels of MTBE were for the
first time identified in four other nearby operating wells. These other
wells were subsequently shut-down in August 1998, to prevent the
further spread of the plume. The total potential impact from the shut-
down of these wells represents a water production loss of approximately
1.25 million gallons per day to the District and the South Lake Tahoe
community.
__________
Public Health Goal for Methyl Tertiary Butyl Ether (MTBE) in
Drinking Water
summary
A Public Health Goal (PHG) of 0.013 mg/L (13 g/L or 13
ppb) is adopted for methyl tertiary butyl ether (MTBE) in drinking
water. The PHG is based on carcinogenic effects observed in
experimental animals. Carcinogenicity has been observed in both sexes
of the rat in a lifetime gavage study (Belpoggi et al. 1995, 1997,
1998), in male rats of a different strain in a 24-month inhalation
study (Chun et al. 1992, Bird et al. 1997), and in male and female mice
in an 18-month inhalation study (Burleigh-Flayer et al. 1992, Bird et
al. 1997). In Sprague-Dawley rats receiving MTBE by gavage,
statistically significant increases in Leydig interstitial cell tumors
of the testes were observed in males, and statistically significant
increases in lymphomas and leukemias (combined) were observed in
females. In Fischer 344 rats exposed to MTBE by inhalation,
statistically significant increases in the incidences of Leydig
interstitial cell tumors of the testes were also observed in males, as
well as renal tubular tumors. In CD-1 mice exposed to MTBE by
inhalation, statistically significant increases in the incidences of
liver tumors were observed in females (hepatocellular adenomas,
hepatocellular adenomas and carcinomas combined) and males
(hepatocellular carcinomas). The two inhalation studies (Burleigh-
Flayer et al. 1992, Chun et al. 1992, Bird et al. 1997) and one gavage
study (Belpoggi et al. 1995, 1997, 1998) cited in this document for the
development of the PHG provided evidence for the carcinogenicity of
MTBE in multiple sites and in both sexes of the rat and mouse. While
some reviews have given less weight to the findings of Belpoggi et al.
(1995, 1997, 1998) due to the limitations of the studies, Office of
Environmental Health Hazard Assessment (OEHHA) scientists found that
they contribute to the overall weight of evidence. We reviewed these
studies and the reported criticisms carefully, and found the studies
are consistent with other MTBE findings, and are of similar quality to
studies on many other carcinogens. This conclusion is consistent with
the findings in the MTBE report (UC 1998) submitted by the University
of California (UC). The results of all available studies indicate that
MTBE is an animal carcinogen in two species, both sexes and at multiple
sites, and five of the six studies were positive.
For the calculation of the PHG, cancer potency estimates were made,
based on the recommended practices of the 1996 United States
Environmental Protection Agency (U.S. EPA) proposed guidelines for
carcinogenic risk assessment (U.S. EPA 1996f), in which a polynomial
[similar to that used in the linearized multistage (LMS) model, but
used empirically and without linearization] is fit to the experimental
data in order to establish the lower 95 percent confidence bound on the
dose associated with a 10 percent increased risk of cancer
(LED10). It is plausible that the true value of the human
cancer potency has a lower bound of zero based on statistical and
biological uncertainties. Part of this uncertainty is due to a lack of
evidence to support either a genotoxic or nongenotoxic mechanism.
However, due to the absence of specific scientific information
explaining why the animal tumors are irrelevant to humans at
environmental exposure levels, a standard health protective approach
was taken to estimate cancer risk. The cancer potency estimate derived
from the geometric mean of the cancer slope factors (CSFs) of the
combined male rat kidney adenomas and carcinomas, the male rat Leydig
cell tumors, and the leukemia and lymphomas in female rats was 1.8
10-3 (mg/kg-day)-1.
The PHG was calculated assuming a de minimis theoretical excess
individual cancer risk level of 10-6 (one in a million) from
exposure to MTBE. Based on these considerations, OEHHA adopts a PHG of
0.013 mg/L (13 g/L or 13 ppb) for MTBE in drinking water using
a CSF of 1.8 10-3 (mg/kg-day)1. This
value also incorporates a daily water consumption (DWC) rate of three
liters equivalent per day (Leq/day). The range of possible values,
based either on different individual tumor sites, or on different
multi-route exposure estimates and the average cancer potency of the
three sites (male rat kidney adenomas and carcinomas, male rat Leydig
interstitial cell tumors, and leukemia and Lymphomas in female rats)
was 2.7 to 16 ppb. The adopted PHG is considered to contain an adequate
margin of safety for the potential noncarcinogenic effects including
adverse effects on the renal and neurological systems.
In addition to the 13 ppb value based on carcinogenicity, a value
of 0.047 mg/L (47 ppb) was calculated based on noncancer effects of
increased relative kidney weights in the Robinson et al. (1990) 90-day
gavage study in rats. The kidney effect is the most sensitive
noncarcinogenic effect by the oral route observed in experimental
animals with a no observable adverse effect level (NOAEL) of 100 mg/kg/
day. This value of 47 ppb incorporates four 10-fold uncertainty factors
(UFs) for a less than lifetime study, interspecies and interindividual
variation and possible carcinogenicity. This value also incorporates a
DWC rate of three Leq/day and a relative source contribution (RSC)
default value of 20 percent. The default value for water ingestion is
the same as used by U.S. EPA, Office of Water and is also documented in
OEHHA's draft technical support document ``Exposure Assessment and
Stochastic Analysis'' (OEHHA 1996). The three Leq/day DWC value
represents approximately the 90 percent upper confidence level on tap
water consumption and the average total water consumption. The three
Leq/day incorporates two liters of direct consumption and one liter for
inhalation of MTBE volatilized from drinking water. The use of 20
percent RSC indicates that most of the exposure occurs from ambient air
levels. It is used in the noncancer risk assessment, but, consistent
with standard practice, is not incorporated into the cancer risk
assessment. While the lower value of 13 ppb is adopted as the PHG the
difference in the two approaches is less than four-fold.
introduction
The purpose of this document is to establish a PHG for the gasoline
additive MTBE in drinking water. MTBE is a synthetic solvent used
primarily as an oxygenate in unleaded gasoline to boost octane and
improve combustion efficacy by oxygenation. Reformulated fuel with MTBE
has been used in 32 regions in 19 states in the United States (U.S.) to
meet the 1990 Federal Clean Air Act Amendments (CAAA) requirements for
reducing carbon monoxide (CO) and ozone (O3) levels (CAAA of
1990, Title II, Part A, Section 211) because the added oxygenate
promotes more complete burning of gasoline. California's cleaner-
burning reformulated gasoline (California RFG) has been implemented to
meet statewide clean air goals [California Code of Regulations (CCR),
Title 13, Sections 2250 to 2297]. While neither Federal nor State
regulations require the use of a specific oxygenate, MTBE is most
commonly utilized. MTBE is currently used (11 percent by volume) in
California RFG to improve air quality (Demon and Masur 1996).
California is the third largest consumer of gasoline in the world. Only
the rest of the U.S. and the former Soviet Union surpasses it.
Californians use more than 13.7 billion gallons of gasoline a year and
another one billion gallons of diesel fuel.
MTBE and other oxygenates such as ethyl tertiary butyl ether
(ETBE), tertiary butyl alcohol (TBA) and ethanol are currently being
studied to determine the extent of their presence in drinking water and
what, if any, potential health implications could result from exposure
to them (Freed 1997, Scheible 1997, U.S. EPA 1998a, 1998b). California
Senate Office of Research last February released a position paper on
MTBE (Wiley 1998). California Energy Commission last October released a
mandated report entitled ``Supply and Cost of Alternatives to MTBE in
Gasoline'' (Schremp et al. 1998) evaluating alternative oxygenates and
a possible MTBE phaseout. California Bureau of State Audits last
December released a report entitled `` California's Drinking Water:
State and Local Agencies Need to Provide Leadership to Address
Contamination of Groundwater by Gasoline Components and Additives''
emphasizing the needs for improvements to better protect groundwater
from contamination by MTBE (Sjoberg 1998). Maine, New Jersey and Texas
are considering alternatives to MTBE in reducing air pollution in their
State (Renner 1999).
MTBE was the second most-produced chemical in the U.S. in 1997,
whereas previously it was ranked the twelfth in 1995 and eighteenth in
1994 (Cal/EPA 1998, Kirschner 1996, Reisch 1994). In 1994 and 1995, it
was estimated that about 70 million Americans were exposed to
oxygenated gasoline (oxyfuel) and approximately 57 million were exposed
to reformulated gasoline (RFG) (ATSDR 1996, HEI 1996, NRC 1996, NSTC
1996, 1997). About 40 percent of the U.S. population live in areas
where MTBE is used in oxyfuel or RFG (USGS 1996) and most people find
its distinctive terpene-like odor disagreeable (CDC 1993a, 1993b,
1993c, Kneiss 1995, Medlin 1995, U.S. EPA 1997a). MTBE is now being
found in the environment in many areas of the U.S. because of its
increased use over the last several years.
Recently MTBE has become a drinking water contaminant due to its
high water solubility and persistence. When gasoline with 10 percent
MTBE by weight comes in contact with water, about five grams per liter
(g/L) can dissolve (Squillace et al. 1996, 1997a). MTBE has been
detected in groundwater as a result of leaking underground storage
tanks (USTs) or pipelines and in surface water reservoirs via
recreational boating activities. MTBE does not appear to adsorb to soil
particles or readily degrade in the subsurface environment. It is more
expensive to remove MTBE-added gasoline than gasoline without MTBE from
contaminated water (Cal/EPA 1998, U.S. EPA 1987a, 1992c, 1996a, 1997a).
The discussion of improvements in air quality versus the vulnerability
of drinking water surrounding MTBE has raised concerns from the public
as well as legislators (Hoffert 1998, McClurg 1998). The controversy
and new mandated requirements have made MTBE an important chemical
being evaluated by OEHHA.
Background--Prior and Current Evaluations
MTBE is not regulated currently under the Federal drinking water
regulations. The California Department of Health Services (DHS)
recently established a secondary maximum contaminant level (MCL) for
MTBE as 0.05 mg/L (5 g/L or 5 ppb) based on taste and odor
effective January 7, 1999 (22 CCR Section 64449). An interim non-
enforceable Action Level (AL) of 0.035 mg/L (35 g/L or 35 ppb)
in drinking water was established by DHS in 1991 to protect against
adverse health effects. OEHHA (1991) at that time recommended this
level based on noncarcinogenic effects of MTBE in laboratory animals
(Greenough et al. 1980). OEHHA applied large uncertainty factors to
provide a substantial margin of safety for drinking water. Since
February 13, 1997, DHS (1997) regulations (22 CCR Section 64450) have
included MTBE as an unregulated chemical for which monitoring is
required. Pursuant to this requirement, data on the occurrence of MTBE
in groundwater and surface water sources are being collected from
drinking water systems in order to document the extent of MTBE
contamination in drinking water supplies.
In California, the Local Drinking Water Protection Act of 1997
[Senate Bill (SB) 1189, Hayden, and Assembly Bill (AB) 592, Kuehl]
requires DHS to develop a two-part drinking water standard for MTBE.
The first part is a secondary MCL that addresses aesthetic qualities
including taste and odor. The second part is a primary MCL that
addresses health concerns, to be established by July 1, 1999. DHS is
proceeding to establish drinking water standards for MTBE and requested
OEHHA to conduct a risk assessment in order to meet the mandated
schedule to set this regulation by July 1999. As mentioned above, DHS
(1998) also adopts a secondary MCL of five ppb for MTBE to protect the
public from exposure to MTBE in drinking water at levels that can be
smelled or tasted, as an amendment to Table 64449-A, Section 64449,
Article 16, Chapter 15, Division 4, Title 22 of the CCR.
The 1997 act (SB 1189) also requires the evaluation of MTBE for
possible listing under the Safe Drinking Water and Toxic Enforcement
Act of 1986 (Proposition 65) as a chemical known to the State to cause
cancer or reproductive and developmental toxicity on or before January
1, 1999. This involves consideration of the evidence that MTBE causes
these effects by the State's qualified experts for Proposition 65--the
Carcinogen Identification Committee (CIC) and the Developmental and
Reproductive Toxicant (DART) Identification Committee of OEHHA's
Science Advisory Board (OEHHA 1998a, 1998b). These Committees evaluated
MTBE in December 1998; MTBE was not recommended for listing under the
Proposition 65 by either CIC or DART Committee.
The MTBE Public Health and Environmental Protection Act of 1997 (SB
521, Mountjoy) appropriates funds to the UC for specified studies of
the human health and environmental risks and benefits of MTBE. The UC
Toxic Substances Research and Teaching Program is managing the
following six funded projects: (1) an evaluation of the peer-reviewed
research literature on the effects of MTBE on human health, including
asthma, and on the environment by UC Los Angeles (UCLA), (2) an
integrated assessment of sources, fate and transport, ecological risk
and control options for MTBE in surface and ground waters, with
particular emphasis on drinking water supplies by UC Davis, (3)
evaluation of costs and effectiveness of treatment technologies
applicable to remove MTBE and other gasoline oxygenates from
contaminated water by UC Santa Barbara (UCSB), (4) drinking water
treatment for the removal of MTBE from groundwater and surface water
reservoirs by UCLA, (5) evaluation of automotive MTBE combustion
byproducts in California RFG by UC Berkeley, and (6) risk-based
decisionmaking analysis of the cost and benefits of MTBE and other
gasoline oxygenates by UCSB.
Among the SB 521 mandated projects, only the first project
regarding human health effects (Froines 1998, Froines et al. 1998) and
a part of the second project regarding human exposure to MTBE from
drinking water (Johnson 1998) mentioned above are pertinent to the
scope of this report. Their report has been submitted to the Governor
and posted on their web site (www.tsrtp.ucdavis.edu/mtbept/) on
November 12, 1998. In this report, Froines et al. (1998) concluded that
MTBE is an animal carcinogen with the potential to cause cancers in
humans. Also in this report, Johnson (1998) performed a risk analysis
of MTBE in drinking water based on animal carcinogenicity data. The act
requires the report be reviewed and two hearings be held (February 19
and 23, 1999) for the purpose of accepting public testimony on the
assessment and report. The act also requires the Governor to issue a
written certification as to the human health and environmental risks of
using MTBE in gasoline in California.
The American Conference of Governmental Industrial Hygienists
(ACGIH) lists MTBE as an A3 Animal Carcinogen (ACGIH 1996). That is,
MTBE is carcinogenic in experimental animals at relatively high
dose(s), by route(s) of administration, at site(s), of histologic
type(s), or by mechanism(s) that are not considered relevant to
workplace exposure. ACGIH considers that available epidemiological
studies do not confirm an increased risk of cancer in exposed humans.
Available evidence suggests that the agent is not likely to cause
cancer in humans except under uncommon or unlikely routes of exposure
or levels of exposure.
In August 1996 the U.S. Agency for Toxic Substances and Disease
Registry (ATSDR) released the final report ``Toxicological Profile for
MTBE'' which evaluated the toxic effects of MTBE including
carcinogenicity in detail. The cancer effect levels of MTBE through
both inhalation and oral exposure routes have been developed based on
data of carcinogenicity in animals (ATSDR 1996).
The U.S. National Toxicology Program (NTP) did not find MTBE to be
``reasonably anticipated to be a human carcinogen'' in December 1998
(NTP 1998a). The National Institute of Environmental Health Sciences
(NIEHS) Review Committee for the Report on Carcinogens first
recommended (four yes votes to three no votes) that the NTP list MTBE
as ``reasonably anticipated to be a human carcinogen'' in the Ninth
Report on Carcinogens in January 1998 (NTP 1998b). The NTP Executive
Committee Interagency Working Group for the Report on Carcinogens then
voted against a motion to list MTBE (three yes votes to four no votes).
Later in December 1998, the NTP Board of Scientific Counselors Report
on Carcinogens Subcommittee voted against a motion to list MTBE as
``reasonably anticipated to be a human carcinogen. . .'' (five yes
votes to six no votes with one abstention). The conclusions of these
meetings are summarized on the NTP website, however, the supporting
documentation on how these conclusions were reached is still under
preparation and not available to us for evaluation (NTP 1998a). NTP
solicited for final public comments through February 15, 1999 on these
actions.
MTBE has been reviewed by the Environmental Epidemiology Section of
the North Carolina Department of Environment, Health, and Natural
Resources (NCDEHNR) and it was determined that there was limited
evidence for carcinogenicity in experimental animals and that the
compound should be classified as a Group B2 probable human carcinogen
(Rudo 1995). The North Carolina Scientific Advisory Board on Toxic Air
Contaminants (TAC) considered MTBE to be eligible as a Group C possible
human carcinogen (Lucier et al. 1995). New Jersey (NJDWQI 1994, Post
1994) also classified MTBE as a possible human carcinogen. The State of
New York Department of Health is drafting a fact sheet to propose an
ambient water quality value for MTBE based on animal carcinogenicity
data.
The International Agency for Research on Cancer (IARC) of the World
Health Organization (WHO) found ``limited'', but not ``sufficient''
evidence of MTBE carcinogenicity in animals. IARC has recently
classified MTBE as a Group 3 carcinogen (i.e., not classifiable as to
carcinogenicity in humans), based on inadequate evidence in humans and
limited evidence in experimental animals. The conclusions of this
October 1998 IARC Monographs Working Group Meeting are summarized on
the IARC website, however, the supporting documentation on how these
conclusions were reached is still under preparation to be published as
the IARC Monographs Volume 73 (IARC 1998a).
The International Programme on Chemical Safety (IPCS) of WHO has
issued the second draft Environmental Health Criteria on MTBE (IPCS
1997) which was scheduled to be finalized in December 1998. IPCS stated
that carcinogenic findings in animal bioassays seem to warrant some
concern of potential carcinogenic risk to humans, but the document does
not contain a risk characterization. However, the final document is not
available as of February 1999.
European Centre for Ecotoxicology and Toxicology of Chemicals
(ECETOC) prepared a technical report (ECETOC 1997) on MTBE health risk
characterization mainly on occupational inhalation exposure. ECETOC
concluded that MTBE has some potential to increase the occurrence of
certain tumors in female mice or male rats after chronic high-dose
inhalation exposure.
In February 1996 the Office of Science and Technology Policy (OSTP)
through the Committee on Environment and Natural Resources (CENR) of
the White House National Science and Technology Council (NSTC) released
a draft report titled ``Interagency Assessment of Potential Health
Risks Associated with Oxygenated Gasoline'' (NSTC 1996). This report
focused primarily on inhalation exposure to MTBE and its principal
metabolite, TBA. In March 1996 NSTC released the draft document
``Interagency Oxygenated Fuels Assessment'' which addressed issues
related to public health, air and water quality, fuel economy, and
engine performance associated with MTBE in gasoline relative to
conventional gasoline. This document was peer reviewed by the National
Academy of Sciences (NAS) under guidance from the National Research
Council (NRC) which then published its findings and recommendations in
the document ``Toxicological and Performance Aspects of Oxygenated
Motor Vehicle Fuels'' (NRC 1996). The limited review on the potential
health effects of MTBE in the NRC report (1996) considered the animal
carcinogenicity evidence to be positive. The NRC findings were used to
revise the NSTC document and the final report was released in June
1997. The NSTC (1997) concluded: ``there is sufficient evidence that
MTBE is an animal carcinogen''. NSTC (1997) also concluded: ``. . . the
weight of evidence supports regarding MTBE as having a carcinogenic
hazard potential for humans.''
In April 1996 the Health Effects Institute (HEI) released ``The
Potential Health Effects of Oxygenates Added to Gasoline, A Special
Report of the Institute's Oxygenates Evaluation Committee'' (HEI 1996).
HEI (1996) concluded: ``the possibility that ambient levels may pose
some risk of carcinogenic effects in human populations cannot be
excluded''. HEI in summary of studies of long-term health effects of
MTBE concluded: ``Evidence from animal bioassays demonstrates that
long-term, high-level exposures to MTBE by either the oral or
inhalation routes of exposure cause cancer in rodents.''
The U.S. EPA has not established primary or secondary MCLs or a
Maximum Contaminant Level Goal (MCLG) for MTBE but included MTBE on the
Drinking Water Contaminant Candidate List (CCL) published in the
Federal Register on March 2, 1998 (U.S. EPA 1998c, 1997b, 1997d). An
advisory released in December 1997 recommended that MTBE concentration
in the range of 20 to 40 ppb or below would assure both consumer
acceptance of the water and a large margin of safety from any toxic
effects (U.S. EPA 1997a, Du et al. 1998).
On November 30, 1998, the U.S. EPA (1998a) announced the creation
of a blue-ribbon panel to review the important issues posed by the use
of MTBE and other oxygenates in gasoline so that public health concerns
could be better understood. The Panel on Oxygenate Use in Gasoline
under the Clean Air Act Advisory Committee (CAAC), including 12 members
and eight Federal representatives serving as consultants to the Panel,
is to make recommendations to the U.S. EPA on how to ensure public
health protection and continued improvement in both air and water
quality after a 6-month study.
In its 1997 advisory, U.S. EPA agreed with the 1997 NSTC
conclusions and concluded: ``Although MTBE is not mutagenic, a
nonlinear mode of action has not been established for MTBE. In the
absence of sufficient mode of action information at the present time,
it is prudent for EPA to assume a linear dose-response for MtBE.
Although there are no studies on the carcinogenicity of MtBE in humans,
there are multiple animal studies (by inhalation and gavage routes in
two rodent species) showing carcinogenic activity and there is
supporting animal carcinogenicity data for the metabolites. The weight
of evidence indicates that MtBE is an animal carcinogen, and the
chemical poses a carcinogenic potential to humans (NSTC, 1997, page 4-
26).'' The U.S. EPA (1994a, 1994c) proposed in 1994 to classify MTBE as
a Group C possible human carcinogen based upon animal inhalation
studies (published in 1992). At that time, U.S. EPA noted that a Group
B2 probable human carcinogen designation may be appropriate if oral
MTBE exposure studies in animals (published later in 1995) result in
treatment-related tumors.
In 1987, MTBE was identified by the U.S. EPA (1987a) under Section
Four of the Toxic Substances Control Act (TSCA) for priority testing
because of its large production volume, potential widespread exposure,
and limited data on long-term health effects (Duffy et al. 1992). The
results of the testing have been published in a peer-reviewed journal
(Bevan et al. 1997a, 1997b, Bird et al. 1997, Daughtrey et al. 1997,
Lington et al. 1997, McKee et al. 1997, Miller et al. 1997, Stern and
Kneiss 1997).
California Environmental Protection Agency (Cal/EPA) has reported
some background information and ongoing activities on MTBE in
California's ``cleaner-burning fuel program'' in a briefing paper (Cal/
EPA 1998). U.S. EPA (1996d, 1996e) published fact sheets on MTBE in
water in addition to several advisory documents. While concerns have
been raised about its potential health impacts, based on hazard
evaluation of the available data, MTBE is substantially less hazardous
than benzene (a Group A human carcinogen) and 1,3-butadiene (a Group B2
probable human carcinogen), two carcinogenic chemicals it displaces in
California's new gasoline formulations (Spitzer 1997). Potential health
benefits from ambient O3 reduction related to the use of
MTBE in RFG were evaluated (Erdal et al. 1997). Whether the addition of
MTBE in gasoline represents a net increase in cancer hazard is beyond
the scope of this document.
In this document, the available data on the toxicity of MTBE
primarily by the oral route based on the reports mentioned above are
evaluated, and information available since the previous assessment by
NSTC (1997) and U.S. EPA (1997a) is included. As indicated by the
summaries provided above, there has been considerable scientific
discussion regarding the carcinogenicity of MTBE and the relevance of
the animal cancer study results to humans. Also indicated above,
especially by some of the reported votes of convened committees, there
is a considerable disagreement regarding the quality and relevance of
the animal data among scientists. However, some of the disagreement
stems from the differences in the level of evidence considered adequate
for different degrees of confidence by the scientists considering the
evidence. There is a greater level of evidence required to conclude
that the data clearly show that humans are at cancer risk from exposure
than to conclude that there may be some cancer risk or that it is
prudent to assume there is a cancer risk to humans. In order to
establish a PHG in drinking water, a nonregulatory guideline based
solely on public health considerations, the prudent assumption of
potential cancer risk was made. To determine a public health-protective
level of MTBE in drinking water, relevant studies were identified,
reviewed and evaluated, and sensitive groups and exposure scenarios are
considered.
chemical profile
Chemical Identity
MTBE [(CH3)3C(OCH3), CAS Registry
Number 1634-04-4] is a synthetic chemical without known natural
sources. The chemical structure, synonyms, and identification numbers
are listed in Table I and are adapted from the Merck Index (1989),
Hazardous Substances Data Bank (HSDB) of the National Library of
Medicine (1997), Integrated Risk Information Systems (IRIS) of U.S. EPA
(1997c), TOMES PLUS (Hall and Rumack 1998) computerized data
base, and the ATSDR (1996), Cal/EPA (1998), ECETOC (1997), HEI (1996),
NRC (1996), NSTC (1996, 1997), and U.S. EPA (1997a) documents.
TOMES (Toxicology and Occupational Medicine System) PLUS
is a computerized data base which includes the data systems of Hazard
Management, INFOTEXT, HAZARDTEXT,
MEDITEXT, REPROTEXT, SERATEXT, HSDB,
IRIS, Registry of Toxic Effects of Chemical Substances
(RTECS) of National Institute for Occupational Safety and
Health (NIOSH), Chemical Hazard Response Information System (CHRIS) of
U.S. Coast Guard, Oil and Hazardous Materials/Technical Assistance Data
System (OHM/TADS) of U.S. EPA, Department of Transportation (DOT)
Emergency Response Guide, New Jersey Hazardous Substance Fact Sheets
(NJHSFS), North American Emergency Response Guidebook Documents (NAERG)
of U.S. DOT, Transport Canada and the Secretariat of Communications and
Transportation of Mexico, REPROTOX System of the Georgetown
University, Shepard's Catalog of Teratogenic Agents of the Johns
Hopkins University, Teratogen Information System (TERIS) of the
University of Washington, and NIOSH Pocket Guide(TM). For
MTBE, TOMES PLUS (Hall and Rumack 1998) contains entries in
HAZARDTEXT, MEDITEXT, REPROTEXT,
REPROTOX, HSDB, IRIS, RTECS, NAERG and NJHSFS.
Physical and Chemical Properties
Important physical and chemical properties of MTBE are given in
Table 2 and are adapted from Merck Index (1989), HSDB (1997), TOMES
PLUS (Hall and Rumack 1998), and the ATSDR (1996), Cal/EPA
(1998), HEI (1996), NRC (1996), NSTC (1996, 1997), and U.S. EPA (1997a)
documents.
MTBE, an aliphatic ether, is a volatile organic compound (VOC) with
a characteristic odor. It is a colorless liquid at room temperature. It
is highly flammable and combustible when exposed to heat or flame or
spark, and is a moderate fire risk. Vapors may form explosive mixtures
with air. It is unstable in acid solutions. Fire may produce
irritating, corrosive or toxic gases. Runoff from fire control may
contain MTBE and its combustion products (HSDB 1997).
MTBE is miscible in gasoline and soluble in water, alcohol, and
other ethers. It has a molecular weight of 88.15 daltons, a vapor
pressure of about 245 mmHg at 25 +C, an octane number of 110, and
solubility in water of about 50 g/L at 25 +C. It disperses evenly in
gasoline and water and stays suspended without requiring physical
mixing. It does not increase volatility of other gasoline components
when it is mixed in the gasoline. MTBE released to the environment via
surface spills or subsurface leaks was found to initially partition
between water and air (Jeffrey 1997). The log of the octanol-water
partition coefficient (log Kow) is reported to range from
0.94 to 1.24 which indicates that there is 10 times more partitioning
of MTBE in the lipophilic phase than in the aqueous phase of solvents.
The molecular size and log Kow of MTBE are characteristic of
molecules which are able to penetrate across biological membranes of
the skin, lungs and gastrointestinal tracts (Mackay et al. 1993, Nihlen
et al. 1995). The octanol-water partition coefficient is reported to be
16 by Nihlen et al. (1997). Fujiwara et al. (1984) reported laboratory-
derived octanol-water partition coefficients ranging from 17.2 to 17.5
with a log Kow of 1.2. The blood-air, urine-air, saline-air,
fat-air and oil-air partition coefficients (lambda) are reported to be
20, 15.6, 15.3, 142 and 138, respectively (Imbriani et al. 1997). One
part per million (ppm) of MTBE, volume to volume in air, is
approximately 3.6 mg/m3 of air at 20 +C (ATSDR 1996).
organoleptic properties
Taste or odor characteristics, often referred to as organoleptic
properties, are not used by U.S. EPA or DHS for developing primary
drinking water standards, but are used for developing secondary
standards. The estimated thresholds for these properties of MTBE
reported in the literature are given in Table 3 and are adapted from
the ATSDR (1996), Cal/EPA (1998), HEI (1996), HSDB (1997), NSTC (1996,
1997), and U.S. EPA (1997a) documents. Taste and odor may alert
consumers to the fact that the water is contaminated with MTBE (Angle
1991) and many people object to the taste and odor of MTBE in drinking
water (Killian 1998, Reynolds 1998). However, not all individuals
respond equally to taste and odor because of differences in individual
sensitivity. It is not possible to identify point threshold values for
the taste and odor of MTBE in drinking water, as the concentration will
vary for different individuals, for the same individuals at different
times, for different populations, and for different water matrices,
temperatures, and many other variables.
The odor threshold ranges from about 0.32 to 0.47 mg/m3
(about 90 to 130 ppb) in air and can be as low as five ppb (about 0.02
mg/m3) for some sensitive people. In gasoline containing 97
percent pure MTBE at mixture concentrations of 3 percent, 11 percent
and 15 percent MTBE, the threshold for detecting MTBE odor in air was
estimated to be 50 ppb (about 0.18 mg/m3), 280 ppb (about
one mg/m3), and 260 ppb (about 0.9 mg/m3),
respectively (ACGIH 1996). A range of 5 ppb to 53 ppb (about 0.19 mg/
m3) odor threshold in the air was reported in an American
Petroleum Institute (API) document (API 1994).
The individual taste and odor responses reported for MTBE in water
are on average in the 15 to 180 ppb (g/L) range for odor and
the 24 to 135 ppb range for taste (API 1994, Prah et al. 1994, Young et
al. 1996, Dale et al. 1997b, Shen et al. 1997, NSTC 1997). The ranges
are indicative of the average variability in individual response. U.S.
EPA (1997a) has analyzed these studies in detail and recommended a
range of 20 to 40 ppb as an approximate threshold for organoleptic
responses. The study (Dale et al. 1997b) by the Metropolitan Water
District of Southern California (MWDSC) found people more sensitive to
the taste than odor. This result is consistent with API's (1994)
findings for MTBE taste and odor thresholds. But in the study by Young
et al. (1996), test subjects were more sensitive to odor than taste.
The subjects described the taste of MTBE in water as ``nasty'',
``bitter'', ``nauseating'', and ``similar to rubbing alcohol'' (API
1994)
It is noted that chlorination and temperature of the water would
likely affect the taste and odor of MTBE in water. Thresholds for the
taste and odor of MTBE in chlorinated water would be higher than
thresholds of MTBE in nonchlorinated water. Thresholds for the taste
and odor of MTBE in water at higher temperatures (e.g., for showering)
would likely be lower than those of MTBE in water at lower
temperatures.
There were undoubtedly individuals who could only detect the odor
of MTBE at even higher concentrations than 180 ppb (Prah et al. 1994).
Odor thresholds as high as 680 ppb have been reported (Gilbert and
Calabrese 1992). On the other hand, some subjects in these studies were
able to detect the odor of MTBE in water at much lower concentrations,
i.e. 2.5 ppb (Shen et al. 1997), five ppb (McKinnon and Dyksen 1984),
or 15 ppb (Young et al. 1996). Some sensitive subjects in the taste
studies were able to detect MTBE in water at concentrations as low as
two ppb (Dale et al. 1997b), 10 ppb (Barker et al. 1990), 21 ppb (Dale
et al. 1997b), or 39 ppb (Young et al. 1996). Thus, in a general
population, some unknown percentage of people will be likely to detect
the taste and odor of MTBE in drinking water at concentrations below
the U.S. EPA (1997a) 20 to 40 ppb advisory level. DHS (1997) has
recently proposed five ppb as the secondary MCL for MTBE. The lowest
olfaction threshold in water is likely to be at or about 2.5 ppb (Shen
et al. 1997). The lowest taste threshold in water is likely to be at or
about two ppb (Dale et al. 1997b).
______
Table 1.--Chemical Identity of Methyl Tertiary Butyl Ether (MTBE)
------------------------------------------------------------------------
Characteristic Information Reference
------------------------------------------------------------------------
Chemical Name................... Methyl tertiary Merck 1989
butyl ether.
Synonyms........................ Methyl tertiary- Merck 1989
butyl ether;.
Methyl tert-butyl
ether; tert-butyl
methyl ether;
tertiary-butyl
methyl ether;
methyl-1, 1-
dimethylethyl
ether; 2-methoxy-
2-methylpropane;
2-methyl-2-
methoxypropane;
methyl t-butyl
ether; MTBE; MTBE.
Registered trade names.......... No data........... ..................
Chemical formula................ C5H12O or Merck 1989
(CH3)3C(OCH3).
Chemical structure
Identification numbers:
Chemical Abstracts Service 1634-04-4......... Merck 1989
(CAS) Registry number.
National Institute for KN5250000......... HSDB 1997
Occupational Safety and
Health (NIOSH) Registry of
Toxic Effects of Chemical
Substances (RTECS) number.
Department of Transportation/ UN 2398,IMO 3.2... HSDB 1997
United Nations/North America/
International Maritime
Dangerous Goods Code (DOT/UN/
NA/IMCO) Shipping number.
Hazardous Substances Data Bank 5847.............. HSDB 1997
(HSDB) number.
North American Emergency 127............... HSDB 1997
Response Guidebook Documents
(NAERG) number.
National Cancer Institute No data........... ..................
(NCI) number.
U.S. Environmental Protection No data........... ..................
Agency (U.S. EPA) Hazardous
Waste number.
U.S. EPA Oil and Hazardous No data........... ..................
Materials/Technical
Assistance Data System (OHM/
TADS) number.
European EINECS number........ 216.653.1......... ECETOC 1997
------------------------------------------------------------------------
Table 2.--Chemical Physical Properties of MTBE
------------------------------------------------------------------------
Value or
Property information Reference
------------------------------------------------------------------------
Molecular weight................ 88.15 g/mole...... Merck 1989
Color........................... colorless......... Merck 1989
Physical state.................. liquid............ Merck 1989
Melting point................... -109C............. HSDB 1997
Boiling point................... 53.6-55.2C........ Mackay et al. 1993
Density at 20C.................. 0.7404-0.7578 g/mL Squillace et al.
1997a
Solubility:
in water...................... 4.8 g/100 g water. Merck 1989
in water...................... 23.2-54.4 g/L Garrett et al.
water. 1986, Mackay et
al. 1993
in water...................... 43-54.3 g/L water. Squillace et al.
1997a
in water, 20C................. 4-5 percent....... Gilbert and
Calabrese 1992
in water, 25C................. 51 g/L water...... HSDB 1997
Partition coefficients
octanol-water................. 16................ Nihlen et al. 1997
17.2-17.5......... Fujiwara et al.
1984
Log Kow....................... 0.94-1.16......... Mackay et al. 1993
1.2............... Fujiwara et al.
1984
1.24.............. U.S. EPA 1997a
Log Koc....................... 1.05 (estimated).. Squillace et al.
1997a
2.89 (calculated). U.S. EPA 1995b
Vapor pressure:
at 25C........................ 245-251 mm Hg..... Mackay et al. 1993
at 100 F...................... 7.8 psi (Reid ARCO 1995a
Vapor Pressure).
Henry's law constant............ 0.00058-0.003 atm- Mackay et al. 1993
m3/mole.
at 25C........................ 5.87 10- ATSDR 1996
4 atm-m3/mole.
at 15C........................ 0.011 Robbins et a. 1993
(dimensionless).
Ignition temperature............ 224C.............. Merck 1989
Flash point..................... -28C.............. Merck 1989
28C (closed cup).. Gilbert and
Calabrese 1992
Explosion limits................ 1.65 to 8.4 Gilbert and
percent in air. Calabrese 1992
Heat of combustion.............. 101,000 Btu/gal at HSDB 1997
25C.
Heat of vaporization............ 145 Btu/lb at 55C. HSDB 1997
Stability....................... MTBE is unstable Merck 1989
in acidic
solution.
Conversion factors:
ppm (v/v) to mg/m3 in air at 1 ppm = 3.61 mg/m3 ACGIH 1996
25C.
mg/m3 to ppm (v/v) in air at 1 mg/m3 = 0.28 ppm ACGIH 1996
25C.
------------------------------------------------------------------------
Table 3.--Organoleptic Properties of MTBE
------------------------------------------------------------------------
Value or
Property information Reference
------------------------------------------------------------------------
Odor Taste...................... terpene-like at Gilbert and
25C. Calabrese 1992
Threshold in air.............. 300 ppb........... Smith and Duffy
1995
0.32-0.47 mg/m3... ACGIH 1996
(90-13 ..................
0 ppb).
5-53 ppb API 1994
(detection).
99 percent pure MTBE........ 8 ppb API 1994
(recognition).
97 percent pure MTBE........ 125 ppb API 1994
(recognition).
97 percent pure MTBE in
gasoline.
15 percent MTBE........... 260 ppb........... ACGIH 1996
11 percent MTBE........... 280 ppb........... ACGIH 1996
3 percent MTBE............ 50 ppb............ ACGIH 1996
Threshold in water............ 680 ppb........... Gilbert and
Calabrese 1992
180 ppb........... Prah et al. 1994
95 ppb............ ARCO 1995a
55 ppb API 1994
(recognition).
45 ppb (detection) API 1994
15-95 ppb (mean 34 Young et al. 1996
ppb).
15-180 ppb........ U.S. EPA 1997a
13.5-45.4 ppb..... Shen et al. 1997
5-15 ppb.......... McKinnon and
Dyksen 1984
2.5 ppb........... Shen et al. 1997
Taste........................... solvent-like at U.S. EPA 1997a
25C.
Threshold in water............ 21-190 ppb........ Dale et al. 1997b
24-135 ppb........ U.S. EPA 1997a
39-134 ppb (mean Young et al. 1996
48 ppb).
39-134 ppb........ API 1994
10-100 ppb........ Barker et al. 1990
2 ppb (one Dale et al. 1997b
subject).
------------------------------------------------------------------------
Production and Uses
MTBE is manufactured from isobutene; also known as isobutylene or
2-methylpropene (Merck 1989), which is a product of petroleum refining.
It is made mainly by combining methanol with isobutene, or dervied from
combining methanol and TBA. It is used primarily as an oxygenate in
unleaded gasoline, in the manufacture of isobutene, and as a
chromatographic effluent especially in high pressure liquid
chromatography (ATSDR 1996, HSDB 1997). MTBE also has had a limited use
as a therapeutic drug for dissolving cholesterol gallbladder stones
(Leuschner et al. 1994).
MTBE is the primary oxygenate used in gasoline because it is the
least expensive and in greatest supply. It is promoted as a gasoline
blending component due to its high octane rating, low cost of
production, ability to readily mix with other gasoline components, ease
in distribution through existing pipelines, distillation temperature
depression, and beneficial dilution effect on undesirable components of
aromatics, sulfur, olefin and benzene. In addition, the relatively low
co-solvent volatility of MTBE does not result in a more volatile
gasoline that could be hazardous in terms of flammability and
explosivity. The use of MTBE has helped offset the octane specification
loss due to the discontinued use of higher toxicity high octane
aromatics and has reduced emissions of benzene, a known human
carcinogen, and 1,3-butadiene, an animal carcinogen (Cal/EPA 1998,
Spitzer 1997).
MTBE has been commercially used in Europe since 1973 as an octane
enhancer to replace lead in gasoline and was approved as a blending
component in 1979 by U.S. EPA. Since the early 1990's, it has been used
in reformulated fuel in 18 states in the U.S. Under Section 211 of the
1990 CAAA, the Federal oxyfuel program began requiring gasoline to
contain 2.7 percent oxygen by weight which is equivalent to roughly 15
percent by volume of MTBE be used during the four winter months in
regions not meeting CO reduction standards in November 1992. In January
1995, the Federal RFG containing 2 percent oxygen by weight or roughly
11 percent of MTBE by volume was required year-round to reduce
O3 levels. Oxygenates are added to more than 30 percent of
the gasoline used in the U.S. and this proportion is expected to rise
(Squillace et al. 1997a).
In California, Federal law required the use of Phase I RFG in the
worst polluted areas including Los Angeles and San Diego as of January
1, 1995, and in the entire State as of January 1, 1996. By June 1,
1996, State law required that all gasoline sold be California Phase 2
RFG and Federal Phase II RFG will be required by the year 2000
(Cornitius 1996). MTBE promotes more complete burning of gasoline,
thereby reducing CO and O3 levels in localities which do not
meet the National Ambient Air Quality Standards (ATSDR 1996, USGS
1996). Almost all of the MTBE produced is used as a gasoline additive;
small amounts are used by laboratory scientists (ATSDR 1996). When used
as a gasoline additive, MTBE may constitute up to 15 percent volume to
volume of the gasoline mixture. Currently, MTBE is added to virtually
all of the gasoline consumed in California (Cal/EPA 1998).
The amount of MTBE used in the U.S. has increased from about 0.5
million gallons per day in 1980 to over 10 million gallons per day in
early 1997. Of the total amount of MTBE used in the U.S., approximately
70 percent are produced domestically, about 29 percent are imported
from other countries, and about 1 percent is existing stocks. Over 4.1
billion gallons of MTBE are consumed in the U.S. annually, including
1.49 billion gallons--more than 36 percent of the national figure--in
California (Wiley 1998). California uses about 4.2 million gallons per
day of MTBE, about 85 percent of which is imported into the state,
primarily by ocean tankers from the Middle East (Cal/EPA 1998).
California also imports MTBE from Texas and other major MTBE-producing
states in the U.S.
MTBE production in the U.S. began in 1979 and increased rapidly
after 1983. It was the second most-produced chemical, in terms of
amount, in the U.S. in 1997, whereas previously it was ranked the
twelfth in 1995 and eighteenth in 1994 (Cal/EPA 1998, Kirschner 1996,
Reisch 1994). The production was 13.61 million pounds in 1994 and 17.62
million pounds in 1995 (Kirschner 1996). MTBE production was estimated
at about 2.9 billion gallons in the U.S. and about 181 million gallons
in California in 1997 (Wiley 1998). MTBE is manufactured at more than
40 facilities by about 27 producers primarily concentrated along the
Houston Ship Channel in Texas and the Louisiana Gulf Coast. Texas
supplies about 80 percent of the MTBE produced in the U.S. with about
10 percent produced in Louisiana and about 5 percent in California
(Cal/EPA 1998). The major portion of MTBE produced utilizes, as a co-
reactant, isobutylene that is a waste product of the refining process
(Wiley 1998).
environmental occurrence and human exposure
The NSTC (1997) report provides extensive occurrence data for MTBE
and other fuel oxygenates, as well as information on applicable
treatment technologies. Similar information, specifically based on data
in California, can be found in the recent UC (1998) report mandated
under SB 521. For additional information concerning MTBE in the
environment, the NSTC report can be accessed through the NSTC Home Page
via a link from the OSTP. The U.S. Geological Survey (USGS) has been
compiling data sets for national assessment of MTBE and other VOCs in
ground and surface water as part of the National Water-Quality
Assessment (NAWQA) Program (Buxton et al. 1997, Lapham et al. 1997,
Squillace et al. 1997a, 1997b, Zogorski et al. 1996, 1997). Information
on analytical methods for determining MTBE in environmental media is
compiled in the ATSDR (1996) Toxicological Profile document.
The U.S. EPA (1993, 1995a) estimated that about 1.7 million
kilograms (kgs) MTBE were released from 141 facilities reporting in the
Toxics Release Inventory (TRI) per year, 97.3 percent to air, 2.44
percent to surface water, 0.25 percent to underground injection, and
0.01 percent to land. Cohen (1998) reported that an estimated 27,000
kgs or 30 tons per day were emitted from 9,000 tons of MTBE consumed in
California per day. The California Air Resources Board (ARB) estimated
that the exhaust and evaporative emission was about 39,000 kgs or 43
tons per day in California in 1996 (Cal/EPA 1998).
A multimedia assessment of refinery emissions in the Yorktown
region (Cohen et al. 1991) indicated that the MTBE mass distribution
was over 73 percent in water, about 25 percent in air, less than 2
percent in soil, about 0.02 percent in sediment, about 10-6
percent in suspended solids, and 10-7 percent in biota. A
recent laboratory study on liquid-gas partitioning (Rousch and
Sommerfeld 1998) suggests that dissolved MTBE concentrations can vary
substantially from nominal. The main route of exposure for occupational
and non-occupational groups is via inhalation, ingestion is considered
as secondary, and dermal contact is also possible.
The persistence half-life of MTBE (Jeffrey 1997) is about 4 weeks
to 6 months in soil, about 4 weeks to 6 months in surface water, and
about 8 weeks to 12 months in groundwater based on estimated anaerobic
biodegradation, and about 20.7 hours to 11 days in air based on
measured photooxidation rate constants (Howard et al. 1991, Howard
1993). Church et al. (1997) described an analytical method for
detecting MTBE and other major oxygenates and their degradation
products in water at sub-ppb concentrations. MTBE appears to be
biodegraded under anaerobic conditions (Borden et al. 1997, Daniel
1995, Jensen and Arvin 1990, Mormile et al. 1994, Steffan et al. 1997).
Brown et al. (1997) and Davidson and Parsons (1996) reviewed state-of-
the-art remediation technologies for treatment of MTBE in water.
McKinnon and Dyksen (1984) described the removal of MTBE from
groundwater through aeration plus granulated activated charcoal (GAC).
Koenigsberg (1997) described a newly developed bioremediation
technology for MTBE cleanup in groundwater. Cullen (1998) reported a
one-year field test of a polymer-enhanced carbon technology for MTBE
removal at the drinking water supply source.
Air, Soil, Food, and Other Sources
The presence of MTBE in ambient air is documented and likely to be
the principal source of human exposure. MTBE is released into the
atmosphere during the manufacture and distribution of oxyfuel and RFG,
in the vehicle refueling process, and from evaporative and tailpipe
emissions from motor vehicles. The general public can be exposed to
MTBE through inhalation while fueling motor vehicles or igniting fuel
under cold startup conditions (Lindstrom and Pleil 1996). The level of
inhaled MTBE at the range relevant to human exposures appears to be
directly proportional to the MTBE concentrations in air (Big/dynamics,
Inc. 1981, 1984c, Niblen et al. 1994). In air, MTBE may represent 5 to
10 percent of the VOCs that are emitted from gasoline-burning vehicles,
particularly in areas where MTBE is added to fuels as part of an
oxygenated fuel program (ARCO 1995a). MTBE has an atmospheric lifetime
of approximately 4 days and its primary byproducts are tert-butyl
formate (TBF), formaldehyde (HCHO), acetic acid, acetone, and TBA.
MTBE was found in urban air in the U.S. (Zogorski et al. 1996,
1997) and the median concentrations ranged from 0.13 to 4.6 parts per
billion by volume (ppbv). Fairbanks, Alaska reported concentrations
ranging from two to six ppbv when the gasoline contained 15 percent
MTBE (CDC 1993a). Grosjean et al. (1998) reported ambient
concentrations of ethanol and MTBE at a downtown location in Porto
Alegre, Brazil where about 74 percent of about 600,000 vehicles use
gasoline with 15 percent MTBE, from March 20, 1996 to April 16, 1997.
Ambient concentrations of MTBE ranged from 0.2 to 17.1 ppbv with an
average of 6.6 4.3 ppbv. This article also cited
unpublished data including Cape Cod (four samples, July to August
1995): 39 to 201 parts per trillion by volume (pptv or 1/1,000 ppbv),
Shenandoah National Park (14 samples, July to August 1995): less or
equal to (>) seven pptv, Brookhaven (16 samples, July to August 1995):
33 to 416 pptv, Wisconsin (62 samples, August 1994 to December 1996,
with all but five samples yielding no detectable MTBE with a detection
limit of 12 pptv): >177 pptv, and downtown Los Angeles, California (one
sample, collected in 1993 prior to the introduction of California RFG
with MTBE): 0.8 ppbv.
Ambient levels of MTBE in California are similar or slightly higher
than the limited data suggest for other states. The results of two
recent (from 1995 to 1996) monitoring surveys (Poore et al. 1997,
Zielinska et al. 1997) indicate that ambient levels of MTBE averaged
0.6 to 7.2 ppbv with sampling for 3 hours at four southern California
locations, and 1.3 to 4.8 ppbv with sampling for 24 hours at seven
California locations. The Bay Area Air Quality Management District
(BAAQMD) has an 18-station network and has been monitoring for MTBE
since 1995. The average concentration of MTBE in the San Francisco Bay
area is approximately one ppbv (Cal/EPA 1998).
The ARB established a 20-station TAC air-monitoring network in
1985, and began analyzing ambient air for MTBE in 1996 (ARB 1996).
Preliminary data suggest a statewide average of approximately two ppbv
with higher concentrations in the South Coast of about four ppbv. The
limit of detection is 0.2 ppbv. The Desert Research Institute, under
contract to ARB as a part of the 1997 Southern California Ozone Study
(Fujita et al. 1997), monitored for MTBE in July through September 1995
and 1996 in Southern California, at the Asuza, Burbank, and North Main
monitoring sites. The monitoring was designed to determine peak morning
rush hour concentrations (6 to 9 a.m.) and was part of a comprehensive
study to analyze reactive organics in the South Coast Air Basin. The
results showed a mean of approximately four ppbv with a range of one to
11 ppbv. These concentrations are similar to the ARB findings. Although
ARB sampled for 24 hours, the highest concentrations are seen in the
morning rush hour traffic because MTBE is a tailpipe pollutant.
Industrial hygiene monitoring data for a MTBE operating unit shows
an average 8-hour exposure of 1.42 ppm. Average exposure for
dockworkers was determined to be 1.23 ppm. Occupational exposure to
gasoline containing two to 8 percent MTBE is estimated at one to 1.4
ppm per day (ARCO 1995a, 1995b). In a New Jersey study, MTBE
concentrations as high as 2.6 ppm were reported in the breathing zone
of individuals using self-service gasoline stations without vapor
recovery equipment, and the average MTBE exposure among service station
attendants was estimated to be below one ppm when at least 12 percent
MTBE was used in fuels (Hartle 1993). The highest Canadian predicted
airborne concentration of 75 ng/m3 is 3.9
107 times lower than the lowest reported effect level of
2,915 mg/m3 in a subchronic inhalation study in rats
(Environmental Canada 1992, 1993, Long et al. 1994).
In a Finnish study based on inhalation exposure (Hakkola and
Saarinen 1996), oil company road tanker drivers were exposed to MTBE
during loading and delivery at concentrations between 13 and 91 mg/m3
(about 3.6 to 25 ppm) and the authors suggested some improvement
techniques to reduce the occupational exposure. A recent Finnish study,
Saarinen et al. (1998) investigated the exposure and uptake of 11
drivers to gasoline vapors during road-tanker loading and unloading. On
average the drivers were exposed to vapors for 21 14
minutes, three times during a work shift. The mean concentration of
MTBE was 8.1 8.4 mg/m3 (about 2.3 ppm).
Vainiotalo et al. (1999) studied customer breathing zone exposure
during refueling for 4 days in summer 1996 at two Finnish self-service
gasoline station with ``stage 1'' vapor recovery systems. The MTBE
concentration ranged from less than 0.02 to 51 mg/m3. The
geometric mean concentration of MTBE in individual samples was 3.9 mg/
m3 at station A and 2.2 mg/m3 at station B. The
average refueling (sampling) time was 63 seconds at station A and 74
seconds at station B. Mean MTBE concentration in ambient air (a
stationary point in the middle of the pump island) was 0.16 mg/
m3 for station A and 0.07 mg/m3 for station B.
Exposure to CO, MTBE, and benzene levels inside vehicles traveling
in an urban area in Korea was reported (Jo and Park 1998). The in-
vehicle concentrations of MTBE were significantly higher (p < 0.0001),
on the average 3.5 times higher, in the car with a carbureted engine
than in the other three electronic fuel-injected cars. The author
considered the in-auto MTBE levels, 48.5 g/m3
(about 13 ppb) as a median, as two to three times higher than the
measurements in New Jersey and Connecticut. Goldsmith (1998) reported
that vapor recovery systems could reduce risks from MTBE.
Unlike most gasoline components that are lipophilic, the small,
water-soluble MTBE molecule has low affinity for soil particles and
moves quickly to reach groundwater. In estuaries, MTBE is not expected
to stay in sediment soil but can accumulate at least on a seasonal
basis in sediment interstitial water (ATSDR 1996). There are no
reliable data on MTBE levels in food, but food is not suspected as a
significant source of exposure to MTBE. There is little information on
the presence of MTBE in plants or food chains. The bioconcentration
potential for MTBE in fish is rated as insignificant based on the
studies with Japanese carp by Fujiwara et al. (1984) generating
bioconcentration factors for MTBE ranging from 0.8 to 1.5. Limited data
suggest that MTBE will not bioaccumulate in fish or food chains (ATSDR
1996). Based on fugacity modeling and limited information on
concentrations in shellfish, it is estimated that the average daily
intake of MTBE for the age group of the Canadian population most
exposed on a body weight basis, i.e., 5 to 11-year-olds, is 0.67 ng/kg/
day (Environmental Canada 1992, 1993, Long et al. 1994).
Water
MTBE, being a water-soluble molecule, binds poorly to soils and
readily enters surface and underground water. MTBE appears to be
resistant to chemical and microbial degradation in water (ATSDR 1996).
When it does degrade, the primary product is TBA. Two processes,
degradation and volatilization, appear to reduce the concentrations of
MTBE in water (Baehr et al. 1997, Borden et al. 1997, Schirmer and
Baker 1998). The level of ingested MTBE from drinking water at the
range relevant to human exposures appears to be directly proportional
to the MTBE concentrations in water (Big/dynamics, Inc. 1981, 1984c,
Nihlen et al. 1994). The concentrations of MTBE in Canadian surface
water predicted under a worst-case scenario is six ppt (or six ng/L),
which is 1.12 108 times lower than the 96-hour
LC50 for fathead minnow of 672 ppm (or 672 mg/L)
(Environmental Canada 1992, 1993). The transport, behavior and fate of
MTBE in streams have been summarized by the USGS NAWQA Program (Rathbun
1998).
MTBE can be a water contaminant around major production sites,
pipelines, large tank batteries, transfer terminals, and active or
abandoned waste disposal sites. It tends to be the most frequently
detected VOC in shallow groundwater (Bruce and McMahon 1996). The
primary release of MTBE into groundwater is from leaking USTs. Gasoline
leaks, spills or exhaust, and recharge from stormwater runoff
contribute to MTBE in groundwater. In small quantities, MTBE in air
dissolves in water such as deposition in rain (Pankow et al. 1997).
Recreational gasoline-powered boating and personal watercraft is
thought to be the primary source of MTBE in surface water. MTBE has
been detected in public drinking water systems based on limited
monitoring data (Zogorski et al. 1997). Surveillance of public drinking
water systems in Maine, begun in February 1997, has detected MTBE at
levels ranging from 1 to 16 ppb in 7 percent of 570 tested systems with
a median concentration of three ppb (IPCS 1997, Smith and Kemp 1998).
Sampling program conducted during summer of 1998 found trace levels of
MTBE in 15 percent of Maine's drinking water supplies. Concentrations
above 38 ppb were found in 1 percent of the wells (Renner 1999).
MTBE is detected in groundwater following a reformulated fuel spill
(Garrett et al. 1986, Shaffer and Uchrin 1997). MTBE in water can be
volatilized to air, especially at higher temperature or if the water is
subjected to turbulence. However, it is less easily removed from
groundwater than other VOCs such as benzene, toluene, ethylbenzene, and
xylenes (BTEX) that are commonly associated with gasoline spills. MTBE
and BTEX are the most water-soluble fractions in gasoline and therefore
the most mobile in an aquifer system. Based on equilibrium fugacity
models and especially during warm seasons, the high vapor pressure of
MTBE leads to partitioning to air and half-lives in moving water are
estimated around 4.1 hours (Davidson 1995, Hubbard et al. 1994). In
shallow urban groundwater, MTBE was not found with BTEX. Landmeyer et
al. (1998) presented the areal and vertical distribution of MTBE
relative to the most soluble gasoline hydrocarbon, benzene, in a
shallow gasoline-contaminated aquifer and biodegradation was not a
major attenuation process at this site. MTBE may be fairly persistent
since it is refractory to most types of biodegradation (Borden et al.
1997, Daniel 1995, Jensen and Arvin 1990). Adsorption is expected to
have little effect and dissolved MTBE will move at the same rate as the
groundwater. MTBE may be volatilized into air or into soil gas from
groundwater and these mechanisms may account for the removal of MTBE
from groundwater.
MTBE has been detected in water, mainly by the USGS, in Colorado
(Livo 1995, Bruce and McMahon 1996), California (Boughton and Lico
1998), Connecticut (Grady 1997), Georgia, Indiana (Fenelon and Moore
1996), Maine (Smith and Kemp 1998), Maryland (Daly and Lindsey 1996),
Massachusetts (Grady 1997), Minnesota, Nevada (Boughton and Lico 1998),
New Hampshire (Grady 1997), New Jersey (Terracciano and O'Brien 1997,
O'Brien et al. 1998), New Mexico, New York (Stackelberg et al. 1997,
Lince et al. 1998, O'Brien et al. 1998), North Carolina (Rudo 1995),
Pennsylvania (Daly and Lindsey 1996), South Carolina (Baehr et al.
1997), Texas, Vermont (Grady 1997), Wisconsin and other states. A
recent USGS NAWQA survey (Boughton and Lico 1998) reported the
detection of MTBE in Lake Tahoe, Nevada and California, from July to
September 1997, in concentrations ranging from 0.18 to 4.2 ppb and to
depths of 30 meters. Zogorski et al. (1998) summarized the findings and
research by the USGS in ground and surface water that MTBE has been
detected in 14 percent of urban wells and 2 percent of rural wells
sampled from aquifers used for drinking water.
USGS has published the results of the NAWQA Program (Squillace et
al. 1995, 1996, 1997a, 1997b, 1998) of monitoring wells, which are not
drinking water wells. This program analyzed concentrations of 60 VOCs
from 198 shallow wells and 12 springs in eight urban areas (none in
California) and 549 shallow wells in 21 agricultural areas (including
the San Joaquin Valley). MTBE was detected in 27 percent of the urban
wells and springs and I.3 percent of the agricultural wells. The
average MTBE concentration found in shallow groundwater was 0.6 ppb.
MTBE was the second most frequently detected VOC (behind chloroform) in
shallow groundwater in urban wells with a detection frequency of 27
percent of the 210 wells and springs sampled (Anonymous 1995, Squillace
et al. 1996, Zogorski et al. 1998). No MTBE was detected in 100
agricultural wells in the San Joaquin Valley.
A recent evaluation of MTBE impacts to California groundwater
resources (Happel et al. 1998), jointly sponsored by the Underground
Storage Tank (UST) Program of the California State Water Resources
Control Board (SWRCB), the Office of Fossil Fuels of U.S. Department of
Energy (DOE), and the-Western States Petroleum Association (WSPA),
found evidence of MTBE in nearly 80 percent of the 1,858 monitoring
wells from 236 leaking underground fuel tank (LUFT) sites in 24
counties examined by the Lawrence Livermore National Laboratory (LLNL).
LLNL originally estimated that more than 10,000 LUFT sites out of the
recognized 32,409 sites in California are contaminated with MTBE.
Recent ongoing monitoring report (UC 1998) confirms that at least 3,000
to 4,500 LUFT sites are contaminated with MTBE. Maximum concentrations
found at these sites ranged from several ppb to approximately 100,000
ppb or 100 ppm, indicating a wide range in the magnitude of potential
MTBE impacts at gasoline release sites. MTBE plumes are more mobile
than BTEX plumes, and the plumes are usually large migrates. Primary
attenuation mechanism for MTBE is dispersion. LLNL concluded that MTBE
might present a cumulative contamination hazard.
In response to the growing concern over the detection of MTBE in
California's groundwater and surface water bodies, the SWRCB was
requested to convene an advisory panel to review the refueling
facilities and practices at marinas located on surface water bodies
serving as drinking water sources to determine if any upgrades should
be made to eliminate releases to the water body (Patton et al. 1999a).
In addition, SWRCB's advisory panel was asked to review existing data
base of UST contamination sites to determine if there is a leak history
and identify appropriate measures to assure the prevention and
detection of oxygenate releases from retail marketing facilities
(Patton et al. 1999b).
MTBE was detected in municipal stormwater in 7 percent of the 592
samples from 16 U.S. cities during 1991 to 1995 with a range of 0.2 to
8.7 ppb and a median of 1.5 ppb (Delzer et al. 1997). MTBE was found to
be the seventh most frequently detected VOCs in municipal stormwater.
Among the stormwater samples that had detectable concentrations of
MTBE, 87 percent were collected between October 1 and March 31 which is
the period of time when oxygenated gasoline is used in CO nonattainment
areas (Squillace et al. 1998). Surveys by the U.S. EPA found that 51
public water suppliers in seven responding states had detected MTBE.
There are ongoing regional studies of MTBE occurrence in California,
New England, Long Island, New Jersey and Pennsylvania (Wiley 1998).
MTBE was detected in aquifers (Landmeyer et al. 1997, 1998, Lindsey
1997).
Cal/EPA and other State agencies have taken a proactive approach
toward investigating MTBE in water in California. MTBE has recently
been detected in shallow groundwater at over 75 percent of about 300
leaking UST sites in the Santa Clara Valley Water District (SCVWD), at
90 out of 131 fuel leak sites under jurisdiction of the San Francisco
Regional Water Quality Control Board (SFRWQCB) and at over 200 leaking
sites in the Orange County Water District. According to the Santa Ana
Regional Water Quality Control Board, MTBE has been found at
concentrations higher than 200 ppb at 68 percent of the leaking UST
sites in its jurisdiction and at concentrations above 10,000 ppb at 24
percent of the leaking sites. In Solano County, concentrations of MTBE
as high as 550,000 ppb have been reported in groundwater at sites with
leaking USTs. However, these wells are not sources for drinking water
(SCDEM 1997). At sites of gasoline leakage, MTBE concentrations as high
as 200,000 ppb have been measured in groundwater (Davidson 1995,
Garrett et al. 1986).
In July 1998, the SFRWQCB (1998) has compiled a list of 948 LUFT
sites in the nine Bay Area counties in which groundwater has been
contaminated with MTBE to a concentration of more than five ppb, which
is the detection limit. The MTBE concentrations from the monitoring
wells ranged from six ppb to as high as 19,000,000 ppb or 19,000 ppm.
The monitoring well with 19,000,000 ppb of MTBE also was reported with
benzene contamination in groundwater at 1,900 ppb and a maximum
concentration of 6,100 ppb during the past 2 years. The range of MTBE
concentrations was from 7 to 390,000 ppb in Alameda County, 6 to
240,000 ppb in Contra Costa County, 6 to 210,000 ppb in Marin County,
12 to 60,000 ppb in Napa County, 6 to 710,000 ppb in San Francisco
County, 7 to 2,400,000 ppb in San Mateo County, 6 to 140,000 ppb in
Santa Clara County, 9 to 19,000,000 ppb in Solano County, and 7 to
390,000 ppb in Sonoma County.
In 1994, SB 1764 (Thompson, California Health and Safety Code,
Section 25299.38) established an independent advisory committee to the
SWRCB to review the cleanup of USTs including requesting companies to
monitor MTBE (Farr et al. 1996). State and Federal statues require that
all USTs including LUFTs be removed, replaced or upgraded to meet
current standards by December 22, 1998. In June 1996, the SWRCB asked
local regulatory agencies to require analysis at all leaking UST sites
with affected groundwater. MTBE has been detected at a majority of the
sites. Concentrations of MTBE in shallow groundwater near the source of
the fuel release can exceed 10,000 ppb or 10 ppm (Cal/EPA 1998).
In 1995, ARB requested DHS' Division of Drinking Water and
Environmental Management to test for MTBE in the state's drinking
water. In February 1996, DHS sent an advisory letter to water suppliers
it regulates, requesting voluntary testing for MTBE while a monitoring
regulation was being developed. The regulation was adopted on February
13, 1997, and requires monitoring of MTBE as an unregulated chemical by
the water suppliers from a drinking water well or a surface water
intake at least once every 3 years. DHS routinely updates the reported
detection of MTBE in groundwater and surface water sources on its
website. DHS uses a detection limit for purposes of reporting (DLR) for
MTBE of five ppb based on consideration of the State's commercial
laboratories' use of MTBE in other common analyses and the potential
for sample contamination and the reporting of false positives.
Laboratories are only required to report MTBE analytical results at or
above the five ppb DLR, but some laboratories are reporting lower
concentrations.
According to the DHS report, from February 13 to June 13, 1997,
MTBE had been detected in 14 of the 388 drinking water systems that had
been monitored. As of December 22, 1997, 18 of the 516 systems
monitored had reported MTBE detection. These are drinking water wells
tapping deep aquifers and some aquifers at depths of 200 feet or
greater. In addition, approximately 2,500 public drinking water sources
had been sampled and reported. Only 33 sources including 19 groundwater
sources and 14 surface water sources, 9 of which are reservoirs, had
reported detectable concentrations of MTBE. Three groundwater sources
including city of Santa Monica (up to 300 ppb in February 1996), city
of Marysville (up to 115 ppb in January 1997), and Presidio of San
Francisco (up to 500 ppb in July 1990 from a currently abandoned well)
had reported concentrations above the U.S. EPA (1997a) advisory level
of 20 to 40 ppb. Otherwise, the range of reported values was less than
(<) one to 34.1 ppb in groundwater sources and < one to 15 ppb in
surface water sources (DHS 1997).
The city of Santa Monica has shut down two well fields, Charnock
and Arcadia, due to MTBE contamination. These well fields used to
supply 80 percent of the drinking water to the city residents.
Concentrations as high as 610 ppb were observed in the Charnock aquifer
and the seven wells in the field have been closed. In the Arcadia well
field, two wells have been closed due to MTBE contamination from an UST
at a nearby gasoline station (Cal/EPA 1998, Cooney 1997). DHS (1997)
reported MTBE concentrations up to 130 ppb in a Charnock well and 300
ppb in another Charnock well in February 1996, and up to 72.4 ppb in an
Arcadia well in August 1996. In Santa Clara County, the Great Oaks
Water Company has closed a drinking water well in South San Jose due to
trace MTBE contamination. The Lake Tahoe Public Utilities District has
shut down 6 of their 36 drinking water wells because of MTBE
contamination.
MTBE has also been found in many surface water lakes and reservoirs
(DHS 1997). The reservoirs allowing gasoline powerboat activities have
been detected with MTBE at higher concentrations than those reservoirs
prohibiting boating activities. DHS reported MTBE in Lake Tahoe, Lake
Shasta, Whiskeytown Lake in the city of Redding, San Pablo Reservoir in
East Bay Municipal Utility District (EBMUD) in the San Francisco Bay
area, Lobos Creek in Presidio of San Francisco, Del Valle and Patterson
Pass of Zone Seven Water Agency serving east Alameda County, Clear Lake
in Konocti County Water District, Canyon Lake in the Elsinore Valley
Municipal Water District, Lake Perris in the MWDSC in the Los Angeles
area, and Alvarado, Miramar, and Otay Plant influent in city of San
Diego. MTBE concentrations ranged from < 1 to 15 ppb. Donner Lake, Lake
Merced, Cherry and New Don Pedro Reservoirs in EBMUD, Anderson and
Coyote Reservoirs in the SCVWD, Modesto Reservoir in the Stanislaus
Water District, and Castaic Reservoir in MWDSC also had detectable
levels of MTBE.
The city of Shasta Lake domestic water supply intake raw water was
reported with 0.57 ppb MTBE in September 1996 although Lake Shasta had
88 ppb in a surface water sample next to a houseboat at a marina dock.
BTEX were found in lower concentrations than MTBE. Water was analyzed
for hydrocarbons before and after organized jet ski events held in the
summer and fall of 1996 in Orange County and Lake Havasu (Dale et al.
1997a). MTBE was measured in the water at the small holding basin in
Orange County at concentrations of up to 40 ppb a few days after the
event while there was only negligible BTEX. At the larger Lake Havasu,
the MTBE concentrations increased from below the level of detection to
13 ppb. A recent report to the SCVWD described the detection of an
average concentration of three ppb MTBE in Anderson, Calero, and Coyote
Reservoirs which are drinking water sources where powerboating is
allowed. Calero Reservoir banned jet skis in July 1998. The National
Park Service is proposing a systemwide ban on similar types of personal
watercraft, which are presently allowed in 34 of America's 375 national
park units.
The Carson publicly-owned treatment works (POTW) in Carson,
California has also reported MTBE in its wastewater. The Carson POTW
processes the largest volume of refinery wastewater in the Nation (13
refineries sporadically discharge wastewater to the POTW). Refineries
in California perform their own pretreatment prior to discharging to
sewers. The refineries' discharges contain average levels from one to
7,000 ppb (seven ppm) with concentrations occasionally as high as
40,000 ppb. California refineries are situated mainly along the coast
and discharge directly or indirectly to marine waters. No California
refineries discharge their wastewater to sources of drinking water.
metabolism and pharmacokinetics
The available information on the metabolism and pharmacokinetics of
MTBE is limited to humans and rats with little information from mice.
MTBE can be absorbed into the body after inhalation in humans (Johanson
et al. 1995, Nihlen et al. 1998a, 1998b, Vainiotalo et al. 1998) and
rats (Buckley et al. 1997, Miller et al. 1997, Prah et al. 1994,
Savolainen et al. 1985), ingestion or skin contact in rats (Miller et
al. 1997). It is metabolized and eliminated from the body within hours.
MTBE caused lipid peroxidation in the liver and induction of hepatic
microsomal cytochrome P450 content in mice (Katoh et al.
1993). The major metabolic pathway of MTBE in both animals and humans
is oxidative demethylation leading to the production of TBA (Poet et
al. 1997c). In animals, HCHO is also a metabolite (Hutcheon et al.
1996). This reaction is catalyzed by cytochrome P450 enzymes
(Brady et al. 1990, Hong et al. 1997b).
MTBE and TBA have been detected in blood, urine, and breath of
humans exposed to MTBE via inhalation for 12 hours. Nihlen et al.
(1998b) in a chamber study exposing human subjects for 2 hours suggests
that TBA in blood or urine is a more appropriate biological exposure
marker for MTBE than the parent ether itself. Bonin et al. (1995) and
Lee and Weisel (1998) described analytical methods for detecting MTBE
and TBA in human blood and urine at concentrations below one ppb. A
recent Finnish study, Saarinen et al. (1998) investigated the uptake of
11 drivers to gasoline vapors during road-tanker loading and unloading.
The total MTBE uptake during the shift was calculated to be an average
of 106 65 mmole. The mean concentrations of MTBE and TBA
detected in the first urine after the work shift were 113
76 and 461 337 nanomole/L, and those found 16 hours later
in the next morning were 18 12 and 322 213
nanomole/L, respectively.
Absorption
There is limited information on the rate and extent that MTBE
enters the systemic circulation. MTBE is lipophilic which will
facilitate its absorption across the lipid matrix of cell membranes
(Nihlen et al. 1997). In its liquid or gaseous state, MTBE is expected
to be absorbed into the blood stream (Nihlen et al. 1995). MTBE is
absorbed into the circulation of rats following oral, intraperitoneal
(i.p.), intravenous (i.v.), or inhalation exposures (Bioresearch
Laboratories 1990a, 1990b, 1990c, 1990d, Miller et al. 1997, NSTC
1997). Dermal absorption of MTBE is limited, as compared with other
routes.
The concentration-time course of MTBE in blood plasma of male rats
administered 40 mg/kg/day by oral, dermal, or i.v. routes was followed
(Miller et al. 1997). Peak blood concentrations of MTBE
(Cmax) were obtained within 5 to 10 minutes. Higher levels
of MTBE were seen after oral versus i.v. exposure indicating
elimination of the latter via the lungs. Miller et al. (1997) compared
the areas under the concentration-time curves (AUC) for MTBE following
i.v. and oral administrations and concluded that MTBE was completely
absorbed from the gastrointestinal tract. Plasma levels of MTBE
following dermal exposure were limited; peak concentrations were
achieved 2 to 4 hours after dosing. Absorption ranged from 16 to 34
percent of applied doses of 40 mg/kg/day and 400 mg/kg/day
respectively. After inhalation exposure, plasma concentrations of MTBE
reached apparent steady State within 2 hours at both low (400 ppm) and
high (8,000 ppm) doses. Peak MTBE concentrations were reached at four
to 6 hours and were 14 and 493 ppb, respectively.
Distribution
Once in the blood, MTBE is distributed to all major tissues in the
rat. Due to its hydrophilic properties, neither MTBE nor its
metabolites would be expected to accumulate in body tissues. TBA
appears to remain longer, and chronic exposure could result in
accumulation to some steady-state level, but this needs further study.
Once absorbed, MTBE is either exhaled as the parent compound or
metabolized. Oxidative demethylation by cytochrome P450-
dependent enzymes is the first step in the metabolism that yields HCHO
and TBA. TBA is detected in blood and urine and appears to have a
longer half-life in blood than MTBE (Poet et al 1996, Prah et al. 1994,
Prescott-Mathews et al. 1996, Savolainen et al. 1985).
Metabolism
The metabolism of absorbed MTBE proceeds in a similar fashion
regardless of route of exposure. MTBE is metabolized via microsomal
enzymes in the cells of organs (Turini) et al. 1998). MTBE undergoes
oxidative demethylation in the liver via the cytochrome
P450-dependent enzymes (P450 IIE1,
P450IIB1, and P450IIA6 are thought to be
involved) to give TBA and HCHO (Brady et al. 1990, Hong et al. 1 997b).
Rat olfactory mucosa displays a high activity in metabolizing MTBE via
the cytochrome P450-dependent enzymes (Hong et al. 1997a).
In vitro studies of MTBE in human (Poet and Borghoff 1998) and rat
(Poet and Borghoff 1 997b) liver microsomes confirm that MTBE is
metabolized by P450-dependent enzymes and suggest that the
metabolism of MTBE will be highly variable in humans. TBA may be
eliminated unchanged in expired air or may undergo secondary metabolism
forming 2-methyl-1,2-propanediol and -hydroxyisobutyric acid.
Both of these latter metabolites are excreted in the urine and account
for about 14 percent and 70 percent respectively of urine radioactivity
for 14C-MTBE dosed rats (Miller et al. 1997). Two
unidentified minor metabolites are also excreted in urine.
Bernauer et al. (1998) studied biotransformation of 12C-
and 2-13C-labeled MTBE and TBA in rats after inhalation or
gavage exposure to identify 2-methyl-1,2-propanediol and 2-
hydroxyisobutyrate as major metabolites in urine by 13C
nuclear magnetic resonance and gas chromatography/mass spectrometry. In
one human individual given five mg 13C-TBA/kg orally, 2-
methyl-1,2-propanediol and 2-hydroxyisobutyrate were major metabolites
in urine. The results suggest that TBA formed from MTBE be extensively
metabolized by further oxidation reactions. In vitro evidence suggests
that TBA may also undergo oxidative demethylation to produce HCHO and
acetone (Cederbaum and Cohen 1980). Identification of
14CO2 in expired air of 14C-MTBE
treated rats suggests some complete oxidation of MTBE or metabolites
occurs, probably via HCHO. Studies in humans are more limited but TBA
has been observed as a blood metabolite of MTBE. The participation of
hepatic cytochrome P450-dependent enzymes also indicates a
potential role of co-exposure to other environmental chemicals in
affecting MTBE metabolism and toxicity (Hong et al. 1997b, NSTC 1997).
Excretion
Elimination of MTBE and its metabolites by Fischer 344 rats is
primarily via the lungs (expired air) and the kidneys (urine). In
expired air, MTBE and TBA are the predominant forms. After i.v.
administration of 14C-MTBE to male rats most of the
radioactivity was excreted in the exhaled air (60 percent) and urine
(34.9 percent) with only 2 percent in the feces and 0.4 percent
remaining in the tissues/carcass. Most of the administered dose was
eliminated as MTBE during the first 3 hours following administration.
About 70 percent of the dose recovered in the urine were eliminated in
the first 24 hours and 90 percent in 48 hours. After dermal exposure to
MTBE for 6 hours, 70 to 77 percent of the applied radioactivity was
unabsorbed while 7.6 to 18.9 percent was excreted in expired air, 6.3
to 16.2 percent in urine, and 0.25 to 0.39 percent in feces at 40 and
400 mg/kg/day respectively. A negligible amount (< 0.2 percent) was
found in tissues/carcass. The composition of 14C-radiolabel
in expired air was 96.7 percent MTBE and 3.3 percent TBA at the high
dose. After inhalation exposures most of the 14C was
eliminated in the urine with 64.7 percent after single and 71.6 percent
after repeated low doses. At the high dose, a larger fraction was
eliminated in exhaled air: 53.6 percent compared to 17 percent for
single or 21 percent for repeated low doses. Less than 1 percent of the
dose was recovered in the feces and < 3.5 percent in the tissues/
carcass. The composition of 14C-radiolabel in exhaled breath
in the first 6 hours following administration of MTBE was 66 to 69
percent MTBE and 21 to 34 percent TBA. By 24 hours post-dose 85 to 88
percent of the urine radioactivity was eliminated in rats from all
exposure groups (Miller et al. 1997).
Pulmonary elimination of MTBE after intraperitoneal injection in
mice (Yoshikawa et al. 1994) at three treated doses (50, 100 and 500
mg/kg) indicated an initial rapid decrease of the elimination ratio
followed by a slow decrease at the doses of 100 and 500 mg/kg. The
calculated half-lives of the two elimination curves obtained by the
least squares method were approximately 45 minutes and 80 minutes. The
pulmonary elimination ratios at the three different doses were from
23.2 percent to 69 percent. Most of the excreted MTBE was eliminated
within 3 hours.
In a human chamber study (Buckley et al. 1997), two subjects were
exposed to 1.39 ppm MTBE, that is comparable to low levels which might
be found in the environment for 1 hour, followed by clean air for 7
hours. The results showed that urine accounted for less than 1 percent
of the total MTBE elimination. The concentrations of MTBE and TBA in
urine were similar to that of the blood ranging from 0.37 to 15
g/L and two to 15 g/L, respectively. Human breath
samples of end-expiration volume were collected from two individuals
during motor vehicle refueling, one person pumping the fuel and a
nearby observer, immediately before and for 64 minutes after the
vehicle was refueled with premium grade gasoline (Lindstrom and Pleil
1996). Low levels of MTBE were detected in both subjects breaths before
refueling and levels were increased by a factor of 35 to 100 after the
exposure. Breath elimination indicated that the half-life of MTBE in
the first physiological compartment was between 1.3 and 2.9 minutes.
The breath elimination of MTBE during the 64-minute monitoring period
was about four-fold for the refueling subject comparing to the observer
subject.
Johanson et al. (1995) and Nihlen et al. (1998a, 1998b) reported
toxicokinetics and acute effects of inhalation exposure of 10 male
subjects to MTBE vapor at 5, 25, and 50 ppm for 2 hours during light
physical exercise. MTBE and TBA were monitored in exhaled air, blood,
and urine. The elimination of MTBE from blood was multi-phasic with no
significant differences between exposure levels. The elimination phases
had half-lives of 1 minute, 10 minutes, 1.5 hours, and 19 hours
respectively. Elimination of MTBE in urine occurred in two phases with
average half-lives of 20 minutes and 3 hours. Excretion of MTBE
appeared to be nearly complete within 10 hours. For TBA excretion the
average post-exposure half-lives in blood and urine were 10 and 8.2
hours respectively. Some exposure dependence was noted for the urinary
half-life with shorter values seen at the highest exposure level (50
ppm 2 hour). A low renal clearance for TBA (0.6 to 0.7 mL/
hour/kg) may indicate extensive blood protein binding or renal tubular
reabsorption of TBA.
Pharmacokinetics
The plasma elimination half-life (t1/2) of MTBE in male
rats was about 0.45 to 0.57 hour after i.v., oral (low dose), and
inhalation exposures. A significantly longer t1/2 of 0.79
hour was observed with the high oral dose of 400 mg/kg/day. For dermal
exposure the initial MTBE elimination t1/2 was 1.8 to 2.3
hours. TBA elimination t1/2 values were 0.92 hour for i.v.,
0.95 to 1.6 hours for oral, 1.9 to 2.1 hours for dermal, and 1.8 to 3.4
hours for inhalation exposures. The apparent volume of distribution for
MTBE ranged from 0.25 to 0.41 L after i.v., oral, and inhalation dosing
and from 1.4 to 3.9 liters (L) after dermal exposures. The total plasma
clearance of MTBE, corrected for relative bioavailability, ranged from
358 to 413 mL/hour in i.v., oral, and dermal administrations.
Inhalation values ranged from 531 mL/hour for low single dose to 298
mL/hour for high single dose. For oral administration of 40 or 400 mg/
kg/day MTBE the AUC values were 17 and 230 (g/mL) hour for
MTBE and 39 and 304 (g/mL)hour for TBA (Miller et al. 1997).
The disposition and pharmacokinetics observed in these studies are
similar to those observed in human volunteers following inhalation and
dermal exposures (U.S. EPA 1993). For inhalation exposure to 5 mg/
m3 for 1 hour the t1/2 value for MTBE was 36
minutes. Blood TBA levels rose during exposure and remained steady for
up to 7 hours post-exposure suggesting a longer t1/2 for TBA
in humans compared to rats. Other more recent data (cited in NSTC 1997)
indicate a multi-exponential character to MTBE elimination from human
blood with t1/2 values of 2 to 5 minutes, 15 to 60 minutes
and greater than 190 minutes. These results possibly indicate a more
complex distribution or binding of MTBE in humans than observed in
rats. Such differences probably are related to larger fat compartments
in humans compared to rats.
Overall, these studies show that following i.v., oral, or
inhalation exposures MTBE is absorbed, distributed, and eliminated from
the body with a half-life of about 0.5 hour. Dermal absorption is
limited. The extent of metabolism to TBA (and HCHO) the major
metabolite is somewhat dependent on route and dose. TBA is eliminated
from the body with a half-life of 1 to 3 hours or longer in humans.
Virtually all MTBE is cleared from the body 48 hours post-exposure.
Physiologically-Based Pharmacokinetic (PBPK) Models
Computer-based PBPK models have been developed for rats (Borghoff
et al. 1996a, Rao and Ginsberg 1997). These models vary in complexity,
metabolic parameters, and one chemical specific parameter. The Borghoff
et al. (1996a) model uses five compartments for MTBE and either five or
two for TBA. While model predictions of MTBE blood concentrations and
clearance following inhalation or oral exposures were generally good,
the model underpredicted MTBE blood levels at 8,000 ppm by a factor of
two. Accurate model predictions of TBA blood levels and clearance were
more elusive with the two compartment model giving more accurate
predictions at lower oral and inhalation doses than at higher doses or
than the five compartment model. The Rao and Ginsberg (1997) model is
more complex using eight compartments for MTBE and eight for TBA. While
both models assume two Michaelis-Menten processes (Vmaxc/Km) from MTBE
to TBA namely high capacity to low affinity (Vmaxc2/
Km2), and low capacity to high affinity (Vmaxc1/
Km1), the Rao and Ginsberg (1997) model uses different
parameters than Borghoffet al. (1996a) with a lower Vmaxc1/
Km1. Rao and Ginsberg (1997) use a lower tissue/blood
partition coefficient for TBA in the slowly perfused compartment (e.g.,
muscle) of 0.4 versus 1. Predictions of blood levels and clearance
rates for MTBE and TBA with MTBE inhalation exposures appear to be more
accurate with this model. Similar validation is claimed for the oral
and i.v. routes for MTBE exposure and for i.p. exposure to TBA although
these data have not been seen in detail. Rao and Ginsberg (1997) used
their model to evaluate some key uncertainties of acute inhalation
exposures to MTBE during bathing and showering and concluded that the
acute central nervous system (CNS) toxicity is likely due to MTBE
rather than to its TBA metabolite. The simulated brain TBA
concentration for CNS effects was in the 500 to 600 mg/L range. In
contrast, the simulated brain concentration for MTBE's CNS effects was
considerably lower (89 to 146 mg/L). By comparing TBA only versus MTBE
exposure studies the authors concluded that under conditions where MTBE
dosing produced acute CNS toxicity, the simulated TBA brain
concentrations were too low to be effective.
Despite the lack of human data on tissue/blood partition
coefficients and other key parameters, both models have been adjusted
to human anatomical and physiological values and estimated metabolic
and chemical parameters and compared with limited human blood data.
Although the Borghoff et al. (1996a) model was able to predict MTBE
levels seen in Cain et al. (1996) during inhalation exposure, it
underpredicted MTBE blood concentrations after exposure, resulting in a
faster clearance than seen experimentally. The Rao and Ginsberg (1997)
model more closely simulated the data (1.7 ppm MTBE for 1 hour) of Cain
et al. (1996) but underpredicted the peak and postexposure
concentrations at higher inhalation exposures of 5 and 50 ppm MTBE for
2 hours (Johanson et al. 1995). It is clear that while human MTBE PBPK
models may be improved considerably, they may prove useful in their
present State to assess risks associated with some environmental
exposures to MTBE (e.g., exposures when taking a shower).
toxicology
The toxicology profile of MTBE has been summarized in the U.S. (Von
Burg 1992, ATSDR 1996) and in Great Britain (BIBRA 1990). Zhang et al.
(1997) used computer modeling to predict metabolism and toxicological
profile of gasoline oxygenates including MTBE based on structure
activity relationships. Health risk assessment of MTBE has been
performed (Gilbert and Calabrese 1992, Hartly and Englande 1992,
Hiremath and Parker 1994, Stern and Tardiff 1997, Tardiff and Stern
1997). The general toxicity of MTBE is not considered as ``highly
hazardous'' in a hazard ranking system for organic contaminants in
refinery effluents (Siljeholm 1997) and is considered as less hazardous
than most chemicals in 10 ranking systems in the Chemical Scorecard of
the Environmental Defense Fund (EDF 1998). A substantial amount of
health-related research has been conducted or initiated on MTBE in
recent years (ATSDR 1996, U.S. EPA 1997a). A recent literature review
(Borak et al. 1998) summarizes the exposure to MTBE and acute human
health effects including nine epidemiological studies, 10 industrial
hygiene studies, and 12 clinical studies. However, most of the studies
and reviews focus on the inhalation route of exposure in human health
effects and laboratory animal toxicities. No studies were located
regarding toxic effects in humans after oral exposure to MTBE alone.
Because this document is mainly concerned with the effects of MTBE in
drinking water, it focuses on oral toxicity studies in animals. There
is limited information on dermal exposure effects in humans and
animals. Very little is known about the toxic effects of MTBE in plants
and ecosystems.
Toxicological Effects in Animals
Table 4 summarizes the lowest concentrations resulting in toxicity
in laboratory animals via inhalation or oral exposure as reported in
the ATSDR (1996) document and the latest U.S. EPA (1997c) advisory.
Clary (1997) reviewed the systemic toxicity of MTBE including 12
inhalation and four oral studies. Stelljes (1997) summarized similar
information based on only the ATSDR (1996) document. The various
noncancer health effects via oral route of exposure in all tested
species and the duration of exposure are summarized in Table 5. The
highest NOAELs and all the lowest observed adverse effect level
(LOAELs) are also included in Table 5. Details of each of the studies
listed in Table 5 are described in the following sections on acute,
subacute, subchronic and chronic toxicity. The cancer effects observed
in animals are discussed in a separate section on carcinogenicity in
this chapter. There were no studies located regarding cancer in humans
after oral, or any other exposure to MTBE.
In animal studies, oral exposure to MTBE for acute, subacute,
subchronic, or chronic duration appears to be without effects on the
cardiovascular, musculoskeletal, dermal, ocular, or reproductive
systems. In acute and subacute oral exposure studies, limited effects
on the respiratory, gastrointestinal, hematological, hepatic, renal, or
neurological systems and some minor systemic toxicities have been
observed. In subchronic oral exposure, limited effects on
gastrointestinal, hematological, hepatic, or renal systems and some
minor systemic toxicities have been observed. In chronic oral exposure,
the main observation is cancer and preneoplastic effects (ATSDR 1996).
In this document, all the potential toxic effects of MTBE have been
reviewed with an emphasis on the oral exposure; particularly the
potential reproductive, developmental and carcinogenic effects have
been extensively reviewed by OEHHA staff.
Some acute, intermediate or chronic duration minimal risk levels
(MRLs) have been derived by the ATSDR for inhalation or oral exposure
to MTBE (ATSDR 1996). U.S. EPA (1997c) lists in IRIS a Reference
Concentration (RfC) for inhalation that is similar to the ATSDR's
inhalation MRL. However, the current IRIS (U.S. EPA 1997c) does not
list a Reference Dose (RfD) for ingestion (U.S. EPA 1987b) that
is.similar to the ATSDR's ingestion MRL. In addition to the key
documents from governmental agencies and literature search articles
mentioned above, toxicology information in the TOMES PLUS
data base (Hall and Rumack 1998) also has been used in the following
summary of toxic effects of MTBE.
Table 4.--Summary of Selected Data on MTBE: Noncancer Toxic Effects in Animals*
----------------------------------------------------------------------------------------------------------------
Inhalation (mg/m3) Oral (mg/kg/day)
----------------------------------------------------------------
Dose level Subacute/ Subacute/
Acute Subchronic Chronic Acute Subchronic
----------------------------------------------------------------------------------------------------------------
NOAEL.......................................... 1,440 1,440 1,440 40 100
LOAEL.......................................... 3,600 2,880 10,800 90 300
Lethal Dose.................................... 649,000 NA NA 3,866 NA
----------------------------------------------------------------------------------------------------------------
*Values represent the lowest reported in ATSDR (1996) and U.S. EPA (1997a)
______
Table 5.--Significant Noncancer Health Effects and Levels of Oral Exposure to MTBE in Animals*
--------------------------------------------------------------------------------------------------------------------------------------------------------
Exposure/Duration/
Species/(Strain) Frequency (Specific System NOAEL (mg/kg/day) LOAEL (mg/kg/day) Reference
route)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Acute Exposure
--------------------------------------------------------------------------------------------------------------------------------------------------------
Death:
Rat.............................. once (gavage)......... ...................... ..................... 3,866 (LD50)......... ARCO 1980
Mouse............................ once (gavage)......... ...................... ..................... 4,000 (LD50)......... Little et.al. 1979
Syntemic Toxicity:
Rat.............................. once (gavage)......... Respiratory........... ..................... 4,080 (labored ARCO 1980
respiration).
...................... Neurological.......... ..................... 1,900 (slight to .....................
marked CNS
depression 2,450
(ataxia).
Rat (Sprague-Dawley)............. once (gavage in oil).. Gastrointestinal...... ..................... 100 (diarrhea)....... Robinson et al. 1990
...................... Neurological.......... 900.................. 1,200 (profound but .....................
transient
anesthesia).
Rat (Fischer 344)................ once (gavage in water) Neurological.......... 40................... 400 (drowsiness)..... Bioresearch Labs.
1990b)
Rat (Sprague-Dawley)............. once (gavage)......... Neurological.......... ..................... 90 (salivation) 440 Johnson et al. 1992,
(Male) Klan et al. 1992
(hypoactivity,
ataxia) 1,750
(Female).
--------------------------------------------------------------------------------------------------------------------------------------------------------
Subacute Exposure
--------------------------------------------------------------------------------------------------------------------------------------------------------
Systemic Toxicity:
Rat (Sprague-Dawley)............. 14 days............... Respiratory........... 1,428................ ..................... Robinson et al. 1990
7 days/week........... Cardiovascular........ 1,428................ ..................... .....................
once/day (gavage in Gastrointestinal...... ..................... 357 (diarrhea)....... .....................
oil).
...................... Hematological......... 1,428 (Female)....... 357 (Male) (decreased .....................
monocytes).
...................... Hepatic............... 714 (Male)........... 1,071 (Male) .....................
[increased serum
glutamic-oxaloacetic
transaminase (SGOT)
and lactic
dehydrogenase] 1,428
(Female) [decreased
blood urea nitrogen
(BUN) values].
...................... Renal................. 1,071 (Male)......... 1,428 (Male) .....................
(increased hyaline
droplets).
...................... ...................... 1,428 (Female)....... ..................... .....................
...................... Endocrine............. 1,428................ ..................... .....................
...................... Body weight........... 714 (Female)......... 1,071 (Female)....... .....................
...................... ...................... ..................... (unspecified reduced .....................
weight gain).
...................... Immunological/ ..................... 1,428................ .....................
Lymphoreticular.
...................... Neurological.......... 1,071................ 1,428 (profound but .....................
transient
anesthesia,
hypoactivity,
ataxia).
...................... Reproductive.......... 1,428................ ..................... .....................
...................... Other................. 1,071 (Male)......... 1,428 (Male)......... .....................
...................... ...................... 357 (Female)......... 714 (Female) .....................
(elevated
cholesterol).
Mouse (CD-1)..................... 3 weeks,.............. Body weight........... 1,000................ ..................... Ward et al. 1994,
1995
5 days/week (gavage in Reproductive.......... 1,000................ ..................... .....................
oil).
--------------------------------------------------------------------------------------------------------------------------------------------------------
Subchronic Exposure
--------------------------------------------------------------------------------------------------------------------------------------------------------
Death:
Rat (Sprague-Dawley)............. 16 weeks, 4 days/week, ...................... ..................... 250 (Female) Belpoggi et al. 1995
once/day, (gavage in (increased
oil). mortality).
Systemic Toxicity:
Rat (Sprague-Dawley)............. 4 weeks............... Respiratory........... 1,750................ ..................... Johnson et al. 1992,
Klan et al. 1992
5 days/week........... Cardiovascular........ 1,750................ ..................... .....................
once/day (gavage)..... Gastrointestinal...... 440.................. 1,750 (inflammation, .....................
submucosal edema,
epithelial
hyperplasia, stomach
ulcers).
...................... Hematological......... 1,750................ ..................... .....................
...................... Muscle/skeleton....... 1,750................ ..................... .....................
...................... Hepatic............... 440.................. 1,750 (increased .....................
relative liver
weights).
...................... Renal................. 1,750 (Female)....... 440 (Male) (increased .....................
hyaline droplets in
proximal convoluted
tubules and
increased relative
kidney weights).
...................... Endocrine............. 1,750................ ..................... .....................
...................... Dermal................ 1,750................ ..................... .....................
...................... Ocular................ 1,750................ ..................... .....................
...................... Body weight........... 1,750................ ..................... .....................
...................... Immunological/ 1,750................ ..................... .....................
Lymphoreticular.
...................... Neurological.......... ..................... 440 (hypoactivity, .....................
ataxia).
...................... Reproductive.......... 1,750................ ..................... .....................
...................... Other................. 440.................. 1,750 (increased .....................
serum cholesterol).
Rat (Sprague-Dawley)............. 90 days............... Respiratory........... 1,200................ ..................... Robinson et al. 1990
7 days/week........... Cardiovascular........ 1,200................ ..................... .....................
once/day (gavage in Gastrointestinal...... ..................... all treated doses .....................
oil). (diarrhea).
...................... Hematological......... 900.................. 1,200 (increased .....................
monocytes, decreased
mean corpuscular
volume in males,
increased red blood
cell, hemoglobin,
hematocrit and
decreased white
blood cells in
females).
...................... Hepatic............... ..................... all treated doses .....................
(decreased BUN
values).
...................... Renal................. 900 (Male)........... 1,200 (Male)......... .....................
...................... ...................... 1,200 (Female)....... (hyaline droplets, .....................
granular casts).
...................... ...................... 100.................. 300 (alterations in .....................
kidney weights).
...................... Endocrine............. 1,200................ ..................... .....................
...................... Body weight........... 1,200................ ..................... .....................
...................... Immunological/ ..................... 1,200................ .....................
Lymphoreticular.
...................... Reproductive.......... 1,200................ ..................... .....................
...................... Other................. 300 (Male)........... 900 (Male)........... .....................
...................... ...................... ..................... 100 (Female) .....................
(elevated
cholesterol).
--------------------------------------------------------------------------------------------------------------------------------------------------------
Chronic Exposure
--------------------------------------------------------------------------------------------------------------------------------------------------------
Systemic Toxicity:
Rat (Sprague-Dawley)............. 104 weeks............. Respiratory........... 1,000................ ..................... Belpoggi et al. 1995
4 days/week........... Cardiovascular........ 1,000................ ..................... .....................
once/day (gavage in Gastrointestinal...... 1,000................ ..................... .....................
oil).
...................... Muscle/skeleton....... 1,000................ ..................... .....................
...................... Hepatic............... 1,000................ ..................... .....................
...................... Renal................. 1,000................ ..................... .....................
...................... Endocrine............. 1,000................ ..................... .....................
...................... Dermal................ 1,000................ ..................... .....................
...................... Body weight........... 1,000................ ..................... .....................
...................... Immunological/ 1,000 male........... 250 (Female) .....................
Lymphoreticular. (dysplastic
proliferation of
lymphoreticular
tissues, possibly
preneoplastic).
...................... Reproductive.......... 1,000................ ..................... .....................
--------------------------------------------------------------------------------------------------------------------------------------------------------
* adapted from ATSDR (1996) and U.S. EPA (1997c)
acute toxicity
Studies of the systemic effects of MTBE have been conducted in
animals, but the majority involves inhalation exposure (Clary 1997).
Inhalation or contact with MTBE may irritate or burn skin and eyes.
Vapors may cause dizziness or suffocation. Acute toxicity studies in
animals demonstrate the extremely low toxicity of MTBE (ARCO 1980,
Little et al. 1979, Reese and Kimbrough 1993).
The oral LD50s (lethal doses with 50 percent kill) are
approximately 3,866 mg/kg or four mL/kg in rats, and approximately
4,000 mg/kg or 5.96 mL/kg in mice. The inhalation 4-hour
LC50s (lethal concentrations with 50 percent kill) in rats
have been calculated to be approximately 39,395 ppm for 96.2 percent
MTBE, 33,370 ppm for 99.1 percent MTBE and 23,576 ppm for MTBE. The
inhalation 10-minute LC50 in mice is approximately 180,000
ppm and the inhalation 15-minute LC50 in mice is
approximately 141 g/m3. The inhalation LT50 (time
at which death occurs in 50 percent of the exposed animals) in mice
exposed to 209,300 ppm MTBE is 5.6 minutes (ATSDR 1996). The dermal
LD50 is estimated to be greater than 10 mL/kg in New Zealand
rabbits (HSDB 1997). The i.p. LD50 is 1.7 mL/kg or
approximately 1,100 mg/kg in mice and greater than 148 mg/kg in rats
(Arashidani et al. 1993, RTECS 1997).
Zakko et al. (1997) reported cytotoxicity of MTBE to intestinal
mucosa of rats via i.p. injection similar to the effects of MTBE
treatment for gallstone dissolution in humans. MTBE infused
intraduodenally for 3 hours in male New Zealand rabbits caused local
intestinal cytotoxic and systemic hepatoxic effects (Clerici) et al.
1997).
At lethal doses, ocular and mucous membrane irritation, ataxia,
labored breathing, CNS depression, and general anesthetic effects
precede death. An inhalation study also demonstrated inflammation in
the nasal mucosa of rats at a dose of 3,000 ppm for 6 hours per day for
9 days (HSDB 1997). Mice that inhaled up to approximately 8,400 ppm
MTBE for 1 hour had approximately a 52 percent decrease in breathing
frequency (Tepper et al. 1994). The decrease occurred immediately,
reached a maximum by 10 minutes and returned to baseline 15 minutes
after exposure. High oral doses of greater than 4,080 mg of MTBE/kg
caused labored respiration in rats (ARCO 1980). A 4-hour direct
exposure to MTBE vapor at concentrations greater than 18,829 ppm in an
inhalation study resulted in ocular discharges in rats (ARCO 1980). A
6-hour inhalation study produced signs of reversible CNS depression
following exposure to 8,000 ppm and, to a lesser extent, to 4,000 ppm
vapor with a NOAEL of 800 ppm (Dodd and Kintigh 1989, Daughtrey et al.
1997). As indicated in Tables 4 and 5, a NOAEL of 40 mg/kg/day and a
LOAEL of 90 mg/kg/day are established by these acute oral exposure
experiments based on the neurological effects (Bioresearch Laboratories
1990b, Johnson et al. 1992, Klan et al. 1992).
subacute toxicity
In a consecutive 14-day study, Sprague-Dawley rats (10/sex/dose)
were administered MTBE in corn oil by gavage at 0, 357, 714, 1,071 or
1,428 mg/kg/day. MTBE appears to be irritating to the gastrointestinal
tract of rats as evidenced by diarrhea and histological lesions at all
levels of MTBE by the third day of dosing throughout the 14-day study.
Decreased lung weight was observed in female rats at all MTBE doses and
at 714 mg/kg/day in male rats. Decreased levels of monocytes in blood
were observed in male rats at all MTBE doses. Increased liver enzymes
in males at 1,071 mg/kg/day and decreased blood urea nitrogen (BUN)
values in females at 1,428 mg/kg/day were observed. At the highest
dose, anesthesia was immediate, but recovery was complete within 2
hours. Ataxia and hyperactivity, an increase in the weight of kidneys,
adrenal glands, and livers in both genders at 1,428 mg/kg/day, and an
increase in hyaline droplet formation in kidneys of male rats at 1,428
mg/kg/day were observed. Increases in relative kidney weights were
noted in the males at 1,071 and at 1,428 mg/kg/day and in females at
the 1,428 mg/kg/day dose. Although there was a dose-related decrease in
body weight gain, it was significant only in females at the highest
treatment regimen. At 1,428 mg/kg/day in males and at 714 mg/kg/day in
females, elevated cholesterol was observed. There were no gross lesions
seen at any treatment level. Based on the increases in relative kidney
weight, a NOAEL of 714 mg/kg/day and a LOAEL of 1,071 mg/kg/day are
established by these experiments (Robinson et al. 1990). These studies
indicate that the male kidney is the primary target of short-term
toxicity at relatively high doses. Subchronic toxicity studies of TBA
indicated that, in rodents, the urinary tract is a target system and
males are more sensitive to TBA toxicity than females (NTP 1995).
subchronic toxicity
In a 104-week gavage cancer study, increased mortality was observed
in female Sprague-Dawley rats at 250 mg/kg/day beginning at 16 weeks
from the start of the study (Belpoggi et al. 1995). Daily oral
administration in rats for 4 weeks resulted in increased hyaline
droplets and kidney weight in males at 440 mg/kg/day and higher doses,
and stomach ulcers, increased liver weights and serum cholesterol at
1,750 mg/kg/day (Johnson et al. 1992, Klan et al. 1992).
Sprague-Dawley rats (10/sex/dose) were treated orally with MTBE in
corn oil for 90 days at 0, 100, 300, 900, or 1,200 mg/kg/day.
Anesthesia was evident at the highest dose, but as in the 14-day study,
full recovery occurred in 2 hours. There was a significant decrease in
final body weight of females only at the highest level of treatment.
The diarrhea seen in the treated animals was considered to be the
consequence of the bolus dosing regime. In female rats, there were
significantly increased heart weights at 900 mg/kg/day and increases in
relative kidney weights at 300, 900, and 1,200 mg/kg/day. In male rats,
increases were noted only at the two highest treatment levels. BUN
levels were significantly reduced in both males and females at all MTBE
doses. Reductions in serum calcium and creatinine were observed in
males and a reduction in cholesterol in females was reported, but there
were no clear dose-dependent results. Based on the alterations in
kidney weights, a NOAEL and LOAEL of 100 and 300 mg/kg/day,
respectively, are identified from this study (Robinson et al. 1990).
The subchronic data from the study by Robinson et al. (1990) were
proposed by U.S. EPA (1996a) to develop a draft RfD and a draft
Drinking Water Equivalent Level (DWEL) for kidney effects from MTBE.
The increase in kidney weights at doses of 300 mg/kg/day and higher was
considered to be an adverse effect, since increases in organ weights
are a marker for adverse organ effects (Weil 1970). The diarrhea
observed was considered to be a gastrointestinal complication of the
gavage dosing. Based on the NOAEL of 100 mg/kg/day, a DWEL for kidney
effects of 3,500 ppb can be derived for a 70 kg male adult with two
liters (L) of daily water consumption (DWC), using an uncertainty
factor of 1,000. The uncertainty factor reflects a 10 for the less-
than-lifetime duration of the study, a 10 for interspecies variability,
and a 10 for intraspecies variability. Using an additional uncertainty
factor of 10 for potential carcinogenicity and a 20 percent default
relative source contribution (RSC), U.S.EPA (1996a) drafted a lifetime
Health Advisory (HA) of 70 ppb or 70 g/L. Details of the
equation and calculation of the HA are described later in the chapter
on the calculation of the PHG.
genetic toxicity
The results of genetic toxicity studies for MTBE were generally
negative; however, positive results have been reported in one in vitro
test system in studies that included information on mechanisms of
action, and in one in vivo test system. As detailed later in this
section, MTBE was not mutagenic in bacteria and tissue culture gene
mutation assays, a sister chromatic exchange assay, a Drosophila sex-
linked recessive lethal test, in vitro and in vivo chromosomal
aberration assays, in vivo and in vitro unscheduled DNA synthesis
assays, an in vivo DNA repair assay, an in vivo cytotoxicity assay, and
in vitro and in vivo micronucleus assays. The only positive in vitro
genotoxicity test was for forward mutations in the mouse lymphoma assay
with exogenous activation (ARCO 1980, Mackerer et al. 1996) and
Mackerer et al. (1996) suggested that HCHO was the metabolite
responsible for mutagenic activity in the assay (Gamier et al. 1993).
The only positive in vivo genotoxicity test was for DNA strand breaks
in the rat lymphocyte comet assay (Lee et al. 1998). ATSDR (1996)
indicated that MTBE has little or no genotoxic activity. However, the
positive results in the mouse lymphoma and rat lymphocyte assays
indicate that the genetic toxicity of MTBE needs to be investigated
further.
MTBE was negative in the Ames in vitro assay for reverse mutation
in Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98, and
TA100 in the absence or presence of metabolic activation (ARCO 1980,
Cinelli et al. 1992, Life Science Research Roma Toxicology Centre
S.P.A. 1989a). Since MTBE is volatile, a closed system was used in a
recent microsuspension assay (Kado et al. 1998), and negative results
were observed even though some elevated revertant values were seen with
TA100 and TA 104. MTBE produced no evidence of a dose-related increase
for sister chromatic exchange (ARCO 1980), for gene mutation in Chinese
hamster V79 cells (Life Science Research Roma Toxicology Centre S.P.A.
1989b) and for in vitro unscheduled DNA synthesis in primary rat
hepatocytes (Life Science Research Roma Toxicology Centre S.P.A. 1989c,
Vergnes and Chun 1994). It was negative for micronuclei formation in
erythrocytes (Vergnes and Kintigh 1993).
The only in vitro test system in which MTBE has tested positive is
the activated mouse lymphoma forward mutation assay (ARCO 1980,
Mackerer et al. 1996). TBA, one of MTBE's major metabolites, was
negative in this assay (McGregor et al. 1988). MTBE was positive for
forward mutations in mouse lymphoma L5178Y tk+/
tk- cells in the presence, but not the absence, of metabolic
activation (ARCO 1980, Stoneybrook Labs. Inc. 1993). HCHO, another one
of MTBE's metabolites, is genotoxic, causing both gene mutations and
chromosomal damage in the presence of exogenous metabolic activation
systems. HCHOis also a known carcinogen causing nasal tumors in rodents
when inhaled at high concentrations, and may also cause nasopharyngeal
tumors in humans via inhalation. Work by Mackerer et al. (1996)
suggested that HCHO was the MTBE metabolite responsible for mutagenic
activity in the activated mouse lymphoma forward mutation assay.
Additional studies from this laboratory demonstrated that the HCHO was
produced from in vitro metabolism of MTBE in this assay system (Gamier
et al. 1993).
MTBE was assessed for its in vivo mutagenic potential (McKee et al.
1997). It was negative in the sex-linked recessive lethal assay in
Drosophila melanogaster (Sernau 1989). It was negative for chromosomal
aberrations in Fischer 344 rats exposed via inhalation (Vergnes and
Morabit 1989), in Sprague-Dawley rats (ARCO 1980) and CD-1 mice (Ward
et al. 1994) exposed orally. It was negative for hypoxanthine-guanine
phosphoribosyl transferase (hprt) mutant frequency increase in spleen
lymphocytes of CD-1 mice exposed orally for 6 weeks (Ward et al. 1994,
1995), for micronuclei formation in bone marrow in mice exposed via
inhalation (Vergnes and Kintigh 1993) or via i.p. injection (Kado et
al. 1998), for in vivo DNA repair increase in cultured primary
hepatocytes of CD-1 mice exposed via inhalation (Vergnes and Chun 1994)
and for an in vivo cytotoxicity assay in rats exposed via inhalation
(Vergnes and Morabit 1989).
The only in vivo test system in which MTBE has tested positive is
the rat lymphocyte comet assay, as reported in a recent meeting
abstract (Lee et al. 1998). Rats were treated with MTBE by gavage, and
lymphocytes assessed for alkaline-labile strand breaks. A significant
increase in DNA strand breaks was reported for the highest dose group.
An increase in apoptotic comets was also observed in lymphocytes from
exposed rats, but this result was not statistically significant for any
one dose group.
MTBE is volatile and water-soluble. Given the technical
difficulties associated with testing volatile chemicals in bacterial
and cultured cell systems, it is possible that careful delivery to
genetic materials may have yielded data on reasons for the relative
lack of genotoxic activity of MTBE in vitro (Mackerer et al. 1996, Kado
et al. 1998). Additionally, the in vivo test systems used to test MTBE
were primarily chromosomal damage assays, with two exceptions being the
spleen lymphocyte hprt mutation assay (Ward et al. 1994) and the in
vivo-in vitro mouse hepatocyte unscheduled DNA synthesis assay (Vergnes
and Chun 1994). Only one in vivo assay system, the hprt mutation assay,
had the potential to detect gene mutations, and it is relatively
insensitive in detecting genotoxic chemicals with known false
negatives. In vivo genotoxicity and metabolism data is not available
for a number of the organ systems such as rat kidney, testis, and
spleen and bone marrow, which developed tumors in carcinogenicity
bioassays.
developmental and reproductive toxicity
No human studies relevant to MTBE reproductive and developmental
toxicity were located. There are a limited number of animal
developmental and reproductive toxicity studies, all using the
inhalation route of exposure, as listed below:
one developmental toxicity study in rats exposed to 250 to
2,500 ppm for 6 hours per day on gestation days (gd) 6 to 15 (Conaway
et al. 1985, Bio/dynamics, Inc. 1984a),
two developmental toxicity studies in mice exposed to 250
to 2,500 ppm for 6 hours per day on gestation days 6 to 15 (Conaway et
al. 1985, Bio/dynamics, Inc. 1984b), or to 1,000 to 8,000 ppm for 6
hours per day on gestation days 6 to 15 (Bevan et al. 1997b, Tyl and
Neeper-Bradley 1989),
one developmental toxicity study in rabbits exposed to
1,000 to 8,000 ppm for 6 hours per day on gestation days 6 to 18 (Bevan
et al. 1997b, Tyl 1989),
one single generation reproductive toxicity study in rats
exposed to 300 to 3,400 ppm (Biles etal. 1987),
one two-generation reproductive toxicity study in rats
exposed to 400 to 8,000 ppm (Bevan et al. 1997a, Neeper-Bradley 1991).
Study designs and results are outlined in Table 6. Some information
on reproductive organs can also be obtained from subchronic and chronic
toxicity studies (also outlined in Table 6), and there are a few recent
studies of possible endocrine effects.
While no effects on fertility endpoints were reported, these
studies provide evidence for adverse effects of MTBE on development.
Reduced fetal weight and increased frequency of fetal skeletal
variations were reported in mice after MTBE exposure during
organogenesis, with a NOAEL of 1,000 ppm (Bevan et al. 1997b, Tyl and
Neeper-Bradley 1989). Also, in the rat two-generation study, increased
postnatal death and decreased postnatal weights were found; the NOAEL
was 400 ppm MTBE (Bevan et al. 1997a). A provisional RfC of 173 ppm (48
mg/m3) has been derived using U.S. EPA risk assessment
methodology (Sonawane 1994) on the basis of developmental toxicity that
occurred in the two-generation rat study (Bevan et al. 1997a, Neeper-
Bradley 1991). Additionally, a projected no-effect-concentration in
drinking water for humans of 2.3 to 9.2 mg/L has been derived by U.S.
EPA (1997a) based on a range of NOAELs (250 to 1,000 ppm) in the two
developmental toxicity studies in mice. The NSTC (1997) report stated
that ``MTBE is not expected to pose a reproductive or developmental
hazard under the intermittent, low-level exposure experienced by
humans''.
The developmental and reproductive toxicity studies were of good
quality, and generally conformed to U.S. EPA testing guidelines. The
highest inhalation concentration used (8,000 ppm) produced
hypoactivity, ataxia, and reduced auditory responsiveness in adult
males and females during exposure, reflecting the anesthetic properties
of MTBE. Prostration, labored respiration, lacrimation, and periocular
encrustation were among the clinical signs reported. There was no
increase in adult male and female mortality or organ pathology at any
inhalation concentration, but lower food intake and weight gain was
sometimes seen at the 8,000 ppm concentration. The developmental
toxicity study (Conaway et al. 1985) and single generation study (Biles
et al. 1987) in rats, and one of the developmental toxicity studies in
mice (Conaway et al. 1985) did not include a dose that was minimally
toxic to adult males and females. Little developmental or reproductive
toxicity was reported in these studies, but it is difficult to
interpret this lack of findings because the concentrations were not
high enough to induce adult maternal and paternal toxicity.
Developmental Toxicity
Animal Developmental Toxicity Studies
Dose-dependent effects on fetal weight and fetal skeletal
variations were reported in mice; no fetal effects were reported in the
rats and rabbits. Notably, the rat developmental toxicity study
(Conaway et al. 1985, Bio/dynamics, Inc. 1984a) was conducted in a
lower concentration range. In rabbits, maternal toxicity was reported
at the highest concentration (8,000 ppm) as reduced maternal food
intake, maternal weight loss, hypoactivity, and ataxia during treatment
and increased relative liver weights at term. However, no fetal effects
of treatment were reported in rabbits (Tyl 1989).
In mice (Bevan et al. 1997b, Tyl and Neeper-Bradley 1989), an 8,000
ppm concentration produced statistically significant lower pregnancy
weight gain (approximately 30 percent lower compared to controls) as
well as reduced corrected pregnancy weight gain. Food consumption of
dams was lower during the exposure period only. Clinical signs of
toxicity, statistically greater in incidence in the 8,000 ppm group on
gestation day 6 to 15, were hypoactivity, ataxia, prostration, labored
respiration, lacrimation and periocular encrustation. Group
observations during daily exposures included hypoactivity, ataxia and
forced respiration. Fetal toxicity endpoints at the 8,000 ppm
concentration included: increased postimplantation loss, fewer live
fetuses per litter, higher percent of litters with external and
visceral malformations, increased incidence of cleft palate and partial
atelectasis (absence of fetal lung inflation), reduced fetal body
weight (21 percent), and increase in the frequency of a number of
skeletal variations reflecting delayed ossification.
At the 4,000 ppm exposure, two of these fetal effects (reduced
fetal body weight and delayed ossification) were also statistically
significant and no maternal toxicity in the form of body weights or
clinical signs of toxicity occurred. Group observations at the 4,000
ppm concentrations included hypoactivity and ataxia. The fetal body
weight effects and delayed ossification were generally concentration-
related at 4,000 and 8,000 ppm, with no indication of treatment related
effects at 1,000 ppm, the NOAEL. The mouse developmental toxicity study
(Conaway et al. 1985) reported a nonsignificant but apparently
concentration-related pattern of increased fetal skeletal malformations
in mice exposed to 0, 250, 1,000, or 2,500 ppm (7, 11, 16, and 22
percent affected litters), including fused ribs and sternebrae. Conaway
et al. (1985) also evaluated skeletal ossification variations (Big/
dynamics, Inc. 1984b), but data were not provided or discussed.
Animal Reproductive Toxicity Studies
As noted above, the two rat reproductive toxicity studies used
longer exposures than the developmental toxicity studies, beginning
prior to mating and continuing through pregnancy and lactation in the
dams. Developmental toxicity in the two generation rat study included
reduced pup viability and body weights in the postnatal period for both
generations (Bevan et al. 1997a, Neeper-Bradley 1991). Viability, as
indexed by the number of dead pups on postnatal day four, was lower
than controls in the 8,000 ppm group of both the F1 and
F2 generations; survival indices were not affected. Group
difference in pup body weights was not significant on lactation day
one; group differences in body weight appeared later in lactation. Pup
weights were consistently lower than controls in the 8,000 ppm group
after postnatal day 14 in the F1 generation and after
postnatal day 7 in the F2 generation, and in the 3,000 ppm
group after postnatal day 14 in the F2 generation.
The finding of reduced pup weight gain during lactation in the
absence of reduced maternal weight gain is a distinctive finding of the
study. Pups were not directly exposed to MTBE during the lactation
period but may have been indirectly exposed via dam's milk or MTBE
condensation on the dam's fur. The postnatal effects could also have
been the result of MTBE effects on maternal behavior or lactation. The
findings on postnatal effects are partially supported by the earlier
rat single generation study (Biles et al. 1987), which described
reduced pup survival and reduced postnatal weights at exposure
concentrations of 250 to 2,500 ppm. The statistical significance and
dose-related characteristics of these effects varied in the single
generation study (see Table 6).
Reproductive Toxicity
Fertility and general toxicity
The two rat reproductive toxicity studies used exposures beginning
prior to mating and continuing through pregnancy and lactation in the
dams. No indication of reduced fertility was reported in either study.
No evaluations of ovarian cyclicity or sperm parameters were included
in either study.
As mentioned above, a concentration toxic to the adult breeders was
not reached in the single generation study (Biles et al. 1987), but was
included in the two generation study (Bevan et al. 1997a, Neeper-
Bradley 1991). Increased absolute liver weights (8,000 ppm males and
females) and increased relative liver weights (3,000 and 8,000 ppm
males and 8,000 ppm females) were reported in the F1
generation. Liver weights of the F1 generation were the only
organ weights reported.
An unexplained effect was greater lactational body weight gain in
the 3,000 ppm dams (F1) and 8,000 ppm dams (F0
and F1) relative to controls. This was due to less maternal
weight loss at the end of the lactation period, postnatal days 14 to
28. Lactational weight gain through postnatal day 14 did not differ
from controls. Maternal body weight had not been reduced during
gestation or at term. However, pups in the 3,000 and 8,000 ppm groups
were smaller than controls at some postnatal ages (see section on
developmental toxicity above) and this may have resulted in lower
energy requirements for lactation.
Reproductive organs
Information on reproductive organs of rats from single and multi-
generation studies is varied and incomplete. No effects on reproductive
organ weights (testes, epididymides, seminal vesicles, prostate,
ovaries) or pathology (testes, epididymides, ovaries) were reported in
the rat single generation study (Biles et al. 1987). Reproductive organ
weights were not obtained in the rat multi-generation study; no
exposure related histopathology of reproductive organs (vagina, uterus,
ovaries, epididymides, seminal vesicles, testes, prostate) was reported
when 25 rats per sex per generation in the control and 8,000 ppm group
were examined (Bevan et al. 1997a, Neeper-Bradley 1991).
Reproductive organ weights and pathology were sometimes reported in
subchronic and chronic toxicity and oncogenicity studies in rats. No
effects on weight or histopathology of gonads (ovaries and testes) were
noted in 14 and 90-day gavage studies in rats (n = 10/sex/group)
(Robinson et al. 1990). No effects on histopathology (testes, ovaries,
prostate, uterus) were reported in a lifetime (eight weeks to natural
death) gavage study in rats (n = 60/sex/group) (Belpoggi et al. 1995).
Organ weights were not reported in this oncogenicity study.
Endocrine effects
Moser et al. (1996b, 1998) conducted studies in mice of potential
antiestrogenic effects of MTBE. Endocrine modulating effects of MTBE
were suggested by the rodent tumor profile of endocrine sensitive
organs in oncogenicity studies. An additional suggestive finding was
reduced incidence of uterine endometrial hyperplasia in the mouse
inhalation cancer bioassays (Burleigh-Flayer et al. 1991), which
implies reduced estrogen action on the endometrium throughout the
lifetime. Moser et al. (1996b, 1998) demonstrated a number of adverse
effects of MTBE on the reproductive system of mice:
lower relative uterine and ovarian weights compared to
controls,
increase in overall length of estrous cycle, as well as
estrus and nonestrus stages,
lower rate of cell proliferation in the uterine, cervical
and vaginal epithelium,
changes in histology of the uterus, cervix and vagina
indicative of decreased estrogen action.
Body weight gain was also lower in MTBE exposed mice than in
controls.
In investigating the potential mechanism of MTBE-induced reduction
in estrogen action, Moser et al. (1996b) found that estrogen metabolism
was increased twofold in hepatocytes isolated from mice exposed to
1,800 mg MTBE/kg/day by gavage for 3 days. This change was associated
with greater liver weight and P450 content. This series of
experiments suggested that MTBE might lower circulating estrogen
concentrations by increasing estrogen metabolism. However, later
studies failed to confirm effects on serum estrogen when female mice
were exposed to 8,000 ppm MTBE for 4 or 8 months (Moser et al., 1998).
A further series of experiments (Moser et al. 1998) failed to find
evidence that MTBE endocrine effects were mediated by the estrogen
receptor by studying binding of MTBE and its metabolites to the
estrogen receptor, changes in expression of estrogen receptor in MTBE
exposed mice, and alterations of estrogen receptor activation and
translocation in a transfection assay. The authors suggest that MTBE
may exert an antiestrogenic action by a mechanism that does not involve
a change in circulating estrogen or estrogen receptor binding.
The consequences of reduced estrogen action induced by MTBE in mice
are not known; no fertility studies have been conducted in mice. It is
also not clear whether similar effects occur in other species, at other
doses, or with other exposure durations, since parallel studies have
not been done. The specificity of the effect also needs to be
determined. Unleaded gasoline has been found to have some
antiestrogenic effects similar to MTBE (MacGregor et al. 1993, Moser et
al. 1996b, Standeven et al. 1994). Also, an in vivo study reported
recently in abstract form (Okahara et al. 1998) described mild
estrogenic and antiestrogenic effects in pubertal mice (21 to 25 days
old) gavaged with 600 or 1,500 mg MTBE/kg body weight for 5 days.
Other Relevant Data
As discussed in the section on metabolism and pharmacokinetics,
MTBE is distributed to all major tissues studied in the rat. MTBE is
metabolized in the liver to TBA. TBA appears to be widely distributed
(Aarstad et al. 1985, Borghoff et al. 1996a, Savolainen et al. 1985).
No studies specifically examining distribution of MTBE or TBA to male
or female reproductive organs, or the placenta, embryo, or fetus were
located in the general published literature. In view of the general
widespread distribution, it is plausible that MTBE and TBA distribute
to these tissues.
Several studies have examined the developmental toxicity of TBA in
mice (oral) and rats (inhalation and oral). No reproductive studies of
TBA were located. NTP conducted subchronic and carcinogenesis studies
in mice and rats by drinking water that examined some reproductive
endpoints. There is also an in vitro study of TBA and mouse sperm.
The specific studies located were:
one developmental toxicity study in mice, oral (liquid
food), 0, 0.5, 0.75, or 1 percent weight to volume, gestation days 6 to
20 (Daniel and Evans 1982),
one developmental toxicity study in mice, oral (gavage), 0
or 780 mg/kg, twice per day, gestation days 6 to 18 (Faulkner et al.
1989),
one developmental toxicity study in rats, inhalation, 0,
2,000, 3,500, or 5,000 ppm, 7 hours per day, gestation days 1 to 19
(Nelson et al. 1989a),
one developmental toxicity study in rats, inhalation, 0,
6,000, 12,000 mg/m3 (0, 1,660, or 3,330 ppm), 7 hours per
day, gestation days 1 to 19 (abstract only) (Nelson et al. 1989b),
one developmental toxicity study in rats, oral (liquid
food), 0, 0.65, 1.3, or 10.9 percent volume to volume, gestation days 8
to 22 (abstract only) (Abel and Bilitzke 1992),
one developmental toxicity study in rats, gastric cannula,
0, or 0.6 to 2.7 g/kg/day, postnatal day four to seven (Grant and
Samson 1982),
subchronic (13 weeks) and carcinogenesis (2 years) studies
in rats and mice (both sexes), oral (water), various concentrations
(NTP 1995),
one in vitro study of mouse sperm fertilization capacity
(Anderson et al. 1982).
With the exception of Nelson et al. (1989a), reporting of the data
in the developmental studies was incomplete. Developmentally toxic
effects were observed in mice and rats orally administered TBA,
including prenatal and postnatal death (Abel and Bilitzke 1992,
Faulkner et al. 1989, Daniel and Evans 1982) and postnatal
developmental retardation (Daniel and Evans 1982). Malformations were
not observed (Faulkner et al. 1989). The inhalation study in rats by
Nelson et al. (1989a) found developmental retardation, as manifested in
lower fetal weights, at concentrations of 2,000, 3,500 and 5,000 ppm
TBA, and a higher percent of skeletal variations compared to controls
at 3,500 and 5,000 ppm. No increases in resorptions or malformations
were observed. Lower maternal weight was reported at 5,000 ppm.
Maternal neurobehavioral effects associated with the exposures
(narcosis at 5,000 ppm, unsteady gait at 3,500 and 5,000 ppm, unsteady
at 2,000 ppm) were also observed in the Nelson et al. (1989a) study.
The NTP subchronic and carcinogenesis studies in mice and rats by
drinking water used various concentrations of TBA. In these studies,
systemic toxicity was observed at the high concentration, usually
including death, reduced weight gain, and altered kidney weight. The
studies found little indication of potential reproductive toxicity.
Specifically, no effects on testis weight or sperm were observed. Minor
and inconsistent effects on testis histopathology and estrous cyclicity
were observed at the high concentrations. The in vitro study found no
effect of TBA on mouse sperm fertilization capacity.
Table 6.--MTBE: Developmental and Reproductive Toxic Effects (studies in
alphabetical order by author)
------------------------------------------------------------------------
Reported effects
Study design (1) (2) Reference
------------------------------------------------------------------------
Rat (Sprague-Dawley), oral Male: No increase Belpoggi et. al.
(gavage) death, reduced 1995
body weight gain,
or reduced food
consumption.
Male and female, 104 weeks, 4 No testicular ..................
days/week. histopathological
effects.
0,250, 1,000 Female: No reduced ..................
body weight gain,
or reduced food
consumption.
250, 1,000 mg/kg/ ..................
day: Increased
death (dose-
responsive, SS
not addressed).
No ovarian ..................
histopathological
effects.
Mouse (CD-1) inhalation gd 6-15, No maternal death, Bevan et al. 1997b
6 hours/day. or altered liver Tyl and Neeper-
weight. Bradley 1989
8,000 ppm: Reduced ..................
maternal body
weight (SS),
reduced body
weight gain (SS),
reduced food
consumption
during treatment
period (SS).
Target concentrations: 0, 1,000, Clinical signs ..................
4,000, 8,000 ppm. (individual
observations):
maternal,
hypoactivity
(SS), ataxia (SS)
prostration (SS),
labored
respiration (SS),
lacrimation (SS),
periocular
encrustation (SS).
Analytical concentrations: 0, Clinical signs ..................
1,035, 4,076, 8,153 ppm. (group
observations
during daily
exposure
periods):
maternal
hypoactivity,
ataxia, labored
breathing.
4,000 ppm: ..................
Clinical signs
(group
observations
during daily
exposure
periods):
maternal
hypoactivity,
ataxia.
No increased pre- ..................
implant loss,
early
resorptions, or
skeletal
malformations.
8,000 ppm: ..................
Increased post-
implant loss
(late resorptions
and dead fetuses)
(SS), reduced
live litter size
(SS), altered sex
ratio (less
males) (SS),
increased cleft
palate (SS)
(resulting in
increased pooled
external
malformations,
soft tissue
malformations,
and total
malformations
(SS)), reduced
fetal weight
(SS), increased
incidence of some
skeletal
variations
(mainly reduced
ossification)
(SS).
4,000 ppm: Reduced ..................
fetal weight
(SS), increased
incidence of some
skeletal
variations
(mainly reduced
ossification)
(SS).
Rabbit (New Zealand White)...... No maternal death, Bevan et al.
reduced body 1997b, Tyl 1989
weight, or
clinical signs of
toxicity before
or after daily
exposure periods.
Inhalation gd 6-18, 6 hours/day. 8,000 ppm: Reduced ..................
maternal body
weight gain (gd 6-
12) (SS)
(resulting in
reduced body
weight gain gd 6-
18 (SS)), reduced
food consumption
(gd 6-11, 13-14)
(SS) (resulting
in reduced food
consumption gd 6-
18 (SS)),
increased
relative liver
weight (SS).
Clinical signs
(group
observations
during daily
exposure
periods):
hypoactivity,
ataxia.
Target concentrations: 0, 1,000, 4,000 ppm: Reduced ..................
4,000, 8,000 ppm. maternal body
weight gain (gd 6-
9)(SS), reduced
food consumption
(gd 6-8, 9-
10)(SS).
Analytical concentrations: 0, No increased pre-
1,021, 4,058, 8,021 ppm. or post-implant
loss, reduced
litter size,
altered sex
ratio, reduced
fetal weight,
increased
malformations, or
increased
skeletal
variations..
Rat (Sprague-Dawley)............ No adult male or Bevan et al.
female deaths (F0 1997a, Neeper-
or F1), reduced Bradley 1991
adult female body
weight (F0),
reduced adult
female body
weight gain (F1),
or reduced adult
female food
consumption (F0).
Inhalation 2 generation 8,000 ppm: Reduced ..................
reproductive. adult male body
weight (F0,
F1)(SS), reduced
adult male body
weight gain (F0:
weeks 0-3, 5-7;
F1: weeks 0-2, 5-
6), reduced adult
female body
weight (F1: weeks
0-8, not
gestation or
lactation) (SS),
reduced adult
female body
weight gain (F0:
weeks 0-1, 5-6,
not gestation or
lactation) (SS),
increased female
body weight gain
during lactation
(F0, F1)(SS),
increased adult
male and female
absolute and
relative liver
weights (F1)(SS),
reduced adult
female food
consumption (F1:
lactation days 7-
14, not pre-breed
or gestation)
(SS).
Target concentrations: 0,400, Clinical signs ..................
3,000, 8,000 ppm. (individual
observations):
adult male,
perioral wetness
(F0, F1),
perioral
encrustation and
salivation (F1);
adult female,
perioral wetness
(F0, F1),
perioral
encrustation,
salivation and
urine stains (F1).
Analytical concentrations: 0, Clinical signs ..................
402, 3,019, 8,007 ppm. (group
observations
during daily
exposure
periods): adult
male and female,
ataxia (F0, F1),
hypoactivity (F0,
F1),
blepharospasm
(F0, F1), lack of
startle reflex
(F0, F1).
Male: 6 hours/day, 10 weeks (5 3,000 ppm: ..................
days/week) + mating + gestation. Increased adult
male relative
liver weights
(F1) (SS),
increased adult
female body
weight gain (F1:
lactation) (SS).
Clinical signs
(group
observations
during daily
exposure
periods): adult
male and female,
hypoactivity (F0,
F1),
blepharospasm
(F0, F1), lack of
startle reflex
(F0, F1).
No ovarian ..................
uterine, or
vaginal
histopathological
effects,
testicular or
other male
reproductive
organ
histopathological
effects, reduced
mating (F0, F1),
reduced fertility
(F0, F1), reduced
live litter size
(F1 F2) reduced
postnatal
survival after
pnd 4 (F1, F2),
reduced live
birth, 4-day
survival, or
lactation indices
(F1, F2), or
reduced lactation
day one weight
(F1, F2).
Female: 6 hours/day, 10 weeks (5 8,000 ppm: ..................
days/week) + mating + gestation Increased dead
(gd 1-19) + lactation (pnd 5- pups pnd 4 (F1,
28). F2)(SS), reduced
litter size at
end of lactation
(F2)(SS), reduced
postnatal weight
(F1:pnd 14-28,
F2:pnd 7-28)
(SS), reduced
postnatal weight
gain (F1:pnd 7-
21, F2:pnd 1-
21)(SS).
Exposures for F0 starting at pnd 3,000 ppm: ..................
42, and F1 starting on pnd 29- Increased dead
31. Pups not placed in pups pnd 4-28
inhalation chambers during (F1)(SS)(NOTR at
lactation. 8,000 ppm),
reduced postnatal
weight (F1: pnd
4, 14, F2: obd 14-
28) (SS), reduced
postnatal weight
gain (F1: pnd 1-
4, 7-14, F2: pnd
7-21) (SS).
Rat (Sprague-Dawley) Inhalation. No adult male or Biles et al. 1987,
female death, or Bio/dynamics
reduced male or 1984c
female body
weight (F0).
Reproductive: 1 generation, 2 2,500, 250 ppm: ..................
litter. Increased
incidence dilated
renal pelves in
females (NOT
1,000 ppm).
Male: 6 hours/day, 12 weeks (5 No altered testes ..................
days/week), + first mating (2 or ovary weight
weeks, daily), + 8 weeks (5 (F0), adverse
days/week), + second mating (2 histopathological
weeks, daily). effects on
ovaries or testes
(F0), reduced
mating, reduced
male fertility,
reduced female
fertility
(pregnancy rate),
reduced litter
size (live or
total) (F1a,
F1b), altered sex
ratio (F1a, F1b),
reduced pup
viability at
birth (live/
total)(F1a),
reduced birth
weight (F1a,
F1b), reduced pup
survival on pnd 4
(F1b), or reduced
pup survival on
pnd 21 (F1a, F1b).
Female: 6 hours/day, 3 weeks (5 2,500 ppm: Reduced ..................
days/week), + first mating pup viability at
(daily) + first gestation (gd 0- birth (live/
20) + first lactation (pnd 5- total) (F1b) (SS)
21) + 2 weeks (5 days/week) + (Note high in
second mating (daily) + second controls: control
gestation (gd 0-20) + second 99 percent, 1,000
lactation (pnd 5-21). and 2,500 ppm
95.5 percent.
Authors discount
biological
significance),
reduced postnatal
weight on pnd 14,
21 (F1a, F1b)
(NOT SS).
Target concentrations in text: 1,000 ppm: Reduced ..................
0, 250, 1,000, 2,500 ppm. pup viability at
birth (live/
total) F1b) (SS)
Note high in
controls: control
99 percent, 1,000
and 2,500 ppm
95.5 percent.
Authors discount
biological
significance),
reduced pup
survival from pnd
0-4 (F1a) (NOT
2,500 ppm),
reduced postnatal
weight on pnd 14,
21 (F1a, F1b)
(NOT SS).
Target concentrations in 250 ppm: Reduced ..................
abstract: 0, 300, 1,300, 3,400 pup survival from
ppm. pnd 0-4 (F1a)
(NOT 2,500 ppm)
(SS).
Nominal concentrations, Male/ ..................
Female: 0/0, 290/300, 1,300/
1,300, 3,400/3,400 ppm.
Analytical concentrations, Male/ ..................
Female: 0/0, 290/300, 1,180/
1,240, 2,860/2,980 ppm.
Mouse (CD-1) Inhalation, Male Male: 8,000 ppm: Burleigh-Flayer et
and female, 6 hours/day, 5 days/ Increased death al. 1992
week, 18 months 0,400, 3,000, (SS), reduced
8,000 ppm. body weight (SS),
increased liver
weight (SS),
blepharospasm,
hypoactivity,
ataxia, lack of
startle reflex,
prostration.
3,000 ppm: ..................
Increased liver
weight (SS),
blepharospasm,
hypo-activity,
ataxia, lack of
startle reflex,
stereotypy.
400 ppm: Increased ..................
liver weight
(SS). No
alteration in
testes weight,
testicular (or
other
reproductive
organ) histo-
pathological
effects.
Female: No ..................
increased death.
8,000 ppm: Reduced ..................
body weight (SS),
increased liver
weight (SS),
blepharospasm,
hypoac- tivity,
ataxia, lack of
startle reflex,
prostration.
3,000 ppm: ..................
Increased liver
weight (SS),
blepharospasm,
hypoac- tivity,
ataxia, lack of
startle reflex,
stereotypy.
No ovarian (or ..................
other
reproductive
organ)
histopathological
effects.
Rat (Fischer 344), Inhalation... Male: No altered Chun et al. 1992
liver weight to
400 ppm (see
note).
Male and female 6 hours/day, 5 ..................
days/week.
Male: 0, 400 ppm, 104 weeks..... 8,000 ppm: ..................
Increased death
(SS), reduced
body weight (SS),
(increased)
nephropathy,
ataxia,
hypoactivity,
blepharospasm,
lack of startle
reflex.
Male: 3,000 ppm, 97 weeks....... 3,000 ppm: ..................
Increased death
(SS),
nephropathy,
ataxia, hypoac-
tivity,
blepharospasm,
lack of startle
reflex.
Male: 8,000 ppm, 82 weeks....... 400 ppm: Increased ..................
death (SS),
nephropathy
Female: 0, 400, 3,000, 8,000 No altered testes ..................
ppm, 104 weeks. weight to 400 ppm
(see note).
8,000, 3,000, 400 ..................
ppm: Increased
testicular
mineralization
(see note).
Note: Remaining
males in 8,000
and 3,000 ppm
groups were
sacrificed early
due to high group
mortality.
Authors attribute
mortality and
mineralization of
``numerous
tissues'' to
nephropathy. No
statistical
evaluation of
testes or other
organ weight, or,
apparently,
histopathological
changes, was
performed by the
authors for the
8,000 or 3,000
ppm groups.
Female: No ..................
increased death.
8,000 ppm: Reduced ..................
body weight (SS),
increased liver
weight (SS),
ataxia,
hypoactivity,
blepharospasm,
lack of startle
reflex,
nephropathy.
3,000 ppm: ..................
Increased liver
weight (SS),
ataxia,
hypoactivity,
blepharospasm,
lack of startle
reflex,
nephropathy.
No ovarian (or ..................
other
reproductive
organ)
histopathological
effects.
Rat (Sprague-Dawley), Inhalation No maternal death, Conaway et al.
gd 6-15, 6 hours/day. reduced maternal 1985, Bio/
body weight, dynamics, Inc.
altered water 1984a
consumption, or
altered liver
weight.
Target concentrations: 0, 250, 2,500, 1,000, 250 ..................
1,000, 2,500 ppm. ppm: Reduced
maternal food
consumption on gd
9-12 (SS).
Analytical concentrations: 0, No increased pre- ..................
250, 1,000, 2,430 ppm. or post-implant
loss, reduced
live litter size,
reduced fetal
weight, reduced
crown-rump
distance, altered
sex ratio,
increased
malformations, or
increased
ossification
variations.
Nominal concentrations: 0, 260, ..................
1,100, 3,300 ppm.
Mouse (CD-1) Inhalation, gd 6- No maternal death, Conaway et al
15, 6 hours/day. reduced maternal 1985, Bio/
body weight, dynamics, Inc.
altered food or 1984b
water
consumption,
altered liver
weight.
Target concentrations: 0, 250, No increased pre- ..................
1,000, 2,500 ppm. or post-implant
losses, reduced
live litter size,
reduced fetal
weight, reduced
crown-rump
distance, altered
sex ratio,
increased
malformations.
Analytical concentrations: 0, [Fetuses with ..................
280, 1,110, 2,710 ppm. skeletal
malformations:
control, 1.6
percent; 250 ppm,
1.7 percent;
1,000 ppm, 2.4
percent; 2,500
ppm, 3.1 percent
(NOT SS). Litters
with skeletal
malformations:
control, 7.4
percent; 250 ppm,
11.5 percent;
1,000 ppm, 16
percent; 2,500
ppm, 22.2 percent
(NOT SS).].
Nominal concentrations: 0, 280, ..................
1,200, 3,500 ppm.
Rat (Sprague-Dawley), oral Male: No increased Robinson et al.
(gavage). death. 1990
Male and female, 14 days, 0, 1,428 mg/kg/day: ..................
357, 714, 1,071, 1,428 mg/kg/ Reduced body
day. weight gain (SS),
anesthesia, loose
stools.
1,071, 714 mg/kg/ ..................
day: Reduced body
weight gain (SS),
loose stools.
357 mg/kg/day: ..................
Loose stools.
No altered ..................
absolute testes
weight, or
testicular
histopathological
effects.
1,071, 714 mg/kg/ ..................
day: Increased
relative testes
weight (NOT at
1,428 mg/kg/day)
(SS).
Female: No ..................
increased death.
1,428 mg/kg/day: ..................
Reduced body
weight gain (SS),
anesthesia, loose
stools.
1,071 mg/kg/day: ..................
Reduced body
weight gain (SS),
loose stools.
714, 357 mg/kg/ ..................
day: Loose stools.
No altered ovary ..................
weight, or
ovarian
histopathological
effects.
Rat (Sprague-Dawley), oral Male: No increased Robinson et al.
(gavage). death. 1990
Male and female, 90 days 0, 100, 1,200 mg/kg/day: ..................
300, 900, 1,200 mg/kg/day. Reduced body
weight (NOT SS),
increased
relative liver
weight (SS),
increased
absolute and
relative kidney
weight (SS),
anesthesia,
diarrhea.
900 mg/kg/day: ..................
Increased
relative liver
weight (SS),
increased
absolute and
relative kidney
weight (SS),
diarrhea.
300, 100 mg/kg/ ..................
day: Diarrhea.
No altered testes ..................
weight, or
testicular
histopathological
effects.
Female: No ..................
increased death.
1,200 mg/kg/day: ..................
Reduced body
weight (SS),
anesthesia,
diarrhea.
900, 300 mg/kg/ ..................
day: Reduced body
weight (NOT SS),
diarrhea.
100 mg/kg/day: ..................
Diarrhea.
No altered ovary ..................
weight, or
ovarian
histopathological
effects.
------------------------------------------------------------------------
(1) Abbreviations: gd = gestation day, pnd = postnatal day.
(2) Effects reported by authors to be statistically significant (SS) or
biologically noteworthy.
immunotoxicity
Oral administration of 1,428 mg MTBE/kg/day for 14 days reduced
absolute spleen weights and absolute and relative thymus weights in
female rats but not in males and did not produce histopathological
lesions in the spleen or thymus. Similar results were observed
following 90 days treatment with an oral dose of 100 to 1,200 mg MTBE/
kg/day (Robinson et al. 1990). An increased incidence of dysplastic
proliferation of lymphoreticular tissues was observed in female rats
gavaged with 250 or 1,000 mg MTBE/kg/day, 4 days per week for 104 weeks
(Belpoggi et al. 1995). The authors discussed the possibility that
these lesions had the potential to develop into the lymphomas and
leukemias also observed in this study.
Administration of MTBE to Sprague-Dawley male rats by daily gavage
for 28 days with 40, 400, or 800 mg MTBE/kg/day produced an overall
increased percentage of apoptotic-type comets in peripheral blood
lymphocytes but no dose produced a statistical increase over vehicle
controls. DNA strand breakage was significantly increased in the 800
mg/kg/day group and depressed body weight gain and high corticosterone
levels were observed at 28 days (Lee et al. 1998).
neurotoxicity
Acute oral exposure in rats caused marked CNS depression at doses
greater than 1,900 mg/kg, ataxia at doses greater than 2,450 mg/kg,
loss of righting reflex at doses greater than 3,160 mg/kg, and tremors
and labored breathing at doses greater than 4,080 mg/kg. A no observed
effect level (NOEL) of 40 mg/kg for adverse but reversible neurological
effects for acute oral exposure was identified (Bioresearch
Laboratories 1990b) and an acute oral MRL of 0.4 mg/kg/day was
calculated by ATSDR (1996).
Scholl et al. (1996) measured the duration of ataxia and hypnosis
in male Fischer 344 rats pretreated with P450 inducers
following a single sub-hypnotic (0.5 mg/kg) and hypnotic (1.2 mg/kg)
i.p. dose of MTBE. Pretreatment with phenobarbital, and to a lesser
extent clofibrate but not beta-naphthoflavone, prolonged the duration
of ataxia or narcosis from MTBE compared with the vehicle control. The
data suggested that the biotransformation status is a major potential
determinant of sensitivity to the CNS depression effects of MTBE.
Two inhalation studies indicated that MTBE might be a weak
neurotoxicant in adult rats with primary effects of acute impairment. A
6-hour inhalation study and a 13-week repeated vapor inhalation study
produced signs of reversible CNS depression following exposure to 8,000
ppm and, to a lesser extent, to 4,000 ppm vapor with a NOAEL of 800 ppm
(Dodd and Kintigh 1989, Daughtrey et al. 1997). MTBE induced some mild
and reversible CNS toxicity but did not appear to be a neurotoxicant
under the conditions of these studies (Fueta et al. 1994).
chronic toxicity
Sprague-Dawley rats (60 animals per sex, per dose group) were given
0, 250 or 1,000 mg MTBE/kg/day in olive oil via gavage, 4 days per
week, for 104 weeks. This dosing regimen gives a 7-day time-weighted
average daily dose of 0, 143, and 571 mg/kg/day. Survival appeared to
be decreased in female rats after 16 weeks, but no statistical
treatments on data were reported. There was no reporting of
hematological, clinical chemistry or urinalysis parameters, or any
indication as to whether or not these endpoints were evaluated. The
authors did not observe any differences in food consumption or final
body weights in the various groups. In addition, they did not report
any noncancer histopathological changes (Belpoggi et al. 1995, 1997,
1998). Due to the limited scope, intermittent treatment schedule and
scant data reporting on noncancer endpoints in this study, it is not
possible to identify an adequate NOAEL or LOAEL.
Kidney toxicity was observed in both males and females in the 2-
year inhalation study in Fischer 344 rats by Chun et al. (1992)
discussed in the next section on carcinogenicity. U.S. EPA derived a
RfC of three mg/m3 based on the kidney and liver effects of
MTBE (U.S. EPA 1993, 1997c). These data support the conclusion that,
after MTBE exposure, kidney toxicity is of toxicological concern.
However, the use of the Robinson et al. (1990) study for evaluation of
kidney effects, as detailed in the previous section on subchronic
toxicity, has two significant uncertainties. One is that the study was
for 90 days and not for a lifetime, and the second is the extrapolation
of dose from a single daily bolus dose in corn oil to the continuous
small doses from drinking water exposure. In general, it would be
anticipated that a 90-day exposure period would tend to underestimate
the toxicity, while the bolus dose (a NOAEL of 100 mg/kg/day) would be
more likely to overestimate the toxic response. However, the relative
effects of these two factors are uncertain.
Animal studies conducted at very high levels of exposure to MTBE,
i.e., at greater than 1,000 ppm, through inhalation caused increased
liver, kidney, spleen, and adrenal weights; decreased brain weight,
body weight, and body weight gain; swollen periocular tissue; and
ataxia in rodents. Increased prostration (lying flat) or exhaustion was
reported in female rodents only.
carcinogenicity
No data on long-term effects of human exposure to MTBE relevant to
cancer risk were found in recent literature searches performed by
OEHHA.
The carcinogenic activity of MTBE has been investigated in male and
female Sprague-Dawley rats administered MTBE by gavage (Belpoggi et al.
1995, 1997, 1998) and in male and female Fischer 344 rats (Chun et al.
1992, Bird et al. 1997) and CD-1 mice (Burleigh-Flayer et al. 1992,
Bird et al. 1997) exposed to MTBE by inhalation. In rats receiving MTBE
by gavage for 24 months, statistically significant increases in Leydig
interstitial cell tumors of the testes were observed in males, and
statistically significant increases in lymphomas and leukemias
(combined) were observed in females. An increase in the incidence of
uterine sarcomas was also observed in MTBE-exposed female rats, but was
not statistically significant at the p < 0.05 level. In rats exposed to
MTBE by inhalation for up to 24 months, statistically significant
increases in the incidences of renal tubular tumors and Leydig
interstitial cell tumors of the testes were observed in males. In mice
exposed to MTBE by inhalation for up to 18 months, statistically
significant increases in the incidences of liver tumors were observed
in females (hepatocellular adenomas; hepatocellular adenomas and
carcinomas combined) and males (hepatocellular carcinomas). These
studies are described in more detail below.
Oral Exposure Studies
Rat gavage exposure studies: Belpoggi et al. (1995, 1997, 1998)
Groups of 60 male and 60 female 8-week old Sprague-Dawley rats were
administered MTBE in olive oil by gavage at doses of 0 (oil only), 250
or 1,000 mg/kg body weight/day, 4 days per week for 104 weeks. Animals
were maintained until natural death; the last animal died at 174 weeks
of age. No difference in water or food consumption, or in mean body
weights was observed between treated and control animals of either sex.
A dose-related decrease in survival was observed in females. At 56
weeks of age, survival was approximately 98 percent, 85 percent, and 78
percent in controls, low- and high-dose females, respectively; at 88
weeks of age, survival in those same groups was approximately 76
percent, 60 percent, and 43 percent. In males, there was no difference
in survival between the controls and the low-dose animals. However,
after 88 weeks, survival in high-dose males exceeded that of low-dose
and control males. At 104 weeks of age, survival was approximately 30
percent in low-dose and control males and 43 percent in high-dose
males; at 120 weeks of age, survival in those same groups was
approximately 11 percent and 32 percent.
A dose-related increase in the combined incidence of lymphomas and
leukemia was observed in female rats (Table 7). The authors reported
that the increase was highly significant (p < 0.01) in the high-dose
group and marginally significant in the low-dose group, when analyzed
using a log-ranked test as described by Mantel (1966) and Cox (1972).
When analyzed using the Fisher Exact test, the combined incidence of
lymphomas and leukemia in high-dose females was significantly different
from controls at the p = 0.001 level. Historical control incidence
rates in this laboratory for lymphomas and leukemias (combined) was <
10 percent in female Sprague-Dawley rats (Belpoggi et al. 1995). The
authors also noted an increase in uterine sarcomas in the low-dose
females (\5/60\ versus \1/60\ in controls), however, this increase did
not reach statistical significance (p = 0.1 by Fisher's Exact test). In
males, a statistically significant increased incidence of Leydig cell
tumors of the testes was observed in the high-dose group (Table 7). The
authors reported that this increase was significant at the p = 0.05
level using a prevalence analysis for nonlethal tumors (Hoer and
Walburg 1972).
Subsequent to the initial report of this study, a pathology review
was undertaken (Belpoggi et al. 1998) in which slides from the original
study were re-examined, and diagnostic criteria reviewed. This was
undertaken by an independent panel of the Cancer Research Centre (where
the study authors are based), assisted by an outside pathologist. Tumor
incidences according to the review are also presented in Table 7. Both
observed types of tumor were re-examined:
1. Testicular tumors.--Diagnosis was carried out according to
criteria developed by NTP, and adenomas and hyperplasia were reported
separately. In addition, adenomas were further characterized as single
or multiple histiotype, and the number of multifocal adenomas in each
dose group was reported. The results confirmed the diagnosis of the
Leydig cell tumors as adenomas, as reported in the initial papers.
According to the NTP diagnostic criteria, the incidence of Leydig cell
adenomas was 3, 5, and 11 in the control, low- and high-dose groups,
respectively. Hyperplasia was found in four, eight, and nine animals of
the three dose groups. This compares with the originally reported
incidences of 2, 2, and 11 in control, low- and high-dose animals. The
latest report indicated that all four multifocal adenomas observed
occurred in the high-dose group. No dose related increase of atrophy or
degeneration of testicular tissue was observed, although these
pathologies were reported. Thus, the tumors were not considered likely
to be secondary to cell death.
2. Lymphoid tumors.--The cell type of origin and tumor sites were
reported. All neoplasms were of lymphoid origin. Corrected incidences
were 2, 7, and 12 in the control, low- and high-dose groups,
respectively. For comparison, the previously reported incidence data
were 2, 6, and 12 in the same groups. Cancers were classified as
lymphoblastic lymphomas, lymphoblastic leukemias and
lymphoimmunoblastic lymphomas. The latter category was the most
prevalent, accounting for one, six, and eight of the tumors observed in
the respective dose groups. The data on distribution by site indicated
that most animals with lymphoid cancers were affected at multiple
sites. The tissues involved in treated animals were lung, liver, spleen
and lymph node, and ``other'', with the lung being the most commonly
affected site in treated animals.
______
Table 7.--Tumors in Sprague-Dawley Rats Receiving MTBE by Gavage, 0, 250 or 1,000 mg/kg/day, 4 days/week for 104
Weeks (Belpoggi et al. 1995, 1997, 1998)
----------------------------------------------------------------------------------------------------------------
Dose a (mg/kg/day)
Tumor site and type -----------------------------------------------
0 250 1,000
----------------------------------------------------------------------------------------------------------------
Females:
Hemolympohoreticular tissue (including mesenteric lymph nodes)
Lymphomas and leukemias (Belpoggi et al. 1995)................ 2/58b 6/51b 12/47 b,c,d,e
(3.4%) (11.8%) (25.5%)
Lymphomas and leukemias of lymphoid origin (Belpoggi et al. 2/58b 7/51b 12/47b,d,e
1998)........................................................ (3.4%) (13.7%) (25.5%)
Males:
Testes
Leydig interstitial cell tumors (Belpoggi et al. (1995)....... 2/26f (7.7%) 2/25f (8.0%) 11/32f,g,h
(34.4%)
Leydig interstitial cell adenomas (Belpoggi et al. 1998)...... 3/26f (11.5%) 5/25f (20.0%) 11/32f,h
(34.4%)
----------------------------------------------------------------------------------------------------------------
a Administered in olive oil, 4 days per week, for 104 weeks.
b Number of lesion-bearing animals/total alive at 56 weeks of age, when the first leukemia was observed.
c Incidence relative to control group was significant (p < 0.01) using a log-ranked test (Mantel 1966, Cox
1972), as reported by Belpoggi et al. (1995).
d Incidence relative to control group was significant by the Fisher Exact test (p = 0.001).
e Dose-related trend was significant by the Cochran-Armitage trend test (p < 0.01).
f Number of lesion-bearing animals/total alive at 96 weeks of age, when the first Leydig cell tumor was
observed.
g Incidence relative to control group was significant at the p = 0.05 level using prevalence analysis for
nonlethal tumors (Hoer and Walburg 1972), as reported by Belpoggi et al. (1995).
h Incidence relative to control group was significant by the Fisher Exact test (p < 0.05).
Inhalation Exposure Studies
Groups of 50 male and 50 female 8-week old Fischer 344 rats were
exposed to 0, 400, 3,000, or 8,000 ppm MTBE vapor by inhalation
(corresponding to analytical mean concentrations of 403, 3,023, or
7,977 ppm, or 1,453, 10,899, 28,760 mg/m3). The animals were
exposed for 6 hours per day, 5 days per week for 24 months, except for
the mid- and high-dose males, which were terminated at 97 and 82 weeks,
respectively, due to a dose-dependent increased mortality rate from
chronic progressive nephropathy. Low-dose males also experienced an
increase in nephropathy that was associated with a slight increase in
mortality and a decrease in survival. Survival times for females were
not significantly different between exposed and control rats. However,
there were slightly more deaths due to chronic progressive nephropathy
in the mid- and high-dose females than in the low-dose and control
females. Body weight gain and absolute body weight were decreased in
both sexes of the high-dose group. Exposure-related increases in kidney
and liver weights were reported in mid- and high-dose females, but not
in males. Chun et al. (1992) concluded that the maximum tolerated dose
(MTD) was exceeded in both sexes at high- and mid-dose levels, based on
increased mortality. Other observed effects of MTBE exposure included
anesthetic effects in rats of both sexes in the mid- and high-dose
groups.
A detailed histopathology examination was performed on all animals
in the control and high-dose groups, and on all animals that died or
were sacrificed moribund. Only a limited histopathology examination was
performed on non-moribund animals from the low- and mid-dose groups
that survived to terminal sacrifice; for males, only the liver,
kidneys, testes and gross lesions were evaluated, while for females,
only the liver and gross lesions were examined microscopically (Bird et
al. 1997). At the request of the MTBE Task Force, Experimental
Pathology Laboratories, Inc. (1993) re-evaluated the histopathologic
slides of kidneys from all male and female rats used in the Chun et al.
(1992) study, and confirmed the study pathologist's conclusion that
MTBE increased the severity of chronic progressive nephropathy in rats
of both sexes. No histopathologic re-evaluation of the kidney tumors
was performed.
In males, a statistically significant increase in renal tubular
adenoma and carcinoma (combined) was observed in the mid-dose group
(Table 8). In high-dose males renal tubular adenomas were increased,
however, this increase did not reach statistical significance (Table
8). The sensitivity of the bioassay to detect a dose-related increase
in renal tumors in the high-dose group is likely to have been reduced
by the high rate of early mortality, and the early termination of this
treatment group at week 82. Despite the reduced sensitivity of the
bioassay, a statistically significant increase in Leydig interstitial
cell testicular tumors was observed in mid- and high-dose males, with a
clear dose-response evident (Table 8). Historical laboratory control
values for Leydig testicular tumors in Fischer rats ranged from 64 to
98 percent (Bird et al. 1997).
In female Fischer 344 rats exposed to MTBE vapor, a single rare
renal tubular cell adenoma was observed in one mid-dose animal; no
treatment-related increases in tumor incidence were observed (Chun et
al. 1992, Bird et al. 1997). MTBE treatment of females was associated
with several nonneoplastic kidney lesions, however. Both female and
male rats exposed to MTBE experienced a dose-related increase in
mortality from chronic progressive nephropathy. Increases in
microscopic kidney changes indicative of chronic nephropathy were seen
in all treated males and in mid- and high-dose females. All treated
males had increases in the severity of mineralization and interstitial
fibrosis of the kidney, while increases in mild to moderate
glomerulosclerosis, interstitial fibrosis, and tubular proteinosis were
observed in females.
Table 8.--Tumors in Male Fischer 344 Rats Receiving MTBE by Inhalation, 0, 400, 3,000, or 8,000 ppm, for up to
24 Monthsa (Chun et al. 1992, Bird et al. 1997)
----------------------------------------------------------------------------------------------------------------
Concentration b (ppm)
Tumor site and type ---------------------------------------------------------------
0 400 3,000 8,000
----------------------------------------------------------------------------------------------------------------
Kidney:
renal tubular adenoma......................... 1/35c 0/32c 5/31c 3/20c
renal tubular carcinoma....................... 0/35c 0/32c 3/31c 0/20c
renal tubular adenoma and carcinoma (combined) 1/35c 0/32c 8/31c,d 3/20c
(3%) (0%) (26%) (15%)
Testes:
Leydig interstitial cell tumors............... 32/50 35/50 41/50e 47/50f
(64%) (70%) (82%) (94%)
----------------------------------------------------------------------------------------------------------------
a Mid- and high-dose animals were terminated at 97 and 82 weeks, respectively, due to a dose-dependent increased
mortality rate from chronic progressive nephropathy.
b Administered as MTBE vapor 6 hours per day, 5 days per week.
c Survival-adjusted tumor incidence rates were used to attempt to control for excess early mortality in the mid-
and high-dose groups (U.S. EPA, 1995c).
d,e,f Incidence relative to control group was significant by the Fisher Exact test (dp < 0.01, ep < 0.05, fp <
0.001).
Groups of 50 male and 50 female 8-week old CD-1 mice were exposed
to 0, 400, 3,000, or 8,000 ppm MTBE vapor by inhalation (corresponding
to analytical mean concentrations of 402, 3,014, or 7,973 ppm or 1,442,
10,816, or 28,843 mg/m3). The animals were exposed for 6
hours per day, 5 days per week, for 18 months. Increased mortality and
decreased mean survival time were observed only for male mice in the
high-dose group. A slightly increased frequency of obstructive
uropathy, a condition that occurs spontaneously in this mouse strain,
was observed in high-dose males, however, deaths due to the condition
were within the range noted for historical controls. Body weight gain
and absolute body weights were decreased in high-dose males and
females. Dose-dependent increases in liver weights were observed in
both sexes. Kidney weights were increased in high-dose females and in
low- and mid-dose males. Burleigh-Flayer et al. (1992) concluded that
the MTD was exceeded in both sexes at the high-dose level. Other
observed effects of MTBE exposure included anesthetic effects in mice
of both sexes in the mid- and high-dose groups.
A detailed histopathology examination was performed on all animals
in the control and high-dose groups, and on all animals that died or
were sacrificed moribund. Only a limited histopathology examination was
performed on non-moribund animals from the low- and mid-dose groups
that survived to terminal sacrifice; for males, only the liver, spleen
and submandibular lymph nodes were evaluated, while for females, only
the liver, uterus and stomach were examined microscopically (Bird et
al. 1997).
In females, a statistically significant increased incidence of
hepatocellular adenomas was observed in the high-dose group (Table 9).
The incidence of hepatocellular adenomas and carcinomas (combined) was
also increased in high-dose females, however, only two hepatocellular
carcinomas were reported, one each in the low- and high-dose groups. In
males, a statistically significant increase in hepatocellular
carcinomas was observed in the high-dose group (Table 9). Bird et al.
(1997) noted that the combined incidence of adenomas and carcinomas in
high-dose males was similar to the historical incidence for male CD-1
mice of 33 percent. However, after correcting for the number of animals
alive at 49 weeks, when the first hepatocellular adenoma was observed
in males, the incidence in the high-dose group was 43 percent (16/37,
see Table 9), representing a clear increase above the cited historical
incidence in male CD-1 mice. Burleigh-Flayer et al. (1992) concluded
that the increased incidence of liver tumors in the high-dose groups
(adenomas in females and carcinomas in males) could be attributed to
MTBE exposure. The ability of this study to detect increases in tumor
incidence was likely decreased by the shortened study length (18 versus
24 months).
Table 9.--Tumors in CD-1 Mice Receiving MTBE by Inhalation, 0, 400, 3,000 or 8,000 ppm, for up to 18 Monthsa
(Burleigh-Flayer et al. 1992, Bird et al. 1997)
----------------------------------------------------------------------------------------------------------------
Doseb (ppm)
Tumor site and type ---------------------------------------------------------------
0 400 3,000 8,000
----------------------------------------------------------------------------------------------------------------
Females (Liver):
hepatocellular adenoma........................ 2/50 1/50 2/50 10/50c
hepatocellular carcinoma...................... 0/50 1/50 0/50 1/50
hepatocellular adenoma and carcinoma 2/50 2/50 2/50 11/50d
(combined)...................................
Males (Liver):
hepatocellular adenoma........................
hepatocellular carcinoma...................... 11/47e 11/47e 9/46e 12/37e
hepatocellular carcinoma...................... 2/42f 4/45f 3/41f 8/34c,f
hepatocellular adenoma and carcinoma 12/47e 12/47e 12/46e 16/37e
(combined)...................................
----------------------------------------------------------------------------------------------------------------
a Male mice in the high-dose group experienced early mortality.
b Administered as MTBE vapor 6 hours per day, 5 days per week.
c,d Incidence relative to control group was significant by the Fisher Exact test (cp < 0.05, p < 0.01).
e Number of lesion-bearing animals per total alive at 49 weeks, when the first hepatocellular adenoma was
observed.
f Number of lesion-bearing animals per total alive at 63 weeks, when the first hepatocellular carcinoma was
observed.
Other Relevant Data
Structure-Activity Comparisons
MTBE and similar ethers generally undergo metabolism at the
ethereal bond to form the corresponding alcohol and an aldehyde
(Savolainen et al. 1985). Other structurally similar ethers include
ETBE and tertiary-amyl methyl ether (TAME). No studies have been
reported to date on the carcinogenicity of ETBE or TAME. Published data
on the genotoxic potential of ETBE and TAME are few in number; ETBE and
TAME tested negative in the Salmonella reverse mutation assay, and TAME
did not induce micronuclei in mouse bone marrow cells following
exposure in vivo (NSTC 1997). In a recent review of gasoline toxicity,
Caprino and Togna (1998) briefly refer to an unpublished report in
which TAME induced ``chromosomal effects'' in Chinese hamster ovary
cells. MTBE is made by isobutene and methanol, or TBA and methanol. NTP
has documented some evidence of carcinogenic activity for isobutene in
male rats (NTP 1997), and for TBA in male rats and female mice (NTP
1995).
Pathology
The tumors observed by Belpoggi et al. (1995, 1997, 1998) in
hemolymphoreticular tissues in the female Sprague-Dawley rat were
diagnosed as lymphomas and leukemias. The re-analysis of the pathology
data (Belpoggi et al. 1998) confirmed that these neoplasms were all of
lymphoid origin, and further identified them as lymphoblastic
lymphomas, lymphoblastic leukemias, and lymphoimmunoblastic lymphomas.
IARC (IARC, 1993) classifies all three of these tumor types as
malignant lymphomas. The aggregation of these tumor types for
carcinogen identification and risk assessment purposes is therefore
appropriate.
The testicular tumors observed in both the Sprague-Dawley (Belpoggi
et al. 1995, 1997, 1998) and Fischer 344 (Chun et al. 1992, Bird et al.
1997) rat strains were diagnosed as Leydig interstitial cell tumors.
The spontaneous incidence of these tumors is typically much lower in
the Sprague-Dawley rat, as compared to the Fischer 344 rat
(approximately 5 percent and 88 percent, respectively at 24 months)
(Clegg et al. 1997). The control incidence of these tumors reported by
Belpoggi et al. (1995) (i.e., 7.7 percent) is consistent with levels
typically observed in the Sprague-Dawley strain. The control incidence
observed by Chun et al. (1992), (i.e., 64 percent) was reported in the
published study (Bird et al. 1997) as being lower than that typically
observed in the Fischer 344 strain. However, this control incidence was
similar to that (i.e., 64.9 percent) reported for male Fischer 344 rats
in another oncogenicity study from the same laboratory (Burleigh-Flayer
et al., 1997), the same as the historical control rate for male Fischer
344 rats in NTP inhalation studies (Nyska et al. 1998), and within the
range (64 to 98 percent) reported for aged male rats of this strain
(Bird et al. 1997, Haseman and Arnold 1990). The lower spontaneous
Leydig cell tumor incidence observed in the Chun et al. (1992) study is
likely to have facilitated the detection of the dose-dependent increase
in Leydig cell tumors in MTBE-treated males, despite the early
termination of the mid- and high-dose groups.
The tumors observed in male Fischer 344 rat kidney tissues (Chun et
al. 1992, Bird et al. 1997) were diagnosed as renal tubular adenomas
and carcinomas. These two tumor phenotypes are generally considered to
be related in origin, with the possibility that adenomas may progress
to carcinomas (Borghoff et al. 1996b). Therefore, they are normally
aggregated for carcinogen identification and risk assessment purposes
(U.S. EPA 1991). The possibility that the male rat-specific
2u-globulin nephropathy plays a significant role in
the pathogenesis of MTBE rat kidney tumors has been investigated, and
reported to be unlikely (NSTC 1997, U.S. EPA 1997a). The data indicate
that MTBE induces only mild accumulation of 2u-
globulin and mild or partial expression of 2u-
globulin associated nephropathy in male rats, while clearly
exacerbating the expression of non-2u-globulin rat
nephropathy in both males and females (NSTC 1997). Support for this
conclusion includes the observation that a dose-dependent increase in
mortality from chronic progressive nephropathy was observed in male
rats at all dose levels, and in females at the mid- and high-dose
levels in the rat inhalation bioassay (Bird et al. 1997). Observed
microscopic kidney changes included increases in the severity of
mineralization and interstitial fibrosis in all treated males, and
increases in mild to moderate glomerulosclerosis, interstitial
fibrosis, and tubular proteinosis in mid- and high-dose females (Chun
et al. 1992). In addition, a rare renal tubular tumor was observed in
one MTBE-treated female rat (Chun et al. 1992). In a separate analysis
of a 13-week inhalation exposure study of male rats conducted at the
Bushy Run Research Center laboratory, Swenberg and Dietrich (1991)
measured the levels of 2u-globulin associated with
hyaline droplets in MTBE-treated and control kidney sections by
immunohistochemical staining techniques. Although a slight increase in
renal cortex staining for 2u-globulin was observed
in MTBE-treated animals, as compared with controls, there was no
relationship between the level of 2u-globulin
staining and the dose of MTBE received (U.S. EPA 1997c, Swenberg and
Dietrich 1991). In a study by Lington et al. (1997), inhalation of
4,000 and 8,000 ppm MTBE for 13 weeks resulted in a moderate increase
in the size of hyaline droplets in male rat kidney, but no MTBE-
associated increase in the area or intensity of 2u-
globulin immunostaining was observed, as reported by Bird et al.
(1997). In a 4-week inhalation study, exposure to 3,000 and 8,000 ppm
MTBE increased the levels of protein accumulated in male rat kidney
tubule epithelial cells, but not the levels of 2u-
globulin, as compared with controls (Bird et al. 1997).
The tumors observed by Burleigh-Flayer et al. (1992) and Bird et
al. (1997) in mouse liver were diagnosed as hepatocellular adenomas and
carcinomas. These two tumor phenotypes are generally considered to be
related in origin, with the possibility that adenomas may progress to
carcinomas. They are normally therefore aggregated for carcinogen
identification and risk assessment purposes. The sensitivity of the
study to detect treatment-related tumors, especially in the low- and
mid-dose groups, may have been compromised by the less-than-lifetime
length of the study (18 months).
Mechanism
The mechanism(s) by which MTBE induces tumors at multiple sites in
rats and mice is unknown at this time. It is unclear whether MTBE
itself plays a direct role in the observed tumorigenesis, or whether
metabolism to one or more active metabolites is required. The two major
metabolites of MTBE, HCHO (Kerns et al. 1983, Sellakumar et al. 1985,
Til et al. 1989, Woutersen et al. 1989) and TBA (NTP 1995), have both
been shown to possess tumorigenic activity in animal studies.
Interestingly, there is a commonality of tumor sites observed for MTBE,
HCHO, and TBA. Leukemias were observed in male and female Sprague-
Dawley rats administered HCHO in drinking water (Soffritti et al.
1989), and renal tubular cell adenomas and carcinomas were observed in
male Fischer 344 rats administered TBA in drinking water (NTP 1995,
Cirvello et al. 1995). IARC (1995) concluded that the evidence on the
carcinogenicity of HCHO was sufficient in animals and limited in
humans, and classified the agent in Group 2A probably carcinogenic to
humans. NTP (1995) in reviewing the results of 2-year drinking water
studies with TBA concluded that ``there was `some' evidence of
carcinogenic activity of TBA in male Fischer 344/N rats based on
increased incidences of renal tubule adenoma or carcinoma (combined)''.
It is presently unknown whether the nature or degree of MTBE
metabolism is tissue- or sex-specific, or whether there is any
relationship between the site of metabolism and target tumor sites.
Comparison of the target tumor sites in rats administered MTBE by two
different routes of administration is inherently limited by the use of
different rat strains in these studies; however, these findings suggest
that route-specific distribution and metabolism of MTBE may be of
importance in the development of some (e.g., leukemias and lymphomas,
renal tumors), but not all treatment-associated tumors (e.g.,
testicular tumors). It has also been suggested that sex-specific
differences in metabolism may underlie the development of leukemias and
lymphomas in female, but not male rats (Belpoggi et al. 1995, 1997,
1998). This hypothesis remains untested, however.
MTBE was negative in a number of genotoxicity assays as noted in
the section on genetic toxicity in this document and by ATSDR (1996),
testing positive only in the activated mouse lymphoma forward mutation
assay (ARCO 1980, Mackerer et al. 1996) and the rat lymphocyte comet
assay (Lee et al. 1998). The MTBE metabolite TBA was not mutagenic in
either the Salmonella assay (Zeiger et al. 1987) or the mouse lymphoma
assay (McGregor et al. 1988). HCHO is genotoxic, testing positive in
numerous assay systems (IARC 1995). Data on HCHO-related genotoxicity
in MTBE tumorigenesis are too limited to draw any conclusions at this
time. Studies conducted in freshly isolated mouse hepatocytes from
female CD-1 mice (Casanova and Heck 1997) did not find any dose-related
increase in HCHO-associated DNA-protein cross-links or RNA-HCHO adducts
following MTBE-treatment. Similar results were obtained with freshly
isolated hepatocytes from male B6C3FI mice and male Fischer 344 rats
(Casanova and Heck 1997). These data suggest that HCHO is not the
active species responsible for MTBE liver tumorigenesis in the mouse.
In studies using the mouse lymphoma assay, however, HCHO has been
implicated as the active species responsible for MTBE's mutagenic
activity (Gamier et al. 1993, Mackerer et al. 1996). DNA-protein cross-
link data and RNA-HCHO adduct data are not available for the other
tumor sites noted after MTBE exposure in laboratory animals.
Several hypotheses have been put forward suggesting that MTBE may
act via a variety of nongenotoxic mechanisms, such as the involvement
of endocrine modulation in mouse liver and rat testicular tumorigenesis
(Bird et al. 1997, Moser et al. 1996b) and 2u-
globulin nephropathy in male rat kidney tumorigenesis (Bird et al.
1997, Poet and Borghoff 1997a, 1997b, Prescott-Mathews et al. 1997a).
While MTBE exposure of the mouse is associated with various endocrine-
related tissue and cellular responses (see the section on developmental
and reproductive toxicity in this document), the available data are
insufficient to support an endocrine-mediated mode of action for MTBE-
associated liver (Moser et al. 1996a, 1996b, Moser et al. 1998, Okahara
et al. 1998) or testicular tumors (Day et al. 1998) at this time.
Data which suggest that 2u-globulin nephropathy
may be involved in MTBE kidney tumorigenesis include the following:
A mild to moderate increase in the number and size of
hyaline droplets in the renal proximal tubule cells of MTBE-treated
male rats has been observed.
LIn a 10-day inhalation study, MTBE increased the number
of protein droplets within the renal proximal tubules of male rats with
a statistically significant concentration-related positive trend
(Prescott-Mathews et al. 1997a).
LIn a 14-day gavage study, MTBE increased the formation
of hyaline droplets in male rat kidney proximal tubular epithelial
cells at the highest dose tested (Robinson et al. 1990).
LIn a 28-day inhalation study, MTBE slightly increased
protein accumulation in male rat kidney tubular epithelial cells (Bird
et al. 1997).
LIn a 13-week inhalation study, MTBE slightly increased
hyaline droplet formation in male rat kidney (Swenberg and Dietrich
1991).
LIn another 13-week inhalation study, MTBE slightly
increased the size of hyaline droplets in male rat kidney (Bird et al.
1997 reporting on findings of Lington et al. 1997).
LIn a 90-day gavage study, MTBE slightly increased the
number of hyaline droplets in male rat kidney proximal tubular
epithelial cells (Robinson et al. 1990).
Protein in the renal proximal tubule cells of MTBE-treated
male rats stains weakly for 2u-globulin.
LIn a 13-week inhalation study, MTBE slightly increased
hyaline droplet formation and staining for 2u-
globulin in male rat kidney but these increases were not dose-dependent
(Swenberg and Dietrich 1991).
LIn a 10-day inhalation study, no dose-related increase
in 2u-globulin staining could be detected in MTBE-
treated male rat kidney by immunohistochemical staining (Prescott-
Mathews et al. 1997a).
Using an ELISA-based method, a mild dose-dependent
increase in 2u-globulin-immunoreactivity
(approximately 150 g2u-globulin/mg total
protein in controls versus 200 g2u-
globulin/mg total protein in the high-dose animals) has been observed
in rat kidney cytosol of male rats exposed to MTBE by inhalation for 10
days (Prescott-Mathews et al. 1997a).
MTBE binds weakly to 2u-globulin in
vitro. Using a kidney homogenate system, only a very weak interaction
between MTBE and male rat renal proteins was detected (Poet and
Borghoff 1997a). This interaction did not survive dialysis or anion
exchange chromatography (Poet and Borghoff 1997a).
A dose-dependent increase in cell proliferation has been
observed in the renal cortex of male rats exposed to MTBE by inhalation
for 10 days (Prescott-Mathews et al. 1997a).
Agents which are thought to induce renal tubular tumors
via an 2u-globulin-mediated mechanism are
nongenotoxic. MTBE has demonstrated little or no genotoxicity in vitro
or in viva.
Data which argue against a significant role for
2u-globulin nephro-
pathy in MTBE kidney tumorigenesis include the following:
Male rat specificity for nephropathy and renal
tumorigenicity has not been observed.
LIn a 2-year inhalation study, MTBE exacerbated chronic
progressive nephropathy and increased mortality associated with chronic
progressive nephropathy in a dose-dependent manner in both in female
and male rats (Chun et al. 1992, Bird et al. 1997).
LA rare kidney tumor was observed in one MTBE-treated
female rat in the 2-year inhalation study (Chun et al. 1992, Bird et
al. 1997).
A clear exposure-related increase in staining for
2u-globulin, an effect typical of classical
2u-globulin nephropathy-inducing agents, has not
been observed in male rats treated with MTBE.
LIn a 13-week inhalation study, MTBE slightly increased
hyaline droplet formation and staining for 2u-
globulin in male rat kidney but these increases were not dose-dependent
(Swenberg and Dietrich 1991).
LIn another 13-week inhalation study, MTBE slightly
increased the size of hyaline droplets in male rat kidney, but no
increase in the area or intensity of 2u-globulin
staining was observed (Bird et al. 1997 reporting on findings of
Lington et al. 1997).
LIn a 28-day inhalation study, MTBE slightly increased
protein accumulation in male rat kidney, but did not increase
2u-globulin immunohistochemical staining (Bird et
al. 1997).
LIn a 10-day inhalation study, no dose-related increase
in 2u-globulin staining could be detected in MTBE-
treated male rat kidney by immunohistochemical staining, but using a
more sensitive ELISA-based assay a mild increase in the concentration
of 2u-globulin (approximately 150
g2u-globulin/mg total protein in controls
versus 200 g2u-globulin/mg total protein
in the high-dose animals) was observed (Prescott-Mathews et al. 1997a).
This small increase is in contrast to the marked increase seen with
classical 2u-globulin nephropathy-inducing agents,
such as 2,2,4-trimethylpentane (approximately 200
g2u-globulin/mg total protein in controls
versus 550 g2u-globulin/mg total protein
in treated animals) (Prescott-Mathews et al. 1997a).
2u-Globulin-positive proteinaceous
casts, another effect typical of classical 2u-
globulin nephropathy-inducing agents, were not seen at the junction of
the proximal tubules and the thin loop of Henle in several short-term
studies, including a 10-day inhalation study (Prescott-Mathews et al.
1997a), a 28-day inhalation study (Bird et al. 1997), or a 13-week
inhalation study (Swenberg and Dietrich 1991, U.S. EPA 1997c). However,
in a 90-day oral study a small number of granular casts were observed
(Robinson et al. 1990).
Linear mineralization of papillary tubules, another effect
typical of classical 2u-globulin nephropathy-
inducing agents, has not been reported in rats exposed to MTBE to date.
To date, published reports have not detected the binding
of MTBE to 2u-globulin or male rat renal proteins
in vivo (Prescott-Mathews et al. 1997b), although Borhgoff and
colleagues report indirect evidence for an in vivo association between
MTBE and male rat renal proteins (Borghoff, personal communication).
Only a very weak interaction between MTBE and male rat renal proteins
has been detected in vitro, using a kidney homogenate system (Poet and
Borghoff 1997a). This interaction did not survive dialysis or anion
exchange chromatography (Poet and Borghoff 1997a), in contrast to
observations with classical 2u-globulin
nephropathy-inducing agents, where typically 20 to 40 percent of bound
ligand is retained after dialysis (NSTC 1997).
The available data on renal tumorigenesis indicate that MTBE
induces only mild accumulation of 2u-globulin and
mild or partial expression of 2u-globulin
associated nephropathy in male rats, while clearly exacerbating the
expression of non-2u-globulin rat nephropathy in
both males and females (NSTC 1997). The U.S. EPA (1991) established
three criteria for causation of an a2u-globulin effect:
(1) increased number and size of hyaline droplets in renal proximal
tubule cells of treated male rats;
(2) accumulating protein in the hyaline droplets is
2u-globulin; and
(3) additional aspects of the pathological sequence of lesions
associated with 2u-globulin nephropathy are
present.
If the response is mild all of the typical lesions may not be
observed, however, some elements consistent with the pathological
sequence must be demonstrated to be present.
Evaluation of the available data indicates that the first U.S. EPA
criterion has been satisfied, but not the second or third (NSTC 1997,
U.S. EPA 1997a).
In late 1997, IARC held a workshop to examine, among other issues,
the scientific basis for possible species differences in mechanisms by
which renal tubular cell tumors may be produced in male rats (IARC
1998b). The final draft of the consensus report from this workshop
outlines seven criteria which all must be met by agents causing kidney
tumors through an 2u-globulin-associated response
in male rats. These criteria are the following:
(1) Lack of genotoxic activity (agent and/or metabolite) based on
an overall evaluation of in vitro and in vivo data
(2) Male rat specificity for nephropathy and renal tumorigenicity
(3) Induction of the characteristic sequence of histopathological
changes in shorter-term studies, of which protein droplet accumulation
is obligatory
(4) Identification of the protein accumulating in tubular cells as
2u-globulin
(5) Reversible binding of the chemical or metabolite to
2u-globulin
(6) Induction of sustained increased cell proliferation in the
renal cortex
(7) Similarities in dose-response relationship of the tumor outcome
with the histopathological end-points (protein droplets,
2u-globulin accumulation, cell proliferation)
The data summarized above indicates that the second, fourth and
seventh IARC (1998b) criteria have not been satisfied. With regard to
the third criterion, the classical 2u-globulin-
associated accumulation of granular casts has not been observed in
several shorter-term studies. Similarly, linear mineralization of
papillary tubules, which is also part of the characteristic sequence of
histopathological changes, has not been observed. With regard to the
fifth criterion, MTBE appears to reversibly bind to
2u-globulin only very weakly. As to the sixth
criterion, there are no data available to evaluate whether MTBE induces
a sustained increase in cell proliferation in the renal cortex.
Thus, based on both the U.S. EPA and IARC criteria,
2u-globulin nephropathy does not appear to play a
significant role in MTBE kidney tumorigenesis.
Summary of the Evidence
Epidemiological studies of the carcinogenic effects of MTBE are not
available. Carcinogenicity of MTBE has been observed in both sexes of
the rat in a lifetime gavage study (Belpoggi et al. 1995, 1997, 1998),
in male rats of a different strain in a 24-month inhalation study (Chun
et al. 1992, Bird et al. 1997), and in male and female mice in an 18-
month inhalation study (Burleigh-Flayer et al. 1992, Bird et al. 1997).
Statistically significant increases in Leydig interstitial cell tumors
of the testes were observed in two different strains of rats by two
separate routes of administration. Other statistically significant
increases in the rat were leukemias and lymphomas (combined) in females
and renal tubular tumors in males. Statistically significant increases
in hepatocellular carcinomas were observed in male mice and
statistically significant increases in adenomas and combined adenomas
and carcinomas were observed in female mice. MTBE has demonstrated
little or no genotoxicity in vitro or in vivo. The mechanism by which
MTBE induces tumors at multiple sites in animals remains unknown (NSTC
1997, Mennear 1995, 1997a, 1997b). Additional supporting evidence is
provided by the carcinogenic activity of HCHO and TBA, two primary
metabolites of MTBE, which share target tumor sites in common with
MTBE. Both TBA and MTBE cause renal tumors in one strain
of rat, and both orally administered HCHO and MTBE were associated with
lymphohematopoietic cancers in a different strain.
Conclusion
Based on the information reviewed in the preparation of this
document, there is evidence for the carcinogenicity of MTBE at multiple
sites in both sexes of the rat and the mouse in five of the six
available studies; MTBE is a two-species, multi-strain, two-sex, two-
route, and multi-site carcinogen. Positive animal carcinogenicity data
for HCHO and TBA, metabolites of MTBE, provide support for this
conclusion.
ecotoxicity
Concern has been raised about the effects of MTBE in water on
plants, animals and ecosystems (UC 1998). Rowe et al. (1997) summarized
aquatic toxicity information and water quality criteria for VOCs
including MTBE being monitored in the NAWQA Program by the USGS. The
species tested so far for toxic effects of MTBE have high thresholds in
the ppm or mg/L range indicating that MTBE has limited acute and
chronic toxicity for aquatic species (Mancini 1997, Stubbleffield et
al. 1997). Acute studies generated MTBE LC50 values with the
freshwater green algae of 184 ppm, the freshwater Ceriodaphnia fleas of
348 ppm, the freshwater Daphnia water fleas of 542 and 681 ppm, the
freshwater fathead minnows of 672, 706, 929 and 979 ppm, the freshwater
rainbow bouts of 887 and 1237 ppm, the freshwater tadpoles of 2,500
ppm, the marine mysid shrimps of 44 and 136 ppm, the marine inland
silverside of 574 ppm, the marine bleak of > 1,000 ppm, the marine
copepod of > 1,000 ppm, and the marine sheepshead minnows of > 2,500
ppm.
Toxicity of MTBE to Daphnia magna and Photobacterium phosphoreum
was reported (Gupta and Lin 1995). A recent laboratory toxicity study
with three unicellular algae suggests that the dissolved MTBE may alter
algal community composition in the natural environment (Rousch and
Sommerfeld 1998). Research by the API and others on ecological hazards
of MTBE exposure is continuing. Because of the large amount of MTBE
usage in California, high water and lipid solubility of MTBE, and lack
of information on toxic effects of long-term exposure to low doses of
MTBE (e.g., reproductive impairment in plants or animals), Cal/EPA
(1998) has a continuing interest in reviewing current and proposed
research to fill in these data gaps.
toxicological effects in humans
No studies were located regarding toxic effects of MTBE in humans
following ingestion or skin contact. No studies were located regarding
toxic effects of ingested or inhaled or skin-contacted MTBE in drinking
water in humans. No studies were located regarding acute effects,
subchronic effects, chronic effects, death, systemic effects including
respiratory, gastrointestinal, cardiovascular, hematological,
musculoskeletal, hepatic, renal, endocrine, dermal, ocular, or body
weight effects, immunological or lymphoreticular effects, neurological
effects, developmental or reproductive effects, genotoxic effects, or
cancer in humans after oral exposure to MTBE alone (ATSDR 1996).
No epidemiological study data on long-term effects and the
carcinogenic effects of human exposure to MTBE were found in an earlier
search by ATSDR (1996) or more recently by OEHHA. The U.S. EPA has not
classified MTBE with respect to potential human carcinogenicity based
on animal studies. The NSTC (1997) report concluded that ``there is
sufficient evidence to indicate that MTBE is an animal carcinogen and
to regard MTBE as having a human hazard potential.'' Nevertheless,
health complaints from the public have raised the concern of Federal
and State health agencies (Begley 1994, Begley and Rotman 1993, CDC
1993a, 1993b, 1993c, Drew 1995, Joseph 1995, Mehlman 1995, 1996, 1998a,
1998b, 1998c, 1998d).
No studies were located regarding death, cardiovascular effects,
hematological effects, musculoskeletal effects, hepatic effects, renal
effects, endocrine effects, body weight effects, developmental and
reproductive effects, genotoxic effects, or cancer in humans after
inhalation exposure to MTBE. No studies were located regarding death,
respiratory effects, gastrointestinal effects, cardiovascular effects,
hematological effects, musculoskeletal effects, hepatic effects, renal
effects, endocrine effects, body weight effects, immunological or
lymphoreticular effects, neurological effects, developmental and
reproductive effects, genotoxic effects, or cancer in humans after
dermal exposure to MTBE (ATSDR 1996).
Acute Toxicity
A recent literature review (Borak et al. 1998) summarizes the
exposure to MTBE and acute human health effects including nine
epidemiological studies, ten industrial hygiene studies, and 12
clinical studies. No studies were located regarding acute toxic effects
of ingested or skin-contacted MTBE in humans. There are very limited
data on the acute toxicity of MTBE in humans through inhalation
exposure. Several studies undertaken over the past four to 5 years were
unable to find any correlation between reported acute health effects
and MTBE exposures experienced by the general public, mainly through
inhalation, from the use of MTBE in gasoline (ATSDR 1996, Balter 1997,
McCoy et al. 1995, NSTC 1996, 1997, U.S. EPA 1997a). The acute effects
of combustion products and atmospheric chemistry of gasoline, and of
gasoline formulated with MTBE, deserve further study within the context
of sensitive populations (McConnell and Taber 1998).
Ingestion of gasoline-MTBE mixtures may result in aspiration and
pneumonitis. Two recent reviews by Mehlman (1998a, 1998d) reported
neurotoxic, allergic, and respiratory effects in humans from water and
air contaminated by MTBE in gasoline. Symptoms reported by 82
participants ingesting water containing MTBE from a spill in North
Carolina for approximately 5 years include headache, anxiety, inability
to concentrate, lightheadedness, ear, nose and throat irritation, skin
rashes, sneezing and breathing problems, shortness of breath and
bronchitis. Similar acute illnesses in petroleum workers were reported.
Acute symptoms in Alaska and New Jersey were summarized and allergic
symptoms from one Alaska resident were detailed.
Complaints of acute effects from exposure to oxygenates such as
MTBE in gasoline, mainly via inhalation, have been received by health
authorities (Fiedler et al. 1994, McCoy et al. 1995, Raabe 1993).
However, the limited epidemiological studies that have been conducted
to date have not demonstrated a causal association between acute
effects and inhalation exposure in a relatively small population (ATSDR
1996). Three human volunteer inhalation studies did not show increased
symptoms among healthy adults (Cain et al. 1996, Johanson et al. 1995,
Prah et al. 1994).
In 1993, the J.B. Pierce Laboratory of Yale University (Cain et al.
1996) and U.S. EPA (Prah et al. 1994), in two separate studies, exposed
individuals to clean air and air mixed with MTBE. In cases where 37 or
43 human volunteers were exposed to low levels of MTBE in air (1.39 or
1.7 ppm) for 1 hour, there was no significant increase in symptoms of
eye, nasal, or pulmonary irritation when the results for periods of
exposure to MTBE were compared to results from exposure to ambient air.
There were also no significant effects on mood or in the results from
several performance-based neurobehavioral tests. In both studies, the
females ranked the general quality of the air containing MTBE lower
than the control atmosphere. However, in the study by Cain et al.
(1996), where the subjects were also exposed to an atmosphere
containing a total of 7.1 ppm mixture of 17 VOCs that are frequent air
contaminants in areas around gasoline stations, the air quality of the
MTBE-containing atmosphere ranked higher than that with the VOC
mixture. No increase in acute symptoms was observed in individuals
exposed to MTBE at concentrations that would be encountered while
refueling a car.
The studies by Hakkola (1994), Hakkola et al. (1996, 1997) and
White et al. (1995) compared the effects in two groups exposed to
different concentrations of MTBE from treated gasoline because of their
lifestyles. The moderately exposed individuals either drove a gasoline
delivery truck, worked in a gasoline station, or worked on car repairs.
The minimally exposed individuals merely used a gasoline-powered
vehicle to go to and from work or as part of their job. In the study by
White et al. (1995), the odds ratio was 8.9 (95 percent confidence
interval = 1.2 to 75.6) for the reporting of one or more symptoms when
11 individuals with blood MTBE levels of > 2.4 g/L were
compared with 33 individuals with lower levels. The odds ratio
increased to 21 (95 percent confidence interval = 1.8 to 539) when
commuters were excluded from the population studied and eight workers
with blood levels of > 3.8 g/L were compared to 22 individuals
with lower blood MTBE levels. All individuals lived and worked in the
area around Stamford, Connecticut.
In a series of studies conducted in Finland where the gasoline
contains 10 percent MTBE, Hakkola (1994) first evaluated
neuropsychological symptoms among 61 male tanker drivers with exposure
to organic solvents at work. The differences between the exposed group
and the two control groups (56 males with occasional exposure at work
and 31 male with no exposure) were found not to be statistically
significant. Hakkola et al. (1996) again found that there were no
statistically significant differences between the signs and symptoms
reported by 101 drivers of tanker trucks and 100 milk truck drivers.
Blood concentrations of MTBE or its metabolites were not monitored.
However, the latest Hakkola et al. (1997) study comparing symptoms and
moods among 101 road tanker drivers with 100 milk delivery drivers
found results different from the previous studies. The tanker drivers
with long exposure to gasoline during the work week reported
significantly higher changes in fatigue scores than drivers with short
exposure, and 20 percent of tanker drivers reported acute symptoms
connected to MTBE exposure.
In the winter of 1992, the State of Alaska began using 15 percent
MTBE in wintertime oxygenated gasoline as part of the Federal
requirements to reduce emissions of CO in Fairbanks and Anchorage.
There were reports of headaches, dizziness, nausea, and spaciness after
refueling and/or working around oxygenated gasoline (Smith and Duffy
1995). The Centers for Disease Control (CDC), U.S. EPA, and the State
of Alaska investigated these complaints but were unable to associate
them with MTBE exposure. Instead, it was suggested that the increase in
price of the new Federal RFG, the odor of MTBE, and the harsh climate
of Alaska resulted in some of the public associating changes in fuel
with the reported symptoms. The State is now using ethanol in its
gasoline during the winter (Belier et al. 1992, Chandler and Middaugh
1992, CDC 1993a). Gordian et al. (1995) reported no increase in claims
for respiratory illness in Anchorage or Fairbanks after introduction of
MTBE in Alaska.
A study in Alaska (Moolenaar et al. 1994) compared effects and
blood levels of MTBE from a time period when oxygenated fuels were in
use (Phase I) to those after the oxygenated fuels use had stopped
(Phase II). The subjects were volunteers who were occupationally
exposed to motor vehicle exhaust or gasoline fumes. Eighteen workers
participated in Phase I and 22 in Phase II. Twelve of those that
participated in Phase I of the study also participated in Phase II. A
questionnaire was used to gather information on signs and symptoms and
blood samples were collected for measurement of MTBE at the beginning
and end of a typical workday. In Phase I, the median post-shift MTBE
level was higher than the pre-shift value (1.80 versus 1.15 ppb).
During Phase II, the values were more comparable (0.25 versus 0.21
ppb). Median post-shift blood measurements of TBA were higher during
Phase I than in Phase II (5.6 versus 3.9 ppb).
Signs and symptoms that could be associated with MTBE exposure were
reported more frequently during Phase I than Phase II (Moolenaar et al.
1994). During Phase I, 50 percent or more of the participants reported
headaches, eye irritations, and nose and throat irritations. Reporting
of these symptoms occurred in less than 10 percent of the participants
during Phase II. However, it is difficult to evaluate if psychosomatic
factors and individual sensitivity had influenced these results. The
volunteers may have chosen to participate because of their sensitivity
to contaminants in the atmosphere. A follow-up survey of workers
exposed to oxygenated fuel in Fairbanks, Alaska (Moolenaar et al. 1997)
detected higher blood benzene concentrations in mechanics than drivers
and other garage workers.
Milwaukee, Wisconsin began to use MTBE in its gasoline as part of
the Federal RFG program in November 1994. Similar health complaints, as
voiced in Alaska (Beller et al. 1992), were registered in Wisconsin.
U.S. EPA, the Wisconsin Department of Health, CDC, and the University
of Wisconsin investigated complaints from approximately 1,500 people.
They wrote two reports (May and September 1995) and concluded that they
could find no relationship between reported health effects and MTBE
exposure. It was suggested that the odor of MTBE, increase in price of
wintertime gasoline, and negative media coverage were responsible for
the reports of health problems associated with exposure to gasoline
(Anderson et al. 1995).
National Institute for Working Life in Sweden (Nihlen et al. 1998a,
1998b) assessed acute effects up to the Swedish occupational exposure
limit value with both objective measurements and questionnaires. The
healthy male volunteers were exposed to MTBE vapor for 2 hours at 5,
25, and 50 ppm during light physical work. In the questionnaire, only
the ratings of solvent smell increased up to 50 percent of the scale as
the volunteers entered the chamber and declined slowly with time. No
ocular effects were observed. Nasal airway resistance blockage index
increased but was not related to exposure levels. Decreased nasal
volume was seen but with no dose-effect relationship. The authors
concluded no or minimal acute effects of MTBE vapor upon short-term
exposure at these relatively high levels.
An interview questionnaire study (Fiedler et al. 1994) was
conducted, first to assess exposure and the symptomatic responses of
individuals with multiple chemical sensitivities (MCS) while using
gasoline products with MTBE, second to compare their responses to
individuals with chronic fatigue syndrome (CFS) which can not
contribute to exposure to chemicals, and third to compare with normal
controls. Fourteen MCS, five CFS, and six normal control subjects of
comparable age, education, gender, and ethnicity completed several
structured interview and assessment sessions. It was concluded that
while the sample was limited, MTBE symptoms were not uniquely
associated with chemical sensitivity or with situations where MTBE was
more prevalent.
Several additional major literature reviews on the acute health
effects of MTBE have been conducted. Reviews from studies in
Connecticut (CDC 1993b, White et al. 1995), Montana (MCCHD 1993), New
Jersey (Mohr et al. 1994), New York (CDC 1993c), Illinois and Wisconsin
(Anderson et al. 1995) and the HEI (1996) could find no evidence
linking acute health effects with exposure to MTBE from gasoline use.
In 1993, the Environmental and Occupational Health Sciences Institute
(EOHSI) surveyed New Jersey garage workers and service station
attendants, some of whom were exposed to MTBE, and some of whom were
not. No significant differences in the frequency of reported symptoms
were observed between the two groups (Hartle 1993, Mohr et al. 1994).
EOHSI is conducting a study on individuals who have reported
sensitivity to MTBE and were recruited from the ``Oxybuster'' group in
New Jersey. The Oxybuster group is a citizens' group which claims their
members experience acute health effects from breathing MTBE (Joseph
1995). Those individuals will be exposed to gasoline with and without
MTBE. Results are expected later in 1998.
In response to the negative publicity associated with the use of
Federal wintertime oxygenated fuel, the White House OSTP through the
NSTC in September 1995 directed Federal agencies to review fuel economy
and engine performance issues, water quality, air quality benefits, and
health effects of oxygenates in fuel with a final report issued in June
1997. NSTC (1997) concluded that with the information collected to date
there was no evidence that MTBE is causing increases in acute symptoms
or illnesses at concentrations experienced by the general population,
but anecdotal reports of acute health symptoms among some individuals
cannot yet be explained or dismissed. NSTC also recommended that
greater attention should be given to the potential for increased
symptom reporting among workers exposed to high concentrations of
oxygenated gasoline containing MTBE. Regarding the issue of acute
sensitivity to MTBE, NRC which peer-reviewed an earlier draft of the
NSTC report, concluded that there was no reason to believe that some
people have extreme sensitivity to MTBE. The final NSTC report
concluded ``an examination of possible predisposing factors might be
useful to better understand the occurrence of various symptoms in the
general public following exposure to MTBE-containing gasoline.''
MTBE has had a limited use as a therapeutic drug for dissolving
cholesterol gallbladder stones (ATSDR 1996, HSDB 1997). Perfusion of
MTBE through the bile duct and gallbladder by a percutaneous
transhepatic catheter under local anesthesia was once used as a medical
treatment to dissolve gallstones as an alternative to surgery (Diaz et
al. 1992, Edison et al. 1993, Lin et al. 1994). Leuschner et al. (1994)
reported identical side effects of manual and automatic gallstone
dissolution with MTBE in 228 patients. Hellstern et al. (1998) surveyed
268 European patients from one hospital comparing with 535 patients
from 20 other centers and reported that method-related lethality
amounted to 0 percent and 30-day-lethality to 0.4 percent. Another
solvent, ethyl propionate, has been suggested to be preferable to MTBE
in this investigational procedure due to intestinal mucosa damages
(Hofmann et al. 1997).
Acute exposure of humans to MTBE has occurred via injection through
the catheter into the gallbladder. During this procedure, some of the
MTBE enters the blood stream and is distributed systemically. Side
effects reported in patients treated by this procedure included nausea,
vomiting, coughing, bronchitis, sleepiness, sedation, perspiration,
bradycardia (slow heart beat), elevation of liver enzymes, apnea, CNS
depression, and respiratory depression (Allen et al. 1985, Juliani et
al. 1985, Wyngaarden 1986). A case of acute renal failure was also
reported (Ponchon et al. 1988). These signs cannot be attributed
totally to MTBE because of the confounding effects of anesthesia and
the infusion process itself. Borak et al. (1998) reviewed 12
dissolution studies and reported that the peak MTBE blood levels
averaged 40,000 g/L in one study and ranged up to 10,000 g/L in another
study.
Immunotoxicity
There are very limited human studies available on the
immunotoxicity of MTBE-added fuels through inhalation or MTBE-
contaminated water. Duffy (1994) concluded that single day exposures to
oxyfuel and its combustion products did not show an immediate effect on
the immune system as measured by serum plasma interleukin six (IL-6)
levels. In this study, blood samples from 22 individuals exposed to
auto emissions derived from oxyfuel were analyzed for effects on the
immune system by monitoring IL-6 levels at the beginning and at the end
of the 8-hour workday during a 4-week period in late November and early
December 1992 (Duffy 1994).
Vojdani et al. (1997b) reported the detection of MTBE antibodies in
seven out of 24 gasoline station attendants (six females and 18 males
ranging in age from 21 to 58 years) who were employed for more than 2
years in service stations, and none out of the 12 healthy control
subjects (four females and eight males 24 to 60 years of age). The
results indicated that these IgG and IgM antibodies were produced
against the methyl or tert-butyl group of MTBE. They also indicated
that the immune reactions to MTBE occurred through hapten carrier
reactions that could be related to airborne exposures to TBF. However,
the antibody response did not correlate with claimed symptoms.
The same group (Mordechai et al. 1997, Vojdani et al. 1997a) also
reported reversible but statistically significant increased rates of
abnormal apoptosis (programmed cell death) and cell cycle progression
in peripheral blood lymphocytes in 20 Southern California residents
exposed to MTBE and benzene contaminated water as compared to ten
healthy human controls. Similar observations on 80 patients were
reported again by the same group (Vojdani and Brautbar, 1998).
Apoptosis is an organism's way of maintaining healthy cell populations,
the process can lead to the development of disease if it is unduly
suppressed or stimulated (Thompson 1995). For example, cancer may be
the result of a failure in the apoptotic process, in which mutant cells
are allowed to proliferate freely rather than being recognized as
damaged and destroyed.
Neurotoxicity
Burbacher (1993) reviewed gasoline and its constituents as
neuroactive substances and recommended future studies to focus on
examining the dose-response relationship between chronic low-level
exposure and subtle toxic effects in CNS functions. The results from
human studies of neurological effects, e.g. headache, dizziness,
disorientation, fatigue, emotional distress, gastrointestinal problems,
e.g. nausea or diarrhea, and symptoms of respiratory irritation in
individuals exposed to MTBE vapors through MTBE-containing fuels are
inconclusive (Hakkola et al. 1996, Hakkola and Saarinen 1996, Moolenaar
et al. 1994, White et al. 1995). The three studies cited were different
in their design and utilized slightly different parameters for
monitoring effects. All studies evaluated exposure to an MTBE-gasoline
mixture and not MTBE alone.
However, in the most recent study by Hakkola et al. (1997)
comparing neuropsychological symptoms and moods among 101 road tanker
drivers from three Finnish oil companies with 100 milk delivery drivers
from two milk companies, the tanker drivers with long exposure to
gasoline during the work week reported significantly higher changes in
fatigue scores than drivers with short exposure, and 20 percent of
tanker drivers reported acute symptoms of headache, dizziness, nausea,
dyspnoea, and irritation of saliva excretion. These symptoms have been
connected to MTBE exposure. The authors suggested that exposure to MTBE
during the workweek could be reason for acute symptoms among the tanker
drivers in this study.
dose-response assessment
Internal Dose Estimation
Due to the lack of a clear mode of action of TBA or other MTBE
metabolites in MTBE-induced carcinogenesis in experimental animals,
OEHHA has necessarily had to treat the parent compound MTBE as the
cause of the observed effects in animal studies for the purpose of
determining dose metrics. In order to estimate internal doses of MTBE,
in addition to simple continuous applied doses, a simplified PBPK model
was employed. This model is based on both the Borghoffet al. (1996a)
model, in that it has five compartments for MTBE and five compartments
for TBA, and the Rao and Ginsberg (1997) model with its MTBE metabolic
parameters and slowly perfused compartment/blood partition coefficient
for TBA. The PBPK model employs compartments loosely representing
``Fat, Liver, Kidneys, Muscle, and rapidly perfused tissues termed as
Vessel Rich Group (VRG)''. The model's fundamental structure is based
on that developed by Hattis et al. (1986) for perchloroethylene and was
formulated in Stellar software (ithink v. 3.0.6b
for the Power Macintosh, High Performance Systems Inc., Hanover, New
Hampshire 03755). The model units for the whole animal are moles, L,
moles/L, hour, moles/hour, L/hour, and ppm in alveolar air. Simulations
of up to 32 hours were run at approximately 1,000 steps per simulated
hour, using the Runge-Kutta four computation method on a Power
Macintosh 7100/80. The model parameters were obtained from Borghoff et
al. (1996a) or Rao and Ginsberg (1997) and are listed in Table 10. In
addition to simulations of the pharmacokinetic data of Miller et al.
(1997) with a model 0.22 kg rat, simulations of cancer bioassay doses
were conducted assuming 0.35 kg for female and 0.5 kg for male lifetime
average body weights. Physiological and metabolic parameters were
scaled to these body weights as described in Borghoff et al. (1996a).
Table 10.--Parameters Used in the PBPK Model Simulations for MTBE and TBA
----------------------------------------------------------------------------------------------------------------
Parameter Female rat Male rat Source
----------------------------------------------------------------------------------------------------------------
Body weight (kg)........................... 0.35 0.5 Estimated from Belpoggi et
al. 1995
Compartment volumes (L):
Liver.................................... 0.014 0.020 Borghoff et al. 1996a
Kidney................................... 0.00245 0.0035 Borghoff et al. 1996a
Muscle................................... 0.2625 0.375 Borghoff et al. 1996a
Fat...................................... 0.0245 0.035 Borghoff et al. 1996a
Vessel Rich Group (VRG).................. 0.01505 0.0215 Borghoff et al. 1996a
Flows (L/hour):
Alveolar ventilation..................... 6.4 8.32 Borghoff et al. 1996a
Cardiac output........................... 6.4 8.32 Borghoff et al. 1996a
Liver.................................... 1.6 2.88 Borghoff et al. 1996a
Kidney................................... 1.6 2.88 Borghoff et al. 1996a
Muscle................................... 0.96 1.248 Borghoff et al.1996a
Fat...................................... 0.576 0.7488 Borghoff et al. 1996a
VRG...................................... 1.664 2.1632 Borghoff et al. 1996a
Partition coefficients (MTBE):
Blood/Air................................ 11.5 11.5 Borghoff et al. 1996a
Liver/Blood.............................. 1.1826 1.1826 Borghoff et al. 1996a
Kidney/Blood............................. 3.113 3.113 Borghoff et al. 1996a
Muscle/Blood............................. 0.565 0.565 Borghoff et al. 1996a
Fat/Blood................................ 10.05 10.05 Borghoff et al. 1996a
VRG/Blood................................ 3.113 3.113 Borghoff et al. 1996a
Partition coefficients (TBA):
Blood/Air................................ 481-75 481-75 Borghoff et al. 1996a*
Liver/Blood.............................. 0.8316 0.8316 Borghoff et al. 1996a
Kidney/Blood............................. 1.1289 1.1289 Borghoff et al. 1996a
Muscle/Blood............................. 0.4 0.4 Rao & Ginsberg 1997
Fat/Blood................................ 0.3971 0.3971 Borghoff et al. 1996a
VRG/Blood................................ 1.1289 1.1289 Borghoff et al. 1996a
Metabolism (MTBE):
Vmax1 (mole/hour)........................ 2.05 10- 2.66 10- Rao & Ginsberg 1997
6 6
Vmax2 (mole/hour)........................ 2.27 10- 2.94 10- Rao & Ginsberg 1997
4 4
Km1 (M).................................. 2.27 10- 2.27 10- Rao & Ginsberg 1997
6 6
Km1 (M).................................. 1.25 10- 1.25 10- Rao & Ginsberg 1997
3 3
Metabolism (TBA):
Vmax (mole/hour)......................... 2.46 10- 3.21 10- Rao & Ginsberg 1997
5 5
Km (M)................................... 3.79 10- 3.79 10- Rao & Ginsberg 1997
4 4
GI absorption (hour-1)..................... 0.8 0.8 Model assumption
----------------------------------------------------------------------------------------------------------------
* Note: see text
The PBPK model simulation results for oral exposures to MTBE are
summarized in Table 11. The italic boldface values are observed
experimental data from Miller et al. (1997). The simulated or predicted
values for 0.215 kg, 0.35 kg female, and 0.5 kg male rats are shown in
normal type. In general, better predictions were obtained for MTBE than
for TBA both for maximum blood concentration and the area under the
blood concentration x time curve, or AUC.
Adequate simulation of TBA blood kinetics became increasingly
difficult with increased body size and lower TBA blood-air partition
coefficients of 150 and 75 had to be employed to achieve stable
simulations. In all cases MTBE doses were cleared within 24 hours and
there was no need for multi-day simulations to estimate an average
daily MTBE AUC for the bioassays. In all cases MTBE AUC was linear with
applied dose for a particular body size.
Table 11.--Comparison of PBPK Predictions with Experimental Data from Oral MTBE Administrations*
----------------------------------------------------------------------------------------------------------------
MTBE mM MTBE AUC mM TBA AUC mM Blood:Air
Oral dose/Body weight Cmax TBA mM Cmax hour hour MTBE/TBA
----------------------------------------------------------------------------------------------------------------
40 mg/kg, 0.215 kg rat......................... 0.068 0.176 0.150 0.863 11.5/481
Observed:
Frat......................................... 0.127 0.12 0.142 0.495
Mrat......................................... 0.195 0.135 0.193 0.526
250 mg/kg:
0.35 kg Frat................................. 0.527 0.974 1.03 6.3 11.5/75
0.5 kg Mrat.................................. 0.813 1.42 2.32 10.7
400 mg/kg:
0.215 kg rat................................. 0.801 2.26 1.88 30.7 11.5/150
Observed:
Frat......................................... 1.30 0.66 2.19 3.90
Mrat......................................... 1.41 0.68 2.61 4.10
1,000 mg/kg:
0.35 kg Frat................................. 2.36 3.03 6.08 30.9 11.5/75
0.5 kg Mrat.................................. 3.81 3.26 11.9 30.6
----------------------------------------------------------------------------------------------------------------
* Note: Mrat = male rat; Frat = female rat, in both cases values are for assumed lifetime average body weights.
Simulation values are single day results and not averaged over a week.
Table 12 gives the average daily doses based on the blood MTBE AUC
values for male and female rat simulations and the linear relations for
each with applied oral dose.
Table 12.--MTBE AUC-Based PBPK Doses
----------------------------------------------------------------------------------------------------------------
Average applied MTBE AUC females MTBE AUC males mg/
Nominal dose mg/kg/day mg/kg/day mg/kg/day kg/day
----------------------------------------------------------------------------------------------------------------
O...................................................... O O 0
250.................................................... 143 116.1 124.2
1,000.................................................. 571 576.0 575.1
----------------------------------------------------------------------------------------------------------------
Males: mg/kg/day = 26.28 + 82.36 (mM hour), r = 0.998;
Females: mg/kg/day = 38.95 + 159.37 (mM hour), r= 0.996.
Table 13 presents similar simulation results for inhalation
exposures with the observed experimental values in italic boldface. The
results are similar to the oral exposures with predictions of MTBE
blood concentrations and AUCs being closer to observed values than TBA
predictions. On the basis of comparison of MTBE AUC values, a 3,000 ppm
6-hour exposure appeared to be equivalent to a 1,000 mg/kg
oral Savage dose to a 0.5 kg rat. As seen in the oral exposures, the
MTBE AUC in mM hour varied linearly with applied dose [ppm 6-
hour/day = 145.84 + 255.17 (mM hour), r = 0.999]. Also given in the
lower part of Table 13 are dose conversions from MTBE AUC to oral mg/
kg/day averaged for lifetime daily intake. This conversion assumes that
the same relation exists between AUC and mg/kg/day as seen above in the
oral simulations. If this assumption holds, the oral equivalent male
doses from the inhalation bioassay would be 0, 82.9, 618.8, and 1,848.3
mg/kg/day. The male oral doses from the Savage bioassay study would be
0, 124.2, and 575.1 mg/kg/day.
Table 13.--Comparison of MTBE PBPK Predictions with Experimental Data:
Rat Inhalation
----------------------------------------------------------------------------------------------------------------
MTBE mM MTBE AUC mM TBA AUC mM Blood:Air
Inhalation dose/Body weight Cmax TBA mM Cmax hour hour MTBE/TBA
----------------------------------------------------------------------------------------------------------------
400 ppm 6 hours:
0.215 kg rat................................. 0.219 1.34 1.31 15.8 11.5/350
Observed 400 ppm:
Mrat......................................... 0.169 0.535 0.956 5.45
Frat......................................... 0.171 0.531 0.884 5.05
400 ppm 6 hours, 0.5 kg Mrat......... 0.182 0.914 1.09 12.2 11.5/350
3,000 ppm 6 hours, 0.5 kg Mrat....... 1.7 5.4 10.2 125est 11.5/150
8,000 ppm 6 hours, 0.215 kg rat...... 5.65 9.83 33.9 22.6 11.5/150
Observed 8,000 ppm:
Mrat......................................... 6.3 7.2 33.6 81.0
Frat......................................... 6.4 3.3 32.6 34.4
8,000 ppm 6 hours, 0.5 kg Mrat....... 5.2 9.6 31.1 487est 11.5/150
----------------------------------------------------------------------------------------------------------------
Nominal
dose ppm MTBE AUC mM Dose from Dose from
Male rats 6 hour MTBE AUC MTBE AUC*
hours ppm mg/kg/day
----------------------------------------------------------------------------------------------------------------
400 1.09 424 82.9
3,000 10.2 2,749 618.8 ...........
8,000 31.1 8,082 1,848.3
----------------------------------------------------------------------------------------------------------------
* Note: This conversion assumes the same relation between AUC and mg/kg/day as seen in oral studies or what
single oral dose would give the predicted MTBE AUC seen during the 6-hour inhalation exposures. See also
Dourson and Felter (1997) for alternative route-to-route extrapolation.
Overall, the PBPK pharmacokinetic correction for delivered dose when based on MTBE blood AUC is relatively
modest compared to the simple applied dose. It is presently uncertain whether other dose metrics would be
superior to MTBE AUC and will probably remain so until a more definitive mode(s) of action of MTBE
carcinogenesis develops.
noncarcinogenic effects
The most sensitive noncarcinogenic effect by oral route is in the
kidney based on the Robinson et al. (1990) 90-day gavage study with a
NOAEL of 100 mg/kg/day. As noted above this value was used by U.S. EPA
(1996a) to derive a proposed lifetime HA of 70 ppb (or 0.07 mg/L) in
drinking water for MTBE. In its more recent document (U.S. EPA 1997a),
U.S. EPA employed this toxicity endpoint along with two other noncancer
endpoints, neurological and reproductive and developmental, as well as
three cancer endpoints in a margin of exposure (MOE) analysis to
develop longer-term HAs. Other states also used this toxicity endpoint
to develop regulatory guidelines for MTBE as described later in this
document.
carcinogenic effects
Possible Modes of Action
There are limited data available on the mechanism of action of
MTBE. It remains unknown whether biotransformation is required for
expression of MTBE's carcinogenic activity. The data from several in
vitro and in viva tests indicate that MTBE lacks significant genotoxic
activity and suggest that a genotoxic mode of action is unlikely. It
has been proposed that MTBE's induction of renal tubular cell tumors in
the male rat is the result of 2u-globulin
nephropathy. Although some characteristic features of
2u-globulin nephropathy have been associated with
MTBE, the absence of others leads to the overall conclusion that
2u-globulin nephropathy is not likely to account
for the induction of kidney tumors by MTBE. Although endocrine-mediated
modes of action have been suggested for MTBE's induction of testicular
tumors in rats and liver tumors in mice, there are insufficient data to
support these hypotheses. In summary, the data available at this time
do not provide sufficient evidence in support of a specific mode of
action of MTBE carcinogenicity.
Estimation of Carcinogenic Potency
According to the proposed guidelines for carcinogen risk assessment
(U.S. EPA 1996f) the type of extrapolation employed for a given
chemical depends on the existence of data supporting linearity or
nonlinearity or a biologically based or case-specific model. When
insufficient data are available supporting either approach the default
is to use a linear extrapolation. MTBE seems to fit this category,
since no mode of action is known (U.S. EPA 1994a, 1994c). Although the
lack of genotoxicity and the nonlinearity of the carcinogenic response
in some studies might be argued as supportive of a mechanism other than
direct genotoxicity via covalent modification of DNA, attempts to
identify positively an alternative mechanism have not so far succeeded.
Dourson and Felter (1997) attempted to perform an extrapolation of the
cancer potency of MTBE from inhalation route (Chun et al. 1992) to oral
route.
Cancer potency or cancer potency factor (CPF) is a slope derived
from a mathematical function used to extrapolate the probability of
incidence of cancer from a bioassay in animals using high doses to that
expected to be observed at the low doses which are likely to be found
in chronic human exposure. The mathematical model, such as the LMS
model, is commonly used in quantitative carcinogenic risk assessments
in which the chemical agent is assumed to be a complete carcinogen and
the risk is assumed to be proportional to the dose at very low doses.
q1* is the upper 95 percent confidence limit on the cancer
potency slope calculated by the LMS model. Or another cancer slope
factor (CSF) is a potency value derived from the lower 95 percent
confidence limit on the 10 percent tumor dose (LED10).
LED10 is the 95 percent lower bound on the dose that is
predicted to give a 10 percent tumor incidence. The CSF equals to 10
percent dividing by LED10.
Earlier guidelines for cancer risk assessment, including those
formerly used by OEHHA (DHS 1985) have required the use of the LMS
model to estimate an upper bound on the low-dose potency
(q1*). However, more recent OEHHA methodologies, and the
draft proposed U.S. EPA (1996f) guidelines for carcinogen risk
assessment, recommend a linear extrapolation approach based on the
LED10. A multistage polynomial is used to fit data in the
observable range, unless some other dose-response curve is specifically
indicated by the available data. Because adequate data do not exist for
MTBE, the default curve-fitting approach is appropriate. Interspecies
scaling for oral doses (and internal doses calculated from a single-
species pharmacokinetic model) is based on (body
weight)\3/4\ as proposed by U.S. EPA (1996f, 1992b) instead
of the (body weight)\2/3\ used previously. For inhalation
exposures U.S. EPA has in the past used an assumption of equivalence
between different species of exposures to a given atmospheric
concentration. This provides roughly similar scaling in effect, due to
the way that breathing rate and related parameters affecting uptake
scale with body weight. More recently PBPK modeling has been seen as a
preferable approach to both dose estimation and interspecies scaling of
inhalation exposures, where data are available to support this. Since
pharmacokinetic data are available for MTBE in the rat, the modeling
approach was feasible in this case for that species only.
Table 14 summarizes the cancer potency values derived by both the
LED10 method and the LMS model (for comparison with earlier
results) from the available statistically significant rodent cancer
bioassay data sets for MTBE described earlier in the section on
carcinogenicity. In all cases the Tox--Risk v.3.5 (Crump et al. 1993)
program was used to fit the multistage model to the quantal data sets.
The qu1 cancer potencies or the 95 percent upper bound on
the LMS linear slope at low dose were calculated directly by the
program. CSF's are based on the LED10. The CSF is 0.1/
LED10, in units of (mg/kg-day) -1. For the curve
fitting to estimate the LED10, we have employed a p * 0.05
criterion for the Chi-squared goodness of fit statistic of the
optimized polynomial. In order to obtain an adequate fit it was
necessary to exclude the data for kidney tumors in the high dose (8,000
ppm) males rats in the study by Chun et al. (1992). As can be seen from
Table 14, the potency estimates for all tumors are similar whether
based on the q1 or the CSF. Results in the inhalation
studies (shun et al. 1992, Burleigh-Flayer et al. 1992) are effectively
the same (within a factor of two) for the different sites in rats and
mice, except that the potency for testicular interstitial cell tumors
in male rats is about five times higher. Comparison between different
routes and experiments for the rat is easiest by examining the data
calculated using the pharmacokinetic model to convert the inhalation
exposures to equivalent oral doses. In this case it is apparent that
all the results are comparable, with the testicular interstitial cell
tumors in the Chun et al. (1992) males again showing a slightly higher
value than those found at other sites or in the testis in the Belpoggi
et al. (1995, 1997, 1998) oral study.
Table 14.--Dose Response Parameters for MTBE Carcinogenicity Studies
----------------------------------------------------------------------------------------------------------------
Tumor site and
Species Sex type q1* (ppm - 1) LED10 (ppm) CSF (ppm -1)
----------------------------------------------------------------------------------------------------------------
(a) Inhalation studies--ppm in air as dose metric
----------------------------------------------------------------------------------------------------------------
Mouse........................ Female.......... hepatocellular 3.2 320 3.2
adenoma + 10