[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 - 4                          10 - 4
                                                  carcinoma.
                               Male............  hepatocellular    7.3              140   7.0 
                                                  adenoma +               10 - 4                          10 - 4
                                                  carcinoma.
Rat..........................  Male............  renal tubular     4.4              240   4.2 
                                                  cell adenoma +          10 - 4                          10 - 4
                                                  carcinoma
                                                  testicular
                                                  interstitial
                                                  cell tumors.
                                                                   2.3               46   2.2 
                                                                          10 - 3                          10 - 3
----------------------------------------------------------------------------------------------------------------
Assumed:
Data reassessment by U.S. EPA (1994c, 1995c).
Duration correction based on (te /t1)3: t1 = 104 weeks for both rats and mice.
Interspecies correction: ppm equivalency.



----------------------------------------------------------------------------------------------------------------
                                                  Tumor site and   q1*  (mg/kg-    LED10  mg/kg/   CSF  (mg/kg-
            Study                     Sex              type           day) -1           day          day) - 1
----------------------------------------------------------------------------------------------------------------
                              (b) Rat oral study--Administered dose as dose metric
----------------------------------------------------------------------------------------------------------------
Belpoggi, et al., 1995, 1998.  Male............  Leydig cell
                                                  tumors:
                                                   Original 1995  1.38               76  1.38 
                                                  report.                 10 - 3                          10 - 3
                                                   Revised 1998   1.63               64  1.55 
                                                  data.                   10 - 3                          10 - 3
                               Female..........  Leukemia/
                                                  lymphoma:
                                                   Original 1995  2.13               49  2.03 
                                                  report.                 10 - 3                          10 - 3
                                                   Revised 1998   2.20               48  2.09 
                                                  data.                   10 - 3                          10 - 3
----------------------------------------------------------------------------------------------------------------
Assumed:
No duration correction: te = t1.
Interspecies correction: BW3/4.




----------------------------------------------------------------------------------------------------------------
                                                 Tumor site and   q1*  (mM.hour/  LED10  mM.hour/ CSF  (mM.hour/
            Route                    Sex              type          day)  -1            day          day) - 1
----------------------------------------------------------------------------------------------------------------
                             (c) Rat oral and inhalation studies--AUC as dose metric
----------------------------------------------------------------------------------------------------------------
Inhalation (Chun et al. 1992)  Male...........  renal tubular              0.037             2.9           0.035
                                                 cell adenoma +
                                                 carcinoma.
                               Male...........  testicular                  0.16            0.66            0.15
                                                 interstitial
                                                 cell tumors.
Gavage (Belpoggi et al         Male...........  Leydig cell
                                                 tumors:
  1995, 1998)                                     Original 1995            0.044             2.4           0.041
                                                 report.
                                                  Revised 1998             0.044             2.4           0.041
                                                 data.
                               Female.........  Leukemia/
                                                 lymphoma:
                                                  Original 1995            0.051             2.1           0.048
                                                 report.
                                                  Revised 1998             0.051             2.1           0.048
                                                 data.
----------------------------------------------------------------------------------------------------------------
Assumed:
Data reassessment by U.S. EPA (1994c, 1995c) for Chun et al. (1992) study.
Duration correction based on (te /t1)3: T1 = 104 weeks for rats.
Interspecies correction: AUC equivalency.



----------------------------------------------------------------------------------------------------------------
                                                  Tumor site and   q1*  (mg/kg-    LED10  mg/kg/   CSF  (mg/kg-
            Route                     Sex              type          day)  - 1          day          day) - 1
----------------------------------------------------------------------------------------------------------------
                             (d) Rat oral study--Equivalent oral dose as dose metric
----------------------------------------------------------------------------------------------------------------
Inhalation (Chun et al. 1992)  Male............  renal tubular     1.9               55   1.8 
                                                  cell adenoma +          10 - 3                          10 - 3
                                                  carcinoma.
                               Male............  testicular        9.2               11   8.7 
                                                  interstitial            10 - 3                          10 - 3
                                                  cell tumors.
Gavage (Belpoggi et al.......  Male............  Leydig cell
                                                  tumors:
  1995, 1998)                                      Original 1995  1.38               76  1.38 
                                                  report.                 10 - 3                          10 - 3
                                                   Revised 1998   1.63               64  1.55 
                                                  data.                   10 - 3                          10 - 3
                               Female..........  Leukemia/
                                                  lymphoma:
                                                   Original 1995  2.13               49  2.03 
                                                  report.                 10 - 3                          10 - 3
                                                   Revised 1998   2.20               48  2.09 
                                                  data.                   10 - 3                          10 - 3
----------------------------------------------------------------------------------------------------------------
Assumed:
Data reassessment by U.S. EPA (1994c, 1995c) for Chun et al. (1992) study.
Duration correction based on (te / t1)3: T1 = 104 weeks for rats.
Interspecies correction: BW 3/4.



------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
             Species                     Route                Sex             Body weight       Study  duration    Lifetime  assumed    Dosing schedule      Concentrations          Study
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                          (e) Oral and inhalation studies--Study design
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Rat.............................  Inhalation........  Male..............  500g..............  97 weeks..........  104 weeks.........  6 hour/day,  5 day/ 0, 400, 3,000,      Chun et al. 1992
                                                                                                                                       week.               8,000* ppm.
Mouse...........................  Inhalation........  Male..............  35g...............  68 weeks..........  104 weeks.........  6 hour/day,  5 day/ 0, 400, 3,000,      Chun et al. 1992
                                                                                                                                       week.               8,000* ppm.
                                                      Female............  30g...............  68 weeks..........  104 weeks.........  6 hour/day,  5 day/ 0, 400, 3,000,      ..................
                                                                                                                                       week.               8,000* ppm.
Rat.............................  Gavage............  Male..............  500g..............  lifetime..........  104 weeks.........  4 day/week........  0, 250, 1,000 mg/   Belpoggi et al.
                                                                                                                                                           kg, day.            1995
                                                      Female............  350g..............  lifetime..........  104 weeks.........  4 day/week........  0, 250, 1,000 mg/
                                                                                                                                                           kg/day.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
*8,000 ppm dose group not used in analysis of male rat renal tubule tumors due to inability of multistage polynomial to achieve adequate fit.

    Carcinogen risk assessment guidelines used by OEHHA normally 
recommend selection of human cancer potency estimates based on the most 
sensitive site and species, unless there is evidence to indicate that 
the most sensitive site(s) are not relevant to human cancer induction, 
or represent data sets with unusually wide error bounds. As an 
alternative, where several equally plausible results are available and 
are sufficiently close to be regarded as concordant, the geometric mean 
of all such estimates may be used.
    The pharmacokinetic model, that allows comparison of different 
routes and corrects for nonlinearities in the relationship between 
applied and internal dose, is not available for the mouse. Therefore, 
the potency estimates obtained in the rat are preferred for risk 
assessment purposes. Because the results in rats and mice are 
comparable, the use of the rat data is consistent with the policy of 
selecting appropriately sensitive species as the basis for the estimate 
of potency in humans.
    In terms of the relevance to human cancer and the mechanism of the 
observed effects, the results of the studies by Chun et al. (1992) and 
Burleigh-Flayer et al. (1992) are limited by the relatively severe 
mortality seen in the highest dose groups, and the less-than lifetime 
exposure given the mice and the male rats. These experimental flaws are 
not so severe as to exclude the use of the data in risk assessment, nor 
more prohibitive than the experimental flaws associated with many 
studies on other compounds that have been successfully used for this 
purpose. There are, however, additional problems in the case of the 
testicular interstitial cell tumors observed in male rats by Chun et 
al. (1992). The study authors stated that the control incidence of 
these tumors was lower than the historical incidence observed in 
animals from the colony from which these experimental animals were 
obtained. In view of this, the slightly divergent value for the potency 
estimate obtained with this data set is regarded with lower confidence 
than the other values obtained in this analysis.
    An attempt was made to allow for the severe impact of mortality on 
the male rat kidney adenoma and carcinoma incidence in the study by 
Chun et al. (1992) by applying the time-dependent version of the LMS 
model to the individual time-to-tumor incidence data in this study. A 
suitable model available in the Tox--Risk program (multistage in dose, 
Weibull in time) was used, and an adequate fit was obtained. The 
program provided an estimate of q1* = 7.6  
10-2, (mg/kg-day)-1, which is substantially 
higher than the value estimated from the quantal data. The calculated 
end-of-life LED10 indicated a CSF of 7.2  
10-2 (mg/kg-day)1. However, the fit obtained 
involved a large Weibull exponent (z = 8.7, whereas more usual values 
are in the range of three to six), implying a very late appearance of 
this tumor. This observation may be of interest in addressing the 
unsolved question of the mechanism of induction of this tumor by MTBE. 
However it implies a marked reduction in the confidence which can be 
placed in the potency estimate using this model. Few tumor data were 
obtained during the final third of the expected lifetime of the exposed 
rats (due to the early death of all the rats dosed with 8,000 ppm, and 
most of the rats dosed with 3,000 ppm by this time). The potency 
estimate therefore involves a substantial extrapolation outside the 
range of the observed data, even using the LED10/CSF 
methodology that is designed to avoid such problems. The extreme time 
dependency, deficiency in genotoxicity data, and other uncertainties 
described previously also raise the question of how appropriate it is 
to use this particular model to fit these data. Its use for 
extrapolation outside the range of observed data (as opposed to merely 
as a curve-fitting device within the range of observed data) implies an 
acceptance of the classic Armitage-Doll theory of action for genotoxic 
carcinogens, which may not be warranted in the case of MTBE. Because 
the mechanistic information and the technical resources which would be 
required to undertake a more appropriate analysis of these time-to-
tumor data are lacking, it was decided not to include the results of 
the time-dependent analysis in the final risk estimate.
    In view of the closeness of the other values obtained in the rat, 
and their similar confidence levels, the preferred value for the cancer 
potency is therefore the geometric mean of the potency estimates 
obtained for the male rat kidney adenomas and carcinomas combined (1.8 
 10-3) (Chun et al. 1992), and the male rat Leydig 
interstitial cell tumors (1.55  10-3) and the 
leukemia and lymphomas in female rats (2.09  10-3) 
(Belpoggi et al. 1995, 1998). The combined use of these data yields an 
estimated CSF of 1.8  10-3 (mg/kg-day). While it is 
theoretically possible that the true human CSF could exceed this value, 
that is considered unlikely. On the other hand it is plausible that the 
lower bound on the human CSF includes zero. This is a result of 
statistical uncertainty with a zero lower bound estimate on 
q1, by the LMS method with some MTBE data sets and 
biological uncertainties due to interspecies extrapolation and mode of 
action.
    A unit risk value is similarly derived from the geometric mean of 
the respective LED10 values for the blood MTBE AUC (Table 
14c) as follows:
    (a) the geometric mean of 2.1 mM  hour is converted to 
external concentration (in ppm) using the regression expression derived 
above i.e., 145.84 + 225.17(2.1) = 618.7 = 619 ppm;
    (b) this value is converted to mg/m3 using the 3.6 mg/
m3/ppm conversion factor, or 619 ppm  3.6 mg/
m3/ppm = 2,230 mg/m3,
    (c) the unit risk is calculated as 0.1/2230 mg/m3 or 4.5 
x 10-5 (mg/m3)-1 or 4.5  
10-8 (g/m3)-1.
    Since the LED values were in human equivalent doses no additional 
interspecies scaling is required. This unit risk would indicate 
negligible theoretical lifetime cancer risk at ambient MTBE air 
concentrations below about 6.2 ppbv (ppb by volume).
                           calculation of phg
    Calculations of public health-protective concentrations of chemical 
contaminants in drinking water associated with negligible risks for 
carcinogens or noncarcinogens must take into account the toxicity of 
the chemical itself, as well as the potential exposure of individuals 
using the water. Tap water is used directly as drinking water, for 
preparing foods and beverages. It is also used for bathing or 
showering, and in washing, flushing toilets, and other household uses 
resulting in potential dermal and inhalation exposures.
Noncarcinogenic Effects
    Calculation of a public health-protective concentration (C, in mg/
L) for MTBE in drinking water for noncarcinogenic endpoints uses the 
following general equation adopted by U.S. EPA (1990, 1 992a, 1 996c): 
C = NOAEL/LOAEL  BW  RSC/UF  DWC

    where:

    NOAEL/LOAEL = no observable adverse effect level or lowest observed 
adverse effect level.
    BW = body weight (a default of 70 kg for a male or 60 kg for a 
female adult).
    RSC = relative source contribution (a default of 20 percent to 80 
percent as explained below).
    UF = Uncertainty factors (UFs) are included to account for gaps in 
our knowledge (uncertainty) about the toxicity of chemicals and for 
recognized variability in human responses to toxic chemicals.

          In determining UFs for chronic effects it is conventional to 
        apply an UF where data are only available from short- or 
        medium-term exposures of animals, rather than full lifetime 
        exposures. In the case of MTBE noncarcinogenic effects, there 
        is no adequate chronic study in experimental animals of the 
        critical effect (increase in kidney weight in rats): the key 
        study is of 90 days duration or about 10 percent the life span 
        of a rat. Because of this, we consider that a 10-fold UF is 
        justified.
          For interspecies extrapolation of toxic effects seen in 
        experimental animals to what might occur in exposed humans an 
        UF of up to 10-fold is generally recommended. This is usually 
        considered as consisting of two parts: one that accounts for 
        metabolic or pharmacokinetic differences between the species; 
        and another that addresses pharmacodynamic differences, i.e. 
        differences between the response of human and animal tissues to 
        the chemical exposure. Based on the limited metabolic studies 
        of MTBE in humans that indicate possible differences from 
        metabolism in rodents, and unresolved questions of its toxic 
        potential for neurological, immunological and endocrine effects 
        we believe a 10-fold UF for interspecies differences is 
        appropriate.
          Exposed humans are known to vary considerably in their 
        response to toxic chemical and drug exposures due to age, 
        disease states, and genetic makeup, particularly in genetic 
        polymorphisms for enzymes (isozymes) for detoxifying chemicals. 
        While little is known about individual variation of MTBE 
        metabolism and toxicity the use of a 10-fold UF seems prudent 
        considering the widespread use of tap water in the population.
          Finally an additional 10-fold UF is used to account for 
        possible carcinogenicity. This follows an U.S. EPA policy 
        applied to their Group C contaminants. OEHHA has previously 
        employed this additional UF for other PHGs in situations where 
        either a nonlinear dose response was applied to a carcinogen or 
        where both linear and nonlinear approaches were used.

    DWC = daily water consumption rate (a default of two L/day for an 
adult has been used by the U.S. EPA (1996b), or L equivalent/day (Leq/
day) to account for additional inhalation and dermal exposures from 
household use of drinking water as explained below).
    Based on the NOAEL of 100 mg/kg/day of the most sensitive 
noncarcinogenic effect in the kidney from the 90-day gavage (Robinson 
et al. 1990) study, the following calculation can be made:

    C = 100 mg/kg/day  70 kg  0.2 = 0.0467 mg/L = 47 
ppb (rounded)/10  1,000  3 Leq/day

    In this calculation an additional UF of 10 is employed to account 
for potential carcinogenicity and a DWC value of three Leq/day is used 
to account for inhalation exposures via typical household use as well 
as ingestion of tap water. The RSC addresses other non-drinking-water 
sources, principally airborne MTBE from vehicular exhaust. Support for 
these values is presented below in a discussion of exposure factors.
Exposure Factors
    The U.S. EPA (1994b) estimated scenarios of potential human 
exposure to MTBE related to RFG. In terms of the equation for 
calculating the public health-protective concentrations of chemical 
contaminants in drinking water as shown above, the first exposure 
factor to be considered is the RSC (OEHHA 1996, U.S. EPA 1994b). The 
RSC is a factor that is based on an estimate of the contribution of 
drinking water exposure relative to other sources such as food, air, 
etc. While food is often a significant source of chronic chemical 
exposure, in the case of MTBE, airborne exposures are likely to be most 
significant, if highly variable. U.S. EPA typically uses 20 percent as 
the default RSC. Maine Department of Human Services used 10 percent RSC 
for their proposed MCL for MTBE of 35 ppb (Smith and Kemp 1998) based 
on the same renal toxicity (Robinson et al. 1990) NOAEL in the 90-day 
oral study.
    Estimates for combined population's airborne exposures and 
occupational subpopulations' exposures vary by three orders of 
magnitude or more and include few California data sets. Some of these 
estimates are collected in Table 15 where RSC values are calculated for 
a range of drinking water concentrations. The analyses of Brown (1997) 
include a combined population grand average of 0.00185 mg/kg/day for 
various activity associated airborne exposures and an average ambient 
water concentration of 0.36 ppb. The NSTC (1997) report gives MTBE 
concentrations in groundwater and surface water ranging from 0.2 to 8.7 
ppb with a median value of 1.5 ppb, presumably resulting from nonpoint 
sources. Although the air exposure analysis of Brown (1997) is the most 
comprehensive it may underestimate MTBE exposures to the general public 
in local areas in California (e.g., the Los Angeles basin), possibly by 
a factor of two. Also due to the year-round and universal use of MTBE 
in California gasoline, commuters, other drivers, gasoline station 
customers and neighbors, and the general public are likely to receive 
greater exposures than elsewhere in the U.S. For this reason a health-
protective value of 0.2 (or 20 percent), equal to the default value 
used by U.S. EPA (1994a, 1994b, 1996a), is used here for the RSC.
    The other exposure factor in the equation to calculate the public 
health-protective concentrations of chemical contaminants in drinking 
water as shown above is DWC, the daily water intake in Leq/day. DWC 
represents the amount of tap water consumed as drinking water as well 
as that mixed with beverages and used in cooking. The default for an 
adult is two L/day. For children a default value of one Leq/day is 
used. For VOCs, additional exposures occur via the inhalation and 
dermal routes (i.e., multi-route) during and after showering, bathing, 
flushing of toilets, washing clothes and dishes, and other domestic 
uses (OEHHA 1996, U.S. EPA 1994b).
    Estimates of inhalation and dermal exposure of MTBE relative to 
ingestion exposure vary from 15 percent at 0.36 ppb in water (Brown 
1997) to 45 percent to 110 percent at 70 ppb in water based on 
predictions of the CalToxTM Model (DTSC 1994) assuming only 
50 percent of inhaled MTBE is absorbed. Nihlen et al. (1998a) observed 
a respiratory uptake of 42 percent to 49 percent in human subjects 
exposed to MTBE for 2 hours at 5, 25, and 50 ppm. A value of 50 percent 
inhalation absorption seems supported by actual human data. Based on 
this assumption and a range of values for Henry's Law constant, the 
estimated total MTBE intake ranges from 2.5 Leq/day to 4 Leq/day as 
shown in Table 16. For this analysis, OEHHA scientists concluded that 
one liter of additional exposure would incorporate the expected 
exposure to MTBE volatilized from water and inhaled. Therefore, three 
Leq/day for total MTBE exposure would appear to be a reasonable 
estimate for the purpose of calculating the PHG. The Henry's Law 
constant for MTBE is about 6  10-4 atm-
m3/mole at 25 +C which is approximately one quarter (\1/4\) 
that of benzene and one fourteenth (\1/14\) that of perchloroethylene, 
the two common VOCs that have been studied previously (Robbins et al. 
1993). MTBE is less volatile and its solubility in water is 
significantly higher than these VOCs. Accordingly, the correction for 
showering and other activities for assumed daily water consumption for 
MTBE is smaller than these other common VOCs. This is consistent with 
the conclusions of Johnson (1998) as documented in the UC (1998) MTBE 
report.

Table 15.--Relative Source Contribution (RSC) Estimates (Percent) for Different Combinations of Air and Drinking
                                            Water Exposures to MTBE*
----------------------------------------------------------------------------------------------------------------
                                                                RSC (In Percent)
Air exposure estimate  (mg/kg/     Air exposure   --------------------------------------------     Reference
             day)                    scenario      0.36 ppb*    2 ppb*    12 ppb*    70 ppb*
----------------------------------------------------------------------------------------------------------------
0.00185.......................  Combined U.S.            0.6          3         16         52  Brown 1997
                                 population grand
                                 average.
0.01..........................  One million              0.1        0.6        3.3         17  Brown 1997
                                 exposed U.S.
                                 nationwide.
0.002.........................  Los Angeles basin        0.5        2.8         15         50  ARB 1996
                                 at 4 ppbv
                                 ambient.
0.0093........................  Scenario I annual        0.1        0.6        3.6         18  NSTC 1996
0.0182........................  Scenario II             0.06        0.3        1.8         10  NSTC 1996
                                 annual.
6.7  10-5............  Milwaukee,                13         46         84         97  HEI 1996
                                 Wisconsin Air.
0.37..........................  MTBE distribution      0.003       0.02       0.09         27  HEI 1996
                                 of fuel mixture
                                 Time-Weighted-
                                 Average (TWA)
                                 for workers.
1.3  10-4............  Albany, New York           7         30         72         94  NSTC 1997
                                 air.
Geometric mean................  .................       0.28        1.5        6.4         34  .................
Arithemetic mean..............  .................        2.6       10.4       24.5       45.6  .................
----------------------------------------------------------------------------------------------------------------
Note:
RSC = (Iwater  100) / (Iwater + Iair). Food and soil sources are considered negligible for MTBE.
Iwater = uptake by ingestion of tap water containing MTBE at the concentrations noted assuming two L/day and 100
  percent intestinal absorption.
Iair = uptake by inhalation of airborne MTBE assuming 20 m3 air inhaled/day and 50 percent absorption.
Both Iwater and Iair are assumed for a 70 kg human.
*The concentrations of MTBE in drinking water were taken from the reports noted rather than using arbitrary
  values: 0.36 ppb (Brown 1997); two ppb (NSTC 1997 rounded); 12 ppb (rounded 10-6 risk estimate, U.S. EPA
  1996a); and 70 ppb (proposed Longer-Term and Lifetime HA, U.S. EPA 1996a). However, any plausible range could
  have been used, e.g., 5, 10, 20, 40, etc.


  Table 16.--CalToxTM Predictions of Inhalation (I), Oral (O) and Dermal (D) Exposures (mg/kg/day) from 70 ppb
      MTBE Contaminated Tap Water: Effects of Varying Henry's Law Constant and Drinking Water Intake Level
----------------------------------------------------------------------------------------------------------------
                                                                Water intake (mL/kg/day)
  Henry's Law constant (PA m3/mole)   --------------------------------------------------------------------------
                                                 19.4                     33.3                     43.9
----------------------------------------------------------------------------------------------------------------
66.5.................................  I = 1.16  10-3  1.16  10-3....  1.16  10-3
                                       O = 1.11  10-3  1.91  10-3....  2.52  10-3
                                       D = 4.41  10-6  4.41  10-6....  4.41  10-6
                                       2.28  10-3....  3.08  10-3....  3.69  10-3
                                       All 2.46 Leq/day.......  3.30 Leq/day...........  3.97 Leq/day
142..................................  I = 1.17  10-3  ND.....................  ND
                                       O = 109  10-3.  .......................  .......................
                                       D = 4.43  10-6  .......................  .......................
                                         = 2.26  10-3  .......................  .......................
                                       All 2.48 Leq/day.......  .......................  .......................
228..................................  I = 1.18  10-3  1.18  10-3....  1.18  10-3
                                       O = 1.09  10-3  1.88  10-3....  2.47  10-3
                                       D = 4.34  10-6  4.3  10-6.....  4.34  10-6
                                       2.27  10-3....  3.06  10-3....  3.65  10-3
                                       All 2.51 Leq/day.......  3.33 Leq/day...........  4.03 Leq/day
----------------------------------------------------------------------------------------------------------------
Note: The CalToxTM model vadose and root zone compartments were loaded to predict 70 ppb MTBE in the groundwater
  used for residential drinking water. Various values for Henry's Law constant and water intake in mL/kg/day for
  a 62 kg female were used. MTBE parameters for molecular weight, octanol-water partition coefficient, melting
  point, vapor pressure, and water solubility were entered. Water intake values (mL/kg/day) correspond to median
  tap water for 20- to 64-year-old females (19.4), median total water intake for 20- to 64-year-old females
  (33.3), and average total water intake for all females (43.9) based on the Western Regional data (Ershow and
  Cantor 1989). Inhalation (I) value assumes 50 percent of inhaled MTBE is absorbed. Oral (O) and dermal (D)
  values assume 100 percent absorption. Total intakes by all routes are also expressed as L equivalents (Leq)
  per day.

Carcinogenic Effects
    For carcinogens, the following general equation can be used to 
calculate the public health-protective concentration (C) for a chemical 
in drinking water (in mg/L):

    C = BW  R/q1* or CSF  DWC = 
mg/L

where:

    BW = adult body weight (a default of 70 kg).
    R = de minimis level for lifetime excess individual cancer risk (a 
default of 10-6).
    q1* or CSF = cancer slope factor. The q1* is 
the upper 95 percent confidence limit on the cancer potency slope 
calculated by the LMS model, and CSF is a potency derived from the 
lower 95 percent confidence limit on the 10 percent (0.1) tumor dose 
(LED10). CSF = 0.1/LED10. Both potency estimates 
are converted to human equivalent [in (mg/kg-day)-1] using 
BW 3/4 scaling.
    DWC = daily volume of water consumed by an adult (a default of two 
L/day or other volume in Leq/day to account for additional inhalation 
and dermal exposures from household use of drinking water as explained 
above).

    Two cancer potency estimates, q1* or CSF, were 
calculated because our current experience with the LMS model is 
extensive whereas the new methodology proposed by U.S. EPA (1996f) in 
its draft guidelines for carcinogen risk assessment is based on the 
LED10 for which little is known about the problems and 
outcome of using this procedure. The LMS model focuses on the linear 
low-dose extrapolation and analysts (e.g., U.S. EPA) have often 
accepted relatively poor fits to the observed tumor incidence data. The 
new method places a higher premium on fitting the observed data to 
estimate the ED10 and the 95 percent lower bound 
LED10, the point from which the low dose extrapolation is 
made (U.S. EPA 1996a). In the case of the estimates obtained for 
carcinogenic potency of MTBE, the values calculated using the LMS model 
are not significantly different from that obtained using the preferred 
LED10 approach.
    The calculated public health-protective concentration accounting 
for carcinogenic effects of MTBE is based on a carcinogenic potency of 
1.8  10-3 (mg/kg-day)-1. This estimate 
is the geometric mean of the potency estimates (CSFs) obtained for the 
combined male rat kidney adenomas and carcinomas in the inhalation 
study by Chun et al. (1992), the male rat Leydig cell tumors in the 
oral study by Belpoggi et al. (1995, 1998), and the leukemia and 
lymphomas in female rats, also in the study by Belpoggi et al. (1995, 
1998). It is consistent with potencies obtained at other sites in 
another species (mice). The estimate for the inhalation route was 
converted to an oral intake using the pharmacokinetic model described 
earlier. The public health-protective concentration was therefore 
calculated using the following values:

    BW = 70 kg (the default male adult human body weight).
    R = 10-6 (default de minimis lifetime excess individual 
cancer risk).
    q1* or CSF = 1.8  10-3 (mg/kg-
day)-1 (CSF estimated as above).
    DWC = 3 Leq/day (daily water consumption. As described previously 
in the section on RSCs, there are various probable routes of exposure 
in addition to ingestion that would result from contamination of water 
supplies. To allow for these additional exposures as shown in 
calculations in Table 16, the assumed daily volume of water consumed by 
an adult is increased from the default of two L/day to three Leq/day).
Thus,

    C = 70  10-6 /1.8  10-3 
 3 = 13  10-3 mg/L = 13 g/L = 13 
ppb

    Since the calculated public health-protective concentration based 
on noncancer toxicity of 47 ppb is less protective of public health 
than the above cancer based value of 13 ppb, the recommended PHG level 
for MTBE is therefore 13 ppb (0.013 mg/L or 13 g/L). The 
adopted PHG is considered to contain an adequate margin of safety for 
the potential noncarcinogenic adverse effects including adverse effects 
on the renal, neurological and reproductive systems.
                         risk characterization
    MTBE is used as an additive in cleaner burning automotive fuel in 
California. This results in opportunities for airborne exposures as 
well as drinking water exposures through leaking USTs and to a lesser 
extent from certain powered watercraft and air deposition. The public 
health risks of exposure to MTBE can be characterized as follows:
Acute Health Effects
    Acute health effects are not expected to result from typical 
exposure to MTBE in drinking water. This includes household airborne 
exposures from showering, flushing toilets, etc. Reports of health 
complaints of various nonspecific symptoms (e.g., headache, nausea, 
cough) associated with exposure to gasoline containing MTBE have not 
been confirmed in controlled studies and remain to be fully evaluated.
Carcinogenic Effects
    Inhalation exposure to MTBE produced increased incidences of kidney 
and testicular tumors in male rats and liver tumors in mice. Oral 
administration of MTBE produced leukemia and lymphoma in female rats 
and testicular tumors in male rats. A summary of our evaluation is 
listed below.
     As a result of this assessment OEHHA considers MTBE to be 
an animal carcinogen and a possible human carcinogen.
     Three cancer bioassays have shown MTBE induced tumors at 
several sites, in two species, in both sexes, by oral and inhalation 
routes of exposure; five of six studies were positive.
     Cancer study results exhibit consistency. For example, 
testicular tumors were induced in rats by both routes of MTBE 
administration.
     The oral rat study by Belpoggi et al. (1995, 1997, 1998) 
was found to be adequate for risk assessment purposes despite early 
mortality in the females.
     The inhalation studies in rats and mice were also 
considered adequate for risk assessment despite early mortality in both 
studies.
     In general the quality of the three studies was as good or 
better than those typically available for chemical risk assessment.
     While there are varying degrees of uncertainty as to the 
relevance to human cancer causation for each of the tumor types induced 
by MTBE in rodents (i.e., hepatocellular adenoma and carcinoma, renal 
tubular adenoma and carcinoma, Leydig interstitial cell tumors of the 
testes, leukemias and lymphomas), the occurrence of tumors at all of 
these sites adds considerably to the weight of evidence supporting the 
conclusion that MTBE should be considered a possible human carcinogen.
     MTBE genotoxicity data is weak, and there is no clear 
evidence that genotoxicity of its metabolites is involved in the 
carcinogenicity observed.
     There is no evidence to support a specific nongenotoxic 
mode of action (e.g., hormone receptor binding) and no evidence that 
metabolism of MTBE is required for carcinogenicity. In the absence of 
sufficient evidence, dose metrics based on the parent compound, MTBE, 
were necessarily chosen for the dose-response assessment.
     In 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.
     Cancer potency estimates derived from different studies, 
sites, and routes of administration are similar.
     Cancer potency estimates are low compared to other known 
carcinogens despite the health conservative default assumptions 
employed.
     The adopted PHG of 13 ppb is based on an average of three 
quantitatively similar CSFs for three sites (kidney tumors, testicular 
tumors, leukemia and lymphoma). If the PHG value was based on 
individual tumor sites instead of an average, the values would range 
from 2.7 to 15 ppb.
     The CSFs are upper-bound estimates defined by the 95 
percent confidence limit on the ED10. It is theoretically 
possible that the true value of the cancer potency of MTBE in humans 
could exceed these values, but that is considered unlikely. It is 
plausible that the true value of the human cancer potency for MTBE has 
a lower bound of zero based on statistical and biological uncertainties 
including interspecies extrapolation and mode of action.
     The estimate of multi-route exposure employed in the PHG 
calculation was three Leq/day. The range of exposure estimates based on 
different Henry's Law constants and water ingestion rates was 2.5 to 
four Leq/day. The range of possible PHGs based on this range and the 
average CSF of 0.0018 (mg/kg-day)-1 is 10 to 16 ppb.
     Additional peer review of all the cancer bioassays would 
be useful, as would be a separate bioassay of MTBE in drinking water. 
However, these supplemental data should be seen in the context of the 
data already available, which are substantial and of better quality 
than is available for some other compounds for which risk assessments 
have been undertaken.
     Lack of knowledge of the mode(s) of action of MTBE or its 
metabolites is a major limitation of this risk assessment.
     Lack of evidence of cancer causation in humans is also a 
significant limitation, although widespread use and potential exposure 
is relatively recent in California and the rest of the U.S.
     Additional pharmacokinetic data in humans and improved 
PBPK models in animals and humans are desirable.
     Lack of information on the role that interindividual 
variability (i.e., stemming from metabolic polymorphisms, age-related 
differences, and concurrent disease conditions) may play in determining 
susceptibility to the carcinogenicity of MTBE severely hinders 
identification of sensitive subgroups in the California population.
    The cancer potency estimate derived from the geometric mean of the 
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. Individual 
tumor endpoint CSFs ranged from 1.55  10-3 (mg/kg-
day)-1 to 8.7  10-3 (mg/kg-
day)-1, or a range of about six-fold. Potencies based on the 
LMS model were similar ranging from 1.63  10-3 (mg/
kg-day)-1 to 9.2  10-3 (mg/kg-
day)-1, also a range of six-fold. A time-to-tumor analysis 
gave much higher values of 0.076 (mg/kg-day)-1 and 0.072 
(mg/kg-day)-1 for the LMS and LED10 approaches, 
respectively. However this latter estimate has a low degree of 
confidence.
    The findings of the oral gavage studies conducted by Belpoggi and 
colleagues have been given less weight by some reviewers, based on 
criticisms of various aspects of the study design, study reporting, and 
data analysis employed. The NAS (NRC 1996) review of the studies of 
Belpoggi et al. (1995) noted the following as study deficiencies: (1) 
the dosage schedule of Monday, Tuesday, Thursday, and Friday, rather 
than five consecutive days; (2) use of doses in apparent excess of the 
Maximum Tolerated Dose (MTD), based on a dose-related decrease in 
survival among treated females; (3) the combining of leukemia and 
lymphoma incidence; (4) incomplete description of tumor pathology and 
diagnostic criteria; and (5) lack of mortality adjusted analysis to 
account for differences in survival times. As noted above, OEHHA has 
considered these criticisms and considers that, although these 
experiments, like the others available for MTBE, do have certain 
limitations or difficulties of interpretation, they contribute 
considerably to the overall evidence available for MTBE risk 
assessment. Further, our conclusion is that the study is valid, not 
critically flawed, and is consistent with other reported results.
    In criticizing the dosing schedule, NAS (NRC 1996) is correct in 
pointing out that 5 days per week is more usual. However, there is no 
evidence from the pharmacokinetic analyses that the proportionately 
higher peak dose and longer recovery periods would make any difference 
relative to the same time-averaged dose given over 5 days. The 
criticism that the MTD was exceeded appears misguided, in that a 
substantial proportion of the animals in all groups survived for a 
major part of the standard lifetime. The authors specifically noted no 
dose-related differences between control and exposed animals in food 
and water consumption or mean body weights (important indicators of 
non-specific toxicity). In any event, such a flaw, if real, would 
reduce rather than enhance the power of the studies to detect a 
positive response. The questions as to the advisability of combining 
leukemias and lymphomas, and the desire for clarification of the 
diagnostic criteria for these and the Leydig cell tumors, have been 
addressed by pathology review undertaken by Belpoggi et al. (1998), and 
reviewed elsewhere in this document. OEHHA shares the NAS preference 
for availability of full mortality data whenever possible, but notes 
that extensive quantal statistical analyses were undertaken by Belpoggi 
et al. (1998), as well as by OEHHA for this report, and considers that 
the data as presented provide an adequate basis for use in this risk 
assessment.
    In its critique of the Belpoggi et al. studies, the NAS (NRC 1996) 
also stated that ``an in-depth review of the data, especially the 
pathology (microscopic slides) of the critical lesions, is warranted 
(as was done with the inhalation studies) before the data are used for 
risk assessment.'' As mentioned above, Belpoggi and colleagues have 
recently published the results of a pathology review in which slides 
from the original study were re-examined, and diagnostic criteria 
reviewed by an independent panel of pathologists from the Cancer 
Research Centre, with the participation of an outside pathologist 
(Belpoggi et al. 1998). This review confirmed the authors' previous 
findings, and addressed the concerns expressed in the NAS report. As 
was correctly pointed out in the NSTC report (1997), the pathological 
findings of the MTBE inhalation studies (Burleigh-Flayer et al. 1992, 
Chun et al. 1992) have not undergone peer review, moreover, 
``independent peer review of pathological findings are not routinely 
performed in carcinogenesis studies used by the risk assessing 
community and (U.S.) EPA.''
    The water concentration associated with a 10-6 
negligible theoretical extra lifetime cancer risk calculated from this 
analysis is 13 ppb. This includes an estimate of inhalation exposure 
from showering in MTBE contaminated water, flushing toilets, and other 
household activities involving tap water. The estimate of one Leq/day 
of additional exposure via the inhalation route is lower than the 
default value of two Leq/day of additional exposure suggested by U.S. 
EPA (1996b) based on average estimated showering exposures of a number 
of typical VOCs. This reflects the fact that MTBE is less volatile and 
more water-soluble than other VOCs commonly found in drinking water. 
The adopted PHG value of 13 ppb also compares favorably with the 
Provisional Health and Consumer Acceptability Advisory range of 20 to 
40 ppb established by U.S. EPA (1997a) using a MOE approach. Since the 
adopted value of 13 ppb was calculated for a 1  
10-6 theoretical lifetime extra risk from a linear 
extrapolation, the values of 130 ppb and 1,300 ppb (1.3 ppm or 1.3 mg/
L) would be associated with the higher risk estimates of 1  
10-5 1  10-4, respectively.
    For PHGs, our use of the RSC has, with a few exceptions, followed 
U.S. EPA drinking water risk assessment methodology. U.S. EPA has 
treated carcinogens differently from noncarcinogens with respect to the 
use of RSCs. For noncarcinogens, RfDs (in mg/kg/day), DWELs (in mg/L) 
and MCLGs (in mg/L) are calculated using UFs, body weights and DWC (in 
Leq/day) and RSC, respectively. The typical RSC range is 20 percent to 
80 percent (0.2 to 0.8), depending on the scientific evidence.
    U.S. EPA follows a general procedure in promulgating MCLGs:
     if Group A and B carcinogens (i.e., strong evidence of 
carcinogenicity) MCLGs are set to zero;
     if Group C (i.e., limited evidence of carcinogenicity), 
either an RfD approach is used (as with a noncarcinogen) but an 
additional UF of 1 to 10 (usually 10) is applied to account for the 
limited evidence of carcinogenicity, or a quantitative method (potency 
and low-dose extrapolation) is used and the MCLG is set in the 
10-5 to 10-6 cancer risk range;
     if Group D (i.e., inadequate or no animal evidence) a Rfl) 
approach is used to promulgate the MCLG.
    For approaches that use low-dose extrapolation based on 
quantitative risk assessment, U.S. EPA does not factor in a RSC. The 
use of low-dose extrapolation is considered by U.S. EPA to be 
adequately health-protective without the additional source 
contributions. In developing PHGs, we have used the assumption that 
RSCs should not be factored in for carcinogens grouped in U.S. EPA 
categories A and B. and for C carcinogens for which we have calculated 
a cancer potency value based on low-dose extrapolation. This is an area 
of uncertainty and scientific debate and it is not clear how this 
assumption impacts the overall health risk assessment.
                       other regulatory standards
    The IPCS of WHO is issuing the final version of an environmental 
health criteria document on MTBE (IPCS 1997). The Dutch Expert 
Committee on Occupational Standards (Wibowo 1994) recommended a health-
based 8 hour-Time-Weighted Average (TWA) exposure limit for MTBE of 180 
mg/m3 or 50 ppm to be averaged over an 8-hour working day, 
and a short-term 15-minute-TWA limit of 360 mg/m3 or 100 ppm 
in the Netherlands. Czechoslovakia has an Occupational Exposure Limit 
(OEL) TWA of 100 mg/m3 and a Short-Term OEL (STEL) of 200 
mg/m3 since January 1993. Russia has a STEL of 100 mg/
m3 since January 1993 (RTECS 1997). Sweden established a TWA 
of 50 ppm and a 15-minute STEL of 75 ppm in 1988 (ACGIH 1996). The 
British Industrial Biological Research Association (BIBRA) compiled a 
toxicological profile on MTBE in 1990. The Danish Environmental 
Protection Administration is considering setting a 30 ppb limit of MTBE 
in groundwater. More recently, ECETOC (1997) recommended an 
occupational exposure limit of 90 mg/m3 or 25 ppm to be 8 
hour-TWA and a short-term peak 15-minute-TWA limit of 270 mg/
m3 or 75 ppm.
    In the U.S., the OSHA and NIOSH established the TLV-TWA as 40 ppm 
in air (144 mg/m3) in 1994 as proposed by ACGIH in 1993. 
ACGIH (1996) also lists MTBE as an A3 animal carcinogen in 1995 as 
proposed in 1994. MTBE is on the Emergency Preparedness and Community 
Right-to-Know Section of the Superfund Amendments and Reauthorization 
Act of 1986 (SARA Title III) Extremely Hazardous Substances (EMS) list 
and in the TSCA Test Submission (TSCATS) Data base. It is one of the 
TRI chemicals to be routinely inventoried. MTBE is on the Hazardous Air 
Pollutant (HAP) list with 189 other chemicals to be regulated under the 
Air Toxics Program of the 1990 CAAA. Article 211 (b) of Title III of 
the CAAA requires that oil companies conduct gasoline inhalation 
studies and U.S. EPA sent the testing requirement notification on 
August 20, 1997. Negotiations with industry on the extent of these 
studies are ongoing. Animal research will focus on short and long-term 
inhalation effects of conventional gasoline and gasoline with MTBE. The 
Article 211 studies will also include human exposure research. The 
research will be completed at varying intervals over the next 5 years. 
HEI is funding three new studies designed to answer key questions on 
the metabolism of MTBE and other ethers in animals and humans.
    MTBE is listed as a California TAC mandated under AB 1807 by virtue 
of its status as a HAP. It is one of the California Air Toxics ``Hot 
Spots'' chemicals mandated under AB 2588. ARB is proposing to place 
MTBE into subcategory b as substances nominated for review for 
development of health values. A chronic Reference Exposure Level, which 
is the same as the three mg/m3 RfC for inhalation of MTBE in 
air as listed in the U.S. EPA (1997c) IRIS data base, is being 
developed in the draft Hot Spots document by OEHHA mandated under SB 
1731. Texas established a half-hour limit in ambient air of 0.6 mg/
m3 and an annual limit of 0.288 mg/m3 in 1992 
(Sittig 1994).
    MTBE is not a priority pollutant under the Clean Water Act and is 
not a target analyte in routine water quality monitoring and assessment 
programs. MTBE is included in the draft and final Drinking Water 
Contaminant Candidate List (CCL) required by the Safe Drinking Water 
Act (U.S. EPA 1997b, 1997d, 1998b). The final list is published on 
March 2, 1998 with descriptions on how to make decisions on whether to 
establish a standard on the contaminants. CCL is divided into 
categories representing next steps and data needs for each contaminant. 
U.S. EPA will choose at least five contaminants from the Regulatory 
Determination Priorities category and determine by August 2001 whether 
or not to regulate them based on occurrence, exposure and risk. If 
regulations are deemed necessary they must be proposed by August 2003 
and promulgated by February 2005. MTBE is proposed for inclusion on the 
Federal ``National Drinking Water Contaminant Occurrence Data Base''.
    In the interim, the Office of Water has initiated a data base based 
on voluntary reporting from some states, USGS data, and other available 
sources. MTBE is on the U.S. EPA Drinking Water Priority List for 
future regulation. The U.S. EPA's Office of Research and Development is 
working to identify MTBE research needs, including monitoring, 
exposure, health effects, and remediation. A workshop was held on 
October 7, 1997 to present an initial assessment of research needs to 
industry and academic groups. A draft report (U.S. EPA 1998b) has been 
issued for public comment ending by August 28, 1998. Other U.S. EPA 
activities include development of a protocol to collect data on 
potential CO reductions using Federal oxygenated gasoline. USGS is 
conducting urban land use studies this year to characterize VOCs, 
including MTBE contamination as a part of the larger national NAWQA 
program.
    Since the early 1990's, U.S. EPA has evaluated MTBE to quantify its 
toxic effects (Farland 1990, Hiremath and Parker 1994, Klan and 
Carpenter 1994, Gomez-Taylor et al. 1997). U.S. EPA (1996a) proposed a 
70 ppb HA for MTBE in its December 1996 draft report based on 
noncarcinogenic kidney and liver effects in laboratory animals with 
large uncertainty factors (U.S. EPA 1996f). U.S. EPA also included an 
extra uncertainty factor in its draft report to account for the 
possible carcinogenicity of the substance. The laboratory animal cancer 
bioassays of MTBE by the inhalation route were performed by Bushy Run 
Research Center (Burleigh-Flayer et al. 1992, Chun et al. 1992) and the 
ones by the oral route were performed by Cancer Research Centre of the 
European Foundation for Oncology and Environmental Sciences ``B. 
Ramazzini'' in Italy (Belpoggi et al. 1995, 1997, 1998). U.S. EPA has 
not had an opportunity to audit the studies even though reviews of 
pathological findings are not routinely performed (NSTC 1997). 
Nevertheless, in the 1996 draft, U.S. EPA indicated that the animal 
studies would suggest that 12.5 ppb would equate to a theoretical risk 
level of one excess fatal case of cancer per million people per 70-year 
lifetime (a 10-6 risk), a level usually viewed as de 
minimis, for MTBE as a Group B2 probable human carcinogen. The 12.5 ppb 
was calculated based on an oral cancer potency estimate 
(q1*) of 3 x 10-3 (mg/kg-day)-1 
derived from the default LMS method and a scaling factor of body weight 
raised to \3/4\ power using the combined lymphoma and leukemia in the 
female rats in the gavage study.
    The U.S. EPA (1997c) IRIS data base lists the RfC for inhalation of 
MTBE in air as three mg/m3 as last revised on September 1, 
1993. The RfC is based on increased liver and kidney weights, increased 
prostration in females, and swollen periocular tissues in male and 
female rats. The RfD for oral exposure to MTBE is under review by U.S. 
EPA (1997c). In 1992, U.S. EPA derived a draft long-term HA range for 
MTBE in drinking water of 20 to 200 ppb (or 0.02 to 0.2 mg/L) based on 
a RfD of 0.1 mg/kg/day from a 90-day rat drinking water study with 
dose-related increases in relative kidney weights in both sexes 
(Robinson et al. 1990). The range is due to the uncertainty for the 
carcinogen classification. The guideline would be either 20 ppb if MTBE 
were classified as a Group B2 or C carcinogen, or 200 ppb if MTBE is a 
Group D carcinogen. In 1994, U.S. EPA drafted a proposal in reviewing 
data from animal studies for the possibility of listing MTBE as a Group 
B2 probable human carcinogen, and derived an oral cancer potency 
estimate (q1*) of 8.6  10-3 (mg/kg-
day)-1 and a HA of four ppb for a 10-6 risk.
    The States of Vermont and Florida established drinking water 
standards for MTBE of 40 ppb and 50 ppb, respectively. The New York 
State Department of Public Water promulgated a MCL of 50 ppb in 1988. 
The New York State Department of Health is drafting an ambient water 
quality value for protection of human health and sources of potable 
water for MTBE based on the evaluation of animal oncogenicity data. The 
New Jersey Department of Environmental Protection (NJDEP) proposed in 
1994 and established in 1996 a health-based MCL for MTBE in drinking 
water of 70 ppb, reducing from 700 ppb. This is in agreement with the 
1993 evaluation of the U.S. EPA except for an uncertainty factor of 
10,000 used by NJDEP instead of the 3,000 applied by the U.S. EPA 
(NJDWQI 1994, Post 1994). The Illinois Environmental Protection Agency 
listed a human threshold toxicant advisory concentration of 230 ppb in 
1994 and has proposed a health-based MCL for MTBE in drinking water 
ranging from 70 to 2,000 ppb. The Massachusetts Department of 
Environmental Protection in 1995 proposed to decrease the guideline for 
MTBE in drinking water from 700 ppb to 70 ppb (MORS 1995). The Maine 
Department of Human Services listed a drinking water threshold of 50 
ppb in 1995 and is considering to adopt 35 ppb based on noncancer 
health effects with a RSC of 10 percent (Smith and Kemp 1998). NCDEHNR 
has proposed a primary MCL of 70 ppb. The Wisconsin Department of 
Natural Resources in 1995 established a groundwater enforcement 
standard for MTBE of 60 ppb (WDOH 1995). The guideline for MTBE in 
drinking water is 35 ppb in Arizona, 40 ppb in Michigan, 50 ppb in 
Rhode Island, and 100 ppb in Connecticut and New Hampshire (ATSDR 1996, 
HSDB 1997, Sittig 1994).
    The UC report mandated under SB521 concluded that MTBE is an animal 
carcinogen with the potential to cause cancers in humans (Froines et 
al. 1998). Using several models for exposure analysis, Johnson (1998) 
calculated a de minimis theoretical excess individual cancer risk level 
of 10-6 from exposure to MTBE of 10 ppb which, the author 
concluded, is comparable to the level recommended in this report.
    DHS has added MTBE to a list of unregulated chemicals that require 
monitoring by drinking water suppliers in California in compliance with 
the California Safe Drinking Water Act, Sections 116300 to 116750. An 
interim Action Level of 35 ppb or 0.035 mg/L for drinking water was 
adopted by the DHS in 1991. The level was recommended by OEHHA (1991) 
using the oral RfD of 0.005 mg/kg/day then reported on the U.S. EPA 
IRIS data base for an anesthetic effect in rats in a 13-week inhalation 
study performed in Europe (Greenough et al. 1980). DHS is proceeding 
with establishing drinking water standards for MTBE in California.
    The initial standard to be developed for MTBE is a secondary MCL. 
The secondary MCL of five ppb is adopted by DHS as a regulation 
effective January 7, 1999. Secondary MCLs address aesthetic qualities 
of drinking water supplies. In the case of MTBE, the focus is on its 
organoleptic qualities, that is, its odor and taste. The purpose of the 
secondary MCL is to protect the public from exposure to MTBE in 
drinking water at levels that can be smelled or tasted. Secondary MCLs 
in California are enforceable standards, which means that drinking 
water should not be served by public water systems if it contains MTBE 
higher than the secondary standard. Enforceable secondary standards are 
unique to California. The proposed secondary MCL for MTBE is based on 
data from experiments that have been performed by researchers, using 
panels of subjects who were exposed to varying concentrations of MTBE 
in water to determine levels at which it could be smelled or tasted. As 
part of the process by which regulations are adopted under California's 
Administrative Procedures Act, the proposed regulation (R-44-97) was 
available for public comment since July 3, 1998, and September 8, 1998 
was the close of the written comment period (DHS 1998).
    The next standard to be developed is a primary MCL that protects 
the public from MTBE at levels that can affect public health. A primary 
MCL for MTBE will include consideration of the health risk assessment, 
the technical feasibility of meeting the MCL (in terms of monitoring 
and water treatment requirements for MTBE) and costs associated with 
compliance. DHS has requested the OEHHA to provide a risk assessment 
for MTBE that is required for the development of the primary standard. 
DHS requested that the risk assessment be completed in order to meet 
the scheduled adoption of this regulation by July 1999. The proposed 
primary MCL is anticipated to be available for public comment in early 
1999.
                               references
    Aarstad K, Zahlsen K, Nilsen OG (1985). Inhalation of butanols: 
Changes in the cytochrome P450 enzyme system. Arch. Toxicol. 
Suppl 8: 418-421.
    Abel EL, Bilitzke PJ (1992). Effects of prenatal exposure to 
methanol and t-butanol in Long Evans rats. Am. J. Obstet. Gynecol. 
166(1, pt 2): 433.
    ACGIH (1996). Methyl Tert-Butyl Ether. In: Documentation of the 
Threshold Limit Values and Biological Exposure Indices. Supplements to 
the Sixth Edition: Methyl Tert-Butyl Ether. pp. 1-12. Cincinnati, Ohio: 
American Conference of Governmental Industrial Hygienists, Inc. 
(ACGIH).
    Allen MJ, Borody TJ, Bugliosi TF, May GR, Thistle JL, Etzel AL 
(1985). Rapid dissolution of gallstones by methyl tertiary-butyl ether: 
Preliminary observations. New Engl. J. Med. 312(4): 217-220. January 
24.
    Anderson HA, Hanrahan L, Goldring J, Delaney B (1995). An 
Investigation of Health Concerns Attributed to Reformulated Gasoline 
(RFG) Use in Southeastern Wisconsin. Final Report. May 30. Addendum. 
September 18. 99 pp. Milwaukee, Wisconsin: Section of Environmental 
Epidemiology and Prevention, Bureau of Public Health, Division of 
Health, Wisconsin Department of Health and Social Services.
    Anderson RAJ, Reddy JM, Joyce C, Willis BR, Van der Ven H, Zaneveld 
LJ (1982). Inhibition of mouse sperm capacitation by ethanol. Biol. 
Reprod. 27(4): 833-40.
    Angle CR (1991). If the tap water smells foul, think MTBE. Letter 
to the Editor. JAMA 266(21): 2985-2986. December 4.
    Anonymous (1995). USGS reports MTBE in groundwater. Oil & Gas J. 
93(16): 21-22. April 17. PennWell Publishing Company.
    API (1994). Odor threshold studies performed with gasoline and 
gasoline combined with MTBE, ETBE and TAME. Prepared by TRC 
Environmental Corporation, Windsor, Connecticut, for American Petroleum 
Institute (API). January. API # 4592. Submitted to the U.S. 
Environmental Protection Agency with cover letter dated February 22, 
1995. EPA/OTS DOC#86950000131. Washington, D.C.: API. API MTBE website: 
http://www.api.org/ehs/othrmtbe.htm
    Arashidani K, Katoh T, Yoshikawa M, Kikuchi M, Kawamoto T, Kodama Y 
(1993). LD50 and weight change in organs of mice following 
intraperitoneal administration of methyl tertiary-butyl ether. Sangyo 
Igaku (Japan) 35(5):404-405. September.
    ARB (1996). Preliminary Ambient Oxygenates Data of the California 
ARB Laboratory Information System, and San Francisco Bay Area Air 
Quality Management District (BAAQMD) Ambient Air Toxics Data on MTBE. 
Laboratory and Monitoring Division, California Air Resources Board 
(ARB), California Environmental Protection Agency (Cal/EPA). 
Sacramento, California: ARB, Cal/EPA.
    ARCO (1995a). MTBE Use and Possible Occurrences in Water Supplies. 
Prepared by William J. Piel. May 10. 4 pp. Newton Square, Pennsylvania: 
ARCO Chemical Company.
    ARCO (1995b). Methyl t-Butyl Ether (MTBE): A status report of its 
presence and significance in U.S. drinking water. Presented by ARCO 
Chemical Company to the Office of Water, U.S. Environmental Protection 
Agency on June 8. Glenolden, Pennsylvania: ARCO Chemical Company.
    ARCO (1980). Methyl tertiary-butyl ether: acute toxicological 
studies. Unpublished study for ARCO Research and Development for ARCO 
Chemical Company. Glenolden, Pennsylvania: ARCO Chemical Company.
    ATSDR (1996). Toxicological profile for methyl tert-butyl ether. 
August. Prepared by Research Triangle Institute for the Agency for 
Toxic Substances and Disease Registry (ATSDR), Centers for Disease 
Control (CDC), Public Health Service (PHS), United States Department of 
Health and Human Services (USDHHS). Atlanta, Georgia: ATSDR, CDC.
    Baehr AL, Baker RJ, Lahvis MA (1997). Transport of methyl tert-
butyl ether across the water table to the unsaturated zone at a 
gasoline-spill site in Beaufort, South Carolina. Paper ENVR 230. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
417-418.
    Balter NJ (1997). Casualty assessment of the acute health 
complaints reported in association with oxygenated fuels. Risk Anal. 
17(6): 705-715. December.
    Barker JF, Hubbard CE, Lemon LA (1990). The influence of methanol 
and MTBE on the fate and persistence of monoaromatic hydrocarbons I 
ground water. Ground Water Manag. 113-117.
    Begley R (1994). MTBE high demand time looms as health questions 
linger. Chemical Week 155: 13. August 31-September 7.
    Begley R, Rotman D (1993). Health complaints fuel Federal concern 
over MTBE. Chemical Week 152(10): 7. March 17.
    Beller M, Schloss M, Middaugh J (1992). Potential Illness Due to 
Exposure to Oxyfuels. Evaluation of Health Effects from Exposure to 
Oxygenated Fuel in Fairbanks, Alaska. December 11. Bulletin Number 26. 
Anchorage, Alaska: Alaska Department of Health and Social Services.
    Belpoggi F, Soffritti M, Maltoni C (1998). Pathological 
characterization of testicular tumours and lymphomas-leukaemias, and of 
their precursors observed in Sprague-Dawlay rats exposed to methyl 
tertiary-butyl ether (MTBE). Eur. J. Oncol. 3(3): 201-206.
    Belpoggi F, Soffritti M, Maltoni C (1995). Methyl tertiary-butyl 
ether (MTBE)--a gasoline additive--causes testicular and 
lymphohaematopoietic cancers in rats. Toxicol. Ind. Hlth. 11(2): 119-
149. March.
    Belpoggi F, Soffritti M, Filippini F. Maltoni C (1997). Results of 
long-term experimental studies on the carcinogenicity of methyl tert-
butyl ether. Annals N. Y. Acad. Sci. 837: 77-95. December 26.
    Bernauer U. Amberg A, Scheutzow D, Dekant W (1998). 
Biotransformation of 12C- and 2-13C-labeled 
methyl tert-butyl ether, ethyl tert-butyl ether, and tert-butyl alcohol 
in rats: Identification of metabolites in urine by 13C 
nuclear magnetic resonance and gas chromatography/mass spectrometry. 
Chem. Res. Toxicol. 11(6): 651-658. June.
    Bevan C, Neeper-Bradley TL, Tyl RW, Fischer LC, Panson RD, Kneiss 
JJ, Andrews LS (1997a). Two-generation reproductive study of methyl 
tertiary-butyl ether (MTBE) in rats. J. Appl. Toxicol. 17(S1): S13-S19. 
May.
    Bevan C, Tyl RW, Neeper-Bradley TL, Fischer LC, Panson RD, Douglas 
JF, Andrews LS (1997b). Developmental toxicity evaluation of methyl 
tertiary-butyl ether (MTBE) by inhalation in mice and rabbits. J. Appl. 
Toxicol. 17(S1): S21-S29. May.
    BIBRA (1990). Methyl t-butyl ether (MTBE) toxicology profile. The 
British Industrial Biological Research Association (BIBRA) Working 
Group. 6 pp. London, Great Britain: BIBRA Toxicology International.
    Biles RW, Schroeder RE, Holdsworth CE (1987). Methyl tert-butyl 
ether inhalation in rats: a single generation reproduction study. 
Toxicol. Ind. Hlth. 3(4): 519-534. December.
    Bio/dynamics, Inc. (1984a). An inhalation teratology study in rats 
with methyl tertiary-butyl ether (MTBE). Project No. 80-2515. 
Unpublished report submitted to API, Washington, D.C. East Millstone, 
New Jersey: Bio/dynamics, Inc.
    Bio/dynamics, Inc. (1984b). An inhalation teratology study in mice 
with methyl tertiary-butyl ether (MTBE). Project No. 80-2516. 
Unpublished report submitted to API, Washington, D.C. East Millstone, 
New Jersey: Bio/dynamics, Inc.
    Bio/dynamics, Inc. (1984c). The metabolic fate of methyl tertiary-
butyl ether (MTBE) following acute intraperitoneal injection. Project 
No. 80089. Unpublished report submitted to API, Washington, D.C. 150 
pp. East Millstone, New Jersey: Bio/dynamics, Inc.
    Bio/dynamics, Inc. (1981). A 9-day inhalation toxicity study of 
MTBE in the rat. Project No. 40-1452. Unpublished report submitted to 
API, Washington, D.C. 352 pp. East Millstone, New Jersey: Bio/dynamics, 
Inc.
    Bioresearch Laboratories (1990a). Pharmacokinetics of methyl 
tertiary-butyl ether (MTBE) and tert-butyl alcohol (TBA) in male and 
female Fischer-344 rats after administration of 14C-MTBE by 
intravenous, oral, and dermal routes. Report #38842. Senneville, 
Quebec, Canada: Bioresearch Laboratories.
    Bioresearch Laboratories (1990b). Mass balance of radioactivity and 
metabolism of methyl tert-butyl ether (MTBE) in male and female 
Fischer-344 rats after administration of 14C-MTBE by 
intravenous, oral, and dermal routes. Report #38843. Senneville, 
Quebec, Canada: Bioresearch Laboratories.
    Bioresearch Laboratories (1990c). Pharmacokinetics of methyl tert-
butyl ether (MTBE) and tert-butyl alcohol (TBA) in male and female 
Fischer-344 rats after single and repeat inhalation nose-only exposure 
to 14C-MTBE. Report #38844. Senneville, Quebec, Canada: 
Bioresearch Laboratories.
    Bioresearch Laboratories (1990d). Disposition of radioactivity of 
methyl tertiary-butyl ether (MTBE) in male and female Fischer-344 rats 
after nose-only inhalation exposure to 14C-MTBE. Report 
#38845. Senneville, Quebec, Canada: Bioresearch Laboratories.
    Bird MG, Burleigh-Flayer HD, Chun JS, Douglas JF, Kneiss JJ, 
Andrews LS (1997). Oncogenicity studies of inhaled methyl tertiary-
butyl ether (MTBE) in CD-1 mice and F-344 rats. J. Appl. Toxicol. 17 
(S1): S45-S55. May.
    Bonin MA, Ashly DL, Cardinali FL, McCraw JM, Wooten JV (1995). 
Measurement of methyl tert-butyl ether and tert-butyl alcohol in human 
blood by purge-and-trap gas chromatography-mass spectrometry using an 
isotope-dilution method. J. Analyt. Toxicol. 19(3): 187-191. May-June.
    Borak J, Pastides H, Van Ert M, Russi M, Herastein J (1998). 
Exposure to MTBE and acute human health effects: A critical literature 
review. Human and Ecological Risk Assess. 4(1): 177-200. February.
    Borden RC, Daniel RA, LeBrun LE IV, Davis CW (1997). Intrinsic 
biodegradation of MTBE and BTEX in a gasoline-contaminated aquifer. 
Water Resources Res. 33(5): 1105-1115. May.
    Borghoff SJ, Murphy JE, Medinsky MA (1996a). Development of a 
physiologically-based pharmacokinetic model for methyl tertiary-butyl 
ether and tertiary-butanol in male Fischer-344 rats. Fundam. Appl. 
Toxicol. 30(2): 264-275. April.
    Borghoff SJ, Prescott-Mathews JS, Poet TS (1996b). The mechanism of 
male rat kidney tumors induced by methyl tert-butyl ether (MTBE) and 
its relevance in assessing human risk. CIIT Activities. 16(10): 1-10. 
October. Research Triangle Park, North Carolina: Chemical Industry 
Institute of Toxicology (CIIT).
    Boughton CJ, Lico MS (1998). Volatile Organic Compounds in Lake 
Tahoe, Nevada and California, July-September 1997. USGS Fact Sheet FS-
055-98. June. 2 pp. Carson City, Nevada: USGS.
    Brady JF, Xiao F, Ning WJ, Yang CS (1990). Metabolism of methyl 
tertiary-butyl ether by rat hepatic microsomes. Arch. Toxicol. 64(2): 
157-160.
    Brown A, Devinny JS, Davis MK, Browne TE, Rodriguez RA (1997). A 
review of potential technologies for the treatment of methyl tertiary-
butyl ether (MTBE) in drinking water. In: Proceedings of the NGWA-API 
Conference on Petroleum Hydrocarbons and Organic Chemicals in Ground 
Water: Prevention, Detection, and Remediation. 16 pp. November 12-14. 
Houston, Texas. Dublin, Ohio: National Ground Water Association (NGWA).
    Brown SL (1997). Atmospheric and potable water exposures to methyl 
tertiary-butyl ether (MTBE). Reg. Toxicol. Pharmacol. 25(3): 256-276. 
June.
    Bruce BW, McMahon PB (1996). Shallow groundwater quality beneath a 
major urban center: Denver, Colorado, USA. J. Hydrology (Amsterdam, 
Netherlands) 186(1-4): 129-151.
    Buckley TJ, Prah JD, Ashley D, Zweidinger RA, Wallace LA (1997). 
Body burden measurements and models to assess inhalation exposure to 
methyl tertiary-butyl ether (MTBE). J. Air Waste Manag. Assoc. 47(7): 
739-752. July.
    Burbacher TM (1993). Neurotoxic effects of gasoline and gasoline 
constituents. Environ. Hlth. Perspect. 101(S6): 133-141. December.
    Burleigh-Flayer HD, Chun JS, Kintigh WJ (1992). Methyl tertiary 
butyl ether: vapor inhalation oncogenicity study in CD-1 mice. Bushy 
Run Research Center Report No. 91N0013A. October 15. Union Carbide 
Chemicals and Plastics Company, Inc. submitted to the U.S. EPA under 
TSCA Section 4 Testing Consent Order 40 CFR 799.5000 with cover letter 
dated October 29, 1992. EPA/OPTS#42098. Export, Pennsylvania: Bushy Run 
Research Center.
    Burleigh-Flayer HD, Doss DE, Bird MG, Ridlon SA (1991). 
Oncogenicity study of inhaled methyl tertiary butyl ether (MTBE) in CD-
1 mouse. MTBE Task Force. Washington, D.C.: Oxygenated Fuels 
Association (OFA).
    Burleigh-Flayer HD, Garman R, Neptun K, Bevan C, Gardiner T, Kapp 
R, Tyler T, Wright G (1997). Isopropanol vapor inhalation oncogenicity 
study in Fischer 344 rats and CD-1 mice. Fund. Appl. Toxicol. 36:95-
111.
    Buxton HT, Landmeyer JE, Baehr AL, Church CD, Tratnyek PG (1997). 
Interdisciplinary investigation of subsurface contaminant transport and 
fate at point-source releases of gasoline containing methyl tert-butyl 
ether (MTBE). In: Proceedings of the Petroleum Hydrocarbons and Organic 
Chemicals in Ground Water: Prevention, Detection, and Remediation 
Conference. pp. 15. November 11-14. Houston, Texas. Dublin, Ohio: NGWA.
    Cain WS, Leaderer BP, Ginsberg GL, Andrews LS, Cometto-Muniz JE, 
Gent JF, Buck M, Berglund LG, Mohsenin V, Monahan E, Kjaergaard S 
(1996). Acute exposure to low-level methyl tertiary-butyl ether (MTBE): 
Human reactions and pharmacokinetic responses. Inhalation Toxicol. 
8(1): 21-49. January.
    Cal/EPA (1998). MTBE (methyl tertiary butyl ether) briefing paper 
by the California Environmental Protection Agency (Cal/EPA). April 24, 
1997, updated September 3, 1998. 33 pp. Sacramento, California: Cal/
EPA. Available at: http:/www.arb.ca.gov/cbg/pub/pub.htm
    Caprino L, Togna GI (1998). Potential health effects of gasoline 
and its constituents: a review of current literature (1990-1997) on 
toxicological data. Environ. Hlth. Perspect. 106:115-125.
    Casanova M, Heck HA (1997). Lack of evidence for the involvement of 
formaldehyde in the hepatocarcinogenicity of methyl tertiary-butyl 
ether in CD-1 mice. Chem. Biol. Interact. 105(2): 131-143. July 11.
    CDC (1993a). An investigation of exposure to methyl tertiary-butyl 
ether (MTBE) in oxygenated fuel in Fairbanks, Alaska. October 22. 
National Center for Environmental Health (NCEH), Centers for Disease 
Control and Prevention (CDC), PHS, USDHHS. Atlanta, Georgia: CDC.
    CDC (1993b). An investigation of exposure to MTBE among motorists 
and exposed workers in Stamford, Connecticut. September 14. NCEH, CDC, 
PHS, USDHHS. Atlanta, Georgia: CDC.
    CDC (1993c). An investigation of exposure to MTBE and gasoline 
among motorists and exposed workers in Albany, New York. August 4. 
NCEH, CDC, PHS, USDHHS. Atlanta, Georgia: CDC.
    Cederbaum AI, Cohen G (1980). Oxidative demethylation of t-butyl 
alcohol by rat liver microsomes. Biochem. Biophys. Res. Comm. 97: 730-
736.
    Chandler B, Middaugh J (1992). Potential illness due to exposure to 
oxyfuels: Anchorage, Alaska. Bulletin Number 1. Middaugh J ed. 
Anchorage, Alaska: Alaska Department of Health and Social Services.
    Chun JS, Burleigh-Flayer HD, Kintigh WJ (1992). Methyl tertiary 
ether: vapor inhalation oncogenicity study in Fisher 344 rats. Bushy 
Run Research Center Report No. 91N0013B. November 13. Union Carbide 
Chemicals and Plastics Company, Inc. submitted to the U.S. EPA under 
TSCA Section 4 Testing Consent Order 40 CFR 799.5000 with cover letter 
dated November 19, 1992. EPA/OPTS#42098. Export, Pennsylvania: Bushy 
Run Research Center.
    Church CD, Isabelle LM, Pankow JF, Rose DL, Tratnyek PG (1997). 
Method for determination of methyl tert-butyl ether and its degradation 
products in water. Environ. Sci. Technol. 31(12): 3723-3726.
    Cinelli S, Ciliutti P, Falezza A, Meli C, Caserta L, Marchetti S, 
Seeberg AH, Vericat JA (1992). Absence of mutagenicity of methyl-
tertiary-butyl ether [abstract No. P36/P10]. Toxicol. Lett. Suppl. 1-
356: 300.
    Cirvello JD, Radovsky JE, Heath DR, Farnell DR, Lindamood, III C 
(1995). Toxicity and carcinogenicity of t-butyl alcohol in rats and 
mice following chronic exposure in drinking water. Toxicol. Ind. Hlth. 
11(2): 151-165.
    Clary JJ (1997). Methyl tertiary butyl ether systemic toxicity. 
Risk Anal. 17(6): 661-672. December.
    Clegg ED, Cook JC, Chapin RE, Foster PMD, Daston GP (1997). Leydig 
cell hyperplasia and adenoma formation: Mechanisms and relevance to 
humans. Reproductive Toxicol. 11(1): 107-121.
    Clerici C, Gentili G, Zakko SF, Balo S, Miglietti M, Giansanti M, 
Modesto R, Guttermuth CF, Morelli A (1997). Local and systemic effects 
of intraduodenal exposure to topical gallstone solvents ethyl 
propionate and methyl tert-butyl ether in the rabbit. Digest. Dis. Sci. 
42(3): 497-502.
    Cohen Y (1998). Multimedia distribution of oxygenated fuel 
additives. Presented at the MTBE Workshop, co-sponsored by the UCLA 
Center for Environmental Risk Reduction, UC Toxic Substances Research 
and Teaching Program, and Southern California Society for Risk 
Analysis. February 28. 29 pp. UCLA, Los Angeles, California.
    Cohen Y, Allen DT, Clay R, Tsai WT, Rosselot K, Klee H. Blewitt D 
(1991). Multimedia assessment of refinery emissions. Paper No. 91-84.6 
presented at the 84th Annual Meeting of the Air and Waste Management 
Association. June 16-21. Vancouver, British Columbia, Canada.
    Conaway CC, Schroeder RE, Snyder NK (1985). Teratology evaluation 
of methyl tertiary-butyl ether in rats and mice. J. Toxicol. Environ. 
Hlth. 16(6): 797-809.
    Cooney CM (1997). California struggles with presence of MTBE in 
public drinking water wells. Environ. Sci. Technol. 31(6): A269. June.
    Cornitius T (1996). California air rules foster MTBE demand. 
Chemical Week 158(27): 33, July 17.
    Cox DR (1972). Regression models and life-tables (with discussion). 
J.R. Stat. Soc. B. 24: 187-220.
    Crump KS, Howe RB, van Landingham C, Fuller WG (1993). TOX--RISK, a 
Toxicology Risk Assessment Program. Version 3.5. October. Ruston, 
Louisiana: K.S. Crump Division, Clement International Corp.
    Cullen PG (1998). MTBE: A remediation headache. Environ. Protect. 
6: 32-35. June.
    Dale MS, Losee RF, Crofts EW, Davis MK (1997a). MTBE: Occurrence 
and fate in source-water supplies. Paper ENVR 101. In: Proceedings of 
the 213th American Chemical Society National Meeting, Division of 
Environmental Chemistry, Environmental Fate and Effects of Gasoline 
Oxygenates. April 13-17. San Francisco, California. 37(1): 376-377.
    Dale MS, Moylan MS, Koch B, Davis MK (1997b). MTBE: Taste and odor 
threshold determinations using the flavor profile method. Presented at 
the Water Quality Technology Conference. November 9-13. Denver, 
Colorado. American Water Works Association (AWWA).
    Daly MH, Lindsey BD (1996). Occurrence and concentrations of 
volatile organic compounds in shallow groundwater in the Lower 
Susquehanna River basin, Pennsylvania and Maryland. USGS Water 
Resources Investigation Report. WRIR 96-4141. 8 pp. USGS.
    Daniel MA, Evans MA (1982). Quantitative comparison of maternal 
ethanol and maternal tertiary butanol diet on postnatal development. J. 
Pharmacol. Exp. Ther. 222(2): 294-300.
    Daniel RA (1995). Intrinsic Bioremediation of BTEX and MTBE: Field, 
Laboratory and Computer Modeling Studies. Graduate Thesis, Department 
of Civil Engineering, North Carolina State University (NCU). Raleigh, 
North Carolina: NCU.
    Daughtrey WC, Gill MW, Pritts IM, Douglas JF, Kneiss JJ, Andrews LS 
(1997). Neurotoxicological evaluation of methyl tertiary-butyl ether in 
rats. J. Appl. Toxicol. 17(S1): S57-S64. May.
    Davidson JM (1995). Fate and transport of MTBE--The latest data. 
In: Proceedings of the Petroleum Hydrocarbons and Organic Chemicals in 
Ground Water: Prevention, Detection, and Remediation Conference. pp. 
285-301. November 29-December 1. Houston, Texas. Dublin, Ohio: NGWA.
    Davidson JM, Parsons R (1996). Remediating MTBE with current and 
emerging technologies. In: Proceedings of the Petroleum Hydrocarbons 
and Organic Chemicals in Ground Water: Prevention, Detection, and 
Remediation Conference. pp. 15-29. November 13-25. Houston, Texas. 
Dublin, Ohio: NGWA.
    Day KJ, de Peyster A, Allgaier BS, Luong A, MacGregor JA (1998). 
Methyl t-butyl ether (MTBE) effects on the male rat reproductive 
endocrine axis [Abstract No. 861 presented at the 1998 Society of 
Toxicology Annual Meeting]. The Toxicologist 42(1-S): 174. March.
    Delzer GC, Zogorski JS, Lopes TJ (1997). Occurrence of the gasoline 
oxygenate MTBE and BTEX compounds in municipal stormwater in the United 
States, 1991-1995. Paper ENVR 100. In: Proceedings of the 213th 
American Chemical Society National Meeting, Division of Environmental 
Chemistry, Environmental Fate and Effects of Gasoline Oxygenates. April 
13-17. San Francisco, California. 37(1): 374-376.
    Denton J. Masur L (1996). California's cleaner burning gasoline and 
methyl tertiary-butyl ether [Abstract]. In: the Proceedings of the 
Society of Environmental Toxicology and Chemistry (SETAC) 17th Annual 
Meeting. p. 115. November 17-21. Washington, D.C.
    DHS (1998). Notice of Proposed Rulemaking. Revision of the 
Secondary Maximum Contaminant Level List, the Unregulated Chemical 
Monitoring Lists, and Associated Requirements for Drinking Water (R-44-
97). California Department of Health Services (DHS). July 3. 
Sacramento, California: DHS, Health and Welfare Agency, State of 
California.
    DHS (1997). Proposed Regulation for a Revision to the Secondary MCL 
List and Revisions to Unregulated Chemical Monitoring List and 
Associated Requirements for Drinking Water. Division of Drinking Water 
Environmental Management. October and December. Sacramento, California: 
DHS, Health and Welfare Agency, State of California.
    DHS (1985). Guidelines for Chemical Carcinogen Risk Assessments and 
Their Scientific Rationale. Sacramento, California: DHS, Health and 
Welfare Agency, State of California.
    Diaz, D, Bories P. Ampelas M, Larrey D, Michel H (1992). Methyl 
tert-butyl ether in the endoscopic treatment of common bile duct 
radiolucent stones in elderly patients with nasobiliary tube. Digest. 
Dis. Sci. 37:97-100.
    Dodd DE, Kintigh WJ (1989). Methyl tertiary butyl ether (MTBE) 
repeated 13-week vapor inhalation study in rats with neurotoxicity 
evaluation. Bushy Run Research Center Project Report 52-507. Final 
Report submitted to the U.S. EPA with cover letter dated September 27, 
1989 with draft submitted dated August 11, 1989. TSCATS/403186. EPA/OTS 
#40-8913440. No. FYI-OTS-0889-0689. WPA/PTS #FYI-OTS-0889-0689. Export, 
Pennsylvania: Bushy Run Research Center.
    Dourson ML, Felter SP (1997). Route-to-route extrapolation of the 
toxic potency of MTBE. Risk Anal. 17(6): 717-725. December.
    Drew RT (1995). Misunderstand MTBE. Letter to the Editor. Environ. 
Hlth. Perspect. 103(5): 420. May.
    DTSC (1994). CalToxTM, A Multimedia Total Exposure Model 
for Hazardous Waste Sites. Spreadsheet User's Guide. Version 1.5. 
Prepared by the University of California, Davis, in corporation with 
Lawrence Livermore National Laboratory for the Department of Toxic 
Substances Control, California Environmental Protection Agency. 
Sacramento, California: DTSC, Cal/EPA.
    Du JT, Abernathy CO, Donohue J. Mahfouz A, Khanna K (1998). 
Provisional health and consumer acceptability advisory for methyl t-
butyl ether (MTBE) [Abstract no. 1123 presented at the 1998 Society of 
Toxicology Annual Meeting]. The Toxicologist 42(1-S): 228. March.
    Duffy JS, Del Pup JA, Kneiss JJ (1992). Toxicological evaluation of 
methyl tertiary-butyl ether (MTBE): Testing performed under TSCA 
consent agreement. J. Soil Contam. 1(1): 29-37. and Hydrocarbon Contam. 
Soils 2: 757-765. Washington, D.C.: American Chemical Society.
    Duffy LK (1994). Oxyfuel in Alaska: Use of interleukins to monitor 
effects on the immune system. Sci. Total Environ. 151(3): 253-256. July 
18.
    ECETOC (1997). Methyl tert-Butyl Ether (MTBE) Health Risk 
Characterization. CAS No. 1634-04-4 (EINECS No. 216.653.1). June. 
European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC) 
Technical Report No. 72. Brussels, Belgium: ECETOC.
    EDF (1998). Methyl tert-butyl ether. In: The Environmental Defense 
Fund (EDF) Chemical Scorecard. It is protected by copyright. Available 
at: www.scorecard.org
    Edison SA, Maier M, Kohler B. Schlauch D, Buttmann A, Gauer E, 
Riemann JF (1993). Direct dissolution of gallstones with MTBE by 
endoscopic cannulation of the gallbladder. Am. J. Gastroenterol. 88(8): 
1242-1248.
    Environmental Canada (1993). Canadian Environmental Protection Act 
Priority Substances List Supporting Document, Methyl Tertiary Butyl 
Ether (MTBE). January. 28 pp. Ottawa, Canada: Canada Communication 
Group Publisher, Government of Canada.
    Environmental Canada (1992). Canadian Environmental Protection Act 
Priority Substances List Assessment Report No. 5, Methyl Tertiary Butyl 
Ether (MTBE). 19 pp. Ottawa, Canada: Canada Communication Group 
Publisher, Government of Canada.
    Erdal S. Gong H Jr., Linn WS, Rykowski R (1997). Projection of 
health benefits from ambient ozone reduction related to the use of 
methyl tertiary butyl ether (MTBE) in the reformulated gasoline 
program. Risk Anal. 17(6): 693-704. December.
    Ershow AG, Cantor KP (1989). Total Water and Tap Water Intake in 
the United States: Population Based Estimates of Quantities and 
Sources. Life Sciences Research Office, Federation of American 
Societies for Experimental Biology (FASEB). Baltimore, Maryland: FASEB.
    Experimental Pathology Laboratories, Inc. (1993). Histopathologic 
Evaluation of Kidneys from Male and Female Rats Utilized on a Vapor 
Inhalation Oncogenicity Study of Methyl Tertiary Butyl Ether. Pathology 
Slide Peer-Review Report. MTBE Task Force Study Number 91N0013B. 
Submitted to Methyl Tertiary Butyl Ether Task Force organized by the 
Oxygenated Fuels Association, Inc. Washington, D.C.: MTBE Task Force, 
OFA.
    Farland WH (1990). Memorandum on Drinking Water Quantification of 
Toxicologic Effects (QTE) for MTBE. Final Draft. ECAO-CIN-DO23. Office 
of Health and Environmental Assessment, U.S. Environmental Protection 
Agency. Washington, D.C.: U.S. EPA.
    Farr J. Apostolakis G. Collins M, Crouch III RC, Fogg G. Reinhard 
M, Scow K (1996). Senate Bill 1764 Advisory Committee Recommendations 
Report Regarding California's Underground Storage Tank (UST) Program. 
May 31. Submitted to the California State Water Resources Control Board 
(SWRCB). Sacramento, California: SWRCB.
    Faulkner TP, Wiechart JD, Hartman DM, Hussain AS (1989). The 
effects of prenatal tertiary butanol administration in CBA/J and C57BL/
6J mice. Life Sci. 45(21): 1989-95.
    Fenelon JM, Moore RC (1996). Occurrence of volatile organic 
compounds in groundwater in the White River basin, Indiana, 1994-1995. 
USGS Fact Sheet FS 138-96. 4 pp. USGS.
    Fiedler N. Mohr SN, Kelly-McNeil K, Kipen HM (1994). Response of 
sensitive groups to methyl tertiary-butyl ether (MTBE). In: Proceedings 
of the 1993 Conference on MTBE and Other Oxygenates, pp. D65-D84. EPA/
600-R95-134. Inhalation Toxicol. 6 (6): 539-552. November-December.
    Freed CN (1997). EPA fuel programs. Paper ENVR 95. In: Proceedings 
of the 213th American Chemical Society National Meeting, Division of 
Environmental Chemistry, Environmental Fate and Effects of Gasoline 
Oxygenates. April 13-17. San Francisco, California. 37(1): 366-368.
    Froines JR, Collins M, Fanning E, McConnell R, Robbins W, Silver K, 
Kun H, Mutialu R. Okoji R. Taber R, Tareen N. Zandonella C (1998). An 
evaluation of the scientific peer-reviewed research and literature on 
the human health effects of MTBE, its metabolites, combustion products 
and substitute compounds. In: Health and Environmental Assessment of 
MTBE. Report to the Governor and Legislature of the State of California 
as Sponsored by SB 521. Volume II: Human Health Effects. 267 pp. 
Submitted through the University of California Toxic Substances 
Research and Teaching Program SB521 MTBE Research Program. November 12. 
Davis, California. Available at: http://tsrtp.ucdavis.edu/mtberpt/
    Froines JR (1998). SB521 MTBE research by UCLA: An evaluation of 
the peer-reviewed research literature on the human health, including 
asthma, and environmental effects of MTBE. Abstract presented at the 
University of California Toxic Substances Research and Teaching Program 
SB521 MTBE Research Workshop. June 16. Davis, California. Available at: 
http://tsrtp.ucdavis.edu/mtbe/
    Fueta Y, Arashidani K, Katoh T, Fukata K, Kodama Y (1994). Effects 
of methyl tertiary-butyl ether on the central nervous system. Sangyo 
Igaku 36(1): 26-27.
    Fujita EM, Bowen JL, Green MC, Moosmuller H (1997). Southern 
California Ozone Study (SCOS97) Quality Assurance Plan. Report prepared 
for California Air Resources Board, Desert Research Institute, Reno, 
Nevada. April 4, 1997. Sacramento, California: ARB, Cal/EPA.
    Fujiwara U, Kinoshita T, Sato H, Kojima I (1984). Biodegradation 
and bioconcentration of alkyl ethers. Yukagaken 33: 111-114.
    Garnier AC, Harper JG, Angelosanto FA, Blackburn GR, Schreiner CA, 
Mackerer CR (1993). The metabolite formaldehyde is responsible for the 
mutagenicity of methyl tertiary butyl ether (MTBE) in the activated 
mouse lymphoma assay. 4 pp. Presented at the Annual Meeting of the 
Genetic Toxicology Association. October 21. Princeton, New Jersey: 
Mobil Oil Corp.
    Garrett P, Moreau M, Lowry JD (1986). MTBE as a groundwater 
contaminant. In: Proceedings of the NWWA-API Conference on Petroleum 
Hydrocarbons and Organic Chemicals in Ground Water--Prevention, 
Detection and Restoration. pp. 227-238. November 12-14. Houston, Texas. 
Dublin, Ohio: National Water Well Association (NWWA).
    Gilbert CE, Calabrese EJ (1992). Developing a standard for methyl 
tertiary-butyl ether in drinking water. In: Regulating Drinking Water 
Quality. pp. 231-252. Gilbert CE, Calabrese EJ eds. Ann Arbor, 
Michigan: Lewis Publishers, Inc.
    Goldsmith JR (1998). Vapor recovery systems can reduce risks from 
MTBE. Letter to the Editor. Environ. Hlth. Perspect. 106 (5): A220. 
May.
    Gomez-Taylor MM, Abernathy CO, Du JT (1997). Drinking water health 
advisory for methyl tertiary-butyl ether. Paper ENVR 98. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
370-372.
    Gordian ME, Huelsman MD, Brecht ML, Fisher DG (1995). Health 
effects of MTBE in gasoline in Alaska. Alaska Med. 37(3): 101-103, 119. 
July-September.
    Grady SJ (1997). Distribution of MTBE in groundwater in New England 
by aquifer and land use. In: Proceedings of the 213th American Chemical 
Society National Meeting, Division of Environmental Chemistry, 
Environmental Fate and Effects of Gasoline Oxygenates. April 13-17. San 
Francisco, California. 37(1): 392-394.
    Grant KA, Samson HH (1982). Ethanol and tertiary butanol induced 
microcephaly in the neonatal rat: Comparison of brain growth 
parameters. Neurobehav. Toxicol. Teratol. 4(3): 315-321.
    Greenough RJ, McDonald P, Robinson P, Cowie J, Maule W, Macnaughtan 
F, Rushton A (1980). MTBE (Driveron) 3-month inhalation toxicity in 
rats. Project No. 413038. Inveresk Research International. Unpublished 
report to Chemise Werke Hols AG, Marl, West Germany. Report No. 1596. 
230 pp. Edinburgh. As cited in the U.S. EPA's IRIS, MTBE, 1991. NTIS 
Publication No. NTIS/OTS 0513483.
    Grosjean E, Grosjean D, Gunawardena R. Rasmussen RA (1998). Ambient 
concentrations of ethanol and methyl tert-butyl ether (MTBE) in Porto 
Alegre, Brazil, March 1996-April 1997. Environ. Sci. Technol. 32(6): 
736-742. March 15.
    Gupta G, Lin YJ (1995). Toxicity of methyl tertiary butyl ether to 
Daphnia magna and Photobacterium phosphoreum. Bull. Environ. Contam. 
Toxicol. 55(4): 618-620. October.
    Hakkola M, Honkasalo ML, Pulkkinen P (1997). Changes in 
neuropsychological symptoms and moods among tanker drivers exposed to 
gasoline during a work week. Occup. Med. (Oxford, London, England) 
47(6): 344-348. August.
    Hakkola M, Honkasalo ML, Pulkkinen P (1996). Neuropsychological 
symptoms among tanker drivers exposed to gasoline. Occup. Med. (Oxford) 
46(2): 125-130. April.
    Hakkola M, Saarinen L (1996). Exposure of tanker drivers to 
gasoline and some of its components. Annals Occup. Hyg. 40(1): 1-10. 
February.
    Hakkola M (1994). Neuropsychological symptoms among tanker drivers 
with exposure to solvents. Occup. Med. (Oxford) 44(5): 243-246. 
December.
    Hall AH, Rumack BH, eds. (1998). TOMES PLUS System. Micromedex, 
Inc., Englewood, Colorado.
    Happel AM, Beckenbach EH, Halden RU (1998). An Evaluation of MTBE 
Impacts to California Groundwater Resources. UCRL-AR-130897. Report 
submitted to the California State Water Resources Control Board, 
Underground Storage Tank Program, Department of Energy, Office of 
Fossil Fuels, and Western States Petroleum Association. Livermore, 
California: Environmental Restoration Division, Environmental 
Protection Department, Lawrence Livermore National Laboratory (LLNL), 
University of California (UC).
    Hartle R (1993). Exposure to methyl tertiary-butyl ether and 
benzene among service station attendants and operators. Environ. Hlth. 
Perspect. 101(S6): 23-26. December.
    Hartley WR, Englande SJ Jr. (1992). Health risk assessment of the 
migration of unleaded gasoline--a model for petroleum products. Water 
Sci. Technol. 25(3): 65-72.
    Haseman JK, Arnold J. (1990). Tumor incidence in Fischer 344 rats: 
NTP historical data. In: Pathology of the Fischer Rat. Boorman GA, 
Eustis SL, Elwell MR, Montgomery CA Jr, MacKenzie WF eds. pp. 555-564. 
San Diego, California: Academic Press.
    Hattis D, Tuler S. Finkelstein L, Luo Z-Q (1986). A 
Pharmacokinetic/Mechanism-based Analysis of the Carcinogenic Risk of 
Perchloroethylene. Center for Technology, Policy and Industrial 
Development, Massachusetts Institute of Technology (MIT). Cambridge, 
Massachusetts: MIT.
    Hellstern A, Leuschner U, Benjaminov A, Ackermann H, Heine T, Festi 
D, Orsini M, Roda E, Northfield TC, Jazrawi R, Kurtz W. Schmeck-
Lindenau HJ, Stumpf J, Eidsvoll BE, Asdland E, Lux G, Boehnke E, Wurbs 
D, Delhaye M, Cremer M, Sinn I, Horing E, von Gaisberg U, Neubrand M, 
Paul F (1998). Dissolution of gallbladder stones with methyl tert-butyl 
ether and stone recurrence: A European survey. Digest. Dis. Sci. 43(5): 
911-920. May.
    HEI (1996). The Potential Health Effects of Oxygenates Added to 
Gasoline: A Review of the Current Literature. April. A special report 
of the Health Effect Institute's Oxygenates Evaluation Committee. 
Cambridge, Massachusetts: Health Effects Institute (HEI). Available at: 
http://www.healtheffects.org/oxysum.htm
    Hiremath CB, Parker JC (1994). Methyl tertiary butyl ether: cancer 
risk assessment issues (U.S. EPA, Office of Research and Development, 
Office of Health and Environmental Assessment). 25 pp. [Abstract No. 
540 presented at the 1994 Society of Toxicology Annual Meeting]. The 
Toxicologist 14(1): 152. March.
    Hoel DG, Walburg HE (1972). Statistical analysis of survival 
experiments. J. Natl. Cancer Inst. 49: 361-372.
    Hoffert SP (1998). Haze of uncertainty surrounds gas additive, 
lawmakers look to scientists for answers. The Scientist 12(13): 1 and 
7.
    Hofmann AF, Amelsberg A, Esch O. Schteingart CD, Lyche K, Jinich H, 
Vansonnenberg E, D'Agostino HB (1997). Successful topical dissolution 
of cholesterol gallbladder stones using ethyl propionate. Digest. Dis. 
Sci. 42(6): 1274-1282. June.
    Hong JY, Wang YY, Bondoc FY, Yang CS, Lee M, Huang WQ (1997a). Rat 
olfactory mucosa displays a high activity in metabolizing methyl tert-
butyl ether and other gasoline ethers. Fund. Appl. Toxicol. 40(2): 205-
210. December.
    Hong JY, Yang CS, Lee M, Wang YY, Huang WQ, Tan Y, Patten CJ, 
Bondoc FY (1997b). Role of cytochrome P450 in the metabolism 
of methyl tert-butyl ether in human livers. Arch. Toxicol. 71(4): 266-
269.
    Howard PH ed. (1993). Handbook of Environmental Fate and Exposure 
Data for Organic Chemicals. Volume IV. pp. 71-75. Ann Arbor, Michigan: 
Lewis Publishers, Inc.
    Howard PH, Boethling RS, Jarvis WF, Meylan WM, Michalenko EM 
(1991). Handbook of Environmental Degradation Rates. pp. 653-654. 
Chelsea, Michigan: Lewis Publishers, Inc.
    HSDB (1997). Hazardous Substances Data Bank (HSDB): t-Butyl Methyl 
Ether. Last revised on April 23, 1997. Bethesda, Maryland: National 
Library of Medicine (NLM), National Toxicology Program (NTP).
    Hubbard, CE, Barker JF, O'Hannesin SF, Vandegriendt M, Gillham RW 
(1994). Transport and fate of dissolved methanol, MTBE, and 
monoaromatic hydrocarbons in a shallow sand aquifer. API Publication 
4601, Appendix H. Ontario, Canada: Institute for Groundwater Research, 
University of Waterloo.
    Hutcheon DE, Arnold JD, ten Hove W, Boyle J III (1996). 
Disposition, metabolism and toxicity of methyl tertiary-butyl ether, an 
oxygenate for reformulated gasoline. J. Toxicol. Environ. Hlth. 47(5): 
453-464. April 5.
    IARC (1998a). IARC Monographs Working Group--Volume 73: Evaluation 
or Re-evaluation of Some Agents Which Target Specific Organs in Rodent 
Bioassays. Workshop, October 28, 1998, Lyon, France. Monograph in 
preparation, summary table available on IARC web site. Lyons, France: 
IARC, WHO. IARC website address: http://www.IARC.FR
    IARC (1998b). Species Differences in Thyroid, Kidney and Urinary 
Bladder Carcinogenesis. Consensus Report. Final Draft. In: Consensus 
Document. Proceedings of the IARC Workshop, November 3-7, 1997, Lyon, 
France. January 8. Lyons, France: IARC, WHO.
    IARC (1995). Formaldehyde. In: International Agency for Research on 
Cancer (IARC) monographs on the evaluation of carcinogenic risks to 
humans: wood dust and formaldehyde. 62: 217-362. Lyon, France: IARC, 
World Health Organization (WHO).
    IARC (1993). International Classification of Rodent Tumours. Part 
I--The Rat. 4. Hematopoietic system. Editor U. Mohr. IARC Scientific 
Publications No. 122, Lyon, France: IARC, World Health Organization 
(WHO).
    IARC (1987). Monographs on the Evaluation of the Carcinogenic Risk 
of Chemicals to Humans: An Updating of IARC Monographs Volumes I to 42, 
Supplement 7. Lyons, France: IARC, WHO.
    Imbriani M, Ghittori S. Pezzagno G (1997). Partition coefficients 
of methyl tert-butyl ether (MTBE). G. Ital. Med. Lav. Ergon. 
(Occupational Medicine, Pisa, Italy) 19(3): 63-65. July-September.
    IPCS (1997). International Programme on Chemical Safety (IPCS), 
Environmental Health Criteria (EHC), Methyl Tertiary-Butyl Ether. Task 
Group Draft. PCS/EHC/97. January. Final expected in December 1998 as 
EHC Series No. 206 Geneva, Switzerland: United Nations Environmental 
Programme (UNEP), International Labour Organization, WHO.
    Jeffrey D (1997). Physical-chemical properties of MTBE and 
preferred environmental fate and compartmentalization. Paper ENVR 209. 
In: Proceedings of the 213th American Chemical Society National 
Meeting, Division of Environmental Chemistry, Environmental Fate and 
Effects of Gasoline Oxygenates. April 13-17. San Francisco, California. 
37(1):397-399.
    Jensen HM, Arvin E (1990). Solubility and degradability of the 
gasoline additive MTBE and gasoline compounds in water. In: 
Contaminated Soils, 90: 445-448. Netherlands: Kluwer Academic 
Publishers.
    Jo WK, Park KH (1998). Exposure to carbon monoxide, methyl-tertiary 
butyl ether (MTBE), and benzene levels inside vehicles traveling on an 
urban area in Korea. J. Expo. Anal. Environ. Epidemiol. 8(2): 159-171.
    Johanson G. Nihlen A, Lof A (1995). Toxicokinetics and acute 
effects of MTBE and ETBE in male volunteers. Toxicol. Lett. (Shannon, 
Ireland) 82/83: 713-718. December.
    Johnson ML (1998). Exposure of humans to MTBE from drinking water. 
In: Health and Environmental Assessment of MTBE. Report to the Governor 
and Legislature of the State of California as Sponsored by SB 521. 
Volume V: Risk assessment, Exposure Assessment, Water Treatment and 
Cost-Benefit Analysis, Chapter 1. 11 pp. Submitted through the 
University of California Toxic Substances Research and Teaching Program 
SB521 MTBE Research Program. November 12. Davis, California. Available 
at: http://tsrtp.ucdavis.edu/mtberpt/
    Johnson WD, Findlay J. Boyne RA (1992). 28-day oral (gavage) 
toxicity study of methyl tert-butyl ether in rats. Prepared for Amoco. 
ITT Research Institute Project No. L08100. Chicago, Illinois: ITT 
Research Institute.
    Joseph P (1995). Illness due to methyl tertiary butyl ether. Letter 
to the Editor. Arch. Environ. Hlth. 50(5): 395-396. Available at: 
http://www.oxybusters.com/oxybustr.htm
    Juliani G, Gandini G, Gabasio S, Bonardi L, Fascetti E, Gremo L 
(1985). Colelitolisi chimica transcutanea con metil-ter-butil etere 
(MTBE). La Radiol. Med. 71: 569-574.
    Kado NY, Kuzmicky PA, Loarca-Pina G. Mumtaz MM (1998). Genotoxicity 
testing of methyl tertiary-butyl ether (MTBE) in the Salmonella 
microsuspension assay and mouse bone marrow micronucleus test. Mutation 
Res. 412(2): 131-138. January.
    Katoh T, Arashidani K, Kikuchi M, Yoshikawa M, Kodama Y (1993). 
Effects of methyl tertiary-butyl ether on hepatic lipid peroxidation in 
mice. Nippon Eiseigaku Zasshi (Japan) 48(4): 873-878. October.
    Kerns KD, Pavkov KL, Donofrio DJ, Gralla EJ, Swenberg JA (1983). 
Carcinogenicity of formaldehyde in rats and mice after long-term 
inhalation exposure. Cancer Res. 43: 4382-4392.
    Killian W (1998). Oxyfuel advertisement offends readers. Letter to 
the Editor. J. Am. Water Works Assoc. 90(2): 4-4. February.
    Kirschner EM (1996). Growth of top 50 chemicals slowed in 1995 from 
very high 1994 rate. C&EN (Chemical and Engineering News) 74(15): 16-
22. April 8.
    Klan MJ, Carpenter MJ (1994). A risk-based drinking water 
concentration for methyl tertiary-butyl ether (MTBE). U.S. EPA. In: 
Proceedings of the Petroleum Hydrocarbons and Organic Chemicals in 
Ground Water: Prevention, Detection and Remediation Conference. pp. 
107-115. November 2-4. Houston, Texas. Dublin, Ohio: National Water 
Well Association.
    Klan MJ, Johnson W. Hatoum NS, Yermakoff JK (1992). 28-day oral 
(gavage) toxicity study of methyl tert-butyl ether (MTBE) in rats 
[Abstract No. 382 presented at the 1992 Society of Toxicology Annual 
Meeting]. The Toxicologist 12(1): 117. February.
    Kneiss J (1995). MTBE--the headache of clean air. Environ. Hlth. 
Perspect. 103(7-8): 666-670. July-August.
    Koenigsberg S (1997). MTBE: Wild card in groundwater cleanup. 
Environ. Protection 8(11): 26-28. November.
    Landmeyer JE, Chapelle FH, Bradley PM, Pankow JF, Church CD, 
Tratnyek PG (1998). Fate of MTBE relative to benzene in a gasoline-
contaminated aquifer (1993-98). 37 pp. In: Ground Water Monitoring & 
Remediation. Accepted April 17. In press.
    Landmeyer JE, Pankow JF, Church CD (1997). Occurrence of MTBE and 
tert-butyl alcohol in a gasoline-contaminated aquifer. Paper ENVR 228. 
In: Proceedings of the 213th American Chemical Society National 
Meeting, Division of Environmental Chemistry, Environmental Fate and 
Effects of Gasoline Oxygenates. April 13-17. San Francisco, California. 
37(1): 413-415.
    Lapham WW, Neitzert KM, Moran MM, Zogorski JS (1997). USGS compiles 
data set for national assessment of VOCs in groundwater. Ground Water 
Monitoring & Remediation. XVII(4): 147-157. Fall.
    Lee LC, Quintana PJE, de Peyster A (1998). Comet assay evaluation 
of the effect of methyl t-butyl ether (MTBE) on rat lymphocytes 
[Abstract No. 923 presented at the 1998 Society of Toxicology Annual 
Meeting]. The Toxicologist 42(1-S): 187. March.
    Lee CW, Weisel CP (1998). Determination of methyl tert-butyl ether 
and tert-butyl alcohol in human urine by high-temperature purge-and-
trap gas chromatography-mass spectrometry. J. Analyt. Toxicol. 22(1): 
1-5. January/February.
    Leuschner U. Hellstern A, Ansell A, Gatzen M, Guldutuna S. 
Leuschner M (1994). Manual and automatic gallstone dissolution with 
methyl tert-butyl ether. Digest. Dis. Sci. 39(6): 1302-1308. June.
    Life Science Research Roma Toxicology Centre S.P.A. (1989a). 
Reverse mutation in Salmonella typhimurium, test substance: MTBE. 
Report No. 216001-M-03489. Rome, Italy: Roma Toxicology Centre S.P.A.
    Life Science Research Roma Toxicology Centre S.P.A. (1989b). Gene 
mutation in Chinese hamster V79 cells, test substance: MTBE. Report No. 
216002-M-03589. Rome, Italy: Roma Toxicology Centre S.P.A.
    Life Science Research Roma Toxicology Centre S.P.A. (1989c). 
Unscheduled DNA synthesis (UDS) in primary rat hepatocytes 
(autoradiographic method), test substance: MTBE. Report No. 216003-M-
03689. Rome, Italy: Roma Toxicology Centre S.P.A.
    Lin XZ, Chou TC, Lin PW, Chow YL, Li CC, Chen SK (1994). Chemical 
dissolution of gallstones in Taiwan: An in vitro study. J. 
Gastroenterol. Hepatol. 9(2): 143-147.
    Lince DP, Wilson LR, Carlson GA (1998). Methyl tert-butyl ether 
(MTBE) contamination in private wells near gasoline stations in upstate 
New York. Bull. Environ. Contam. Toxicol. 61 (4): 484-488.
    Lindsey BD, Breen KJ, Daly MH (1997). MTBE in water from fractured-
bedrock aquifers, southcentral Pennsylvania. Paper ENVR 210. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
399-400.
    Lindstrom SB, Pleil JD (1996). Alveolar breath sampling and 
analysis to exposures to methyl tertiary-butyl ether (MTBE) during 
motor vehicle refueling. J. Air Waste Manag. Assoc. 46: 676-682. July.
    Lington AW, Dodd DE, Ridlon SA, Douglas JF, Kneiss JJ, Andrew LS 
(1997). Evaluation of 13-week inhalation toxicity study on methyl t-
butyl ether (MTBE) in Fischer 344 rats. J. Appl. Toxicol. 17(SI): S37-
S44. May.
    Little CJ, Dale AD, Whatley JA (1979). Methyl tert-butyl ether: A 
new chromatographic effluent. J. Chromatogr. 169: 381-385.
    Livo KB (1995). Overview of public's perspective of health effects 
from oxyfuels in Colorado. Presented at the HEI Workshop on Acute 
Health Effects on Oxygenates and Oxygenated Gasolines. July 27. 
Chicago, Illinois.
    Long G, Meek ME, Savard S (1994). Methyl tertiary-butyl ether 
(MTBE): Evaluation of risks to health from environmental exposure in 
Canada. J. Environ. Sci. Hlth., Part C, Environ. Carcinog. Ecotoxicol. 
Rev. C12(2): 389-395.
    Lucier G, Genter MB, Lao YJ, Stopford W, Starr T (1995). Summary of 
the carcinogenicity assessment of MTBE conducted by the Secretary's 
Scientific Advisory Board on Toxic Air Pollutants. Report to the North 
Carolina Department of Environment, Health, and Natural Resources. 
Environ. Hlth. Perspect. 103(5): 420-422. May.
    MacGregor JA, Richter WR, Magaw RI (1993). Uterine changes in 
female mice following lifetime inhalation of wholly vaporized unleaded 
gasoline: A possible relationship to liver tumors? Am. Coll. Toxicol. 
12: 119-126.
    Mackay D, Shiu WY, Ma KC (1993). Illustrated Handbook of Physical-
Chemical Properties and Environmental Fate for Organic Chemicals. V. 
III. Volatile Organic Chemicals. p. 756. Chelsea, Michigan: Lewis 
Publishers.
    Mackerer CR, Angelosanto FA, Blackburn GR, Schreiner CA (1996). 
Identification of formaldehyde as the metabolite responsible for the 
mutagenicity of methyl tertiary-butyl ether in the activated mouse 
lymphoma assay. Proc. Soc. Exp. Biol. Med. 212(4): 338-341. September.
    Mancini ER (1997). Aquatic toxicity data for methyl tertiary-butyl 
ether (MTBE): Current status, future research. Paper ENVR 245. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1):427-
429.
    Mantel N (1966). Evaluation of survival data on two new rank order 
statistics arising in its consideration. Cancer Chemother. Rep. 50: 
163-170.
    MCCHD (1993). Oxygenated Fuel Data Collection: Missoula Physician 
Screening. Missoula, Montana: Missoula City-County Health Department 
(MCCHD).
    McClurg S (1998). The challenge of MTBE: clean air vs. clean water? 
Western Water July/August: 4-13.
    McConnell R. Taber R (1998). Acute effects of exposure to methyl 
tert-butyl ether in gasoline. West. J. Med. 169(6): 375. December.
    McCoy M Jr, Abernethy J. Johnson T (1995). Anecdotal Health-Related 
Complaint Data Pertaining to Possible Exposures to MTBE: 1993 and 1994 
Follow-up Survey (1984-1994). API Publication 4623. Washington, D.C.: 
API.
    McGregor DB, Brown A, Cattanach P, Edwards I, McBride D, Caspony WJ 
(1988). Responses of the LS178y tk+/tk- mouse 
lymphoma cell forward mutation assay. II: 18 coded chemicals. Environ. 
Mol. Mutagen. 11: 91-118.
    McKee RH, Vergnes JS, Galvin JB, Douglas JF, Kneiss JJ, Andrews LS 
(1997). Assessment of the in vivo mutagenic potential of methyl 
tertiary-butyl ether. J. Appl. Toxicol. 17(S1): S31-S36. May.
    McKinnon RJ, Dyksen JE (1984). Removing organics from groundwater 
through aeration plus GAC. J. Am. Water Works Assoc. 76: 42-47. May.
    Medlin J (1995). MTBE: The headache of clean air. Environ. Hlth. 
Perspect. 103: 666-670. July-August.
    Mehlman MA (1998a). Human health effects from exposure to gasoline 
containing methyl tertiary butyl ether (MTBE). Eur. J. Oncol. 3(3): 
171-189.
    Mehlman MA (1998b). Concluding remarks on the hazards of MTBE in 
gasoline. Eur. J. Oncol. 3(3): 207-208.
    Mehlman MA (1998c). Pollution by gasoline containing hazardous 
methyl tertiary butyl ether (MTBE). [Editorial] Arch. Environ. Hlth. 
53(4): 245-246.
    Mehlman MA (1998d). Dangerous and cancer-causing properties of 
products and chemicals in the oil-refining and petrochemical industry: 
Part XXV, neurotoxic, allergic, and respiratory effects in humans from 
water and air contaminated by methyl tertiary butyl ether in gasoline. 
J. Clean Technol., Environ. Toxicol. & Occup. Med. 7(1): 65-87.
    Mehlman MA (1996). Dangerous and cancer-causing properties of 
products and chemicals in the oil-refining and petrochemical industry: 
Part XXII, health hazards from exposure to gasoline containing methyl 
tertiary butyl ether, study of New Jersey residents. Toxicol. Ind. 
Hlth. 12(5): 613-627. September-October.
    Mehlman MA (1995). Dangerous and cancer-causing properties of 
products and chemicals in the oil-refining and petrochemical industry: 
Part XV, health hazards and health risks from oxygenated automobile 
fuels (MTBE), lessons not heeded. Int. J. Occup. Med. Toxicol. 4(2): 
219-236.
    Mennear JH (1997a). Carcinogenicity studies on Methyl tertiary 
butyl ether (MTBE): Critical review and interpretation. Risk Anal. 
17(6): 673-681. December.
    Mennear JH (1997b). Methyl tertiary butyl ether (MTBE) 
carcinogenesis: Hazard identification and safety assessment. Toxicol. 
Ecotoxicol. News (TEN) 4(5): 139-147.
    Mennear JH (1995). MTBE: Not carcinogenic. Letter to the Editor. 
Environ. Hlth. Perspect. 103(11): 985-986. November.
    Merck (1989). The Merck Index: An encyclopedia of Chemicals, Drugs, 
and Biologicals. 11th ed. Budavari S, O'Neil MJ, Smith A, Heckelman PE, 
eds. Rahway, New Jersey: Merck & Co., Inc.
    Miller MJ, Ferdinandi ES, Klan M, Andrews LS, Douglas JF, Kneiss JJ 
(1997). Pharmacokinetics and disposition of methyl t-butyl ether in 
Fischer-344 rats. J. Appl. Toxicol. 17(S1): S3-S12. May.
    Mohr S. Fiedler N. Weisel C, Kelly McNeil K (1994). Health effects 
of MTBE among New Jersey garage workers. Inhalation Toxicol. 6(6): 553-
562. November-December.
    Moolenaar RL, Hefflin BJ, Ashley DL, Middaugh JP, Etzel RA (1997). 
Blood benzene concentrations in workers exposed to oxygenated fuel in 
Fairbanks, Alaska. Int. Arch. Occup. Environ. Hlth. 69(2): 139-143.
    Moolenaar RL, Hefflin BJ, Ashley DL, Middaugh JP, Etzel RA (1994). 
MTBE in human blood after exposure to oxygenated fuel in Fairbanks, 
Alaska. Arch. Environ. Hlth. 49(5): 402-409. September-October.
    Mordechai E, Vojdani A, Magtoto L, Choppa PC, Brautbar N (1997). 
Induction of apoptosis in individuals exposed to methyl tertiary butyl 
ether (MTBE) [Abstract No. 1727 presented at the 1997 Society of 
Toxicology Annual Meeting]. The Toxicologist 36(1, Pt. 2): 340. March.
    Mormile MR, Liu S. Suflita JM (1994). Anaerobic biodegradation of 
gasoline oxygenates: Extrapolation of information to multiple sites and 
redox conditions. Environ. Sci. Technol. 28(9): 1727-1732. September.
    MORS (1995). Justification for Decreasing the ORS Guideline for 
MTBE in Drinking Water from 0.7 mg/L to 0.07 mg/L. Office of Research 
and Standards (ORS), Department of Environmental Protection, the 
Commonwealth of Massachusetts. Boston, Massachusetts: MORS.
    Moser GJ, Wolf DC, Sar M, Gaido KW, Janszen D, Goldsworthy TL 
(1998). Methyl tertiary butyl ether-induced endocrine alterations in 
mice are not mediated through the estrogen receptor. Toxicol. Sci. 
(formerly Fund. Appl. Toxicol.) 41(1): 77-87. January.
    Moser GJ, Wong BA, Wolf DC, Fransson-Steen RL, Goldsworthy TL 
(1996a). Methyl tertiary butyl ether lacks tumor-promoting activity in 
N-nitro-sodiethylamine-initiated B6C3F1 female mouse liver. 
Carcinogenesis 17(12): 2753-2761. December.
    Moser GJ, Wong BA, Wolf DC, Moss OR, Goldsworthy TL (1996b). 
Comparative short-term effects of methyl tertiary-butyl ether and 
unleaded gasoline vapor in female B6C3F1 mice. Fundam. Appl. Toxicol. 
31(2): 173-183. June.
    Neeper-Bradley TL (1991). Two-generation reproduction study of 
inhaled methyl tert-butyl ether (MTBE) in CD Sprague-Dawley rats. Final 
Report. August 13. Bushy Run Research Center Project ID 53-594. 
Submitted to the U.S. EPA with cover letter dated August 16, 1991. EPA/
OTS #40-9113465. Export, Pennsylvania: Bushy Run Research Center.
    Nelson BK, Brightwell WS, Khan A, Burg JR, Goa PT (1989a). Lack of 
selective developmental toxicity of three Butanol isomers administered 
by inhalation to rats. Fundam. Appl. Toxicol. 12(3): 469-79.
    Nelson BK, Brightwell WS, Khan A, Kreig EFJ, Massari VJ (1989b). 
Behavioral teratology investigation of tertiary-butanol administered by 
inhalation to rats. Teratology 39(5): 504.
    Nihlen A, Lof A, Johanson G (1998a). Experimental exposure to 
methyl tertiary-butyl ether I. Toxicokinetics in humans. Toxicol. Appl. 
Pharmacol. 148(2): 274-280. February.
    Nihlen A, Walinder R, Lof A, Johanson G (1998b). Experimental 
exposure to methyl tertiary-butyl ether II. Acute effects in humans. 
Toxicol. Appl. Pharmacol. 148(2): 281-287. February.
    Nihlen A, Lof A, Johanson G (1997). Liquid/air partition 
coefficients of methyl and ethyl t-butyl ethers, t-amyl methyl ether, 
and t-butyl alcohol. J. Clean Technol., Environ. Toxicol., Occup. Med. 
6(2): 205-213.
    Nihlen A, Lof A, Johanson G (1995). Liquid/air partition 
coefficients of methyl and ethyl t-butyl ethers, t-amyl methyl ether, 
and t-butyl alcohol. J. Exposure Analyt. Environ. Epidemiol. 5(4): 573-
592.
    Nihlen A, Walinder R, Lof A, Johanson G (1994). Toxicokinetics and 
irritative effects of MTBE in man. Presented at the International 
Society for Environmental Epidemiology meeting. Durham, North Carolina.
    NJDWQI (1994). Maximum Contaminant Level Recommendations for 
Hazardous Contaminants in Drinking Water, Appendix A: Health-Based 
Maximum Contaminant Level Support Documents and Addenda. September 26. 
Newark, New Jersey: New Jersey Drinking Water Quality Institute 
(NJDWQI).
    NRC (1996). Toxicological and Performance Aspects of Oxygenated 
Motor Vehicle Fuels. 160 pp. Committee on Toxicological and Performance 
Aspects of Oxygenated Motor Vehicle Fuels, Board on Environmental 
Studies and Toxicology, Commission on Life Sciences, National Research 
Council (NRC), National Academy of Sciences (NAS). Washington, D.C.: 
National Academy Press.
    NSTC (1997). Interagency Assessment of Oxygenated Fuels. June. 
National Science and Technology Council (NSTC), Committee on 
Environment and Natural Resources (CENR) and Interagency Oxygenated 
Fuels Assessment Steering Committee. White House Office of Science and 
Technology Policy (OSTP) through the CENR of the Executive Office of 
the President. Washington, D.C.: NSTC. Available at: http://
www.whitehouse.gov/WH/EOP/OSTP/html/OSTP--Home.html
    NSTC (1996). Interagency Assessment of Potential Health Risks 
Associated with Oxygenated Gasoline. February. OSTP through the 
President's NSTC, CENR and Interagency Oxygenated Fuels Assessment 
Steering Committee. Washington, D.C.: NSTC.
    NTP (1998a). Summary of RG1, RG2 and NTP Board Subcommittee 
Recommendations for the Agents, Substances, Mixtures or Exposure 
Circumstances Reviewed in 1998 for Listing in or Delisting from the 
Report on Carcinogens, 9th Edition. December 4. National Toxicology 
Program (NTP) website: http://ntp-server.niebs.nih.gov/NewHomeRoc/
    NTP (1998b). National Toxicology Program January 1998 Update. 
National Toxicology Program (NTP), National Institute of Environmental 
Health Sciences (NIEHS), National Institutes of Health (NIH). Research 
Triangle Park, North Carolina: NTP. January.
    NTP (1997). Toxicology and carcinogenesis studies of isobutene (CAS 
No. 115-11-7) in Fischer 344/N rats and B6C3F1 mice (inhalation 
studies). Board Draft. National Toxicology Program Technical Report 
Series No. 487, NIH Publication No. 97-3977. NTP, NIEHS, NIH. Research 
Triangle Park, North Carolina: NTP.
    NTP (1995). Toxicology and carcinogenesis studies of t-butyl 
alcohol (CAS No. 76-65-0) in Fischer 344/N rats and B6C3F1 mice 
(drinking water studies). National Toxicology Program Technical Report 
Series No. 436, NIH Publication No. 94-3167. NTP, NIEHS, NIH. Research 
Triangle Park, North Carolina: NTP.
    Nyska A, Leininger JR, Maronpot RR, Haseman JK, Hailey JR (1998). 
Effect of individual versus group caging on the incidence of pituitary 
and Leydig cell tumors in F344 rats: proposed mechanism. Med. Hypoth. 
50: 525-529.
    O'Brien AK, Reiser RG, Gylling H (1997). Spatial Variability of 
Volatile Organic Compounds in Streams on Long Island, New York, and in 
New Jersey. USGS Fact Sheet FS-194-97. 6 pp. West Trenton, New Jersey: 
Department of Interior, USGS, NAWQA.
    OEHHA (1998a). Evidence on the Carcinogenicity of Methyl Tertiary 
Butyl Ether (MTBE). Public Review Draft. September. Berkeley, 
California: Office of Environmental Health Hazard Assessment (OEHHA), 
California Environmental Protection Agency.
    OEHHA (1998b). Evidence on the Developmental and Reproductive 
Toxicity of Methyl Tertiary Butyl Ether (MTBE). Public Review Draft. 
September. Berkeley, California: Office of Environmental Health Hazard 
Assessment (OEHHA), California Environmental Protection Agency.
    OEHHA (1996). Air Toxics Hot Spots Program Risk Assessment 
Guidelines. Part IV. Exposure Assessment and Stochastic Analysis. 
Public Review Draft. December. Berkeley, California: Office of 
Environmental Health Hazard Assessment (OEHHA), California 
Environmental Protection Agency.
    OEHHA (1991). MTBE Interim Action Level. February 19. Memorandum 
from the Pesticide and Environmental Toxicology Section (PETS), OEHHA 
to the Office of Drinking Water, DHS. Berkeley, California: PETS, 
OEHHA, DHS.
    Okahara N, de Peyster A, McPherson SE, MacGregor JA (1998). Effect 
of MTBE on estrogen-sensitive tissues of immature female CD-1 mice 
[Abstract No. 862 presented at the 1998 Society of Toxicology Annual 
Meeting]. The Toxicologist 42(1-S): 174-175. March.
    Pankow JF, Thomson NR, Johnson RL, Baehr AL, Zogorski JS (1997). 
The urban atmosphere as a non-point source for the transport of MTBE 
and other VOCs to shallow groundwater. Environ. Sci. Technol. 31(10): 
2821-2828.
    Patton A, Clementsen KL, Farahnak S. Drewry M, Ammon M, Arrieta D, 
Bevan AL, Charles T, Daniels D, Davis M, DiGiovanni D, Fortes F, 
Garrison R, Gebhart G, Jackson D, Kaiser S, Ray J, Rogow M, Rollins B, 
Smith DS, Tikannen M, Wilson D, Wolfe R (1999a). Report of the State 
Water Resources Control Board's Advisory Panel on Fueling and Refueling 
Practices at California Marinas. January. 34 pp. Sacramento, 
California: SWRCB.
    Patton A, Farahnak S, Drewry M, Anderson L, Arrieta D, Bravinder 
JL, Camille D, Gilson D, Hamilton C, Johnson B, Jones J, Sarrantis M, 
Smith J, Steck C, Tulloch C, Welge S, Westbrook P, White J, Winsor C, 
Young T, Zedrick D (1999b). Report of the State Water Resources Control 
Board's Advisory Panel on Leak History of New and Upgraded Underground 
Storage Tank Systems. January. 8 pp. Sacramento, California: SWRCB.
    Poet TS, Borghoff SJ (1998). Metabolism of methyl t-butyl ether in 
human liver microsomes [Abstract No. 464 presented at the 1998 Society 
of Toxicology Annual Meeting]. The Toxicologist 42(1-S): 94. March.
    Poet TS, Borghoff SJ (1997a). In vitro uptake of methyl tert-butyl 
ether (MTBE) in male rat kidney: Use of a two-compartment model to 
describe protein interactions. Toxicol. Appl. Pharmacol. 145(2): 340-
348. August.
    Poet TS, Borghoff SJ (1997b). Metabolism of methyl t-butyl ether in 
methyl tert-butyl ether (MTBE) in F-344 rats liver microsomes [Abstract 
No. 1717 presented at the 1997 Society of Toxicology Annual Meeting]. 
The Toxicologist 36(1, pt. 2): 338. March.
    Poet TS, Lalentine JL, Borghoff SJ (1997c). Pharmacokinetics of 
tertiary butyl alcohol in male and female Fischer 344 rats. Toxicol. 
Lett. 92: 179-186.
    Poet TS, Murphy JE, Borghoff SJ (1996). In vitro uptake of MTBE in 
male and female rat kidney homogenate: Solubility and protein 
interactions [Abstract No. 1563 presented et the 1996 Society of 
Toxicology Annual Meeting]. The Toxicologist 30(1, pt. 2): 305. March.
    Ponchon T, Baroud J, Pujol B, Valette PJ, Perrot D (1988). Renal 
failure during dissolution of gallstone by methyl tert-butyl ether. 
Letter to the Editor. Lancet 2: 276-277. July 30.
    Poore M, Chang B. Niyati F, Madden S (1997). Sampling and analysis 
of methyl t-butyl ether (MTBE) in ambient air at selected locations in 
California. Paper ENVR 215. In: Proceedings of the 213th American 
Chemical Society National Meeting, Division of Environmental Chemistry, 
Environmental Fate and Effects of Gasoline Oxygenates. April 13-17. San 
Francisco, California. 37(1): 407.
    Post G (1994). Methyl Tertiary Butyl Ether, Health-Based Maximum 
Contaminant Level Support Document. July. Division of Science and 
Research, New Jersey Department of Environmental Protection (NJDEP). 
Trenton, New Jersey: NJDEP.
    Prah JD, Goldstein GM, Devlin R. Otto D, Ashley D, House D, Cohen 
KL, Gerrity T (1994). Sensory, symptomatic, inflammatory, and ocular 
responses to and the metabolism of MTBE in a controlled human exposure 
experiment. Inhalation Toxicol. 6(6): 521-538. Erratum. (1995) 
Inhalation Toxicol. 7(4): 575.
    Prescott-Mathews JS, Wolf DC, Wong BA, Borghoff SJ (1997a). Methyl 
tert-butyl ether causes 2u-globulin nephropathy and 
enhanced renal cell proliferation in male F-344 rats. Toxicol. Appl. 
Pharmacol. 143(2): 301-314. April.
    Prescott-Mathews JS, Garrett MJ, Borghoff SJ (1997b). Chemical 
binding to 2u-globulin following gavage dosing of 
14C-methyl tert-Butyl Ether (MTBE) in F-344 rats [Abstract 
No. 1726 presented et the 1997 Society of Toxicology Annual Meeting]. 
The Toxicologist 36(1, pt. 2): 340. March.
    Prescott-Mathews JS, Wolf DC, Wong BA, Borghoff SJ (1996). MTBE-
induced protein droplet nephropathy and cell proliferation in male F-
344 rats [Abstract No. 1559 presented at the 1996 Society of Toxicology 
Annual Meeting]. The Toxicologist 30(1, pt. 2): 304. March.
    Raabe GK (1993). API Health Complaint Survey. EPA/600/R-95/134. In: 
Proceedings of the Conference on MTBE and Other Oxygenates: A Research 
Update. July 26-28. Falls Church, Virginia.
    Rao HV, Ginsberg GL (1997). A physiologically-based pharmacokinetic 
model assessment of methyl t-butyl ether in groundwater for a bathing 
and showering determination. Risk Anal. 17(5): 583-598. October.
    Rathbun RE (1998). Transport, Behavior, and Fate of Volatile 
Organic Compounds in Streams. U.S. Geological Survey (USGS) 
Professional Paper 1589. 151 pp. Washington, D.C.: U.S. Department of 
the Interior, USGS.
    Reese E, Kimbrough RD (1993). Acute toxicity of gasoline and some 
additives. Environ. Hlth. Perspect. 101(S6): 115-131.
    Reisch MS (1994). Top 50 chemicals production rose modestly in the 
U.S. C&EN 72: 12-15. April 8.
    Renner R (1999). Maine seeks to drop MTBE from its clean fuels 
program. Environ. Sci. Technol. 33(1): 9A-10A. January 1.
    Reynolds G (1998). Oxyfuel advertisement offends readers. Letter to 
the Editor. J. Am. Water Works Assoc. 90(2): 4-4.
    Robbins GA, Wang S. Stuart JD (1993). Using the static headspace 
method to determine Henry's Law Constants. Analyt. Chemistry 65(21): 
3113-3118.
    Robinson M, Bruner RH, Olson GR (1990). Fourteen- and ninety-day 
oral toxicity studies of methyl tertiary-butyl ether (MTBE) in Sprague-
Dawley rats. J. Am. Coll. Toxicol. 9(5): 525-540.
    Rousch JM, Sommerfeld MR (1998). Liquid-gas partitioning of the 
gasoline oxygenate methyl tert-butyl ether (MTBE) under laboratory 
conditions and its effect on growth of selected algae. Arch. Environ. 
Contam. Toxicol. 34(1): 6-11. January.
    Rowe BL, Landrigan SJ, Lopes TJ (1997). Summary of published 
aquatic toxicity information and water-quality criteria for selected 
volatile organic compounds. USGS Open-File Report. OFR 97-563. 60 pp. 
USGS.
    RTECS (1997). Registry of Toxic Effects of Chemical Substances 
(RTECS): Ether, Tert-Butyl Methyl. Last revision date: 1997. National 
Institute for Occupational Safety and Health (NIOSH). Cincinnati, Ohio: 
NIOSH.
    Rudo KM (1995). Methyl tertiary butyl ether (MTBE)--evaluation of 
MTBE carcinogenicity studies. Toxicol. Ind. Hlth. 11(2): 167-173. 
March-April.
    Saarinen L, Hakkola M, Pekari K, Lappapainen K, Aitio A (1998). 
Exposure of gasoline road-tanker drivers to methyl tert-butyl ether and 
methyl tert-amyl ether. Int. Arch. Occup. Environ. Hlth. 71(2): 143-
147. March.
    Savolainen H, Pfaffli P, Elovaara E (1985). Biochemical effects of 
methyl tertiary-butyl ether (MTBE) in extended vapor exposure in rats. 
Arch. Toxicol. 57(4): 285-288.
    SCDEM (1997). Groundwater Monitoring Report: Project Status, 
Quarterly Monitoring, and NPDES Report for July to September 1997. 
October. Fairfield, California: Solano County Department of 
Environmental Management (SCDEM).
    Scheible MH (1997). California's cleaner-burning gasoline 
regulations. Paper ENVR 96. In: Proceedings of the 213th American 
Chemical Society National Meeting, Division of Environmental Chemistry, 
Environmental Fate and Effects of Gasoline Oxygenates. April 13-17. San 
Francisco, California. 37(1): 368-369.
    Scholl HR, Seelig B, Thomas PE, Iba MM (1996). Methyl t-butyl ether 
(MTBE) induced central nervous system (CNS) depression: effects of 
metabolism of the compound [Abstract No. 122 presented at the 1996 
Society of Toxicology Annual Meeting]. The Toxicologist 30(1, Part 2): 
24. March.
    Schirmer M, Beker JF (1998). A study of long-term MTBE attenuation 
in the Borden aquifer, Ontario, Canada. Ground Water Monitoring and 
Remediation, Spring 1998: 113-122.
    Schremp G. Glaviano T, Nelson Y, Stoner S, Gopal J, Ganeriwal R, 
Tang C, Bemis G, Nix HD (1998). Supply and Cost of Alternatives to MTBE 
in Gasoline. October. P300-98-013. Sacramento, California: California 
Energy Commission, Energy Information and Analysis Division, Fuel 
Resources Office.
    Sellakumar AR, Snyder CA, Solomon JJ, Albert RE (1985). 
Carcinogenicity of formaldehyde and hydrogen chloride in rats. Toxicol. 
Appl. Pharmacol. 81: 401-406.
    Sernau RC (1989). Mutagenicity test on methyl tertiary butyl ether 
in Drosophila melanogaster sex-linked recessive lethal test. Final 
Report. HLA study no. 10484-0-461. Fiche # OYSO528039. Submitted to the 
U.S. Environmental Protection Agency with cover letter dated April 14, 
1989. EPA/OTS DOC#40-8913430. Kensington, Maryland: Hazelton 
Laboratories America, Inc.
    SFRWQCB (1998). Compilation of MTBE Contamination in Groundwater 
from 948 LUFT Sites in the Nine San Francisco Bay Area Counties. July 
13. Mandated to be updated every 3 months. Leaking Underground Fuel 
Tank Program, San Francisco Regional Water Quality Control Board 
(SFRWQCB). Oakland, California: SFRWQCB. Also available in KTVU, San 
Francisco, web site at: http://bayinsider.com/ktvu/newsroom/mtbe/
    Shaffer KL, Uchrin CG (1997). Uptake of methyl tertiary butyl ether 
(MTBE) by groundwater solids. Bull. Environ. Contam. Toxicol. 59(5): 
744-749. November.
    Shen YF, Yoo LY, Fitzsimmons SR, Yamamoto MK (1997). Threshold odor 
concentrations of MTBE and other fuel oxygenates. Paper ENVR 216. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
407-409.
    Siljeholm J (1997). A hazard ranking of organic contaminants in 
refinery effluents. Toxicol. Ind. Hlth. 13(4): 527-551. July-August.
    Sittig (1994). T-Butyl Methyl Ether. In: World-wide Limits for 
Toxic and Hazardous Chemicals in Air, Water and Soil. p. 135. Park 
Ridge, New Jersey: Noyes Publications.
    Sjoberg KR (1998). California's Drinking Water: State and Local 
Agencies Need to Provide Leadership to Address Contamination of 
Groundwater by Gasoline Components and Additives. December. Report 
Number 98112. Sacramento, California: California State Auditor, Bureau 
of State Audits. Available at: http://www.bsa.ca.gov/bsa/
    Smith SL, Duffy LK (1995). Odor and health complaints with Alaska 
gasolines. Chemical Hlth. Safety 32(3): 2-38.
    Smith AK, Kemp PA (1998). Maximum Contaminant Level for Methyl 
Tertiary Butyl Ether (MTBE). Technical Support Document. February 1. 
Environmental Toxicology Program, Bureau of Health. Augusta, Maine: 
Maine Department of Human Services.
    Soffritti M, Maltoni C, Maffei F, Biagi R (1989). Formaldehyde: an 
experimental multipotential carcinogen. Toxicol. Ind. Hlth. 5: 699-730.
    Sonawane B (1994). Assessment of potential developmental toxicity 
risk of methyl tertiary butyl ether (MTBE). Teratology 49: 388A. May.
    Spitzer HL (1997). An analysis of the health benefits associated 
with the use of MTBE reformulated gasoline and oxygenated fuels in 
reducing atmosphere concentrations of selected volatile organic 
compounds. Risk Anal. 17(6): 683-691. December.
    Squillace PJ, Pankow JF, Korte NE, Zogorski JS (1998). 
Environmental behavior and fate of methyl tert-butyl ether (MTBE). USGS 
Fact Sheet FS-203-96. Revised February 1998. 6 pp. Rapid City, South 
Dakota: Department of Interior, USGS, NAWQA.
    Squillace PJ, Pankow JF, Korte NE, Zogorski JS (1997a). Review of 
the environmental behavior and fate of methyl tert-butyl ether (MTBE). 
J. Environ. Toxicol. Chemistry 16(9): 1836-1844. September.
    Squillace PJ, Zorgorski JS, Wilber WG, Price CV (1997b). 
Preliminary assessment of the occurrence and possible sources of MTBE 
in groundwater in the United States, 1993-1994. Paper ENVR 99. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
372-374.
    Squillace PJ, Zorgorski JS, Wilber WG, Price CV (1996). Preliminary 
assessment of the occurrence and possible sources of MTBE in 
groundwater in the United States, 1993-1994. Environ. Sci. Technol. 
30(5): 1721-1730.
    Squillace PJ, Pope DA, Price CV (1995). Occurrence of the Gasoline 
Additive MTBE in Shallow Groundwater in Urban and Agricultural Areas. 
USGS Fact Sheet FS-114-95. 4 pp. Denver, Colorado: Department of 
Interior, USGS, NAWQA.
    Stackelberg PE, O'Brien AK, Terracciano SA (1997). Occurrence of 
MTBE in surface and groundwater, Long Island, New York, and New Jersey. 
Paper ENVR 208. In: Proceedings of the 213th American Chemical Society 
National Meeting, Division of Environmental Chemistry, Environmental 
Fate and Effects of Gasoline Oxygenates. April 13-17. San Francisco, 
California. 37(1): 394-397.
    Standeven AM, Blazer T. Goldsworthy TL (1994). Investigation of 
antiestrogenic properties of unleaded gasoline in female mice. Toxicol. 
Appl. Pharmacol. 127: 233-240.
    Steffan RJ, McClay K, Vainberg S. Condee CW, Zhang D (1997). 
Biodegradation of the gasoline oxygenates methyl tert-butyl ether 
(MTBE), ethyl tert butyl ether (ETBE), and tert-amyl methyl ether 
(TAME) by propane-oxidizing bacteria. Appl. Environ. Microbiol. 63(11): 
4216-4222. November.
    Stelljes ME (1997). Issues associated with the toxicological data 
on MTBE Paper ENVR 212. In: Proceedings of the 213th American Chemical 
Society National Meeting, Division of Environmental Chemistry, 
Environmental Fate and Effects of Gasoline Oxygenates. April 13-17. San 
Francisco, California. 37(1): 401-403.
    Stern BR, Kneiss JJ (1997). Methyl tertiary-butyl ether (MTBE): Use 
as an oxygenate in fuels. J. Appl. Toxicol. 17(S1): S1-S2. May.
    Stern BR, Tardiff RG (1997). Risk characterization of methyl 
tertiary butyl ether (MTBE) in tap water. Risk Anal. 17(6): 727-743.
    Stoneybrook Laboratories Inc. (1993). Activated mouse lymphoma 
(L5178Y/tk+/tk-) mutagenicity assay supplemented 
with formaldebyde dehyrogenase for methyl tertiary butyl ether. Status 
Report 65579. Princeton, New Jersey: Stoneybrook Laboratories Inc.
    Stubblefield WA, Burnett SL, Hockett JR, Naddy R, Mancini ER 
(1997). Evaluation of the acute and chronic aquatic toxicity of methyl 
tertiary-butyl ether (MTBE). Paper ENVR 246. In: Proceedings of the 
213th American Chemical Society National Meeting, Division of 
Environmental Chemistry, Environmental Fate and Effects of Gasoline 
Oxygenates. April 13-17. San Francisco, California. 37(1): 429-430.
    Swenberg JA, Dietrich DR (1991). Immunohistochemical localization 
of 2u-globulin in kidneys of treated and control 
rats of a 13-week vapor inhalation study undertaken with methyl 
tertiary butyl ether (MTBE). Report to John Kneiss, Manager, MTBE Task 
Force. July 26, 1991. Chapel Hill, North Carolina: University of North 
Carolina.
    Tardiff RG, Stern BR (1997). Estimating the risks and safety of 
methyl tertiary butyl ether (MTBE) and tertiary butyl alcohol (TBA) in 
tap water for exposures of varying duration. Paper ENVR 247. In: 
Proceedings of the 213th American Chemical Society National Meeting, 
Division of Environmental Chemistry, Environmental Fate and Effects of 
Gasoline Oxygenates. April 13-17. San Francisco, California. 37(1): 
430-432.
    Terracciano SA, O'Brien AK (1997). Occurrence of volatile organic 
compounds in streams on Long Island, New York, and New Jersey. USGS 
Fact Sheet. FS 063-97. 4 pp. Washington, D.C.: USGS.
    Thompson CB (1995). Apoptosis in the pathogenesis and treatment of 
disease. Science 267: 1456-1462.
    Til HP, Woutersen RA,. Feron VJ, Hollanders VMH, Falke HE (1989). 
Two-year drinking-water study for formaldehyde in rats. Food Chem. 
Toxicol. 27: 77-87.
    Tepper JS, Jackson MC, McGee JK, Costa DL, Graham JA (1994). 
Estimation of respiratory irritancy from inhaled MTBE in mice. 
Inhalation Toxicol. 6(6): 563-569.
    Turini A, Amato G. Longo V, Gervasi PG (1998). Oxidation of methyl- 
and ethyl-tertiary-butyl ethers in rat liver microsomes: Role of the 
cytochrome P450 isoforms. Arch. Toxicol. 72(4): 207-214. 
March.
    Tyl RW, Neeper-Bradley TL (1989). Developmental toxicity study of 
inhaled methyl tertiary butyl ether (MTBE) in CD-1 mice. Final Report. 
July 20. Bushy Run Research Center Report No. 51-266. Submitted to the 
U.S. EPA with cover letter dated July 26, 1989. TSCATS/403186. EPA/OTS 
#40-8913432. No. FYI-OTS-0889-0689. Export, Pennsylvania: Bushy Run 
Research Center.
    Tyl RW (1989). Developmental toxicity study of inhaled methyl 
tertiary butyl ether (MTBE) in New Zealand white rabbits. Final Report. 
May 12. Bushy Run Research Center Report No. 51-268. Submitted to the 
U.S. EPA with cover letter dated July 12, 1989. EPA/OTS #40-8913426. 
No. FYI-OTS-0889-0689. Export, Pennsylvania: Bushy Run Research Center.
    UC (1998). Health and Environmental Assessment of MTBE. Report to 
the Governor and Legislature of the State of California as Sponsored by 
SB 521. Five Volumes. 874 pp. Submitted through the University of 
California (UC) Toxic Substances Research and Teaching Program SB521 
MTBE Research Program. November 12. Davis, California: University of 
California. Available at: http://tsrtp.ucdavis.edu/mtberpt/
    U.S. EPA (1998a). Press Release: EPA Announces Blue-Ribbon Panel to 
Review Use of MTBE and Other Oxygenates in Gasoline. November 30 5 pp. 
EPA/R-159. U.S. Environmental Protection Agency (U.S. EPA). Washington, 
D.C.: U.S. EPA.
    U.S. EPA (1998b). Research Strategy for Oxygenates in Water. 
External Review Draft. April. 58 pp. EPA/600/R-98/048. National Center 
for Environmental Assessment, Office of Research and Development, U.S. 
EPA. April. Washington, D.C.: U.S. EPA.
    U.S. EPA (1998c). 63 FR 10274. 40 CFR Parts 141 and 142, 
Announcement of the Drinking Water Contaminant Candidate List; Notice. 
U.S. Environmental Protection Agency. Federal Register 63(40): 10274-
10287. Monday, March 2. Washington, D.C.: U.S. EPA.
    U.S. EPA (1997a). Drinking Water Advisory: Consumer Acceptability 
Advice and Health Effects Analysis on Methyl Tertiary-Butyl Ether 
(MTBE). December. Fact Sheet 4 pp. and Advisory 42 pp. EPA-822-F-97-
009. ODW 4304. Health and Ecological Criteria Division, Office of 
Science and Technology, Office of Water, U.S. Environmental Protection 
Agency. Washington, D.C.: U.S. EPA. Available at: http://www.epa.gov/
oust/mtbe/index.htm
    U.S. EPA (1997b). 62 FR 52193 40 CFR Parts 141 and 142, 
Announcement of the Draft Drinking Water Contaminant Candidate List; 
Notice. U.S. Environmental Protection Agency. Federal Register 62(128): 
52193-52219. Monday, October 6. Washington, D.C.: U.S. EPA.
    U.S. EPA (1997c). Integrated Risk Information System (IRIS): Methyl 
Tertiary-Butyl Ether (MTBE). Last revised on September 1, 1993 for 
Reference Concentration (RfC) assessment. U.S. Environmental Protection 
Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1997d). 40 CFR Parts 141 and 142, Drinking Water 
Monitoring Requirements for Certain Chemical Contaminants--Chemical 
Monitoring Reform (CMR) and Permanent Monitoring Relief (PMR); Proposed 
Rule. U.S. Environmental Protection Agency. Federal Register 62(128): 
36100-36136. Thursday, July 3. Washington, D.C.: U.S. EPA.
    U.S. EPA (1996a). Methyl-t-Butyl Ether (MTBE) Drinking Water Health 
Advisory (draft). December. Health and Ecological Criteria Division, 
Office of Science and Technology, Office of Water, U.S. Environmental 
Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1996b). 40 CFR Part 131, National Toxics Rule: Remand of 
Water Quality Criteria for Dioxin and Pentachlorophenol to EPA for 
Response to Comments--Response to Comments from American Forest and 
Paper Association on Two of the Exposure Assumptions Used by EPA in 
Developing the Human Health Water Quality Criteria for Dioxin and 
Pentachlorophenol. U.S. Environmental Protection Agency. Federal 
Register 61(239): 65183-65185. Wednesday, December 11. Washington, 
D.C.: U.S. EPA.
    U.S. EPA (1996c). Benchmark Dose Technical Guidance Document. 
August 6. External Review Draft. EPA/600/P-96/002A. Risk Assessment 
Forum, Office of Health and Environmental Assessment, U.S. 
Environmental Protection Agency. Washington, DC.: U.S. EPA.
    U.S. EPA (1996d). Fact Sheet on MTBE in Water. June. Office of 
Water, U.S. Environmental Protection Agency. Washington, D.C.: U.S. 
EPA.
    U.S. EPA (1996e). Questions and Answers Fact Sheet on MTBE in 
Water. June. Office of Water, U.S. Environmental Protection Agency. 
Washington, D.C.: U.S. EPA.
    U.S. EPA (1996f). 40 CFR Part 131, Proposed Guidelines for 
Carcinogen Risk Assessment. U.S. Environmental Protection Agency. 
Federal Register 61(79): 17959-18011. Wednesday, April 23. Washington, 
D.C.: U.S. EPA.
    U.S. EPA (1995a). Toxics Release Inventory. An online data base 
maintained by the U.S. EPA and accessible via TOXLINE. 1993 data 
accessed June 1995. Office of Toxic Substances Control, U.S. 
Environmental Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1995b). MTBE in Water. Draft. Draft by Evelyn Washington. 
August 1. Office of Ground Water and Drinking Water, U.S. Environmental 
Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1995c). Summary of cancer risk derivations for MTBE, a 
screening evaluation. Appendix A of the NSTC 1996 report. November 29. 
By J. Jinot. Quantitative Risk Methods Group, National Center for 
Environmental Assessment, U.S. Environmental Protection Agency. 
Washington, D.C.: U.S. EPA.
    U.S. EPA (1994a). Health Risk Perspectives on Fuel Oxygenates. EPA 
600/R-94/217. December. Office of Research and Development (ORD), U.S. 
Environmental Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1994b). Estimates of MTBE Exposures Related to 
Reformulated Gasoline. December 8. Environmental Criteria and 
Assessment Office, Office of Health and Environmental Assessment, U.S. 
Environmental Protection Agency. Research Triangle Park, North 
Carolina: U.S. EPA.
    U.S. EPA (1994c). Summary of Cancer Risk Derivatives for MTBE, A 
Screening Evaluation for Internal Consideration Related to Gasoline 
Oxygenates. December 2. Cancer Assessment Statistics and Epidemiology 
Branch, Office of Health and Environmental Assessment, U.S. 
Environmental Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1994d). Reproductive and Developmental Effects from 
Gasoline Vapors, A Screening Evaluation for Internal Consideration 
Related to Gasoline Oxygenates. November 7. Reproductive and 
Developmental Toxicology Branch, Office of Health and Environmental 
Assessment, U.S. Environmental Protection Agency. Washington, D.C.: 
U.S. EPA.
    U.S. EPA (1993). Assessment of Potential Health Risks of Gasoline 
Oxygenated with Methyl Tertiary-Butyl Ether(MTBE). EPA/600/R-93/206. 
NTISPB91-187583/XAB November. Office of Research and Development, U.S. 
Environmental Protection Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1992a). 40 CFR Parts 141 and 142, National Primary 
Drinking Water Regulations (NPDWR); Synthetic Organic Chemicals and 
Inorganic Chemicals, Final Rule. U.S. Environmental Protection Agency. 
Federal Register 57(138):31776-31849. Friday, July 17. Washington, 
D.C.: U.S. EPA.
    U.S. EPA (1992b). Draft Report: A Cross-Species Scaling Factor for 
Carcinogen Risk Assessment Based on Equivalence of mg/kg 3/4/Day. U.S. 
Environmental Protection Agency. Federal Register 57(109): 24152-24173. 
June 5. Washington, D.C.: U.S. EPA.
    U.S. EPA (1992c). Methyl t-Butyl Ether (MTBE) Drinking Water Health 
Advisory. January. Health and Ecological Criteria Division, Office of 
Science and Technology, Office of Water, U.S. Environmental Protection 
Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1991). 2u-globulin association with 
chemically-induced renal toxicity and neoplasia in the male rat. EPA/
625/3-91/019F. Risk Assessment Forum, U.S. Environmental Protection 
Agency. Washington, D.C.: U.S. EPA.
    U.S. EPA (1990). 40 CFR Parts 141, 142 and 143, National Primary 
and Secondary Drinking Water Regulations; Synthetic Organic Chemicals 
and Inorganic Chemicals, Proposed Rule. U.S. Environmental Protection 
Agency. Federal Register 55(143): 30370-30448. Wednesday, July 25. 
Washington, D.C.: U.S. EPA.
    U.S. EPA (1987a). Technical Support Document--MTBE. Prepared for 
Test Rules Development Branch, Existing Chemicals Assessment Division, 
U.S. Environmental Protection Agency. OTS Publication SRC RT-86-394. 
Washington, D.C.: U.S. EPA.
    U.S. EPA (1987b). Reference Dose (RfD): Description and use in 
health risk assessments. IRIS, Appendix A. Integrated risk information 
system documentation, vol. 1. U.S. Environmental Protection Agency. 
EPA/600/8-66/032a. Washington, D.C.: U.S. EPA.
    USGS (1996). Occurrence of the gasoline additive MTBE in shallow 
ground water in urban and agricultural areas. October. United States 
Geological Survey (USGS) Fact Sheet 114.95. Washington, D.C.: USGS. 
Available at: http://water.wr.usgs.gov/mtbe
    Vainiotalo S, Peltonen Y, Ruonakangas A, Pfaffli P (1999). Customer 
exposure to MTBE, TAME, C6 alkyl methyl ethers, and benzene during 
gasoline refueling. Environ. Hlth. Perspect. 107(2): 133-140. February.
    Vainiotalo S, Pekari K, Aitio A (1998). Exposure to methyl tert-
butyl ether and tert-amyl methyl ether from gasoline during tank lorry 
loading and its measurement using biological monitoring. Int. Arch. 
Occup. Environ. Hlth. 71: 391-396.
    Vergnes JS, Chun JS (1994). Methyl tertiary butyl ether: In vivo in 
vitro hepatocyte unscheduled DNA synthesis assay in mice. Bushy Run 
Research Center Laboratory project ID 93N 1316. Submitted to the U.S. 
EPA with cover letter dated June 13, 1994 with draft submitted dated 
October 15, 1993. EPA/OTS DOC#86940000975 and #86940000009. Export, 
Pennsylvania: Bushy Run Research Center.
    Vergnes JS, Kintigh WJ (1993). Methyl tertiary butyl ether: Bone 
marrow micronucleus test in mice. Bushy Run Research Center Laboratory 
project ID 93N1244. Submitted to the U.S. EPA with cover letter dated 
November 15, 1993. EPA/OTS#86940000031. Export, Pennsylvania: Bushy Run 
Research Center.
    Vergnes JS, Morabit ER (1989). Methyl tertiary butyl ether repeated 
exposure vapor inhalation study in rats: In vivo cytogenetic 
evaluation. Bushy Run Research Center Project report 51-635. Fiche 
#OTSO528040 Doc #40-8913431. Export, Pennsylvania: Bushy Run Research 
Center.
    Vojdani A, Brautbar N (1998). Contaminated drinking water with MTBE 
and gasoline: Immunological and cellular effects. Eur. J. Oncol. 3(3): 
191-199.
    Vojdani A, Mordechai E, Brautbar N (1997a). Abnormal apoptosis and 
cell cycle progression in humans exposed to methyl tertiary butyl ether 
and benzene contaminating water. Human Exp. Toxicol. 16(9): 485-494. 
September.
    Vojdani A, Namatalla G, Brautbar N (1997b). Methyl tertiary butyl 
ether antibodies among gasoline service station attendants. Annals N.Y. 
Acad. Sci. 837: 96-104. December 26.
    Von Burg R (1992). Toxicological update: Methyl tertiary butyl 
ether (MTBE). J. Appl. Toxicol. 12(1): 73-74.
    Ward Jr. JB, Au WW, Whorton EB, et al. (1994). Genetic toxicity of 
methyl-tertiary butyl ether. Division of Environmental Toxicology, 
Department of Preventive Medicine and Community Health. Galveston, 
Texas: University of Texas Medical Branch.
    Ward Jr. JB, Daiker DH, Hastings DA, Ammenheuser MM, Legator MS 
(1995). Assessment of the mutagenicity of methyl-tertiary butyl ether 
at the HPRT gene in CD-1 mice [Abstract No. 417 presented at the 1995 
Society of Toxicology Annual Meeting]. The Toxicologist 15: 79.
    WDOH (1995). Methyl Tert-Butyl Ether (MTBE). February. Wisconsin 
Division of Health (WDOH), Department of Natural Resources. Madison, 
Wisconsin: WDOH.
    Weil CS (1970). Significance of organ-weight changes in food safety 
evaluation. In: Metabolic Aspects of Food Safety. Roe FJ eds. pp. 419-
454. New York, New York: Academic Press.
    White MC, Johnson CA, Ashley DL, Buchta TM, Pelletier DJ (1995). 
Exposure to methyl tertiary-butyl ether from oxygenated gasoline in 
Stamford, Connecticut. Arch. Environ. Hlth. 50(3): 183-189. May-June.
    Wibowo AAE (1994). Methyl t-Butyl Ether: Health-Based Recommended 
Occupational Exposure Limit. Dutch Expert Committee on Occupational 
Standards: Werkgroep van Deskundigen ter Vaststeling van MAL-waarden. 
75 pp. Arbete. Och. Halsa, No. 22. 24 pp. Gezondheidsrad, Postbus 
90517, 2509 Lm Den Haag, Netherlands.
    Wiley K (1998). Clean air versus clean water: Does California need 
MTBE? California Senate position paper on MTBE. February. 15 pp. 
Sacramento, California: Senate Office of Research. Available at: http:/
/www.sen.ca.gov/ftp/sen/sor/environ/98mtbe.htm
    Woutersen RA, van Garderen-Hoetmer A, Bruijntjes JP, Swart A, Feron 
VJ (1989). Nasal tumors in rats after severe injury to the nasal mucosa 
and prolonged exposure to 10 ppm formaldehyde. J. Appl. Toxicol. 9: 39-
46.
    Wyngaarden JB (1986). New nonsurgical treatment removes gallstones. 
JAMA 256(13): 1692. October 3.
    Yoshikawa M, Arashidani K, Katoh T, Kawamoto T, Kodama Y (1994). 
Pulmonary elimination of methyl tertiary-butyl ether after 
intraperitoneal administration in mice. Arch. Toxicol. 68(8): 517-519.
    Young WF, Horth H, Crane R, Ogden T, Arnott M (1996). Taste and 
odour threshold concentrations of potential potable water contaminants. 
Water Res. 30(2): 331-340.
    Zakko SF, Scirica JC, Guttermuth MC, Dodge J, Hajjar JJ (1997). 
Ethyl propionate is more effective and less cytotoxic than methyl tert-
butyl ether for topical gallstone dissolution. Gastroenterology 113(1): 
232-237.
    Zeiger E, Anderson B, Haworth S, Lawlor T, Mortelmans K, Speck W 
(1987). Salmonella mutagenicity tests: III. Results from the testing of 
255 chemicals. Environ. Mutagen. 9(S9): 1-110.
    Zhang YP, Macina OT, Rosenkranz HS, Karol MH, Mattison DR, Klopman 
G (1997). Prediction of the metabolism and toxicological profiles of 
gasoline oxygenates. Inhalation Toxicol. 9(3): 237-254. April.
    Zielinska B, Shire J, Harshfield G, Pasek R (1997). Paper 97-
RP139.06. In: Proceedings of the 90th Annual Meeting of the Air and 
Waste Management Association (AWMA). June 8-13. Toronto, Canada.
    Zogorski JS, Delzer GC, Bender DA, Squillace PJ, Lopes TJ, Baehr 
AL, Stackelberg PE, Landmeyer JE, Boughton CJ, Lico MS, Pankow JF, 
Johnson RL, Thomson NR (1998). MTBE: Summary of findings and research 
by the U.S. Geological Survey. In: Proceedings of the 1998 Annual 
Conference of the American Water Works Association. 23 pp. Amherst, 
Massachusetts.
    Zogorski JS, Baehr AL, Bauman BJ, Conrad DL, Drew RT, Korte NE, 
Lapham WW, Morduchowitz A, Pankow JF, Washington ER (1997). Significant 
findings and water-quality recommendations of the Interagency 
Oxygenated Fuel Assessment. In: Proceedings of the 11th Conference on 
Contaminated Soils. pp. 661-679. Amherst, Massachusetts.
    Zogorski JS, Morduchowitz A, Baehr AL, Bauman BJ, Conrad DL, Drew 
RT, Korte NE, Lapham WW, Pankow JF, Washington ER (1996). Fuel 
Oxygenates and Water Quality: Current Understanding of Sources, 
Occurrence in Natural Waters, Environmental Behavior, Fate and 
Significance. Final Report. September. Prepared for Interagency 
Oxygenated Fuel Assessment as Chapter 2 of the NSTC 1997 final report, 
pp. 2-1--2-80. Coordinated by OSTP. Washington, D.C.: NSTC.
                                 ______
                                 
                         List of Abbreviations
AB--Assembly Bill
AL--Action Level
ACGIH--American Conference of Governmental Industrial Hygienists
API--American Petroleum Institute
ARB--California Air Resources Board
ATSDR--Agency for Toxic Substances and Disease Registry, USDHHS
AUC--area under the concentration-time curve
BAAQMD--Bay Area Air Quality Management District, San Francisco, 
    California
BIBRA--British Industrial Biological Research Association
BTEX--benzene, toluene, ethylbenzene, and xylenes
BUN--blood urea nitrogen
BW--body weight
CAAA--1990 U.S. Clean Air Act Amendments
Cal/EPA--California Environmental Protection Agency
CAS--Chemical Abstracts Service
CCL--Drinking Water Contaminant Candidate List, U.S. EPA
CCR--California Code of Regulations
CDC--Centers for Disease Control and Prevention, USDHHS
CFS--chronic fatigue syndrome
CENR--Committee on Environment and Natural Resources, White House OSTP
CHRIS--Chemical Hazard Response Information System, U.S. Coast Guard
CNS--central nervous system
CO--carbon monoxide
CSF--cancer slope factor, a cancer potency value derived from the lower 
    95 percent confidence bound on the dose associated with a 10 
    percent (0.1) increased risk of cancer (LED10) 
    calculated by the LMS model. CSF = 0.1/LED10.
CPF--cancer potency factor, cancer potency, carcinogenic potency, or 
    carcinogenic potency factor
DHS--California Department of Health Services
DOE--U.S. Department of Energy
DOT--U.S. Department of Transportation
DOT/UN/NA/IMCO--U.S. Department of Transportation/United Nations/North 
    America/International Maritime Dangerous Goods Code
DLR--detection limit for purposes of reporting
DWC--daily water consumption
DWEL--Drinking Water Equivalent Level
EBMUD--East Bay Municipal Utility District, California
ECETOC--European Centre for Ecotoxicology and Toxicology of Chemicals
EHS--Extremely Hazardous Substances, SARA Title III
EOHSI--Environmental and Occupational Health Sciences Institute, New 
    Jersey
ETBE--ethyl tertiary butyl ether
GAC--granulated activated charcoal
gd--gestation day
g/L--grams per liter
HA--Health Advisory
HAP--Hazardous Air Pollutant
HCHO--formaldehyde
HEI--Health Effects Institute, Boston, Massachusetts
HSDB--Hazardous Substances Data Bank, U.S. NLM
IARC--International Agency for Research on Cancer, WHO
i.p.--intraperitoneal
IPCS--International Programme on Chemical Safety, WHO
IRIS--Integrated Risk Information Systems, U.S. EPA
i.v.--intravenous
kg--kilograms
L--iter
LC50--lethal concentrations with 50 percent kill
LED50--lethal doses with 50 percent kill
LED10--lower 95 percent confidence bound on the dose 
    associated with a 10 percent increased risk of cancer
Leq/day--liter equivalent per day
LLNL--Lawrence Livermore National Laboratory, California
LMS--linearized multistage
LOAEL--lowest observed adverse effect level
LUFT--leaking underground fuel tank
MCCHD--Missoula City--County Health Department, Montana
MCL--Maximum Contaminant Level
MCLG--Maximum Contaminant Level Goal
mg/L--milligrams per liter
g/L--micrograms per liter
MCS--multiple chemical sensitivities
mL--milliliter
MOE--margin of exposure
MORS--Office of Research and Standards, Department of Environmental 
    Protection, the Commonwealth of Massachusetts
MRL--minimal risk levels
MTBE--methyl tertiary butyl ether
MTD--maximum tolerated close
MWDSC--Metropolitan Water District of Southern California
NAERG--North American Emergency Response Guidebook Documents, U.S., 
    Canada and Mexico
NAS--U.S. National Academy of Sciences
NAWQA--National Water-Quality Assessment, USGS
NCDEHNR--North Carolina Department of Environment, Health, and Natural 
    Resources
NCEH--National Center for Environmental Health, U.S. EPA
NCI--U.S. National Cancer Institute
ng--nanograms
NIEHS--U.S. National Institute of Environmental Health Sciences
NIOSH--U.S. National Institute for Occupational Safety and Health
NJDEP--New Jersey Department of Environmental Protection
NJHSFS--New Jersey Hazardous Substance Fact Sheets
NJDWQI--New Jersey Drinking Water Quality Institute
NLM--National Library of Medicine
NOAEL--no observable adverse effect levels
NOEL--no observable effect levels
NRC--National Research Council, U.S. NAS
NSTC--U.S. National Science and Technology Council
NTP--U.S. National Toxicology Program
OEHHA--Office of Environmental Health Hazard Assessment, Cal/EPA
OEL--Occupational Exposure Limit
OHM/TADS--Oil and Hazardous Materials/Technical Assistance Data System, 
    U.S. EPA
OSTP--White House Office of Science and Technology Policy
O3--ozone
oxyfuel--oxygenated gasoline
PBPK--physiologically-based pharmacokinetic
PHG--Public Health Goal
PHS --Public Health Service, USDHHS
pnd--postnatal day
POTW--publicly-owned treatment works
ppb--parts per billion
ppbv--ppb by volume
ppm--parts per million
ppt--parts per trillion
pptv--ppt by volume
Proposition 65--California Safe Drinking Water and Toxic Enforcement 
    Act of 1986
q1*--a cancer potency value that is the upper 95 percent 
    confidence limit of the low dose extrapolation on cancer potency 
    slope calculated by the LMS model
RfC--Reference Concentration
RfD--Reference Dose
RFG--reformulated gasoline
RSC--relative source contribution
RTECS--Registry of Toxic Effects of Chemical Substances, U.S. NIOSH
SARA--U.S. Superfund (CERCLA) Amendments and Reauthorization Act of 
    1986
SB--Senate Bill
SCVWD--Santa Clara Valley Water District, California
SFRWQCB--San Francisco Regional Water Quality Control Board
SGOT--serum glutamic-oxaloacetic transaminase
SS--statistically significant
STEL--Short-Term Occupational Exposure Limit
Superfund--U.S. Comprehensive Environmental Response, Compensation and 
    Liability Act of 1980, a.k.a. CERCLA
SWRCB--California State Water Resources Control Board
TAC--toxic air contaminant
TAME--tertiary amyl methyl ether
TBA--tertiary butyl alcohol
TBF--tertiary butyl formate
TERIS--Teratogen Information System, University of Washington
TOMES--Toxicology and Occupational Medicine System, Micromedex, Inc.
TRI--Toxics Release Inventory, U.S. EPA
TSCA--U.S. Toxic Substances Control Act
TWA--Time-Weighted Average
te--experimental duration
t1--lifetime of the animal used in the experiment
t1/2--plasma elimination half-life
UC--University of California
UCLA--UC Los Angeles
UCSB--UC Santa Barbara
UF--uncertainty factors
U.S.--United States
USCG--U.S. Coast Guard
USDHHS--U.S. Department of Health and Human Services
U.S. EPA--U.S. Environmental Protection Agency
USGS--U.S. Geological Survey
UST--underground storage tanks
VOC--volatile organic compound
VRG--vessel rich group
WDOH--Wisconsin Division of Health, Department of Natural Resources
WHO--World Health Organization
WSPA--Western States Petroleum Association
  

                                
