EPA 749-F-94-013a

                        CHEMICAL SUMMARY FOR METHANOL
                                 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include online databases, unpublished EPA information, government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 contained in these databases
and secondary sources.

I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES

   The chemical identity and physical/chemical properties of methanol
are summarized in Table 1.

TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF METHANOL
_______________________________________________________________________

Characteristic/Property            Data                   Reference
_______________________________________________________________________
CAS No.                     67-56-1   
Common Synonyms             methyl alcohol, wood 
                            alcohol, wood spirit     Budavari et al. 1989
Molecular Formula           CH4O 
Chemical Structure              H
                                |
                            H - C - OH
                                |
                                H  
Physical State              colorless liquid          Verschueren 1983
Molecular Weight            32.04                     Budavari et al. 1989
Melting Point               -97.8C                   Budavari et al. 1989
Boiling Point               64.7C at 760 mm Hg       Budavari et al. 1989
Water Solubility            miscible                  Budavari et al. 1989
Density                     d20/4, 0.7915 g/mL        Budavari et al. 1989
Vapor Density (air = 1)     1.11                      Budavari et al. 1989
KOC                         9                         CHEMFATE 1994
Log KOW                     -0.77                     HSDB 1994
Vapor Pressure              126 mm Hg at 25C         CHEMFATE 1994
Reactivity                  Flammable; may explode 
                            when exposed to flame     HSDB 1994
Flash Point                 12C                      Budavari et al. 1989
Henry's Law Constant        4.55 x 10-6 atm m3/mol    CHEMFATE 1994
Fish Bioconcentration 
   Factor                   <1 (estimated)            HSDB 1994
Odor Threshold              highly variable, ranges 
                            over several orders
                            of magnitude (10 ppm 
                            to 20,000 ppm in air)     HSDB 1994
Conversion Factors          1 ppm = 1.33 mg/m3
                            1 mg/m3 = 0.76 ppm        Verschueren 1983
_______________________________________________________________________

II. PRODUCTION, USE, AND TRENDS

    A. Production

       Methanol, also called methyl alcohol, is manufactured by 13
       producers in the United States.  Table 2 lists producers, plant 
       locations, and plant capacities.  Annual production capacity is 
       approximately 1,626 million gallons.  In 1992, 1,345 million 
       gallons of methanol were produced in the US, 495 million gallons 
       were imported into the US, and 50 million gallons were exported 
       (Mannsville 1993).
   
    B. Use

       Methanol is used in a variety of industrial applications.  Its
       largest use is as a raw material for the production of methyl
       t-butyl ether (MTBE), a gasoline additive.  It is also used in
       the production of formaldehyde, acetic acid, chloromethanes,
       methyl methacrylate, methylamines, dimethyl terephthalate, and
       as a solvent or antifreeze in paint strippers, aerosol spray
       paints, wall paints, carburetor cleaners, and car windshield
       washer compounds.  Table 3 shows the estimated 1993 US end-use
       pattern for methanol.

    C. Trends

       US consumption of methanol reached an all-time high in 1992,
       with estimated 1993 consumption surpassing this level.  Demand
       is expected to continue to rise, due primarily to predicted
       increases in demand for MTBE as a gasoline additive.  Demand
       for MTBE is expected to at least double by 1995 (Mannsville
       1993).

              TABLE 2.  United States Producers of Methanol
_______________________________________________________________________
Company                   Plant Location           Plant Capacity
                                               (in millions of gallons)
_______________________________________________________________________
                                               
Air Products              Pensacola, FL                  60
Ashland Chemical Co.      Plaquemine, LA                130
Beaumont Methanol         Beaumont, TX                  250
Borden                    Geismar, LA                   210
Coastal Chemical          Cheyenne, WY                   26
Enron (Tenneco)           Pasadena, TX                  140
Georgia Gulf              Plaquemine, LA                140
Hoechst Celanese          Bishop, TX                    160
Lyondell Petrochemicals   Channelview, TX               220
Quantum Chemical          Deer Park, TX                 100
Sand Creek Chemical       Commerce City, CO              25
Tennessee Eastman         Kingsport, TN                  65
Texaco Chemical           Delaware City, DE             100
_______________________________________________________________________
Source:  Mannsville 1993.

  TABLE 3.  Estimated 1993 Unites States End-Use Pattern of Methanol
_______________________________________________________________________

Use of Methanol                                    Percentage of US 
(typical Standard Industrial                         Methanol Use
Classification (SIC) Code) (see end note 1)     
_______________________________________________________________________

Methyl t-butyl ether (production, SIC 2911)               37%
Formaldehyde (production, SIC 2869)                       24%
Acetic acid (production, SIC 2869)                        10%
Chloromethanes (SIC Codes unknown)                         6%
Methyl methacrylate (production, SIC 2821)                 3%
Methylamines (SIC Codes unknown)                           3%
Dimethyl terephthalate (SIC Codes unknown)                 2%
Solvents and automotive 
   chemicals (production, SIC 2842)                        8%
Miscellaneous (no applicable SIC Code(s))                  7%
_______________________________________________________________________
Source:  Mannsville 1993.

III. ENVIRONMENTAL FATE

     A. Environmental Release

        Methanol ranked third in the U.S. among all chemicals for
        total releases into the environment in 1992.  Of the total
        released, 195 million pounds were into the atmosphere, 16.4
        million pounds were into surface water, 27 million pounds into
        underground injection sites, and 3.3 million pounds were onto
        land (TRI92 1994).  Methanol detected in the air from Point
        Barrow, Alaska  averaged 0.77 ppb (CHEMFATE 1994).  Ambient
        concentrations from Stockholm, Sweden ranged from 3.83 to 26.7
        ppb while concentrations from two remote locations in Arizona
        were 7.9 and 2.6 ppb (HSDB 1994).  In one survey, methanol was
        detected in drinking waters from 6 of 10 U.S. cities (HSDB
        1994) but levels were not included.  The chemical has also
        been detected in rainwater collected from Santa Rita, Arizona
        (HSDB 1994).

     B. Transport

        The miscibility of methanol in water and a low KOC (9) indicate
        that the chemical will be highly mobile in soil (HSDB 1994). 
        Volatilization half-lives from a model river and an
        environmental pond were estimated at 4.8 days and 51.7 days,
        respectively (HSDB 1994).  Methanol can be removed from the
        atmosphere in rain water (HSDB 1994).
      
   C. Transformation/Persistence

      1. Air - Once in the atmosphere, methanol exists in the vapor 
         phase with a half life of 17.8 days (HSDB 1994).  The chemical 
         reacts with photochemically produced hydroxyl radicals to 
         produce formaldehyde (HSDB 1994).  Methanol can also react 
         with nitrogen dioxide in polluted air to form methyl nitrite 
         (HSDB 1994).
         
      2. Soil - Biodegradation is the major route of removal of methanol 
         from soils.  Several species of Methylobacterium and Methylomonas 
         isolated from soils are capable of utilizing methanol as a sole 
         carbon source (CHEMFATE 1994).

      3. Water - Most methanol is removed from water by biodegradation.  
         The degradation products of methane and carbon dioxide were 
         detected from aqueous cultures of mixed bacteria isolated from 
         sewage sludge (CHEMFATE 1994).  Aerobic, Gram-negative bacteria 
         (65 strains) isolated from seawater, sand, mud, and weeds of 
         marine origin utilized methanol as a sole carbon source
         (CHEMFATE 1994).  Aquatic hydrolysis, oxidation, and photolysis 
         are not significant fate processes for methanol (HSDB 1994).

      4. Biota - Bioaccumulation of methanol in aquatic organisms
         is not expected to be significant based on an estimated
         bioconcentration factor of 0.2 (HSDB 1994).
         
V. HUMAN HEALTH EFFECTS

   A. Pharmacokinetics

      1. Absorption - Methanol is readily absorbed after oral,
         inhalation, or dermal exposure.  Oral doses in humans of
         71 to 84 mg/kg resulted in blood levels of 4.7 to 7.6
         mg/100 mL of blood within 3 hours (Rowe and McCollister
         1981).  Inhalation of 500 to 1000 ppm methanol for 3 to
         4 hours gave urine concentrations of 1 to 3 mg methanol/100 
         mL of urine at the end of exposure (Rowe and McCollister 1981).  
         Based on urinary methanol levels, the rate of absorption of the 
         chemical appears to be proportional to the concentration of vapor 
         inhaled (HSDB 1994).  The rate of dermal absorption increased
         for 35 minutes then decreased over the next 25 minutes (no 
         other details given) (HSDB 1994). 

      2. Distribution - Methanol distributes rapidly in dogs exposed 
         to 4000 to 15,000 ppm for 12 hours to 5 days; the highest 
         concentrations of the chemical were found in blood, eye fluid, 
         bile, and urine (HSDB 1994).
         
      3. Metabolism - Methanol is oxidized in the human liver by the enzyme 
         alcohol dehydrogenase (Rowe and McCollister 1981).  Metabolic 
         products include formaldehyde and formic acid (HSDB 1994).  The 
         rate of metabolism for methanol (25 mg/kg/hr) is much slower 
         than for ethanol (175 mg/kg/hr) and is independent of concen-
         trations in the blood (HSDB 1994).  Formic acid is responsible 
         for the toxic effects of methanol (ACGIH 1991).

      4. Excretion - Methanol is excreted either as parent compound in 
         the urine or expired air, or as the formic acid metabolite in 
         urine (Rowe and McCollister 1981; HSDB 1994).  The amount of 
         formic acid excreted varies greatly with species from 1% in 
         rabbits to 20% in dogs; humans are intermediate (HSDB 1994).  
         In humans, the half-life of methanol elimination in expired air 
         after oral or dermal exposure is 1.5 hours (HSDB 1994).

   B. Acute Toxicity

      Acute methanol intoxication is manifested initially by signs of 
      narcosis.  This is followed by a latent period in which formic 
      acid accumulates in the body causing metabolic acidosis.  Severe 
      abdominal, leg, and back pain occur and visual degeneration can 
      lead to blindness.

      1. Humans - Ingestion of 80 to 150 mL of methanol is usually fatal 
         to humans (HSDB 1994).  One worker died from exposure to vapor 
         ranging from 4000 to 13,000 ppm over 12 hours (ACGIH 1991).  
         The concentration of 4000 ppm is roughly equivalent to a total of 
         1140 mg/kg over the 12 hour period (see end note 2). Poisoning 
         by nonlethal doses can be described in three stages: (1) narcotic 
         stage similar to ethanol; (2) latent period of 10-15 hours; (3) 
         visual disturbances and central nervous system lesions (Rowe 
         and McCollister 1981).  Visual disturbances can lead to blindness 
         due to edema of the retina and atrophy of the optic nerve head 
         (HSDB 1994).  Third-stage CNS lesions include headache, 
         dizziness, abdominal, back, and leg pain, delirium that can lead 
         to coma, and nausea (HSDB 1994).  Formic acid production causes 
         severe metabolic acidosis (Rowe and McCollister 1981).

      2. Animals - Oral LD50 values for methanol in animals are 0.4 g/kg 
         in the mouse, 6.2 to 13 g/kg in the rat, 14.4 g/kg in the rabbit, 
         and 2 to 7 g/kg in the  monkey (Rowe and McCollister 1981).  The 
         LD50 for dermal application to rabbits is 20 mL/kg (approximately 
         16 g/kg) (Rowe and McCollister 1981).  Dose-response data for 
         inhalation vary with species, dose, and duration (8800 ppm for 8
         hours to 152,800 ppm for 94 minutes).  Symptoms of intoxication 
         include incoordination, salivation, lethargy, narcosis, and death 
         (Rowe and McCollister 1981).

   C. Subchronic/Chronic Toxicity

      Chronic exposure to methanol, either orally or by inhalation, causes 
      headache, insomnia, gastrointestinal problems, and blindness in 
      humans and hepatic and brain alterations in animals.  EPA has derived 
      an oral RfD (reference dose) (see end note 3) for methanol of 0.5 
      mg/kg/day, based on the absence of liver and brain effects in animals 
      exposed by mouth to 500 mg/kg/day.

      1. Humans - "Chronic" exposure to methanol vapors (no time or dose 
         given) caused conjunctivitis, headache, giddiness, insomnia, 
         gastric disturbances, and bilateral blindness (ACGIH 1991).  
         Marked vision loss occurred in one worker exposed to 1200 to 
         8000 ppm vapor for 4 years (ACGIH 1991).

      2. Animals - No effects were seen in rats given 1% (approximately 
         140 mg/kg/day) methanol in drinking water for 6 months (Rowe 
         and McCollister 1981).  Hepatic abnormalities (proteinic 
         degeneration, altered RNA metabolism) occurred in rhesus 
         monkeys given 3 to 6 g/kg for 3 to 20 weeks and in rats given 
         10, 100, or 500 mg/kg/day for one month (Rowe and McCollister 
         1981).  Rabbits chronically fed methanol (no dose or time given)
         had increasing blood levels, brain and eye edema, and myelin 
         thinning (HSDB 1994).  Male and female rats were gavaged with 
         100, 500, or 2500 mg/kg/day for 90 days (U.S. EPA 1994).  
         Increased levels of SGPT and SAP as well as decreased brain 
         weights were seen in both sexes at the highest dose; a no-
         observed-adverse effect level (NOAEL) for the study was 500 
         mg/kg/day.  Based on these data, the U.S. EPA (1994) calculated 
         a chronic RfD (see end note 4) for methanol of 0.5 mg/kg/day.  
         No toxic effects were seen in dogs exposed by inhalation to
         either 10,000 ppm for 3 minutes, 3x/day, for 100 days or
         to 450 or 500 ppm, 8 hours/day for 379 days (Rowe and
         McCollister 1981).  Ultrastructural changes were observed in 
         the photoreceptor cells of rabbits exposed to 46.6 ppm for 
         6 months (Rowe and McCollister 1981).  Rowe and McCollister (1981) 
         concluded that the effects of combined oral and inhalation 
         exposure appear to be additive.  Rats exposed by inhalation to 
         16.8 ppm, 4 hours/day, for 6 months and administered 0.7 mg/kg/day
         orally had changes in blood morphology, oxidation-reduction 
         processes, and liver function (Rowe and McCollister 1981).  

   D. Carcinogenicity

      No information was found on the carcinogenicity of methanol in
      the secondary sources searched.

      1. Humans - No information was found in the secondary sources 
         searched concerning the carcinogenicity of methanol to humans.

      2. Animals - No information was found in the secondary sources 
         searched concerning the carcinogenicity of methanol to animals.  
         The NTP has assigned a project leader for methanol and the design 
         of the study is in progress (NTP 1994).

   E. Genotoxicity

      Methanol was negative for cell transformation in Syrian
      hamster embryo cells (clonal assay and viral enhanced), sister
      chromatid exchange in vitro, and for aneuploidy and chromosome
      aberrations in Neurospora crassa (GENETOX 1992).  The micronucleus 
      test and the assay for chromosome aberrations in mammalian 
      polychromatic erythrocytes were inconclusive (GENETOX 1992).

   F. Developmental/Reproductive Toxicity

      No information was found on the developmental toxicity of methanol 
      in humans.  Methanol can cause adverse effects in the developing 
      offspring in rats at doses that cause overt maternal intoxication.

      1. Humans - No information was found in the secondary sources 
         searched regarding the developmental or reproductive toxicity of 
         methanol to humans.  However, one of the breakdown products of 
         the artificial sweetener asparatame is methanol.  Increased 
         blood methanol levels did not lead to increased formic acid
         levels in women receiving up to 200 mg/kg asparatame (no
         other details reported) and no evidence of fetal risk
         was detected (HSDB 1994).

      2. Animals - Rats were exposed by inhalation, 7 hours/day, to 5000 
         or 10,000 ppm methanol on gestation days 1-19 or to 20,000 ppm 
         on days 7-15.  Maternal intoxication (unsteadiness) occurred at 
         the highest dose and coincided with extra or rudimentary ribs and 
         urinary or cardiovascular defects in the fetuses (ACGIH 1991). 
         Male rats had significantly lowered testosterone levels after 
         inhalation exposure to 200 ppm methanol for 6 weeks; at 10,000 
         ppm a change in luteinizing hormone was also observed (HSDB 1994).

   G. Neurotoxicity

      Methanol causes central nervous system depression in humans and 
      animals as well as degenerative changes in the brain and visual 
      system.

      1. Humans - Methanol causes narcosis similar to ethanol intoxication 
         and nonlethal doses can lead to blindness. Autopsy of individuals 
         after lethal doses revealed edema and hyperemia of the brain and 
         degeneration of the ganglion cells of the retina (Rowe and 
         McCollister 1981).

      2. Animals - Acute methanol intoxication in animals causes CNS 
         depression as observed by narcosis, incoordination, lethargy, 
         drowsiness, and prostration (Rowe and McCollister 1981).

V. ENVIRONMENTAL EFFECTS

   A. Toxicity to Aquatic Organisms

      Methanol has low acute toxicity to aquatic organisms; lethal
      concentrations are much greater than 100 mg/L.  Ninety-six
      hour LC50 values for fish are 28,100 mg/L for Pimephales promelas 
      (fathead minnow), 20,100 mg/L for Oncorhynchus mykiss (rainbow 
      trout), and >28,000 mg/L for Alburnus alburnus (bleak) (AQUIRE 
      1994).  Forty-eight hour LC50 values for Cyprinus carpio 
      (common carp) and Carassius auratus (goldfish) are 28,000 mg/L 
      and 1,700 mg/L, respectively (AQUIRE 1994).  Growth inhibition 
      occurred for 4 strains of Anabaena (blue-green algae) over a range 
      of EC50's of 2.57-3.13% for 10-14 days (AQUIRE 1994).  The LC50 for 
      Artemia salina (brine shrimp) is >10,000 mg/L in 24 hours and that 
      for Culex restuans (mosquito) is 20,000 mg/L in 18 hours 
      (AQUIRE 1994).
      
   B. Toxicity to Terrestrial Organisms

      No information was found in the secondary sources searched regarding 
      the toxicity of methanol to terrestrial organisms.  However, based 
      on the range of oral LD50's, 0.4 to 14.2 g/kg, for monkeys, rats, 
      mice, and rabbits (Rowe and McCollister 1981), it is unlikely that 
      methanol would be toxic to terrestrial animals at environmental 
      levels.

   C. Abiotic Effects

      Methanol reacts with nitrogen dioxide in polluted atmospheres to 
      produce methyl nitrite (HSDB 1994).  According to the definition 
      provided in the Federal Register (1992), methanol is a volatile 
      organic compound (VOC) substance.  As a VOC, methanol 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 methanol as a hazardous
    air pollutant.  Occupational exposure to methanol is regulated by
    the Occupational Safety and Health Administration.  The permissible
    exposure limit (PEL) is 200 parts per million parts of air (ppm) as
    an 8-hour time weighted average (29 CFR 1910.1000).

    Federal agency and other group activities for methanol are
    summarized in Tables 3 and 4.

   TABLE 3.  EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON METHANOL 
________________________________________________________________________
EPA OFFICE            LAW                                PHONE NUMBER
________________________________________________________________________
Pollution Prevention  Toxic Substances Control Act
 & Toxics               (Sec. 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
________________________________________________________________________

             TABLE 4.  OTHER FEDERAL OFFICE/OTHER GROUP 
             CONTACT NUMBERS FOR INFORMATION ON METHANOL
_______________________________________________________________________

Other Agency/Department/Group                      Contact Number
_______________________________________________________________________
Agency for Toxic Substances & Disease Registry    (404) 639-6000
American Conference of Governmental 
   Industrial Hygienists   
(Recommended Exposure Limit (see end note 5): 
   200 ppm)
(Recommended Short Term Exposure Limit (see end 
   note 6):  250 ppm)                             (513) 742-2020
Consumer Product Safety Commission                (301) 817-0994
Food & Drug Administration                        (301) 443-3170
National Institute for Occupational 
   Safety & Health
(Recommended Exposure Limit (see end note 5): 
   200 ppm)                                       (800) 356-4674
Occupational Safety & Health Administration       Check local phone book 
(Permissible Exposure Limit (see end note 7):     for phone number under 
   200 ppm)                                       Department of Labor
_______________________________________________________________________

VII. END NOTES

1. Standard Industrial Classification code is the statistical  
classification standard for all Federal economic statistics.  The code
provides a convenient way to reference economic data on industries of 
interest to the researcher.  SIC codes presented here are not intended to 
be an exhaustive listing; rather, the codes listed should provide an 
indication of where a chemical may be most likely to be found in commerce.

2. Calculated using the factor 1.33 (Verschueren 1983) to convert 4000 ppm
to 5320 mg/m3 which is multiplied by 0.214 (the 12-hour breathing rate, 15
m3 [from the occupational standard 8-hour breathing rate, 10 m3] divided
by the assumed adult body weight, 70 kg) to obtain the dose in mg/kg (U.S.
EPA 1988).

3. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable risk
of deleterious effects during the time period of concern.

4. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable risk
of deleterious effects during the time period of concern.

5. The ACGIH/NIOSH exposure limits are time-weighted average (TWA)
concentrations for an 8-hour workday (ACGIH) and up to a 10-hour workday
(NIOSH) for a 40-hour workweek. 

6. This is a recommended 15-minute exposure limit value that should not be
exceeded at any time.

7. The OSHA exposure limit is a time-weighted-average (TWA) concentration
that must not be exceeded during any 8-hour workshift during a 40-hour
workweek.

VIII.  CITED REFERENCES

ACGIH. 1991. American Conference of Governmental Industrial Hygienists,
Inc. Documentation of the Threshold Limit Values and Biological Exposure
Indices, 6th ed., pp. 903-905.

AQUIRE. 1994. EPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S.
EPA, Duluth, MN. Retrieved March 1994.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck
Index, 11th ed. Merck & Co., Inc., Rahway, NJ, p. 939.

CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data
Bases, retrieved 8/5/94. Syracuse Research Corporation, Syracuse, NY.
 
Federal Register.  1992.  Part 51 - Requirements for Preparation,
Adoption, and Submittal of Implementation Plans. Fed. Reg. 57:3945.

GENETOX. 1992. U.S. EPA GENETOX Program, computerized data base. Retrieved
April 1994.

HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information
Retrieval System, National Library of Medicine. Retrieved August 1994.

NTP. 1994. National Toxicology Program. Management Status Report Produced
from NTP Chemtrack System, 1/11/94. Research Triangle Park, NC: NTP.

Rowe VK, McCollister SB. 1981. Alcohols. In: Patty's Industrial Hygiene
and Toxicology, 3rd ed. Vol. 2C, GD Clayton, FE Clayton, Eds. John Wiley
& Sons, New York, pp. 4528-4541.

TRI92. 1994. 1992 Toxics Release Inventory. Office of Pollution Prevention
and Toxics, U.S. EPA, Washington, D.C., p. 92.

U.S. EPA . 1988. 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. 1994. U.S. Environmental Protection Agency. Integrated Risk
Information System (IRIS) Online. Office of Health and Environmental
Assessment, U.S. EPA, Cincinnati, OH.

Verschueren K, Ed. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Reinhold Company, New York, pp. 818-820.

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.

CHEMFATE.  1994.  Syracuse Research Corporation's Environmental Fate Data
Bases.  Syracuse Research Corporation, Syracuse, NY.

Clayton GD, Clayton FE, Eds.  1981-1982.  Patty's Industrial Hygiene and
Toxicology, 3rd ed.  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 Environmental 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.