X
                                   TECHNICAL REPORT DATA
                            ffleae read tn*auctions on ifit reverse btfort complerint)
 1. REPORT NO.
  EPA/600/8-88/048
                              2.
              3. RECIPIENT'S ACCESSION NO.
                 PB88-179528
 4. TITLE AND SUBTITLE

   Health Effects Assessment  for n-Pentane
              6. REPORT DATE
                                                           6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
                                                            I. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
                                                            10. PROGRAM ELEMENT NO.
                                                            11. CONTRACT/GRANT NO.
 12. SPONSORING AGENCY NAME AND ADDRESS
 Environmental  Criteria and Assessment Office
 Office  of  Research and Development
 U.S.  Environmental Protection Agency
 Cincinnati.  OH  45268	    	
              13. TYPE Of REPORT AND PERIOD COVERED
              14. SPONSORING AGENCY CODE
                EPA/600/22
15. SUPPLEMENTARY NOTES
16. ABSTRACT
   This  report summarizes and  evaluates information relevant  to  a  preliminary interim
 assessment of adverse health  effects  associated with specific chemicals  or compounds.
 The  Office of Emergency and Remedial  Response (Superfund) uses  these  documents in
 preparing  cost-benefit analyses  under Executive Order 12991  for decision-making under
 CERCLA.  All  estimates of acceptable  intakes and carcinogenic potency presented in
 this  document should be considered  as preliminary and reflect limited resources
 allocated  to  this project.  The  intent in these assessments  is  to suggest acceptable
 exposure levels whenever sufficient data are available.  The interim  values  presented
 reflect the relative degree of hazard associated with exposure  or risk to the
 chemical(s) addressed.  Whenever possible, two categories of values have been
 estimated  for systemic toxicants (toxicants for which cancer is not the  endpoint of
 concern).   The first, RfD5 or subchronic reference dose, is  an  estimate  of an exposure
 level that would not be expected to cause adverse effects when  exposure  occurs during
 a limited  time interval.  The RfD is  an estimate of an exposure level  that would not
 be expected to cause adverse effects  when exposure occurs for a significant  portion
 of the  lifespan.  For compounds  for which there is sufficient evidence of
 carcinogen!city, qi*s have been  computed, if appropriate, based on oral  and
 inhalation data if available.
 7.
                                KEY WORDS AND DOCUMENT ANALYSIS
                  DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS  C. COSATI Field/Croup
  DISTRIBUTION STATEMENT
  Public
19. SECURITY CLASS (This Report I

  Unclassified
                           21. NO. Of PAGES
                                              20. SECURITY CLASS (Tha paftj
                                                Unclassified
                           22. PRICE
EPA farm 2220.1 (R«T. 4-77)   PREVIOUS COITION I* OBSOLETE
                                                                          //

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                                            EPA/600/8-88/048
                                            July,  1987
          HEALTH EFFECTS ASSESSMENT
                FOR n-PENTANE
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL  ASSESSMENT
      OFFICE OF RESEARCH AND DEVELOPMENT
    U.S. ENVIRONMENTAL PROTECTION AGENCY
            CINCINNATI, OH 4526fa

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                                  DISCLAIMER


    This   document   has   been   reviewed   In  accordance   with   the   U.S.
Environmental  Protection  Agency's  peer  and  administrative review policies
and approved for publication.  Mention of  trade names  or  commercial products
does not constitute endorsement  or  recommendation  for use.
                                     11

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                                    PREFACE


    This  report  summarizes and evaluates  Information  relevant  to a prelimi-
 nary  Interim assessment  of adverse health effects associated w'ith n-pentane.
 All  estimates of  acceptable Intakes  and carcinogenic potency  presented  1n
 this  document should  be  considered as  preliminary  and reflect  limited  re-
 sources  allocated  to this  project.  Pertinent  toxlcologlc  and  environmental
 data were  located  through  on-Hne  literature  searches  of  the TOXLINE and the
 CHEMFATE/DATALOG data  bases.  The  basic  literature  searched supporting this
 document Is  current up to May, 1986.

    The  Intent In  these  assessments 1s to suggest acceptable exposure levels
 for  noncardnogens  and   risk   cancer  potency  estimates   for  carcinogens
 whenever sufficient  data  were available.  Values were  not  derived  or larger
 uncertainty  factors  were  employed when  the  variable  data  were limited  In
 scope   tending   to  generate  conservative   (I.e.,   protective)  estimates.
 Nevertheless,  the  Interim  values   presented  reflect  the  relative  degree  of
 hazard or risk associated with exposure to the chemlcal(s)  addressed.

    Whenever  possible,  two categories  of values  have been  estimated  for
 systemic  toxicants  (toxicants  for which  cancer  1s   not   the  endpolnt  of
 concern).   The  first,  RfD$  (formerly  AIS)  or subchronlc  reference  dose,  Is
 an estimate  of an  exposure  level  that  would  not be expected to  cause adverse
 effects  when exposure  occurs during a  limited  time Interval  (I.e.,  for  an
 Interval that does not  constitute a  significant  portion  of the Hfespan).
 This type  of exposure  estimate  has not  been  extensively used,  or rigorously
 defined, as  previous  risk  assessment   efforts  have  been  primarily  directed
 towards  exposures  from  toxicants   In  ambient  air  or  water where  lifetime
 exposure   Is  assumed.   Animal  data   used   for   RFD$ estimates  generally
 Include  exposures  with durations   of 30-90  days.   Subchronlc human  data  are
 rarely available.  Reported exposures  are usually from chronic occupational
 exposure  situations  or  from reports  of  acute  accidental   exposure.   These
 values   are  developed  for  both  Inhalation   (RfD$j)  and   oral   (RfDgQ)
 exposures.

    The  RfD  (formerly  AIC)  Is  similar  In  concept  and  addresses  chronic
 exposure.   It Is an estimate  of an exposure  level  that would not be expected
 to cause adverse  effects when exposure  occurs  for a  significant portion  of
 the Hfespan [see  U.S.  EPA (1980) for  a  discussion of this concept].   The
 RfD  1s  route-specific  and  estimates   acceptable  exposure  for either  oral
 (RfOg)  or   Inhalation  (RfDj)  with  the  Implicit  assumption   that  exposure
 by other routes 1s  Insignificant.

    Composite  scores   (CSs)  for   noncardnogens  have   also  been  calculated
where  data  permitted.   These  values  are  used  for  Identifying  reportable
 quantities   and  the methodology for their development  1s  explained  1n  U.S.
 EPA (1983).

    For compounds  for  which there   Is  sufficient evidence of carclnogenldty
 RfD$ and  RfO values  are  not derived.    For a discussion  of  risk  assessment
methodology  for  carcinogens  refer  to  U.S.  EPA (1980).  Since cancer 1s  a
process that  Is  not  characterized  by  a threshold, any exposure contributes
an Increment  of  risk.   For  carcinogens,  q-j*s have been computed,  If appro-
priate, based on  oral  and Inhalation data 1f  available.


                                     111

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                                   ABSTRACT
    Data regarding  n-pentane were  Insufficient  for  quantitative  risk  assess-
ment.  The  more  relevant route of exposure appears  to  be  by  Inhalation.   It
Is  recommended  that  a  complete  pharmacoklnetlc   profile  and  subchronlc
toxlclty testing be performed.

    There are no data  on the cardnogenlclty, chronic  tox1c1ty,  or  pharmaco-
klnetlcs of  n-pentane, and subchronlc toxldty experiments are  not designed
adquately   for   quantitative   assessment   of   risk.    Short-term  Inhalation
exposure  to  either  n-pentane  or  n-hexane  has  produced  respiratory  tract
Irritation  In humans  and nervous  system aberrations 1n both  man and  experi-
mental animals.   N-pentane did not  Increase  the number  of revertants In  a
Salmonella typhlmurlum assay, and had no dominant-lethal effects In mice.   A
complete  pharmacoklnetlcs  profile  and  comprehensive  subchronlc  toxUHy
testing of Inhaled n-pentane are recommended.
                                      1v

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                               ACKNOWLEDGEMENTS


    The  Initial  draft  of  this  report was  prepared  by Syracuse  Research
Corporation  under Contract No.  68-03-3112 for  EPA's  Environmental  Criteria
and  Assessment  Office,  Cincinnati,  OH.   Dr.  Christopher  DeRosa and  Karen
Blackburn  were  the  Technical  Project  Monitors  and John  Helms  (Office  of
Toxic  Substances) was  the  Project Officer.   The  final  documents   In  this
series  were  prepared  for  the  Office  of  Emergency  and Remedial  Response,
Washington, DC.

    Scientists  from  the following  U.S. EPA  offices  provided  review  comments
for this document series:

         Environmental Criteria and Assessment Office, Cincinnati, OH
         Carcinogen Assessment Group
         Office of A1r Quality Planning and Standards
         Office of Solid Waste
         Office of Toxic Substances
         Office of Drinking Water

Editorial review  for the document series was provided by the following:

    Judith Olsen and Erma Durden
    Environmental Criteria and Assessment Office
    Cincinnati, OH

Technical  support services  for  the document  series  was  provided  by  the
following:

    Bette Zwayer, Jacky Bohanon and K1m Davidson
    Environmental Criteria and Assessment Office
    Cincinnati, OH

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                              TABLE  OF  CONTENTS



                                                                       Page



1.  ENVIRONMENTAL CHEMISTRY AND FATE. ... 	     1



2.  ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS 	     3



3.  TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 	     4



4.  CARCINOGENICITY 	     7



5.  REGULATORY STANDARDS AND CRITERIA 	     8



6.  RECOMMENDATIONS 	     9



7.  REFERENCES	    10
                                     v1

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                             LIST OF ABBREVIATIONS

CAS                     Chemical Abstract Service
CBI                     Confidential Business Information
ppm                     Parts per million
STEL                    Short-term  exposure level
TLV                     Threshold limit value
TWA                     Time-weighted average
                                      vll

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                      1.   ENVIRONMENTAL CHEMISTRY AND FATE

    Selected  chemical  and  physical  properties  and  environmental   fate  of
n-pentane are presented  In  Table  1-1.
    In  the  atmosphere,  n-pentane Is expected  to  occur  entirely 1n the vapor
phase.   The atmospheric  half-life  listed  In  Table  1-1 has  been  calculated
based  on HO  radical  reaction rate  constants  ranging  from (3.5H0.13)xlO-12
to  6.55xlO-12 cm3/molecule-sec  at   30°C  and an  ambient  HO  radical  concen-
tration  of  S.OxlO5 molecules/cm3  (Atkinson,  1985).
    In  water, volatilization 1s  expected   to  be a  dominant  fate  process.
Based on an experimentally  determined  value for Henry's Law constant of 1.23
atm-mVmol   at   25°C   (H1ne  and   Mookerjee,   1975),  the   volatilization
half-life of  n-pentane  from a river  1  m deep flowing  1  m/sec with  a  wind
speed of 3  m/sec has been  calculated  to be 2.5 hours  (Lyman  et al.,  1982).
Based  on estimated  bloconcentratlon factors  of  79-220,  bloaccumulation  1n
aquatic  organisms should  not  be significant.
    The  half-life  of n-pentane  1n  soil  could not be located  In the litera-
ture searched.   Based on the  relatively  high  Henry's  Law  constant and vapor
pressure  of  n-pentane   and   assuming  moderate  adsorption  to  soil,  this
compound should  rapidly  volatilize  from  both wet  and  dry soil surfaces.   Its
residence time In soil 1s expected to be higher than In water.
    The  most probable route of human exposure to  n-pentane Is by  Inhalation.
n-Pentane  Is  an extremely  volatile compound  and monitoring  data  Indicates
that It  Is  a  widely occurring atmospheric  pollutant  (Arnts  and Meeks, 1980;
Cavanagh et  al.,  1969; Uno et al., 1985;  Altshuller et al., 1971).
0097h                               -1-                              01/26/87

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                                   TABLE  1-1

                   Selected Chemical  and  Physical  Properties
                      and Environmental Fate  of  n-Pentane
CAS number:

Chemical class:

Molecular weight:

Vapor pressure:


Hater solubility:


Log octanol/water
  partition coefficient:

Bloconcentratlon factor:

Soil adsorption coefficient:

Half-life In
  A1r:
  Water:
  Soil:
109-66-0

aliphatic hydrocarbon

72.15

513 mm Hg at 25°C


38.5 mg/l at 25°C


3.39


79-220 (estimated)

590 (estimated)
2-3 days (estimated)
hours (estimated)
not available
Mackay and Shu1,
1981

Mackay and Shul,
1981

Hansch and Leo,
1985

Lyman et al.,  1982

Lyman et al.,  1982
0097h
   -2-
          10/07/86

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           2.  ABSORPTION  FACTORS  IN  HUMANS AND EXPERIMENTAL ANIMALS







     Pertinent data   regarding  the  absorption  of  n-pentane  after  oral  or



 Inhalation exposure  could  not be  located In  the  available  literature.
0097h                               -3-                              10/07/86

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                3.  TOXICITY IN HUMANS AND EXPERIMENTAL  ANIMALS

    Data  regarding the  oral  toxldty of  n-pentane  are limited to a  single
28-day  experiment  In  rats.   American Petroleum Institute (1985) administered
n-pentane  by  gavage at 0, 0.5 or 2.0  g/kg  5  days/week  for  4  weeks  to  groups
of  10 male  F344  rats.   Control  rats  received  saline  only.    Parameters  of
toxlclty  evaluated  Included  twice  dally  observation  for   mortality  and
clinical  signs  of  toxldty,  terminal body weights and  gross  and  microscopic
appearance of  the  kidneys.   Mortality occurred In 40%  of  high-dose rats  and
20% of  low-dose  rats.   Terminal body weights of  both treated groups were
significantly  less  than controls  (p<0.05).   Absolute  kidney  weights were
lower In  both  treated  groups  (p<0.05)  than In controls.  The  Mstopathologl-
cal appearances  of  the  kidneys was  not remarkable.   This  study  Is  Inadequate
for use 1n risk assessment.
    Data  regarding the  toxldty  of  n-pentane after Inhalation exposure  are
limited.   Gaultler et  al.  (1973)   found polyneuropathy  1n  five  employees
exposed by  Inhalation  to  a  solvent mixture  consisting of 554  n-hexane,  14%
n-heptane and  80% pentane.   Duration of  exposure and exposure  concentration
were  not  specified.   Affected  workers  had anorexia,  paresthesla,  symmetrical
muscle  failure,  asthemla, peripheral  nerve  damage  and  signs of  denervatlon
In the  legs.   Patty and Yant  (1929)  found  no symptoms  of  neuromuscular dis-
order  In  human  volunteers exposed  to  5000  ppm  (-14,750  mg/m3)  n-pentane
for   10   minutes.    Ten  minutes   exposure   to  5000   ppm   (-17,200   mg/m3)
n-hexane,  however, was associated with marked vertigo.
    Male  rats  were exposed  to -3000  ppm (8850  mg/m3)  >99X  pure  n-pentane,
12  hours/day   for  16  weeks,  for study  of nerve  conduction  velocities  and
distal  (tall)   latency to  electrical  stimulation  (Takeuchl  et  al.,  1980,


0097h                                4-                              01/26/87

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 1981).   One  rat  was  sacrificed  at  the end  of  16 weeks,  and  light  and
 electron  microscopy  was  performed on  the gastrocnemlus  and soleus muscles,
 the  dorsal trunk  of  the tall nerve and  the  tibia!  nerve.   N-pentane had no
 effect  on measures  of nerve  conduction,  body weights or  distal  latencies.
 There  was slight  swelling  of the mitochondria and  the  sarcoplasmlc retlcu-
 lum,  and  minor  dilation of  the  myofllaments  of these muscles.   Since  the
 tissues  of only one  rat  were studied  microscopically,  and the nerve conduc-
 tion data  do  not suggest adverse effects, the data of Takeuchl et al. (1980,
 1981) are  Inadequate  for  quantitative  risk assessment.
    Administration of   3000   ppm   (-10,300  mg/m3)   n-hexane,  on  the  same
 treatment  schedule,  resulted In  severe  decreases In  body weight  gain  and
 nerve conduction velocity,  and Increases  In  distal latency (Takeuchl et  al.,
 1980,  1981).   Treated  rats  had  clinical signs  of  neuropathy.   Microscopic
 examination  of  tissues  from  two  n-hexane  .exposed rats  revealed  myelln
 damage,  denervated neuromuscular  Junctions,  muscle  structure  Irregularities
 and axonal degeneration.
    IIT   (1985)  exposed  rats  to  1000  ppm  (-2650  mg/m3)  and  4500   ppm
 (-12,000  mg/m3)  of a  50:50 mixture of n-butane  and  n-pentane,  6 hours/day,
 5 days/week  for  13 weeks.  Exposure was  associated  with  a transient hunched
 appearance, tremors and a nonconcentratlon  related Inhibition  1n body weight
 gain,  which  was  reversible  1n  males.   There   were  no  treatment-related
 changes  on  gross  necropsy   observations,  renal  hlstopathology  or  organ
 weights.
    Lazarew  (1929)  found  that  2-hour  exposure  to  200-300  mg/l  (200-300
 g/m3) n-pentane  caused  mice  to lay  on their sides,  whereas  only  100 mg/i
 (100 g/m3)  n-hexane  for  2  hours  was  needed  for  the same  effect.   Swann  et
0097h                               -5-                              01/26/87

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al.  (1974)  observed no  anesthesia  In mice exposed for  5  minutes  to <16,000
ppm  (-47,200  mg/m3)  n-pentane.   At  32,000  ppm  (-94,400  mg/m3),  light
anesthesia  was  observed during recovery, and  at  higher  concentrations  there
were  signs  of  respiratory  Irritation  and  deep  anesthesia.   NIOSH  (1977)
concluded   that,  within  the  alkane  series  C5-C8,  physiological  potency
Increases as chain  length Increases.
    Epstein  et  al.  (1982)  studied  the potential  dominant-lethal  effects  of
n-pentane,  collected as  fractions  of partlculate atmospheric  pollutants  In
9-60X ether,  In mice.   Before mating, between seven and nine  male mice were
Injected once 1ntraper1toneally  with  between 48 and 666 mg/kg  of  one of the
pentane  fractions.   Females  were  sacrificed  13  days  after  the  midweek  of
their  presumed  mating,  and  autopsled.   Treatment  had  no  effect  on  early
fetal deaths or  prelmplantatlon losses.
    There  are  no  data  on  the  Interactive  effects  of  n-pentane  with  other
toxicants.   CBI   data   Indicate   that  concentrations  of  >10%  n-propane,
n-butane,  Isobutane or   Isopentane  sensitized  dog hearts  to the  effects  of
exogenous eplnephrlne.
0097h                               -6-                              01/26/87

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                              4.  CARCINOGENICITY

    Pertinent  data regarding the carclnogenldty of  n-pentane,  by  any route
of  exposure,  could  not  be  located  1n the  available literature.   The  CBI
files  contained the  results  of an  unpublished  mutagenlclty study  1n which
n-pentane  did  not  Increase the  number  of   revertants  In  six strains  of
Salmonella  typh1mur1um.  with or without metabolic  activation.   NIOSH  (1977)
stated  that C5-C8  alkanes probably  do not  have  carcinogenic  or  mutagenlc
activity  because  they are  not  chemically  related to  compounds  that  express
such activity.
    N-pentane  should  be considered a  U.S.  EPA Group  D  (U.S.  EPA,  1986),  or
IARC  Group 3  compound 1n  terms of  the  available  evidence  of  carcinogenic
potential.   These  classifications  are  for  compounds  with  Inadequate  animal
evidence of carclnogenldty, and no human data.
0097h                               -7-                              03/23/87

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                     5.   REGULATORY STANDARDS AND CRITERIA

    NIOSH  (1977)  recommended  a  TWA  occupational  standard  for  n-pentane
exposure  of  350 rag/m3  and a  15-mlnute celling concentration limit  of  1800
mg/m3.    These   levels   were  determined  by   analogy   to   n-hexane,   which
produces  polyneuropathy  at  levels  <1800  mg/m3.   NIOSH  (1977)  did  not
clearly  Indicate  how  the  standard  was  developed  based  on  these  data.
Because workers  are  typically  exposed to mixtures  of  alkanes, and  because
data  on  the metabolism  of Individual  alkanes  are Incomplete,, NIOSH  (1977)
recommended the same standard for all alkanes.
    ACGIH  (1985)  adopted a TWA  of  600 ppm  (-1800 mg/m3) and a STEL  of  750
ppm  (-2250 mg/m3)  for  n-pentane.   ACGIH  (1986) proposed  that  the TLV  and
the  STEL   should  provide  a  margin  of  safety  for  narcotic  and  Irritant
effects.   They  did  not  rule  out  the possibility  of  polyneuropathy  after
chronic exposure  based  on  the  report  by Gaultler et al.  (1973),  but  stated
that the effect would occur for  n-pentane  at higher  exposure levels than  for
n-hexane.    The  workplace   standard   of   350  mg/m3   (NIOSH,   1977),   based
primarily   on  n-hexane exposure data,  was  therefore  considered unneccesarlly
conservative  for  n-pentane.  The  OSHA (1985) occupational  standard  Is  1000
ppm (-2950 mg/m3) for an 8-hour workday.
0097h                               -8-                              10/07/86

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                              6.  RECOMMENDATIONS

     Because  n-pentane exists In the atmosphere completely In the vapor phase
 (Atkinson,  1985),  and  volatilization  from  both water  (Hlne  and Mookerjee,
 1975)  and soil  1s  apparently  rapid,  1t  Is  likely  that the  more  relevant
 route  of exposure  for  humans  Is  by Inhalation.   Limited  evidence  suggests
 that  the major  toxic  effects  of  Inhaled  short-chain  alkanes  Involve  the
 nervous  system  (Gaultler  et al.,  1973;  Takeuchl  et  a!.,  1980,  1981;  IIT,
 1985;  Lazarew,  1929),  although  there   have  been  few  assessments  of  other
 endpolnts.
     Both  acutely and  subchronlcally,  n-hexane was found  to be consistently
 more toxic than  n-pentane  (NIOSH,  1977) at equlmolar  concentrations, so that
 risk assessment  by  analogy 1s not  recommended.  The ACGIH (1986) TLV appears
 to be too weak a basis  for quantitative  risk assessment.
    Assays  for  reverse mutations  (C8I files)  and dominant-lethal  effects
 (Epstein  et   al.,   1982),  as well  as  the  chemical  structure  of  n-pentane
 (NIOSH, 1977), all  suggest that It  Is not  a carcinogenic or mutagenlc threat.
    It  1s recommended  that  a  complete pharmacoklnetlc profile  of  Inhaled
 n-pentane  In  experimental  animals  be conducted.   Results of  acute  toxldty
 testing In a  relevant species should be a  guideline for the development of a
 multi-concentration  subchronlc  test.   Although  gross  disruption  In  nervous
 system  activity  Is  consistently   found  at  higher  concentrations,  H  Is
 Important  to  establish whether  lower  concentrations  Interfere  with  more
 subtle measures  of  behavioral performance.  Hematologlcal,  blood biochemical
 and  hlstopathologlcal parameters  should also  be assessed at  all  concentra-
 tions 1n a subchronlc study.
0097h                               -9-                              01/26/87

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                                7.  REFERENCES

ACGJH  (American  Conference  of  Governmental  Industrial Hyglenlsts).   1985.
TLVs: Threshold  limit  values  for  chemical  substances  1n the work environment
adopted  by  ACGIH  with  Intended  changes  for   1985-1986.   Cincinnati.  OH.
p. 26.

ACGIH  (American  Conference  of  Governmental  Industrial Hyglenlsts).   1986.
Documentation of  the  Threshold Limit  Values  and Biological  Exposure Indices,
5th ed.  Cincinnati, OH.  p. 463.

Altshuller, A.P., W.A. Lonneman, F.D.  Sutterfleld and S.L.  Kopczynskl.   1971.
Hydrocarbon composition  of  the atmosphere of the Los Angeles  basin -- 1967.
Environ, Scl. Technol.  5: 1009-1016.

American Petroleum  Institute.   1985.   Four-week oral  nephrotoxldty study 1n
male F344 rats.   OTS submission Microfiche #FYI-AY-1284-0280, Addendum  #2.

Arnts, R.R. and  S.A.  Weeks.   1980.  Blogenlc  hydrocarbon contribution  to  the
ambient air  of  selected areas.   U.S.  EPA,  Research Triangle  Park,  NC.   EPA
600/3-80-023.

Atkinson,  R.  1985.   Kinetics and mechanisms of the gas-phase  reactions of
the hydroxyl  radical  with  organic compounds  under atmospheric  conditions:
Chem.  Rev.   85:  83.
0097H                               -10-                             01/26/87

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Cavanaugh,  L.A.,  C.F.  Schadt  and  E.  Robinson.   1969.   Atmospheric  hydro-
carbon  and carbon monoxide  measurements  at Point Barrow, Alaska.   Environ.
Sc1. Technol.  3:  251-257.

Epstein,  S.S.,  E.  Arnold, J.  Andrea,  W.  Bass and Y. Bishop.   1982.   Detec-
tion  of  chemical   mutagens   by  the  dominant  lethal  assay  In  the  mouse.
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