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                                  DISCLAIMER

    This report  1s  an external draft  for  review purposes only  and  does not
constitute  Agency  policy.   Mention  of  trade names  or commercial  products
does not constitute endorsement or recommendation for use.
                                      11

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                              EXECUTIVE SUMMARY

    AdlponHMle Is a colorless  liquid  at  room temperature with no distinc-
tive  odor  (Smiley, 1981).   It  Is soluble  In  many organic  solvents  and  Is
highly soluble  1n  water  (Smiley, 1981).   It  undergoes  reactions typical  of
nltrlles, e.g.,  hydrolysis  to adlpamlde and adlplc add  and alcoholysls  to
substituted amides and esters (Smiley,  1981).   AdlponltrUe can be produced
commercially either by  ammonlatlon of  adlplc  add,  dlmerlzatlon of acrylo-
nltrlle  or  hydrocyanatlon  of butadiene  (Smiley,  1981).   Current  domestic
manufacturers are  E.I.  Dupont In  Orange,  TX  and  Victoria,  TX and Monsanto
Co.  In  Decatur,  AL (SRI,  1986).   As of  January  1,  1986,  the total  adlpo-
nltrlle production capacity  of these  plants  was  estimated to be 929 million
pounds per year  (SRI,  1986).  The most  Important use  for  this compound  1s  as
an Intermediate  In the manufacturer  of  hexamethylened1am1ne, a precursor  of
Nylon 66 (Smiley,  1981).   Ad1pon1tr1le may also be used In  organic  synthesis
and as a solvent (Kuney,  1985; Hawley, 1981;  Smiley, 1981).
    In the atmosphere, adlponltMle  1s  expected  to exist  almost entirely  In
the  vapor  phase.  Reaction  with  photochemically  generated hydroxyl radical
(estimated  t./?  -10  days)   and  physical  removal  by  wet deposition are
predicted to  be Important fate  processes.   Ad1pon1tr1le  Is not susceptible
to reaction with  ozone (U.S. EPA,  1987b).   In water, aerobic blodegradatlon
1s the  Important  removal mechanism.  Based  on results of a blodegradatlon
study,  It  appears that  the  blodegradatlon  half-life  of  adlponUrlle  1n
unaccllmated waters at 20°C  Is -1 week  (Ludzack et al., 1959a).  Acclimation
of  microorganisms should  Increase  the  rate  of  blodegradatlon  and   lower
temperatures  should  decrease  the  rate  of blodegradatlon  (Ludzack  et   al.,
1959a).  Adsorption  to   suspended  solids  and  sediments,  bloaccumulatlon  1n
                                      1v

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aquatic  organism  and volatilization are  not expected  to  be  Important  fate
processes In  water.   In soil, aerobic  blodegradatlon  1s expected to  be  the
Important degradation mechanism.   Adlponltrlle  has the  potential  to  undergo
extensive leaching;  however,  blodegradatlon  of  the compound would limit  the
movement of  this  compound through  soil.   Volatilization 1s not  expected  to
be significant 1n soil.
    Pertinent data regarding  exposure  to ad1pon1tr1le  by  Inhalation,  dermal
contact  or  1ngest1on of food could  not be located In  the  available  litera-
ture as  cited 1n Appendix A.  Adlponltrlle was  tentatively  Identified  1n  the
drinking water obtained from New Orleans, LA, 1n  January 1976  (Lucas,  1984).
Adlponltrlle  was  also detected  1n  the effluent  from  a nylon  manufacturing
plant (Shackelford and Keith,  1980).
    There was  little  Information  concerning  toxldty of  ad1pon1tr1le  to
aquatic  organisms.    The  lowest  reported acutely toxic  concentration  for
freshwater  fishes  was  384 mg/i,   an  LC5Q  for  golden orfe  (Knle  et  al.,
1983).   The  lowest   reported  acutely  toxic  concentration  for  freshwater
Invertebrates was  445  mg/i,  an  EC5Q   for  Immobilization  of  Daphnla  magna
(BMngmann  and   Kuehn.  1982).   Data  for saltwater  species  could  not  be
located  In the available literature as  cited  1n  Appendix A.
    Studies  of  the metabolism of ad1pon1tr1le  Indicate that 1t  Is  absorbed
by the  gastrointestinal tract, metabolized  to  cyanide  and excreted  1n  the
urine as thlocyanate (Svlrbely and  Floyd,  1964;  Gh1r1nghell1,  1955a;  Tan 11
and Hashimoto. 1985).   Tanll  and Hashimoto (1985) found that  the metabolism
of adlponltrlle  to  cyanide In mice  was greatly  Inhibited  by  CC1.  pretreat-
ment, which  Inhibits  certain drug metabolizing enzymes  In the liver.

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    Nylon workers  exposed  to adlponltrlle  and hexamethylenedlamlne  for  2-3
years  showed  a  tendency for  hyperchromlc  anemia  of  the hemolytlc  type  and
slight leukopenla  (Ceresa,  1948a).   Ceresa (1948b) attributed  these effects
to exposure to ad1pon1tr11e and  hexamethylenedlamlne.
    Dogs  fed  adlponltrlle  1n the  diet  at  levels  <500  ppm had  normal  blood
and  urine values  and  tests  for  liver  and  kidney  function  (Svlrbely  and
Floyd, 1964).   During  the  first week of  the study,  dogs  fed  1000  ppm were
not able  to  consume the entire  dose.   In  a  rat  study  (Svlrbely and  Floyd,
1964), females  treated  with adlponltrlle 1n  the  drinking water at  0.5,  5.0
and 50 ppm  and  males at 50 ppm were found  to have advanced adrenal  degen-
eration.
    Vomiting,  tightness In  the  chest,  headache,  profound  weakness  with
difficulty standing,  vertigo,  respiratory  difficulty,   tachycardia  and  low
blood pressure  were  experienced by a human who  consumed  a few ml of  adlpo-
nltrlle (GhlrlnghelH, 1955b).  Zeller et al.  (1969)  reported seven  cases  of
skin Irritation  1n workers  dermally exposed  to adlponltrlle.
    Adlponltrlle rubbed on  the  backs  of  guinea pigs  for 1 month resulted  In
weight loss,  decreased calcium content of  the  blood,  marked  hyperchromlc
hemolytlc  anemia   with  leukopenla  and  lymphomonocytosls.    Hlstologlcal
examinations  revealed swelling  and  congestion of nearly all Internal  organs
(Ceresa,  1948b).
    Rats   exposed  to adlponltrlle  at  0.3 mg/8. for ten  6-hour  exposures  (5
days/week) showed  Increases  In  blood  glucose, urea nitrogen, creatlnlne  and
urine  glucose,  and  decreases  In  erythrocyte count,  hemoglobin,   leukocyte
count and  urine osmolalHy.  At  0.1 mg/l.  Increases  In  urea  nitrogen  and
lymphocytes  and decreases  1n  the  number  of  eoslnophlls  and neutrophlls were
noted.   No   changes   In  clinical  parameters  were  observed  at  0.03  mg/8.
(Smith and Kennedy, 1982).
                                      v1

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    The oral  ID™  In  the rat  was  reported  to  be 960  mg/kg (Plokhova  and
Rubaklna,  1965)  and 300  mg/kg  (NIOSH,  1978).   Mice,  with an  oral  LD5Q  of
172 mg/kg,  may be  somewhat  more  sensitive to  the  acute  oral  toxldty  of
adlponltrlle (Tan 11  and Hashimoto,  1985).
    The carclnogenlcHy of adlponltrlle  following Inhalation, oral or  other
routes of exposure  has not been studied.   Ad1pon1tr1le  tested negative  for
reverse mutation  In   S.  typhlmurlum  at  concentrations  <10,000 yg/plate,
both with  and without  metabolic  activation.
    Johannsen et al.  (1986) orally  dosed  pregnant rats with  adlponltrlle  at
0, 30, 50 or  80 mg/kg/day on gestation days 6-19.  Two rats  at 80 mg/kg/day
and one  rat at  50 mg/kg/day  died.  Fetal  body weights were  significantly
reduced  at   80  mg/kg/day,   but  this   observation was   not   attributed   to
treatment.   No other changes were noted.  No changes  1n  fertility, gestation
or viability were noted  In  two  litters from rats  exposed  to  adlponltrlle  In
the'r drinking water  at  10,  100 or 500 ppm  >jr  2  years  (Svlrbely and  Floyd,
1964).
    Chronic   oral  exposure to  adlponltrlle  resulted  1n  a  LOAEL  of  0.5  ppm
(0.07 mg/kg/day) that was associated with adrenal  degeneration  In the  2-year
rat study (Svlrbely and Floyd,  1964).  This  study  was  unavailable  for  review
and 1n addition appears to be an unpublished abstract.   Data  were  considered
Inadequate for estimation of either an RfD  or  an RQ.   It Is recommended that
comprehensive subchronlc oral testing be Initiated In  the  rat to  determine a
NOAEL.   Data   were   Insufficient  for   derivation   of   cancer-based   risk
assessment   values.    Adlponltrlle  was   assigned  to   EPA  Group 0,   not
classifiable as to human carclnogenldty.

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                              TABLE  OF  CONTENTS
1.  INTRODUCTION	    1

    1.1.   STRUCTURE AND CAS NUMBER	    1
    1.2.   PHYSICAL AND CHEMICAL PROPERTIES 	    1
    1.3.   PRODUCTION DATA	    2
    1.4.   USE DATA	    2
    1.5.   SUMMARY	    2

2.  ENVIRONMENTAL FATE AND TRANSPORT.  .  .	    5

    2.1.   AIR	    5

           2.1.1.   Reaction with Hydroxyl Radicals 	    5
           2.1.2.   Reaction with Ozone  	    5
           2.1.3.   Physical Removal Processes	    5

    2.2.   WATER	    5

           2.2.1.   Hydrolysis. . .	    5
           2.2.2.   Mlcroblal Degradation  	    6
           2.2.3.   Bloconcentratlon	    6
           2.2.4.   Adsorption	    6
           2.2.5.   Volatilization	    7

    2.3.   SOIL	    7

           2.3.1.   Hyd-olysls	    7
           2.3.2.   M1crob1al Degradation  	    7
           2.3.3.   Adsorption	    7
           2.3.4.   Volatilization	    7

    2.4.   SUMMARY	    8

3.  EXPOSURE	    9

4.  AQUATIC TOXICITY	   10

    4.1.   ACUTE TOXICITY	   10
    4.2.   CHRONIC EFFECTS	   10
    4.3.   PLANT EFFECTS	   10
    4.4.   SUMMARY	   11

5.  PHARMACOKINETCS	   12

    5.1.   ABSORPTION	   12
    5.2.   DISTRIBUTION	   12
    5.3.   METABOLISM	   12
    5.4.   EXCRETION	   13
    5.5.   SUMMARY	   13

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                          TABLE OF CONTENTS  (cont.)

                                                                        Page

 6.  EFFECTS	   14

     6.1.   SYSTEMIC TOXICITY	   14

            6.1.1.   Inhalation Exposures	   14
            6.1.2.   Oral Exposures	   14
            6.1.3.   Other Relevant Information	   15

     6.2.   CARCINOGENICITY	   18

            6.2.1.   Inhalation	 .   18
            6.2.2.   Oral	   18
            6.2.3.   Other Relevant Information	   18

     6.3.   MUTAGENICITY	   18
     6.4.   TERATOGENICITY	   18
     6.5.   OTHER REPRODUCTIVE EFFECTS 	   19
     6.6.   SUMMARY	   19

 7.  EXISTING GUIDELINES AND STANDARDS 	   22

     7.1.   HUMAN	   22
     7.2.   AQUATIC	   22

 8.  RISK ASSESSMENT	   23

     8.1.   CARCINOGENICITY	   23

            8.1.1.   Weight of Evidence	   23
            8.1.2.   Quantitative  Risk Estimates  	   23

     8.2.   SYSTEMIC TOXICITY. .	   23

            8.2.1.   Inhalation Exposure 	   23
            8.2.2.   Oral Exposure	   24

 9.  REPORTABLE QUANTITIES 	   26

     9.1.   BASED ON SYSTEMIC TOXICITY 	   26
     9.2.   BASED ON CARCINOGENICITY	   26

10.  REFERENCES	   29

APPENDIX A: LITERATURE SEARCHED	   36
APPENDIX B: SUMMARY TABLE FOR ADIPONITRILE  	   39
                                      1x

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                               LIST  OF TABLES

No.                              TUIe                                Page

1-1     Current Domestic  Manufacturers of AdiponHMle ........    3

6-1     LD50 Values  for Ad1pon1tr1le .................   17
9-1     Oral Toxlclty  Summary  for AdlponHMTe Using Female
        Wlstar Rats  .........................   27

9-2     Ad1pon1tr1le:  Minimum  Effective Dose (MED) and
        Reportable Quantity  (RQ) ...................   28

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                             LIST OF  ABBREVIATIONS

BCF                     B1oconcentrat1on factor
BOD                     Biological oxygen demand
CAS           "         Chemical Abstract Service
CS                      Composite score
EC5Q                    Concentration effective to 50% of recipients
                        (and all other subscripted concentration levels)
Koc                     Soil sorptlon coefficient standardized
                        with respect to organic carbon
Kow                     Octanol/uater partition coefficient
LC5Q                    Concentration lethal to 50% of recipients
                        (and all other subscripted dose levels)
                        Dose lethal to 50% of recipients
LOAEL                   Lowest-observed-adverse-effect level
MED                     Minimum effective dose
NOAEL                   No-observed-adverse-effect level
ppm                     Parts per million
RfD                     Reference dose
RQ                      Reportable quantity
RV,j                     Dose-rating value
RVe                     Effect-rating value
TWA                     Time-weighted average
                                      x1

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                               1.   INTRODUCTION
1.1.   STRUCTURE AND CAS NUMBER
    AdlponHMle  1s  also  known  as  hexanedlnHMle,  adlplc add  nHrlle,
tetramethyl  cyanide  and  1,4-d1cyanobutane  (SANSS,  1987).   The  structure,
empirical formula, molecular  weight and CAS Registry number are as follows:
                           N=C-CH2-CH2-CH2-CH2-CEN
Empirical formula:   C,H0N.
                     o o e.
Molecular weight:   108.14
CAS Registry number:   111-69-3
1.2.   PHYSICAL AND CHEMICAL  PROPERTIES
    Pure  adlponltrlle  Is  a  colorless  liquid  at  room  temperature  with  no
distinctive  odor  (Smiley,   1981).    It   undergoes  reactions  typical  of
nltrlles, e.g., hydrolysis to adlpamlde and adlplc add  and alcoholysls  to
substituted amides  and esters  (Smiley,  1981).   Adlponltrlle  Is  soluble  In
methanol, ethanol, chloroalkane and aromatic solvents  and has low solubility
1n  carbon  dlsulflde,  ethyl ether  and aliphatic  hydrocarbons (Smiley, 1981).
Selected physical  properties  are given below:

Melting point,  °C:           2.49                    Smiley,  1981
Boiling point,  °C:           295                    Smiley,  1981
Vapor pressure at  20°C:      3.0xlO~3 mm Hg          Neely  and Blau, 1985
Water solubllHy,  20°C:      8xl04 mg/l              Smiley,  1981
Log Kow:                     -0.32                  Tanll  and Hashimoto, 1985
                             -0.42                  U.S. EPA, 1987a
Density, 20°C:                0.965 g/cm3            Smiley,  1981
Refractive Index,  njj :       1.4343                 Smiley,  1981
Flashpoint, °C:              159 (closed cup)        Smiley,  1981
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1.3.   PRODUCTION DATA
    Adlponltrlle  can  be  prepared  commercially  using  either  adlplc  acid,
acrylonltrlle or butadiene  as  feedstock  (Smiley,  1981).  In the adlplc  add
process,  the  feedstock Is allowed to  react  with  ammonia  over a catalyst  to
produce adiponltrlle.   In one butadiene-based production process,  butadiene
1s  directly  hydrocyanated 1n  two  successive steps to  produce  adiponltrlle.
Another  process  Involves  d1mer1zat1on of  acrylonUrlle  In  an electrolyte
cell  to  produce  adiponltrlle (Smiley,  1981).   Table  1-1  lists  production
Information  concerning   current   domestic   manufacturers   of   adiponltrlle.
Although  closed  since  1980,  the  Monsanto  plant  In  Pensacola,  PL,  has  a
yearly  production  capacity  of 185  million  pounds; this  plant continues  to
hydrogenate  adiponltrlle  produced  at  other  Monsanto  locations  to   make
hexamethylened1am1ne (SRI, 1986).
1.4.   USE DATA
    The most Important commercial use  for adlponltrlle  1s as an  Intermediate
In  the manufacture of  hexamethylenedlamlne, a p.^cursor of  Nylon 66  (Smiley,
1981).  Adiponltrlle may  also  be  used  In organic  synthesis and as a  solvent
(Kuney, 1985; Hawley, 1981;  Smiley, 1981).
1.5.   SUMMARY
    Adiponltrlle 1s  a  colorless  liquid at  room temperature with no  distinc-
tive  odor (Smiley,  1981).   It Is soluble  In many organic  solvents and  Is
highly  soluble  In  water  (Smiley, 1981).  It undergoes  reactions  typical  of
nUMles, e.g.. hydrolysis  to  adlpamlde  and  adlplc acid,  and  alcoholysls  to
substituted amides and esters  (Smiley, 1981).  Adiponltrlle can be  produced
commercially either  by ammonlatlon of  adlplc  add, dlmeMzatlon  of  acrylo-
nltrlle  or  hydrocyanatlon  of butadiene  (Smiley,  1981).   Current  domestic
manufacturers are  E.I. Dupont In  Orange,  TX and  Victoria, TX and  Monsanto

0071d                               -2-                              06/25/87

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                                  TABLE 1-1
                Current Domestic Manufacturers of Ad1pon1tr1lea
            Company
  Location
  Annual  Capacity0
(millions of pounds)
          E.I. Dupont
          E.I. Oupont
          Monsanto Co.
Orange, TX
Victoria, TX
Decatur, AL
            441
            293
            195
     Total   929
aSource: SRI, 1986
^Estimates as of January 1,  1986
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       -3-
                     09/14/87

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Co.  In  Decatur, AL  (SRI,  1986).   As  of  January  1,  1986  the total adlpo-
nHMle production capacity of  these  plants  was estimated to  be 929 million
pounds per year (SRI, 1986).  The most Important use  for  this  compound  Is as
an Intermediate 1n  the  manufacturer of hexamethylenedlamlne, a precursor of
Nylon 66 (Smiley,  1981).  Adlponltrlle may also be used  In organic  synthesis
and as a solvent (Kuney, 1985;  Hawley,  1981;  Smiley,  1981).
0071d                               -4-                              06/25/87

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                     2.  ENVIRONMENTAL FATE  AND TRANSPORT

    Limited  experimental   data   pertaining  to  the  environmental  fate  and
transport of  adlponltrlle could be  located In  the  available literature  as
cited  1n  Appendix A.   When possible,  therefore,  Information  concerning  the
fate and  transport  of  this compound  was derived from  physical property data
or molecular structure.
2.1.   AIR
    Based  on  the  estimated  vapor  pressure  of 3.0xlO~3  mm  Hg  at  20°C,
adlponltrlle 1s expected  to be present  almost  entirely  1n  the vapor phase 1n
the atmosphere (E1senre1ch et  al.,  1981).
2.1.1.   Reaction with  Hydroxyl  Radicals.   The estimated  rate constant  for
the  reaction   of  adlponltrlle   with  photochemically  generated   hydroxyl
radicals  Is  ~10~10 cmVmolecule-sec  at 25°C  using  the method  of  Atkinson
(1985).   Given  the average hydroxyl  radical  concentration  In  air   of  8xlOs
molecules/cm3 (U.S.  EPA,  1987b), the  estimated half-life  for this  reaction
Is -10 days (Atkinson,  1985).
2.1.2.   Reaction with  Ozone.  Adlponltrlle  1s  not  susceptible to  oxidation
by ozone 1n the atmosphere (U.S.  EPA, 1987b).
2.1.3.   Physical  Removal  Processes.   Based  on  a   water   solubility   of
8x10*  mg/i  at  20°C  (Smiley,  1981),  1t appears  that  significant  amounts
of adlponltrlle may be removed from the atmosphere  by wet deposition.
2.2.   HATER
2.2.1.   Hydrolysis.   In   an  abstract  of  a  Russian  study  (Llnetskll  and
Serebryakov,  1965), the   first-order  hydrolysis  rate  constant  for  adlpo-
n1tr1le  1n  2-5%  NaOH  solution  at  100°C was  reported  as 1.18 mln'1.   Under
environmental conditions,  however,  adlponltrlle 1s  not likely to  hydrolyze
significantly (U.S. EPA, 1986b).

OOTld                               -5-                              09/14/87

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2.2.2.   M1crob1al   Degradation.   Results  of  a  blodegradatlon   screening
study,  which   used   a  natural   water  sample   as   seed,   Indicate   that
blodegradatlon Is likely  to  be the  most  significant route  of decomposition
for adlponUrlle under aerobic  conditions  In  water (Ludzack et  al.,  1959a).
Incubation  of  0.5-10  mg/i  adiponltrlle  In  unaccllmated  Ohio  River  water
resulted In BOO values equivalent to theoretical oxygen  demands  of 0,  40 and
>100X after 2,  5  and 12 days,  respectively.   Acclimation  of  microorganisms
was  examined  by  redoslng,  and degradation  occurred  twice  as  fast  after
acclimation was achieved.   The effect  of  temperature on blodegradatlon  was
also  studied;  blodegradatlon  at   5°C   required  -3.5  times longer  than  at
20°C.  Ludzack et al.  (1959b)  studied  the blodegradatlon of adiponltrlle by
activated  sludge 1n  a continuous  feed  test  at  22-25°C; 93-98% BOD  removal
was measured with a mean aerator detention time of 7-13  hours  at an Influent
adiponltrlle   concentration   equivalent   to   a  BOO   of   275-350   mg/l.
Adiponltrlle  at  500  mg/l  Incubated  for   72  hours   In   three   different
activated  sludge Inocula, was  found  to  be resistant  to  biological  oxidation
(Lutln,  1970).   Ludzack et al.  (1959a)  found  that  nltrlle oxidation proceeds
by  enzymatic  hydrolysis  leading  to  the  formation of  ammonia,  followed  by
nitrification.
2.2.3.  Bloconcentratlon.   A BCF  of 1  was  estimated for adlponUrlle  using
a  water  solubility  of  8.0x10*  mg/l  at   20°C  (Smiley,  1981)   and  the
following  linear regression equation (Lyman et al., 1982):  log BCF  = 2.791 -
0.564 log  S.  This BCF  value suggests  that adiponltrlle will  not  bloaccumu-
late significantly  In aquatic organisms.
2.2.4.  Adsorption.    An  estimated  K    value  of  9  for    adiponltrlle
(Section 2.3.3.) suggests  that adsorption to sediments  or  suspended  solids
In water would  not  be significant.

0071d                               -6-                               09/14/87

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2.2.5.   Volatilization.   Henry's  Law constant  for  adlponHMle  was  esti-
mated  to  be ~7xlO~9  atm-m3/mol  at 25°C  using  a method  of  group contribu-
tions  to  Intrinsic  hydrophlUc character  (Hlne  and  Mookerjee,  1975).  This
value of Henry's  Law  constant  suggests  that volatilization from water would
not be an Important  removal  mechanism  (Lyman et al.,  1982).
2.3.   SOIL
2.3.1.   Hydrolysis.  Because of the  lack  of experimental data the  signifi-
cance of this reaction cannot be determined.
2.3.2.   H1crob1al Degradation.  In the  only study  available  regarding  the
blodegradatlon  of  ad1pon1tr1le  by   soil  microorganisms,  Kuwahara   et  al.
(1980)  found  that Aeromonas  sp.  BN  7013  Isolated  from  soil  1s  capable of
using  ad1pon1tr1le   as  Us  sole   source   of  nitrogen.   Relatively  rapid
blodegradatlon of adlponUrlle 1n natural water  samples and activated  sludge
Inocula suggests  that  blodegradatlon  may also  be the most Important removal
mechanism 1n soil.
2.3.3.   Adsorption.   A  K    of  9  was  estimated  using  a  water  solubility
of  8.0x10*  mg/l  at 20°C  (Smiley,  1981)  and  the following  linear  regres-
sion  equation  (Lyman  et al.,  1982):   log  K   = -0.55 log S  * 3.64.  This
K   value  Indicates that adlponltrlle should  be highly  mobile In soil and
susceptible to significant  leaching (Swann  et al.,  1983).
2.3.4.   Volatilization.   Based  on a vapor pressure  of  3.0xlO~9 mm  Hg at
20°C  and  a  Henry's Law  constant  of 7xlO"9 atm-mVmol  at  25°C, volatili-
zation of  ad1pon1tr1le from moist  and dry  soil  surfaces  1s  not expected to
be a significant fate process.
007 Id                               -7-                               09/14/87

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2.4.   SUMMARY
    In the atmosphere,  adlponltrlle  1s expected to exist  almost  entirely In
the vapor  phase.   Reaction  with  photochemically generated  hydroxyl  radical
(estimated  t,/2  -10  days)   and  physical  removal  by  wet  deposition  are
predicted  to  be  Important fate  processes.   Ad1pon1tr1le  Is  not  susceptible
to reaction with  ozone (U.S. EPA, 1987b).  In  water,  aerobic blodegradatlon
1s  the  Important  removal  mechanism.   Based on  results  of  a blodegradatlon
study,  1t appears   that  the  blodegradatlon   half-life  of   adlponltrlle  In
unaccllmated waters at  20°C  1s ~1 week (Ludzack et  al.,  1959a).  Acclimation
of  microorganisms  should  Increase  the  rate  of   blodegradatlon  and  lower
temperatures  should  decrease  the rate  of blodegradatlon  (Ludzack  et  al.,
1959a).   Adsorption  to  suspended  solids and  sediments,  bloaccumulatlon  1n
aquatic  organism  and volatilization are not  expected  to  be  Important  fate
processes  In  water.   In soil, aerobic blodegradatlon  1s  expected  to be the
Important degradation  mechanism.   Adlponltrlle has the  potential  to  undergo
extensive leaching;  however, blodegradatlon of the compound  would  limit the
movement of this  compound  through soil.   Volatilization Is  not  expected to
be significant In  soil.
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                                 3.   EXPOSURE

    Pertinent data regarding  exposure  to ad1pon1tr1le by  Inhalation,  dermal
contact or  Ingestlon  of  food could  not  be  located 1n the  available  litera-
ture as cited In Appendix A.  Adlponltrlle was  tentatively  Identified  In  the
drinking water obtained from New Orleans, LA,  1n  January  1976  (Lucas,  1984).
Adlponltrlle was  also detected  In  the effluent  from  a  nylon  manufacturing
plant (Shackelford and Keith,  1976).
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                             4.  AQUATIC TOXICITY
4.1.   ACUTE TOXICITY
    Two available  studies  reported acute  toxldty  data  for fish  or  aquatic
Invertebrates  exposed  to  adiponltrlle.  Henderson  et al.  (1961)  reported
96-hour LC5Q values  of  820 and  1250 mg/l  for  fathead minnows,  Plmephales
promelas.  1n hard and soft water,  respectively.  These authors  also reported
96-hour LC5_ values  of 720  mg/l  for  bluegllls,   Lepomls  macrochlrus.  and
775 mg/l  for gupples,  Leblstes  retlculatus. both  1n  soft water.   Hardness
1n  these  studies was 20  mg/l for  soft  water and  380 mg/l for  hard  water.
An  LC,Q  of 384  mg/l  was  reported  for  the  golden  orfe,  Leudscus  1dus
(Kn1e et al., 1983).
    The only Invertebrate  species  for  which  there  was  Information  about
adiponltrlle  toxlclty  was  the  cladoceran,  Daphnla  magna.   Brlngmann  and
Kuehn  (1982)  reported  a  24-hour  EC,,   for  Immobilization  of  445  mg/l,
while Knle et al. (1983) reported an EC5Q of 1250 mg/l.
4.2.   CHRONIC EFFECTS
    Pertinent  data  regarding  chronic toxlclty  of  ad1pon1tr1le to  aquatic
organisms   could  not  be  located   In  the  available  literature  as  cited  1n
Appendix A.
4.3.   PLANT EFFECTS
    Knle  et al.  (1983) reported  that   408  mg/l  was  a  30-mlnute EC...  for
Inhibition  of  culture  growth  of  the bacterium Pseudomonas  put Ida.   Other
data for  aquatic plants or  bacteria  could  not  be located 1n  the  available
literature as cited In Appendix A.
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4.4.   SUMMARY
    There  was  little  Information  concerning toxldty  of  adlponltrUe  to
aquatic  organisms.   The  lowest  reported acutely  toxic  concentration  for
freshwater  fishes  was  384  mg/i,  an  LC5Q  for   the  golden  orfe  (Knle  et
al., 1983).   The lowest  reported  acutely toxic concentration for freshwater
Invertebrates was  445 mg/l,  an  EC—  for  Immobilization  of  Daphnla  magna
(Brlngmann  and  Kuehn,  1982).   Data  for  saltwater  species  could not  be
located 1n the available  literature  as  cited  1n Appendix  A.
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                             5.   PHARHACOKINETICS
5.1.   ABSORPTION
    Approximately 50%  of  the adlponltrlle  consumed In  the  diet by  mongrel
female dogs  was  recovered  1n the  urine  as  thlocyanate  (Svlrbely and Floyd,
1964).  Dietary concentrations  ranged from 10-1000 ppm.
5.2.   DISTRIBUTION
    Cyanide,  an  Important  metabolite of  ad1pon1tr1le,  has  been  shown  to
cross the blood-brain  barrier and  locate 1n the  brain.   Tan 11  and  Hashimoto
(1985) measured  cyanide  at -0.71  wg/g of  wet tissue  In the brains  of  male
ddY mice  given an oral  4.8 mmol/kg  (519 mg/kg)  dose of adlponltrlle.   The
brains were harvested at the time  of  death, -83  minutes  after treatment.  In
mice  pretreated  with  CC1.  to  Inhibit   the  hepatic  mixed   function  oxldase
system  (and  presumably prevent  degradation of  adlponltrlle to cyanide),  a
519 mg/kg dose of adlponltrlle did not cause  death  and  cyanide was  not found
1n the brain 83 ml.utes after treatment.
5.3.   METABOLISM
    A  number  of  studies   Indicate  that   adlponltrlle  Is   metabolized  to
cyanide.  Svlrbely and Floyd  (1964)  found  that dogs  fed adlponltrlle In the
diet at  10-1000  ppm  showed a dose-related  Increase In  thlocyanate excreted
In  the  urine,  which  Is equivalent  to -50% of  the dose  of adlponltrlle.   The
amount   of   thlocyanate   In   the   bloodstream   of  guinea   pigs   Injected
subcutaneously  with  adlponltrlle  at  3-30 mg/kg  was   proportional  to  the
administered   dose   (Gh1r1nghell1,   1955a).    Tan11  and  Hashimoto   (1985)
    <•
Identified  cyanide  In  the  brains  of mice  orally  dosed with  adlponltrlle.
The  metabolism of ad1pon1tr1le  to  cyanide was  greatly  Inhibited  In  mice
pretreated with  CC1.,  as  evidenced  by  the fact  that cyanide was  not  found
1n the brains of pretreated mice.


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    In an  hi vitro  study  using mouse  liver  mlcrosomes,  6.23  ng  cyan1de/mg
protein/minute  were  formed  from  an  ad1pon1tr1le  concentration  of  3.1  mM
(Tan11  and  Hashimoto,  1985).   When  mice were  treated  with  CC1.  before
mlcrosomes were  harvested,  cyanide was  not  detected after  adiponltrlle  was
added to  the  cultures.  Tanll  and Hashimoto  (1985)  stated  that ad1pon1tr1le
1s  probably  hydroxylated  at   the  a-carbon  to   form  cyanohydMn,   which
degrades spontaneously 1n  alkaline medium to form hydrogen cyanide.
5.4.   EXCRETION
    Approximately  79% of  the  adiponltrlle   (3-30  mg/kg)  Injected  subcuta-
neously  Into  guinea  pigs  was  accounted for  as thlocyanate excreted  1n  the
urine (Gh1r1nghel11,  1955a).   Dogs excreted  -50%  of an oral  dose of  adipo-
nltrlle as urinary thlocyanate;  negligible amounts  of  thlocyanate  were found
1n the feces (Svlrbely and Floyd, 1964).
5.5.   SUMMARY
    Studies of  the metabolism of  adiponltrlle  Indicate that  1t  1s absorbed
by  the  gastrointestinal  tract,  metabolized  to cyanide  and excreted  1n  the
urine as  thlocyanate (Svlrbely  and  Floyd,  1964; Gh1r1nghell1,  1955a;  Tanll
and Hashimoto,  1985).  Tan11  and Hashimoto (1985)  found  that  the  metabolism
of  adiponltrlle  to cyanide In  mice  was greatly Inhibited  by  CC1. pretreat-
ment, which Inhibits certain drug metabolizing enzymes 1n the liver.
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                                 6.  EFFECTS
6.1.   SYSTEMIC  TOXICITY
6.1.1.    Inhalation  Exposures.
    6.1.1.1.   SUBCHRONIC  —  Pertinent   data   regarding  the   toxldty   of
ad1pon1tr1le  following subchronlc  Inhalation exposure  could  not be  located
1n the  available literature as  cited  In  Appendix A.
    6.1.1.2.   CHRONIC  —  Ceresa  (1948a)  reported that  27  Individuals  who
had worked In  the nylon  Industry, handling adiponltrlle and  hexamethylene-
dlamlne for 2-3  years,  showed a definite tendency for hyperchromlc  anemia  of
the hemolytlc  type and  slight leukopenla or  lymphomonocytosls.
6.1.2.    Oral  Exposures.
    6.1.2.1.   SUBCHRONIC  ~  Pertinent   data   regarding  the   toxldty   of
adiponltrlle  following  subchronlc oral  exposure could  not be  located  In  the
available literature as dted In  Appendix  A.
    6.1.2.2.   CHRONIC  —  NIOSH  (1978)  reviewed  chronic   oral   studies   of
adiponltrlle  In  dogs and  rats  completed by  Svlrbely  and Floyd  (1964).   The
original study  report  could  not  be  obtained.  However,  the original  report
from the  fourth  portion  of  this  series  (SvUbely,   n.d.)   was   located.
Apparently each  of the segments were only reported Vn abstract  form.   In  the
dog  study,  an   unspecified  number  of    female  mongrel   dogs  were   fed
adiponltrlle  In the  diet  at  "the equivalent  of"  10,  100,  500 and 1000  ppm
for an  unspecified  period of  time.   Blood  and  urine values  and tests  for
liver  and kidney  function were normal  In  dogs fed adiponltrlle  at  <500 ppm.
During  the first week,  dogs   fed 1000 ppm were  not able  to consume the entire
dose;  the dogs vomited  or  failed  to eat  a  portion  of H.
    In  the rat  study,  an  unspecified number  of male  and female  Wlstar rats
were provided with  0.5,  5.0  or  50 ppm  adiponltrlle  In their  drinking water


0071d                               -14-                             11/17/87

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for  2  years.   Throughout  the  study,  body  weights  remained  normal  and  no
hematologlc abnormalities were observed.  At  the  end of the study, advanced
adrenal  degeneration  was  found  In  female  rats  at  all  three ad1pon1tr1le
concentrations and  1n  male rats  exposed  to  50  ppm.  Degeneration of  other
organs   was  also  noted,  but   was   not  considered  to  be   compound-related.
Determination  of  organ  (spleen,   liver,   kidney)   to   body   weight   ratios
revealed no significant differences.  No effect  on survival  was  reported.
6.1.3.    Other Relevant  Information.   NIOSH  (1978)  summarized a  report  by
GhlMnghelH  (1955b)   concerning  a  case  of acute  poisoning  In  which  an
18-year-old  man  consumed  a  few  ml of  ad1pon1tr1le.    The man  experienced
vomiting,  tightness  1n  the chest,  headache, profound  weakness with  diffi-
culty  standing,  vertigo,  respiratory difficulty,  tachycardia  and low  blood
pressure.  The man recovered after  being treated with sodium thlosulfate.
    As  reviewed  by  NIOSH (1978),  Zeller et  al.  (1969)   reported seven  cases
of dermal  exposure  to adlponUrlle.  Mild  skin Irritation and  Inflammation
developed  1n  six  of  the workers  within  5-15  r.inutes of  exposure.   The
seventh worker,  whose  shoe had been  drenched with ad1pon1tr1le, had  exten-
sive destruction  of  the skin  of   the  foot.   The  Injury   required surgical
treatment and the worker was  Incapacitated  for 117 days.
    To  determine 1f the effects observed 1n  humans occupatlonally  exposed to
ad1pon1tr1le  and  hexamethylenedlamlne  (see  Section   6.1.1.2.)   could  be
attributed  to ad1pon1tr1le, Ceresa  (1948b)  and  Ceresa and  De  Blaslls  (1950)
examined  the toxlclty  of adlponUrlle  and  hexamethylenedlamlne  1n  guinea
pigs.  An  unspecified dose of  ad1pon1tr1le was  rubbed on the  backs  of  guinea
pigs dally  for  1 month  (Ceresa,  1948b).   This  treatment resulted  In  weight
loss,  decreased  calcium  content  of  the blood, marked hyperchromlc  hemolytlc
anemia   with  leukopenia   and   lymphomonocytosU.   Hlstologlcal  examinations
revealed  swelling  and  congestion   of  nearly all  Internal  organs.   Because

0071d                               -15-                             11/17/87

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hemolytlc anemia  with  leukopenla and degenerative  changes  In the  liver  and
kidney were  also  noted 1n guinea  pigs  treated with  subcutaneous  Injections
of  hexamethylenedlamlne,  Ceresa and  De Blas11s  (1950)  concluded  that  both
adlponltMle and  hexamethylenedlamlne may contribute  to  the  effects observed
1n humans.
    Smith and Kennedy  (1982) exposed groups of  10 male  Charles  River CD rats
to  ad1pon1tr1le  vapor  at  0,   0.03,  0.1 or  0.3 mg/l   (0,  30,  100 or  300
mg/m3)  for   ten  6-hour periods  (5  days/week).   After   the  ninth  exposure,
blood and  urine analyses were  completed.   Following the  tenth exposure,  5
rats/exposure group were  sacrificed and comprehensive  hlstologlcal examina-
tions were  conducted.   The  remaining  rats  were allowed  to recover for  14
days when they were sacrificed for  hlstologlcal  examinations.
    During  the  exposures,  the   signs  of toxlclty  observed  In  all  exposed
groups  Included Irregular breathing  and mild  salivation.   Rats exposed  at
0.3  mg/l showed  weight  loss  during the  first  5  exposures,  and   af.er  10
exposures had  changes   1n clinical  pa-ho-logy parameters Including. Increases
1n blood glucose, urea  nitrogen, creatlnlne and  urine glucose,  and  decreases
1n erythrocyte  count,  hemoglobin,  leukocyte count and  urine  osmolalHy.   At
0.1  mg/l,  rats  showed Increased  blood urea  nitrogen   and  lymphocytes  and
decreased numbers  of  eoslnophlls  and  neutrophlls.   No changes  1n clinical
chemistry parameters  were observed  at  0.03 mg/l.   No   hlstologlcal  changes
were  noted  at   any  exposure   concentration.   Fourteen  days  postexposure,
clinical  pathology  parameters  of   all  groups  were  normal  and  microscopic
changes  1n the organs were not observed.
    LD-Q values  for  ad1pon1tr1le are presented  1n  Table 6-1.   Plokhova  and
Rubaklna (1965) reported  effects of acute  lethal oral  doses  of  ad1pon1tr1le
as excitation,  convulsions,  dyspnea, coma with  death 1n 2-6 hours.   H1sto-
pathologlc  changes   Included hyperemla and  dystrophlc  changes   In  brain,

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                                  TABLE 6-1

                              Values  for AdlponHMle
 Species
   Route of
Administration
1050 Value
Reference
Rat
Rat
Rat
Mouse3
House5
Guinea pig
Rat
House
Inhalation
oral
oral
oral
oral
subcutaneous
subcutaneous
Intraperltoneal
1.71 mg/l
{1710 mg/m3)
(4-hour LC5o)
960 mg/kg
300 mg/kg
1.59 mmol
(-172 mg/kg)
2.65 mmol
(-287 mg/kg)
50 mg/kg
200 mg/kg
40 mg/kg
Smith and
Kennedy. 1982
Plokhova and
Rubaklna, 1965
NIOSH, 1978
Tan 11 and
Hashimoto, 1985
Tan 11 and
Hashimoto, 1985
Gh1r1nghell1,
1955b
NIOSH, 1978
Plzak and
Doull, 1969
aH1ce pretreated  with an  Intraperltoneal  Injection  of olive  oil  served  as
 controls  1n  an  experiment  with  mice  pretreated  with  CC14  (see  Section
 5.2).

bH1ce  were pretreated  with  an  Intraperltoneal   Injection  of  CC14.   Mice
 appear  to  be  somewhat  more  sensitive  than  rats  to  the acute oral  tox1c1ty
 of adlponltrlle.
007 Id
                  -17-
                           06/25/87

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 liver,  kidney and  myocardium.   Mice  appear  to  be  somewhat more  sensitive
 than  rats  to  the acute oral toxldty of ad1pon1tr1le.
 6.2.    CARCINOGENICITY
 6.2.1.    Inhalation.   Pertinent   data  regarding   the   cardnogenlcHy   of
 adiponltrlle  following  Inhalation  exposure  could  not  be  located  In  the
 available  literature as cited 1n Appendix A.
 6.2.2.    Oral.  A  NIOSH  (1978)  summary of a  2-year  drinking water study  of
 adiponltrlle  1n VHstar rats  did not report carcinogenic effects.  Additional
 Information  concerning the  cardnogenlcHy  of  adiponltrlle following  oral
 exposure   could  not  be  located  In  the  available  literature   as  dted  1n
 Appendix  A.   The  chemical  1s not  currently  scheduled for  cancer  testing  by
 the NTP (1987).
 6.2.3.    Other Relevant Information.   Pertinent  data regarding   the carclno-
 genldty  of adiponltrlle by  other  routes  of  exposure could not  be located In
 the available literature as cited In Appendix A.
 6.3.    MUTAGENICITY
    NIOSH   (1978)   reported   that   adiponltrlle   was  negative   for  reverse
 mutation  1n Salmonella typhlmurlum strains  TA1536,  TA1537,  TA1538 and  TA98
.at   concentrations   <10,000   yg/plate,  both  with   and   without  metabolic
 activation.
 6.4.    TERATOGENICITY
    Johannsen et  al.  (1986)  dosed  groups of  25  mated Charles River,  COBD CD
 rats  by gavage with ad1pon1tr1le  at 0,  30,  50 or 80 mg/kg/day  on gestation
 days  6-19.  The  dams were sacrificed  on  gestation day 20 and the number and
 location  of viable and  nonvlable   fetuses, early  and late  resorptlons,  and
 the total  number  of  Implants  and  corpora  lutea were  determined.   The fetuses
 were  examined for gross  malformations and half  were examined  for  visceral
 malformations while the remaining were examined for  skeletal anomalies.
 0071d                               -18-                             11/17/87

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    During the  study,  two  80 mg/kg/day  rats  and  one 50 mg/kg/day rat  died.
No  differences  were  found  In  uterine  and  fetal  parameters  measured   at
sacrifice.   Fetal  body  weights  were  reduced significantly  (p<0.05)  at  80
mg/kg/day  but  not  at  30  mg/kg/day,  although  the fetal  body weights were
essentially  the same  at  these  two  dose   levels.   Because  a  dose-related
change  In  fetal body weight  was not  observed,  the Investigators concluded
that  there was  no treatment-related  effect  on  fetal   body  weight.   Fetal
examinations revealed no treatment-related  malformations.
6.5.   OTHER REPRODUCTIVE EFFECTS
    Svlrbely  (n.d) reported  In an  unpublished  abstract  that  exposure  of
Holtzman  rats  (number  unspecified) to  10, 100 or  500  ppm ad1pon1tr1le  for
three  generations   (2  Utters/generation)   did  not result   1n  any   adverse
effects.   Endpolnts  monitored  Included   fertility,   gestation   (NOS)   and
viability.
6.6.   SUMMARY
    Nylon  workers  exposed  to  adlponUrlle and hexamethylened1am1ne  for  2-3
years  showed  a  tendency for  hyperchromlc  anemia  of  the hemolytlc  type  and
slight  leukopenla  (Ceresa,  1948a).   Ceresa (1948b) attributed  these effects
to exposure to ad1pon1tr1le and hexamethylenedlamlne.
    Dogs  fed  adlponUrlle  In  the  diet at   levels  <500  ppm had  normal  blood
and  urine  values  and  tests  for  liver  and  kidney function (Svlrbely  and
Floyd,  1964).   During  the first week  of  the study, dogs fed 1000  ppm were
not  able  to consume the entire  dose.   In   a  rat  study   (Svlrbely  and  Floyd,
1964),  females  treated  with ad1pon1tr1le  In  the  drinking water at  0.5,  5.0
and  50 ppm and males at  50 ppm were  found to have advanced adrenal  degen-
eration.
    Vomiting,  tightness  In  the  chest,   headache,  profound  weakness  with
difficulty  standing,  vertigo,  respiratory difficulty,  tachycardia   and  low

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blood pressure  were  experienced by a human  who  consumed  a few ml of  adlpo-
nHMle (Gh1r1nghell1, 1955b).  Zeller et al.  (1969) reported  seven  cases  of
skin Irritation In workers dermally exposed  to adlponltrlle.
    Adlponltrlle rubbed on  the  backs  of  guinea pigs for 1 month  resulted  1n
weight  loss,  decreased  calcium content  of   the  blood,  marked  hyperchromlc
hemolytlc  anemia  with   leukopenla  and  lymphomonocytosls.    Hlstologlcal
examinations revealed  swelling  and congestion of nearly all Internal  organs
(Ceresa, 1948b).
    Rats  exposed  to   adlponUMle  at  0.3 mg/j. for ten  6-hour exposures  (5
days/week) showed  Increases  1n  blood  glucose, urea nitrogen,  creatlnlne and
urine  glucose,  and  decreases  1n  erythrocyte count,  hemoglobin, leukocyte
count and  urine osmolalHy.   At   0.1 mg/i,   Increases 1n  urea nitrogen and
lymphocytes and decreases  In  the  number  of  eoslnophlls and neutrophlls were
noted.   No  changes   In   clinical  parameters  were  observed  at  0.03 mg/i.
(Smith and Kennedy, 1982).
    The oral  LD.Q 1n  the rat  was reported  to  be 960  mg/kg  (Plokhova and
Rubaklna,   1965)  and  300  mg/kg  (NIOSH,  1978).   Mice,  with an  oral  LD5Q  of
172 mg/kg,  may be  somewhat more  sensitive   to  the  acute oral  toxldty  of
adlponltrlle (Tan11 and Hashimoto,  1985).
    The carclnogenlcHy of  adlponltrlle  following Inhalation,  oral or other
routes of  exposure has not been studied.  Adlponltrlle  tested negative for
reverse  mutation   1n  S.   typhlmurlum  at  concentrations  <10,000 yg/plate,
both with and without metabolic  activation.
    Johannsen et al.   (1986)  orally dosed  pregnant rats with adlponltrUe  at
0, 30, 50  or  80 mg/kg/day on gestation  days   6-19.  Two rats at  80 mg/kg/day
and one  rat at  50  mg/kg/day  died.   Fetal   body  weights  were  significantly
0071d                               -20-                             09/14/87

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reduced at  80  mg/kg/day,  but  this  observation  was not  attributed  to treat-
ment.  No  other  changes  were  noted.   No  changes  In  fertility,  gestation or
viability  were  noted  1n  two  litters  from rats  exposed to  adlponltrlle In
their drinking water  at  10,  100 or 500 ppm for  2  years  (Svlrbely and Floyd,
1964).
0071d                               -21-                             06/25/87

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                    7.  EXISTING GUIDELINES AND STANDARDS
7.1.   HUMAN
    NIOSH  (1978)  recommended  that  employee  exposure  to  adlponltrlle  not
exceed  4 ppm  (18 mg/m3)  as  a  TWA  for  up  to  a 10-hour  work shift  1n  a
40-hour  workweek.   This  recommendation  Is based  on the  comparative acute
toxlclty  of IsobutyronHrlle  and   adlponUrlle  Injected  subcutaneously  1n
female  rats.   Other  guidelines  or  standards  could not  be located  In  the
available literature as  dted  In  Appendix A.
7.2.   AQUATIC
    Guidelines  and  standards  for  the protection of aquatic  organisms from
the effects of  adlponltrlle could not be located In  the available literature
as cited In Appendix A.
0071d                               -22-                            06/25/87

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                             8.  RISK ASSESSMENT
8.1.   CARCINOGENICITY
    Pertinent  data  regarding  the  cardnogenlcHy  of  adlponltrlle  by  any
route of  exposure could  not  be located In the available  literature as  cited
1n Appendix A.
8.1.1.   Weight of Evidence.   Data  were not  located regarding the cardno-
genldty  of  adlponltrlle  1n  humans  or  experimental  animals;   therefore,
ad1pon1tr1le 1s placed 1n EPA Group D  (U.S. EPA,  1986c),  not  classifiable as
to human carclnogenlclty.
8.1.2.   Quantitative   Risk  Estimates.   The  lack  of   data   concerning   the
carclnogenlclty of ad1pon1tr1le  precludes  the derivation of  risk  assessment
values based on carclnogenlclty.
8.2.   SYSTEMIC TOXICITY
8.2.1.   Inhalation  Exposure.
    8.2.1.1.   LESS  THAN LIFETIME   EXPOSURES  (SUBCHRONIC) '— The lack   of
data concerning the toxlclty of  adlponltrlle  following  subchronlc  Inhalation
exposure precludes the derivation of a  subchronlc  Inhalation RfD.
    8.2.1.2.   CHRONIC  EXPOSURES -- Nylon  workers  exposed  to adlponltrlle
and hexamethylenedlamlne for  2-3 years showed a definite  tendency  for  hyper-
chromic anemia of the  hemolytlc  type  and slight  leukopenla (Ceresa,  1948a).
The  study  1s  Inadequate for  the  derivation  of  an  Inhalation RfD  because
exposure was to a mixture of  chemicals and because  of  the lack of quantita-
tive  exposure  data.    The  recommended  occupational standard  of   4  ppm  (18
mg/m3)  (NIOSH,  1978)   based  on acute  subcutaneous  toxlclty   of ad1pon1tr1le
compared with 1sobutyron1tr1le In female rats 1s  not adequate for  determina-
tion of an RfD for Inhalation  exposure.
0071d                               -23-                             09/14/87

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8.2.2.   Oral Exposure.
    8.2.2.1.   LESS THAN  LIFETIME  EXPOSURES (SUBCHRONIC) — The toxUHy  of
adlponHMle following subchronlc oral exposure has not been studied.
    8.2.2.2.   CHRONIC  EXPOSURES — In  a   study   by   Svlrbely  and  Floyd
(1964), blood and  urine  values  and tests for  liver  and  kidney  function  were
normal  In  dogs  fed  adlponltrlle at  <500  ppm for  an  unspecified  length  of
time.   During  the  first  week of the  study,  dogs  fed 1000 ppm  were not  able
to consume the entire dose.
    Female rats  provided  with adlponltrlle  1n  their drinking water at  0.5,
5.0 or  50  ppm and males  at 50  ppm for  2  years were found to  have advanced
adrenal degeneration (Svlrbely and Floyd, 1964).   No changes  In body weight,
organ  weights  or   hematologlcal  values  were  noted   and  no   Increase  1n
mortality was  reported.   Advanced adrenal  degeneration  was observed  1n all
treated groups of  females,  but  1n males only  at  50  ppm.   These observations
suggest  that 0.5  ppm may  be  near  the threshold  for  adrenal  effects  In
females.  Increased mortality was not  reported  1n  any  treatment group, which
suggests that  the  effects  on the  adrenal  were  not life  threatening.   The
drinking water concentration of  0.5  ppm,  therefore, constitutes a NOAEL  1n
male rats and  may  be considered a LOAEL In  female rats.   The fact  that  this
study was  not  available  for  review and  that 1t appears  from the  evaluation
of  other   reports  from  this  series   that   the  report  only  existed  as  an
unpublished abstract precludes use of  these data for RfO development.
    It  1s known  that adlponltrlle  1s  metabolized  to  cyanide.  Therefore, the
possibility  that an  RfD  for  adlponltrlle  could  be derived  by analogy  to
cyanide  was  Investigated.   However,  the  effects  on  the  adrenal   gland
reported by  Svlrbely  and  Floyd  (1964)  are  Inconsistent  with   the reported
critical  effects  of  cyanide  which   are  predominately  CNS  lesions.    In
addition  the dose  of  adlponltrlle  causing  these adrenal  lesions Is  much

0071d                               -24-                      ,       11/17/87

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lower than reported effect levels for cyanide (ATSDR, 1988).  As a result of
discrepancy  1n  both critical  effects  and effective  doses  for adlponltrlle
compared with cyanide,  an RfO based on analogy 1s not derived.  Adlponltrlle
has not been  examined  for  carclnogenldty,  and  the  one teratogenlclty study
(Johannsen et a!.,  1986)  located did not  find  fetal  effects  at doses below
those that caused maternal  toxldty.
0071d                               -25-                             11/17/87

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                          9.  REPORTABLE QUANTITIES
9.1.   BASED ON SYSTEMIC TOXICITY
    The toxldty of adlponltrUe was  discussed  1n  Chapter 6.  The only data
potentially  suitable  for the  derivation  of  an  RQ are  summarized  In Table
9-1.   In  the 2-year  rat study  (Svlrbely  and  Floyd,  1964), advanced adrenal
degeneration was observed  In  female rats provided with  ad1pon1tr1le  In the
drinking water  at  0.5  ppm.   Due  to  reporting  deficiencies  as discussed 1n
Sections  6.1.2.  and  8.2.2.,   these  data  are not  used  to  estimate  an  RQ
(Table 9-2).
9.2.   BASED ON CARCINOGENICITY
    Data were  not  located regarding  the  carclnogenldty  of  ad1pon1tr1le 1n
humans or animals and  the  compound  was  assigned to EPA Group D, not classi-
fiable  as  to  human  carclnogenldty.    Hazard ranking based  on carclnogen-
Iclty, therefore.  Is  not possible.
OOVld                               -26-                             11/17/87

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                                  TABLE 9-1

      Oral Toxldty Summary for  AdlponHrlle  Using  Female Wlstar  Ratsa»b
Average   Vehicle/                 Transformed     Equivalent
Weight    Physical    Exposure     Animal  Dosec    Human  Dose^
 (kg)      State                   (mg/kg/day)     (mg/kg/day)
                               Response
0..356



drinking
water


0.5 ppm In 0.07
the drinking
water for
2 years
0.01 advanced
adrenal
degeneration

aSo.urce: Svlrbely and Floyd,  1964;  NIOSH,  1978

^Number of  animals  at start  of  experiment and purity  of  compound were  not
 reported.^

cCalculated  by  multiplying   the  0.5  ppm  drinking  water  level   by  0.049
 I/day, the  reference  water  Intake for a 0.35 kg  rat  (U.S.  EPA,  1985)  and
 by dividing by the rat body  weight.

^Calculated by multiplying the  animal transformed  dose  by the cube  root  of
 the  ratio' of" the  animal  body  weight  to  the reference  human  body weight
 (70 kg).

Reference rat body weight  (U.S.  EPA,  1985)
0071d
-27-
06/25/87

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                                  TABLE 9-2
                                 AdlponHMle
          Minimum Effective Dose  (MED) and Reportable Quantity (RQ)


Route:
Dose*:
Effect:
Reference:
                           Data are  Insufficient  to evaluate an RQ.
RVd:
RVe:
Composite Score:
RQ:
'Equivalent human dose
0071d                               -28-                             11/17/87

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                               10.  REFERENCES

Atkinson, R.   1985.   Kinetics and  mechanisms  of the  gas-phase reaction  of
the  hydroxyl  radical  with  organic  compounds  under  atmospheric conditions.
Chem. Rev.  85: 69-201.

ATSDR   (Agency   for   Toxic   Substance   and   Disease   Registry).     1987.
lexicological Profile  on Cyanide.  Atlanta, GA.

BMngmann, G.  and R.  Kuehn.   1982..  Results of toxic action of water  pollu-
tants on  Daphnla  magna  Straus  tested  by an Improved standardized  procedure.
Z. Wasser Abwasser Forsch.   15(1): 1-16.

Ceresa,  C.    1948a.   The  blood picture   of  certain workers   1n  the  nylon
Industry.  Med. Lavoro.   39:  162-165.   (Hal.)

Ceresa,  C.   1948b.   Experimental  research on  adiponltrlle poisoning.   Med.
Lavoro.  39: 274-281.   (Hal.)

Ceresa,  C.  and M.  DeBlaslls.  1950.   Poisoning with  hexamethylenedlamlne.
Med. Lavoro.  41:  78-85.  (CA 44:8530e)

E1senre1ch,  S.J.,  B.B.  Looney  and  J.O. Thornton.   1981.  Airborne  organic
contaminants  of  the Great Lakes ecosystem.   Environ.  Scl. Technol.   15(1):
30-38.
0071d                               -29-                             11/17/87

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Gh1r1nghell1, L.  1955a.   ToxIcHy  of adlplc nUrlle.   II.  Study of Influ-
ence exercised on blood constituents by continuous supply and possibility of
absorption through skin.   Hed.  Lavoro.   46:  229-234.   (CA 49:15093fg)

Gh1r1nghell1, L.  1955b.   ToxIcHy  of  adlplc n1tr1le.  CUnlcalplcture and
mechanism of poisoning.   Med.  Lavoro.   46:  221-28.  (Cited In NIOSH, 1978)

Hawley,  G.G.   1981.   The Condensed  Chemical   Dictionary,  10th  ed.   Van
Nostrand Relnhold Co.,  New York.   p.  21.

Henderson,  C.,  Q.H.  Pickering  and  A.E. Lemke.   1961.   The effect  of  some
organic cyanides (nltrlles) on fish.  Proc. Fifteenth Ind. Waste  Conf., Eng.
Bull. Purdue Univ.,  Ser.  No.  106.  65(2): 120-130.

H1ne, J.  and  P.K. HookerJee.   1975.   The Intrinsic hydrophlUc character oi
organic compounds.   Correlations  1n terms  of  structural Contributions.  J.
Org. Chem.  40(3): 292-298.

Johannsen,  F.R., G.J.  Levlnskas,  P.E. Berteau  and  D.E.   Rodwell.    1986.
Evaluation  of  the  teratogenlc  potential of  three  aliphatic  nltrlles  1n the
rat.  Fund. Appl. Toxlcol.  7(1):  33-40.

Kn1e, J.,  A.  Haelke,  I.   Juhnke and  W.  Schiller.   1983.   Results of  studies
of  chemical  substances   using  four  blotests.    Dtsch.   Gewaesserkd.  HHt.
27(3): 77-79.

Kuney,  J.E.,  Ed.  1985.   Chemcyclopedla 1986.   Vol.  4.   American Chemical
Society, Washington,  DC.

0071d                               -30-                            11/17/87

-------
Kuwahara, M.,  H.  Yanase, Y.  Klkuchl  and K.  Okuzuml.   1980.  Metabolism  of
sucdnonltrlle 1n Aeromonas  sp.   Hakkokogaku  Ka1sh1.  58:  441-448.

L1netsk11,  V.A.  and  B.R.  Serebryakov.    1965.   Alkaline   hydrolysis   of
nltrlles  as  a method  of detoxification  of  wastes.   Izv.  Vysshlrh  Uchebn:
Zavedenll, Neft 1 Gaz.   8:  72.   (CA 62:11521c)

Lucas, S.V.   1984.  GC/MS analysis  of  organlcs  In drinking water  concentrates
and advanced waste treatment concentrates.   Vol.  2. Computer-printed  tabula-
tions  of compound   Identification  results  for  large-volume concentrates.
Columbus  Labs.  Health  Eff.  Res.  Lab.,  Columbus, OH.   EPA  600/1-84-0208.
NTIS PB85-128239.

Ludzack,  F.J..  R.B.  Schaffer,   R.N.  Bloomhuff  and M.B.  Ettlnger.   1959a.
Biochemical   oxidation   of  some  commercially   Important  organic   cyanides.
Sewage Ind.  Wastes.   31:  33-44.

Ludzack,  F.3.,  R.B.   Schaffer   and  R.N.  Bloomhuff.    1959b.   Experimental
treatment of   organic  cyanides   by  conventional  sewage  disposal  processes.
In:  Proc.  of  the  14th Ind. Waste  Con.,  Engineering  Ext.  Series  No.   104:
547-565.

Lutln, P.A.   1970.  Removal of  organic  nltrlles  from wastewater  systems.   J.
Water Pollut. Control Fed.  42:  1632-1642.

Lyman,  W.J.,  W.F. Reehl  and  D.H.  Rosenblatt.   1982.   Handbook  of  Chemical
Property  Estimation Methods.  McGraw  Hill Book Co., New  York.   p.  4-9,  5-5,
7-5, 15-27.

0071d                               -31-                             11/17/87

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Neely,  W.B.  and  G.E.  Blau.  1985.   Environmental  Exposure from  Chemicals.
Vol. 1.  CRC Press Inc., Boca Raton,  FL.   p.  31.

NIOSH   (National  Institute  for  Occupational   Safety  and   Health).    1978.
Criteria  for  a  Recommended  Standard...Occupational  Exposure  to  Nltrlles.
Equitable Environ. Health, Inc., Rockvllle,  MD.   p.  166.

NTP  (National  Toxicology  Program).   1987.  Management Status Report.   Dated
1/9/87.

Plokhova, E.I.  and A.P.  Rubaklna.   1965.  lexicological characteristics  of
the  dlnltnie  of adlplc  acid.   G1g1ena  Truda  1  Prof.  Zabolevanlya.   9(9):
56-58.  (CA 64:2650h)

Plzak,  V. and  J.  Ooull.   1969.   A further survey of  compounds  for  radiation
protection,   SAM-7R-69-1.   Brooks  Air   Force  Base.  TX,   USAF   School   of
Aerospace Medicine, Aerospace medical Division  (AFSC).  p.  33-39.   (Cited  In
NIOSH, 1978)

SANSS  (Structure  and  Nomenclature Search System).  1987.   Chemical  Informa-
tion System (CIS) computer data  base.   Online:  February,  1987.

Shackelford, W.M.  and  L.H.  Keith.   1980.   Frequency  of  organic  compound
Identified In water.   U.S. EPA,  Athens, GA.   EPA 600/4-76-062.

Smiley,  R.A.   1981.   NltrHes.  In:  K1rk-0thmer  Encyclopedia  of  Chemical
Technology,  3rd ed.,  Vol. 15, M.  Grayson  and D.  Eckroth,  Ed.  John  WHey and
Sons, New York.  p. 897-901.

0071d                               -32-                              09/14/87

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Smith,  L.W.  and  G.L.  Kennedy,  Jr.   1982.   Inhalation  toxlclty  of  adlpo-
nltrlle 1n rats.  Toxlcol.  Appl.  Pharmacol.   65(2):  257-263.

SRI  (Stanford  Research   Institute).    1986.    1986  Directory   of   Chemical
Producers: United States  of America.   SRI  International,  Menlo  Park,  CA.

Svlrbely,  J.L.   n.d.   Chronic  studies  of  adiponltrlle,  acrylonltrlle  and
B,Bi-oxyprop1on1tr1le.    IV.  Reproduction  studies   In  rats   and  metabolic
studies   In   rats  and  dogs.    Sanitary  Engineering  Center,  U.S.   PHS,
Cincinnati, OH.

Svlrbely, J.L. and E.P. Floyd.   1964.   Toxlcologlc  studies  of  acrylonltrlle,
adiponltrlle and  B,  Bl-oxyd1prop1on1tr1le  —  II.  Chronic  studies.   Cincin-
nati,  U.S.  Dept.  of Health.  Education  and Welfare.  Public Health  Service,
Bureau  of  State  Services,  Robert  A.  Taft  Sanitary  Engineering   Center.
p. 100.  (Cited 1n NIOSH,  1978)

Swann, R.L., D.A. Laskowskl,  P.J. McCall, K. Vander  Kuy  and H.J. Dlshburger.
1983.   A rapid  method  for the  estimation of  the  environmental  parameters
octanol/water partition  coefficient,  soil  sorptlon constant,  water  to  air
ratlio and water solubility.  Res. Rev.   85:  17-28.

Tan1i1, H. and K.  Hashimoto.  1985.  Structure-acute toxlclty  relationship of
dlnUrlles 1n mice.  Arch.  Toxlcol.   57(2):  88-93.

Tullar,  P.E.    1947.   Final  report  on  the pharmacology  and   toxicology  of
acrylonltrlle  and  acrylon.   Kalusowskl   Memorial  Research   Laboratories,
George Washington University.
0071d                               -33-                             11/18/87

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U.S.  EPA.   1980.   Guidelines  and  Methodology Used  In  the  Preparation  of
Health  Effect  Assessment  Chapters  of  the  Consent  Decree  Water  Criteria
Documents.  Federal Register.  45(231): 49347-49357.

U.S.  EPA.    1984.   Methodology  and   Guidelines  for   Reportable  Quantity
Determinations  Based  on Chronic Toxlclty  Data.   Prepared  by  the Office  of
Health  and  Environmental Assessment,  Environmental  Criteria and  Assessment
Office, Cincinnati, OH  for the Office  of Solid Waste  and Emergency Response,
Washington,  DC.

U.S.  EPA.   1985.   Reference  Values for  Risk Assessment.   Prepared by  the
Office  of  Health  and  Environmental Assessment,  Environmental  Criteria  and
Assessment Office, Cincinnati, OH for  the  Office of Solid Waste,  Washington,
DC.

U.S.  EPA.   1986a.   Methodology for  Evaluating Potential  Cardnogenlclty  In
Support of  Reportable   Quantity Adjustments  Pursuant  to  CERCLA Section  102.
Prepared  by  the  Office of  Health  and  Environmental  Assessment,  Cancer
Assessment  Group  for   the Office   of  Solid  Waste  and   Emergency  Response,
Washington,  DC.

U.S.  EPA.  1986b.   OHMTADS (Oil and Hazardous  Materials  Technical  Assistance
Data Systems).  On-Hne: February,  1987.

U.S.  EPA.   1986c.  Guidelines  for   Carcinogen  Risk  Assessment.   Federal
Register.   51(185): 33992-34003.
0071d                               -34-                             11/17/87

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U.S.  EPA.   1987a.   Graphical   Exposure   Modeling   System   (GEMS).   CLOGP
computer program.   Office of Toxic Substances,  U.S.  EPA,  Washington, DC.

U.S. EPA.  19875.   Graphical  Exposure  Modeling System  (GEMS).  Fate of Atmo-
spheric Pollutants (FAP).   Office of  Toxic  Substances, U.S.  EPA, Washington,
DC.

Zeller,  H.V.,  H.T. Hofmann,  A.M.  Thless  and  W.  Hey.   1969.   Toxlclty of
nUMles.  Zentralbl.  ArbeHsmed.  ArbeUsschutz.   19:  225-238.   (CUed 1n
NIOSH, 1978)
0071d                               -35-                             11/17/87

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                                  APPENDIX A

                              LITERATURE  SEARCHED



    This  HEED  1s  based  on  data  Identified  by  computerized  literature

searches of the following:
         TSCATS
         CASR online (U.S. EPA Chemical Activities Status Report)
         TOXLINE
         TOXBACK 76
         TOXBACK 65
         RTECS
         OHM TADS
         STORET
         SRC Environmental Fate Data Bases
         SANSS
         AQUIRE
         TSCAPP
         NTIS
         Federal Register
These searches were conducted  In  February,  1987.   In  addition,  hand searches

were made of  Chemical  Abstracts  (Collective Indices J5-9),  and  the following

secondary sources should be reviewed:


    ACGIH (American  Conference of Governmental  Industrial  Hyglenlsts).
    1986.  Documentation  of the  Threshold  L1mVt Values  and  Biological
    Exposure Indices, 5th ed.  Cincinnati, OH.

    ACGIH (American  Conference of Governmental  Industrial  Hyglenlsts).
    1986-1987.  TLVs: Threshold Limit  Values for  Chemical Substances In
    the  Work  Environment  adopted by  ACGIH with  Intended Changes  for
    1986-1987.  Cincinnati, OH.  Ill  p.

    Clayton,  G.D.  and  F.E.  Clayton,  Ed.   1981.   Patty's  Industrial
    Hygiene and  Toxicology,  3rd  rev.  ed., Vol.  2A.   John  Wiley  and
    Sons, NY.   2878 p.

    Clayton,  G.D.  and  F.E.  Clayton,  Ed.   1981.   Patty's  Industrial
    Hygiene and  Toxicology,  3rd  rev.  ed., Vol.  28.   John  Wiley  and
    Sons, NY.   p. 2879-3816.

    Clayton,  G.D.  and  F.E.  Clayton,  Ed.   1982.   Patty's  Industrial
    Hygiene and  Toxicology,  3rd  rev.  ed., Vol.  2C.   John  Wiley  and
    Sons, NY.   p. 3817-5112.
007 Id
-36-
09/14/87

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    Grayson,  H. and  D.  Eckroth,  Ed.   1978-1984.  Klrk-Othmer  Encyclo-
    pedia of  Chemical Technology, 3rd ed.  John WHey and Sons,  NY.   23
    Volumes.             ^

    Hamilton,  A. and H.L.'.  Hardy.  1974.  Industrial Toxicology,  3rd  ed.
    Publishing Sciences  Group,  Inc.,  Littleton,  MA.  575  p.

    IARC  (International  Agency  for  Research  on Cancer).   IARC  Mono-
    graphs on   the  Evaluation  of Carcinogenic Risk  of  Chemicals   to
    Humans.   WHO,  IARC,  Lyons,  France.

    Jaber, H.M.,  W.R.  Mabey,  A.T.  Lieu,  T.W.  Chou and H.L.  Johnson.
    1984.   Data  acquisition  for  environmental  transport  and  fate
    screening for compounds  of Interest to the Office  of Solid Waste.
    SRI  International,   Menlo   Park,   CA.   EPA  600/6-84-010.   NTIS
    PB84-243906.

    NTP  (National Toxicology  Program).   1986.   Toxicology Research  and
    Testing   Program.   Chemicals  on   Standard Protocol.    Management
    Status.

    Ouellette,   R.P.  and  J.A.  King.   1977.    Chemical  Week Pesticide
    Register.   McGraw-Hill  Book Co.,  NY.

    Sax, I.N.  1984.  Dangerous  Properties of Industrial  Materials,  6th
    ed.  Van  Nostrand Relnhold Co., NY.

    SRI  (Stanford  Research  Institute).   1986.   Directory  of  Chemical
    Producers.   Menlo Park,  CA.

    U.S. EPA.   1986.   Report  on Status Report 1n the  Special Review
    Program,   Registration   Standards   Program   and  the   Data  Call   In
    Programs.    Registration  Standards  and  the  Data Call  1n Programs.
    Office of Pesticide  Programs, Washington, DC.

    U.S. EPA.  1985.  CSB Existing Chemical Assessment Tracking System.
    Name and  CAS  Number Ordered  Indexes.   Office  of  Toxic  Substances,
    Washington.  DC.

    USITC  (U.S.  International  Trade   Commission).   1985.   Synthetic
    Organic  Chemicals.  U.S.   Production and  Sales, 1984,  USITC  Publ.
    1422, Washington.  DC.

    Verschueren, K.   1983.   Handbook of Environmental  Data  on  Organic
    Chemicals,  2nd ed.   Van Nostrand  Relnhold Co.,  NY.

    Wlndholz,  M.,  Ed.  1983.  The Merck  Index,  10th ed.   Merck  and Co.,
    Inc., Rahway,  NJ.

    Worthing,  C.R.  and  S.B. Walker, Ed.   1983.  The Pesticide  Manual.
    British  Crop Protection Council.  695 p.
0071d                               -37-                             09/14/87

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    In  addition,  approximately 30  compendia of  aquatic  toxiclty data  were

reviewed, Including the following:


    Battelle's  Columbus  Laboratories.   1971.   Water  Quality  Criteria
    Data  Book.   Volume  3.  Effects  of  Chemicals   on   Aquatic   Life.
    Selected  Data  from the Literature  through  1968.   Prepared for  the
    U.S. EPA under Contract No. 68-01-0007.   Washington,  DC.

    Oohnson,  W.H.  and  H.T. Flnley.   1980.   Handbook  of  Acute  Toxldty
    of  Chemicals  to   Fish and  Aquatic  Invertebrates.    Summaries   of
    Toxldty  Tests  Conducted  at  Columbia  National  Fisheries  Research
    Laboratory.   1965-1978.    U.S.  Dept.  Interior,  Fish  and  Wildlife
    Serv. Res. Publ. 137,  Washington, DC.

    HcKee, J.E. and H.W.  Wolf.  1963.  Water Quality Criteria, 2nd  ed.
    Prepared  for  the   Resources   Agency  of  California,  State   Water
    Quality Control Board.   Publ.  No. 3-A.

    Plmental, D.  1971.  Ecological  Effects  of  Pesticides  on  Non-Target
    Species.  Prepared  for the U.S.  EPA, Washington, DC.   PB-269605.

    Schneider, B.A.  1979.  Toxicology  Handbook.  Mammalian and Aquatic
    Data.  Book 1: Toxicology  Data.   Office  of  Pesticide  Programs, U.S.
    EPA, Washington, DC.   EPA 540/9-79-003.   NTIS PB 80-196876.
0071d                               -38-                             09/14/87

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o
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                                                 APPENDIX B
                                       Summary Table for Adlponltrlle
                            Species
                                         Exposure
                                  Effect
RfD or qj*
Reference
I
01
Inhalation Exposure
Subchrontc
Chronic
Carclnogentclty

Oral Exposure
Subchronlc
ID
ID
ID


ID
   Chronic
                           ID
   Carctnogenlclty
                           ID
   REPORTABLE  QUANTITIES
   Based on  Chronic  Toxlctty:

   Based on  Carclnogenlclty:
                                      ID

                                      ID
oo
   ID =  Insufficient  Data

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