EPA 749-F-94-017a
              CHEMICAL SUMMARY FOR METHYL-TERT-BUTYL ETHER
                                 prepared by
                   OFFICE OF POLLUTION PREVENTION AND TOXICS
                     U.S. ENVIRONMENTAL PROTECTION AGENCY
                                 August 1994
     This summary is based on information retrieved from a systematic 
search limited to secondary sources (see Appendix A).  These sources 
include online databases, unpublished EPA information, government 
publications, review documents, and standard reference materials.  No 
attempt has been made to verify information in these databases and 
secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
     The chemical identity and physical/chemical properties of methyl
tertiary-butyl ether are summarized in Table 1.
          TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL 
              PROPERTIES OF METHYL-tert-BUTYL ETHER
_________________________________________________________________________
Characteristic/Property             Data               Reference
_________________________________________________________________________
CAS No.                    1634-04-4 
Common Synonyms            MTBE; 2-Methoxy-
                             2-methyl-propane          U.S. EPA 1993a
Molecular Formula          C5H12O    
Chemical Structure               CH3
                                 |
                           CH3-O-C-CH3
                                 | 
                                 CH3
Physical State             Colorless liquid            U.S. EPA 1993a
Molecular Weight           88.15                       Budavari et al. 1989
Melting Point              -109C                      Budavari et al. 1989
Boiling Point              55.2C                      Budavari et al. 1989
Water Solubility           51.26 g/L at 25C           U.S. EPA 1993a
Density                    d20/4, 0.7404 g/mL          Budavari et al. 1989
Vapor Density (air = 1)    3.1                         U.S. EPA 1993a
KOC                        12.3; 11.0 (estimated)      U.S. EPA 1993a
Log KOW                    1.24                        CHEMFATE 1994
Vapor Pressure             245 mm Hg at 25C           Budavari et al. 1989
Reactivity          
Flash Point                Flammable                   HSDB 1994
Henry's Law Constant       5.5 x 10-4 atm m3/mol 
                              at 25C                  U.S. EPA 1993a
Fish Bioconcentration 
           Factor           <2 (measured); 
                             <4 (estimated)            U.S. EPA 1993a
Odor Threshold              0.32-0.47 mg/m3            U.S. EPA 1993c
Conversion Factors          1 ppm = 3.605 mg/m3;        
                            1 mg/m3 = 0.277 ppm        U.S. EPA, 1993
_____________________________________________________________________________
II. PRODUCTION, USE, AND TRENDS
    A. Production       
       There are 27 companies producing methyl-tert-butyl ether (MTBE) at 
       32 facilities in the United States.  Table 2 lists U.S. producers, 
       plant locations, and plant capacities.  In 1992, 9.1 billion pounds 
       of MTBE were produced in the United States.  During that same year, 
       capacity was estimated at 11.6 billion pounds.
    B. Use
       The largest use for MTBE is as a gasoline additive, accounting 
       for almost all U.S. consumption.  Small amounts of MTBE are used 
       as a chemical intermediate to produce high purity isobutylene.  
       The estimated 1993 end-use pattern for MTBE reports that 100 
       percent of MTBE use was in gasoline additives (produced in SIC 
       Code 2911, used in many industries).
    C. Trends
        The U.S. market for MTBE is expected to grow rapidly well into 
        the 1990s.  This growth is due, in part, to Clean Air Act pro-
        visions regarding gasoline reformulation.  
          
                           
                           TABLE 2.  U.S. Producers of MTBE
__________________________________________________________________________
     Company                  Plant Location(s)         Plant Capacity
                                                   (in millions of pounds)
___________________________________________________________________________
     Amoco                    Whiting, IN                     285
                              Yorktown, VA                     50
     ARCO Chemical            Channelview, TX               3,610
                              Corpus Christi, TX            1,140
     ARCO Petroleum           Carson, CA                      240
     Ashland Oil              Catlettsburg, KY                305
     Champlin Refining Co.    Corpus Christi, TX              165
     Chevron                  El Segundo, CA                  190
                              Pascagoula, MS                  200
     Citgo                    Lake Charles, LA                255
     Conoco, Inc.             Ponca City, OK                  133a
                              Westlake, LA                    133a
     Crown Central Petroleum  Pasadena, TX                    285
     Diamond Shamrock         Sunray, TX                      200
     Enron                    LaPorte, TX                   1,425
     Exxon Chemical           Baytown, TX                     285
     Fina Oil & Chemical      Big Spring, TX                   48
     Global Octanes (Mitsui)  Deer Park, TX                 1,188
     Hill Petroleum (Phibro)  Houston, TX                     130
     Kerr McGee               Corpus Christi, TX              171
     Lyondell Petrochemical   Channelview, TX                 285
     Marathon Oil (USX)       Detroit, MI                     133a
                              Robinson, IL                    133a
     Mark West                South Shore, KY                 162
     Mobil                    Beaumont, TX                    240
     Oxychem                  Chocolate Bayou, TX             190
     Phillips                 Sweeny, TX                      285
     Star Enterprises 
        (Texaco/Aramco)       Convent, LA                     190
     Sun Refining 
         & Marketing Co.      Marcus Hook, PA                 240
     Texaco                   Port Neches, TX                 950
     Texas Petrochemicals 
        Corp.                 Houston, TX                   2,090
     Valero Refining Co.      Corpus Christi, TX              160
___________________________________________________________________________
a  Estimated. Combined capacity was reported for both locations listed.
Source:  Mannsville 1993.
III. ENVIRONMENTAL FATE
     A. Environmental Release
        Environmental releases of MTBE may occur at industrial sites
        involved in the manufacture of MTBE or in the blending of MTBE
        with gasoline; during the storage, distribution and transfer of
        MTBE-blended gasoline; and from spills or leaks or fugitive
        emissions at automotive service stations.  Total annual industrial 
        emissions of MTBE in the U.S. in 1992, as reported on the Toxics 
        Release Inventory, were 3 million pounds: 2.8 million pounds to 
        air, 100 thousand pounds to surface water, 68 thousand pounds to 
        underground injection sites, and 288 lb to land (TRI92 1994).  
        Vapor emissions of MTBE from gasoline blended with MTBE may also 
        contribute substantially to atmospheric levels (U.S. EPA 1988a).  
        The annual mean concentration of MTBE in the atmosphere in the 
        United States during 1987-1988 was estimated to be <0.2 ppb (U.S. 
        EPA 1993b).  MTBE has been detected in potable well water samples 
        in several locations; maximum reported concentrations ranged from 
        20  micrograms/L to more than 200 mg/L (U.S. EPA 1993b).
     B. Transport
        MTBE is highly volatile (vapor pressure 245 mm Hg, Henry's Law
        Constant 5.5 x 10-4 atm-m3/mole), and would be expected to
        volatilize rapidly from soil surfaces or water (U.S. EPA, 1993). 
        Calculations based on the environmental partitioning model
        (ENPART) in the Graphical Exposure Modeling System (GEMS) indicate 
        that 99.99% of MTBE will partition to air (U.S. EPA 1993a). 
        However, MTBE leaking from underground gasoline storage tanks may 
        not readily reach the atmosphere.  With estimated organic carbon 
        partitioning coefficients (Koc) of 12.3 (derived from water 
        solubility data) and 10.96 (derived from Kow data) (U.S. EPA 
        1993a), MTBE is expected to be highly mobile in soils, and leaching 
        of the chemical into groundwater is likely (U.S. EPA 1993a).  
     C. Transformation/Persistence
        1. Air - MTBE is not expected to persist in the atmosphere
           because of its rapid reaction with hydroxyl radicals.  The rate 
           constant for this reaction is 2.84 x 10-12 cm3/molecule-sec at 
           25C (HSDB 1994).  MTBE does not absorb light of greater than 
           210 nm; therefore, direct photolysis by UV absorption is 
           not expected to be environmentally significant.  Atmospheric 
           half-lives of 3.0 days in polluted air and 6.1 days in non-
           polluted air have been calculated (U.S. EPA 1993a).
        2. Soil - MTBE is expected to volatilize rapidly from soil surfaces 
           (U.S. EPA 1993a).  MTBE released in subsoils as a result of 
           leaks from underground storage tanks may be persistent.  There 
           is little evidence that MTBE is susceptible to either aerobic 
           or anaerobic biodegradation (U.S. EPA 1993a).
        3. Water - MTBE is expected to volatilize from surface waters
           (U.S. EPA 1993a).  Volatilization half-lives of MTBE from 
           streams, rivers and lakes were estimated to be 2.5 h, 9.5 h and 
           3,296 h (137 days), respectively (U.S. EPA 1993a). MTBE is not 
           expected to hydrolyze, photolyze, or be adsorbed to sediments or 
           suspended particulate matter (HSDB 1994).
        4. Biota - Bioconcentration factors (BCF) of 1.5 and 1.4 were
           reported for Japanese carp exposed to 10 and 80 mg/L MTBE
           (U.S. EPA 1993a).   Bioconcentration factors of 3.70 and 1.56 
           were estimated from regression equations based on Kow values 
           (U.S. EPA 1993a).  These BCFs indicate a low potential for 
           bioconcentration.
IV. HEALTH EFFECTS
    A. Pharmacokinetics
       1. Absorption - Animal studies have shown that MTBE is rapidly
          absorbed following oral or inhalation exposures.  Bioavailability 
          following dermal exposure is reported to be 39% or less than that 
          for oral exposures (U.S. EPA 1993a)
          
       2. Distribution - Animal studies indicate that MTBE is rapidly
          distributed in the blood to all parts of the body including
          the brain.  Peak blood levels occur within 15 min of i.p. 
          injection, and highest tissue levels were reported to occur
          in the liver and kidneys (U.S. EPA 1993a).
       3. Metabolism - The major metabolites of MTBE are tertiary butyl 
          alcohol (TBA) and formaldehyde (U.S. EPA 1993a).  The 
          formaldehyde is likely further metabolized to formic acid and 
          carbon dioxide, with the possible formation of methanol as well.  
          2-Methyl-1,2-propanediol and -hydroxyisobutyric acid have also 
          been identified in the urine of MTBE-exposed animals.
       4. Excretion - Animal studies have shown that MTBE is rapidly
          excreted following oral or inhalation exposures (U.S. EPA 1993a). 
          Following oral exposures, MTBE is eliminated mainly in expired 
          air (46-69%) with smaller amounts excreted in the urine (11-36%). 
          Following inhalation exposures, most MTBE and metabolites are 
          excreted in the urine (53-72%) with smaller amounts in expired 
          air (17-22%) (U.S. EPA 1993a).  
    B. Acute Effects
     
       Limited information indicate that ambient levels of MTBE do not
       pose a health risk to healthy individuals; however, susceptible
       subpopulations living under unique climatic condition (i.e.,
       subartic) may be adversely affected by volatile emissions from
       MTBE-blended gasoline.  Animal lethality data indicate that MTBE
       is low in acute toxicity.  The main target organ of acutely toxic
       doses of MTBE is the nervous system.
       1. Humans - In controlled clinical tests in which healthy 
          individuals were exposed to 5 mg MTBE/m3 for 1 hour, no symptoms 
          of adverse effects were observed (U.S. EPA 1993c).  The concen-
          tration of 5 mg/m3 for 1 hour is roughly equivalent to a dose of 
          0.09 mg/kg (see end note 1).  The individuals were evaluated for 
          symptomatic responses (headaches, throat and nasal irritation, 
          cough, and dizziness), neurobehavioral changes, upper airway 
          inflammation, and eye inflammation.  Complaints of headaches, eye 
          irritation, nose and throat irritation, cough, nausea, dizziness, 
          and spaci-ness were recorded in two cities in Alaska following 
          the introduction of MTBE-blended gasoline during the fall of 1992 
          (U.S. EPA 1993c).  Similar effects could not identified in popu-
          lations in New Jersey or Connecticut where MTBE-blended gasoline 
          was also used.  U.S. EPA (1993c) notes that "There is unlikely to 
          be a substantial risk of acute health symptoms among members of 
          the public receiving 'typical' environmental exposures under 
          temperate conditions (i.e., not subarctic temperature).  This 
          leaves open the question about more subtle health risks, espe-
          cially among susceptible subpopulations.  If acute symptoms are 
          being caused by MTBE, they appear to be mild and transient".
          Humans are acutely exposed to MTBE as part of a medical treatment 
          to dissolve cholesterol gallstones (U.S. EPA 1994).  Injection of 
          the gall bladder with MTBE can result in nausea, vomiting, 
          sleepiness, and minor transient mucosal damage in the
gallbladder.  
          Intravascular hemolysis and renal failure have occurred following 
          inadvertent extravasation of a large bolus of MTBE (U.S. EPA 
          1994).  
       2. Animals - Oral LD50 values of 1.6-3.9 g/kg have been reported 
          for rodents (U.S. EPA 1993a).  Acutely toxic oral doses can 
          result in nervous system effects (see section G) as well as 
          muscular weakness and inflammation of the stomach and small 
          intestines.  Inhalation LC50 values of 85-142 g/m3 have been 
          reported in rodents (U.S. EPA 1993a).  Symptoms of inhalation 
          exposure include nervous system effects (see section G), as well 
          as inflammation of the nasal mucosa and trachea.  MTBE also 
          causes mild skin irritation (slight erythema and edema) and 
          moderate eye irritation (corneal opacities, chemosis and 
          conjunctival redness) (U.S. EPA 1993a).  A skin penetration LD50 
          of >10 mL/kg has been reported for rabbits (Clayton and Clayton 
          1981-82).  MTBE is not expected to be a primary skin irritant 
          (HSDB 1994).
    C. Subchronic/Chronic Effects
       Information on the subchronic and chronic toxicity of MTBE to humans 
       was not found in the secondary sources searched.  Laboratory rodents 
       exposed to high doses or concentrations of MTBE exhibit blood 
       chemistry changes and kidney abnormalities.  
       
       1. Humans - No information specific to MTBE was found in the 
          available literature.
       2. Animals - The subchronic oral toxicity of MTBE was evaluated in 
          a 90-day bioassay in which Sprague-Dawley rats were dosed by 
          gavage with 0, 100, 300, 900 or 1200 mg MTBE/kg/day.  Animals 
          in all treatment groups exhibited diarrhea.  A dose level of 
          1200 mg/kg/day resulted in an increase in hyaline droplets and 
          blockage of renal tubules with granular cysts; increased kidney 
          and liver weights; increases in hemoglobin, hematocrit, and 
          erythrocytes; decreases in blood glucose, blood urea nitrogen 
          (BUN), and calcium; and elevations in cholesterol and aspartate
          aminotransferase (AST) (U.S. EPA 1993a).  Pathological changes 
          in the kidney were not seen at the lower dose levels; however, 
          males and females treated with 900 mg/kg MTBE and females 
          treated with 300 mg/kg/day exhibited increases in relative 
          kidney weight as well as several changes in blood chemistry such 
          as a decrease in BUN.  The oral reference dose (RfD) for MTBE 
          is currently under review by EPA (U.S. EPA 1994).
          In tests in which rats were exposed to MTBE concentrations of
797, 
          3920, or 8043 ppm (6 h/day, 5 days/wk for 13 wk), the two highest 
          concentrations resulted in increased liver, kidney and adrenal 
          weights; changes in hematologic parameters (increased hemoglobin, 
          decreased erythrocyte counts and increased reticulocyte counts); 
          altered serum chemistry [increases in calcium and protein, and 
          decreases in blood glucose, and AST and alanine aminotransferase 
          (ALT) activities]; lymphoidal hyperplasia; splenic hemosiderosis;
          and an increase in the size of hyaline droplets in the renal
          proximal tubular epithelial cells (U.S. EPA 1993a).  No adverse 
          effects were seen at 797 ppm.  The concentration of 8043 ppm is 
          roughly equivalent to 4,639 mg/kg/day (see end note 2).
          Exposure of mice and rats to concentrations of 0, 403, 3023,
          or 7977 ppm MTBE for 6 h/day, 5 days/week, for up to 18 months 
          (mice) or 24 months (rats) resulted in clinical signs of toxicity 
          at the two highest exposure levels (U.S. EPA 1993a).  Effects 
          seen in rats included: increased incidences of swollen periocular 
          tissue; decreases in absolute body weight and body weight gain; 
          increases in absolute and relative liver weight in females; an 
          increase in kidney weight; and an increase in the incidence of 
          chronic nephropathy (glomerulosclerosis, tubular proteinosis,
          interstitial nephritis, and interstitial fibrosis).  Effects seen 
          in mice included increases in absolute and relative liver and 
          kidney weights; increases in absolute and relative adrenal 
          weights in males; increases in hepatocellular hypertrophy and 
          liver masses; and a slightly increased frequency of urinary 
          bladder dilation/distension in males. The 403 ppm exposure level 
          was considered a NOAEL.  Based on the results of the rat study, 
          the U.S. EPA (1994) calculated a chronic RfC (reference concen-
          tration) of 3 mg/m3 for MTBE.
     D. Carcinogenicity
        Information on the potential carcinogenicity of MTBE in humans is
        lacking and the results of animal studies are still under review
        within EPA; however, the current unfinished assessment supports a
        hazard classification of "possible" human carcinogen based upon
        "limited" animal evidence (U.S. EPA 1993c; Anderson 1994).
         1. Humans - No studies were found in the available secondary 
            sources evaluating the potential carcinogenicity of MTBE to
            humans.
         2. Animals - The carcinogenicity of MTBE has been evaluated in
            inhalation exposure studies using CD-1 mice and F344 rats
            (U.S. EPA 1993a).  In female mice, the incidence of liver
            adenomas was significantly increased over control values 
            (10/50 vs. 2/50) in animals exposed to 7973 ppm MTBE (6 h/day, 
            5 days/week, for 18 months).  Male mice exposed to the same 
            MTBE concentration exhibited a slight increase in the combined 
            incidence of liver adenomas and carcinomas (16/49 vs. 12/49 
            in controls), but this increase was not statistically signifi-
            cant and was within the range of historical control values 
            (316/891).  In male rats, the incidence of renal tubular cell 
            tumors (adenomas and carcinomas) was 8/50 for animals exposed 
            to 3023 ppm (6 h/day, 5 days/week, for up to 97 weeks), 3/50 
            for animals exposed to 7977 ppm (for up to 82 weeks), but only 
            1/50 in the control group (statistical significance not 
            reported). In female rats, the only reported kidney tumor was a 
            renal cell adenoma in an animal exposed to 3023 ppm MTBE.  The 
            incidence of testicular tumors (interstitial cell adenomas) was 
            increased above control values (41/50 in the 3023 ppm group and 
            47/50 in the 7977 ppm group vs. 32/50 for the controls).  It 
            was noted by the investigators that the frequency of testicular 
            tumors in the MTBE-exposed animals was within the range 
            (64-98%) reported for aged Fischer 344 rats, and that the 
            frequency of these tumors in the control group was lower than 
            historical controls from the same laboratory.
     E. Genotoxicity
        The genotoxicity of MTBE has been evaluated in microbial mutation
        assays, a sister chromatid exchange (SCE) assay, a mouse lymphoma
        assay, and in a Drosophila sex-linked recessive lethal test (U.S.
        EPA 1993a).  The only study in which MTBE gave a positive response 
        was the mouse lymphoma forward mutation assay, and this response 
        occurred only in the presence of a metabolic activation system.  
          
     F. Developmental/Reproductive Toxicity
        Information on the developmental or reproductive toxicity of MTBE
        in humans was not found in the available secondary sources.  In
        animal studies, high concentrations of MTBE produced develop-
        mental and reproductive toxicity in mice and rats (U.S. EPA 1993a).
        1. Humans - No data were found in the secondary sources searched to 
           indicate that MTBE is a developmental/reproductive toxicant in 
           humans.  
        2. Animals - In tests on CD-1 mice, exposure to 14,400 mg/m3
           and 28,800 mg/m3 on gestation days 6-15 resulted in reduced
           pup viability. An increase in the incidence of cleft palate
           was seen at the higher concentration.  Exposure to 3,600 mg/m3 
           resulted in no adverse effects (EPA, 1993c).  In a one-
           generation study on Sprague-Dawley rats, no adverse develop-
           mental effects occurred at 1,082 mg/m3, but reduced pup 
           viability was seen at 4,470 mg/m3.  In a two-generation study 
           conducted on the same strain of rats, an exposure level of 
           1,453 mg/m3 caused no adverse effects; however, 10,899 mg/m3 
           (3019 ppm) resulted in maternal toxicity, a significant increase 
           in dead pups on day 4, a significant reduction in litter 
           size on days 21 and 28, and a significant reduction in mean 
           pup weight throughout lactation (Anderson, 1994; EPA, 1993c).  
           EPA (1993c) applied an uncertainty factors of 3 (to extrapolate 
           from rats to humans) and 10 (for sensitive subpopulations) to 
           the rat NOAEL of 1,453 mg/m3, to derive a human NOAEL for
           developmental effects of 48 mg/m3 (with uncertainty spanning
           at least an order of magnitude).
     G. Neurotoxicity
        Information on the potential neurotoxicity of MTBE to humans was
        not found in the secondary sources searched.  Laboratory rodents
        exposed to high concentrations of MTBE exhibit neurotoxic effects.
        1. Humans - No information available.
        2. Animals - Acutely toxic oral doses can result in hypoactivity; 
           muscular weakness; hyperpnea; prostration; lacrimation; and a 
           general anesthetic effect at doses of  1200 mg/kg (U.S. EPA 
           1993a).  Symptoms of inhalation exposures include: hyper-
           activity; ataxia; loss of righting; unconsciousness; clonia; 
           sporadic convulsive seizures.  The median effective concen-
           tration (EC50) for anesthesia is 200 g/m3 (55,400 ppm) in mice.  
           Rats exposed to 4000 ppm (6 h/day, 5 days/wk for 13 wk) 
           exhibited mild neurotoxic effects (transient episodes of ataxia, 
           reduced grip strength, and altered motor activity) (U.S. EPA 
           1993a).
           Exposure of mice and rats to target concentrations of 0, 400, 
           3000, or 8000 ppm MTBE for 6 h/day, 5 days/week, for up to 
           18 months (mice) or 24 months (rats) resulted in several 
           clinical signs of neurotoxicity at the two highest exposure
           levels.  Effects seen in rats included: blepharospasm; hypo-
           activity; ataxia, lack of a startle reflex; salivation; and 
           tremors.  Effects seen in mice included blepharospasm, 
           hypoactivity, ataxia, lack of a startle reflex, stereotypy, and 
           prostration (U.S. EPA 1993a).  
V. ENVIRONMENTAL EFFECTS
     
   A. Toxicity to Aquatic Organisms
     
       Limited information indicate that MTBE has low acute toxicity to
       aquatic organisms; lethal concentrations are generally greater
       than 100 mg/L.  Ninety-six-hour LC50 values of 706 mg/L for the 
       fathead minnow (Pimephales promelas), and >1000 mg/L for the 
       bleak Alburnus alburnus and for the harpacticoid copepod, Nitocra 
       spinipes, have been reported (U.S. EPA 1993a). Quantitative 
       Structure Activity Relationship (QSAR) calculations predict a 
       fish acute LC50 of 510 mg/L; a fish chronic value (ChV) of 57 
       mg/L; a daphnid acute LC50 of 510 mg/L; a daphnid ChV of 17 mg/L; 
       a green algal acute LC50 of 300 mg/L; and a green algal ChV of 
       18 mg/L (U.S. EPA 1993a).  An LC50 of 2,500 mg/L have been reported 
       for tadpoles of the frog Rana temporaria; a concentration of 
       200 mg/L was not lethal, and a concentration of 100 mg/L resulted 
       in accelerated tadpole development and marked increases in body 
       weight of tadpoles and frogs that had undergone metamorphosis 
       (U.S. EPA 1993a).
    B. Toxicity to Terrestrial Organisms
        No information was found in the available secondary sources on 
        the toxicity of MTBE to terrestrial organisms.  The reported rat 
        oral LD50 values of 1.6-3.9 g/kg and LC50 values of 85-142 g/m3 
        suggest that the chemical would not be acutely toxic to terres-
        trial animals unless present in very high concentrations.  
     C. Abiotic Effects
        Although MTBE is added to gasoline to improve air quality by
        enhancing combustion and reducing emissions of carbon monoxide 
        and benzene, emissions of other pollutants, such as formaldehyde 
        may increase (U.S. EPA 1993c).  The ozone forming potential of 
        MTBE is estimated to be lower than that for most other non-methane 
        components of urban air including alkenes, aldehydes, nontoluene 
        aromatics, and ethene (U.S. EPA 1993a).  According to the 
        definition provided in the Federal Register (1992), MTBE is a 
        volatile organic compound (VOC) substance.  As a VOC, MTBE can 
        contribute to the formation of photochemical smog in the presence 
        of other VOCs.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
    The Clean Air Act Amendments of 1990 list MTBE as a hazardous air
    pollutant.
    Federal agency and other group activities for MTBE are summarized in
    Tables 3 and 4.
                 TABLE 3.  EPA OFFICES AND CONTACT NUMBERS 
              FOR INFORMATION ON METHYL TERTIARY-BUTYL ETHER
________________________________________________________________________
EPA OFFICE            LAW                                PHONE NUMBER
________________________________________________________________________
Pollution Prevention  Toxic Substances Control Act
 & Toxics               (Sec. 4/8A/8D/8E)               (202) 554-1404
                      Emergency Planning and Community
                       Right-to-Know Act (EPCRA)
                        Regulations (Sec. 313)           (800) 424-9346
                        Toxics Release Inventory data    (202) 260-1531
Air                   Clean Air Act                      (919) 541-0888
Solid Waste &         Comprehensive Environmental
 Emergency Response    Response, Compensation, and
                       Liability Act (Superfund)/
                      Resource Conservation and Recovery
                       Act / EPCRA (Sec. 304/311/312)    (800) 424-9346
Water                 Safe Drinking Water Act            (800) 426-4791
_________________________________________________________________________
             TABLE 4.  OTHER FEDERAL OFFICES/OTHER GROUPS 
               CONTACT NUMBERS FOR INFORMATION ON MTBE
___________________________________________________________________________
Other Agency/Department/Group                               Contact Number
___________________________________________________________________________
Agency of Toxic Substances & Disease Registry               (404) 639-6000
American Industrial Hygiene Association Workplace 
   Environmental Exposure Level (AIHAWEEL) Guide
   (Recommended Exposure Limit (see end note 3):  100 ppm)  (703) 849-8888
Consumer Product Safety Commission                          (301) 504-0994
___________________________________________________________________________
VII. END NOTES
1. Calculated using a factor of 0.0179 (the standard 8-hour occupational
breathing rate of 10 m3 divided by 8, divided by the assumed adult body
weight of 70 kg) to obtain the dose in mg/kg (U.S. EPA 1988b).
2. Calculated using the factor 3,605 (U.S. EPA 1993) to convert 8043 ppm
to 28,995 mg/m3 which is multiplied by 0.16 (the 6-hour breathing rate, 
0.056 m3 [standard 24-hour breathing rate, 0.223 m3] divided by the  
assumed adult rat body rat weight, 0.350 kg, and assuming 100% absorption)
to obtain the dose in mg/kg/day (U.S. EPA 1985).
3. The AIHAWEEL exposure limit is a time-weighted average (TWA) 
concentration that should not be exceeded during an 8-hour workday during 
a 40-hour workweek.
VIII.  CITED REFERENCES
Anderson L.  1994.  Methyl Tertiary-Butyl Ether Risk Management 1 Screening
Document, April 1994 Draft.  Chemical Screening and Risk Assessment 
Division, U.S. EPA, Washington, DC.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Merck & Co., Inc., Rahway, NJ, p. 951.
CHEMFATE.  1994.  Syracuse Research Corporation's Environmental Fate Data
base.  Syracuse Research Corporation, Syracuse, NY.
Clayton GD, Clayton FE.  1981-1982.  Patty's Industrial Hygiene and
Toxicology, 3rd ed., Vol. 2C.  New York:  John Wiley & Sons. p. 2503.
Federal Register.  1992.  Part 51 - Requirements for Preparation, Adoption,
and Submittal of Implementation Plans. Fed. Reg. 57:3945.
HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information
Retrieval System, National Library of Medicine.  Retrieved August, 1994.
Mannsville.  1993.  Chemical Products Synopsis, MTBE.  Mannsville Chemical
Products Corporation.  January, 1993.  
TRI92.  1994.  1992 Toxics Release Inventory.  Office of Pollution 
Prevention and Toxics, U.S. EPA, Washington, DC.  EPA 745-R-94-001.
U.S. EPA.  1985.  U.S. Environmental Protection Agency.  Reference Values 
for Risk Assessment.  Environmental Criteria and Assessment Office, U.S. 
EPA, Cincinnati, OH, Table 1-2.
U.S. EPA.  1988a.  U.S. Environmental Protection Agency.  Fuel and Fuel
Additives: waiver decision. Notice.  Federal Register 44:33846-33847.  
(cited in U.S. EPA 1993a)
U.S. EPA.  1988b.  U.S. Environmental Protection Agency.  Methodology for
Evaluating Potential Carcinogenicity in Support of Reportable Quantity
Adjustments Pursuant to CERCLA Section 102.  Carcinogen Assessment Group,
Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C., 
pp. 21, 22.  OHEA-C-073.
U.S. EPA.  1993a.  U.S. Environmental Protection Agency.  Technical
Information Review.  Methyl tertiary Butyl Ether (CAS No. 1634-04-4).  
Office of Pollution Prevention and Toxics, U.S. EPA, Washington, D.C.
U.S. EPA.  1993b.  U.S. Environmental Protection Agency.  Revised and 
Updated Drinking Water Quantification of Toxicological Effects for Methyl 
tert-Butyl Ether (MTBE).  Final Draft.  Environmental Criteria and 
Assessment Office, U.S. EPA, Cincinnati, OH.  ECAO-CIN-DO23.
U.S. EPA.  1993c.  U.S. Environmental Protection Agency.  Assessment of
Potential Health Risks of Gasoline Oxygenated with Methyl Tertiary Butyl 
Ether (MTBE).  Office of Research and Development, U.S. EPA, Washington, 
DC.  EPA/600/R-93/206.
U.S. EPA.  1994.  Integrated Risk Information System (IRIS) Online. 
Coversheet for Methyl tertiary Butyl Ether.  Office of Health and
Environmental Assessment, U.S. EPA, Cincinnati, OH,  Retrieved 8/2/94.
APPENDIX A.  SOURCES SEARCHED FOR FACT SHEET PREPARATION
AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical
Information Systems, Inc., a subsidiary of Fein-Marquart Assoc.
ATSDR.  1989-1994.  Agency for Toxic Substances and Disease Registry. 
Toxicological Profiles.  Chamblee, GA: ATSDR.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Rahway, N.J.:  Merck & Co., Inc.
Clayton GD, Clayton FE.  1981-1982.  Patty's Industrial Hygiene and
Toxicology, 3rd ed., Vol. 2C.  New York:  John Wiley & Sons.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. 
HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information
Retrieval System, National Library of Medicine.
IARC. 1979-1994. International Agency for Research on Cancer.  IARC 
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. 
Lyon: IARC.
NIOSH (National Institute for Occupational Safety and Health).  1992.  
NIOSH Recommendations for Occupational Safety and Health.  Compendium of 
Policy Documents and Statements.  Cincinnati, OH:  NIOSH.
NTP.  1994.  National Toxicology Program.  Toxicology and Carcinogenesis
Studies.  Tech Rep Ser.
NTP.  1994.  National Toxicology Program.  Management Status Report.  
Produced from NTP Chemtrack system.  April 8, 1994.  National Toxicology 
Program, Research Triangle Park, NC.
OSHA.  1994.  Occupational Safety and Health Administration.  Table Z-2. 
Limits for Air Contaminants.
RTECS.  1994.  Registry of Toxic Effects of Chemical Substances.  MEDLARS
Online Information Retrieval System, National Library of Medicine.
U.S. Air Force.  1989.  The Installation Restoration Toxicology Guide, 
Vols. 1-5.  Wright-Patterson Air Force Base, OH.
U.S. EPA (U.S. Environmental Protection Agency).  1991.  Table 302.4 List 
of Hazardous Substances and Reportable Quantities 40 CFR, part 302.4:3-271.
U.S. EPA.  Most current.  Drinking Water Regulations and Health Advisories. 
Office of Drinking Water, U.S. Environmental Protection Agency, Washington,
D.C.
U.S. EPA.  Most Current.  Health Effects Assessment Summary Tables. 
Cincinnati, OH:  Environmental Criteria and Assessment Office, U.S.EPA.
U.S. EPA reviews such as Health and Environmental Effects Documents, Health
and Enviornmental Effect Profiles, and Health and Environmental 
Assessments.
U.S. EPA.  1994.  Integrated Risk Information System (IRIS) Online. 
Cincinnati, OH:  Office of Health and Environmental Assessment.