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                          EPA/600/8-88/070
                               JULY 1988
   SUMMARY REVIEW OF HEALTH
    EFFECTS ASSOCIATED WITH
            PROPYLENE
       Health Issue Assessment
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
    OFFICE OF HEALTH AND ENVIRONMENTAL
             ASSESSMENT
    OFFICE OF RESEARCH AND DEVELOPMENT
   U.S. ENVIRONMENTAL PROTECTION AGENCY
     RESEARCH TRIANGLE PARK, NC 27711

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                        Disclaimer
This document has  been  reviewed  in  accordance with U.S.
Environmental Protection Agency policy and approved for publication.
Mention of trade names or commercial products does not constitute
endorsement or recommendation for use.

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                            Preface

     The  Office  of Health  and  Environmental Assessment  has
 prepared  this health  issue assessment  to  serve as  a  source
 document for  EPA use. The health assessment was developed for
 use by the Office  of Air Quality Planning and  Standards to support
 decision  making regarding  possible regulation of  propylene as  a
 hazardous air pollutant under the Clean Air Act,  as amended in 1977.

     In the development  of the assessment  document, the scientific
 literature has been  inventoried, key studies have been evaluated and
 summary/conclusions have been  prepared  so  that the chemical's
 toxicity  and  related characteristics  are  qualitatively  identified
 Observed  effect  levels  and other measures of  dose-response
 relationships are discussed, where appropriate,  so that the nature of
 the adverse health  responses is  placed in perspective with observed
 environmental levels.
through"
                                             ha8 been reviewed
    Information  regarding  sources,  emissions,  atmospheric
 transformation, ambient air concentrations, and human exposure  is
 summarized  to  provide  a preliminary  indication  of  the potential
 presence of  this substance in the ambient  air. While the available
 information  is  presented  as  accurately  as  possible  it  is
 acknowledged to be  limited  and dependent in many instances on
 assumption  rather than  specific data.  This  information  is  not
 intended  and,  therefore, should not  be used  as  an  exposure
 assessment by which to estimate risk to public health.

    If a review of  the  health information indicates  that the Aqencv
 should consider  regulatory action for this substance, a considerable
 effort will  be undertaken to obtain  appropriate, more detailed
 information regarding  sources,  emissions, and  ambient air con-
centrations. Such data will provide additional information for drawina
regulatory conclusions regarding the extent and significance of public
exposure to this substance.
                              in

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                     Table of Contents

                                                        Page

 Figures and Tables  	        vj
 Authors, Contributors, and Reviewers  	'.'.'.'.	   vjj
 1.  Background Information   	'.'.'.'.'.'.'.'.'.'.'.'    1
    1.1  Chemical Characterization and Measurement  . '. '. '. .     1
    1.2  Environmental Release, Transformation
          and Exposure  	         2
    1.3  Environmental Effects	      	11
 2.  Health Effects	.'.'.'.'.'.'.'.""   13
    2.1  Pharmacokinetics and Metabolism		   13
    2.2  Biochemical Effects	        13
    2.3 Acute Toxicity	      14
    2.4 Subchronic Toxicity	   15
    2.5 Chronic Toxicity	      15
    2.6 Mutagenicity  	'.'.'.'.	   -\Q
    2.7 Carcinogenicity  	        	   18
    2.8 Other Health Effects	'...'.'.'.'.'.'/.	  20
3.  Summary	  21
4.  References	       23

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                           Figures

Number
1-1    Daytime propylene reaction sequences in the

1-2
   urban troposphere
Hydroxyl radical-initiated gas-phase oxidation
   of propylene  	
                                                   Page
                            Tables
Number
                                                         Page
 1 -1   Propylene concentrations in selected ambient
          air samples  	   4
 1-2   Reactants and products in the propylene-NOx-air
          photooxidation system	• •	   °
 2-1   Incidence of epithelial changes in the nasal cavities
          of rats exposed to propylene via inhalation  	   16
 2-2   Incidence of tumors in mice exposed to propylene
          via inhalation   	   19
                                VI

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          Authors, Contributors, and Reviewers

    The following personnel of Dynamac Corporation were involved
 in the preparation of this document: Dr. Finis Cavender (Department
 Director); Dr  Nicolas P. Hajjar  (Project  Manager/Principal Author);
 Dr. William McLellan, and Louis  Borghi (Authors);  Dr. Norbert Paqe
 (Technical Reviewer); Anne Gardner (Technical Editor); and Gloria
 Fine  (Information  Specialist). This  document was prepared  bv
 Dynamac Corp., Rockville,  MD under contract to the Environmental
 Criteria and Assessment Office,  Research Triangle  Park   NC (Dr
 Dennis J. Kotchmar, Project Manager/Author).

    Drafts of this document have also been  reviewed for scientific
 and technical merit by the following scientists: Dr. E.  E. Sandmever
 Transcontec,  Inc.,  Pittsburgh, PA;  Dr. Dennis  Lynch, Experimental
 Toxicology Branch, NIOSH, Cincinnati,  OH;  Dr.  Michael  Farrow
 Experimental  Pathology Laboratories,  Inc.,  Herndon   VA- Dr'
 noT6!/!?6^- Valcovic'  Reproductive Effects  Assessment Group'
 EPA,  Washington, DC; Dr. Jerry N. Blancato,  Exposure Assessment
 Group,  EPA  Washmgton,  DC;  and  Dr.  Arthur Chiu, Carcinoqen
Assessment Group, EPA, Washington, DC.

   .The information presented in this document is based on  literature
searches of databases and  updates, the  most recent of which was
conducted during March 1988.
                             VII

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             1. BACKGROUND INFORMATION
    This overview provides a brief summary of the data available on
 the health effects of exposure to propylene. Emphasis is placed on
 determining whether  there  is evidence to suggest  that propylene
 exerts effects on human health under conditions and  at  concen-
 trations commonly experienced by the general public.  Both acute and
 chronic  effects  are addressed, including  general toxicity,  muta-
 genicity, and carcinogenicity. To place  the health effects discussion
 in perspective, this report also summarizes  air quality  aspects of
 propylene in the  United States,  including sources, distribution, fate,
 and concentrations associated with certain point sources.

 1.1 Chemical Characterization and Measurement

    Propylene (CAS  No. 115-07-1) has the  chemical structure
 CHaCH = CH2- It is a colorless gas with a molecular weight of 42.08
 It is only slightly soluble in water (44.6 ml/100 ml at 20°C and  1  atm
 or 82.1  mg/100  ml)  and has  a high  vapor pressure (10 atm at
 19.8°C) (TDB; Schoenberg et al., 1982).

    Although infrared  spectrophotometry can be  used to  detect
 propylene in gaseous mixtures (International Agency for Research on
 Cancer,  1979), gas chromatography (GC) is  the analytical  method
 most commonly used to measure concentrations of the compound in
 environmental  media and combustion gases. For the  qualitative and
 quantitative determination, gas chromatography with flame ionization
 detection  (GC/FID) and mass spectroscopy  (MS) have been used
 extensively,  e.g., Nelson and Quigley (1982) and Crow et al.  (1982)
 for  ambient air  concentrations;  Hoff et al.  (1982)  for  pyrolysis
 products; and  Yoshida et al.  (1978)  for polymer combustion gases.
 Cryogenic collection and the  use of solid adsorbents have been used
 as sample preconcentration  steps preceding  GC analyses.  The GC
 method used by Westberg et al. (1974) for the separation of Ca-Ce
 hydrocarbons  in ambient  air uses  a  special chemically bonded
 stationary phase and has a detection limit of 0.5  ppb. Single run C2-
 GIO  HC analysis was accomplished using  the  open trap  cryo-
 focusing/GC-reinjection technique (Matuska -et al.,  1986).  An  aver-
 age retention time of 4.322 minutes was  reported  for propylene.

   Rudolph  et  al.  (1981)  developed  a  GC/FID  method  for
determination of low levels of Ca-Cs hydrocarbons  in  grab samples
 (0.5-2  cm3) of  air.   Hydrocarbons  in the samples are  first
concentrated on  a packed  pre-column with  porous silica  and

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Carbosieve B  kept at -35°C  and then  separated on  a column
packed  with untreated porous  silica  (Spherosil  XOB  075).  The
detection limit  for propylene using this method is  4 ppt. A  similar
GC/FID  method  for determining  C2-Cs hydrocarbons  has recently
been  described  by Reineke and Bachmann (1985).  This method
employs a three-detector setup and   reproducibly  quantifies
propylene at concentrations as low as 12 ppt.
    A GC/FID  method, with detection limits of  2 x  10-12 M for gas
and 5x10-8 ml  for gas dissolved in 1  liter of sea  water at standard
temperature and pressure, was used by Swinnerton and  Linnenbom
(1967) to measure  propylene concentrations in sea water  samples.
Frisch et  al.  (1982)  used a  gas radio  chromatographic  liquid
scintillation spectrophotometric method to  detect  propylene  in the
smoke  of  cigarettes  made with a tobacco filler treated  with  a
radiolabeled insecticide.

1.2 Environmental Release, Transformation,  and Exposure

    Domestic  production capacity of  propylene, as  of  January  1,
1984,  was estimated  to  be about 22.3  billion pounds  annually,
involving 37 companies operating at 61  plant sites  (SRI International,
1984). The compound is  produced as a  by-product of petroleum
refining and as  a coproduct of  ethylene  manufacture. Propylene  is
used in  both chemical and refinery applications. Refinery-generated
propylene is the main source of the compound for nonchemical uses,
whereas the ethylene coproduct material  is used mainly  in chemical
applications. Chemical applications accounted for about 58 percent  of
 domestic consumption of the compound in 1979; refinery applications
 accounted for the  remaining 42 percent.  Propylene is marketed  in
three grades:  refinery  (50-70  percent  pure),  chemical  (90-96
 percent pure),  and  polymer   (>99  percent  pure)  (Chemical
 Economics Handbook, 1980; Schoenberg et al., 1982).

    The current demand  of 14.6 billion  pounds of propylene annually
 for chemical applications is expected to grow at an average rate of 5
 percent per year through 1988, to  a level of 17.7  billion  pounds
 annually (Chemical Marketing  Reporter,  1984). Propylene  is used
 both in the chemical and the petroleum industries as  a  monomer in
 the production of polypropylene (27 percent),  and  as  a  raw  material
 in the  production of acrylonitrile (18 percent), propylene oxide (9.7
 percent), and cumene (7.9 percent of the consumption). Production
 of isopropyl  alcohol,  other alcohols,  and numerous  miscellaneous
 chemicals (e.g., propylene oligomers, butyraldehydes,  acrylic acid,
 ally!  chloride, and  acrolein) account for the remainder of propylene
 chemical  consumption  (Chemical  Economics  Handbook,  1980;
 Schoenberg et al., 1982; Chemical Marketing Reporter, 1984).

     Data on the current demand for propylene  in refinery applications
 were not  available. In refinery applications, propylene is used as a
 feedstock for high-octane blending components  of  gasoline (e.g.,

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  alkylate and polymer gasoline)  and as a fuel  (Chemical  Economics
  Handbook, 1980; Schoenberg et al., 1982).

     Propylene is expected to be released to the environment mainly
  in pyrolysis gases from the combustion processes and incidentally in
  gaseous emissions from industrial manufacturing and use  operations
  However,  quantitative estimates of such industrial releases were  not
  found. Sivertsen (1983) identified propylene as a constituent of  the
  fugitive hydrocarbon emissions of an  ethylene  cracking unit at a
  petrochemical  plant  in  Norway,  but  quantitative  data  were  not
  presented.

     Propylene  is also expected to be released to the environment in
  the combustion gases of  hydrocarbon  fuels, wood, cigarettes and
  synthetic  polymers,  refuse, etc.  Jackson  (1978) found that the
  propylene  content  of the  exhaust  gases  of  automobiles  burning
  leaded  and unleaded gasoline  was  lower  in  late-model  cars
  equipped with  oxidative catalytic converters (2.9 percent as carbon)
 than earlier  models  without converters (6.5 percent as carbon)
 Sigsby et  al.  (1987)  found similar  results with propylene  content
 decreasing further to  1.9 percent  as carbon in 1982 models
 Propylene  has also  been detected in the  exhaust  gases  of  diesel-
 fuel-powered  automobiles,  emitted  at a  rate  of 0.0207  g/mile
 (International Agency for Research on Cancer, 1979), and j'et engines
 at  maximum concentrations of about 130-143 ppm (Katzman and
 Libby,  1975).  The  compound has been  found in  the combustion
 gases and smoke from plant materials such as white pine wood
 (OMara,  1974) and  cigarette  tobacco treated  with  radiolabeled
 methoprene,  an insect growth regulator  (at 0.2 per  cent of the total
 radioactivity recovered in the smoke)  (Frisch et al.,  1982). Levels  of
 < 0.4-1.5  ppm propylene  were  found in  the  flue  gases  of   a
 municipal incinerator (Carotti and Kaiser,  1972).

    Propylene can be released to the environment as emissions from
 incinerators burning hazardous waste. Allen et al. (1986)  monitored
 stack emissions from an incinerator burning hazardous (infectious)
 hospital  waste  (infectious  and noninfectious)  and calculated  an
 emission factor for propylene of < 0.0011 g/kg.  Propylene was not
 found above the detection limit (0.5 ppm) in any of 22 samples  taken.

    Thermal  decomposition  products  of polymers   such as
 polyethylene (Hoff et  al., 1982),  polyamides (Yoshida et al   1978)
 and polyacrylonitrile  (Woolley, 1982)  have  been found to'contain
 propylene.  Woolley  reported that propylene  was present  at  a
 concentration of about 10.7 ppm in the  combustion  gases following
 the burning of 5 kg of polypropylene in a 27-m3 room (closed  door)
 In addition  to  these  sources,  propylene is  produced as  a natural
 metabolite of trees and germinating beans,  corn, cotton, and  peas
 (Vancura and  Stotzky,  1976; Kusy and  Kusy, 1982).

    Propylene concentrations in  ambient air samples  have  been
found to vary diurnally and  with wind direction (Bos et al.,  1977).

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Sexton  and  Westberg  (1984)  reported  that  ground-level
concentrations of propylene in urban air samples collected in seven
US  cities ranged from 4 to 17  ppbC  (geometric mean), whereas
concentrations in rural surface air samples from six  domestic sites
ranged from <0.5 to 3.0 ppbC (geometric mean). Selected ambient
air monitoring data are presented  in Table 1-1.
Table 1-1. Propylene Concentrations in Selected Ambient Air
Samples
        Location          Concentration             Reference
Azusa, CA
Los-Angeles, CA
Philadelphia, PA3
Rural Southern Ontario
Atlantic Ocean (marine air)
Arctic air
(spring haze)
(summer)
Bombay, India3
Delft The Netherlands
Japan (industrial area near
petrochemical plant)
Julich, FRG (semirural)
Sydney, Australia
Lancaster, England

United Kingdom (rural)

4 ppb avg.
10.5 ppb avg.
7-32 ppb (vol.)
7-260 ppb
18-141 ppt
0.05 ppb
1180 ppt avg.
5 pptb
24 ppt
187 ppt
0.4-18.7 ppb
9.1 ppb (vol.) avg.
8 ppb max.
10-100 ppb
5 ppb
7.4 ppb (vol.) avg.
5.1 ppbc
Geometric mean
0.7 ppb avg.;
0.10-4.8 ppb
ranqe
Altshuller et al. (1971)
Altshuller et al. (1971)
Grosjean and Fung (1 984)
Giannovario et al. (1 976)
Anlauf etal. (1985)
Rudolph etal. (1981)
Schmidbauer and Oehme (1985)
Khalil and Rasmussen (1984)
Hovetal. (1984)
Hovetal. (1984)
Netravalkar and Mohan Rao (1984)
Mohan Rao and Pandit (1 988)
Bos etal. (1977)
International Agency for Research
on Cancer (1 979)
Rudolph etal. (1981)
Nelson and Quigley (1982)
Colbeck and Harrison (1985)

International Agency for Research
on Cancer (1979)

 ^Suburban location near industrial complexes.
 ^Difference in concentration in and out of haze layers.
     Propylene concentrations have been  shown to be higher inside
 the home than outside.  Lamb  et al.  (1985)  detected propylene  at
 concentrations of 0.6, 7.1, and 2.2  yg/m.3 inside a home  in August
 1981, December 1981, and June 1982, respectively. The ambient air
 concentrations outside  the home  were  0.9 and  0.5  ixg/m.3  jn
 December 1981  and June 1982, respectively. The authors attributed
 the increased levels of propylene (and other hydrocarbons) in the
 home  to  sources such  as gas  heating, automobile exhaust, and
 aerosol propellents.
     Surface water samples taken from the Gulf of Mexico,  Caribbean
 Sea, Atlantic Ocean, and Pacific Ocean have been found  to contain

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  propylene at  concentrations of  0.1-16  ng/l  (Swinnerton  and
  Lamontagne, 1974).

     Estimates of occupational  exposures to propylene have  been
  reported in industrial hygiene  surveys performed by the National
  Institute  for  Occupational  Safety and Health. According  to the
  National  Occupational Hazard Survey (NOHS), 10,274 workers were
  potentially exposed to propylene in domestic  workplace environments
  in 1970.  Preliminary  data  for  1980 by  the National  Occupational
  Exposure Survey (NOES) indicate that  4,548 workers, including 136
  women, were exposed to the compound.

     Atmospheric concentration limits in  the workplace have not been
  established for  propylene  by either the  Occupational Safety  and
  Health Administration  or the American  Conference of  Governmental
  industrial Hygienists.  However, a suggested maximum permissible
  exposure  limit  of 4,000 ppm  (6,984  mg/m3) (one-fifth the  lower
  flammable limit) has been suggested by  Gerarde (1963).

     Propylene'has odor  thresholds of 5.7-28.6 ppm (10-50 ma/m3
  detection)  and  about 57.3  ppm (100  mg/m3, recognition)  an
 organoleptic (taste) limit of 0.5 mg/l, and a light sensitivity to the  eves
 of approximately  6.3  ppm  (11  mg/m3)  (Verschueren,  1983-
 Krasovitskaya and Malyarova, 1966).

    Propylene released to the environment from point  and  nonpoint
 sources is expected to partition into  the atmosphere due to its hiqh
 vapor pressure. However, its mobility may be limited because of the
 relatively higher density of propylene (1.45) as compared to air (1 0)
 Moreover, since propylene is also highly reactive, chemical reactions
 and degradative processes will probably limit  its transport  and
 decrease  its residence time in the atmosphere.

    The chemical properties of propylene  are  characterized  by its
 double bond and allylic hydrogen atoms. The carbon-carbon double
 bond serves as a source of electrons and thus will easily  undergo
 electrophilic addition  reactions that  are characteristic  of alkenes
 Several types of reactions that occur at room temperature include the
 addition of  halogens  and hydrogen halides, hydroxylation  glycol
 formation, and ozonolysis (Morrison  and Boyd,  1973)  Propylene
 reacts vigorously with  oxidizing materials such as  NO2, N2O4  and
  t2?; Fu1rthermore' ''Quid propylene  will explode on contact with water
 at 315-348 K (Schoenberg et al., 1982).

    The atmospheric fate and photochemical reactions of propylene
 such  as the formation of photochemical oxidants and  smog  have
 been  studied  by several investigators.  Graedel et  al  (1976)
 developed a mathematical model  of  photochemical processes to
 study the  fundamental atmospheric chemistry of the troposphere
The model included chemical kinetics, time-related appearances of
trace contaminated sources,  solar flux variations, bulk airflow and a
geographical matrix of "reaction volumes."  Data  on the diurnal rates

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of several groups of reactions between atmospheric components and
propylene indicated  that the  principal reactant was  the hydroxyl
radical (OH), which accounted for more than 75 percent of the total
propylene removed. The reactions of propylene with ozone occurred
predominantly in the evening. The reactions of  propylene with atomic
oxygen or excited SOa were reported  to  be  insignificant in the
environment  because  of  their relatively low  concentration.  Eight
daylight photochemical reaction chains involved  in the removal  of
propylene from the atmosphere are shown in  Figure 1-1.  Pathways
1  2. and 3  produced two aldehyde molecules for each  propylene
molecule, whereas pathways  4-7 produced  one aldehyde molecule
and  one free radical. The free radicals, in turn, produced additional
hydrogen radicals  by other reactions. The  authors concluded that
once the chain of propylene attack began, the production  of
aldehydes, organic radicals,  and  organic nitrate products was  self-
sustaining.

Figure 1-1. Daytime propylene reaction sequences in the uitoan troposphere.
         Source: Graedel ef al. (1976).

          CH262  + CH3CHO  Q       Oa   CH3CH02 + HCHO

                        ^CH^HCHaO*
                     03       ±         °3
                           O
CH3CH = CHSOj.H-4	—"CH3CH
                   (8)
                                (3)
                     (7)
       CH3C(OH)HCH2
                                                        CH2 + HO
           INO


    HCHO + CHgCHOH
                        CH3CHCH2OH
     Formaldehyde
                            CH3CH2CHO
                              3  z
                           Propionaldehyde
                                              CH2 = CHCHO + HO2


                                                 Acraleiin
                                           CH3CHO + CH3O


                                           Acetaldehyde
     The OH-initiated  gas-phase  oxidation  of several compounds,
  including  propylene,  was  studied by  Edney et al.  (1982).  The

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 mechanism  of _ this oxidation  reaction with  propylene is  shown in
 Figure 1-2.  Using  the rate constant and average OH concentration
 values,  the  atmospheric half-life of propylene was calculated to be
 7.7 hours at approximately 23°C.

  Figure 1-2. Hydroxyl radical-initiated gas-phase oxidation of propylene
          Source: Edney et a/. (1982).

                         CH3CH = CH2 + OH*


                                        O,
                     /*  .          \
CH3CHOH - CH2O2
NO 4- NO2
CH3CHOH - CH2O*
V
HCHO + CH3CHO n
CH3CHO2 - CH2OH
NO 4- NO2
CH3CHO*- CH2OH
°*/
y HO2
    The  atmospheric  residence  time (T) of  propylene can be
estimated using the method of Lyman et al. (1982), which estimates
residence time as a function of reaction rates  with hydroxyl radicals
and ozone but does not consider reactions with other substances or
photodissociation.  Therefore, T must  be  considered  a  maximum
value.  Using  the  rate  constants for reactions of propylene with  OH
(koH  =  1-5  x 1010 liter-mo 1-1-sec-l) and O3  (kQa =  7.8  x  103
liter-moM-sec-1), and  average  concentrations  for  OH  (global
annual average, 1.8 x 10-15 mo| / I) and O3 (urban annual average,
5.0 x  10-9 mof/ I), the estimated  TQH is 10.3 hours  and the TO, is
7.1 hours.
            et al.  (1979,  1980)  studied  the  photo-oxidation of
           in an  evacuable  photochemical smog  chamber.
    Akimoto
*    ""*          	'  ™~ w — •—«««•'•'-'  f-r>ivs«.v/vsll{^llllOCll  Ol I lt_/U  UlldlllUCr
Quantitative analysis of the products was  made  in situ  by a long-
path Fourier  transform infrared spectrometer.  The products formed
under dry or humid conditions (relative humidity 40 percent) in  the
photo-oxidation system containing propylene, NOX, and air are listed
in Table 1-2. Maximum  ozone formation  was obtained when  the
initial concentration ratio  of propylene to NOX  was larger than 3  In
the presence of water vapor,  maximum ozone  formation was slightly
lower compared to the dry air system. There  was no effect on  the
yield of  other  chemicals.  However, the  addition of  water  vapor
markedly enhanced the yield of formic acid (from about 0.16 to 0 53

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ppm  maximum  yield), which was ascribed  to  the reaction of
propylene with formed ozone.  The  authors suggested that the
mechanism may involve the following reactions:
                                x°
                  CH2OO--> CH2  I  -» HCOOH

        •CH2OO-  +  H2O-> [CH2OO-H2O]-»HCOOH + H2O

    Mutagenic, genotoxic, and cytotoxic effects of the photochemical
reaction products of propylene plus NOX have been reported. These
are briefly discussed in Section 3.6.
    The effects of water vapor and carbon monoxide on the photo-
oxidation of propylene in the presence of NOX were also investigated
by Nguyen  and Phillips (1979). Water vapor (<11,000 ppm) had no
effect on the photo-oxidation rate of propylene by  NOX  or on the
yield of NO2  and  03.  The formation  of  formic acid  was  not
investigated by the authors.  Carbon monoxide (<200  ppm), on the
other  hand, increased the rate of  propylene  photo-oxidation  and
product formation.

    Table 1-2. Reactants and Products in the Propylene-NOx-Air
    Photo-Oxidation System
                             Initial Concentration, ppm
Experiment
1
2
3
4
C3H6
3.05
3.04
3.06
3.01
NOX
1.500
1.403
1.583
1.516
NO
1.477
1.358
0.016
0.012
Maximum Yield,
Experiment
1
2
3
4
03
1.20
1.04
1.30
1.15
HCHO CH3CHO
1.75 1.30
1.82 1.32
1.92 1.18
1.82 1.32
PAN&
0.75
0.64
0.76
0.59
NO2
0.023
0.045
1.567
1.504
ppm
PGDN0
0.10
0.11
0.10
0.09
H2Oa
<1
1.7X104
<•<
1.7X104

N205 HNO3
0.03 0.23
0.05 NDd
0.06 0.19
0.04 NDd
     aRH=40% at30°C.
     bperoxyacetyl nitrate.
     CT ,2-Propanediol dinitrate.
     dNot determined due to H2O interference.

     Source: Akomoto et al. (1980).

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    Propylene  glycol dinitrate  was the major  product  in the  gas-
 phase reaction  of N2Os with propylene in dry air  in an evacuable
 smog chamber (Hoshino  et  al., 1978).  Other  products  were
 acetaldehyde,  propylene oxide,  NC>2, and HNO3.  The  ratio  of
 propylene glycol dinitrate,  acetaldehyde, and propylene oxide
 appeared to be  independent of the N2C>5 concentration.  The authors
 suggested that the  formation  of  propylene  glycol dinitrate  in the
 propylene-NOx-air  photo-oxidation   system  resulted from the
 reaction of propylene with  generated N2O5 or  N03  (nitric oxide)
 radical (Hoshino et al., 1978; Akimoto et al., 1979, 1980).

    The gas-phase  reactions of  nitrate radicals with  a series  of
 organic compounds, including propylene, in air  at room  temperature
 were recently reported by Atkinson et al. (1984). The reactions with
 alkenes were, shown to proceed via initial NO3 radical addition to the
 double bond:

                                 ONO2

    • N03 + CH3CH = CH2 -> CH3CHCH2   + CH3 CHCH2ONO2

    Under atmospheric conditions, the two radicals  formed are
 expected to  react with  O2  rapidly to  yield the nitroxyperoxyalkyl
 nitrate and dinitrate  as final  products, although the exact  reaction
 pathway for dinitrate  formation  is  not  known. The rate constant for
 the gas-phase  reaction of  propylene with nitrate radicals  was
 reported to be  4.2   ±  0.9  x  10-12   liter-moM-sec-i. Based on
 the kinetic data generated in this  study together with  the observed
 ambient  atmospheric concentrations of the NO3 radicals that are
 more prevalent during the nighttime, the authors suggested  that the
 reactions  of the  NO3 radicals with the more reactive alkenes  and
 hydroxy-substituted  aromatic compounds may  be an important
 nighttime sink for the radicals and the reactive organic compounds.

    Shepson  et al.  (1985) conducted  smog chamber  studies of
 C3H6/N2Os reactions at low (ppm) reaction levels to determine the
 various reaction mechanisms and yields for the production of organic
 nitrates.  The concentration  of  N2Os  and  propylene  in the  dark
 reaction  were 0.68  and 1.85  ppm  respectively.  Major products
 positively  identified were propylene glycol  dinitrate,  2-hydroxypropyl
 nitrate, and 2-(nitrooxy) propyl  alcohol.  Limited evidence was also
 presented  for  the  formation  of  a-(nitrooxy)  acetone, which is
 produced by a series of reactions summarized as follows:

                     02
         C3H6  + NO3 -* CH3C(O)CH2ONO2 (unbalanced)

    The authors reported that under their experimental  conditions,
which more closely approximate atmospheric conditions, the yields of
propylene glycol dinitrate are not nearly or large  as has been shown
experimentally at higher  initial concentrations of N2Os/C3H6.  This
was due to the competing reactions  producing formaldehyde and
acetaldehyde, or a-(nitrooxy) acetone. The formation  of  a-(nitro-

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oxy) acetone was considered to be a significant finding, since it has
been shown to be mutagenic (Shepson et al.,  1985;  Kleindienst et
al.f 1985; see also the mutagenicity section).
    Upon  release to surface waters,  a small amount of propylene
may dissolve in water, but most of the released  material  is expected
to volatilize to the atmosphere.  Propylene has  been detected in
marine and fresh waters, in trace amounts. Propylene  surface levels
in the Gulf of Mexico have been determined at  9.3 x 10-'ml / I and
In the North Atlantic at 5.9 x 1Q-7ml / I water. Fresh water  levels in
Russia  have been determined at  0.5  mg propylene in  1965
(Sandmeyer, 1985).  In water bodies,  propylene is readily degraded
by microorganisms.  Therefore, propylene is  not  expected to
bioaccumulate  or bioconcentrate in  organisms  and  food  chains.
Under calm  atmospheric conditions, it  has  been  reported  that
propylene  will  sink  to  the  ground because it is denser  than air
(OHMTADS). However,  due  to its high vapor pressure, it is expected
that releases of propylene to soil would be readily transported to air
or water.
    Two studies were  reported on  the microbial oxidation and
metabolism of  propylene  (Cerniglia   et  al.,  1976;  Perry,  1980).
Propane-grown  cells  of  Mycobacterium  convolutum  oxidized
propylene rapidly to acrylate. The rate of oxidation was 51 u' Oa/mg
cells/hour. However, microbial growth  was not observed because the
acrylate inhibited  fatty  acid  oxidation by these  microorganisms. A
mixed culture of two microbial species capable  of utilizing propylene
as the  sole source of carbon and energy was also  isolated by soil
enrichment (Cerniglia  et al.,  1976). One  was  a red-pigmented
organism  designated  YS-3R and identified as being similar  to
 Thermus aquaticus (a thermophilic heterotrophic  organism), and the
other was a small,  white,  colony-forming organism  designated YS-
3  (Perry,  1980).  An axenic culture  isolated from marine  soil  and
 designated as strain PL-1 also metabolized propylene and  utilized  it
 as the  sole  carbon source. The rate of oxidation was 81 ul O2/mg
 cells/hour.  Radiolabeled experiments with  [1~14C]  propylene  and
 14CO2 in the  presence or absence  of arsenite  (an   inhibitor of
 pyruvate metabolism)  indicated  that propylene  was not metabolized
 into pyruvate, but rather was cleaved into two  products,  the  first
 containing one carbon atom and the second containing two. Isocitrate
 lyase activity and fatty acid  profile determination further indicated that
 the mixed culture and  strain PL-1 oxidized propylene at the double
 bond, resulting  in cleavage of the molecule.
     In  contrast, the ratio of propylene's 5-day biochemical oxygen
 demand to its chemical oxygen demand (5-day BOD/COD), used as
 an estimate of biodegradability,  was  zero, indicating  that it  was
 relatively undegradable  (Lyman et al.,  1982).  However,  the
 experimental conditions for  BOD determination were not presented,
 and a complete evaluation of this finding could not be made.
                                10

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 1.3 Environmental Effects

    The available literature on the ecological effects of propylene was
 very limited. Data were found only on the in vivo and in vitro effects
 of propylene on  higher  plants.  No toxicity  data  were found  on  the
 effects of propylene on aquatic plants, invertebrates, microorganisms,
 or fish. Van Haut and Prinz (1979) reported that propylene's  toxicity
 to plants  was  essentially insignificant when compared to ethylene,
 and  they  concluded  that propylene emissions would have  practically
 no  adverse effects  on  plant growth. In a  short-term test,  plants,
 including  the  bushbean,  radish, cress,  petunia,  and  geranium,
 showed characteristic damage  following exposure  to ethylene  at
 concentrations  ranging from 0.1  to 1.44  mg/m3 for varied periods of
 time; i.e.,  0.5-14.0 days. Propylene concentrations ranging from 360
 to 1500 times  those of ethylene (actual concentrations  not given)
 were needed to achieve comparable growth inhibition, but such high
 propylene  concentrations  are  not expected  to  be found  in the
 ambient air.

    In  an  in vitro  study of the mechanism of action of ethylene as a
 plant growth inhibitor, Smith  et al.  (1983)  examined the effect  of
 ethylene  and  some  of  its analogs,   including propylene,  on the
 oxidation  of indole-3-acetic acid. Ethylene and its analogs inhibited
 the  oxidation  of indole-3-acetic   acid   by peroxidase  under
 conditions where the  Fep + + ±?  Compound  III  (an oxy-ferrous
 complex of peroxidase) shuttle was activated. Inhibition occurred only
 in the  presence of the superoxide anion radical (O2~). Spectral and
 kinetic data indicated that ethylene and its analogs enhanced the rate
of reaction of C>2~ with peroxidase; i.e., the  Fep+ + ±s Compound III
shuttle, resulting in the formation of Compound III. Propylene was a
 less effective inhibitor than ethylene.
                               11

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                   2.  HEALTH EFFECTS

 2.1 Pharmacokinetics and Metabolism

    Limited information was  available on the  metabolism of
 propylene. The kinetics of  uptake and metabolism of propylene in
 male CBA mice  was  studied by  Svensson  and Osterman-Golkar
 (1984). Groups of 15 mice were placed in a closed recirculation 11-
 liter chamber  and  exposed to propylene at eight  concentrations
 ranging from 95 to 1,715 ppm. The level of propylene in the air was
 determined by gas chromatography and was followed for at least one
 half-life  during  the exposure period.  The  rate  of uptake at
 equilibrium (between 100 and 150 minutes after onset of exposure)
 was estimated  from the slope of  the  concentration-time  curve and
 expressed in milligrams of propylene per kilogram of body weight per
 hour.  The metabolism of propylene followed  Michaelis-Menton
 kinetics. A double reciprocal plot  of  these  rates versus chamber
 concentration   (which  is a Lineweaver-Burk  representation  of
 Michaelis-Menton  kinetics)  allowed determination  of  the Km  and
 Vmax-  The Km (concentration in  air  at which uptake proceeds at
 half-maximum  velocity)  was  800  ± 60  ppm, and the  Vmax
 (maximum rate  of uptake) was 8 ± 0.5 mg/kg/hour. Since propylene
 was expected to be oxidized to  propylene oxide in a manner similar
 to that previously demonstrated for ethylene in mice,  the combined
 uptake of both ethylene and propylene was studied. It was found that
 the uptake of  14C-ethylene (0.01  ppm), in the presence of a high
 concentration of  propylene (1,260 ppm), was lower  than  in  the
 absence  of propylene.  This finding  suggested  a  competitive
 interaction  of both  compounds in their metabolic pathways and
 indicated that propylene is converted in vivo to propylene oxide. The
 authors reported that the metabolic pathway of propylene involved
 oxidation to the corresponding oxide  and subsequent alkylation of
 nucleophilic sites  in  macromolecules. Alternatively, propyiene and/or
 propylene oxide were  metabolized by other pathways and excreted
 (see also below).

2.2 Biochemical Effects

    Svensson  and  Osterman-Golkar (1984)  also  studied  the
alkylation of macromolecules in mice exposed to 14C-propylene to
demonstrate the transient appearance of propylene oxide in tissues.
In  one  experiment,  the mice were  exposed for  1  hour to an
atmosphere containing  2830  ppm of  14C-propylene and  then
sacrificed  13 hours later. Hemoglobin from blood and DNA from, the
                              13

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liver, testes, spleen, lungs, and kidneys  were isolated, and labeled
alkylation  products  in  these  macromolecules were  identified.  The
amount of radioactivity bound to the DNA of the liver and pooled
organs  was below  the level  of detection.  The hemoglobin  was
hydrolyzed, and the resulting amino acids  chromatographed by ion
exchange after adding carrier  amino acids  and 2-hydroxypropylated
derivatives of  cysteine, histidine, and valine.  The major part of the
radioactivity of hemoglobin (about  70 percent)  eluted with serine,
glycine, and alanine, indicating extensive biodegradation of propylene
followed by  biosynthetic incorporation  of  1  and  2  I4c-carbon
fragments into amino acids. Hemoglobin hydrolysates also  showed
radioactivity associated with  S-(2-hydroxypropyl)  cysteine,  N-(2-
hydroxypropyl) valine,  and N-(2-hydroxypropyl)  histidine. The  de-
gree of alkylation of cysteine  and valine  was 2 nmol/g  of hemo-
globin,  and that for  histidine  was  0.9  nmol/g  of  hemoglobin. In
another experiment, mice were exposed to  20,000 ppm of unlabeled
propylene for 4  hours/day for  8  days.  Blood  was  collected
immediately after the last exposure and  hemoglobin  alkylation
assessed.  The  degree of alkylation was  2.2 nmol  N-(2-hydroxy-
propyl)  histidine/g of hemoglobin per hour.  Two  diastereoisomers of
the histidine  derivative were isolated, which were  similar to  those
obtained from the reaction of DL-propylene oxide with histidine. The
authors suggested  that  these  results indicate nonstereospecific
oxidation  of  propylene  to  propylene  oxide.  However, the  data
presented do not necessarily support such a mechanism.

    The role of the cytochrome P-450 system in the hepatotoxicity
of propylene was investigated by Osimitz and Conolly (1985).  Male
Sprague-Dawley  rats  (200-  275  g) were  pretreated  with  either
polychlorinated biphenyls  (PCB,  Aroclor 1254),  phenobarbital (PB),
0-naphthoflavone (BNF), or  BNF  + PB to  maximally  induce the
appropriate isozymes  of  cytochrome P-450.  Appropriate vehicle
control groups were also included. The animals (at least four rats per
group)  were then exposed to  CP-grade propylene (>99.5 percent
pure) at 0 or 50,000 ppm for 4 hours. All animals were sacrificed 20
hours  postexposure,  and  measurements  of serum sorbitol
dehydrogenase (SDH) and  alanine leucine transaminase  (ALT)
activities  were taken as  indicators  of hepatotoxicity.  Propylene  was
not  hepatotoxic  in untreated,  PB-, BNF-,  or BNF  +  PB-treated
animals, but  it  was hepatotoxic in rats pretreated with  PCB.  The
authors concluded  that an  isozyme  of  cytochrome  P-450 induced
by PCB is required to convert  propylene to a hepatotoxic metabolite
in pretreated rats.

2.3 Acute Toxicity

    No LDso values or lethal  dose estimates were found in the
literature. Reports in the early literature indicate that propylene is not
very  toxic. Exposure  of  white mice  to a  mixture  of 50  percent
propylene and  50 percent air ^produced  anesthesia in  8  minutes
 (Riggs, 1925). Riggs (1925) performed a study in which white rats of
                                14

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 a "pure strain and great uniformity" were  exposed to a gas mixture
 containing propylene (purity,  99 percent)  at concentrations ranging
 from 40 to 70 percent. Oxygen levels were maintained at 25 percent,
 whereas  the  concentrations of nitrogen were  varied. The sex and
 number of animals exposed  were not reported. At 40  percent,
 propylene produced  a light anesthesia  within  15-20  minutes-
 exposure  up  to 6  hours  produced no  visible  signs  of toxicity!
 Exposure  to  propylene  at 55, 65, 70 percent produced a  deep
 anesthesia within  3-6,  2-5,  1-3  minutes, respectively.  Animals
 exposed to 55 percent propylene for  7.5  hours recovered within 2
 minutes postexposure  and  exhibited  no  signs  of  overt toxicity.
 However,  propylene  concentrations of 65 or  70 percent led to
 respiratory  failure  and  death  after 2 hours  or 20-25  minutes
 respectively.

    Brown (1924) reported similar effects in  cats. Anesthesia  was
 induced and maintained at  propylene concentrations between 37 and
 50 percent. At propylene concentrations of 65 and 70 percent,  a fall
 in blood pressure was reported. In dogs, propylene has been shown
 to be a cardiac sensitizer  (Krantz et al.,  1948).  Two mongrel  dogs
 were administered intravenous injections of epinephrine hydrochloride
 at 0.01  mg/kg and then allowed to  breathe a  propylene/air mixture
 (propylene concentration not specified) for 10 minutes. Propylene
 caused  a sensitization of the myocardium to the epinephrine in both
 dogs, resulting in multifocal ventricular tachycardia that progressed to
 ventricular fibrillation and caused death.

    No  further information  was found  on cardiac sensitization to
 epinephrine following propylene exposure.

 2.4 Subchronic Toxicity

    No  compound-related  toxic effects  were observed in male  and
 female F344/N rats and B6C3F! mice following repeated exposure to
 propylene  for  14 days (5  animals/sex/dose)  or 14  weeks  (10
 animals/sex/dose) at concentrations  of 0,  625,  1,250, 2,500, 5,000,
 and  10,000 ppm  for 6 hours/day,  5  days/week (National Toxicology
 Program, 1985). In an early study (Reynolds, 1926), six white mice of
 unspecified strain and sex  were exposed to  impure propylene  at a
 concentration  of 35 percent for five exposures of 90 minutes each
 over a  10-day period. No  toxic effects were  noted  except for the
 liver of  one  animal,  which  showed moderate  fatty  degeneration.
 Subchronic exposure of single mice for 60 minutes (11 exposures in
 33 days, 14 exposures in 41 days,  and 20 exposures in 58 days) did
 not  cause any  obvious  toxic  effects  except for slight fatty
 degeneration of the livers of the mice receiving 14 and  20 exposures.
2.5 Chronic Toxicity

    Quest  et  al.  (I984) recently reported  the  results of  an NTP
carciriogenicity/chronic toxicity bioassay with  propylene  in F344/N
rats arid B6C3F! mice. Groups of 50 rats and mice of  each sex were
                               15

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exposed to  air containing propylene at concentrations of 5,000 or
10,000  ppm for 6 hours/day,  5  days/week for 103 weeks.  Control
groups  were exposed in the same manner but to clean, filtered air.
For safety reasons, the highest dose  level used was based  on a
concentration  that was  one-half  the  lower  flammability limit of
propylene, and may have  been below the maximum tolerated dose.
Propylene had no effect on weight gain or mortality when  compared
to controls in either species or  sex.
    Histopathologic  findings  indicated  a positive   trend  in the
incidence of C-cel! hyperplasia in the  thyroid glands of propylene-
exposed rats.  In  addition, increased  incidences of  nonneoplastic
lesions  developed  in the nasal cavities  of the  exposed rats (Table 2-
1). These lesions included epithelial hyperplasia in the anterior part of
the nasal cavity in  females  exposed  at  10,000  ppm;  squamous
metaplasia  in  males  and females exposed  at  5,000 ppm and  in
females exposed at  10,000  ppm;  and  inflammatory  changes,
characterized   by  an  influx  of  lymphocytes,  macrophages,  and
granulocytes,   in  the  nasal  lumen of  males  exposed at  both
concentration levels.
Table 2-1. Incidence of Epithelial Changes in  the Nasal Cavities of Rats
Exposed to Propylene via Inhalation
                                    Exposure level
Observation
Epithelial hyperplasia
Male
Female
Squamous metaplasia
Male
Female
Inflammation
Male
Female
0
2/50 (4%)
0/49 (0%)
2/50 (4%)
0/49 (0%)
11/50(22%)
8/49 (16%)
5,000 ppm
2/50 (4%)
4/50 (8%)
19/50 (38%)a
15/50 (30%)a
21/50 (42%)a
10/50 (20%)
10,000 ppm
5/50 (10%)
9/50(18%)a
7/50 (14%)
6/50 (12%)a
19/50 (38%)
13/50 (26%)
 ^Significantly (p<0.05) higher than control values.

 Source: Quest et al. (1984).

     There were  no corresponding lesions of the nasal cavities in
 mice  exposed to  propylene.  However,  there  was an  increased
 incidence of chronic, focal, renal inflammation in males (0  of 50, 17
 of 49, and  9 of 49) and in females (1 of 50, 7  of 49, and 6 of 49)
 exposed to propylene at 0, 5,000, and 10,000 ppm, respectively.

 2.6 Mutagenicity
     Two studies have evaluated the mutagenic potential of propylene.
 The compound was nonmutagenic in  an £.  coli survival assay and
 the  Sa/mone//a/microsomal  reverse  mutation  assay.  Landry  and
 Fuerst (1968) reported that propylene was not mutagenic to E. coli B.
 The pure gas was bubbled through a  10-ml  suspension of the cells
 for 10  minutes  and the  cells subsequently maintained  under the
                                16

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  gaseous atmosphere for 24  hours. Mutation rates were  determined
  by counting the survival cells, which, formed colonies after treatment
  with penicillin and neutralization with penicillinase.

     Propylene  was also evaluated for mutagenicity  in  the Ames
  reversion assay  and  found to  be nonmutagenic  in  Salmonella
  typhtmurium tester  strains TA97, TA98, and  TA100 (Hughes et al
  1984). The compound, diluted in ethanol,  was tested at dose levels
  ranging from  6.3 to  626.0  pg/plate, in triplicate,  with and  without
  metabolic activation. Metabolic activation  consisted of  two liver S9
  systems (rat and hamster) induced with Aroclor 1254.

     Recently, two reports have described  the mutagenic, genotoxic
  and cytotoxic effects  of the photochemical reaction  products of
  propylene and NOX.  The  photooxidation  products  of  CsHfi/NOv
  showed  increased mutagenic  activity  when compared  to  the
  reactants in the Ames assay using  Salmonella  typhimurium tester
  strain TA100 (Kleindienst et al., 1985). The tester strain was exposed
  for 20 hours to the irradiated products of the reactants CaHe  NO
  and NOX-NO  at initial concentrations  of  826, 505, and 20o' ppb'
  respectively. Metabolic activation  (S9 from livers of male CD-1  rats
  induced with Aroclor 1254) had  no significant effect on  mutagenic
 activity; however, the number  of revertants  did increase as a function
 of exposure time (-160 excess  revertants/plate after 2.7  hours  and
  -625 revertants/plate after 7.5 hours of exposure). An attempt was
 made  to account  for the  excess  revertants by summing  the
 contributions of the individual major and minor reaction products (the
 major reaction  products of this system are described in  Section 1 2)
 Of the major and minor reaction products, only HCHO and PAN had
 mutagenic activities above the detection limit, contributing 19 and 27
 revertants/plate, respectively, after 7.5 hours of exposure  When  the
 number of  revertants  contributed  by minor products  such  as
 peroxide,  was added to those contributed by PAN and HCHO, only
 20 percent of the observed mutagenic response could be accounted
 for.  Another  possible  product of the  photochemical  reaction of
 propylene and  N2Os  suggested  by  Shepson et  al.  (1985)  is a-
 (nitrooxy) acetone which has been shown to be mutagenic.

    S.  typhimurium strain TA100 was also  exposed to the products
 of  the  C3H6/N2O5  dark  reaction to  determine  to what extent
 CaHe/NOs reactions  contributed to the mutagenic response. A  small
 mutagenic response was  observed  for this mixture  (180 excess
 revertants/plate above controls),  with  S9  activation  having  no
 significant effect on mutagenic activity. The contribution to the total
 response for reaction products a-nitratoacetone, HCHO  and  PAN
 was estimated  to  be  22, 2,  and 8  revertants/plate, respectively
 However, the contribution of all known reaction products accounted
for only a small fraction  of the  total  observed  response  (-19
percent). A  number of possible  explanations for the  observed
mutagenic effect were  suggested by  the  authors,  including the
presence of an unknown potent mutagen not detected in  the analysis
                              17

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of reaction products, the production of  a mutagen from  a reaction
that occurred in the test medium, and the combined effect of two or
more reaction products  acting  synergistically  (Klemdienst et al.,
1985).
    The  photochemical reaction  products  of propylene  and
increased the frequency of sister-chromatid exchanges (SCE's) and
the rate  of growth inhibition in cultured Chinese hamster V79 cells
(Shiraishi and Bandow, 1985). Cultured cells were exposed  for 2
hours to the photochemical reaction products produced  in a  smog
chamber using  four initial  concentration  ratios  of   reactants
(propylene: NOa): 0.5:0.25, 1.0:0.5, 2.0:1.0, and 3.0:1.5 ppm. At the
lowest concentration of reaction products, the mean SCE frequency
was significantly  higher when compared to control  cells  (14.18  per
cell versus  6.84 per cell,  p  < 0.001).  At  higher concentrations, a
greater frequency of  SCE was observed, approximately two to four
times greater than control cells (significantly different at p < 0.001).
The photochemical  reaction  products  inhibited  cell  growth  in a
dose-dependent  manner,  with  a mean  inhibition  rate of 7, 22, 44,
and 59  percent, respectively,  for the  four levels of concentrations
tested. In contrast, propylene and NOa  alone failed  to induce SCE s
in V79 cultures.
     Cell cultures were also  exposed for 2 hours  to  NOa and 03
 concentrations  ranging  from 0.5  to  8.0 and  0.13  to  1.0 ppm,
 respectively. Both compounds significantly increased the frequency
 of SCE's in V79 cells, but their effects were weaker than those
 induced by the photochemical  reaction products of propylene  and
 NO2- The authors concluded that the strong induction of SCE's  in
 V79 cells by  the  photochemical reaction products  was  due to  a
 multiple  effect resulting  from  an interaction  between reaction
 products (Shiraishi and Bandow, 1985).
     One study reports the  mutagenic effects of the  reaction products
 of Oa and propylene on E. coli K 12 343/113. Nover and  Botzenhart
 (1985) showed  induction  of gal*,  arg+  and  MTR-mutations  in
 qrowing cells after treatment with ozonized propylene. The treatment
 with  ozone was  carried  out under  UV irradiation (3000-4000
 angstroms) to  increase the concentration of the  reaction products
 which were hydrocarbon radicals, peroxides,  aldehydes and ketones.
 Similar reaction products of propylene  with Os are shown in Figure
 1-1  Nover and Botzenhart (1985) relate the mutagenic effects  to
 the "photochemical smog" reaction products but not to propylene or
 other hydrocarbons studied.

 2.7 Carcinogenicity
      Two studies have been  reported on the carcinogenic potential of
  propylene  in rats and mice.  In one, Maltoni et al. (1982) presented
  the results  of carcinogenicity studies  with  several  chemicals,
  including propylene,  conducted in an  attempt  to identify  potential
  brain  carcinogens.  In  the  study  with propylene,  groups  of 120
                                 18

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  Sprague-Dawley  rats were  exposed  to  propylene  in  air at 200
  1,000  or 5,000 ppm for 7 hours/day,  5  days/week for 104 weeks'
  One female rat exposed at 1,000 ppm  had a meningioma. However'
  since 2  of the total 325  female controls  in  the  study also had
  menmgiomas,  the authors concluded  that propylene did not cause
  brain tumors  in  rats.  No  data  were  presented for  any  other
  parameters of the study.

     The more  definitive study was the NTP carcinogenicity/chronic
 toxicity bioassay  with propylene in F344/N  rats and B6C3Fi  mice
 reported by Quest et al. (1984). There was no increase noted in the
 incidence  of any  neoplasm  in the propylene-exposed rats when
 compared with the controls. In fact, a negative (p  <0.05) trend was
 observed in the incidence of total  thyroid tumors in female rats with
 the incidence of C-cell adenomas of the  thyroid in the 10000-pDm
 group significantly (p  <0.05)  lower than in controls. However  as
 indicated  above, there was a positive  trend in  the incidence of  C-
 cell hyperplasia in female rats.

     In the exposed mice, both  increases and decreases were noted
 in  the incidences of certain  tumors  (Table 2-2). In female  mice
 sigmf.cant (p <0.05) positive trends in the incidences of hemanqio-
 sarcomas,  combined hemangiomas and  hemangiosarcomas  and
 uterine endometrial stromal polyps were observed in the  high' dose
 group but  the ^ncidences  were  not   significantly  different from
 controls. Similarly, in exposed males, significant (p <0.05) decreases
 onmh6 in.cidences of hepatocellular  adenomas, lung adenomas, and
 combined  lung adenomas and carcinomas  were observed in the low
 dose group although this was not seen in the high dose group  There
 was, however, a significant (p <0.05) negative trend in the incidence
 of  lung  adenomas and carcinomas in males,  but  the  biological
meaning of this is questionable, since the  matched control rate  was
considerably higher than the historical control rate.

                                  Exposed *° p«>pylene via

                                         Exposure level, ppm

Females
Hemangiosarcomas
Hemangiomas and hemangiosarcomas
Uterine endometrial stromal polyps
Mates
Hepatocellular adenomas
Lung adenomas
Luna adenomas and carcinomas
0

0/50
0/50
0/47

5/50
9/50
16/50
5,000

0/49
1/49
0/47

0/49
1/49
4/49
10,000

3/50
4/50
3/48

3/49
4/50
7/50b
  aOnly neoplasms with incidences apparently different from controls
  ^Significant (p < 0.05) negative trend.
  Source: Quest et al. (1984).
                              19

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    Under the conditions  of  the  study  and at the  concentrations
tested, it was concluded that propylene is not carcinogenic in F344/N
rats and B6C3Fi mice.
    In addition to these two studies, Quest et al. (1984) reported that
in a preliminary report  by Maltoni,  no  carcinogenic response  was
found  in  Swiss mice exposed  by  inhalation  for  18 months, to
propylene at  concentrations  of  200, 1000, or 5000 ppm  for  7
hours/day, 5 days/week.
    A weight of evidence characterization for propylene using  EPA's
Guidelines for Carcinogen Risk Assessment involves taking account
of several types of information:
•  The  NTP  bioassays in rats and  mice provide some indication of
    carcinogenic activity, such as positive trends in  the incidence of
    hemangiosarcomas  and  combined  hemangiomas  and
    hemangiosarcomas  in  female mice  and a  hint  of bladder
    hyperplasia in female rats.
•  Propylene is metabolized to propylene oxide (the strength of this
    data  base  requires  further scrutiny). Propylene oxide  and
    ethylene oxide are alkylating agents,  and there is sufficient animal
    evidence for their carcinogenicity.
 •  The  similarity of  endpoints in  the mouse between  propylene
    (trend of hemangiomas)  and  propylene   oxide  (incidence  of
    hemangiomas)   provides additional  indication  of potential
    carcinogenic activity.
 Since no epidemiological data are available, the human data base  is
 inadequate. The available direct animal bioassay data for propylene
 can be  viewed as inadequate but  bordering on limited. The animal
 evidence is  elevated to the limited category by  considering the
 supporting information  on metabolites to include  the carcinogenicity
 of metabolites and  the commonality of site of action between the
 metabolites  and  parent  compound  propylene.  Thus the  overall
 weight-of-evidence  becomes Group  C, possibly  a human  carcin-
 ogen.
     A quantitative cancer unit risk derivation is not  warranted at this
 time  qiven  that there is not a statistically significant animal  dose-
  response study available, and thus the quantitative analysis cannot
  be developed.

  2.8 Other Health Effects
     No studies were found  on  teratogenicity, reproductive  effects,
  neurotoxicity, or other types of health effects on hurnans.
                                20

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                         3. SUMMARY

     Propylene is an olefinic hydrocarbon with the chemical structure
    3CH = CH2. It is  highly soluble  in  water  and has a high  vapor
 pressure. Current domestic production capacity has  been estimated
 to be about 22 billion pounds. Propylene is a product obtained from
 crude oil by distillation  and used in  several chemical  and refinery
 processes. In  the chemical industry, propylene is used as a starting
 material  in the manufacture of polypropylene, acrylonitrile, propylene
 oxide, and as  a component in fuel. In  refinery applications, it is used
 as a feedstock or additive to gasoline and fuels.

     Propylene  may be  released  to the environment  in  gaseous
 emissions from industrial production, chemical utilization, and various
 combustion processes. Ambient concentrations in  urban  areas of the
 United States have generally been found to range from about 1  to 10
 ppb, whereas  concentrations in rural air  samples are approximately
 an order of magnitude lower.

    Gas  chromatography with  flame ionization detection and  mass
 spectrqscopy has been  used extensively  to measure concentrations
 of propylene in environmental media.

    Propylene  released to the environment from  point and  nonpoint
 sources  is expected to partition into the atmosphere  due to its high
 vapor pressure. However, propylene has a relatively higher density
 and is also highly reactive; therefore, its transport will be limited.

    Propylene  is  one of  several  "volatile organic compounds" that
 are precursors  of  photochemical  oxidants  and  other smog
 components. In ambient  air, propylene is susceptible to attack by
 nydroxyl  radicals and  ozone, although the former accounts for  more
 than  75  percent of the  total propylene removed. The reactions of
 propylene with hydroxyl  radicals  occur mainly during the daytime-
 with ozone, during the evening; and with NO3  radicals, at night The
 end products of these reactions are several aldehydes  (e.g  acrolein
 formaldehyde, and acetaldehyde),  acids, ketones, and nitrates, but
 other products  have also been identified. The atmospheric half-life
 of propylene has been estimated to be 7.7  hours.

    Trace levels of propylene have  been detected  in marine and
fresh  waters. In water, propylene  would  probably be subjected to
chemical and degradative processes. Propylene  is not expected to
bioconcentrate  or bioaccumulate in organisms  and food chains  and
has been reported  to be  metabolized by some  microorganisms
Available  environmental effects data are limited  to studies  with higher
                              21

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plants. Some toxic effects were reported at very high concentrations;
however, these concentrations are not expected to be found in the
environment, except for cases  associated with industrial  leaks or
spills.
    One study on the uptake and metabolism of propylene in  mice
following inhalation exposure  indicates  that  propylene is  readily
metabolized, having Km and Vmax values of 800  ± 60 ppm and 8 ±
05  mg/kg/hour,  respectively.  Propylene  is apparently oxidized to
propylene oxide and also metabolized into 1 and 2 carbon fragments,
which are  readily incorporated into  certain amino acids.  Propylene
and/or propylene oxide  also alkylates blood hemoglobin in mice via
conjugation with  cysteine,  valine,  or histidine  to form  the
corresponding S- and  N-(2-hydroxypropyl)  derivatives.

    Limited data from acute toxicity studies indicate that propylene is
not  very  toxic to  rats  (strain  and sex  not  reported);  only  light
anesthesia  was noted following exposure  to  a  40  percent
concentration of prppylene for  6  hours. Similarly, no compound-
related toxic effects were  found in  subchronic studies with F344/N
rats and B6C3F-J mice exposed to propylene at concentrations up to
 10,000 ppm for 6 hours/day, 5 days/week for 14 days or 14 weeks.
 Propylene was  also  not carcinogenic in F344/N  rats  and B6C3Fi
 mice following exposure at concentrations up to  10,000  ppm for 6
 hours/day,  5 days/week for  103  weeks. However, nonneoplastic
 lesions such as  inflammation,  epithelial  hyperplasia,  and squamous
 metaplasia developed in the nasal cavities of exposed rats, and renal
 inflammation was noted in exposed mice.
     Propylene was not mutagenic in an Escherichia coli assay when
 bubbled  through  the  cells  for 10  minutes,  nor  in  Salmonella
 typhimurium strains TA97,  TA98, and TA100 at dose levels up to 626
 ug  in ethanol   per  plate.  Mutagenic   and  cytotoxic effects  of
 photochemical reaction products of propylene and NOX have recently
 been reported in S. typhimurium strain TA100 and cultured Chinese
 hamster  V79 cells without activation;  mutagenic  effects  of the
 reaction products of  03 and propylene on E. coli K12 343/113 have
 also been reported; no other mutagenicity studies were available. No
 teratogenicity,  reproductive effects,  or neurotoxicity  studies of
 propylene  with  laboratory animals were found in the  available
 literature. Similarly, there  were no epidemiologic  or  case  studies
 available to assess its effects on humans.
     According to EPA's carcinogen risk assessment guidelines, the
 animal evidence for the carcinogenicity  of propylene is judged  to be
 only  limited. This equates to  a Group  C classification,  given that
 there is no epidemiologic data and the animal evidence is limited.
                                 22

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0 U.S.GOVEHNMENTPniNTINQOmCEM988 - 548-158/87007
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